sileod/deberta-v3-small-tasksource-nli
Zero-Shot Classification
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Open-angle glaucoma<unk> eye drops, marketed by Pfizer<unk> in Japanese-language packaging In people with ocular hypertension (intraocular pressure (IOP) ≥21 mm Hg) including open-angle glaucoma, treatment with<unk> reduced IOP levels by 22 to 39% over 1 to 12 months’ treatment.<unk> was more effective than timolol 0.5% twice daily in 3 of 4 large (n = 163 to 267) randomised, double-blind trials.<unk> demonstrated a stable long-term IOP-lowering effect in 1- or 2-year continuations of these trials, with no sign of diminishing effect during prolonged treatment. Meta-analysis suggests that<unk> is more effective than timolol in lowering intraocular pressure (IOP). However, it often causes iris pigmentation. While current evidence suggests that this pigmentation is benign, careful lifetime evaluation of patients is still justified. Closed-angle glaucoma Patients who had elevated IOP despite iridotomy and/or iridectomy (including patients of Asian descent),<unk> was significantly more effective than timolol in two double-blind, monotherapy trials (8.2 and 8.8 mm Hg vs 5.2 and 5.7 mm Hg for<unk> vs timolol at 12 and 2 weeks, respectively). | Latanoprost | Travoprost | Carboprost | Iloprost | Bimatoprost | Travoprost/timolol | Bimatoprost/timolol | Bifluranol | 00
| 27,512 |
The syndrome has been hypothesized to be a variant of alopecia areata diffusa or autoimmune non-scarring hair loss that selectively affects all pigmented hairs, leaving only the white hair behind. Marie Antoinette syndrome is caused by high levels of emotional stress, which, in turn, causes less pigmentation of the hair. These form the basis of most uses of the idea in fictional works. It has been found that some hairs can become colored again when stress is reduced. One study with experiments on mice found that stress caused white hair even if the immune system was suppressed (ruling out auto-immune response) and if the glands producing cortisol were removed. The study concluded that over-activation of the sympathetic nervous system was causing stem cells to stop producing pigment cells in hair follicles. | Canities subita | The Fountain of Age | Blind man of Bethsaida | MedCity | Black Death migration | Juven | Plague doctor costume | Biovail | 00
| 56,471 |
Sensorineural hearing loss may be genetic or acquired (i.e. as a consequence of disease, noise, trauma, etc.). People may have a hearing loss from birth (congenital) or the hearing loss may come on later. Many cases are related to old age (age-related). Genetic Hearing loss can be inherited. More than 40 genes have been implicated in the cause of deafness. There are 300 syndromes with related hearing loss, and each syndrome may have causative genes. Recessive, dominant, X-linked, or mitochondrial genetic mutations can affect the structure or metabolism of the inner ear. Some may be single point mutations, whereas others are due to chromosomal abnormalities. Some genetic causes give rise to a late onset hearing loss. Mitochondrial mutations can cause SNHL i.e. m.1555A>G, which makes the individual sensitive to the ototoxic effects of aminoglycoside antibiotics. * The most common cause of recessive genetic congenital hearing impairment in developed countries is DFNB1, also known as Connexin 26 deafness or GJB2-related deafness. * The most common syndromic forms of hearing impairment include (dominant) Stickler syndrome and Waardenburg syndrome, and (recessive) Pendred syndrome and Usher syndrome. * Mitochondrial mutations causing deafness are rare: MT-TL1 mutations cause MIDD (Maternally inherited deafness and diabetes) and other conditions which may include deafness as part of the picture. * TMPRSS3 gene was identified by its association with both congenital and childhood onset autosomal recessive deafness. This gene is expressed in fetal cochleae and many other tissues, and is thought to be involved in the development and maintenance of the inner ear or the contents of the perilymph and endolymph. It was also identified as a tumor associated gene that is overexpressed in ovarian tumors. * Charcot–Marie–Tooth disease an inherited neurological disorder with delayed onset that can affect the ears as well as other organs. The hearing loss in this condition is often ANSD (auditory neuropathy spectrum disorder) a neural cause of hearing loss. * Muckle–Wells syndrome, a rare inherited autoinflammatory disorder, can lead to hearing loss. * Autoimmune disease: although probably rare, it is possible for autoimmune processes to target the cochlea specifically, without symptoms affecting other organs. Granulomatosis with polyangiitis, an autoimmune condition, may precipitate hearing loss. Congenital * Infections: *Congenital rubella syndrome, CRS, results from transplacental transmission of the rubella virus during pregnancy. CRS has been controlled by universal vaccination (MMR or MMRV vaccine). *Cytomegalovirus (CMV) infection is the most common cause of progressive sensorineural hearing loss in children. It is a common viral infection contracted by contact with infected bodily fluids such as saliva or urine and easily transmitted in nurseries and thus from toddlers to expectant mothers. CMV infection during pregnancy can affect the developing foetus and lead to learning difficulties as well as hearing loss. *Toxoplasmosis, a parasitic disease affecting 23% of the population in the U.S., can cause sensorineural deafness to the fetus in utero. * Hypoplastic auditory nerves or abnormalities of the cochlea. Abnormal development of the inner ear can occur in some genetic syndromes such as LAMM syndrome (labyrinthine aplasia, microtia and microdontia), Pendred syndrome, branchio-oto-renal syndrome, CHARGE syndrome * GATA2 deficiency, a grouping of several disorders caused by common defect, viz., familial or sporadic inactivating mutations in one of the two parental GATA2 genes. These autosomal dominant mutations cause a reduction, i.e. a haploinsufficiency, in the cellular levels of the gene's product, GATA2. The GATA2 protein is a transcription factor critical for the embryonic development, maintenance, and functionality of blood-forming, lympathic-forming, and other tissue-forming stem cells. In consequence of these mutations, cellular levels of GATA2 are deficient and individuals develop over time hematological, immunological, lymphatic, and/or other disorders. GATA2 deficiency-induced abnormalities in the lymphatic system are proposed to be responsible for a failure in generating the perilymphatic space around the inner ear's semicircular canals, which in turn underlies the development of sensorineural hearing loss. Presbycusis Progressive age-related loss of hearing acuity or sensitivity can start as early as age 18, primarily affecting the high frequencies, and men more than women. Such losses may not become apparent until much later in life. Presbycusis is by far the dominant cause of sensorineural hearing loss in industrialized societies. A study conducted in Sudan, with a population free from loud noise exposures, found significantly less cases of hearing loss when compared with age-matched cases from an industrialized country. Similar findings were reported by a study conducted of a population from Easter island, which reported worse hearing among those that spent time in industrialized countries when compared with those that never left the island. Researchers have argued that factors other than differences in noise exposure, such as genetic make up, might also have contributed to the findings. Hearing loss that worsens with age but is caused by factors other than normal aging, such as noise-induced hearing loss, is not presbycusis, although differentiating the individual effects of multiple causes of hearing loss can be difficult. One in three persons have significant hearing loss by age 65; by age 75, one in two. Age-related hearing loss is neither preventable nor reversible. Noise Most people living in modern society suffer from some degree of progressive sensorineural (i.e. permanent) noise-induced hearing loss (NIHL) resulting from overloading and damaging the sensory or neural apparatus of hearing in the inner ear. NIHL is typically a drop-out or notch centered at 4000 Hz. Both intensity (SPL) and duration of exposure, and repetitive exposure to unsafe levels of noise contribute to cochlear damage that results in hearing loss. The louder the noise is, the shorter the safe amount of exposure is. NIHL can be either permanent or temporary, called a threshold shift. Unsafe levels of noise can be as little as 70 dB (about twice as loud as normal conversation) if there is prolonged (24-hour) or continuous exposure. 125 dB (a loud rock concert is ~120 dB) is the pain level; sounds above this level cause instant and permanent ear damage. Noise and ageing are the primary causes of presbycusis, or age-related hearing loss, the most common kind of hearing loss in industrial society. The<unk> rs of environmental and occupational noise exposure are widely recognized. Numerous national and international organizations have established standards for safe levels of exposure to noise in industry, the environment, military, transportation, agriculture, mining and other areas. Sound intensity or sound pressure level (SPL) is measured in decibels (dB). For reference: + db Level Example 45 dB Ambient noise level around the home 60 dB Quiet office 60–65 dB Normal conversation 70 dB City street noise at 25' or average TV audio 80 dB Noisy office 95–104 dB Nightclub dance floor 120 dB Close-by thunder or a loud rock concert 150–160 dB Gunshot from a handheld gun An increase of 6 dB represents a doubling of the SPL, or energy of the sound wave, and therefore its propensity to cause ear damage. Because human ears hear logarithmically, not linearly, it takes an increase of 10 dB to produce a sound that is perceived to be twice as loud. Ear damage due to noise is proportional to sound intensity, not perceived loudness, so it's misleading to rely on subjective perception of loudness as an indication of the risk to hearing, i.e. it can significantly underestimate the<unk> r. While the standards differ moderately in levels of intensity and duration of exposure considered safe, some guidelines can be derived. The safe amount of exposure is reduced by a factor of 2 for every exchange rate (3 dB for NIOSH standard or 5 dB for OSHA standard) increase in SPL. For example, the safe daily exposure amount at 85 dB (90 dB for OSHA) is 8 hours, while the safe exposure at 94 dB(A) (nightclub level) is only 1 hour. Noise trauma can also cause a reversible hearing loss, called a temporary threshold shift. This typically occurs in individuals who are exposed to gunfire or firecrackers, and hear ringing in their ears after the event (tinnitus). * Ambient environmental noise: Populations living near airports, railyards and train stations, freeways and industrial areas are exposed to levels of noise typically in the 65 to 75 dBA<unk> . If lifestyles include significant outdoor or open window conditions, these exposures over time can degrade hearing. U.S. Dept. of Housing and Urban Development sets standards for noise impact in residential and commercial construction zones. HUD’s noise standards may be found in 24 CFR Part 51, Subpart B. Environmental noise above 65 dB defines a noise-impacted area. * Personal audio electronics: Personal audio equipment such as iPods (iPods often reach 115 decibels or higher), can produce powerful enough sound to cause significant NIHL. * Acoustic trauma: Exposure to a single event of extremely loud noise (such as explosions) can also cause temporary or permanent hearing loss. A typical source of acoustic trauma is a too-loud music concert. * Workplace noise: The OSHA standards 1910.95 General Industry Occupational Noise Exposure and 1926.52 Construction Industry Occupational Noise Exposure identify the level of 90 dB(A) for 8 hour exposure as the level necessary to protect workers from hearing loss. | symptoms of Jervell and Lange-Nielsen syndrome | symptom of Jervell and Lange-Nielsen syndrome | symptom of Andersen–Tawil syndrome | symptom of Klippel–Feil syndrome | symptom of Maroteaux–Lamy syndrome | symptoms of Rotor syndrome | symptom of Prader–Willi syndrome | symptom of Laron syndrome | 00
| 21,372 |
The World Health Organization classification of testicular tumours subdivides ITGCN into (1) a more common, unspecified type (ITGCNU), and (2) other specific subtypes. The most common specific subtypes are intratubular embryonal carcinoma and intratubular seminoma. | Germ cell neoplasia in situ | In situ lymphoid neoplasia | Surface epithelial-stromal tumor | Sclerosing polycystic adenosis | Keratin implantation cyst | Microcystic adnexal carcinoma | Ductal carcinoma in situ | Intraepithelial neoplasia | 00
| 51,740 |
There are three antiepileptic drugs that have been used for the first-line treatment of<unk> ; these are ethosuximide (ETX), valproic acid (VPA), and lamotrigine (LTG). ETX is an effective first-line treatment for the<unk> seizures only by blocking the low-threshold calcium currents produced by T-type calcium channels in the thalamus. The peak level occurs after 3-5 hours of intake; steady levels of the drug in the blood are achieved after 7-10 days of the same daily dose. The usual dosage is 20-30 mg/kg/day divided into two doses. Common side effects include gastrointestinal disturbances such as hiccups, vomiting, abdominal discomfort, diarrhea, and exceptionally other symptoms like fatigue, insomnia, dizziness, or ataxia. Valproate (VPA) has also been proven effective as a monotherapy in<unk> although ETX is usually preferred as it has a lower impact on attention according to the<unk> Epilepsy study. There are several mechanisms related to VPA’s antiepileptic action, including raising the level of gamma-aminobutyric acid (GABA), calcium-dependent potassium activating and blocking of voltage-sensitive sodium channels, but there is no specific evidence for the mechanism by which VPA controls the<unk> seizures. VPA has a wide range of side effects (high-frequency tremor, altered mental status, increased appetite and weight gain, pancreatitis, hepatic failure, thrombocytopenia, teratogenesis during pregnancy) although serious side effects are rare and usually dose-dependent. Usual maintenance dose in children is 20–30 mg/kg/day. Lamotrigine (LTG) could be used as alternative/ add-on treatment for<unk> along with VPA and ETX. Other possible treatments in the rare cases of pharmacoresistant include levetiracetam, clobazam, topiramate, zonisamide. | Childhood absence epilepsy | Benign infantile epilepsy | Benign familial infantile epilepsy | Benign familial neonatal seizures | Northern epilepsy syndrome | Musicogenic epilepsy | Juvenile myoclonic epilepsy | Temporal lobe epilepsy | 00
| 40,660 |
Prevention of atrial fibrillation focuses primarily on preventing or controlling its risk factors. Many of its risk factors, such as obesity, smoking, lack of physical activity, and excessive alcohol consumption, are modifiable and preventable with lifestyle modification or can be managed by a healthcare professional. Lifestyle modification Several healthy lifestyle behaviors are associated with a lower likelihood of developing atrial fibrillation. Accordingly, consensus guidelines recommend abstaining from alcohol and recreational drugs, stopping tobacco use, maintaining a healthy weight, and regularly participating in moderate-intensity physical activities. Consistent moderate-intensity aerobic exercise, defined as achieving 3.0-5.9 METs of intensity, for at least 150 minutes per week may reduce the risk of developing new-onset atrial fibrillation. Few studies have examined the role of specific dietary changes and how it relates to the prevention of atrial fibrillation. | complications of Rheumatic fever | medical cause of Rheumatic fever | complications of Diphtheria | complications of Behçet's disease | complications of West Nile fever | complications of Stevens–Johnson syndrome | picture of Rheumatic fever | medical cause of Stevens–Johnson syndrome | 00
| 53,339 |
Inheritance Pattern The disease<unk> is inherited in an autosomal recessive manner. Individuals with this disease exhibit a mutation or pathogenic effect in both copies of the TFR2 in each cell. People with only one copy of TFR2 that is affected are labeled as carriers. Carriers typically do not exhibit signs or symptoms of the disease. This disease is shown to have reduced penetrance. Thus, some people with pathogenic variants of the TFR2 gene may never present symptoms related to the disease. Gene Involved The gene involved with patients diagnosed with type 3 hemochromatosis is TFR2 ( or HFE3). HFE is most often the cause of hereditary hemochromatosis. The HFE gene provides instructions for producing a protein that is located on the surface of cells, primarily liver and intestinal cells. The HFE protein is also found on some immune system cells. The HFE protein interacts with other proteins on the cell surface to detect the amount of iron in the body. When the HFE protein is attached to a protein called transferrin receptor 1, the receptor cannot bind to a protein called transferrin. When transferrin receptor 1 is bound to transferrin, iron enters liver cells. So, it is likely that the HFE protein regulates iron levels in liver cells by preventing transferrin from binding to transferrin receptor 1. The HFE protein regulates the production of a protein called hepcidin. Hepcidin is produced by the liver, and it determines how much iron is absorbed from the diet and released from storage sites in the body. When the HFE protein is not bound to transferrin receptor 1, it binds to a group of other proteins that includes hepcidin. The formation of this protein complex triggers the production of hepcidin. So when the HFE protein is bound to transferring receptor 1, hepcidin production is turned off and when the HFE protein is not bound to transferring receptor 1, hepcidin production is turned on. The transferrin receptor 2 (TFR2) gene is responsible for encoding a single-pass type II membrane protein. This protein mediates cellular uptake of transferrin-bound iron, and may be involved in iron metabolism, hepatocyte function and erythrocyte differentiation. Type of Mutations Majority of the cases of hemochromatosis are caused by mutations in the HFE gene. More specifically, Type 3 HH is characterized by mutations in transferrin receptor 2. HH type 3 is linked to mutations in a gene on chromosome 7q22, encoding TFR2. A deletion in the DNA sequence at this location is associated with causing type 3 hemochromatosis. Location of the Chromosome The heterozygous mutation in the transferrin receptor-2 gene (TFR2) and the mutation in the<unk> gene (HFE3) are the causes of<unk> . These mutations are found on chromosome 7q22. The location of the genes affected are at 7:100,620,419 on the DNA chromosome. Effects on Gene Products The gene product is a member of the major histocompatibility complex class I-like family and holds a mutation, Cys-292 to Tyr (C282Y), in 85% of patient chromosomes. The mutation eliminates the ability of HFE to prevent cell-surface expression. There are also other mutations that prevent association of the mutant HFE protein with transferrin receptor. Spectrum of Disease Severity The disease can manifest itself without showing any symptoms, but these symptoms can emerge over time and the disease can therefore become more severe. Symptoms that emerge early on in the disease are generally less severe, and may include conditions such as fatigue, weakness, skin discoloration, loss of sex drive and joint pain. Late in the disease, people may experience liver disease as well as disease to other major organs as excess iron is deposited over time. People can also develop diabetes, heart problems, and abdominal pain. | Haemochromatosis type 3 | Hereditary haemochromatosis | Hemochromatosis type 4 | Juvenile hemochromatosis | Niemann–Pick disease, type C | Wilson's disease | Wilson–Mikity syndrome | Type 3c diabetes | 00
| 54,578 |
The best-validated treatment for OCPD is cognitive therapy (CT) or cognitive behavioral therapy (CBT), with studies showing an improvement in areas of personality impairment, and reduced levels of anxiety and depression. Group CBT is also associated with an increase in extraversion and agreeableness and reduced neuroticism. Interpersonal psychotherapy has been linked to even better results when it came to reducing depressive symptoms. | Obsessive–compulsive personality disorder | Substance use disorder | Haltlose personality disorder | Personality disorder | Emotional spectrum disorder | Obsessive–compulsive disorder | Self-defeating personality disorder | Immature personality disorder | 00
| 10,193 |
The<unk> is a recently described disease manifestation in females that includes multiple paragangliomas or pheochromocytomas and somatostatinomas (in some), both neuroendocrine tumors, and secondary polycythemia associated with high erythropoietin levels. Paragangliomas in these patients are mainly localized to the abdomen whereas somatostatinomas are found in the second portion of the duodenum, as shown by imaging or biochemistry. This syndrome is of special interest as finding more than one type of neuroendocrine tumor in one individual is unusual. Such co-occurrences are usually seen in patients carrying hereditary syndromes like multiple endocrine neoplasia (MEN), neurofibromatosis 1 (NF1), or von Hippel-Lindau (VHL) disease. | Pacak–Zhuang syndrome | Brugada syndrome | Lown–Ganong–Levine syndrome | Bhaskar–Jagannathan syndrome | Burnside–Butler syndrome | Raine syndrome | Bowen–Conradi syndrome | Woodhouse–Sakati syndrome | 00
| 66,260 |
The<unk> forbids all nightshade vegetables such as eggplants, red peppers and tomatoes The<unk> (also known as the Plant Paradox diet) is a fad diet which claims that avoiding all foods that contain high amounts of<unk> s will prevent or reverse arthritis, cancer, cardiovascular disease, inflammation and autoimmune diseases. There is no clinical evidence that a<unk> is effective to treat any disease and its claims have been criticized as pseudoscientific. | Lectin-free diet | Macrobiotic diet | Low-fiber/low-residue diet | Gluten-free diet | Gluten-free, casein-free diet | Elimination diet | Feingold diet | Liquid diet | 00
| 74,723 |
<unk> containing propane, butane, and ethanol, for dental applications<unk> (cold<unk> or vapocoolant) is a type of aerosol<unk> product containing a liquified gas used for rapidly cooling surfaces, in medical and industrial applications. It is usually sold in hand-held<unk> cans. It may consist of various substances, which produce different temperatures, depending on the application. Some of them are highly flammable. Several other types of compressed gas<unk> s also have a<unk> ng effect: for example, tetrafluoroethane, Gas dusters, liquid nitrogen, and carbon dioxide fire extinguishers. | Freeze spray | Hug machine | Sterile insect technique | Florida shuffle | Throat lozenge | Depot injection | Kambo cleanse | Caphosol | 00
| 68,307 |
The pathophysiology of<unk> is still not well understood, despite extensive research. Animal models The lack of animal models that are relevant to<unk> has left many key questions in<unk> pathophysiology unanswered. Earliest rodent models of<unk> used atropine (a muscarinic acetylcholine receptor blocker) to induce cognitive and electroencephalography (EEG) changes similar to<unk> , and other anticholinergic drugs, such as biperiden and hyoscine, have produced similar effects. Along with clinical studies using various drugs with anticholinergic activity, these models have contributed to a "cholinergic deficiency hypothesis" of<unk> . Profound systemic inflammation occurring during sepsis is also known to cause<unk> (often termed sepsis-associated encephalopathy). Animal models used to study the interactions between prior degenerative disease and overlying systemic inflammation have shown that even mild systemic inflammation causes acute and transient deficits in working memory among diseased animals. Prior dementia or age-associated cognitive impairment is the primary predisposing factor for clinical<unk> and "prior pathology" as defined by these new animal models may consist of synaptic loss, abnormal network connectivity, and "primed microglia" brain macrophages stimulated by prior neurodegenerative disease and aging to amplify subsequent inflammatory responses in the central nervous system (CNS). Cerebrospinal fluid Studies of cerebrospinal fluid (CSF) in<unk> are difficult to perform. Apart from the general difficulty of recruiting participants who are often unable to give consent, the inherently invasive nature of CSF sampling makes such research particularly challenging. However, a few studies have exploited the opportunity to sample CSF from persons undergoing spinal anesthesia for elective or emergency surgery. A 2018 systematic review showed that, broadly,<unk> may be associated with neurotransmitter imbalance (namely serotonin and dopamine signaling), reversible fall in somatostatin, and increased cortisol. The leading "neuroinflammatory hypothesis" (where neurodegenerative disease and aging leads the brain to respond to peripheral inflammation with an exaggerated CNS inflammatory response) has been described, but current evidence is still conflicting and fails to concretely support this hypothesis. Neuroimaging Neuroimaging provides an important avenue to explore the mechanisms that are responsible for<unk> . Despite progress in the development of magnetic resonance imaging (MRI), the large variety in imaging-based findings has limited our understanding of the changes in the brain that may be linked to<unk> . Some challenges associated with imaging people diagnosed with<unk> include participant recruitment and inadequate consideration of important confounding factors such as history of dementia and/or depression, which are known to be associated with overlapping changes in the brain also observed on MRI. Evidence for changes in structural and functional markers include: changes in white-matter integrity (white matter lesions), decreases in brain volume (likely as a result of tissue atrophy), abnormal functional connectivity of brain regions responsible for normal processing of executive function, sensory processing, attention, emotional regulation, memory, and orientation, differences in autoregulation of the vascular vessels in the brain, reduction in cerebral blood flow and possible changes in brain metabolism (including cerebral tissue oxygenation and glucose hypometabolism). Altogether, these changes in MRI-based measurements invite further investigation of the mechanisms that may underlie<unk> , as a potential avenue to improve clinical management of people suffering with this condition. Neurophysiology Electroencephalography (EEG) allows for continuous capture of global brain function and brain connectivity, and is useful in understanding real-time physiologic changes during<unk> . Since the 1950s,<unk> has been known to be associated with slowing of resting-state EEG rhythms, with abnormally decreased background alpha power and increased theta and delta frequency activity. From such evidence, a 2018 systematic review proposed a conceptual model that<unk> results when insults/stressors trigger a breakdown of brain network dynamics in individuals with low brain resilience (i.e. people who already have underlying problems of low neural connectivity and/or low neuroplasticity like those with Alzheimer's disease). Neuropathology Only a handful of studies exist where there has been an attempt to correlate<unk> with pathological findings at autopsy. One research study has been reported on 7 patients who died during ICU admission. Each case was admitted with a range of primary pathologies, but all had acute respiratory distress syndrome and/or septic shock contributing to the<unk> , 6 showed evidence of low brain perfusion and diffuse vascular injury, and 5 showed hippocampal involvement. A case-control study showed that 9<unk> cases showed higher expression of HLA-DR and CD68 (markers of microglial activation), IL-6 (cytokines pro-inflammatory and anti-inflammatory activities) and GFAP (marker of astrocyte activity) than age-matched controls; this supports a neuroinflammatory cause to<unk> , but the conclusions are limited by methodological issues. A 2017 retrospective study correlating autopsy data with MMSE scores from 987 brain donors found that<unk> combined with a pathological process of dementia accelerated MMSE score decline more than either individual process. | symptom of Delirium tremens | symptom of Narcolepsy | symptom of Conversion disorder | medical cause of Panic attack | symptoms of Delirium | symptom of Botulism | symptom of Panic attack | symptom of Akathisia | 00
| 6,606 |
<unk> , also called<unk> albinism-deafness syndrome or albinism and deafness of<unk> , is an autosomal dominant congenital disorder characterized by deafness and leucism. It is caused by a mutation in the microphthalmia-associated transcription factor (MITF) gene.<unk> was first described in 1963 by Walter<unk> (1927–2003) a German Physician working in California. | Tietz syndrome | Laurence–Moon syndrome | Landau–Kleffner syndrome | Kapur–Toriello syndrome | Smith–Magenis syndrome | Langer–Giedion syndrome | Aagenaes syndrome | Pelger–Huët anomaly | 00
| 10,766 |
Globally, acne affects approximately 650 million people, or about 9.4% of the population, as of 2010. It affects nearly 90% of people in Western societies during their teenage years, but can occur before adolescence and may persist into adulthood. While acne that first develops between the ages of 21 and 25 is uncommon, it affects 54% of women and 40% of men older than 25 years of age and has a lifetime prevalence of 85%. About 20% of those affected have moderate or severe cases. It is slightly more common in females than males (9.8% versus 9.0%). In those over 40 years old, 1% of males and 5% of females still have problems. Rates appear to be lower in rural societies. While some research has found it affects people of all ethnic groups, acne may not occur in the non-Westernized peoples of Papua New Guinea and Paraguay. Acne affects 40–50 million people in the United States (16%) and approximately 3–5 million in Australia (23%). Severe acne tends to be more common in people of Caucasian or Amerindian descent than in people of African descent. | symptom of XYY syndrome | symptom of Klinefelter syndrome | symptom of Kallmann syndrome | symptom of Prader–Willi syndrome | symptom of Laron syndrome | medical cause of Precocious puberty | symptom of Scheuermann's disease | symptom of Angelman syndrome | 00
| 5,157 |
The clinical diagnosis of<unk> is based on a history of LUTS (lower urinary tract symptoms), a digital rectal exam, and exclusion of other causes of similar signs and symptoms. The degree of LUTS does not necessarily correspond to the size of the prostate. An enlarged prostate gland on rectal examination that is symmetric and smooth supports a diagnosis of<unk> . However, if the prostate gland feels asymmetrical, firm, or nodular, this raises concern for prostate cancer. Validated questionnaires such as the American Urological Association Symptom Index (AUA-SI), the International Prostate Symptom Score (I-PSS), and more recently the UWIN score (urgency, weak stream, incomplete emptying, and nocturia) are useful aids to making the diagnosis of<unk> and quantifying the severity of symptoms. Laboratory investigations Urinalysis is typically performed when LUTS are present and<unk> is suspected to evaluate for signs of a urinary tract infection, glucose in the urine (suggestive of diabetes), or protein in the urine (suggestive of kidney disease). Bloodwork including kidney function tests and prostate specific antigen (PSA) are often ordered to evaluate for kidney damage and prostate cancer, respectively. However, checking blood PSA levels for prostate cancer screening is controversial and not necessarily indicated in every evaluation for<unk> .<unk> and prostate cancer are both capable of increasing blood PSA levels and PSA elevation is unable to differentiate these two conditions well. If PSA levels are checked and are high, then further investigation is warranted. Measures including PSA density, free PSA, rectal examination, and transrectal ultrasonography may be helpful in determining whether a PSA increase is due to<unk> or prostate cancer. Imaging and other investigations Uroflowmetry is done to measure the rate of urine flow and total volume of urine voided when the subject is peeing. Abdominal ultrasound examination of the prostate and kidneys is often performed to rule out hydronephrosis and hydroureter. Incidentally, cysts, tumours, and stones may be found on ultrasound. Post-void residual volume of more than 100 ml may indicate significant obstruction. Prostate size of 30 cc or more indictes enlargement of the prostate. On transrectal ultrasound (TRUS),<unk> calcifications can be seen. Calcifications is due to solidification of<unk> secretions or calcified corpora amylacea (hyaline masses on prostate gland). Calcifications is also found in variety of other conditions such as<unk> is, chronic pelvic pain syndrome, and prostate cancer. For those with elevated levels of PSA, TRUS guided biopsy is performed to take a sample of the prostate for investigation. Although MRI is more accurate than TRUS in determining prostate volume, TRUS is less expensive and almost as accurate as MRI. Therefore, TRUS is still preferred to measure prostate volume. Differential diagnosis Medical conditions The differential diagnosis for LUTS is broad and includes various medical conditions, neurologic disorders, and other diseases of the bladder, urethra, and prostate such as bladder cancer, urinary tract infection, urethral stricture, urethral calculi (stones), chronic<unk> is, and prostate cancer. Neurogenic bladder can cause urinary retention and cause symptoms similar to those of<unk> . This may occur as a result of uncoordinated contraction of the bladder muscle or impairment in the timing of bladder muscle contraction and urethral sphincter relaxation. Notable causes of neurogenic bladder include disorders of the central nervous system such as Parkinson's disease, multiple sclerosis, and spinal cord injuries as well as disorders of the peripheral nervous system such as diabetes mellitus, vitamin B12 deficiency, and alcohol-induced nerve damage. Individuals affected by heart failure often experience nighttime awakenings to urinate due to redistribution of fluid accumulated in swollen legs. Medications Certain medications can increase urination difficulties by increasing bladder outlet resistance due to increased smooth muscle tone at the prostate or bladder neck and contribute to LUTS. Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In contrast, calcium channel blockers and anticholinergic medications can worsen urinary retention by promoting bladder muscle relaxation. Diuretic medications such as loop diuretics (e.g., furosemide) or thiazides (e.g., chlorthalidone) can cause or worsen urinary frequency and nighttime awakenings to urinate. File:Nodular<unk> of the prostate.Micrograph showing nodular<unk> (left off center) of the prostate from a transurethral resection of the prostate (TURP). H&E stain. File:Prostate histology.Microscopic examination of different types of prostate tissues (stained with immunohistochemical techniques): A. Normal (non-neoplastic)<unk> tissue (NNT). B.<unk> . C. High-grade<unk> intraepithelial neoplasia. D.<unk> adenocarcinoma (PCA). | Benign prostatic hyperplasia | Prostate cancer | Chronic bacterial prostatitis | Heart failure | Acute prostatitis | Diabetes | Granulomatous prostatitis | Urinary bladder disease | 00
| 5,579 |
Suspicion of a chromosome abnormality is typically raised due to the presence of developmental delays or birth defects. Diagnosis of<unk> is usually made via a blood sample. A routine chromosome analysis, or karyotype, is usually used to make the initial diagnosis, although it may also be made by microarray analysis. Increasingly, microarray analysis is also being used to clarify breakpoints. Prenatal diagnosis is possible via amniocentesis of chorionic villus sampling. MRI In some children without "classic" holoprosencephaly, microforms of holoprosencephaly may be noted on MRI, including missing olfactory tracts and bulbs and absent or hypoplastic corpus callosum. | 18p- | RUB A535 | ZF2001 | 714-X | Rc-o319 | MIS416 | SOS box | T-47D | 00
| 51,240 |
Human exposure to aerosols has been documented to give rise to a variety of adverse health effects.<unk> occupants complain of symptoms such as sensory irritation of the eyes, nose, or throat; neurotoxic or general health problems; skin irritation; nonspecific hypersensitivity reactions; infectious diseases; and odor and taste sensations. Exposure to poor lighting conditions has led to general malaise. Extrinsic allergic alveolitis has been associated with the presence of fungi and bacteria in the moist air of residential houses and commercial offices. A study in 2017 correlated several inflammatory diseases of the respiration tract with objective evidence of damp-caused damage in homes. The WHO has classified the reported symptoms into broad categories, including: mucous membrane irritation (eye, nose, and throat irritation), neurotoxic effects (headaches, fatigue, and irritability), asthma and asthma-like symptoms (chest tightness and wheezing), skin dryness and irritation, gastrointestinal complaints and more. Several<unk> occupants may report individual symptoms which do not appear to be connected. The key to discovery is the increased incidence of illnesses in general with onset or exacerbation within a fairly close time frame – usually within a period of weeks. In most cases,<unk> symptoms will be relieved soon after the occupants leave the particular room or zone. However, there can be lingering effects of various neurotoxins, which may not clear up when the occupant leaves the<unk> . In some cases – particularly in sensitive individuals – there can be long-term health effects. | Sick building syndrome | FACES syndrome | Roemheld syndrome | Death-grip syndrome | Pfeiffer syndrome | MASA syndrome | Tension myositis syndrome | Raine syndrome | 00
| 11,967 |
<unk> solely measures hemoglobin saturation, not ventilation and is not a complete measure of respiratory sufficiency. It is not a substitute for blood gases checked in a laboratory, because it gives no indication of base deficit, carbon dioxide levels, blood pH, or bicarbonate (HCO3−) concentration. The metabolism of oxygen can be readily measured by monitoring expired CO2, but saturation figures give no information about blood oxygen content. Most of the oxygen in the blood is carried by hemoglobin; in severe anemia, the blood contains less hemoglobin, which despite being saturated cannot carry as much oxygen. Because<unk> imeter devices are calibrated in healthy subjects, the accuracy is<unk> or for critically ill patients and preterm newborns. Erroneously low readings may be caused by hypoperfusion of the extremity being used for monitoring (often due to a limb being cold, or from vasoconstriction secondary to the use of vasopressor agents); incorrect sensor application; highly calloused skin; or movement (such as shivering), especially during hypoperfusion. To ensure accuracy, the sensor should return a steady<unk> and/or<unk> waveform.<unk> technologies differ in their abilities to provide accurate data during conditions of motion and low perfusion. Obesity, hypotension (low blood pressure), and some hemoglobin variants can reduce the accuracy of the results. Some home<unk> imeters have low sampling rates which can significantly underestimate dips in blood oxygen levels. The accuracy of<unk> deteriorates considerably for readings below 80%.<unk> also is not a complete measure of circulatory oxygen sufficiency. If there is insufficient bloodflow or insufficient hemoglobin in the blood (anemia), tissues can suffer hypoxia despite high arterial oxygen saturation. Since<unk> measures only the percentage of bound hemoglobin, a falsely high or falsely low reading will occur when hemoglobin binds to something other than oxygen: * Hemoglobin has a higher affinity to carbon monoxide than it does to oxygen, and a high reading may occur despite the patient's actually being hypoxemic. In cases of carbon monoxide<unk> isoning, this inaccuracy may delay the recognition of hypoxia (low cellular oxygen level). * Cyanide<unk> isoning gives a high reading because it reduces oxygen extraction from arterial blood. In this case, the reading is not false, as arterial blood oxygen is indeed high in early cyanide<unk> isoning. * Methemoglobinemia characteristically causes<unk> readings in the mid-80s. * COPD especially chronic bronchitis may cause false readings. A noninvasive method that allows continuous measurement of the dyshemoglobins is the<unk> CO-oximeter, which was built in 2005 by Masimo. By using additional wavelengths, it provides clinicians a way to measure the dyshemoglobins, carboxyhemoglobin, and methemoglobin along with total hemoglobin. Research has suggested that error rates in common<unk> imeter devices may be higher for adults with dark skin color, leading to claims of encoding systemic racism in countries with multi-racial<unk> pulations such as the United States.<unk> is used for the screening of sleep apnea and other types of sleep-disordered breathing which in the United States are conditions more prevalent among minorities. Equipment In addition to<unk> imeters for professional use, many inexpensive "consumer" models are available. Opinions vary about the reliability of consumer oximeters; a typical comment is "The research data on home monitors has been mixed, but they tend to be accurate within a few percentage<unk> ints". Some smart watches with activity tracking incorporate an oximeter function. An article on such devices, in the context of diagnosing COVID-19 infection, quoted João Paulo Cunha of the University of<unk> rto,<unk> rtugal: "these sensors are not precise, that's the main limitation ... the ones that you wear are only for the consumer level, not for the clinical level".<unk> imeters used for diagnosis of conditions such as COVID-19 should be Class IIB medical grade oximeters. Class IIB oximeters can be used on patients of all skin colors, low pigmentation and in the presence of motion. When a<unk> imeter is shared between two patients, it should be either cleaned with alcohol wipes after each use or a disposable probe or finger cover to be used to prevent cross-infection. According to a report by iData Research the US<unk> monitoring market for equipment and sensors was over $700 million in 2011. Mobile apps Mobile app<unk> imeters use the flashlight and the camera of the phone, instead of infrared light used in conventional<unk> imeters. However, apps don't generate as accurate readings because the camera can't measure the light reflection at two wavelengths, so the oxygen saturation readings that are obtained through an app on a smartphone are inconsistent for clinical use. At least one study has suggested these are not reliable relative to clinical<unk> imeters. | Pulse oximetry | Plethysmograph | Oxygenation index | Hyperoxia test | Oxygen saturation | Oxygen saturation | Fraction of inspired oxygen | Respiratory pressure meter | 00
| 17,457 |
People with the<unk> type of CP typically have muscles that are "tight" or stiff due to high muscle tone. Symptoms of<unk> vary as the disability can affect individuals differently. However, they typically appear in infancy and early childhood and most children are diagnosed in the first two years of life. The main indicator of<unk> is a delay in reaching motor milestones. The following are some common early signs, though the presence of a listed symptom does not definitively mean that a child has<unk> CP: Prior to 6 months * Legs crossing when a child is picked up, also called scissoring * Stiffness * Head "lagging" when the child is picked up 6–10 months * Fisting one hand * Difficulty rolling * Difficulty bringing hands together Older than 12 months of age * Difficulty crawling * Difficulty standing even with support * Walking with an unsteady, uneven, or stiff gait<unk> CP is distinguished from other forms of cerebral<unk> by its prominent symptom of<unk> ity or stiff, tight movements and gait patterns such as the scissor gait. However,<unk> ity as a symptom is also seen in other conditions such as stroke and multiple sclerosis. Thus, the presence of<unk> ity alone does not warrant a conclusive diagnosis of<unk> . Changes in<unk> ity and corresponding postures may also occur with other brain activity, such as excitement, fear or anxiety, or even pain, which increase muscle tension. A person with<unk> CP will commonly show, in addition to higher muscle tone, persistent primitive reflexes, greater stretch reflexes, plantar reflex, and ankle clonus. A third of people with cerebral<unk> have seizures - this is most common in<unk> CP. Audiovisual, cognitive compromise and behavioral disorders can occur. | Spastic cerebral palsy | Athetoid cerebral palsy | Dyskinetic cerebral palsy | Ataxic cerebral palsy | Cerebral palsy | Klumpke paralysis | Infantile progressive bulbar palsy | Oculopharyngeal muscular dystrophy | 00
| 61,391 |
The atypical features seen in cells displaying<unk> sis result from the action of the E5 and E6 oncoproteins produced by HPV. These proteins break down keratin in HPV-infected cells, resulting in the perinuclear halo and nuclear enlargement typical of<unk> s. The E6 oncoprotein, along with E7, is also responsible for the dysregulation of the cell cycle that results in squamous cell dysplasia. The E6 and E7 oncoproteins do this by binding and inhibiting the tumor suppressor genes p53 and RB, respectively. This promotes progression of cells through the cell cycle without appropriate repair of DNA damage, resulting in dysplasia. Due to the ability of HPV to cause cellular dysplasia,<unk> s are found in a number of potentially precancerous lesions. | Koilocyte | Echinocyte | Podocyte | Respirocyte | Prolymphocyte | Centrocyte | Nurse cell | Lymphoblast | 00
| 35,037 |
The<unk> is a randomized controlled<unk> in Manchester, England using Motivational Interventions for Drugs & Alcohol misuse in Schizophrenia. It is led by Professor Christine Barrowclough and operates in both Manchester and London. The<unk> is, along with the Danish CapOpus<unk> , among the only<unk> s aimed at this particular group of comorbid substance abusers with schizophrenia. | MIDAS Trial | QRISK | MOMS Trial | Risk panel | NACA score | RECOVERY Trial | EuroSCORE | Joint replacement registry | 00
| 46,014 |
Anatomy of a Nephron; functional unit of the kidney<unk> <unk> is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. The disorder is caused by genetic mutations resulting in improper function of the thiazide-sensitive sodium-chloride symporter (SLC12A3, also known as NCC, NCCT, or TSC) located in the distal convoluted tubule of the kidney. The distal convoluted tubule of the kidney plays an important homoestatic role in sodium and chloride absorption as well as of the reabsorption of magnesium and calcium. Genetic mutations of NCC, lead to loss of function and subsequently, reduced transport of sodium and chloride via NCC. Secondary derangement of calcium, magnesium, and potassium concentrations are caused by secondary effects in the distal tubule and collecting duct. The effect is an electrolyte imbalance similar to that seen with thiazide diuretic therapy (which causes pharmacological inhibition of NCC activity).<unk> was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified. Bartter syndrome is also an autosomal recessive cause of hypokalemic metabolic alkalosis, but it derives from a mutations of a number of genes that reduce NKCC2 activity. NKCC2 is found in the thick ascending limb of the loop of Henle. | Gitelman syndrome | Angelman syndrome | FG syndrome | Omenn syndrome | Perlman syndrome | Irvine–Gass syndrome | Malouf syndrome | Gleich's syndrome | 00
| 26,153 |
Most common causes of hyperthyroidism by age. There are several causes of hyperthyroidism. Most often, the entire gland is overproducing thyroid hormone. Less commonly, a single nodule is responsible for the excess hormone secretion, called a "hot" nodule. Thyroiditis (inflammation of the thyroid) can also cause hyperthyroidism. Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions. The major causes in humans are: * Graves' disease. An autoimmune disease (usually, the most common cause with 50–80% worldwide, although this varies substantially with location- i.e., 47% in Switzerland (Horst et al., 1987) to 90% in the USA (Hamburger et al. 1981)). Thought to be due to varying levels of iodine in the diet. It is eight times more common in females than males and often occurs in young females, around 20 – 40 years of age. * Toxic thyroid adenoma (the most common cause in Switzerland, 53%, thought to be atypical due to a low level of dietary iodine in this country) * Toxic multinodular goiter High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons: * Inflammation of the thyroid is called thyroiditis. There are several different kinds of thyroiditis including Hashimoto's thyroiditis (Hypothyroidism immune-mediated), and subacute thyroiditis (de Quervain's). These may be initially associated with secretion of excess thyroid hormone but usually progress to gland dysfunction and, thus, to hormone deficiency and hypothyroidism. * Oral consumption of excess thyroid hormone tablets is possible (surreptitious use of thyroid hormone), as is the rare event of eating ground beef or pork contaminated with thyroid tissue, and thus thyroid hormones (termed hamburger thyrotoxicosis or alimentary thyrotoxicosis). Pharmacy compounding errors may also be a cause. * Amiodarone, an antiarrhythmic drug, is structurally similar to thyroxine and may cause either under-or overactivity of the thyroid. * Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment. * A struma ovarii is a rare form of monodermal teratoma that contains mostly thyroid tissue, which leads to hyperthyroidism. * Excess iodine consumption notably from algae such as kelp. Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis). Hypersecretion of thyroid stimulating hormone (TSH), which in turn is almost always caused by a pituitary adenoma, accounts for much less than 1 percent of hyperthyroidism cases. | medical cause of Insomnia | medical cause of Panic attack | symptom of Narcolepsy | symptom of Delirium | symptom of Bipolar disorder | symptoms of Delirium | symptom of Opioid use disorder | complications of Panic attack | 00
| 1,090 |
<unk> (also known as diabetic-bearded woman syndrome) is a rare disorder mainly occurring in postmenopausal women. It is characterized by type II diabetes mellitus and signs related to the overproduction of androgens. The disease is named for Emile<unk> and Joseph<unk> . | Achard–Thiers syndrome | McGillivray syndrome | Bart–Pumphrey syndrome | Lelis syndrome | Cole-Carpenter syndrome | Brunner syndrome | Achard syndrome | Bart syndrome | 00
| 23,787 |
<unk> is indicated for treatment of neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME). | Faricimab | Altbib | Odesivimab | Oseltamivir | Maftivimab | Regdanvimab | Atoltivimab | Sotrovimab | 00
| 71,684 |
Side effects of<unk> can be divided into acute (those occurring while receiving chemotherapy) and delayed (those occurring months to years after completion of chemotherapy). Delayed side effects have assumed particular importance because many patients treated for Hodgkin lymphoma are cured and can expect long lives after completion of chemotherapy. Acute side effects * Hair loss, or alopecia, is a fairly common but not universal side effect of<unk> . Hair that is lost returns in the months after completion of chemotherapy. * Nausea and vomiting can occur with<unk> , although treatments for chemotherapy-induced nausea and vomiting have improved substantially (see Supportive care below). * Low blood counts, or myelosuppression, occur about 50% of the time with<unk> . Blood cell growth factors are sometimes used to prevent this (see Supportive care below). Blood counts are checked frequently while receiving chemotherapy. Any fever or sign of infection that develops needs to be promptly evaluated; severe infections can develop rapidly in a person with a low white blood cell count due to chemotherapy. * Allergic reactions to bleomycin can occur. A small test dose of bleomycin is often given prior to the first round of<unk> to screen for patients who may be allergic. * Neuropathy: Chemotherapy-induced peripheral neuropathy, a progressive and enduring tingling numbness, intense pain, and hypersensitivity to cold, beginning in the hands and feet and sometimes involving the arms and legs. Delayed side effects * Infertility is probably infrequent with<unk> . Several studies have suggested that, while sperm counts in men decrease during chemotherapy, they return to normal after completion of<unk> . In women, follicle-stimulating hormone levels remained normal while receiving<unk> , suggesting preserved ovarian function. Regardless of these data, fertility options (e.g. semen cryopreservation, oocyte cryopreservation, embryo cryopreservation) should be discussed with an oncologist before beginning<unk> therapy. * Pulmonary toxicity, or lung damage, can occur with the use of bleomycin in<unk> , especially when radiation therapy to the chest is also given as part of the treatment for Hodgkin lymphoma. This toxicity develops months to years after completing chemotherapy, and usually manifests as cough and shortness of breath. High concentrations of oxygen, such as those often used in surgery, can trigger lung damage in patients who have received bleomycin, even years later. Pulmonary function tests are often used to assess for bleomycin-related damage to the lungs. One study found bleomycin lung damage in 18% of patients receiving<unk> for Hodgkin disease. Retrospective analyses have questioned whether bleomycin is necessary at all; however, at this point it remains a standard part of<unk> . * Cardiac toxicity, or cardiomyopathy, can be a late side effect of adriamycin. The occurrence of adriamycin-related cardiac toxicity is related to the total lifetime dose of adriamycin, and increases sharply in people who receive a cumulative dose of more than 400 mg/m2. Almost all patients treated with<unk> receive less than this dose (for 6 cycles of<unk> , the cumulative adriamycin dose is 300 mg/m2); therefore, adriamycin-related cardiac toxicity is very uncommon with<unk> . * Secondary malignancies. Patients cured of Hodgkin lymphoma remain at increased risk of developing other (secondary) cancers. Treatment-related leukemias are uncommon with<unk> , especially as compared with MOPP. However, one study found a risk of second cancers as high as 28% at 25 years after treatment for Hodgkin lymphoma, although most of the patients in this study were treated with MOPP chemotherapy rather than<unk> . Many of these second cancers were lung cancers or, in women, breast cancers, emphasizing the importance of smoking cessation and regular preventive care after completion of treatment. Radiation and chemotherapy probably both play a role in the development of these secondary malignancies; the exact contribution of chemotherapy such as<unk> can be difficult to tease out. | ABVD | CAREN | SWAP-200 | PAIR | SBAR | PVSRIPO | Birmingham gauge | Sampaolesi line | 00
| 38,465 |
<unk> is a series of<unk> lessons on<unk> presented by Robert D.<unk> . Dr.<unk> was a professor of surgery in the division of plastic and reconstructive surgery at the University of Louisville School of Medicine. The<unk> was originally released as a series of VHS tapes, published individually between 1995 and 2003. The series was re-released in 2003 on DVD as<unk> 's DVD<unk> of<unk><unk> . The series uses unembalmed<unk> specimens to illustrate<unk> cal structures. Intended for use by medical, dental and medical science students, the<unk> teaching aid uses simple language and high quality images. The authors claim: "Each minute of the finished product took twelve hours to produce: five in creating the script, five in making the shots, and two in post-production." | Acland's Video Atlas of Human Anatomy | Anatomical theatre of the Archiginnasio | Sigmund Freud bibliography | Fares Scale of Injuries due to Cluster Munitions | UFAW Handbook | The Anatomy Lesson of Dr. Nicolaes Tulp | Lloyd Library and Museum | Amsler grid | 00
| 33,566 |
<unk> is a clinical sign in which vigorous abduction followed by the sudden release of the little toe causes an extensor plantar reflex. It is found in patients with pyramidal tract lesions, and is one of a number of Babinski-like responses. The sign is named after the Viennese neurologist Erwin<unk> (1877-1962). | Stransky's sign | Winterbottom's sign | Baastrup's sign | Bancroft's sign | Dance's sign | Kelly's sign | Hamman's sign | Joffroy's sign | 00
| 55,281 |
Common causes of<unk> include: External ear * Cerumen (earwax) or foreign body in the external auditory canal * Otitis externa, infection or irritation of the outer ear * Exostoses, abnormal growth of bone within the ear canal * Tumor of the ear canal * Congenital stenosis or atresia of the external auditory canal (narrow or blocked ear canal). * Ear canal stenosis & atresia can exist independently or may result from congenital malformations of the auricle such as microtia or anotia. * Acquired stenosis (narrowing) of the external auditory canal following surgery or radiotherapy Middle ear Fluid accumulation is the most common cause of<unk> in the middle ear, especially in children. Major causes are ear infections or conditions that block the eustachian tube, such as allergies or tumors. Blocking of the eustachian tube leads to decreased pressure in the middle ear relative to the external ear, and this causes decreased motion of both the ossicles and the tympanic membrane. * Acute or Serous otitis media * Chronic suppurative otitis media (CSOM) * Perforated eardrum * Tympanosclerosis or scarring of the eardrum * Cholesteatoma * Eustachian Tube Dysfunction, inflammation or mass within the nasal cavity, middle ear, or eustachian tube itself * Otosclerosis, abnormal growth of bone in or near the middle ear * Middle ear tumour * Ossicular discontinuity as a consequence of infection or temporal bone trauma * Congenital malformation of the ossicles. This can be an isolated phenomenon or can occur as part of a syndrome where development of the 1st and 2nd branchial arches is seen such as in Goldenhar syndrome, Treacher Collins syndrome, branchio-oto-renal syndrome etc. * Barotrauma unequal air pressures in the external and middle ear. This can temporarily occur, for example, by the environmental pressure changes as when shifting altitude, or inside a train going into a tunnel. It is managed by any of various methods of ear clearing manoeuvres to equalize the pressures, like swallowing, yawning, or the Valsalva manoeuvre. More severe barotrauma can lead to middle ear fluid or even permanent sensorineural<unk> loss. Inner ear Third window effect caused by: * Superior canal dehiscence – which may require surgical correction. * Enlarged vestibular aqueduct * Labyrinthine fistula | Conductive hearing loss | Sensorineural hearing loss | Spatial hearing loss | Prelingual deafness | Unilateral hearing loss | Cortical deafness | Auditory exclusion | Noise-induced hearing loss | 00
| 21,361 |
Micrograph of an excised aortic valve<unk> showing that the avascular branching papillae are covered by endothelium. H&E stain.<unk> are typically found and accurately diagnosed by imaging. The diagnosis is confirmed by pathology. Histologically,<unk> s have branching avascular papillae, composed of collagen, that are covered by endothelium. | Papillary fibroelastoma | Fibrin ring granuloma | Actinic elastosis | Acrokeratoelastoidosis of Costa | Lipofibromatosis | Pyogenic granuloma | Eosinophilic granuloma | Silicone granuloma | 00
| 49,291 |
The<unk><unk> mechanism occurs as the result of the length-tension relationship observed in striated muscle, including for example skeletal muscles, arthropod muscle and cardiac (heart) muscle. As a muscle fiber is stretched, active tension is created by altering the overlap of thick and thin filaments. The greatest isometric active tension is developed when a muscle is at its optimal length. In most relaxed skeletal muscle fibers, passive elastic properties maintain the muscle fibers length near optimal, as determined usually by the fixed distance between the attachment points of tendons to the bones (or the exoskeleton of arthropods) at either end of the muscle. In contrast, the relaxed sarcomere length of cardiac muscle cells, in a resting ventricle, is lower than the optimal length for contraction. There is no bone to fix sarcomere length in the heart (of any animal) so sarcomere length is very variable and depends directly upon blood filling and thereby expanding the heart chambers. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in a normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For longer sarcomere lengths, this is the result of there being less overlap of the thin and thick filaments; for shorter sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. An increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length. The stretching of the muscle fibers augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils, causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. Specifically, the sensitivity of troponin for binding Ca2+ increases and there is an increased release of Ca2+ from the sarcoplasmic reticulum. In addition, there is a decrease in the spacing between thick and thin filaments, when a cardiac muscle fiber is stretched, allowing an increased number of cross-bridges to form. The force that any single cardiac muscle fiber generates is related to the sarcomere length at the time of muscle cell activation by calcium. The stretch on the individual fibers, caused by ventricular filling, determines the sarcomere length of the fibres. Therefore the force (pressure) generated by the cardiac muscle fibres is related to the end-diastolic volume of the left and right ventricles as determined by complexities of the force-sarcomere length relationship. Due to the intrinsic property of myocardium that is responsible for the<unk><unk> mechanism, the heart can automatically accommodate an increase in venous return, at any heart rate. The mechanism is of functional importance because it serves to adapt left ventricular output to right ventricular output. If this mechanism did not exist and the right and left cardiac outputs were not equivalent, blood would accumulate in the pulmonary circulation (were the right ventricle producing more output than the left) or the systemic circulation (were the left ventricle producing more output than the right). | Frank–Starling law | Mitrofanoff principle | Mandelbaum effect | Arndt–Schulz rule | Haldane effect | Bell–Magendie law | Windkessel effect | Goldwater rule | 00
| 14,827 |
*<unk> ilation Curve – Plot VE vs. VO2 or Watts or Time – The point at which there is a non‐linear increase in<unk> ilation * V‐Slope Method – Plot VO2 vs. VCO2 – The point at which the increase in VCO2 is greater than the increase in VO2 *<unk> ilatory Equivalents Method – Plot VE/VO2 and VE/VCO2 vs. Watts or time or VO2 – Point at which VE/VO2 increases while VE/VCO2 decreases or stays the same. | Ventilatory threshold | Mandatory minute ventilation | Lung compliance | Cardiac reserve | Tidal volume | Minute ventilation | Gas exchange | Peak inspiratory pressure | 00
| 66,651 |
T2 MRI of cervical spine demonstrating normal cord signal (green circle) and increased T2 signal in the central cord (red circle). Diagnostic criteria In 2002, the<unk> Consortium Working Group proposed the following diagnostic criteria for idiopathic acute<unk> : Investigations Individuals who develop<unk> are typically transferred to a neurologist who can urgently investigate the patient in a hospital. If breathing is affected, particularly in upper spinal cord lesions, methods of artificial ventilation must be on hand before and during the transfer procedure. The patient should also be catheterized to test for and, if necessary, drain an over-distended bladder. A lumbar puncture can be performed after the MRI or at the time of CT myelography. Corticosteroids are often given in high doses when symptoms begin with the hope that the degree of inflammation and swelling of the spinal cord will be lessened, but whether this is truly effective is still debated. Differential diagnosis The differential diagnosis of acute<unk> includes demyelinating disorders, such as multiple sclerosis and neuromyelitis optica, infections, such as herpes zoster and herpes simplex virus, and other types of inflammatory disorders, such as systemic lupus erythematosus and neurosarcoidosis. It is important to also rule out an acute cause of compression on the spinal cord. | Transverse myelitis | Lhermitte's sign | Vascular myelopathy | Acute flaccid myelitis | Amyotrophic lateral sclerosis | Surfer's myelopathy | CMV polyradiculomyelopathy | Primary lateral sclerosis | 00
| 2,296 |
Most sources treat low-fiber and low-residue diets as identical, but some make a distinction based on the difference between<unk> and<unk> . Dietary<unk> is the indigestible part of food made from plants.<unk> includes not only<unk> but also other materials found in the colon after digestion. When this distinction is made, a low-fiber diet simply reduces<unk> intake by eliminating or limiting high-fiber foods such as raw fruits and vegetables. A low-residue diet includes restrictions on foods such as dairy products, which do not contain<unk> but do develop<unk> after digestion. The American Academy of Nutrition and Dietetics’ removed the low-residue diet from its Nutrition Care Manual because there is no scientifically accepted quantitative definition of<unk> and there is no method to determine the<unk> produced by a food. | Low-fiber/low-residue diet | Low-FODMAP diet | Gluten-free diet | Specific carbohydrate diet | Plant-based diet | Macrobiotic diet | Lectin-free diet | Low-carbohydrate diet | 00
| 30,700 |
<unk> or brain<unk> peptide (BNP), also known as B-type<unk> peptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased<unk> blood volume. The 32-amino acid polypeptide BNP is secreted attached to a 76–amino acid N-terminal fragment in the prohormone called NT-proBNP (BNPT), which is biologically inactive. Once released, BNP binds to and activates the atrial<unk> factor receptor NPRA, and to a lesser extent NPRB, in a fashion similar to atrial<unk> peptide (ANP) but with 10-fold lower affinity. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better targets than ANP for diagnostic blood testing. The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. | Ventricular natriuretic peptide | N-terminal prohormone of brain natriuretic peptide | Prorenin | Plasma renin activity | Orexin | Leptin | Aldosterone-to-renin ratio | C-peptide | 00
| 72,842 |
The mainstay of treatment involves two broad strategies: treat the cancer that usually occurs with the disease, and give medications that suppress the body's immune system attack on the nervous system. Because current treatments are not successful at eliminating the disease, the goal of treatment is often to reduce symptoms rather than attempt to cure it. To date, treatments have been unsuccessful in achieving a sustained reduction of symptoms or survival in the vast majority of patients. Some treatments may directly combat the mechanisms by which the disease may be caused. To suppress the immune system, steroids, antibodies, or even<unk> man cells may be injected into a patient. Certain types of antibodies called intravenous immunoglobulins (IVIG) also have shown to lead to reduced symptoms due to their ability to reduce and eliminate anti-Hu antibodies. A drug called rituximab, a molecule that targets B cells, helps reduce the symptoms of anti-Hu encephalitis and decreases the number of anti-Hu antibodies. Cancer treatment may involve surgical removal of the tumor, or medications that may shrink or eliminate the tumor. Treatment with cyclophosphamide, a chemotherapy drug, has shown promise, in addition to adrenocorticotropic hormone (ACTH). This hormone is involved in regulating many body functions including stress level and blood pressure. Steroids such as dexamethasone may help reduce disease burden by reducing the antibody-building activity of the disease. Despite the fact that steroids can be used to reduce the immunological antibody-building activity of the disease in all people, many other anti-Hu encephalitis treatments are most effective in children. Treatments may also be focused purely on symptoms rather than targeting the potential causes of the disease. For seizures, anticonvulsant medications may be used, such as valproic acid, levetiracetam, or lamotrigine. For hallucinations, delusions, and mood disturbances, second generation antipsychotic agents (e.g., olanzapine, clozapine) are also used for symptom control. | Anti-Hu associated encephalitis | Anti-NMDA receptor encephalitis | Anti-VGKC-complex encephalitis | Powassan encephalitis | Post viral cerebellar ataxia | Anti-neurofascin demyelinating diseases | Viliuisk encephalomyelitis | Limbic-predominant age-related TDP-43 encephalopathy | 00
| 70,740 |
In herpes labialis, the duration of healing, pain and detectable virus is reduced by up to one day, compared with the total duration of 2–3 weeks of disease presentation. | Penciclovir | Aciclovir | Valganciclovir | Famciclovir | Ganciclovir | Alcaftadine | Letermovir | Amantadine | 00
| 38,070 |
Symptoms vary from case to case, and may correlate to how much of the chromosome is missing. Symptoms that are frequently observed with the condition include: * Low birth weight * Malformations of the head * Eye abnormalities * Defects of the hands and feet, polydactyly * Reproductive abnormalities (males) * Psychological and motor retardation | Partial monosomy 13q | Distal trisomy 10q | 2q37 monosomy | Tetrasomy 18p | Chromosome 2q deletion | Tetrasomy 9p | Chromosome 15q partial deletion | Monosomy 9p | 00
| 50,032 |
<unk> , also known as 3-deketo-17α-ethyl-19-nortestosterone or as 17α-ethylestr-4-en-17β-ol, is a synthetic estrane steroid and a 17α-alkylated derivative of nandrolone (19-nortestosterone; 19-NT). It is specifically the 17α-ethyl and 3-deketo derivative of nandrolone as well as the 3-deketo derivative of norethandrolone (17α-ethyl-19-NT). Other related AAS include bolenol (3-deketo-17α-ethyl-19-nor-5-androstenediol), ethyldienolone (17α-ethyl-δ9-19-NT), norboletone (17α-ethyl-18-methyl-19-NT), propetandrol (17α-ethyl-19-NT 3β-propionate), and tetrahydrogestrinone (THG; 17α-ethyl-18-methyl-δ9,11-19-NT). The progestins allylestrenol (3-deketo-17α-allyl-19-NT) and lynestrenol (3-deketo-17α-ethynyl-19-NT) are also closely related to<unk> , differing only by the C17α substitution. | Ethylestrenol | Lynestrenol | Allylestrenol | Bisoctrizole | Norethandrolone | Nandrolone propionate | Oxandrolone | Allenestrol | 00
| 37,287 |
A temporary loss of smell can be caused by a blocked nose or infection. In contrast, a permanent loss of smell may be caused by death of olfactory receptor neurons in the nose or by brain injury in which there is damage to the olfactory nerve or damage to brain areas that process smell (see olfactory system). The lack of the sense of smell at birth, usually due to genetic factors, is referred to as congenital<unk> . Family members of the patient suffering from congenital<unk> are often found with similar histories; this suggests that the<unk> may follow an autosomal dominant pattern.<unk> may very occasionally be an early sign of a degenerative brain disease such as Parkinson's disease and Alzheimer's disease. Another specific cause of permanent loss could be from damage to olfactory receptor neurons because of use of certain types of nasal spray; i.e., those that cause vasoconstriction of the nasal microcirculation. To avoid such damage and the subsequent risk of loss of smell, vasoconstricting nasal sprays should be used only when absolutely necessary and then for only a short amount of time. Non-vasoconstricting sprays, such as those used to treat allergy-related congestion, are safe to use for prescribed periods of time.<unk> can also be caused by nasal polyps. These polyps are found in people with allergies, histories of sinusitis, and family history. Individuals with cystic fibrosis often develop nasal polyps. Amiodarone is a drug used in the treatment of arrhythmias of the heart. A clinical study demonstrated that the use of this drug induced<unk> in some patients. Although rare, there was a case in which a 66-year-old male was treated with amiodarone for ventricular tachycardia. After the use of the drug he began experiencing olfactory disturbance, however after decreasing the dosage of amiodarone, the severity of the<unk> decreased accordingly, suggesting a relationship between use of amiodarone to the development of<unk> . COVID-19-related<unk> Chemosensory disturbances, including loss of smell or taste, are the predominant neurological symptom of COVID-19. As many as 80% of COVID-19 patients exhibit some change in chemesthesis, including smell. Loss of smell has also been found to be more predictive of COVID-19 than all other symptoms, including fever, cough or fatigue, based on a survey of 2 million participants in the UK and US. Google searches for "smell", "loss of smell",<unk> ", and other similar terms increased since the early months of the pandemic, and strongly correlated with increases in daily cases and deaths. Research into the mechanisms underlying these symptoms is currently ongoing. Many countries list<unk> as an official COVID-19 symptom, and some have developed "smell tests" as potential screening tools. In 2020, the Global Consortium for Chemosensory Research, a collaborative research organization of international smell and taste researchers, formed to investigate loss of smell and related chemosensory symptoms. List of causes | Anosmia | Dysosmia | Phantosmia | Aspermia | Hyperhidrosis | Hyperosmia | Buphthalmos | Xerophthalmia | 00
| 5,619 |
<unk><unk> disease responds well, and often dramatically, to glucocorticoid therapy, provided that advanced fibrotic lesions have not resulted in irreversible damage, and this has included resolution of radiologic findings. Men given glucocorticoids to treat<unk><unk> disease at other anatomical sites sometimes report relief of their lower urinary tract symptoms, suggesting that<unk> may be underdiagnosed. Cases are however likely to get misdiagnosed as benign prostatic hyperplasia and to get treated alternatively with medications such as alpha blockers. The efficacy of alpha blockers in<unk> remains unclear. | IgG4-related prostatitis | Granulomatous prostatitis | Asymptomatic inflammatory prostatitis | Chronic bacterial prostatitis | Non-gonococcal urethritis | Urogenital tuberculosis | Eosinophilic cystitis | Genitourinary amoebiasis | 00
| 67,338 |
Several well regarded institutions of medical research have produced clinical criteria useful in diagnosing TTS. One of the first sets of guidelines was initially published in 2004 and again in 2008 by the Mayo Clinic. Other research institutions proposing diagnostic criteria include the Japanese<unk> Study Group, Gothenburg University, Johns Hopkins University, the<unk> Italian Network and the Heart Failure Associates TTS Taskforce of the European Society of Cardiology. All of the research institutions agree on at least two main criteria needed to accurately diagnose TTS: 1) transient left ventricular wall motion abnormality and 2) the absence of a condition obviously explaining this wall motion abnormality (coronary artery lesion, hypoperfusion, myocarditis, toxicity, etc.). Other commonly acknowledged criteria necessary for diagnosis include characteristic EKG changes and mild to modest elevation in cardiac troponin. Transient apical ballooning syndrome or<unk> is found in 1.7–2.2% of patients presenting with acute coronary syndrome. While the original case studies reported on individuals in Japan,<unk> has been noted more recently in the United States and Western Europe. It is likely that the syndrome previously went undiagnosed before it was described in detail in the Japanese literature. Evaluation of individuals with<unk> typically includes a coronary angiogram to rule out occlusion of the left anterior descending artery, which will not reveal any significant blockages that would cause the left ventricular dysfunction. Provided that the individual survives their initial presentation, the left ventricular function improves within two months. The diagnosis of<unk> may be difficult upon presentation. The ECG findings often are confused with those found during an acute anterior wall myocardial infarction. It classically mimics ST-segment elevation myocardial infarction, and is characterised by acute onset of transient ventricular apical wall motion abnormalities (ballooning) accompanied by chest pain, shortness of breath, ST-segment elevation, T-wave inversion or QT-interval prolongation on ECG. Cardiac enzymes are usually negative and are moderate at worst, and cardiac catheterization usually shows absence of significant coronary artery disease. The diagnosis is made by the pathognomonic wall motion abnormalities, in which the base of the left ventricle is contracting normally or is hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities. Although apical ballooning has been described classically as the angiographic manifestation of<unk> , it has been shown that left ventricular dysfunction in this syndrome includes not only the classic apical ballooning, but also different angiographic morphologies such as mid-ventricular ballooning and, rarely, local ballooning of other segments. The ballooning patterns were classified by Shimizu et al. as<unk> type for apical akinesia and basal hyperkinesia, reverse<unk> for basal akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning accompanied by basal and apical hyperkinesia, and localised type for any other segmental left ventricular ballooning with clinical characteristics of<unk> -like left ventricular dysfunction. In short, the main criteria for the diagnosis of<unk> are: the patient must have experienced a stressor before the symptoms began to arise; the patient's ECG reading must show abnormalities from a normal heart; the patient must not show signs of coronary blockage or other common causes of heart troubles; the levels of cardiac enzymes in the heart must be elevated or irregular; and the patient must recover complete contraction and be functioning normally in a short amount of time. File:Takotsubo ventriculography.Left ventriculography during systole showing apical ballooning akinesis with basal hyperkinesis in a characteristic<unk> ventricle File:Takotsubo left ventriculogram.Left ventriculogram during systole displaying the characteristic apical ballooning with apical motionlessness in a patient with<unk> File:Takotsubo ultrasound.(A) Echocardiogram showing dilatation of the left ventricle in the acute phase (B) Resolution of left ventricular function on repeat echocardiogram six days later File:Takotsubo ECG.ECG showing sinus tachycardia and non-specific ST and T wave changes from a person with confirmed<unk> File:UOTW 74 - Ultrasound of the Week 2.Echocardiogram showing the effects of the disease | Takotsubo cardiomyopathy | Bubo | Wooden chest syndrome | Acute pericarditis | Acute coronary syndrome | Tamponade | Toxic anterior segment syndrome | Acute chest syndrome | 00
| 41,566 |
<unk> catalyzes the reversible phosphorylation of<unk> , deoxyuridine, and their analogs (except deoxycytidine) to their respective bases (thymine/uracil) and 2-deoxyribose 1-phosphate. The enzyme follows a sequential mechanism, where phosphate binds before<unk> (or deoxyuridine, etc.) and 2-deoxyribose 1-phosphate leaves after the nitrogenous base. The<unk> is bound in a high-energy conformation, in which the glycosidic bond weakens as the phosphate attacks the C1 position of the ribose ring, as shown below. The enzyme can then transfer deoxyribose 1-phosphate to other nitrogenous bases.<unk> mechanism Further experiments have shown that thymine inhibits the enzyme via both substrate inhibition and nonlinear product inhibition. This suggests that thymine can inhibit the enzyme via multiple sites. The enzyme also displays cooperativity with respect to both<unk> and phosphate in the presence of thymine, which suggests that<unk> has several allosteric and/or catalytic sites as well. | Thymidine phosphorylase | Xanthine oxidase | Asparaginase | Galactose-1-phosphate uridylyltransferase | Dispase | Iduronate-2-sulfatase | Transaminase | Biotinidase | 00
| 48,284 |
Lateral cross section of female reproductive system, illustrating the vesicovaginal and rectovaginal areas As pelvic organ prolapse and stress urinary incontinence can be present separately or simultaneously, surgical<unk> is implanted into vesicovaginal and rectovaginal region through the vaginal route in different approaches, to manage patients’ condition properly. Pelvic organ prolapse (POP) surgery The goal of POP repair with<unk> is to increase longevity in patients by reconstructing organ position and preventing pelvic organs from bulging into the vagina. Generally, the position and incisions for<unk> are determined by the corresponding pelvic muscle defect, which differs from patient to patient. The implantation usually starts with anterior colpotomy, which is an incision on the anterior vaginal wall to assess the vesicovaginal space in front of the vagina. For patients who have undergone hysterectomy or will be preserving their uterus, only longitudinal anterior incision can be performed. For patients who are also receiving a concomitant hysterectomy, an anterior colpotomy, a Cross-T-shaped incision that cuts around the cervix, or a single incision around the cervix and across the vagina will be performed. Tissue Fixation System (TFS) invented in Australia, an example of<unk> implant to repair pelvic organ prolapse and stress urinary incontinence. In consideration of the patient's specific conditions, the<unk> can be positioned in front of the vaginal wall (cystocele correction), behind the vaginal wall (rectocele correction), or on top of the vagina (uterine prolapse correction). For cystocele corrections, horizontal arms will be inserted on the lateral bladder walls through the obturator foramen by an Emmet needle. Meanwhile, vertical straps will be placed onto the fibrous thickenings of pelvic fascia anteriorly and posteriorly in order to reposition the bladder. Alternatively, an incision on the posterior vaginal wall will be needed to place the<unk> through the perineal skin for rectocele correction. To hold the rectum upright, the horizontal straps are inserted into space surrounding the rectum, brought out of the body and pulled below the anus. If both corrections are required,<unk> can be cut into two pieces before operation and adjusted for accurate reconstruction. After putting the prolapsed organs back to its original position and reinforcing the vaginal wall, the incision is closed with sutures.<unk> surgery is expected to show improved pelvic support after the first few weeks, particularly for non-absorbable<unk> es which have a higher biocompatibility and permanent outcome. For absorbable<unk> es, longer recovery time and lower durability are expected as native tissues need to grow into the pores to support the weakened organs. Stress urinary incontinence (SUI) surgery<unk> , also known as midurethral or bladder neck sling for SUI repair, can be used to support the urethra or the neck of the bladder in two surgical approaches, namely the retropubic and transobturator. In the retropubic approach, two incisions above the pubic bone and one incision in the vagina are performed. The<unk> is then placed under the urethra through the retropubic space, which is anterior to bladder and posterior to pubic symphysis, and brought out to the suprapubic area. In the transobturator approach, two incisions in the groin area and one incision in the vagina are performed. The<unk> is inserted through the obturator foramen to avoid damage of pelvic organs, and brought out to the skin in the groin area. Since 2008, mini-slings with single vaginal incision have been introduced to reduce complications without comprising the successful rate. | Transvaginal mesh | Cervical pessary | Macy catheter | Vaginoplasty | Perineal dilator | Vaginal dilator | Hymenorrhaphy | Progesterone vaginal ring | 00
| 74,344 |
Six factors can contribute to the formation of edema: # increased hydrostatic pressure; # reduced colloidal or oncotic pressure within blood vessels; # increased tissue colloidal or oncotic pressure; # increased blood vessel wall permeability (e.g., inflammation); # obstruction of fluid clearance in the lymphatic system; # changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidneys. Generation of interstitial fluid is regulated by the forces of the Starling equation. Hydrostatic pressure within blood vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood plasma and tissue. As a result, the colloidal or oncotic pressure of the higher level of protein in the plasma tends to draw water back into the blood vessels from the tissue. Starling's equation states that the rate of leakage of fluid is determined by the difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with a fall in reflection coefficient. Changes in the variables in Starling's equation can contribute to the formation of edemas either by an increase in hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in vessel wall permeability. The latter has two effects. It allows water to flow more freely and it reduces the colloidal or oncotic pressure difference by allowing protein to leave the vessel more easily. Another set of vessels known as the lymphatic system acts like an "overflow" and can return much excess fluid to the bloodstream. But even the lymphatic system can be overwhelmed, and if there is simply too much fluid, or if the lymphatic system is congested, then the fluid will remain in the tissues, causing swellings in legs, ankles, feet, abdomen or any other part of the body. | symptom of Thoracic outlet syndrome | symptom of Carpal tunnel syndrome | symptom of Dysautonomia | symptom of Motion sickness | symptom of Myasthenia gravis | symptom of Pulmonary heart disease | symptom of Legius syndrome | symptom of Pulmonary embolism | 00
| 5,005 |
Legal scholars, economists, activists, policymakers, industries, and trade organizations have held differing views on<unk> and engaged in contentious debates on the subject. Critical perspectives emerged in the nineteenth century that were especially based on the principles of free trade. Contemporary<unk> s have echoed those arguments, claiming that<unk> block innovation and waste resources that could otherwise be used productively, and also block access to an increasingly important "commons" of enabling technologies (a phenomenon called the tragedy of the anticommons), apply a "one size fits all" model to industries with differing needs, that is especially unproductive for industries other than chemicals and pharmaceuticals and especially unproductive for the software industry. Enforcement by<unk> trolls of poor quality<unk> has led to<unk> of the<unk> office as well as the system itself.<unk> on pharmaceuticals have also been a particular focus of<unk> , as the high prices they enable puts life-saving drugs out of reach of many people. Alternatives to<unk> have been proposed, such Joseph Stiglitz's suggestion of providing "prize money" (from a "prize fund" sponsored by the government) as a substitute for the lost profits associated with abstaining from the monopoly given by a<unk> These debates are part of a larger discourse on intellectual property protection which also reflects differing perspectives on copyright. | Criticism of patents | Patient trade-off | Patient group directions | Cost sharing | Component causes | Public security | Guaranteed issue | Prescription charges | 00
| 50,616 |
<unk> is a technique for genetic sex determination in those species where XX chromosome pair is present.<unk> can be done by identifying Barr body, a drumstick like appendage located in the rim of the nucleus in somatic cells. Barr body is the inactive X chromosome which lies condensed in the nucleus of somatic cells. A typical human (or other XY-based organism) female has only one Barr body per somatic cell, while a typical human male has none. Though a Barr body can be sought in any human<unk> ed cell, circulating mononuclear cells are commonly used for this purpose. These cells are cultured, and treated with chemicals such as colcemid to arrest mitosis in metaphase. A minimum of 30 percent of sex chromatin indicates genetic female sex. | Nuclear sexing | Structural inheritance | Fetal programming | Sex-chromosome dosage compensation | Sex selection | Genetics of obesity | Genomic imprinting | Germline mosaicism | 00
| 69,860 |
Pyle two-channel<unk><unk> Important applications include public address systems, theatrical and concert sound reinforcement systems, and domestic systems such as a stereo or home-theatre system. Instrument<unk> s including guitar<unk> s and electric keyboard<unk> s also use<unk> s. In some cases, the<unk><unk> for an instrument<unk> is integrated into a single<unk> "head" which contains a preamplifier, tone controls, and electronic effects. These components may be mounted in a wooden speaker cabinet to create a "combo<unk> ". Musicians with unique performance needs and/or a need for very<unk> ful amplification may create a custom setup with separate rackmount preamplifiers, equalizers, and a<unk><unk> mounted in a 19" road case.<unk><unk> s are available in standalone units, which are used by hi-fi audio enthusiasts and designers of public address systems (PA systems) and sound reinforcement systems. A hi-fi user of<unk><unk> s may have a stereo<unk><unk> to drive left and right speakers and a single-channel (mono)<unk><unk> to drive a subwoofer. The number of<unk><unk> s used in a sound reinforcement setting depends on the size of the venue. A small coffeehouse may have a single<unk> amp driving two PA speakers. A nightclub may have several<unk> amps for the main speakers, one or more<unk> amps for the monitor speakers (pointing towards the band) and an additional<unk> amp for the subwoofer. A stadium concert may have a large number of<unk> amps mounted in racks. Most consumer electronics sound products, such as TVs, boom boxes, home cinema sound systems, Casio and Yamaha electronic keyboards, "combo" guitar amps and car stereos have<unk><unk> s integrated inside the chassis of the main product. | Audio power amplifier | Eye chart | Computational audiology | Solar viewer | Optometry | Head mirror | Snellen chart | Reading machine | 00
| 5,716 |
Electrode placement for<unk> ; RL electrode (green), not shown, remains on leg A<unk> (also called the S5<unk> is a modified ECG<unk> used to detect atrial flutter waves when atrial flutter is suspected clinically, based on signs and symptoms, but is not definitely demonstrated on the standard 12<unk> ECG. In order to create the<unk> , the right arm electrode is moved to the manubrium adjacent to the sternum. Then the left arm electrode is moved to the right, fifth intercostal space adjacent to the sternum. The left leg electrode is placed on the right lower costal margin. The<unk> is then read as<unk> I on the ECG and, since in most patients it will be roughly perpendicular to the wave of ventricular depolarization, atrial flutter waves may be more apparent. | Lewis lead | Sybil | Pubmeth | Metaldehyde | Lewisite | Vinyl chloride | Basilicon | Heptachlor | 00
| 47,450 |
<unk> is a medical condition with an unknown cause that shows symptoms of short stature, congenital optic atrophy and brachytelephalangy. This condition is extremely rare with only two cases being found. | Berk–Tabatznik syndrome | Townes–Brocks syndrome | Fryns-Aftimos syndrome | Bannayan–Riley–Ruvalcaba syndrome | McKittrick-Wheelock syndrome | Cortes Lacassie syndrome | Teunissen–Cremers syndrome | Barakat-Perenthaler syndrome | 00
| 52,373 |
Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.Replacing white bread with whole wheat may help reduce hyperglycemia In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc. Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control. Dipeptidyl peptidase 4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in hospital. Increasing aerobic exercise to at least 30 minutes will make better use of glucose accumulated in the body since glucose is being used for energy by the muscle. Calorie restriction would be one of the main lifestyle changes because it reduces over eating which contributes to hyperglycemia. Diets higher in healthy unsaturated fats and whole wheat carbohydrates such as the Mediterranean diet can help reduce carbohydrate intake to better control hyperglycemia. Diets such as intermittent fasting and ketogenic diet help reduce calorie consumption which could significantly reduce hyperglycemia. Carbohydrates are the main cause for hyperglycemia, non whole wheat items should be substituted for whole wheat items. Fruits are a part of a complete nutritious diet, but the intake of fruit should be limited due to its high sugar content. | diagnosis of Diabetic ketoacidosis | complications of Diabetic ketoacidosis | medical cause of Cardiogenic shock | medical cause of Hyperthermia | symptom of Diabetic ketoacidosis | symptom of Syndrome of inappropriate antidiuretic hormone secretion | symptoms of Toxic shock syndrome | medical cause of Hypoglycemia | 00
| 5,330 |
<unk><unk> 2011 tropospheric column density. The EPA have some regulations and guidelines for monitoring<unk><unk> levels. Historically, some states in the U.S including Chicago, Northeast corridor and L.A have had high levels of<unk><unk> . In 2006, the WHO estimated that over 2 million deaths result annually from air pollution in which<unk><unk> constitute one of the pollutants. While over 50% of the disease that results from these pollutants are common in developing countries and the effects in developed countries is also significant. An EPA survey in the U.S. suggests that 16 percent of United States' housing units are sited close to an airport, highway or railroad increasing in the United States the exposure risk of approximately 48 million people. A feasibility study of the ozone formed from the oxidation of<unk><unk> in ambient air reported by the WHO suggested that daily deaths of 1 to 2% is attributed to exposure to ozone concentration above 47.3 ppb and exposure above 75.7ppb is attributed to 3 to 5% increase in daily mortality. A level of 114 ppb was attributed to 5 to 9% increase daily mortality. Silo filler's disease is pervasive during the harvest seasons of food grains. In May 2015, the National Green Tribunal directed Delhi and other states in India to ban diesel vehicles over 10 years old as a measure to reduce<unk><unk> emission that may result in<unk> . In 2008, the report of United Kingdom Committee on the Medical Effects of Air Pollutants (COMEAP) suggested that air pollution is the cause of about 29,000 deaths in UK. The WHO urban air quality database estimated Delhi's mean annual PM 10 levels in 2010 as 286 μg /m3 and London as 23 μg /m3. In 2014, the database estimated Delhi's annual mean PM 2.5 particulate matter levels in 2013 as 156 μg /m3 whereas, London have only 8 μg /m3 in 2010 but the<unk><unk> in London breach the European Union's standard. In 2013, the annual mean<unk><unk> level in London was estimated as 58 μg /m3 but the save and "threshold limit value" is 40 μg /m3. In March 2015, Brussels took the United Kingdom into court for breaching emissions limits of<unk><unk> at its coal-fired Aberthaw power stations in Wales. The plant operated under a permit allowing emissions of 1200 mg/Nm3, which is more than twice the 5 mg/Nm3 limit specified in the EU's large combustion plant directive. | Nitrogen dioxide poisoning | Carbon monoxide poisoning | Chlorine gas poisoning | Organophosphate poisoning | Oxygen toxicity | Cyanide poisoning | Barbiturate overdose | Nitrogen narcosis | 00
| 67,683 |
The earliest and probably most widely accepted scientific theory of<unk> action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce<unk> effects, which was later linked to their inhibitory effects on monoamine oxidase, the enzyme that catalyses the breakdown of the monoamine neurotransmitters. All currently marketed<unk> s have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual melatonergic-serotonergic pathway. Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic<unk> s have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not<unk> equately respond to monoaminergic<unk> s. A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, epigenetic, cortisol hypersecretion and inflammatory hypotheses. | Antidepressant | Antipsychotic | Appetite stimulant | Mood stabilizer | Tetracyclic antidepressant | Tricyclic antidepressant | Atypical antidepressant | Antimanic drugs | 00
| 253 |
Generic<unk> 7.5/200 mg<unk> (INNs), sold under the brand name Vicoprofen, is a fixed-dose combination analgesic medication used in short-term therapy to relieve severe pain. Vicoprofen combines the analgesic and antitussive properties of hydrocodone with the analgesic, anti-inflammatory, and antipyretic properties of<unk> . In contrast to hydrocodone/acetaminophen combination analgesics such as Vicodin, this<unk> avoids some of the liver toxicity which may occur from acetaminophen, but still presents significant dangers in hydrocodone overdose, namely respiratory depression. Vicoprofen is supplied in a fixed dose combination tablet which contains hydrocodone bitartrate, USP 7.5 mg with<unk> , USP 200 mg. Additional strengths of generic Vicoprofen are now available, in combinations of 5 mg/200 mg and 10 mg/200 mg respectively. | Hydrocodone/ibuprofen | Oxycodone/ibuprofen | Ibuprofen/paracetamol | Hydrocodone/paracetamol | Naproxen/diphenhydramine | Hydrocodone/aspirin | Celecoxib/tramadol | Butalbital/acetaminophen | 00
| 60,302 |
A titanium hip prosthesis, with a ceramic head and polyethylene acetabular cup Ceramics are now commonly used in the medical fields as dental and bone implants. Surgical cermets are used regularly. Joint replacements are commonly coated with<unk> materials to reduce wear and inflammatory response. Other examples of medical uses for<unk> s are in pacemakers, kidney dialysis machines, and respirators. The global demand on medical ceramics and ceramic components was about U.S. $9.8 billion in 2010. It was forecast to have an annual growth of 6 to 7 percent in the following years, with world market value predicted to increase to U.S. $15.3 billion by 2015 and reach U.S. $18.5 billion by 2018. Mechanical properties and composition<unk> s are meant to be used in extracorporeal circulation systems (dialysis for example) or engineered bioreactors; however, they're most common as implants. Ceramics show numerous applications as biomaterials due to their physico-chemical properties. They have the advantage of being inert in the human body, and their hardness and resistance to abrasion makes them useful for bones and teeth replacement. Some ceramics also have excellent resistance to friction, making them useful as replacement materials for malfunctioning joints. Properties such as appearance and electrical insulation are also a concern for specific biomedical applications. Some<unk> s incorporate alumina (Al2O3) as their lifespan is longer than that of the patient's. The material can be used in middle ear ossicles, ocular prostheses, electrical insulation for pacemakers, catheter orifices and in numerous prototypes of implantable systems such as cardiac pumps. Aluminosilicates are commonly used in dental prostheses, pure or in ceramic-polymer composites. The ceramic-polymer composites are a potential way to filling of cavities replacing amalgams suspected to have toxic effects. The aluminosilicates also have a glassy structure. Contrary to artificial teeth in resin, the colour of tooth ceramic remains stable Zirconia doped with yttrium oxide has been proposed as a substitute for alumina for osteoarticular prostheses. The main advantages are a greater failure strength, and a good resistance to fatigue. Vitreous carbon is also used as it is light, resistant to wear, and compatible with blood. It is mostly used in cardiac valve replacement. Diamond can be used for the same application, but in coating form. Calcium phosphate-based ceramics constitute, at present, the preferred bone substitute material in orthopaedic and maxillofacial applications, as they are similar to the main mineral phase of bone in structure and chemical composition. Such synthetic bone substitute or scaffold materials are typically porous, which provides an increased surface area that encourages osseointegration, involving cell colonisation and revascularisation. However, such porous materials generally exhibit lower mechanical strength compared to bone, making highly porous implants very delicate. Since the elastic modulus values of ceramic materials are generally higher than that of the surrounding bone tissue, the implant can cause mechanical stresses at the bone interface. Calcium phosphates usually found in<unk> s include hydroxyapatite (HAP) Ca10(PO4)6(OH)2; tricalcium phosphate β (β TCP): Ca3 (PO4)2; and mixtures of HAP and β TCP. Table 1:<unk> s Applications Devices Function Biomaterial Artificial total hip, knee, shoulder, elbow, wrist Reconstruct arthritic or fractured joints High-density alumina, metal bioglass coatings Bone plates, screws, wires Repair fractures Bioglass-metal fibre composite, Polysulphone-carbon fibre composite Intramedullary nails Align fractures Bioglass-metal fibre composite, Polysulphone-carbon fibre composite Harrington rods Correct chronic spinal curvature Bioglass-metal fibre composite, Polysulphone-carbon fibre composite Permanently implanted artificial limbs Replace missing extremities Bioglass-metal fibre composite, Polysulphone-carbon fibre composite Vertebrae Spacers and extensors Correct congenital deformity Al2O3 Spinal fusion Immobilise vertebrae to protect spinal cord Bioglass Alveolar bone replacements, mandibular reconstruction Restore the alveolar ridge to improve denture fit Polytetra fluro ethylene (PTFE) - carbon composite, Porous Al2O3, Bioglass, dense-apatite End osseous tooth replacement implants Replace diseased, damaged or loosened teeth Al2O3, Bioglass, dense hydroxyapatite, vitreous carbon Orthodontic anchors Provide posts for stress application required to change deformities Bioglass-coated Al2O3, Bioglass coated vitallium Table 2: Mechanical Properties of Ceramic Biomaterials Material Young's Modulus (GPa) CompressiveStrength (MPa) Bond strength (GPa) Hardness Density (g/cm3) Inert Al2O3 380 4000 300-400 2000-3000(HV) >3.9 ZrO2 (PS) 150-200 2000 200-500 1000-3000(HV) ≈6.0 Graphite 20-25 138 NA NA 1.5-1.9 (LTI)Pyrolitic Carbon 17-28 900 270-500 NA 1.7-2.2 Vitreous Carbon 24-31 172 70-207 150-200(DPH) 1.4-1.6 Bioactive HAP 73-117 600 120 350 3.1 Bioglass ≈75 1000 50 NA 2.5 AW Glass Ceramic 118 1080 215 680 2.8 Bone 3-30 130-180 60-160 NA NA Multipurpose A number of implanted ceramics have not actually been designed for specific biomedical applications. However, they manage to find their way into different implantable systems because of their properties and their good biocompatibility. Among these ceramics, we can cite silicon carbide, titanium nitrides and carbides, and boron nitride. TiN has been suggested as the friction surface in hip prostheses. While cell culture tests show a good biocompatibility, the analysis of implants shows significant wear, related to a delaminating of the TiN layer. Silicon carbide is another modern-day ceramic which seems to provide good biocompatibility and can be used in bone implants. Specific use In addition to being used for their traditional properties, bioactive ceramics have seen specific use for due to their biological activity. Calcium phosphates, oxides, and hydroxides are common examples. Other natural materials — generally of animal origin — such as bioglass and other composites feature a combination of mineral-organic composite materials such as HAP, alumina, or titanium dioxide with the biocompatible polymers (polymethylmethacrylate): PMMA, poly(L-lactic) acid: PLLA, poly(ethylene). Composites can be differentiated as bioresorbable or non-bioresorbable, with the latter being the result of the combination of a bioresorbable calcium phosphate (HAP) with a non-bioresorbable polymer (PMMA, PE). These materials may become more widespread in the future, on account of the many combination possibilities and their aptitude at combining a biological activity with mechanical properties similar to those of the bone. | Bioceramic | Bioactive glass | Biopharmaceutical | Covid-Organics | Biomaterial | Inhalant | Mold | Cathartic | 00
| 55,009 |
<unk> is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic. | Hypermagnesemia | Rhabdomyolysis | Hyponatremia | Hypercalcaemia | Lithium toxicity | Hypophosphatemia | Hyperkalemia | Hypernatremia | 00
| 20,254 |
Edema, also spelled oedema, and also known as fluid retention, dropsy, hydropsy and swelling, is the build-up of fluid in the body's tissue. Most commonly, the legs or arms are affected.<unk> s may include skin which feels tight, the area may feel heavy, and affected joints may be hard to move. Other<unk> s depend on the underlying cause. Causes may include venous insufficiency,<unk><unk> , kidney problems, low protein levels, liver problems, deep vein thrombosis, infections, angioedema, certain medications, and lymphedema. It may also occur after prolonged sitting or standing and during menstruation or pregnancy. The condition is more concerning if it starts suddenly, or pain or shortness of breath is present. Treatment depends on the underlying cause. If the underlying mechanism involves sodium retention, decreased salt intake and a diuretic may be used. Elevating the legs and support stockings may be useful for edema of the legs. Older people are more commonly affected. The word is from the Greek oídēma meaning 'swelling'. | symptom of Heart failure | symptom of Myocardial infarction | symptom of Arrhythmia | symptom of Pneumonia | symptom of Coronary artery disease | symptom of Pulmonary embolism | symptom of Acute liver failure | symptom of Cardiovascular disease | 00
| 4,984 |
The inheritance pattern is autosomal dominant. It is related to a mutation in the TIMP3 gene. | Sorsby's fundus dystrophy | Reis–Bucklers corneal dystrophy | Kjer's optic neuropathy | Peyronie's disease | Fleischer ring | Kayser–Fleischer ring | Meesmann corneal dystrophy | Leber's hereditary optic neuropathy | 00
| 69,791 |
<unk> is a condition where a lymphangioma is not present in a single localised mass, but in a widespread or multifocal manner. It is a rare type of tumor which results from an abnormal development of the lymphatic system. It is thought to be the result of congenital errors of lymphatic development occurring prior to the 20th week of gestation.<unk> is a condition marked by the presence of cysts that result from an increase both in the size and number of thin-walled lymphatic channels that are abnormally interconnected and dilated. 75% of cases involve multiple organs. It typically presents by age 20 and, although it is technically benign, these deranged lymphatics tend to invade surrounding tissues and cause problems due to invasion and/or compression of adjacent structures. The condition is most common in the bones and lungs and shares some characteristics with Gorham’s disease. Up to 75% of patients with<unk> have bone involvement, leading some to conclude that<unk> and Gorham’s disease should be considered as a spectrum of disease rather than separate diseases. When it occurs in the lungs,<unk> has serious consequences and is most aggressive in the youngest children. When the condition extends into the chest it commonly results in the accumulation of chyle in the linings of the heart and/or lungs. Chyle is composed of lymph fluid and fats that are absorbed from the small intestine by specialized lymphatic vessels called lacteals during digestion. The accumulations are described based on location: chylothorax is chyle in the chest; chylopericardium is chyle trapped inside the sack surrounding the heart; chyloascites is chyle trapped in the linings of the abdomen and abdominal organs. The presence of chyle in these places accounts for many of the symptoms and complications associated with both<unk> and Gorham’s disease. The incidence of<unk> is unknown and it is often misdiagnosed. It is separate and distinct from lymphangiectasis, lymphangioleiomyomatosis (LAM), pulmonary capillary hemangiomatosis, Kaposi’s sarcoma, and kaposiform hemangioendothelioma. Its unusual nature makes<unk> (and Gorham’s disease) a diagnostic and therapeutic challenge. A multidisciplinary approach is generally necessary for optimal diagnosis and symptom management. The term literally means lymphatic system (lymph) vessel (angi) tumor or cyst (oma) condition (tosis). | Lymphangiomatosis | Lymphangitis carcinomatosa | Angiomatosis | Papillomatosis | Universal angiomatosis | Fibromatosis | Chorangiosis | Tuberculous gumma | 00
| 40,862 |
Only some<unk> s such as influenza are contagious and commonly believed infectious. The microorganisms that cause these<unk> s are known as pathogens and include varieties of bacteria, viruses, protozoa, and fungi. Infectious<unk> s can be transmitted, e.g. by hand-to-mouth contact with infectious material on surfaces, by bites of insects or other carriers of the<unk> , and from contaminated water or food (often via fecal contamination), etc. Also, there are sexually transmitted<unk> s. In some cases, microorganisms that are not readily spread from person to person play a role, while other<unk> s can be prevented or ameliorated with appropriate nutrition or other lifestyle changes. Some<unk> s, such as most (but not all) forms of cancer, heart<unk> , and mental<unk> orders, are non-infectious<unk> s. Many non-infectious<unk> s have a partly or completely genetic basis (see genetic<unk> order) and may thus be transmitted from one generation to another. Social determinants of health are the social conditions in which people live that determine their health. Illnesses are generally related to social, economic, political, and environmental circumstances. Social determinants of health have been recognized by several health organizations such as the Public Health Agency of Canada and the World Health Organization to greatly influence collective and personal well-being. The World Health Organization's Social Determinants Council also recognizes Social determinants of health in poverty. When the cause of a<unk> is poorly understood, societies tend to mythologize the<unk> or use it as a metaphor or symbol of whatever that culture considers evil. For example, until the bacterial cause of tuberculosis was<unk> covered in 1882, experts variously ascribed the<unk> to heredity, a sedentary lifestyle, depressed mood, and overindulgence in sex, rich food, or alcohol, all of which were social ills at the time. When a<unk> is caused by a pathogenic organism (e.g., when malaria is caused by Plasmodium), one should not confuse the pathogen (the cause of the<unk> with<unk> itself. For example, West Nile virus (the pathogen) causes West Nile fever (the<unk> . The misuse of basic definitions in epidemiology is frequent in scientific publications. Types of causes Regular physical activity, such as riding a bicycle or walking, reduces the risk of lifestyle<unk> s. ;Airborne: An airborne<unk> is any<unk> that is caused by pathogens and transmitted through the air. ;Foodborne: Foodborne illness or food poisoning is any illness resulting from the consumption of food contaminated with pathogenic bacteria, toxins, viruses, prions or parasites. ;Infectious: Infectious<unk> s, also known as transmissible<unk> s or communicable<unk> s, comprise clinically evident illness (i.e., characteristic medical signs or symptoms of<unk> resulting from the infection, presence and growth of pathogenic biological agents in an individual host organism. Included in this category are contagious<unk> s – an infection, such as influenza or the common cold, that commonly spreads from one person to another – and communicable<unk> s – a<unk> that can spread from one person to another, but does not necessarily spread through everyday contact. ; Lifestyle: A lifestyle<unk> is any<unk> that appears to increase in frequency as countries become more industrialized and people live longer, especially if the risk factors include behavioral choices like a sedentary lifestyle or a diet high in unhealthful foods such as refined carbohydrates, trans fats, or alcoholic beverages. ; Non-communicable: A non-communicable<unk> is a medical condition or<unk> that is non-transmissible. Non-communicable<unk> s cannot be spread directly from one person to another. Heart<unk> and cancer are examples of non-communicable<unk> s in humans. | Disease | Precancerous condition | Cancer | Psychopathology | Drug | Drug | Cancer cluster | Suboptimal health | 00
| 773 |
<unk> incidence; most common in Asia, Africa, Central and South America In 2000,<unk> caused an estimated 21.7 million illnesses and 217,000 deaths. It occurs most often in children and young adults between 5 and 19 years old. In 2013, it resulted in about 161,000 deaths – down from 181,000 in 1990. Infants, children, and adolescents in south-central and Southeast Asia have the highest rates of typhoid. Outbreaks are also often reported in sub-Saharan Africa and Southeast Asia. In 2000, more than 90% of morbidity and mortality due to<unk> occurred in Asia. In the U.S., about 400 cases occur each year, 75% of which are acquired while traveling internationally. Before the antibiotic era, the case fatality rate of<unk> was 10%–20%. Today, with prompt treatment, it is less than 1%, but 3%–5% of people who are infected develop a chronic infection in the gall bladder. Since S. enterica subsp. enterica serovar Typhi is human-restricted, these chronic carriers become the crucial reservoir, which can persist for decades for further spread of the disease, further complicating its identification and treatment. Lately, the study of S. enterica subsp. enterica serovar Typhi associated with a large outbreak and a carrier at the genome level provides new insight into the pathogenesis of the pathogen. In industrialized nations, water sanitation and food handling improvements have reduced the number of typhoid cases. Developing nations, such as those in parts of Asia and Africa, have the highest rates. These areas lack access to clean water, proper sanitation systems, and proper health-care facilities. In these areas, such access to basic public-health needs is not expected in the near future. In 2004–2005 an outbreak in the Democratic Republic of Congo resulted in more than 42,000 cases and 214 deaths. Since November 2016, Pakistan has had an outbreak of extensively drug-resistant (XDR)<unk> . In Europe, a report based on data for 2017 retrieved from The European Surveillance System (TESSy) on the distribution of confirmed typhoid and paratyphoid<unk> cases found that 22 EU/EEA countries reported a total of 1,098 cases, 90.9% of which were travel-related, mainly acquired during travel to South Asia. | Typhoid fever | Leptospirosis | Trench fever | Lassa fever | Cotton fever | Boutonneuse fever | Yellow fever | Paratyphoid fever | 00
| 2,273 |
It is an inhibitor of the enzyme janus kinase 1 (JAK1) and janus kinase 3 (JAK 3), which means that it interferes with the JAK-STAT signaling pathway, which transmits extracellular information into the cell nucleus, influencing DNA transcription. In a mouse model of established arthritis,<unk> rapidly improved disease by inhibiting the production of inflammatory mediators and suppressing STAT1-dependent genes in joint tissue. This efficacy in this disease model correlated with the inhibition of both JAK1 and JAK3 signaling pathways, suggesting that<unk> may exert therapeutic benefit via pathways that are not exclusive to inhibition of JAK3. | Tofacitinib | Ocrelizumab | Belatacept | Etanercept | Ibalizumab | Sarilumab | Theralizumab | Atezolizumab | 00
| 60,446 |
A demonstration of a common mechanism of a<unk> in a car accident. The mechanism of the injury is forcible hyperextension of the head, usually with distraction of the neck. Traditionally this would occur during judicial hanging, when the noose was placed below the condemned subject's chin. When the subject was dropped, the head would be forced into hyperextension by the full weight of the body, a sufficient force to cause the fracture. However, despite its long association with judicial hangings, one study of a series of such hangings showed that only a small minority of hangings produced a<unk> . Apart from hangings, the mechanism of injury—a sudden forceful hyperextension centered just under the chin—occurs mainly with deceleration injuries in which the victim's face or chin strike an unyielding object with the neck in extension. The most common scenario is a frontal motor vehicle accident with an unrestrained passenger or driver, with the person striking the dashboard or windshield with their face or chin. Other scenarios include falls, diving injuries, and collisions between players in contact sports. Although a<unk> is unstable, survival from this fracture is relatively common, as the fracture itself tends to expand the spinal canal at the C2 level. It is not unusual for patients to walk in for treatment and have such a fracture discovered on X-rays. Only if the force of the injury is severe enough that the vertebral body of C2 is severely subluxed from C3 does the spinal cord become crushed, usually between the vertebral body of C3 and the posterior elements of C1 and C2. | Hangman's fracture | Pott's fracture | Smith's fracture | Bennett's fracture | Bosworth fracture | Smith fracture | Duverney fracture | March fracture | 00
| 38,810 |
Vertebrobasillar<unk> * Hemifacial spasm * Paresis * Trigeminal neuralgia Internal carotid<unk> * Progressive visual field defect | Intracranial dolichoectasias | Vein of Galen aneurysmal malformations | Chiari malformation | Porencephaly | Periventricular leukomalacia | Hydrocephalus | Cavernous venous malformation | Intraventricular hemorrhage | 00
| 39,638 |
<unk> , also known as red burning skin and<unk> dermatitis, has been reported in people who apply topical<unk> s for 2 weeks or longer and then discontinue use. Symptoms affect the skin and include redness, a burning sensation, and itchiness, which may then be followed by peeling. This condition generally requires the daily application of a topical<unk> for more than 2 weeks but sometimes can occur with even less<unk> use. It appears to be a specific adverse effect of topical corticosteroid use. People with atopic dermatitis are most at risk. Treatment involves discontinuing the use of topical<unk> s, either gradually or suddenly. Counselling and cold compresses may also help. The condition is common, with thousands of people congregating in online communities to support one another throughout the healing process. Many cases have been reported in both adults and children. It was first described in 1979. | Topical steroid withdrawal | Topical glucocorticoids | Eyelid revision | Phototherapeutic keratectomy | Topical medication | Ozone therapy | Artificial tears | Corneal transplantation | 00
| 68,492 |
A<unk> <unk> , also known as an intensive care nursery (ICN), is an intensive care unit (ICU) specializing in the care of ill or premature newborn infants.<unk> refers to the first 28 days of life.<unk> care, as known as specialized nurseries or intensive care, has been around since the 1960s. The first American newborn intensive care unit, designed by Louis Gluck, was opened in October 1960 at Yale New Haven Hospital.<unk> is typically directed by one or more<unk> ogists and staffed by resident physicians, nurses, nurse practitioners, pharmacists, physician assistants, respiratory therapists, and dietitians. Many other ancillary disciplines and specialists are available at larger units. The term<unk> comes from neo, "new", and natal, "pertaining to birth or origin". | Neonatal intensive care unit | Pediatric intensive care unit | Outline of cardiology | Post-anesthesia care unit | Birthing center | Operating theater | Intensive care unit | Operating room management | 00
| 23,293 |
The initial symptoms of<unk> intoxication include central nervous system depression, headache, dizziness, nausea, lack of coordination, and confusion. Sufficiently large doses cause unconsciousness and death. The initial symptoms of<unk> exposure are usually less severe than the symptoms from the ingestion of a similar quantity of<unk> . Once the initial symptoms have passed, a second set of symptoms arises, from 10 to as many as 30 hours after the initial exposure, that may include blurring or complete loss of vision, acidosis, and putaminal hemorrhages, an uncommon but serious complication. These symptoms result from the accumulation of toxic levels of formate in the blood, and may progress to death by respiratory failure. Physical examination may show tachypnea, and eye examination may show dilated pupils with hyperemia of the optic disc and retinal edema. | Methanol toxicity | Toxic alcohol | Tin poisoning | Infection | Sulfuric acid poisoning | Serotonin syndrome | Hydrocarbon poisoning | Diabetic ketoacidosis | 00
| 65,591 |
<unk> is a corticosteroid drug with<unk> ominant glucocorticoid and low mineralocorticoid activity, making it useful for the treatment of a wide range of inflammatory and autoimmune conditions such as asthma, uveitis, pyoderma gangrenosum, rheumatoid arthritis, urticaria, angioedema, ulcerative colitis, pericarditis, temporal arteritis and Crohn's disease, Bell's palsy, multiple sclerosis, cluster headaches, vasculitis, acute lymphoblastic leukemia and autoimmune hepatitis, systemic lupus erythematosus, Kawasaki disease, dermatomyositis, and sarcoidosis.<unk> acetate ophthalmic suspension (eye drops) is an adrenocortical steroid<unk> oduct,<unk> epared as a sterile ophthalmic suspension and used to reduce swelling, redness, itching, and allergic reactions affecting the eye. It has been explored as a treatment option for bacterial keratitis.<unk> can also be used for allergic reactions ranging from seasonal allergies to drug allergic reactions.<unk> can also be used as an immunosuppressive drug for organ transplants.<unk> in lower doses can be used in cases of<unk> imary adrenal insufficiency (Addison's disease). Corticosteroids inhibit the inflammatory response to a variety of inciting agents and, it is<unk> esumed, delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary<unk> oliferation, fibroblast<unk> oliferation, deposition of collagen, and scar formation with inflammation. | Prednisolone | Methylprednisolone | Prednisone | Methylprednisolone succinate | Methylprednisolone acetate | Cyclofenil | Methylprednisolone aceponate | Triamcinolone | 00
| 15,356 |
A number of preventative measures are recommended, including avoiding straining while attempting to defecate, avoiding constipation and diarrhea either by eating a high-fiber diet and drinking plenty of fluid or by taking fiber supplements, and getting sufficient exercise. Spending less time attempting to defecate, avoiding reading while on the toilet, and losing weight for overweight persons and avoiding heavy lifting are also recommended. | Hemorrhoid | Anal cancer | Anal fissure | Anorectal varices | Hematocolpos | Pyometra | Rectitis | Anal fistula | 00
| 7,029 |
<unk> is a diagnostic classification for some DSM-IV Axis II<unk> disorders not<unk> listed in DSM-IV. The DSM-5 does not have an equivalent to<unk> Disorder NOS. However<unk> disorder-trait specified (PD-TS) remains under consideration for future revisions. The DSM 5 "Unspecified Disorder" is not a<unk> disorder, it is used to enhance specificity of an existing disorder or it is an emergency diagnosis unto itself (i.e. Unspecified Mental Disorder, 300.9), without being attached to another disorder. | Personality disorder not otherwise specified | Disruptive mood dysregulation disorder | Dissociative disorder not otherwise specified | Bipolar disorder not otherwise specified | Depressive personality disorder | Bipolar I disorder | Other specified dissociative disorder | Bipolar II disorder | 00
| 54,180 |
The precise mechanism of action for<unk> is not known, although efforts to identify<unk> 's teratogenic action generated 2,000 research papers and the proposal of 15 or 16 plausible mechanisms by 2000. As of 2015, the main theories were inhibition of the process of angiogenesis, its inhibition of cereblon, a ubiquitin ligase, and its ability to generate reactive oxygen species which in turn kills cells. In 2018, results were first published which suggested that<unk> 's teratogenic effects are mediated through degradation of the transcription factor, SALL4, an as yet unverified finding.<unk> also binds to and acts as an antagonist of the androgen receptor (AR) and hence is a nonsteroidal antiandrogen (NSAA) of some capacity. In accordance, it can produce gynecomastia and sexual dysfunction as side effects in men.<unk> is provided as a racemic mixture of two enantiomers; while there are reports that only one of the enantiomers may cause birth defects, the body converts each enantiomer into the other through mechanisms that are not well understood. | Thalidomide | Pomalidomide | Vincristine | Lenalidomide | Mercaptopurine | Febuxostat | Ifosfamide | Ixazomib | 00
| 3,495 |
The pathogenesis of<unk> is not well understood or documented like other diseases of this nature. Even though<unk> is a disease that results in neurological defects, its pathogenesis occurs in areas that reside outside of the nervous system. There was a strong deposition of PrPSc initially located in the ileal Peyer's patches of the small intestine. The lymphatic system has been identified in the pathogenesis of scrapie. It has not, however, been determined to be an essential part of the pathogenesis of<unk> . The Ileal Peyer's patches have been the only organ from this system that has been found to play a major role in the pathogenesis. Infectivity of the Ileal Peyer's patches has been observed as early as 4 months after inoculation. PrPSc accumulation was found to occur mostly in tangible body macrophages of the Ileal Peyer's patches. Tangible body macrophages involved in PrPSc clearance are thought to play a role in PrPSc accumulation in the Peyer's patches. Accumulation of PrPSc was also found in follicular dendritic cells; however, it was of a lesser degree. Six months after inoculation, there was no infectivity in any tissues, only that of the ileum. This led researchers to believe that the disease agent replicates here. In naturally confirmed cases, there have been no reports of infectivity in the Ileal Peyer's patches. Generally, in clinical experiments, high doses of the disease are administered. In natural cases, it was hypothesized that low doses of the agent were present, and therefore, infectivity could not be observed. | Bovine spongiform encephalopathy | Variant Creutzfeldt–Jakob disease | Creutzfeldt–Jakob disease | Powassan encephalitis | Saint Louis encephalitis | Eastern equine encephalitis | Japanese encephalitis | Viliuisk encephalomyelitis | 00
| 51,781 |
The efficacy of<unk> s has been assessed on various wound types. There is some evidence to suggest that<unk> s are effective dressings for chronic wounds including pressure ulcers, diabetic ulcers, and venous ulcers although the results are uncertain.<unk> s have been shown to accelerate healing in partial and full thickness burn wounds of varying size. Other studies have shown that<unk> s accelerate healing in radioactive skin injuries and dog bite wounds.<unk> s decrease the healing time of traumatic skin injuries by an average 5.28 days and reduce the pain reported by patients. | Hydrogel dressing | Hydrocolloid dressing | Alginate dressing | Occlusive dressing | Wound closure strip | Surgical tape | Surgical suture | Polymer sponge | 00
| 69,857 |
The primary manifestations are thrombocytopenia and megakaryocytopenia, or low numbers of platelets and megakaryocytes. There is an absence of megakaryocytes in the bone marrow with no associated physical abnormalities. | Congenital amegakaryocytic thrombocytopenia | X linked thrombocytopenia | Drug-induced thrombocytopenic purpura | Gray platelet syndrome | Quebec platelet disorder | Immune thrombocytopenic purpura | Essential thrombocythemia | Harris platelet syndrome | 00
| 54,107 |
Despite outgoing research, the cause of<unk> is not entirely clear. Inflammation is thought to play a role as well as damage to the venous valves from the thrombus itself. This valvular incompetence combined with persistent venous obstruction from thrombus increases the pressure in veins and capillaries. Venous hypertension induces a rupture of small superficial veins, subcutaneous hemorrhage and an increase of tissue permeability. That is manifested by pain, swelling, discoloration, and even ulceration. | Post-thrombotic syndrome | Fibrinolysis syndrome | Thrombotic storm | Acute limb ischaemia | Painful bruising syndrome | Deep vein thrombosis | Superficial vein thrombosis | Orthostatic purpura | 00
| 40,255 |
<unk> is a radiation therapy modality, in which the patient is scanned across a modulated strip-beam, so that only one “slice” (Greek prefix “tomo-”) of the target is exposed at any one time by the linear accelerator (linac) beam. The three components distinctive to this modality are: (1) a collimator pair that defines the length of the strip, (2) a binary multileaf collimator whose leaves open and close during treatment to modulate the strip’s intensity, and (3) a couch that scans the patient across the beam at a fixed speed during the treatment delivery. | Tomotherapy | Chemoradiotherapy | External beam radiotherapy | Selective internal radiation therapy | Plaque radiotherapy | Image-guided radiation therapy | Irradiation | Radiation therapy | 00
| 44,855 |
Class switch recombination Different genetic defects cause HIgM syndrome, the vast majority are inherited as an X-linked recessive genetic trait and most sufferers are male. IgM is the form of antibody that all B cells produce initially before they undergo class switching. Healthy B cells efficiently switch to other types of antibodies as needed to attack invading bacteria, viruses, and other pathogens. In people with hyper IgM syndromes, the B cells keep making IgM antibodies because can not switch to a different antibody. This results in an overproduction of IgM antibodies and an underproduction of IgA, IgG, and IgE. | Hyper-IgM syndrome type 4 | Hyper-IgM syndrome type 5 | Hyper-IgM syndrome type 2 | Hyper-IgM syndrome type 3 | Hyper-IgM syndrome type 1 | Hyper IgM syndrome | Anti-IgLON5 disease | Wiskott–Aldrich syndrome | 00
| 51,826 |
Affected anatomy Human ear anatomy. Note: The complete anatomy of the human ear is extensive, and can be divided into the inner ear and outer ear. The remainder of this article mainly references the cochlea, outer hair cells, and organ of Corti. In general, structural damages to any anatomical part of the human ear can cause hearing-related problems. Usually, minor bending of the stereocilia of the inner ear is associated with temporary hearing loss and is involved in<unk> . Complete loss of the stereocilia causes permanent hearing damage and is more associated with noise-induced hearing loss and other<unk> diseases. The outer hair cells, or OHCs, can be thought of as microamplifiers that provide stimulation to the inner hair cells. The OHCs are the most fragile of the hair cells, hence their involvement in<unk> and other hearing impairments. The hearing organ in fish is called an otolith, which is sensitive to particle motion, not sound pressure. Some fish also have a lateral line. + Location of anatomical parts 350px 350px 350px Inner ear showing cochlea Cochlea showing organ of Corti Organ of Corti showing hair cells Affected mechanisms Traveling wave theory Temporary threshold shifts related to<unk> are related to the amplitude of a stimulus-driven traveling wave. This is believed to be true because the vibration propagated by the active process is not usually at the center of the maximum amplitude of this wave. Instead, it is located much further down and the differences associated between them explain the shift in threshold. The TTS that is experienced is the exhaustion of the active system located at the locus of the traveling wave driven by the cochlear amplifier described below.<unk> can be explained by the relative activity of the active process at low-level stimulation (<30 dB). Classical passive system There are two different systems associated with the mechanics of the cochlea: the classical passive system and an active process. The passive system works to stimulate the inner hair cells directly and works at levels above 40 dB. At stimulation levels that prevent the excitation of the passive system, prolonged noise exposure results in a decrease in the loudness heard over time, even when the actual intensity of the noise has not changed. This is caused by the exhaustion of the active process. Active process The active process is also known as the cochlear amplifier. This amplification increases vibrations of the basilar membrane through energy obtained from the Organ of Corti. As the stimulation increases, it is assumed that basilar membrane displacement, caused by the traveling wave, becomes continually more basal in regards to the cochlea. A sustained low-level stimulus can cause an energetic exhaustion of the active system which in turn prevents the passive system from activating. Excessive vibrations Currently it is believed that<unk> and NIHL are related to excessive vibrations of the inner ear which may cause structural damages. Metabolic activity is required in order to maintain the electrochemical gradients used in mechano-electrical and electro-mechanical transduction during noise exposure and sound recognition. The metabolic activity is associated with active displacements which are components of the sound-induced vibration involving prestin, a motor protein that causes OHC motility. Excess vibrations require increased metabolic energy. In addition, these extra vibrations can cause the formation of free radicals known as reactive oxygen species or ROS. Elevated levels of ROS continue to increase the metabolic demands of the system. These increasing demands fatigue the system and eventually lead to structural damages to the Organ of Corti. Recovery In all cases of<unk> , sufficient recovery time should allow full correction of the hearing impairment and return threshold levels to their baseline values. There is currently no way to estimate the amount of time needed to recover from<unk> because it is not usually detectable until after the injury has already occurred. Studies that measured recovery time have noted that the time required is related to the magnitude of the initial hearing loss. The most significant recovery was found to occur during the first 15 minutes following cessation of the noise exposure. When sufficient recovery time is not allotted, the effects become permanent, resulting in acquired noise-induced hearing loss. Up to 120 minutes of recovery time can be required of noises of only 95 dB. For comparison, common items that can produce noise at this level are motorcycles and subways. Protective measures Toughening and energy spread Two protective measures have been investigated related to the amount of noise exposure and the duration of that exposure. Although these would be hard to regulate in spontaneous occurrences, they could have a positive effect on work conditions if guidelines could be set for machining times or for other systems that produce loud noises over a long period of time. The toughening effect is put in place by increasing the system's resistance to noise over time. Currently, the specific mechanisms that cause the cochlear toughening are not known. However, the OHCs and related processes are known to play a role. The other toughening measure is to spread a given amount of energy to the system over a longer amount of time. This would allow recovery processes to take place during the quiet interludes that are gained by increasing the exposure duration. So far, studies have not shown a direct correlation between the amount of toughening and the amount of threshold shift experienced. This suggests that even a toughened cochlea may not be completely protected. Substances Both furosemide and salicylic acid are considered ototoxic at certain doses. Research has been done to determine their ability to protect against<unk> and permanent damage through toughening phenomena, a state described by reduced active cochlear displacements. Although limited research has been done with these two substances in terms of protective drug regimes because of their associated risks, both have shown positive results in reducing<unk> by the decrease in ROS formation through individual mechanisms described below. Furosemide Furosemide injections prior to noise exposure have been shown to decrease the endocochlear potential. This decrease results in a reduction of active cochlear displacements and it is believed that the protection by furosemide stems from the limitation of excessive vibrations while the cochlear amplifier is depressed. Salicylic acid Salicylic acid competitively interferes with anion binding to OHC prestin which thereby reduces motility. This reduction in active displacement is again associated with depression of the cochlear amplifier which decreases the excessive vibrations experienced during noise-exposure. Antioxidants Vitamins A, C and E have been shown to be 'free radical scavengers' by studies looking for protective tendencies of antioxidants. In addition, NAC, or N-acetyl-L-cysteine (acetylcysteine), has been shown to reduce ROS formation associated with the excessive vibrations induced by the noise exposure. Limitations Although<unk> and NIHL protective measures would be helpful for those who are constantly exposed to long and loud noises, current research is limited due to the negative associations with the substances. Furosemide is used in congestive heart failure treatments because of its diuretic properties. Salicylic acid is a compound most frequently used in anti-acne washes, but is also an anticoagulant. Further uses of these substances would need to be personalized to the individual and only under close monitoring. Antioxidants do not have these negative effects and therefore are the most commonly researched substance for the purpose of protecting against<unk> . However, at this time there has been no marketed application. In addition, no synergistic relationships between the drugs on the degree of reduction of<unk> have been discovered at this time. | Auditory fatigue | Olfactory fatigue | Auditory exclusion | Nyctalopia | Ocular dysmetria | Physiological anisocoria | Mechanical anisocoria | Cyclopia | 00
| 60,056 |
Focal epilepsy<unk> is effective as single-drug treatment for newly diagnosed focal epilepsy in adults. It reduces focal seizures by 50% or more as an add-on medication. Partial-complex epilepsy<unk> is effective as add-on treatment for partial (focal) epilepsy. Generalized epilepsy<unk> is effective for treatment of generalized tonic-clonic epilepsy. It has been approved in the United States as add-on treatment for myoclonic, and tonic-clonic seizures.<unk> has been approved in the European Union as a monotherapy treatment for epilepsy in the case of partial seizures or as an adjunctive therapy for partial, myoclonic, and tonic-clonic seizures.<unk> is sometimes used off label to treat status epilepticus. Prevention of seizures Based on low-quality evidence,<unk> is about as effective as phenytoin for prevention of early seizures after traumatic brain injury. It may be effective for prevention of seizures associated with subarachnoid hemorrhages. Other<unk> has not been found to be useful for treatment of neuropathic pain, nor for treatment of essential tremors.<unk> has not been found to be useful for treating autism, but is an effective treatment for partial, myoclonic, or tonic-clonic seizures associated with autism spectrum disorder. Special groups Studies in female pregnant rats have shown minor fetal skeletal abnormalities when given maximum recommended human doses of<unk> orally throughout pregnancy and lactation. Studies were conducted to look for increased adverse effects in the elderly population as compared to younger patients. One such study published in Epilepsy Research showed no significant increase in incidence of adverse symptoms experienced by young or elderly patients with central nervous system (CNS) disorders.<unk> may be safely used with caution in children over the age of four. However, it has not been determined whether it can be safely given to children under the age of four. | Levetiracetam | Piracetam | Phenylpiracetam | Mesuximide | Dimiracetam | Brivaracetam | Lamotrigine | Ethosuximide | 00
| 16,107 |
CHAPLE is characterized by severe protein-losing enteropathy leading to hypoproteinemia. Symptoms can include abdominal pain, nausea, vomiting, diarrhea, loss of appetite, weight loss, and edema. People also have chronic malabsorption, which causes deficiencies in iron, ferritin, calcium, magnesium, folate, vitamin D and vitamin B12. Some patients may have recurrent respiratory infections associated with hypogammaglobulinemia. Severe thrombotic vascular occlusions may also be found among these patients. | CD55 deficiency | CD25 deficiency | MBL deficiency | Complement 2 deficiency | Complement 3 deficiency | Leukocyte adhesion molecule deficiency | Caspase-8 deficiency | CDKL5 deficiency disorder | 00
| 70,886 |
During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mmHg) than the right ventricle (~20 mmHg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms. In serious cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure. This reverses the left to right shunt, so that blood then flows from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation. This effect is more noticeable in patients with larger<unk> s, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller<unk> s may be asymptomatic. Four different septal<unk> s exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly. | Ventricular septal defect | Heart septal defect | Atrioventricular septal defect | Atrial septal defect | Aortopulmonary septal defect | Tricuspid atresia | Double aortic arch | Double inlet left ventricle | 00
| 18,147 |
Seizures are managed with anticonvulsive medications. Laser coagulation or cryoablation (freezing) of the retina can be used to destroy the abnormal blood vessels. Retinal detachment is repaired with a scleral buckle or with vitrectomy. Removal or enucleation of the eye is a last resort option if the eye already has become blind and painful. Repeated blood transfusions may be needed to control anemia, and thrombocytopenia can be managed with splenectomy. | Cerebroretinal microangiopathy with calcifications and cysts | Intraretinal microvascular abnormalities | Punctate inner choroiditis | Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations | Chronic relapsing inflammatory optic neuropathy | Diffuse unilateral subacute neuroretinitis | Progressive outer retinal necrosis | Giant retinal ganglion cells | 00
| 62,630 |
Under the law of England and Wales regarding insanity and unfitness to plead, once a court has determined that the defendant is subject to a disability that prevents their<unk> progressing, there may be a<unk> " in which the truth of the allegations against the defendant, as opposed to their guilt or innocence of a crime, is to be determined. The court's options are: to order an absolute discharge; a supervision order; or a hospital order (with or without a restriction order). The<unk> is not a criminal<unk> to determine guilt or otherwise; it is "limited to ensuring that the interference with the liberty of the defendant consequent upon whatever order might be made following an adverse finding can be justified by reference to what can be proved about what he or she did, even if intention might have been clouded by delusion or other incapacity." | Trial of the facts | Theory of indispensable attributes | Partner notification | Manning criteria | Sustainability and transformation plan | Chain of survival | Outline of medicine | Certificate of medical necessity | 00
| 68,287 |
Frequent serum GH measurements in normal subjects (left panel) demonstrate that GH can fluctuate between undetectable levels most of the time interspersed with peaks of up to 30 μg/L (90 mIU/L); in acromegaly (right panel) GH hypersecretion is continuous with no undetectable levels. If acromegaly is suspected, medical laboratory investigations followed by medical imaging if the lab tests are positive confirms or rules out the presence of this condition. IGF1 provides the most sensitive lab test for the diagnosis of acromegaly, and a GH suppression test following an oral glucose load, which is a very specific lab test, will confirm the diagnosis following a positive screening test for IGF1. A single value of the GH is not useful in view of its pulsatility (levels in the blood vary greatly even in healthy individuals).Magnetic resonance image of a pituitary macroadenoma that caused acromegaly with compression of the optic chiasm GH levels taken 2 hours after a 75- or 100-gram glucose tolerance test are helpful in the diagnosis: GH levels are suppressed below 1 μg/L in normal people, and levels higher than this cutoff are confirmatory of acromegaly. Other pituitary hormones must be assessed to address the secretory effects of the tumor, as well as the mass effect of the tumor on the normal pituitary gland. They include thyroid stimulating hormone (TSH), gonadotropic hormones (FSH, LH), adrenocorticotropic hormone, and prolactin. An MRI of the brain focusing on the sella turcica after gadolinium administration allows for clear delineation of the pituitary and the hypothalamus and the location of the tumor. A number of other overgrowth syndromes can result in similar problems. Differential diagnosis Pseudoacromegaly is a condition with the usual acromegaloid features, but without an increase in growth hormone and IGF-1. It is frequently associated with insulin resistance. Cases have been reported due to minoxidil at an unusually high dose. It can also be caused by a selective post receptor defect of insulin signalling, leading to the impairment of metabolic, but preservation of mitogenic, signalling. | symptom of Congenital generalized lipodystrophy | symptom of Laron syndrome | symptoms of Rotor syndrome | symptom of Prader–Willi syndrome | picture of Congenital hypothyroidism | symptom of Scheuermann's disease | symptom of Maroteaux–Lamy syndrome | symptom of Rotor syndrome | 00
| 53,451 |
<unk> (or<unk> sex or penitentiary sex) consists of sexual relationships between<unk> ers or between a<unk> er and a<unk> employee or other persons to whom<unk> ers have access. Since<unk> s are usually separated by sex, most sexual activity is with a same-sex partner. Exceptions to this consist of sex during conjugal visits and sex with an employee of the opposite sex.<unk> is an issue that has been commonly misunderstood and misrepresented due not only to the taboo nature of the subject, but also because of a lack of research. The most common kind of sexual activity in<unk> s is consensual sex. A 2011 study developed a taxonomy for different types of sexual behaviors in women's<unk> . They include suppression, in which an inmate chooses celibacy (i.e. refrains from sexual activity while in<unk> , most commonly to stay loyal to a partner who is outside of<unk> ; autoeroticism (i.e. masturbation); true homosexuality (consensual sex between inmates who were already homosexual before entering<unk> ; situational homosexuality (consensual sex between inmates who have homosexual experiences for the first time in<unk> ; and sexual violence (which can be between inmates or between a staff member and an inmate. Sexual violence includes coercion, manipulation, and compliance. Manipulation is performed for power or some kind of reward. Compliance occurs to obtain safety, protection, or out of fear). In general,<unk> er-prisoner relationships are same-sex relationships because<unk> s are generally segregated by sex. An example of an exception to this general rule took place in Canada at the Sainte-Anne-des-Plaines<unk> . There, two convicted killers of the opposite sex, Karla Homolka and Jean-Paul Gerbet, were able to engage in sexual activity through a chain-link fence, which was the only barrier separating men and women. This<unk> is Canada's highest security<unk> in which inmates of either sex may be sent if considered especially dangerous. | Prison sexuality | Self-hatred | Bullying in medicine | Sexual addiction | Sexually active life expectancy | Extended female sexuality | Effects and aftermath of rape | Somatic experiencing | 00
| 9,807 |
<unk> , sold under many brand names, is a benzodiazepine. It is mainly an anti-anxiety agent with similar side effects to diazepam (Valium). In addition to being used to treat anxiety or panic states,<unk> may be used as a premedicant prior to minor surgery.<unk> typically comes in doses of 3 mg and 6 mg tablets. It was patented in 1961 by Roche and approved for medical use in 1974. | Bromazepam | Triazolam | Quazepam | Halazepam | Oxazepam | Adinazolam | Remimazolam | Flutazolam | 00
| 20,763 |
Established in 1969, the<unk> is one of America's longest running treatment<unk> s for individuals who struggle with excess weight, a sedentary lifestyle, and associated health problems. The<unk> is designed for adults age 18 and up and dedicated to education about and exploration of major components of successful lifestyle change including nutrition,<unk> , behavioral health, medical management, and ongoing support. | Duke Diet and Fitness Center | Licensed behavior analyst | Handbook on Drug and Alcohol Abuse | PhenX Toolkit | Suffolk GP Federation | Mental health counselor | Hellenic Athletic Federation of the Deaf | Mental health tribunal | 00
| 41,697 |
<unk> (), sold under the brand name Koselugo, is a medication for the treatment of children, two years of age and older, with neurofibromatosis type I (NF-1), a genetic disorder of the nervous system causing tumors to grow on nerves. It is taken by mouth. Common side effects include headache, abdominal pain and other problems of the gastrointestinal tract, fatigue, muscle pain, as well as dry skin and other skin problems.<unk> was approved for medical use in the United States in April 2020. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication. | Selumetinib | Binimetinib | Cobimetinib | Pralsetinib | Lestaurtinib | Axitinib | Mobocertinib | Gefitinib | 00
| 61,433 |
Conservative treatment involves the long term use of laxatives and enemas, and has limited success. Dietary changes in order to control the disease are ineffective and high fiber diets often worsen the symptoms in children. As a last resort, surgical treatment (internal sphincter myectomy or colon resection) is used. In extreme cases, the only effective cure is a complete transplant of the affected parts. | Intestinal neuronal dysplasia | Autoimmune gastrointestinal dysmotility | Small intestinal bacterial overgrowth | Foreign body in alimentary tract | Exocrine pancreatic insufficiency | Non-celiac gluten sensitivity | Small intestine neuroendocrine tumor | Familial multiple intestinal atresia | 00
| 28,584 |
<unk> is a general term for inflammation or infection of the ear, in both humans and other animals. When infection is present, it may be viral or bacterial. When inflammation is present due to fluid build up in the middle ear and infection is not present it is considered<unk> media with effusion. It is subdivided into the following: *<unk> externa, external<unk> , or "swimmer's ear", involves the outer ear and ear canal. In external<unk> , the ear hurts when touched or pulled. *<unk> media, or middle ear infection, involves the middle ear. In<unk> media, the ear is infected or clogged with fluid behind the ear drum, in the normally air-filled middle-ear space. This the most common infection and very common in babies below 6 months sometimes requires a surgical procedure called myringotomy and tube insertion. *<unk> interna, or labyrinthitis, involves the inner ear. The inner ear includes sensory organs for balance and hearing. When the inner ear is inflamed, vertigo is a common symptom. Other symptoms in adults include pain and drainage from ear or problems with hearing. Symptoms in children can include excessive crying, touching at ears, drainage, and fever. Treatment can range from increasing fluids and over the counter medicine to manage symptoms to antibiotics prescribed by medical providers. | Otitis | Chorditis | Rhinitis | Posthitis | Pouchitis | Placentitis | Orchitis | Chondritis | 00
| 27,858 |
<unk> Combat Gauze<unk> is a brand of hemostatic dressing, wound dressing that contains an agent that promotes blood clotting. | QuikClot | Rape kit | QTY Code | ThermoSensor | Kick chart | Diff-Quik | AutoAnalyzer | Pest House | 00
| 68,123 |
Cytosine Uracil The mechanism of SHM involves deamination of cytosine to uracil in DNA by the enzyme activation-induced cytidine deaminase, or AID. A cytosine:guanine pair is thus directly mutated to a uracil:guanine mismatch. Uracil residues are not normally found in DNA, therefore, to maintain the integrity of the genome, most of these mutations must be repaired by high-fidelity Base excision repair enzymes. The uracil bases are removed by the repair enzyme, uracil-DNA glycosylase. Error-prone DNA polymerases are then recruited to fill in the gap and create mutations. The synthesis of this new DNA involves error-prone DNA polymerases, which often introduce mutations at the position of the deaminated cytosine itself or neighboring base pairs. During B cell division the immunoglobulin variable region DNA is transcribed and translated. The introduction of mutations in the rapidly proliferating population of B cells ultimately culminates in the production of thousands of B cells, possessing slightly different receptors and varying specificity for the antigen, from which the B cell with highest affinities for the antigen can be selected. The B cells with the greatest affinity will then be selected to differentiate into plasma cells producing antibody and long-lived memory B cells contributing to enhanced immune responses upon reinfection. The<unk> process also utilizes cells that auto-select against the 'signature' of an organism's own cells. It is hypothesized that failures of this auto-selection process may also lead to the development of an auto-immune response. | Somatic hypermutation | Hair cloning | Osseoincorporation | Prime editing | Gene duplication | Exon shuffling | Autoamputation | Genome editing | 00
| 60,559 |
The true incidence of<unk> is unknown because of the difficulty in making the diagnosis and because of underreporting. It is estimated to occur in 1:1300 to 1:5000 transfusions of plasma-containing products.<unk> is the leading reported cause of death related to transfusion in the United States; more than 20 cases were reported per year from 2003 to 2005. The immune mediated form of<unk> occurs approximately once every 5000 transfusions and has a mortality of 6–9%. | Transfusion-related acute lung injury | Transfusion associated circulatory overload | Culture-bound syndrome | Macrophage activation syndrome | Transfusion-related immunomodulation | Systemic inflammatory response syndrome | Transfusion transmitted infection | Transfusion-associated graft-versus-host disease | 00
| 35,439 |
X-ray showing lung cancer in the left lung Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy. The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment. Cytogenetics and immunohistochemistry are other types of tissue tests. These tests provide information about molecular changes (such as mutations, fusion genes and numerical chromosome changes) and may thus also indicate the prognosis and best treatment. Cancer diagnosis can cause psychological distress and psychosocial interventions, such as talking therapy, may help people with this. | symptom of Arsenic poisoning | symptom of Lead poisoning | symptom of Carbon monoxide poisoning | symptom of Alcohol intoxication | symptom of Shigellosis | symptom of Sulfhemoglobinemia | symptoms of Toxic shock syndrome | symptom of Tuberculosis | 00
| 5,907 |
Treatment can involve operations to lengthen the leg bones, which involves many visits to the hospital. Other symptoms can be treated with medicine or surgery. Most female patients with the syndrome can live a long and normal life, while males have only survived in rare cases. | Conradi–Hünermann syndrome | Hermansky–Pudlak syndrome | Zimmermann–Laband syndrome | Wells-Jankovic syndrome | Keppen–Lubinsky syndrome | Hallermann–Streiff syndrome | Lujan–Fryns syndrome | Sakati–Nyhan–Tisdale syndrome | 00
| 40,012 |
<unk> refers to thyroid dysfunction occurring in the first 12 months after pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. According to the National Institute of Health,<unk> affects about 8% of pregnancies. There are, however, different rates reported globally. This is likely due to the differing amounts of average<unk> follow times around the world, and due to our own innate differences. For example, in Bangkok, Thailand the rate is 1.1%, but in Brazil it is 13.3%. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with<unk> , one in five will develop permanent hypothyroidism requiring lifelong treatment.<unk> is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a subacute lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism.<unk> is a member of the group of thyroiditis conditions known as resolving thyroiditis. | Postpartum thyroiditis | Radiation-induced thyroiditis | Subacute thyroiditis | Autoimmune thyroiditis | Ord's thyroiditis | Subacute lymphocytic thyroiditis | De Quervain's thyroiditis | Riedel's thyroiditis | 00
| 43,511 |
<unk> s may be discovered on medical imaging incidentally (i.e. an incidentaloma), or may be present in patients as an abdominal mass or<unk> cyst, hematuria, abdominal pain, or manifest first in a paraneoplastic syndrome that seems unrelated to the<unk> . Other markers or complications that may arise from<unk> s can appear to be more subtle, including; low hemoglobin, fatigue, nausea, constipation, and/or hyperglycemia. | Kidney tumour | Renal cyst | Kidney cancer | Liver tumor | Ureteral cancer | Pyonephrosis | Hydronephrosis | Kidney stone disease | 00
| 56,514 |
<unk> is a malignant tumor of the pineal gland. A<unk> is a supratentorial midline primitive neuroectodermal tumor.<unk> may occur in patients with hereditary uni- or bilateral retinoblastoma. When retinoblastoma patients present with<unk> this is characterized as "trilateral retinoblastoma". Up to 5% of patients with hereditary retinoblastoma are at risk of developing trilateral retinoblastoma. Prognosis of patients with trilateral retinoblastoma is dismal, only a few patients have survived more than 5 years after diagnosis; all survivors were diagnosed with small tumors in a subclinical stage. Recent advances in (high-dose) chemotherapy treatment regimens and early detection have improved survival of patients with trilateral retinoblastoma to up to 50%. | Pineoblastoma | Sialoblastoma | Medulloblastoma | Ameloblastoma | Neurothekeoma | Hemangioblastoma | Cementoblastoma | Pilocytic astrocytoma | 00
| 54,947 |
The accuracy of diagnosis by<unk> depends on whether the correct site is<unk> ed. There is a risk that a diagnosis can be missed if the<unk> misses the diseased part of heart muscle, particularly with myocardial inflammation or fibrosis. An experienced pathologist trained in<unk> analysis and interpretation also reflects<unk> ’s reliability. Variability between pathologists has been observed. | Endomyocardial biopsy | Ballistocardiography | Magnetocardiography | Phonocardiogram | Tissue Doppler echocardiography | Electrocorticography | Electrocochleography | Coronary CT calcium scan | 00
| 71,697 |
Public health The<unk> is generally used as a means of correlation between groups related by general<unk> and can serve as a vague means of estimating adiposity. The duality of the<unk> is that, while it is easy to use as a general calculation, it is limited as to how accurate and pertinent the data obtained from it can be. Generally, the<unk> is suitable for recognizing trends within sedentary or overweight individuals because there is a smaller margin of error. The<unk> has been used by the WHO as the standard for recording obesity statistics since the early 1980s. This general correlation is particularly useful for consensus data regarding obesity or various other conditions because it can be used to build a semi-accurate representation from which a solution can be stipulated, or the RDA for a group can be calculated. Similarly, this is becoming more and more pertinent to the growth of children, since the majority of children are sedentary. Cross-sectional studies indicated that sedentary people can decrease<unk> by becoming more physically active. Smaller effects are seen in prospective cohort studies which lend to support active mobility as a means to prevent a further increase in<unk> . Clinical practice<unk> categories are generally regarded as a satisfactory tool for measuring whether sedentary individuals are underweight, overweight, or obese with various exceptions, such as athletes, children, the elderly, and the infirm. Also, the growth of a child is documented against a<unk> -measured growth chart. Obesity trends can then be calculated from the difference between the child's<unk> and the<unk> on the chart. In the United States,<unk> is also used as a measure of underweight, owing to advocacy on behalf of those with eating disorders, such as anorexia nervosa and bulimia nervosa. Legislation In France, Italy, and Spain, legislation has been introduced banning the usage of fashion show models having a<unk> below 18. In Israel, a<unk> below 18.5 is banned. This is done to fight anorexia among models and people interested in fashion. | Body mass index | Body adiposity index | Obesity | Lean body mass | Family history | Body fat percentage | Body composition | Sedentary lifestyle | 00
| 454 |
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