Fedor Jeftichew ("Jo-Jo the Dog-faced Man"), Stephan Bibrowski ("Lionel the Lion-faced Man"), Jesús "Chuy" Aceves ("Wolfman"), Annie Jones ("the bearded woman") and Alice Elizabeth Doherty ("The Minnesota Woolly Girl") all had hypertrichosis. [8] Extensive hypertrichosis carries an emotional burden and can cause cosmetic embarrassment; however, some people attempt no treatments because they say it defines who they are. [2] [28] The Gonsalvus family [ edit ] Main article: Petrus Gonsalvus Petrus Gonsalvus (1537–1618) was referred to by Italian naturalist Ulisse Aldrovandi as "the man of the woods". [29] Four of his seven children were also afflicted with hypertrichosis and painted. [30] Barbara van Beck [ edit ] Main article: Barbara van Beck Barbara van Beck (1629–1668?) ... (Supattra Sasupan's Thai national ID card is visible.) ^ "11-Year-Old 'Delighted' After Being Named World's Hairiest Girl" . Fox News. February 28, 2011 . Retrieved 2011-03-07 . ^ Rashid, Rashid M.; White, Lucile E. (2007).
The cutter is usually an older woman, but in communities where the male barber has assumed the role of health worker he will also perform FGM. [25] [c] When traditional cutters are involved, non-sterile devices are likely to be used, including knives, razors, scissors, glass, sharpened rocks and fingernails. [27] According to a nurse in Uganda, quoted in 2007 in The Lancet , a cutter would use one knife on up to 30 girls at a time. [28] In several countries, health professionals are involved; in Egypt 77 percent of FGM procedures, and in Indonesia over 50 percent, were performed by medical professionals as of 2008 and 2016. [29] [3] Classification Variation The WHO, UNICEF and UNFPA issued a joint statement in 1997 defining FGM as "all procedures involving partial or total removal of the external female genitalia or other injury to the female genital organs whether for cultural or other non-therapeutic reasons". [13] The procedures vary according to ethnicity and individual practitioners; during a 1998 survey in Niger, women responded with over 50 terms when asked what was done to them. [17] Translation problems are compounded by the women's confusion over which type of FGM they experienced, or even whether they experienced it. [30] Studies have suggested that survey responses are unreliable. ... The estimate was based on a study conducted on 28,393 women attending delivery wards at 28 obstetric centres in Burkina Faso, Ghana, Kenya, Nigeria, Senegal and Sudan. ... [A 10] 1960s : Central African Republic, Ghana and Guinea, after gaining independence, pass laws restricting FGM. 1969 : Guinean gynaecologist Aja Tounkara Diallo Fatimata begins 28-year practice of performing fake clitoridectomies to satisfy families.
In this study, [49] after two cycles of ABVD chemotherapy, 83% of people were free of disease at 3 years if they had a negative PET versus only 28% in those with positive PET scans. ... August 3, 2016. Archived from the original on 28 July 2016 . Retrieved 12 August 2016 . ^ a b c World Cancer Report 2014 . ... August 3, 2016. Archived from the original on 28 July 2016 . Retrieved 13 August 2016 . ^ a b c d e "SEER Stat Fact Sheets: Hodgkin Lymphoma" . ... Archived from the original on June 28, 2009 . Retrieved June 18, 2009 . ^ Bobrove AM (June 1983). ... Human Reproduction Update . 18 (1): 12–28. doi : 10.1093/humupd/dmr038 . PMID 21896559 . ^ Estcourt L, Stanworth S, Doree C, Hopewell S, Murphy MF, Tinmouth A, Heddle N, et al.
Description Classic Hodgkin lymphoma is a malignancy of B-cell origin in which the neoplastic cells, known as 'Reed-Sternberg' (RS) cells, are characteristically binucleated (summary by Salipante et al., 2009). See also 236000. Inheritance Hafez et al. (1985) estimated that the heritable component of Hodgkin disease is as high as one-third. Additional evidence supporting an inherited predisposition comes from twin studies, racial-incidence patterns, and occurrences of multiplex families. Observations in a small number of affected relative pairs suggested the presence of an HLA-linked locus (Chakravarti et al., 1986), but this could account for only a minority of the familial risk observed in proband studies (Shugart and Collins, 1998). Leri-Weill dyschondrosteosis (LWD; 127300) is a skeletal dysplasia characterized by short stature, shortened forelimbs, and distal radioulnar (Madelung) deformity.
Population Genetics Ferraris et al. (1997) quoted an estimate of 4.5% as the proportion of all cases of Hodgkin disease represented by familial Hodgkin disease. They reviewed 28 articles on familial Hodgkin disease, published between 1972 and 1995, with detailed analysis of data from 18 papers, reporting on 328 patients.
Hodgkin lymphoma (HL) is a heterogeneous group of malignant lymphoid neoplasms of B-cell origin characterized histologically by the presence of Hodgkin and Reed-Sternberg (HRS) cells in the vast majority of cases. Epidemiology HL is an uncommon cancer with an incidence of about 1/40,000 in North America and Europe. There are about 8500 new cases reported in the U.S. each year. Clinical description HL is comprised of 2 major forms: classical Hodgkin lymphoma (CHL; see this term), seen in 95% of all HL cases, and nodular lymphocyte predominant Hodgkin lymphoma (NLPHL; see this term), seen in only 5% of all HL cases. Disease onset occurs most frequently in young adults (age 15-35) followed by older adults (over the age of 55) and usually begins with the painless swelling of a lymph node in the upper body. Disease can spread to multiple lymph node regions or lymphoid structures and associated systemic symptoms (weight loss > 10% of baseline, fevers, night sweats) are observed in about 20% of patients.
Classical Hodgkin lymphoma (CHL) is a B-cell lymphoma characterized histologically by the presence of large mononuclear Hodgkin cells and multinucleated Reed-Sternberg (HRS) cells. Epidemiology The annual incidence of CHL in developed countries is approximately 1/40,000. It accounts for 95% of HL cases. Clinical description Onset most commonly occurs in young adults aged 15-30, followed by adults over the age of 55. In the early stages of the disease many patients are asymptomatic. The most common sign of CHL is the painless enlargement or swelling of upper body lymph nodes (most frequently in the neck, axillae or mediastinum). Itchy skin, fatigue and decreased appetite can also be presenting symptoms.
The risk of progression from Barrett's to dysplasia is uncertain, but is estimated at about 20% of cases. [22] Due to the risk of chronic heartburn progressing to Barrett's, EGD every five years is recommended for people with chronic heartburn, or who take drugs for chronic GERD. [23] Causes [ edit ] A comparison of a healthy condition to GERD Acid reflux is due to poor closure of the lower esophageal sphincter , which is at the junction between the stomach and the esophagus. [5] Factors that can contribute to GERD: Hiatal hernia , which increases the likelihood of GERD due to mechanical and motility factors. [24] [25] Obesity : increasing body mass index is associated with more severe GERD. [26] In a large series of 2,000 patients with symptomatic reflux disease, it has been shown that 13% of changes in esophageal acid exposure is attributable to changes in body mass index. [27] Factors that have been linked with GERD, but not conclusively: Obstructive sleep apnea [28] [29] Gallstones , which can impede the flow of bile into the duodenum , which can affect the ability to neutralize gastric acid [ medical citation needed ] In 1999, a review of existing studies found that, on average, 40% of GERD patients also had H. pylori infection. [30] The eradication of H. pylori can lead to an increase in acid secretion, [31] leading to the question of whether H. pylori -infected GERD patients are any different than non-infected GERD patients. ... American Journal of Gastroenterology . 108 (3): 308–28. doi : 10.1038/ajg.2012.444 . PMID 23419381 . ^ a b c d e f g Kahrilas PJ, Shaheen NJ, Vaezi MF, et al. ... PMID 16831610 . ^ "Infant acid reflux - Diagnosis and treatment - Mayo Clinic" . www.mayoclinic.org . Retrieved 28 September 2018 . ^ Tighe MP, Afzal NA, Bevan A, Beattie RM (2009). ... American Journal of Gastroenterology . 108 (3): 308–28. doi : 10.1038/ajg.2012.444 . PMID 23419381 .
Overview Gastroesophageal reflux disease (GERD) occurs when stomach acid repeatedly flows back into the tube connecting your mouth and stomach (esophagus). This backwash (acid reflux) can irritate the lining of your esophagus. Many people experience acid reflux from time to time. However, when acid reflux happens repeatedly over time, it can cause GERD . Most people are able to manage the discomfort of GERD with lifestyle changes and medications. And though it's uncommon, some may need surgery to ease symptoms. Symptoms Common signs and symptoms of GERD include: A burning sensation in your chest (heartburn), usually after eating, which might be worse at night or while lying down Backwash (regurgitation) of food or sour liquid Upper abdominal or chest pain Trouble swallowing (dysphagia) Sensation of a lump in your throat If you have nighttime acid reflux, you might also experience: An ongoing cough Inflammation of the vocal cords (laryngitis) New or worsening asthma When to see a doctor Seek immediate medical care if you have chest pain, especially if you also have shortness of breath, or jaw or arm pain.
Description Gastroesophageal reflux (GER) is characterized by the retrograde movement of stomach contents into the esophagus. In its most severe form, GER results in extensive tissue damage caused by acid reflux. In adolescents and adults, and even infrequently in children, chronic GER is associated with the risk of developing Barrett metaplasia (614266), a premalignant lesion of the esophageal mucosa (Hu et al., 2000). In turn, Barrett metaplasia is correlated with the development of adenocarcinoma of the esophagus (see 614266), estimated as the fifth most prevalent neoplasia in the Western world (Lagergren et al., 1999). Mapping To identify a genetic locus that cosegregates with a severe pediatric GER phenotype in families with multiple affected members, Hu et al. (2000) performed a genomewide scan using microsatellite markers spaced at an average interval of 8 cM.
Preliminary report", by Richard Doll and Austin Hill , [28] [14] and the 1950 Wynder and Graham Study , entitled "Tobacco Smoking as a Possible Etiologic Factor in Bronchiogenic Carcinoma: A Study of Six Hundred and Eighty-Four Proved Cases". ... The other three studies also reported that, to quote one, "smoking was powerfully implicated in the causation of lung cancer". [27] The Doll and Hill paper reported that "heavy smokers were fifty times as likely as non-smokers to contract lung cancer". [28] [27] Causality [ edit ] The case-control studies clearly showed a close link between smoking and lung cancer , but were criticized for not showing causality .
Overactivation of glutamate receptors damages neurons; for example it leads to the formation of free radicals. [8] Excitotoxicity is a possible factor in the development of PTE; [13] it may lead to the formation of a chronic epileptogenic focus. [8] An epileptic focus is the part of the brain from which epileptic discharges originate. [28] In addition to chemical changes in cells, structural changes that lead to epilepsy may occur in the brain. [3] Seizures that occur shortly after TBI can reorganize neural networks and cause seizures to occur repeatedly and spontaneously later on. [4] The kindling hypothesis suggests that new neural connections are formed in the brain and cause an increase in excitability. [19] The word kindling is a metaphor: the way the brain's response to stimuli increases over repeated exposures is similar to the way small burning twigs can produce a large fire. [29] This reorganization of neural networks may make them more excitable. [4] Neurons that are in a hyperexcitable state due to trauma may create an epileptic focus in the brain that leads to seizures. [12] In addition, an increase in neurons' excitability may accompany loss of inhibitory neurons that normally serve to reduce the likelihood that other neurons will fire; these changes may also produce PTE. [4] Diagnosis [ edit ] EEG shows abnormal activity in some types of seizure disorder, but may or may not display abnormal findings in PTE. ... "Pediatric posttraumatic seizures: Epidemiology, putative mechanisms of epileptogenesis and promising investigational progress". Dev. Neurosci . 28 (4–5): 354–363. doi : 10.1159/000094162 .
However, some still have problems with pain and instability after one year (5–30%). Re-injury is also very common. [28] Epidemiology [ edit ] Adolescents vs general population ankle sprain instances Ankle Sprain Epidemiology- U.S. ... "An epidemiological survey on ankle sprain" . Journal of Sports Medicine . 28 (2): 112–6. doi : 10.1136/bjsm.28.2.112 .
Overview A sprained ankle is an injury that occurs when you roll, twist or turn your ankle in an awkward way. This can stretch or tear the tough bands of tissue (ligaments) that help hold your ankle bones together. Ligaments help stabilize joints, preventing excessive movement. A sprained ankle occurs when the ligaments are forced beyond their normal range of motion. Most sprained ankles involve injuries to the ligaments on the outer side of the ankle. Treatment for a sprained ankle depends on the severity of the injury.
In one study of patients with liver injury, 64% reported alcohol intakes of greater than 80 grams a day, while 35% took 60 grams a day or less. [27] Whether chronic alcoholism should be considered a risk factor has been debated by some clinical toxicologists. [28] [29] For chronic alcohol users, acute alcohol ingestion at the time of a paracetamol overdose may have a protective effect. [28] [30] For non-chronic alcohol users, acute alcohol consumption had no protective effect. ... Journal of Clinical Pharmacy and Therapeutics . 28 (4): 307–10. doi : 10.1046/j.1365-2710.2003.00497.x .
Benzodiazepines taken in overdose in combination with alcohol , barbiturates , opioids , tricyclic antidepressants , or sedating antipsychotics , anticonvulsants , or antihistamines are particularly dangerous. [26] Additionally, emergency department visits involving benzodiazepines compared to other sedative-hypnotics have much higher odds of hospitalization, patient transfer, or death. [27] In the case of alcohol and barbiturates, not only do they have an additive effect but they also increase the binding affinity of benzodiazepines to the benzodiazepine binding site , which results in a very significant potentiation of the CNS and respiratory depressant effects. [28] [29] [30] [31] [32] In addition, the elderly and those with chronic illnesses are much more vulnerable to lethal overdose with benzodiazepines. ... Pharmaceutica Acta Helvetiae . 62 (1): 28–32. PMID 2882522 . ^ a b c d e Whyte, IM (2004).
While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS. [27] Geography MS is more common in people who live farther from the equator , although exceptions exist. [5] [28] These exceptions include ethnic groups that are at low risk far from the equator such as the Samis , Amerindians , Canadian Hutterites , New Zealand Māori , [29] and Canada's Inuit , [2] as well as groups that have a relatively high risk close to the equator such as Sardinians , [2] inland Sicilians , [30] Palestinians , and Parsi . [29] The cause of this geographical pattern is not clear. [2] While the north–south gradient of incidence is decreasing, [28] as of 2010 it is still present. [2] MS is more common in regions with northern European populations [5] and the geographic variation may simply reflect the global distribution of these high-risk populations. [2] Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation. [31] [32] [33] A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life. [34] Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk to MS. ... Please update this article to reflect recent events or newly available information. ( September 2020 ) Deaths from multiple sclerosis per million persons in 2012 0-0 1-1 2-2 3–5 6–12 13–25 MS is the most common autoimmune disorder of the central nervous system . [15] As of 2010, the number of people with MS was 2–2.5 million (approximately 30 per 100,000) globally, with rates varying widely in different regions. [16] [2] It is estimated to have resulted in 18,000 deaths that year. [150] In Africa rates are less than 0.5 per 100,000, while they are 2.8 per 100,000 in South East Asia, 8.3 per 100,000 in the Americas, and 80 per 100,000 in Europe. [16] Rates surpass 200 per 100,000 in certain populations of Northern European descent. [2] The number of new cases that develop per year is about 2.5 per 100,000. [16] Rates of MS appear to be increasing; this, however, may be explained simply by better diagnosis. [2] Studies on populational and geographical patterns have been common [40] and have led to a number of theories about the cause. [12] [27] [31] MS usually appears in adults in their late twenties or early thirties but it can rarely start in childhood and after 50 years of age. [2] [16] The primary progressive subtype is more common in people in their fifties. [60] Similarly to many autoimmune disorders, the disease is more common in women, and the trend may be increasing. [5] [28] As of 2008, globally it is about two times more common in women than in men. [16] In children, it is even more common in females than males, [5] while in people over fifty, it affects males and females almost equally. [60] History Medical discovery Detail of Carswell's drawing of MS lesions in the brain stem and spinal cord (1838) Robert Carswell (1793–1857), a British professor of pathology , and Jean Cruveilhier (1791–1873), a French professor of pathologic anatomy, described and illustrated many of the disease's clinical details, but did not identify it as a separate disease. [151] Specifically, Carswell described the injuries he found as "a remarkable lesion of the spinal cord accompanied with atrophy". [5] Under the microscope, Swiss pathologist Georg Eduard Rindfleisch (1836–1908) noted in 1863 that the inflammation-associated lesions were distributed around blood vessels. [152] [153] The French neurologist Jean-Martin Charcot (1825–1893) was the first person to recognize multiple sclerosis as a distinct disease in 1868. [151] Summarizing previous reports and adding his own clinical and pathological observations, Charcot called the disease sclerose en plaques . ... His diary began in 1822 and ended in 1846, although it remained unknown until 1948. His symptoms began at age 28 with a sudden transient visual loss ( amaurosis fugax ) after the funeral of a friend.
Overview Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). In MS , the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body. Eventually, the disease can cause permanent damage or deterioration of the nerve fibers. Signs and symptoms of MS vary widely between patients and depend on the location and severity of nerve fiber damage in the central nevous system. Some people with severe MS may lose the ability to walk independently or ambulate at all.
The Notani classification of stages is based on the radiographic and clinical findings, with studies describing low grade ORN being treated conservatively and advanced ORN including pathological fractures, and oro-cutaneous fistula treated surgically. [25] Prevention [ edit ] Prior to radiotherapy [ edit ] Dental assessment [ edit ] It is recommended to have a multi-disciplinary approach to care and dental assessment before the patient undergoes radiotherapy. [27] It has been reported, [28] that analysis of patients who have a strict preventive regime paired with IMRT resulted in no cases of ORN. ... "Infectious diseases of the jaws". Journal of Oral Surgery . 28 (1): 17–26. PMID 5262227 . ^ a b c Marx RE (May 1983).
Dermal edema [solid arrows in (A,B)] and a sparse superficial predominantly perivascular and interstitial infiltrate of lymphocytes and eosinophils without signs of vasculitis (dashed arrow). [25] Diagnosis is typically based on the appearance. [2] The cause of chronic hives can rarely be determined. [26] Patch testing may be useful to determine the allergy. [2] In some cases regular extensive allergy testing over a long period of time is requested in hopes of getting new insight. [27] [28] No evidence shows regular allergy testing results in identification of a problem or relief for people with chronic hives. [27] [28] Regular allergy testing for people with chronic hives is not recommended. [26] Acute versus chronic [ edit ] Acute urticaria is defined as the presence of evanescent wheals which completely resolve within six weeks. [29] Acute urticaria becomes evident a few minutes after the person has been exposed to an allergen.
The vascular theory has been called into question [26] and other mechanisms are being considered. [27] The Third Edition of the Internal Classification of Headache disorders classifies CH as belonging to the trigeminal autonomic cephalalgias. [28] Nerves [ edit ] Two nerves are thought to play an important role in CH: the trigeminal nerve and the facial nerve . [29] Genetics [ edit ] Cluster headache may run in some families in an autosomal dominant inheritance pattern. [30] [25] People with a first degree relative with the condition are about 14–48 times more likely to develop it themselves, [1] and around 8 to 10% of persons with CH have a positive family history. [30] [31] Several studies have found a higher number of relatives affected among female. [31] Others have suggested these observations may be due to lower numbers of females in these studies. [31] Possible genetic factors warrant further research, current evidence for genetic inheritance is limited. [25] Genes that are thought to play a role in the disease are the hypocretin/orexin receptor type 2 (HCRTR2), alcohol dehydrogenase 4(ADH4), G protein beta 3 (GNB3), pituitary adenylate cyclase-activating polypeptide type I receptor (ADCYAP1R1), and membrane metalloendopeptidase (MME) genes. [30] Tobacco smoking [ edit ] About 65% of persons with CH are, or have been, tobacco smokers. [1] Stopping smoking does not lead to improvement of the condition and CH also occurs in those who have never smoked (e.g. children); [1] it is thought unlikely that smoking is a cause. [1] People with CH may be predisposed to certain traits, including smoking or other lifestyle habits. [32] Hypothalamus [ edit ] A review suggests that the suprachiasmatic nucleus of the hypothalamus , which is the major biological clock in the human body, may be involved in cluster headaches, because CH occurs with diurnal and seasonal rhythmicity. [33] Positron emission tomography (PET) scans indicate the brain areas which are activated during attack only, compared to pain free periods. ... "The Incidence and Prevalence of Cluster Headache: A Meta-Analysis of Population-Based Studies". Cephalalgia . 28 (6): 614–8. doi : 10.1111/j.1468-2982.2008.01592.x . ... S2CID 10284630 . ^ Nalini Vadivelu; Alan David Kaye; Jack M. Berger (28 November 2012). Essentials of palliative care .
Overview Cluster headaches, which occur in cyclical patterns or cluster periods, are one of the most painful types of headache. A cluster headache commonly awakens you in the middle of the night with intense pain in or around one eye on one side of your head. Bouts of frequent attacks, known as cluster periods, can last from weeks to months, usually followed by remission periods when the headaches stop. During remission, no headaches occur for months and sometimes even years. Fortunately, cluster headache is rare and not life-threatening. Treatments can make cluster headache attacks shorter and less severe.
The fact that 40% of diabetics who carefully controlled their blood sugar nevertheless developed neuropathy made clear other factors were involved. [25] In a 2013 meta-analysis of 6 randomized controlled trials involving 27,654 patients with Type 2 diabetes, tight blood glucose control reduced the risk for some macrovascular and microvascular events but without effect on all-cause mortality and cardiovascular mortality. [26] Autoimmune processes [ edit ] Research from 2007 suggested that in type 1 diabetics, the continuing autoimmune disease which initially destroyed the beta cells of the pancreas may also cause neuropathy, [27] and nephropathy. [28] In 2008 it was even suggested to treat retinopathy with drugs to suppress the abnormal immune response rather than by blood sugar control. [29] Genetic factors [ edit ] The known familial clustering of the type and degree of diabetic complications indicates that genetics play a role in causing complications: the 2001 observation, that non-diabetic offspring of type 2 diabetics had increased arterial stiffness and neuropathy despite normal blood glucose levels, [30] the 2008 observation, that non-diabetic first-degree relatives of diabetics had elevated enzyme levels associated with diabetic renal disease [31] and nephropathy. [32] the 2007 finding that non-diabetic family members of type 1 diabetics had increased risk for microvascular complications, [33] such as diabetic retinopathy [34] Some genes appear to provide protection against diabetic complications, as seen in a subset of long-term diabetes type 1 survivors without complications. [35] [36] Mechanisms [ edit ] Chronic elevation of blood glucose level leads to damage of blood vessels called angiopathy . ... "Autoantibodies to autonomic nerves associated with cardiac and peripheral autonomic neuropathy" . Diabetes Care . 28 (8): 1959–64. doi : 10.2337/diacare.28.8.1959 . ... Nutrition (Burbank, Los Angeles County, Calif.) . 28 (7–8): e23–26. doi : 10.1016/j.nut.2012.01.005 . ^ Selhub, J., Jacques, P., Dallal, G., Choumenkovitch, S., & Rogers, G. (2008).
In addition to modification of custody, Gardner recommended therapy for the child. [22] [24] Gardner's proposed intervention for moderate and severe PAS, which include court-ordered transfer to the alienated parent, fines, house arrest, and incarceration, have been critiqued for their punitive nature towards the alienating parent and alienated child, and for the risk of abuse of power and violation of their civil rights. [25] [26] With time, Gardner revised his views and expressed less support for the most aggressive management strategies. [25] Reception [ edit ] Gardner's original formulation, which labeled mothers almost exclusively as the alienating parent, was endorsed by fathers' rights groups, as it allowed fathers to explain the reluctance of their children to visit them and assign blame to their former wives. [25] [27] In contrast, women's groups criticized the syndrome, concerned that it permitted abusers to claim that allegations of abuse by mother or child were reflective of brainwashing. [25] Gardner himself emphasized that PAS only applied in situations where there was no actual abuse or neglect had not occurred, [7] [28] but by 1998, noted an increase in the awareness of PAS had led to an increase in its misapplication as an exculpatory legal maneuver. [29] PAS has been cited in high-conflict divorce and child custody cases, particularly as a defense against accusations of domestic violence or sexual abuse. [5] [22] The status of the syndrome, and thus its admissibility in the testimony of experts, has been the subject of dispute, with challenges raised about its acceptance by professionals in the field, whether it follows a scientific methodology that is testable, whether it has been tested and has a known error rate, and the extent to which the theory has been published and peer-reviewed. [22] PAS has not been accepted by experts in psychology , child advocacy or the study of child abuse [6] or legal scholars. [7] PAS has been extensively criticized by members of the legal and mental health community, who state that PAS should not be admissible in child custody hearings based on both science and law. [5] [6] [7] [22] [30] No professional association has recognized PAS as a relevant medical syndrome or mental disorder. ... "Recommendations for Dealing with Parents who Induce a Parental Alienation Syndrome in their Children". Journal of Divorce & Remarriage . 28 (3/4): 1–21. doi : 10.1300/J087v28n03_01 . ^ a b c d Gardner, Richard (2004).
In one study of 143 pediatric outcomes, a failure rate of 1.4% was reported in the loop group versus 10.5% in the packing group (P<.030), [26] while a separate study reported a 5.5% failure rate among loop patients. [27] Primary closure [ edit ] Closing an abscess immediately after draining it appears to speed healing without increasing the risk of recurrence. [10] This may not apply to anorectal abscesses as while they may heal faster, there may be a higher rate of recurrence than those left open. [28] Prognosis [ edit ] Even without treatment, skin abscesses rarely result in death, as they will naturally break through the skin. [3] Other types of abscess are more dangerous. ... PMID 6397949 . ^ Bokhari, Maria R.; Mesfin, Fassil B. (2019), "Brain Abscess" , StatPearls , StatPearls Publishing, PMID 28722871 , retrieved 2019-07-28 ^ Tomolillo, CM; Crothers, LJ; Aberson, CL (2007).
Non-infectious diseases that can be confused with MVD are acute promyelocytic leukemia , hemolytic uremic syndrome , snake envenomation , clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura , hereditary hemorrhagic telangiectasia , Kawasaki disease , and even warfarin intoxication. [28] [29] [30] [31] The most important indicator that may lead to the suspicion of MVD at clinical examination is the medical history of the patient, in particular the travel and occupational history (which countries and caves were visited?) ... Boca Raton: CRC Press. p. 458. ISBN 9781439884317 . Retrieved 28 October 2017 . CS1 maint: extra text: authors list ( link ) ^ Peterson, A. ... "Marburg virus vaccines based upon alphavirus replicons protect guinea pigs and nonhuman primates". Virology . 251 (1): 28–37. doi : 10.1006/viro.1998.9367 .
Marburg hemorrhagic fever (MHF), caused by Marburg virus, is a severe viral hemorrhagic disease characterized by initial fever and malaise followed by gastrointestinal symptoms, bleeding, shock, and multi-organ system failure. Epidemiology MHF is endemic to Central Africa and is generally recognized in sporadic small outbreaks (<50 cases), although one large (>250 cases) nosocomial outbreak occurred in Angola in 2004-2005. Less than 500 cases have been reported to date. Clinical description After an incubation period of about 8 days (range 3-21 days), patients typically present with the abrupt onset of non-specific signs and symptoms including fever, malaise, headache, chest pain and myalgia/arthralgia, followed rapidly by gastrointestinal manifestations (vomiting, diarrhea, abdominal pain) and, in some cases, a maculopapular skin rash. Severe cases develop bleeding (sub-conjunctival hemorrhage, epistaxis, bleeding from the mouth and rectum, oozing from venipuncture sites), neurologic involvement (disorientation, convulsions, coma), shock and multi-organ system failure. Mild-to-moderate leukopenia and thrombocytopenia are often present and disseminated intravascular coagulation (DIC) commonly develops, best indicated by the presence of D-dimers.
The Sydney Morning Herald . August 28, 2008 . Retrieved August 28, 2008 . ^ "A baby boy born with two heads has died after developing a fever and breathing difficulties, a Bangladeshi doctor says" . Sky News . August 28, 2008. Archived from the original on January 23, 2009 . Retrieved August 28, 2008 . ^ "Conjoined twins born with one body" . ... February 19, 2009. ^ "Life Is Confusing For Two-Headed Snakes" . National Geographic . October 28, 2010 . Retrieved September 19, 2011 . ^ a b "Life Is Confusing For Two-Headed Snakes" . National Geographic . October 28, 2010 . Retrieved September 19, 2011 . ^ "Georgia Capitol Museum" .
There are many causes, which can be broadly grouped into three mechanisms: primary (internal bleeding and swelling); secondary (vigorous fluid replacement as an unintended complication of resuscitative medical treatment, leading to the acute formation of ascites and a rise in intra-abdominal pressure); and recurrent (compartment syndrome that has returned after the initial treatment of secondary compartment syndrome). [28] There have been cases of compartment syndrome associated with hypothyroidism. [29] Chronic [ edit ] When compartment syndrome is caused by repetitive use of the muscles, it is known as chronic compartment syndrome (CCS). [30] [31] This is usually not an emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscles. ... Imaging studies (X-ray, CT, MRI) can be useful in ruling out the more common diagnoses. [37] Additionally, MRI has been shown to be effective in diagnosing chronic exertional compartment syndrome. [38] The average duration of symptoms prior to diagnosis is 28 months. [39] Treatment [ edit ] Acute [ edit ] Use of a skin graft to close a fasciotomy wound.
NMDA receptors can be found presynaptically on central terminals of primary afferent neurons and postsynaptically on spinal dorsal horn neurons. [28] it has been shown experimentally that introduction of an NMDA receptor antagonist to mice and rats greatly reduces or even prevents OIH. [29] B-arrestin 2 transcripts (Arrb2) are implicated in OIH because of their upregulation during analgesic tolerance in the periaqueductal gray , cortex and striatum . [30] NMDA receptor antagonists combined with morphine in OIH conditions have been shown to reduce Arr2b in the entirety of the mouse's brain. [31] These findings implicate Arr2b activity as a factor in OIH. ... "Numbers, Densities, and Colocalization of AMPA- and NMDA-Type Glutamate Receptors at Individual Synapses in the Superficial Spinal Dorsal Horn of Rats" . Journal of Neuroscience . 28 (39): 9692–9701. doi : 10.1523/JNEUROSCI.1551-08.2008 .
