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  • Idiopathic Pulmonary Fibrosis GARD
    Common symptoms include shortness of breath and a dry, hacking cough. In some cases fibrosis happens quickly, while in others, the process is much slower.
    ABCA3, SFTPC, RTEL1, PARN, TERC, TERT, SFTPA1, DPP9, MUC5B, DSP, STN1, SFTPA2, FAM13A, ATP11A, IL6, CFTR, IL4, CXCL8, IL13, IRF5, ATL1, KRT20, PNO1, TGFB1, TNF, USF2, NLRP1, CXCL13, TLR9, MAK16, RBMS3, SRRM2, PTGS2, STAT4, SDC4, TNFRSF8, CHI3L1, VCAN, CCN2, DCN, FN1, HNF4A, IFNG, IL1B, IL1RN, IL4R, CXCR1, CXCR2, COX2, SERPINE1, SERPINA1, PTBP1, MS4A1, S100A4, MTCO2P12
    • Pulmonary Fibrosis, Idiopathic OMIM
      A wide range of agents was implicated, including coal dust, wood dust, metal dust, and adhesives; the exposure was occupational in only 2 cases and in most the exposure was in the home. ... Screening the TERT and TERC genes in 100 consecutive patients, including the 62 individuals in whom telomere length had been measured, revealed a mutation in TERC in only 1 patient (602322.0010). The authors noted that a subset of patients (10%) with no family history and no detectable mutations in telomerase had telomere lengths in the range of known mutation carriers. ... The shared haplotype harbored 2 functionally uncharacterized genes, ELMOD2 (610196) and LOC152586 (610310), of which only ELMOD2 was expressed in lung and showed significantly decreased mRNA expression in lung from idiopathic pulmonary fibrosis when compared with that of healthy lung. ... Induction of pulmonary fibrosis in these chimeric mice by endotracheal bleomycin (BLM) injection caused large numbers of GFP+ cells to appear in active fibrotic lesions, whereas only a few GFP+ cells could be identified in control lungs.
    • Pulmonary Fibrosis And/or Bone Marrow Failure, Telomere-Related, 3 OMIM
      A number sign (#) is used with this entry because of evidence that telomere-related pulmonary fibrosis and/or bone marrow failure-3 (PFBMFT3) is caused by heterozygous mutation in the RTEL1 gene (608833) on chromosome 20q13. For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742). Clinical Features Stuart et al. (2015) reported 5 unrelated families with susceptibility to pulmonary fibrosis and/or unspecified lung disease. Affected family members had shortened telomeres (less than 1-2% of control length). None were noted to have features of bone marrow failure. Cogan et al. (2015) reported 9 families in which multiple individuals were diagnosed with interstitial pneumonia between 45 and 87 years of age (mean, 64.8 years).
    • Pulmonary Fibrosis And/or Bone Marrow Failure, Telomere-Related, 4 OMIM
      A number sign (#) is used with this entry because of evidence that telomere-related pulmonary fibrosis and/or bone marrow failure-4 (PFBMFT4) is caused by heterozygous mutation in the PARN gene (604212) on chromosome 16p13. For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742). Clinical Features Stuart et al. (2015) reported 6 unrelated families with pulmonary fibrosis and/or unspecified lung disease. Affected family members had shortened telomeres (less than 1-30% of control length). A few patients had premature graying of the hair, but none were noted to have features of bone marrow failure.
    • Acute Interstitial Pneumonia GARD
      Acute interstitial pneumonia (AIP) is a rare and serious condition that affects the lungs. The signs and symptoms generally develop and progress rapidly. In the early stages of the condition, affected people may experience upper respiratory and/or viral-like symptoms such as cough, shortness of breath, and fever. This is followed by the rapid onset of respiratory failure and the need for mechanical ventilation in the majority of cases. The underlying cause of AIP is unknown. Most cases occur sporadically in people with no family history of the condition. There is, unfortunately, no proven treatment for AIP. Supportive care is generally recommended to address the signs and symptoms of the condition.
  • Plasma Cell Leukemia GARD
    For detailed information on the available treatment options, please visit the following link. http://www.cancer.gov/cancertopics/pdq/treatment/myeloma/Patient/page4
    IL6, CDKN2A, MYC, TP53, CCND1, IGH, FGFR3, RASSF1, RB1, HLA-A, H3P10, CDKN2B, CD40, CKS1B, SOCS3, TMSB4X, BCR, VEGFA, NSD2, CXCR4, BCL10, PKD2L1, SFRP5, MAFB, NES, BCL2, PHF19, MUC16, RBM45, TIMP3, SFRP1, FLT4, SAT1, BRAF, PTEN, PSMB5, NCAM1, MLH1, MGMT, MDM2, KRAS, CD40LG, IL3, CD79A, ICAM1, FRZB, PLIN2
    • Plasma Cell Leukemia Orphanet
      A rare plasma cell neoplasm characterized by peripheral plasmacytosis, usually with extensive and diffuse infiltration of the bone marrow, and monoclonal paraproteinemia. Neoplastic plasma cells may also be found in extramedullary sites, such as the liver or spleen, among others. Most cases present as primary plasma cell leukemia without previous diagnosis of myeloma. The condition can also represent leukemic transformation of plasma cell myeloma (secondary plasma cell leukemia). Clinical manifestations include lymphadenopathy, organomegaly, renal failure, bone marrow failure, and peripheral neuropathies.
    • Plasma Cell Leukemia Wikipedia
      It is the terminal phase of these patients myeloma disease. sPCL patients typically are highly symptomatic due to extensive disease with malignant plasma cell infiltrations in, and failures of, not only the bone marrow but also other organs.
  • Baby Acne Mayo Clinic
    Preparing for your appointment If you're following a standard well-baby exam schedule, your baby will likely visit with your family's health care provider or a pediatrician soon. ... For baby acne, some basic questions to ask your doctor include: Is my baby's condition likely temporary or long lasting? What treatments are available? What advice do you have for my baby's skin care? Will this acne scar my baby's face?
  • Abortion In Mexico Wikipedia
    Retrieved 31 July 2016 . ^ "Se han interrumpido legalmente 138 mil embarazos en ocho años" . Excélsior (in Spanish). ... Retrieved 2009-10-18 . ^ "Temen se extienda prohibición al aborto en el país" . El Financiero en línea (in Spanish). ... ISBN 978-3659527661 . ^ "La legalidad del aborto en México a discusión en la Suprema Corte" . ... "Una de cada 3 mujeres que interrumpe su embarazo en el DF es ama de casa" . CNN: Mexico . Retrieved 16 March 2014 . ^ a b Grupo de Informacion en Reproduccion Elegida. "Aborto: Capitulo Uno" (PDF) .
  • Usog Wikipedia
    Usog or balis is a topic in psycho-medicine in Filipino Psychology (but considered just as a Filipino superstition in Western Psychology) where an affliction or psychological disorder is attributed to a greeting by a stranger, or an evil eye hex . It usually affects an unsuspecting child, usually an infant or toddler, who has been greeted by a visitor or a stranger. [1] In some limited areas, it is said that the condition is also caused by the stranger having an evil eye or masamang mata in Tagalog , lurking around. ... There are observations that a stranger (or a newcomer or even a visiting relative) especially someone with a strong personality (physically big, boisterous, has strong smell, domineering, etc.) may easily distress a child. ... Some have observed that at times even praising a shy child by a visiting relative caused an usog . [4] [7] The saliva from the stranger, granted that he or she is healthy and consistent with his or her oral hygiene , is relatively clean [8] and contains enough antimicrobial compounds such as lactoferrin , lactoperoxidase , and secretory immunoglobulin A which can help clear pathogens from the child and benefit the child against infection. [9] Furthermore, human saliva has opiorphin , a newly researched pain-killing substance. ... More than the superstitious folks, researchers dealing with Filipino Psychology say they have observed this phenomenon with regularity and suggest that this be added to the Psychiatric Disorders Handbook DSM-V . [4] See also [ edit ] Evil eye Lihi Albulario Saliva Opiorphin References [ edit ] ^ PWE-USOG / PWE-BUYAG: Miscellaneous Therapies in Philippine Alternative Medicine ^ http://www.viloria.com/secondthoughts/archives/00000176.html ^ Fadul, J. ... ISBN 978-971-542-570-4 . ^ Youtube Usog ^ http://neurophilosophy.wordpress.com/2006/11/14/lick-your-wounds/ Neurophilosophy: Lick your wounds ^ Discover Magazine, "The Biology of ...Saliva" October 2005 ^ Wisner, Anne; Evelyne Dufour; Michaël Messaoudi; Amine Nejdi; Audrey Marcel; Marie-Noelle Ungeheuer; Catherine Rougeot (November 13, 2006).
  • Abortion In Norway Wikipedia
    Current Norwegian legislation and public health policy provides for abortion on request in the first 12 weeks of gestation, by application up to the 18th week, and thereafter only under special circumstances until the fetus is viable, which is usually presumed at 21 weeks and 6 days. ... ("Grundlaget for al frihet er rådighet over egen krop og hvad i den er. Det motsatte er en slaves tilstand") In the period between 1920 and 1929, about 100 individuals were sentenced for an illegal abortion. ... Gradual liberalization and a core feminist cause [ edit ] Year Number of abortions Rate 1965 3455 n/a 1970 7941 n/a 1975 15132 n/a 1976 14754 0.542 1980 (on request) 13531 0.468 In 1960, a new law allowed abortion by application approved by a commission of two physicians, and only on the basis of medical, eugenic, or criminal criteria; and with the consent of the husband if the applicant was married. ... Sage . 24 (1): 23–38. doi : 10.1177/1350506815619878 . References [ edit ] ^ https://www.regjeringen.no/no/dokumenter/about-the-abortion-act/id419252/ ^ https://www.regjeringen.no/no/dokumenter/about-the-abortion-act/id419252/ ^ http://www.ssb.no/vis/magasinet/slik_lever_vi/art-2005-02-18-01.html ^ Christine Svendsen (12 May 2012) Aborterte fostre levde i over en time før hjertet hadde sluttet å slå NRK.
  • Mirizzi's Syndrome Wikipedia
    Cholecystectomy and bilioenteric anastomosis may be required. Roux-en-Y hepaticojejunostomy has shown good outcome in some studies. [4] Epidemiology [ edit ] Mirizzi's syndrome occurs in approximately 0.1% of patients with gallstones . [5] It is found in 0.7 to 2.5 percent of cholecystectomies . [1] It affects males and females equally, but tends to affect older people more often. ... Mirizzi was educated and trained in his hometown and later visited some of the best hospitals throughout the United States for further education and training. ... Society for Surgery of the Alimentary Tract. http://www.ssat.com/cgi-bin/abstracts/09ddw/P7.cgi ^ "eMRCS" . www.emrcs.com .
    AZU1, HDLBP, SLBP, STAM2, HEBP1, BTBD8
    • Mirizzi Syndrome Orphanet
      A rare biliary tract disease characterized by external compression and subsequent obstruction of an extrahepatic biliary duct by one or more gallstones in the cystic duct or the gallbladder. Patients may present with acute or chronic cholecystitis with right upper abdominal pain, nausea, and vomiting, jaundice, or cholangitis. Cholecystobiliary or -enteric fistulae can arise due to chronic inflammation and ulceration.
  • Episcleritis Wikipedia
    Episcleritis Eye with Episcleritis Specialty Ophthalmology Symptoms Eye redness without pain Watery eyes Types Nodular and simple/diffuse Diagnostic method History and physical examination Differential diagnosis Scleritis Treatment Artificial tears , supportive care Medication Topical corticosteroids Non-steroidal anti-inflammatory drugs . Prognosis Good Episcleritis is a benign, self-limiting inflammatory disease affecting part of the eye called the episclera . The episclera is a thin layer of tissue that lies between the conjunctiva and the connective tissue layer that forms the white of the eye ( sclera ). ... Contents 1 Signs and symptoms 2 Pathophysiology 3 Diagnosis 4 Treatment 5 Prognosis 6 Epidemiology 7 References 8 External links Signs and symptoms [ edit ] Episcleritis of a 40 years old female Symptoms of episcleritis typically include painless redness of the eye (mild pain is possible but atypical), and watery eyes . [1] The pain of episcleritis is typically mild, less severe than in scleritis , [2] and may be tender to palpation. [3] There are two types of episcleritis: the diffuse type, where the redness involves the entire episclera, and the nodular type, where the redness appears more nodular , involving only a small, well-circumscribed area ( sectoral ). [4] The diffuse type of episcleritis may be less painful than the nodular type. Sometimes, small nodules are present within the episclera, which move slightly over the sclera with gentle pressure. [4] Discharge is absent with episcleritis, and vision is unaffected. [4] Patients with episcleritis experience far less photophobia than patients with uveitis . [1] Episcleritis does not cause the presence of cells or flare in the anterior chamber of the eye. [1] In 80 percent of cases, episcleritis affects only one eye, [5] whereas scleritis often affects both eyes. ... ISBN 978-0071769648 . ^ a b c d e f Kunimoto, Derek; Kunal Kanitkar; Mary Makar (2004). The Wills eye manual: office and emergency room diagnosis and treatment of eye disease (4 ed.).
    DNASE1L3, PSMB8, MBTPS2, SLC29A3, NLRP3, HLA-DRB1, INSRR, DBR1, RBM45
  • Cholera Mayo Clinic
    If you develop severe diarrhea after visiting an area with active cholera, see your doctor. ... If soap and water aren't available, use an alcohol-based hand sanitizer. Drink only safe water, including bottled water or water you've boiled or disinfected yourself. ... Diagnosis Although signs and symptoms of severe cholera can be unmistakable in areas where it's common, the only way to confirm a diagnosis is to identify the bacteria in a stool sample. ... When you make your appointment, ask if there are restrictions you need to follow before your visit. Make a list of: Your symptoms, when they began and how severe they are Recent exposure to possible sources of infection, particularly if you've traveled abroad recently Key medical information, including other conditions for which you're being treated All medications, vitamins or other supplements you take, including doses Questions to ask your doctor Some questions to ask your doctor about cholera include: Are there other possible causes for my symptoms? ... Am I at risk of any long-term complications from cholera? Am I contagious? How can I reduce my risk of passing my illness to others?
    PCYT1B, CTBS, CFTR, SPINK1, EGF, ATP8B1, ANXA5, IL1B, NBAS, WASF2, CYP27A1, ATN1, CYP2B6, GLB1, HSP90AA1, FBXW7, POMC, IL17A, VEGFA, TYRP1, TRPC1, NAGLU, NPY, SOD1, ABO, SLC9A3, SCN7A, ACE2, EVPL, CAV1, VIP, TM7SF2, TNF, TRAF3, TRP-AGG2-5, MIR132, TICAM2, CAVIN1, EZR, WARS1, ZNRD2, PTF1A, BAP1, TNFSF9, NRSN1, SPHK1, WASF1, TPH2, ART5, THBS1, NOD2, MIR146A, MIR155, RANBP2, S100A4, S100A8, CLEC11A, H3P23, SLC5A1, LOC102724197, LOC102723971, TMED7-TICAM2, MFT2, SPR, STAR, SYP, TAPBP, H3P37, TRBV20OR9-2, TF, CAP1, NLRP3, CRLF2, BPIFB1, IL22, TMED7, VPS54, GGTLC1, IL23A, TSLP, PPIL1, MAP1LC3A, KRT20, CTTNBP2, SEPTIN3, CMIP, NSFL1C, PHF12, XYLT2, GOLPH3, TNMD, DUOX2, EFEMP2, DCTN6, PYCARD, WASF3, FASTK, TMED2, SNRNP35, TPPP, AKAP13, FOXP2, CHP1, CNOT1, SLC39A6, SUMF2, LDLRAP1, IFT172, PTH, LAT, ARFIP1, SLC6A16, PTHLH, SERPINA3, PTEN, CYLD, CETP, CHRM1, CHRM3, CKB, COX8A, CRP, CSF2, CCN2, CTSD, CYP11A1, CD81, CYP19A1, CYP26A1, CD55, ACE, DECR1, DLG4, EGFR, ENO1, ERBB2, CDK2, CD44, ESRRA, KLK3, ADCY6, ADPRH, AKT1, AKT2, ALB, ANGPT1, APOB, APOE, APRT, STS, CD40LG, ALDH7A1, BCL2, TSPO, CACNA1E, CAMP, CASR, CAV3, CD9, MS4A1, ESR1, F9, PSMD9, PIK3CA, LEP, LHCGR, MBL2, MBP, MFAP1, MMP9, NT5E, NTF4, ABCB4, PIK3CB, KIT, PIK3CD, PIK3CG, PLEK, POU4F1, PRF1, PRG2, PRSS1, PRSS8, PSEN1, LCN1, ITGB1, PTK2B, HSPA4, FCGR3A, FDX1, FLII, ACKR1, GLP1R, GPR39, HIVEP1, HMGB1, HSD17B1, HSPA8, ING1, HSPD1, ICAM1, IFI27, IFNA1, IFNA13, IKBKB, IL6, CXCL8, IDO1, H3P19
    • Cholera GARD
      Cholera is an infection of the small intestines that is caused by the bacterium Vibrio cholera . The condition can range from mild to severe and many affected people may have no obvious signs or symptoms. Approximately 5-10% of infected people will have severe disease with watery diarrhea and vomiting leading to rapid fluid loss, dehydration, and shock. If left untreated, this can cause acute renal failure, severe electrolyte imbalances, coma, or even death. People develop cholera when they eat food or drink water that is contaminated with Vibrio cholera .
    • Cholera Orphanet
      The majority of infected individuals will be asymptomatic, a smaller percentage will develop mild to moderate symptoms, and only a small proportion will develop severe dehydration. ... Signs of dehydration and electrolyte imbalance soon occur and include sunken eyes, lethargy, dry mouth, decreased skin turgor, wrinkled hands and feet, and cold clammy skin. ... Etiology Cholera is due to an infection with Vibrio cholerae , a Gram negative rod bacteria that grows best in coastal waters and estuaries and is spread by the fecal-oral route. Over 200 serogroups exist but only 2 cause epidemic cholera: O1 and O139.
    • Cholera Wikipedia
      Bacterial infection of the small intestine Cholera Other names Asiatic cholera, epidemic cholera [1] A person with severe dehydration due to cholera causing sunken eyes and wrinkled hands and skin. Specialty Infectious disease Symptoms Large amounts of watery diarrhea , vomiting , muscle cramps [2] [3] Complications Dehydration , electrolyte imbalance [2] Usual onset 2 hours to 5 days after exposure [3] Duration A few days [2] Causes Vibrio cholerae spread by fecal-oral route [2] [4] Risk factors Poor sanitation , not enough clean drinking water , poverty [2] Diagnostic method Stool test [2] Prevention Improved sanitation, clean water , hand washing , cholera vaccines [2] [5] Treatment Oral rehydration therapy , zinc supplementation , intravenous fluids , antibiotics [2] [6] Frequency 3–5 million people a year [2] Deaths 28,800 (2015) [7] Cholera is an infection of the small intestine by some strains of the bacterium Vibrio cholerae . [4] [3] Symptoms may range from none, to mild, to severe. [3] The classic symptom is large amounts of watery diarrhea that lasts a few days. [2] Vomiting and muscle cramps may also occur. [3] Diarrhea can be so severe that it leads within hours to severe dehydration and electrolyte imbalance . [2] This may result in sunken eyes , cold skin, decreased skin elasticity, and wrinkling of the hands and feet. [5] Dehydration can cause the skin to turn bluish . [8] Symptoms start two hours to five days after exposure. [3] Cholera is caused by a number of types of Vibrio cholerae , with some types producing more severe disease than others. [2] It is spread mostly by unsafe water and unsafe food that has been contaminated with human feces containing the bacteria. [2] Undercooked seafood is a common source. [9] Humans are the only animal affected. [2] Risk factors for the disease include poor sanitation , not enough clean drinking water , and poverty . [2] There are concerns that rising sea levels will increase rates of disease. [2] Cholera can be diagnosed by a stool test . [2] A rapid dipstick test is available but is not as accurate. [10] Prevention methods against cholera include improved sanitation and access to clean water . [5] Cholera vaccines that are given by mouth provide reasonable protection for about six months. [2] They have the added benefit of protecting against another type of diarrhea caused by E. coli . [2] The primary treatment is oral rehydration therapy —the replacement of fluids with slightly sweet and salty solutions . [2] Rice-based solutions are preferred. [2] Zinc supplementation is useful in children. [6] In severe cases, intravenous fluids , such as Ringer's lactate , may be required, and antibiotics may be beneficial. [2] Testing to see which antibiotic the cholera is susceptible to can help guide the choice. [3] Cholera affects an estimated 3–5 million people worldwide and causes 28,800–130,000 deaths a year. [2] [7] Although it is classified as a pandemic as of 2010 [update] , it is rare in the developed world . [2] Children are mostly affected. [2] [11] Cholera occurs as both outbreaks and chronically in certain areas . [2] Areas with an ongoing risk of disease include Africa and Southeast Asia . [2] The risk of death among those affected is usually less than 5% but may be as high as 50%. [2] No access to treatment results in a higher death rate. [2] Descriptions of cholera are found as early as the 5th century BC in Sanskrit . [5] The study of cholera in England by John Snow between 1849 and 1854 led to significant advances in the field of epidemiology . [5] [12] Seven large outbreaks have occurred over the last 200 years with millions of deaths. [13] Play media Video summary ( script ) Contents 1 Signs and symptoms 2 Cause 2.1 Transmission 2.2 Susceptibility 3 Mechanism 3.1 Genetic structure 3.2 Antibiotic resistance 4 Diagnosis 5 Prevention 5.1 Surveillance 5.2 Vaccination 5.3 Sari filtration 6 Treatment 6.1 Fluids 6.2 Electrolytes 6.3 Antibiotics 6.4 Zinc supplementation 7 Prognosis 8 Epidemiology 9 History 9.1 Research 10 Society and culture 10.1 Health policy 10.2 Notable cases 10.3 In popular culture 11 Country examples 11.1 Zambia 11.2 India 11.3 Democratic Republic of Congo 12 References 13 Further reading 14 External links Signs and symptoms Typical cholera diarrhea that looks like "rice water" The primary symptoms of cholera are profuse diarrhea and vomiting of clear fluid. [14] These symptoms usually start suddenly, half a day to five days after ingestion of the bacteria. [15] The diarrhea is frequently described as "rice water" in nature and may have a fishy odor. [14] An untreated person with cholera may produce 10 to 20 litres (3 to 5 US gal) of diarrhea a day. [14] Severe cholera, without treatment, kills about half of affected individuals. [14] If the severe diarrhea is not treated, it can result in life-threatening dehydration and electrolyte imbalances. [14] Estimates of the ratio of asymptomatic to symptomatic infections have ranged from 3 to 100. [16] Cholera has been nicknamed the "blue death" [17] because a person's skin may turn bluish-gray from extreme loss of fluids. [18] Fever is rare and should raise suspicion for secondary infection. Patients can be lethargic and might have sunken eyes, dry mouth, cold clammy skin, or wrinkled hands and feet. ... One such recipe calls for 1 liter of boiled water, 1/2 teaspoon of salt, 6 teaspoons of sugar, and added mashed banana for potassium and to improve taste. [61] Electrolytes As there frequently is initially acidosis , the potassium level may be normal, even though large losses have occurred. [14] As the dehydration is corrected, potassium levels may decrease rapidly, and thus need to be replaced. [14] This may be done by consuming foods high in potassium, like bananas or coconut water. [62] Antibiotics Antibiotic treatments for one to three days shorten the course of the disease and reduce the severity of the symptoms. [14] Use of antibiotics also reduces fluid requirements. [63] People will recover without them, however, if sufficient hydration is maintained. [31] The WHO only recommends antibiotics in those with severe dehydration. [62] Doxycycline is typically used first line, although some strains of V. cholerae have shown resistance . [14] Testing for resistance during an outbreak can help determine appropriate future choices. [14] Other antibiotics proven to be effective include cotrimoxazole , erythromycin , tetracycline , chloramphenicol , and furazolidone . [64] Fluoroquinolones , such as ciprofloxacin , also may be used, but resistance has been reported. [65] Antibiotics improve outcomes in those who are both severely and not severely dehydrated. [66] Azithromycin and tetracycline may work better than doxycycline or ciprofloxacin . [66] Zinc supplementation In Bangladesh zinc supplementation reduced the duration and severity of diarrhea in children with cholera when given with antibiotics and rehydration therapy as needed. ... ] so cholera was able to spread. [95] Cholera morbus is a historical term that was used to refer to gastroenteritis rather than specifically cholera. [96] Drawing of Death bringing cholera, in Le Petit Journal (1912). Emperor Pedro II of Brazil visiting people with cholera in 1855. Hand bill from the New York City Board of Health , 1832—the outdated public health advice demonstrates the lack of understanding of the disease and its actual causative factors. ... Affordability of vaccines can be a problem; if the governments do not provide vaccinations, only the wealthy may be able to afford them and there will be a greater toll on the country's poor. [115] [116] The speed with which government leaders respond to cholera outbreaks is important. [117] Besides contributing to an effective or declining public health care system and water sanitation treatments, government can have indirect effects on cholera control and the effectiveness of a response to cholera. [118] A country's government can impact its ability to prevent disease and control its spread.
  • Tree Nut Allergy Wikipedia
    Someone allergic to walnuts or pecans may not have an allergy to cashews or pistachios, because the two groups are only distantly related and do not necessarily share related allergenic proteins. ... Argentina decided to prohibit precautionary allergen labeling since 2010, and instead puts the onus on the manufacturer to control the manufacturing process and label only those allergenic ingredients known to be in the products. ... Retrieved 12 January 2018 . ^ a b c d e f Allen KJ, Turner PJ, Pawankar R, Taylor S, Sicherer S, Lack G, Rosario N, Ebisawa M, Wong G, Mills EN, Beyer K, Fiocchi A, Sampson HA (2014). ... CS1 maint: extra text: authors list ( link ) ^ https://acaai.org/allergies/types/food-allergies/types-food-allergy/tree-nut-allergy ^ https://kidshealth.org/en/parents/allergy.html ^ https://acaai.org/allergies/types/food-allergies/types-food-allergy/tree-nut-allergy ^ https://acaai.org/allergies/types/food-allergies/types-food-allergy/tree-nut-allergy ^ a b Bublin M, Breiteneder H (2014). ... J Pharm Sci . 107 (5): 1263–1268. doi : 10.1016/j.xphs.2017.12.021 . PMID 29287928 . ^ Mills EN, Valovirta E, Madsen C, Taylor SL, Vieths S, Anklam E, Baumgartner S, Koch P, Crevel RW, Frewer L (2004).
    HLA-DRB1, CCR1, HLA-A, STAT6, RBM45, NUTM1
  • Giant Cell Arteritis Mayo Clinic
    Complications Giant cell arteritis can cause serious complications, including: Blindness. Diminished blood flow to your eyes can cause sudden, painless vision loss in one or, rarely, both eyes. ... For giant cell arteritis, questions to ask your doctor include: What's the most likely cause of my symptoms? What are other possible causes? What tests will I need? What are my treatment options? What side effects can I expect from the medication? How long do I need to stay on medication, and what's my long-term prognosis? Will giant cell arteritis come back? ... How can I best manage them together? Do I need to change my diet? Do I need to take supplements?
    PTPN22, IL6, HLA-DRB1, IFNG, SMUG1, TNF, CRP, RBM45, GCA, TLR4, IL10, ICAM1, ESR1, TP53, MMP2, MMP9, IL17A, PLCE1, CCL5, HLA-DQA1, IL32, NOS3, CTNNB1, IL6R, MTHFR, IL23A, ACR, CCR5, CD68, CCL2, RASSF1, CD274, IL1B, TGFB1, COX2, FASLG, IFNA1, IFNA13, ESR2, HLA-B, MTCO2P12, MMP3, TNFSF13B, PTGS2, PDCD1, CD40, CDKN2A, IL4, IL33, VEGFA, TGFBR1, EDN1, TGFBR2, HT, RABEPK, TSBP1, LANCL1, ANP32B, SPATA2, IL1RL1, ARHGEF2, CD83, ACHE, CXCR4, P4HA2, MBD4, HLTF, SNCA, STAT1, STAT4, TAZ, TERT, TNFAIP3, TP53BP1, TP73, TRAF1, TRAF6, TYMS, VCAM1, XRCC1, XRCC2, XRCC3, SEMA3B, CCDC6, PLA2G6, TP63, TNFSF13, TNFRSF11A, CDK5R1, CD226, SETD2, GADD45G, EBNA1BP2, CDCA5, IL23R, CBLL2, RASSF6, IL27, ARMH1, IL31, MIR141, MIR203A, MIR22, MIR135B, MIR146B, MIR628, CCR2, MIR770, HOTAIR, CD24, MIR3196, MICA, RPL17-C18orf32, KLRC4-KLRK1, C5orf66-AS1, MIR6872, UPK3B, H3P13, LMLN, TMPRSS13, FAM167A, IL17D, FAF1, KLRK1, POU2F3, WWTR1, DKK3, IL37, SELE, IL21R, IL22, MBL3P, WWOX, BANK1, RASSF5, MOCOS, MEG3, ZC4H2, MYDGF, SLC12A9, IL21, SLC25A19, MUL1, COL18A1, FIP1L1, ARHGAP24, SHMT1, PLCL1, CX3CL1, CXCL11, EGFR, ELN, ERBB2, ERCC5, F9, FCGR2A, FCGR2B, FCGR3A, FCGR3B, FCN2, FGF2, FGF13, FOLR2, GALNT2, GCHFR, CXCR3, GYPA, HIF1A, HLA-DQB1, HLA-DRB3, IFNGR1, CCN1, IKBKB, IL1A, IL1RN, EDNRB, ECE1, DNMT3B, CD6, ACTB, JAG1, ALB, AKR1B1, ANGPT1, ANGPT2, ANXA1, FAS, CCND1, BLK, CAV1, CD40LG, GADD45A, CDKN1A, CDKN2D, CDS1, CCR6, CRH, CSF2, CSF3, CSK, CTLA4, CX3CR1, DAP, IL2, IL2RA, IL3, PLA2G1B, NEDD4, NFKB1, NOS2, PEBP1, PRKN, PCNA, PIK3C3, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PLA2G2A, MX1, PLG, MAPK1, MAPK8, PSMD7, PTEN, PTX3, REG1A, RHCE, RPL17, S100A8, S100A9, GADD45B, MTRR, CXCL8, LMNA, IL9, IL12A, IL12RB2, CXCL10, IRAK1, IRF5, ITGA2B, ITGAM, ITGB3, KRT15, RPSA, LTB, MST1, SMAD4, MBL2, SMCP, MDM2, MECP2, MFGE8, MIF, MMP12, MNAT1, MPO, MSMB, H3P28
    • Temporal Arteritis OMIM
      This sequence stretch translated into a polymorphic site in the antigen-binding groove of the HLA-DR molecule, suggesting a crucial role in the selection and presentation of antigen to T lymphocytes. Eyes - Retinal arteritis - Blindness Inheritance - Autosomal dominant Misc - Response to adrenal glucocorticoids Lab - Elevated sedimentation rate Vascular - Temporal arteritis - Giant cell arteritis - Polymyalgia rheumatica (PMR) ▲ Close
    • Giant Cell Arteritis Orphanet
      Giant cell arteritis (GCA) is a large vessel vasculitis predominantly involving the arteries originating from the aortic arch and especially the extracranial branches of the carotid arteries. Epidemiology GCA is the most common adulthood vasculitis with an annual incidence of 1/3,000-1/25,000 adults over 50 years old. It is more frequent in populations of northern European background. GCA affects people of more than 50 years old (median age at diagnosis between 70-75 years old) and occurs twice as frequently in women as in men. Clinical description GCA often starts insidiously with general symptoms, cranial manifestations (headache, jaw claudication, scalp tenderness, visual loss), and, in about 50% of patients, polymyalgia rheumatica. Visual symptoms due to an ischemic optic neuropathy occur in 20-30% of patients, and can rapidly lead to irreversible monocular blindness.
    • Giant Cell Arteritis GARD
      Giant cell arteritis (GCA) is a form of vasculitis , a group of disorders that cause inflammation of blood vessels. GCA most commonly affects the arteries of the head (especially the temporal arteries, located on each side of the head), but arteries in other areas of the body can also become inflamed. The inflammation causes the arteries to narrow, resulting in poor blood flow. Signs and symptoms when arteries in the head are involved may include a throbbing headache on one side or the back of the head, tenderness of the scalp, flu-like symptoms, and/or problems with eyesight. Symptoms when other arteries are involved depend on the location of those arteries.
  • Chiari Malformation Mayo Clinic
    For Chiari malformation, some basic questions to ask your doctor include: What is likely causing my symptoms or condition? Other than the most likely cause, what are possible causes for my symptoms or condition? ... If you don't think I need to be treated now, how will you monitor me for changes in my condition? If you recommend surgery, what should I expect from my recovery? What is the risk of complications from surgery? What is my long-term prognosis after surgery? ... Should I see a specialist? What will that cost, and will my insurance cover seeing a specialist? ... Have you developed any problems with your eyes and ears, such as blurred vision or a ringing or buzzing in your ears?
    ERF, FUZ, FGFR3, SKI, POLR3A, CHD4, SON, CLIP2, ZIC1, HMGA2, BAZ1B, GTF2IRD1, TMEM94, SIK3, SALL1, LEMD3, TBL1XR1, TBL2, SETD2, DACT1, MKS1, RFWD3, FANCI, SC5D, RFC2, PORCN, PTEN, VANGL1, DNMT3A, ELN, FBN1, FGFR1, FGFR2, GNAQ, GTF2I, KMT2C, LIMK1, MECP2, NOTCH2, NOTCH3, PIK3CA, POR, PTCH1, LRP5, UCN2, PPP1R2C, AQP1, UNC50, ZRSR2, LAMC2, CSF2, CREBBP, UTS2B
    • Chiari Malformation Type Ii OMIM
      CM2 is uniquely associated with myelomeningocele (open spina bifida; see 182940) and is found only in this population (Stevenson, 2004). ... INHERITANCE - Multifactorial HEAD & NECK Eyes - Nystagmus RESPIRATORY - Inspiratory stridor - Expiratory apnea with cyanosis ABDOMEN Gastrointestinal - Dysphagia - Choking - Poor feeding NEUROLOGIC Central Nervous System - Herniation and elongation of the cerebellar tonsils, cerebellar vermis, brainstem, and fourth ventricle through the foramen magnum - Small, thin cerebellum - Absent cisterna magna - Polygyria - Ventricular anomalies - Partial or total agenesis of the corpus callosum (33%) - Hypotonia - Opisthotonos - Bulbar signs - Heterotopias - Cervical myelopathy - Upper limb weakness - Spasticity - Ataxia - Headache, occipital - Subnormal intelligence (62%) - Hydrocephalus - Open spina bifida (myelomeningocele, 182940 ) - Associated with syringomyelia ( 186700 ) MISCELLANEOUS - Symptom onset at birth or infancy Arnold-Chiari type II is uniquely associated with myelomeningocele ( 182940 ) ▲ Close
    • Chiari Malformation Wikipedia
      In normal adults, the posterior fossa comprises 27% of the total intracranial space, while in adults with Chiari Type I, it is only 21%. [51] H. neanderthalensis had platycephalic (flattened) skulls. ... Archived from the original on November 21, 2010 . Retrieved November 4, 2011 . ^ https://abcnews.go.com/GMA/OnCall/story? ... "The Chiari 3.5 malformation: a review of the only reported case". Child's Nervous System . 32 (12): 2317–2319. doi : 10.1007/s00381-016-3255-3 . ... Retrieved February 4, 2015 . ^ [1] [ dead link ] ^ [2] Archived October 17, 2011, at the Wayback Machine ^ "Rizzoli & Isles 7x03 - Cops vs Zombies - Recap" . June 15, 2016. ^ https://twitter.com/RizzoliIslesWB/status/742526140837855233 [ non-primary source needed ] ^ https://www.youtube.com/watch? ... H24info (in French) . Retrieved September 22, 2018 . ^ https://www.newcastleherald.com.au/story/5197651/updated-siblings-give-cuddles-to-ease-the-tears-of-sabre-norris/ .
    • Arnold-Chiari Malformation Type Ii Orphanet
      A rare, central nervous system malformation characterized by caudal displacement of the cerebellum, pons, medulla and fourth ventricle through the foramen magnum into the spinal canal, and is typically associated with myelomeningocele. Variable other central nervous system abnormalities might be present (partial or complete agenesis of the corpus callosum, a small fourth ventricle, obstructive hydrocephalus, falx and tentorium defects, and polygyria). Symptoms include hypotonia, apnea with cyanosis, dysphagia, opisthotonus, nystagmus, spasticity, ataxia, and occipital headache.
    • Chiari Malformation Type 2 GARD
      Chiari malformation type 2 (CM type II) is a type of Chiari malformation in which both the cerebellum and brain stem tissue extend into the foramen magnum (the hole at the skull base for passing of the spinal cord). CM type II is usually accompanied by a myelomeningocele (a form of spina bifida that occurs when the spinal canal and backbone do not close before birth), which can result in partial or complete paralysis of the area below the spinal opening. While the severity of CM type II can vary greatly, it can potentially cause severe, life-threatening complications during infancy or childhood. The exact cause of CM type II is not known but it appears to be due to defects in the brain and spinal cord that occur during fetal development. Treatment includes surgery to ease symptoms and/or stop the progression of damage to the nervous system.
  • Dipsomania Wikipedia
    Contents 1 History 1.1 Examples in fiction 1.2 Examples in science 2 See also 3 References 4 External links History [ edit ] The term was coined by the German physician Christoph Wilhelm Hufeland in 1819, when, in a preface to an influential book by German-Russian doctor C. von Brühl-Cramer, [1] he translated Brühl-Cramer's term " trunksucht " as "dipsomania". [2] [3] [4] Brühl-Cramer classified dipsomania in terms of continuous, remittent, intermittent, periodic and mixed forms, and in his book he discussed its cause, pathogenesis , sequelae , and treatment options, all influenced by prevailing ideas about the laws of chemistry and concepts of excitability. [5] Due to the influence of Brühl-Cramer's pioneering work, dipsomania became popular in medical circles throughout the 19th century. [6] Political scientist Mariana Valverde describes dipsomania as "the most medical" of the many terms used to describe habitual drunkenness in the 19th century. [7] Along with terms such as "inebriety", the idea of dipsomania was used as part of an effort of medical professionals and reformers to change attitudes about habitual drunkenness from being a criminally punishable vice to being a medically treatable disease. [8] As historian Roy MacLeod wrote about this dipsomania reform movement, it "illuminates certain features of the gradual transformation taking place in national attitudes towards the prevention and cure of social illnesses during the last quarter of the 19th century." [8] Although dipsomania was used in a variety of somewhat contradictory ways by different individuals, by the late 19th century the term was usually used to describe a periodic or acute condition, in contrast to chronic drunkenness. [9] In his 1893 book Clinical Lessons on Mental Diseases: The Mental State of Dipsomania , Magnan characterized dipsomania as a crisis lasting from one day to two weeks, and consisting of a rapid and huge ingestion of alcohol or whatever other strong, excitatory liquid was available. [9] Magnan further described dipsomania as solitary alcohol abuse, with loss of all other interests, and these crises recurred at indeterminate intervals, separated by periods when the subject was generally sober. [9] Similarly, in 1892 the influential English physician and mental health expert Daniel Hack Tuke defined dipsomania as a syndrome involving "an irresistible obsession and impulse to drink, coming on in attacks, during which the patients are in a condition of impotence of will and manifest great anguish." [10] Tuke clarifies that dipsomania can be distinguished from what was at the time considered alcoholism by six key factors. ... Alcoholism has no definite course." [12] Fourth, "a dipsomaniac satisfies a pathological and imperious want; he does not like alcohol, and takes it against his will," whereas "an alcoholic individual has no actual want; he only obeys a vice, a proclivity, and an alteration of his moral sense." [12] Fifth, a dipsomaniac is conscious and ashamed of his condition, whereas an alcoholic is sometimes unaware of, but more often indifferent to it. ... "All this time I have been liable to fits of ether dipsomania, kept away at intervals only by rigorous abstention from thought on the subject." ... London: Macmillan and Co., Limited. p. 1065. Works cited Tuke, Daniel Hack (1892). A Dictionary of Psychological Medicine: Giving the Definition, Etymology and Synonyms of the Terms Used in Medical Psychology with the Symptoms, Treatment, and Pathology of Insanity and the Law of Lunacy in Great Britain and Ireland . 1 . ... CS1 maint: ref=harv ( link ) External links [ edit ] Bucknill, John Charles; Daniel Hack Tuke (1879). A Manual of Psychological Medicine: Containing the Lunacy Laws, the Nosology, Aetiology, Statistics, Description, Diagnosis, Pathology, and Treatment of Insanity (Fourth ed.).
    GABRA2, ALDH2, HTR2A, ADH1C, ADH1B, CYP2E1, OPRM1, NPY, PDYN, SLC6A4, SNCA, CHRNA5, GABBR1, TACR1, TAS2R38, CCKAR, CHRNA3, NPY2R, GABRG2, SLC29A1, SHBG, TACR3, GGT1, ADH4, FTO, SERINC2, CTNNA2, KIAA0040, PKNOX2, LINC02694, KCNJ6, THSD7B, AKR1A1, BDNF, CHRM2, POMC, DBH, MAOA, ANKK1, HTR1B, DRD2, DRD3, DRD4, CRHR1, COMT, SLC6A3, OPRK1, CRH, ALDH1A1, MAOB, GRIN2B, CNR1, TPH1, ADH7, HTR2C, TH, HTR1A, MTHFR, NFKB1, TRH, GATA4, GAD1, APOE, GRIN2A, OPRL1, GABRB1, IL6, GABRA6, HTR3A, CCK, MPDZ, GABRB3, GABRA1, HTR7, SGIP1, IL1RN, IL10, GRM8, LEP, IL1B, GRIN1, MMP9, OPRD1, NR4A2, GLUL, GH1, NTRK2, GAL, GAD2, GABRG1, DRD1, HNMT, SLC6A2, ADH1A, CLOCK, HTR3B, CHRNB4, ADH5, ARSA, CHRNA4, ZNF699, SLC18A2, GRIK1, SNRNP70, GABRB2, SRD5A1, TAC1, CDH11, CDH13, GABRG3, ACE, GRIK3, SLC1A2, TP53, GRM1, TTC12, PTP4A1, ADRA2A, IL1R1, IL1A, SGCE, AKR1C3, SDHAF3, ABO, HMGB1, TKT, CAT, FYN, NTSR1, PHF3, CNTNAP2, DKK2, OXT, CREB1, CHRNB3, CRHBP, NTS, GHS, SLC6A5, RFX4, PENK, XRCC5, KPNA3, AGO1, LRP8, UBAP2, SEMA5A, CXCL8, SLC17A5, GEMIN4, TESK2, TIPARP, PIK3R1, SAT1, LILRA1, KLF11, GALR3, MGLL, GALR2, ZCCHC14, ANKRD7, ARC, RGS4, NRXN3, SLCO3A1, NCAM1, NQO2, TAS2R16, SIGMAR1, KANK1, SLC6A9, C1D, IPO11, SRD5A2, HERPUD1, PCDH12, NEUROD2, PDE10A, AGO2, TFAP2B, SPG21, CYTL1, CARTPT, NRDC, MOG, MOBP, HOMER1, SLC6A1, NPY5R, CNTN6, NAT1, DSCAML1, EPHX1, GRM3, GABRR1, GRM2, CAMK2A, NKAIN1, THEMIS, DPYSL2, OSBPL5, CYP2A13, CDH12, CDH15, GNB3, CNTN4, GLI2, GHSR, GABRA5, AKR1C4, CNR2, NKAIN2, GAPDH, GAP43, GALR1, CALCA, CAMK4, DUSP8, PTK2B, HLA-DRA, PER3, ADCY7, ADH6, NLGN4X, STON2, HAMP, ALDH3B2, ALK, GSTM1, DTNBP1, AR, GRM7, FABP2, CASC4, ASTN1, GABRR2, EP300, EGF, RFC1, CYP2B6, SLC46A1, EGFR, RASGRF2, ECHS1, PDE4B, REN, CDK20, RACK1, CFTR, ADCY5, TBX19, VWF, PHLDA2, SNORA54, NPS, BAG3, MIR382, BHMT, TF, ST18, CARS1, GPHN, NPSR1, CDH5, CDH8, CDH9, EPHA8, CDH18, CDH10, GGH, FOLR1, MMP2, MBP, NAP1L4, FKBP5, LHB, GFAP, IL17A, FSHB, ANAPC1, TAGLN3, PCDH10, PPP1R1B, HDAC2, NMUR2, SLC22A18, AVPR1B, BRAP, SEMA3A, UTP20, ARL15, AGBL4, STAT3, RARA, PECR, LHPP, MREG, ANKS1B, KLF12, PML, STK40, C1orf220, CCSER1, FIP1L1, NCALD, FSTL5, AVP, NUMA1, NRXN1, PPP1R16B, RHOG, SLC39A8, GSS, STX18-AS1, TRPC4AP, LINC02268, ZBTB16, FAM162A, LINC01818, LINC02661, ESRRG, RN7SL697P, ADAMTSL1, AOX3P, PLGRKT, NSG1, AOX3P-AOX2P, STAT5B, BCOR, MBNL2, SLC6A6, C15orf32, NPM1, GCKR, STAG3, CSRNP3, IGSF22, IGSF9B, PRKAR1A, IRF2BP2, SETD5, TBL1XR1, GRK5, MICB, NCOA6, LYZ, MAP3K4, PLCL2, NABP1, RHBDL2, TMEM260, C16orf72, GRM5, ALLC, DDX53, LINC02210-CRHR1, LOC110806262, PRL, TSPO, SAGE1, GLP1R, GYPE, GYPB, GYPA, TPH2, FLNA, OR2AG1, FAAH, MIR21, ADIPOQ, KL, PER2, PPARA, F9, PNOC, TDO2, CCKBR, APRT, RET, TLR4, SMPD1, SMARCA1, PER1, CFP, PRDM2, NGF, CYP2A6, CCDC6, PTCH1, ESR1, DMTN, F2, EBPL, EPO, IL18R1, WDR20, ELK3, FAT1, PLCD3, EDNRB, ATN1, NLRP3, DNASE1L3, MRGPRF, DBI, OPN4, NPL, FGF2, PARP9, HTT, PCDH19, HCRTR1, CPNE5, HARS1, GUSB, GSTT1, GSR, DCLRE1C, GSK3B, NR3C1, GRIN2C, EFHD2, GPT, GM2A, GDNF, OPA3, EFHC2, PNPLA3, SLC19A3, GCG, CYP3A5, FN1, CYP19A1, COL6A3, CNIH3, AGT, ARNTL, LINC00273, GGTLC5P, GGTLC3, GGT2, GGTLC4P, AIRE, MIR4456, ALDH1B1, THRA1/BTR, MDD2, AGER, AP2B1, ADCYAP1, RN7SL263P, ADCY9, ADCY1, ADA, STIN2-VNTR, LOC111216288, OPN1SW, MDD1, TMEM161B, CDK5, CRP, ZNF366, HHEX, CHRNB1, H19, CHRM5, BTBD8, EYS, CHM, CD40, DST, CD36, CACNA1C, DAGLA, BRCA1, MIR126, MIR141, MIR155, MIR183, MIR19A, NLN, RETN, SLC17A6, PTPN11, RXRB, ARFGEF2, PDLIM5, RNU1-4, BRD2, PPARGC1A, PRSS21, RAB40B, SPACA9, SCN11A, SRSF5, MAPK8, PPAT, KDM6B, PPARG, PPARD, ABAT, PLG, HEY2, RBFOX2, SORT1, SLC1A3, TFIP11, TIMP1, NOL3, ST8SIA4, HGS, XRCC4, UMOD, DLGAP2, PPIG, TYR, TNF, THRA, SMS, THOP1, TGFB1, TFF3, TAT, SYN2, HDAC6, EBI3, SST, DHRS9, PIK3CG, PIK3CD, HLA-B, IL16, MFAP1, MEF2C, MC4R, MARK1, LOX, ABLIM1, KCNN3, KCNK3, IMPA1, IL12B, GDAP1, HTR1E, ACSS2, HSPG2, NPDC1, KCNK13, ARHGEF7, HSD11B2, HRAS, HP, MYC, MYT1, PIK3CB, HPGDS, PIK3CA, AUTS2, PHEX, PGC, PECAM1, PDGFRB, PDE4A, SALL3, PC, OXTR, NF1, NUCB2, NRGN, NPY1R, NOS3, HDGFL3, NGFR, ASCC1, HERC5, NF2, H3P40
    • Alcohol Dependence OMIM
      Abnormalities in platelet monoamine oxidase activity were found only in type 2 alcoholics (Von Knorring et al., 1985). ... By using 2 discovery GWAS datasets of the Study of Addiction: Genetics and Environment (SAGE) and the Collaborative Study on the Genetics of Alcoholism (COGA), Han et al. (2013) identified a subnetwork of 39 genes that not only was enriched for genes associated with alcohol dependence, but also collectively associated with alcohol dependence in both European Americans (p less than 0.0001) and African Americans (p = 0.0008). ... The combined SNP associations with early- and late-stage metabolism only accounted for approximately 20% of the total genetic variance linked to the ADH region, and most of the variance for in vivo alcohol metabolism linked to this region is yet to be explained. ... There were study-wide significant associations between rs1229984 (103720.0001) and flushing and consumption, but only nominally significant associations (p less than 0.01) with alcohol dependence. ... Association with the DKK2 gene on Chromosome 4q25 Kalsi et al. (2010) conducted a systematic, gene-centric association study of alcohol dependence using 518 SNPs within the 65 genes of the linkage peak on chromosome 4q21-q32 identified by Prescott et al. (2006). Case-only regression analysis with the quantitative variable of alcohol-dependent symptoms was performed in 562 genetically independent cases of the Irish Affected Sib Pair Study of Alcohol Dependence (IASPSAD) sample.
    • Alcoholism Wikipedia
      The alcohol dehydrogenase allele ADH1B*3 also causes a more rapid metabolism of alcohol. The allele ADH1B*3 is only found in some individuals of African descent and certain Native American tribes. ... It defines a standard drink as one 12-ounce bottle of beer, one 5-ounce glass of wine, or 1.5 ounces of distilled spirits. [97] Despite this risk, a 2014 report in the National Survey on Drug Use and Health found that only 10% of either "heavy drinkers" or "binge drinkers" defined according to the above criteria also met the criteria for alcohol dependence, while only 1.3% of non-binge drinkers met the criteria. ... Much of the treatment community for alcoholism supports an abstinence-based zero tolerance approach; however, some prefer a harm-reduction approach. [125] Detoxification Main article: Alcohol detoxification Alcohol detoxification or 'detox' for alcoholics is an abrupt stop of alcohol drinking coupled with the substitution of drugs, such as benzodiazepines , that have similar effects to prevent alcohol withdrawal . Individuals who are only at risk of mild to moderate withdrawal symptoms can be detoxified as outpatients. ... Alcohol causes the body to release endorphins, which in turn release dopamine and activate the reward pathways; hence in the body reduces the pleasurable effects from consuming alcohol. [141] Evidence supports a reduced risk of relapse among alcohol-dependent persons and a decrease in excessive drinking. [140] Nalmefene also appears effective and works in a similar manner. [140] The Sinclair method is another approach to using naltrexone or other opioid antagonists to treat alcoholism by having the person take the medication about an hour before they drink alcohol and only then . [142] [143] The medication blocks the positive reinforcement effects of ethanol and hypothetically allows the person to stop drinking or drink less. [143] Disulfiram prevents the elimination of acetaldehyde , a chemical the body produces when breaking down ethanol. ... Suicide is also very common in adolescent alcohol abusers, with 25 percent of suicides in adolescents being related to alcohol abuse. [164] Among those with alcohol dependence after one year, some met the criteria for low-risk drinking, even though only 25.5 percent of the group received any treatment, with the breakdown as follows: 25 percent were found to be still dependent, 27.3 percent were in partial remission (some symptoms persist), 11.8 percent asymptomatic drinkers (consumption increases chances of relapse) and 35.9 percent were fully recovered – made up of 17.7 percent low-risk drinkers plus 18.2 percent abstainers. [165] In contrast, however, the results of a long-term (60-year) follow-up of two groups of alcoholic men indicated that "return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence." [134] There was also "return-to-controlled drinking, as reported in short-term studies, is often a mirage."
    • Alcohol Use Disorder MedlinePlus
      Alcohol use disorder is a diagnosis made when an individual has severe problems related to drinking alcohol. Alcohol use disorder can cause major health, social, and economic problems, and can endanger affected individuals and others through behaviors prompted by impaired decision-making and lowered inhibitions, such as aggression, unprotected sex, or driving while intoxicated. Alcohol use disorder is a broad diagnosis that encompasses several commonly used terms describing problems with drinking. It includes alcoholism, also called alcohol addiction, which is a long-lasting (chronic) condition characterized by a powerful, compulsive urge to drink alcohol and the inability to stop drinking after starting. In addition to alcoholism, alcohol use disorder includes alcohol abuse, which involves problem drinking without addiction.
    • Alcohol Dependence Wikipedia
      Other alcohol-related disorders [ edit ] Because only 3 of the 7 DSM-IV criteria for alcohol dependence are required, not all patients meet the same criteria and therefore not all have the same symptoms and problems related to drinking. ... However, many definitions of alcoholism exist, and only some are compatible with alcohol abuse. ... Alcohol dependence refers to an entity in which only alcohol is the involved addictive agent. ... In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. ^ http://www.alcoholcostcalculator.org/business/about/dsm.html ^ "ICD-9-CM Diagnosis Codes 303.* : Alcohol dependence syndrome" . www.icd9data.com . ^ Clark, David, Background Briefing, Alcohol Dependence, Drink and Drug News, 7 February 2005, p. 11 ^ "Alcohol use screening tests – GOV.UK" . www.gov.uk .
  • Lichen Sclerosus Mayo Clinic
    If you've already been diagnosed with lichen sclerosus, see your health care provider every 6 to 12 months. These visits are important to check for any skin changes or side effects of treatment. ... After several weeks, your health care provider will likely suggest that you use it only twice a week to prevent symptoms from returning. ... Some basic questions to ask your health care provider about possible lichen sclerosus include: What's the most likely cause of my symptoms? What treatment approach do you suggest, if any? If the first treatment doesn't work, what will you suggest next? How much do you expect my symptoms will improve with treatment — and how soon? Will I need treatment for this condition for the rest of my life? What self-care steps can I follow to ease my symptoms?
    TP53, CDKN2A, ECM1, H3P10, TNF, IL1B, CAT, RBP2, S100A7, CCL4, CCL4L2, SOD1, TRBV20OR9-2, THBS1, RARB, PTGS1, CRISP2, ARHGEF1, FSCN1, RASSF2, SERPINA1, MMRN1, CADM1, KRT20, MIB1, SPZ1, MIR155HG, PRSS55, CXCL17, CCL4L1, MIR155, LINC01191, DEFB4B, PTCH1, AFM, PCNA, IL1A, CCND1, CALCA, MS4A1, CRABP2, CCN2, DEFB4A, FLG, GATA3, CXCR3, GZMB, HLA-B, HSPA4, IL1RN, AR, IL13, CXCL10, IRF6, KRAS, KRT1, KRT17, SMAD3, MAL, MGMT, MKI67, MMP9, COX1, MUC2
    • Lichen Sclerosus Et Atrophicus OMIM
      Lichen sclerosus et atrophicus is a relatively uncommon cutaneous disorder that may affect any area. There is a particular predilection, however, for involvement of the female genitalia. Although typically the patient is a middle-aged female, prepubertal females may also develop this disorder. Shirer and Ray (1987) stated that about 18 cases of familial LSA had been reported. They concluded that 'heredity plays a role in some, if not all, cases.'
    • Lichen Sclerosus Wikipedia
      In a prospective longitudinal cohort study of 507 women throughout 6 years, cancer occurred for 4.7% of patients who were only "partially compliant" with corticosteroid treatment, while it occurred in 0% of cases where they were "fully compliant". [39] In a second study, of 129 patients, cancer occurred in 11% of patients, none of which were fully compliant with corticosteroid treatment. [35] Both these studies however also said that a corticosteroid as powerful as clobetasol is not necessary in most cases. ... External links [ edit ] Classification D ICD - 10 : L90.0 ICD - 9-CM : 701.0 MeSH : D018459 External resources eMedicine : derm/234 NIAMS – Questions and Answers About Lichen Sclerosus NIAMS – Fast Facts About Lichen Sclerosus dermnetnz.org better medicine Medscape Reference Author: Jeffrey Meffert, MD; Chief Editor: Dirk M Elston, MD Medical Pictures http://www.dermlectures.com/LecturesWMV.cfm?lectureID=88 https://web.archive.org/web/20070927210529/http://dermis.multimedica.de/dermisroot/de/34088/diagnose.htm https://web.archive.org/web/20071008130921/http://dermnetnz.org/immune/ls-imgs.html v t e Cutaneous keratosis, ulcer, atrophy, and necrobiosis Epidermal thickening keratoderma : Keratoderma climactericum Paraneoplastic keratoderma Acrokeratosis paraneoplastica of Bazex Aquagenic keratoderma Drug-induced keratoderma psoriasis Keratoderma blennorrhagicum keratosis : Seborrheic keratosis Clonal seborrheic keratosis Common seborrheic keratosis Irritated seborrheic keratosis Seborrheic keratosis with squamous atypia Reticulated seborrheic keratosis Dermatosis papulosa nigra Keratosis punctata of the palmar creases other hyperkeratosis : Acanthosis nigricans Confluent and reticulated papillomatosis Callus Ichthyosis acquisita Arsenical keratosis Chronic scar keratosis Hyperkeratosis lenticularis perstans Hydrocarbon keratosis Hyperkeratosis of the nipple and areola Inverted follicular keratosis Lichenoid keratosis Multiple minute digitate hyperkeratosis PUVA keratosis Reactional keratosis Stucco keratosis Thermal keratosis Viral keratosis Warty dyskeratoma Waxy keratosis of childhood other hypertrophy: Keloid Hypertrophic scar Cutis verticis gyrata Necrobiosis / granuloma Necrobiotic/palisading Granuloma annulare Perforating Generalized Subcutaneous Granuloma annulare in HIV disease Localized granuloma annulare Patch-type granuloma annulare Necrobiosis lipoidica Annular elastolytic giant-cell granuloma Granuloma multiforme Necrobiotic xanthogranuloma Palisaded neutrophilic and granulomatous dermatitis Rheumatoid nodulosis Interstitial granulomatous dermatitis / Interstitial granulomatous drug reaction Foreign body granuloma Beryllium granuloma Mercury granuloma Silica granuloma Silicone granuloma Zirconium granuloma Soot tattoo Tattoo Carbon stain Other/ungrouped eosinophilic dermatosis Granuloma faciale Dermis / localized CTD Cutaneous lupus erythematosus chronic: Discoid Panniculitis subacute : Neonatal ungrouped: Chilblain Lupus erythematosus–lichen planus overlap syndrome Tumid Verrucous Rowell's syndrome Scleroderma / Morphea Localized scleroderma Localized morphea Morphea–lichen sclerosus et atrophicus overlap Generalized morphea Atrophoderma of Pasini and Pierini Pansclerotic morphea Morphea profunda Linear scleroderma Atrophic / atrophoderma Lichen sclerosus Anetoderma Schweninger–Buzzi anetoderma Jadassohn–Pellizzari anetoderma Atrophoderma of Pasini and Pierini Acrodermatitis chronica atrophicans Semicircular lipoatrophy Follicular atrophoderma Linear atrophoderma of Moulin Perforating Kyrle disease Reactive perforating collagenosis Elastosis perforans serpiginosa Perforating folliculitis Acquired perforating dermatosis Skin ulcer Pyoderma gangrenosum Other Calcinosis cutis Sclerodactyly Poikiloderma vasculare atrophicans Ainhum / Pseudo-ainhum
    • Lichen Sclerosus GARD
      Lichen sclerosus (LS) affects the skin leading to scarring around the genital and anal areas. It can occur at any age but mainly occurs in women over the age of 50. It mainly affects the skin around the vagina, anus, and tip of the penis. Symptoms can include white lesions or plaques, pain during urination, itching, and pain during intercourse. Some people have no symptoms, while others may experience itchiness (sometimes severe), discomfort, or blistering.
  • Uterine Fibroids Mayo Clinic
    Many women who are told that hysterectomy is their only option can have an abdominal myomectomy instead. ... This surgery removes the uterus. It remains the only proven permanent solution for uterine fibroids. ... Use it to note important information during your visit. Prepare a list of questions to ask. ... Are the fibroids located on the inside or outside of my uterus? What kinds of tests might I need? ... Will I need a medication before or after surgery? Will my uterine fibroids affect my ability to become pregnant?
    TSC2, HMGA2, ESR1, SMAD3, SFRP1, WNT5B, INHBA, FH, TP53, BET1L, TNRC6B, CCDC57, KANK1, SCFD2, DNAH2, NEK10, PTPRR, NIPAL1, SULT1B1, C11orf65, DNM3, MSH3, ZNF346, SIRT3, CYP19A1, CTNNB1, SYNE1, PGR, IGF1, POGLUT3, LNX1, IGF2, STN1, CSMD1, RIC8A, HK3, MCM8, ACTRT3, SLC7A3, SLC66A3, SLAIN2, MRTFA, NLGN2, COG6, ITPR1, FOXO1, CDC42, WNT4, CDC73, PDLIM5, CD6, TNFSF13, MIR3681HG, LINC00598, ATM, BABAM2, TGFB3, TNFSF12-TNFSF13, MED12, GREB1, COMT, KIT, FN1, AR, VCAN, ESR2, VEGFA, BCL2, EGF, TNF, DES, CDKN2A, MMRN1, ACTB, CYP17A1, AKT1, FGF2, KAT6B, TGFB1, CYP1B1, CUX1, CYP1A1, EDN1, HOXA10, MDM2, PDGFRB, PRL, GPER1, IFI27, CXCL8, RAD51B, GSTM1, KANSL1, CYP2B6, H3P23, MIR197, CCND1, TMED7, BAX, TMED7-TICAM2, MIR200C, DCTN6, HPSE2, CCN1, KRAS, ALK, XRCC1, EPO, ALDH1A1, HMGA1, PTGS2, DNMT1, DPT, EGR1, PSMD9, EGFR, CD34, ZNRD2, PLAG1, SMUG1, TICAM2, PCNA, MIR29C, IL1B, IL2, MYLK, SMN2, IL4, SPIN1, HTC2, TSHZ1, SQSTM1, XRCC3, SMN1, PPARG, INSR, SLPI, ATG7, IL18R1, IGFBP3, IGFBP2, MAPK3, PTCH1, PIK3CG, ITGAV, PIK3CD, SMAD4, DLEC1, PTEN, NOS3, MED13, MMP2, SERPINE1, PBX3, SRF, MCL1, SMAD7, RELA, PTTG1, SMAD2, LGALS3, LEP, RTN4, EBI3, PIK3CA, TXN, PPIG, SHBG, PIK3CB, CD274, H3P10, KLF11, MUC16, GJA1, MSTN, MTOR, FMOD, BCR, FASN, EZH2, EWSR1, EDNRB, CALD1, CASP3, CAV1, ATN1, DNMT3A, MIR21, CDH1, ACE, CDK2, CCN2, CDK8, CDKN1A, COL4A6, COL4A5, ANGPT2, COL1A1, HIF1A, PRLHR, AKT2, CD24, HSD17B1, GNRHR, GNRH1, HSD17B2, MIR29B2, CCN5, COG5, FST, NCOA2, POSTN, BET1, RNA5SP202, MIR29B1, MIR29A, PGR-AS1, MIR221, TNFSF9, MTCO2P12, HOTAIR, SPINT2, KHDRBS1, TNFSF10, EBP, NFAT5, NES, WASF3, TRADD, FERMT2, BECN1, SDS, SLC27A4, MIR182, AKAP13, NCOA1, LOC110806263, RAD50, MIR7-1, POTEM, MIR363, NCOR1, MIR146B, CXCL14, ADAMTS4, ATG5, POU5F1P3, EDIL3, CHST3, TSIX, ADIPOQ, KLF4, POU5F1P4, POTEF, NCOR2, WSCD2, DEPDC5, GPR166P, MIR15B, MVP, EBAG9, MIR93, MIR7-3, ARTN, SNURF, AKT3, HDAC6, MIR7-2, TRG-GCC5-1, PDCD6, GJC1, VN1R17P, SNIP1, MIR150, CDK19, AZIN2, HDAC8, MBD6, GNRHR2, ADCY10, EDEM2, ATF7IP, MRGPRX3, MRGPRX4, MEG3, CYCSP25, RXFP2, PACC1, ANO1, WIPI1, UGT1A8, OSCP1, MED8, NACC1, MYOCD, FERMT3, FSD1, GGCT, TP63, TET1, PPP1R2C, PDCD1LG2, TSPYL2, FSD1L, LINC00473, ADGRV1, LGR6, NLRC5, SPZ1, ATAD1, RXFP1, CCNB1IP1, HSD17B7, GPR151, DCTN4, GADL1, GPRC6A, TAC4, MRGPRX1, IL4I1, LPAR3, HCAR2, SLC7A8, LHFPL3, PRSS55, NANOG, SLC27A1, TBPL2, CASC15, RFTN1, SERTM2, MIRLET7C, TBATA, NUP62, MAGEC3, AGO2, DNAJB7, SLC27A6, SGSM3, PCDH11X, HPGDS, OXER1, PDCD4, FOXP1, TET3, LAT, SNORD56, ADAMTS15, FAM9A, PTPN22, TES, PLD5, SATB2, ACR, IFITM1, GLI1, GJB2, GHR, GH1, GAPDH, FZD2, FOXO3, FKBP5, FGR, FGFR4, FGFR1, EFEMP1, FBN1, PTK2B, F3, ERCC2, EPHB2, ENO1, ENG, EGR2, EFNA4, EDNRA, ECM1, TSC22D3, GLB1, GNRH2, DRD1, GPR17, IKBKB, IGFBP7, IGFBP5, IGFBP1, IFNA13, IFNA1, TNC, HSPA1B, HSPA1A, HRAS, HPV18I2, HPGD, HOXA13, HOXA11, HMGCR, HMGN2, HMGB1, NRG1, GTF2H1, GSTT1, GRM2, NR3C1, GRIA2, DRD2, SARDH, CXCR1, CASP1, VPS51, BSG, BRCA1, DST, BMP8B, BMP2, BCL6, BAK1, ATF3, ASIP, ARNT, FAS, APEX1, AMHR2, AMH, AKR1B1, AHR, AGTR2, AGTR1, AGRP, PLIN2, ACVRL1, ACTG1, CA2, CCNC, DHCR24, CCND2, DHCR7, TIMM8A, DFFB, DFFA, DBI, DAXX, DAPK1, DAP, CYP24A1, CTSL, CSF2, CR2, CPN2, CPN1, COX6C, COL4A2, COL3A1, CKS2, CEBPB, CEBPA, CD44, CD38, CCNG1, IL1RN, IL18, RECK, TACR1, TACR2, TAC1, SYP, STK11, SST, SRC, SPP1, SPINT1, SOX2, SORD, SNRPN, SMARCB1, SLC5A3, SMTN, SLC3A2, SLC2A4, SLC2A1, SFRP4, SDHB, CXCL12, CCL2, SATB1, SALL1, TAC3, TACR3, RXRA, TFAP2C, FZD4, TKTL1, MLRL, SLC7A5, NR4A3, YWHAG, XRCC4, XRCC2, XPC, XIST, WNT7A, LAT2, VIM, VDR, TSC1, CRISP2, TP53BP1, TLR3, SEC62, TIMP2, THBS2, THBS1, NR2F2, ACP1, RGS7, ITGA2, OGG1, NTS, NPPA, NGF, NEUROG1, COX2, MSH2, MPO, MMP14, MMP1, MME, MKI67, MEST, MEN1, MECP2, MAP2, LTBP2, LTBP1, CYP4F3, LAMB1, KRT19, ITGB1, ITGA5, ITGA2B, NTSR1, ORC5, TRIM27, OXTR, REST, RBP1, PLAAT4, RAD51, PTHLH, PTH, PSMB9, PROS1, PRLR, MAPK1, PPP4C, POU5F1, PON1, PLXNA2, PLP1, PLA2G1B, PGAM1, PER1, PDGFRA, PCP4, PCOLCE, PAEP, PEBP1, S100A4
    • Leiomyoma, Uterine OMIM
      A number sign (#) is used with this entry because at least one form of uterine leiomyoma (UL) is known to be due to fusion between an isoform of the recombinational repair gene RAD51B (602948) and the high mobility group protein gene HMGIC (HMGA2; 600698). Uterine leiomyomas have been observed with other fusion partners of the HMGIC gene, namely ALDH2 (100650), COX6C (124090), and HEI10 (608249). Uterine leiomyomata also occur in association with skin leiomyomata and renal cell cancer on the basis of mutations in the gene encoding fumarate hydratase (FH; 136850; see 150800). There is evidence also that leiomyoma development involves a myofibroblast phenotype characterized by dysregulation of genes encoding extracellular matrix proteins, particularly reduced expression of dermatopontin (125597), a feature shared with keloids (148100). Cytogenetics In histologically benign uterine leiomyomas from 34 patients, Heim et al. (1988) found an apparently identical reciprocal translocation t(12;14)(q14-15;q23-24) in the tumors of 4 patients.
    • Uterine Fibroid Wikipedia
      The abdomen can grow larger mimicking the appearance of pregnancy. [1] Some large fibroids can extend out through the cervix and vagina. [7] While fibroids are common, they are not a typical cause for infertility, accounting for about 3% of reasons why a woman may not be able to have a child. [9] The majority of women with uterine fibroids will have normal pregnancy outcomes. [10] [11] In cases of intercurrent uterine fibroids in infertility, a fibroid is typically located in a submucosal position and it is thought that this location may interfere with the function of the lining and the ability of the embryo to implant . [9] Risk factors [ edit ] Some risk factors associated with the development of uterine fibroids are modifiable. [12] Fibroids are more common in obese women. [13] Fibroids are dependent on estrogen and progesterone to grow and therefore relevant only during the reproductive years. Diet [ edit ] Diets high in fruits and vegetables tend to lower the risk of developing fibroids. [12] Fibers, vitamin A, C and E, phytoestrogens, carotenoids, meat, fish, and dairy products are of unclear effect. [12] Normal dietary levels of vitamin D may reduce the risk of developing fibroids. [12] Genetics [ edit ] Fifty percent of uterine fibroids demonstrate a genetic abnormality. ... If a mother had fibroids, risk in the daughter is about three times higher than average. [14] Black women have a 3-9 times increased chance of developing uterine fibroids than white women. [15] Only a few specific genes or cytogenetic deviations are associated with fibroids. [16] 80-85% of fibroids have a mutation in the mediator complex subunit 12 ( MED12 ) gene. [17] [18] Familial leiomyomata [ edit ] Further information: Hereditary leiomyomatosis and renal cell cancer A syndrome ( Reed's syndrome ) that causes uterine leiomyomata along with cutaneous leiomyomata and renal cell cancer has been reported. [19] [20] [21] This is associated with a mutation in the gene that produces the enzyme fumarate hydratase , located on the long arm of chromosome 1 (1q42.3-43). ... Laparoscopic myomectomy has less pain and shorter time in hospital than open surgery. [54] Hysterectomy [ edit ] Hysterectomy was the classical method of treating fibroids. Although it is now recommended only as last option, fibroids are still the leading cause of hysterectomies in the US. Endometrial ablation [ edit ] Endometrial ablation can be used if the fibroids are only within the uterus and not intramural and relatively small. ... PMID 22895965 . ^ Malartic C, Morel O, Akerman G, Tulpin L, Desfeux P, Barranger E (2008). "La mifépristone dans la prise en charge des fibromes utérins". Gynécologie Obstétrique & Fertilité . 36 (6): 668–74. doi : 10.1016/j.gyobfe.2008.01.017 .
  • Thrush (Horse) Wikipedia
    Daily cleaning of the hooves also contributes to the prevention of thrush. [2] In general, thrush is relatively easy to treat, although it can easily return and it can take up to a year for a fully healthy frog to regrow after a severe infection. References [ edit ] ^ https://www.thehorse.com/articles/27319/the-lowdown-on-thrush ^ a b c d Ensminger, M. ... ISBN 0-8134-2883-1 . Further reading [ edit ] http://www.equisearch.com/horses_care/health/hoof_care/eqthrush305/ https://www.thehorse.com/articles/26470/brushing-up-on-thrush https://www.thehorse.com/articles/32743/thrush-that-black-smelly-gooey-stuff https://www.thehorse.com/articles/20341/thwarting-thrush https://practicalhorsemanmag.com/health-archive/how-to-treat-my-horses-thrush-27863
  • Epidermal Nevus Syndrome Orphanet
    Epidermal nevus syndrome (ENS) is a rare congenitally acquired syndrome, characterized by the presence of epidermal nevi in association with various developmental abnormalities of the skin, eyes, nervous, skeletal, cardiovascular and urogenital systems. ... Most are present at birth, occur sporadically and affect both sexes. All well-defined ENS are lethal gene syndromes, except nevus comedonicus syndrome. ... Management and treatment No ideal medical therapy for the cutaneous lesions of ENS exists. The skin lesions may be amenable to surgery.
    FGFR3, NRAS, PIK3CA, HRAS, KRAS, PTEN, AKT1, COL7A1, KRT10, EGFR, KRT1, RMRP, FGF23, NSDHL
    • Epidermal Nevus MedlinePlus
      One group of epidermal nevi, called keratinocytic or nonorganoid epidermal nevi, includes nevi that involve only keratinocytes. Keratinocytic epidermal nevi are typically found on the torso or limbs. ... The tumor is usually benign, although rarely cancerous (malignant ) tumors develop. Some affected individuals have only an epidermal nevus and no other abnormalities. However, sometimes people with an epidermal nevus also have problems in other body systems, such as the brain, eyes, or bones. In these cases, the affected individual has a condition called an epidermal nevus syndrome. ... Mutations associated with an epidermal nevus are present only in the cells of the nevus, not in the normal skin cells surrounding it.
    • Epidermal Nevus Syndrome Wikipedia
      Epidermal nevus syndrome Other names Solomon's syndrome Specialty Dermatology , medical genetics Epidermal nevus syndrome (also known as " Feuerstein and Mims syndrome ", [1] [2] and " Solomon's syndrome " [1] : 775 [3] ) is a rare disease that was first described in 1968 and consists of extensive epidermal nevi with abnormalities of the central nervous system (CNS), skeleton, skin, cardiovascular system , genitourinary system and eyes. [2] : 634 However, since the syndrome's first description, a broader concept for the " epidermal nevus " syndrome has been proposed, with at least six types being described: [1] : 776 [4] Schimmelpenning syndrome Nevus comedonicus syndrome Pigmented hairy epidermal nevus syndrome Proteus syndrome CHILD syndrome Phakomatosis pigmentokeratotica See also [ edit ] Epidermis List of cutaneous conditions References [ edit ] ^ a b c Freedberg, et al. (2003).
  • Obesity In Mexico Wikipedia
    Mexico’s government has created nutrition programs, to deal with nutritional issues such as obesity; especially in vulnerable people and low-income sectors. [18] These include food distribution among low-income communities, micronutrient supplementation, and fortification of food. [18] All of this is made to fight the deficiency of vitamins and minerals. ... The House passed the proposed measure to charge a 5% tax on packaged food that contains 275 calories (1,150 kJ) or more per 100 grams, on grounds that such high-energy items typically contain large amounts of salt and sugar and few essential nutrients. [22] Subsequent studies have indicated that the one peso per liter tax rate has only led to a small reduction in soft drink consumption, and the fall in calorie consumption was described as "nothing compared to the drop in calories people needed to consume in order to not be obese". [23] The effectiveness of the tax on junk food was subject to debate. [ citation needed ] See also [ edit ] List of countries by Body Mass Index (BMI) References [ edit ] ^ a b c d e Popkin, Barry (2004). ... PMID 15387482 . ^ The nutrition transition and obesity : Food and Agricultural Order of the United Nations. ^ a b c d Sobrepeso y obesidad, Gobierno Del Distrito Federal, April 2013, http://www.who.int/topics/obesity/en/index.html . ^ a b "Fat Mexico - Obesity on the rise in Mexico" , The Economist . ^ a b c d e Bermudez, Odilia I.; Tucker, Katherine L. (2003). ... Retrieved 24 April 2013 . ^ Tuckman, 2008 ^ Lucha libre vs Obesidad, April 2013, http://www.seguro-popular.gob.mx/index.php?option=com_content&view=article&id=547&Itemid=472 . ^ CAMPAÑA "MÍDETE Y ACTÍVATE, April 2013, http://www.cns.salud.gob.mx/contenidos/midete.html . ^ Mexico Tries Taxes to Combat Obesity, https://www.wsj.com/articles/SB10001424052702304864504579141462546165166 ^ editor, Denis Campbell Health policy (2016-03-17).
  • Hiv/aids In Malawi Wikipedia
    For example, older women have demonstrated higher levels of knowledge regarding HIV/AIDS than younger women in Malawi. [2] Because men typically have greater access to education and other social resources, they are often more knowledgeable about HIV prevention and transmission than women. [2] While men are, on average, able to list 2.2 ways to prevent HIV transmission, women are only able to list 1.5 ways. [2] Only 38% of women surveyed in 2003-2004 understood that their husbands would be less likely to contract HIV if they used condoms during intercourse with prostitutes and other women from high-risk groups. [9] In addition, men who are raised in urban environments are, on average, more informed about HIV/AIDS than men who are raised in rural environments, presumably because urban children typically have greater access to educational resources than rural children. [2] Among both men and women, higher levels of education correspond to increased knowledge about HIV/AIDS: men and women who have received secondary school educations are significantly more likely to understand complex aspects of the disease, such as the fact that people who appear healthy can still be HIV-positive, than those who have not. [2] Finally, people who have lost friends or family members to the disease are likely to have greater knowledge about HIV/AIDS due to their personal, firsthand exposure to the problem. [2] The aforementioned study by Barden-O'Fallon et al., which surveyed 940 women and 661 men, indicated that, despite their knowledge and awareness, many people in Malawi do not feel personally susceptible to HIV infection. [2] On average, only 23% of the adults who were surveyed during this study, both male and female, believed that they were likely to contract HIV and die of AIDS. [2] Greater HIV/AIDS awareness among men does not seem to correspond with increased perceived risk; on the other hand, increased levels of knowledge about HIV/AIDS do correlate positively to perceived risk among women. [2] Another study conducted in rural Malawi between 1998 and 2001 by Kirsten P. ... In Malawi, HIV/AIDS is usually transmitted through heterosexual sex , but the epidemic has also significantly impacted the homosexual male population in Malawi. [1] In addition, women in Malawi are more likely to be HIV-positive than men, suggesting that women are particularly vulnerable to HIV/AIDS. [1] Finally, the disease has affected children and young adults both directly and indirectly; 170,000 Malawian children were HIV-positive in 2011, and the number of orphans in Malawi has increased dramatically since the epidemic began in 1985. [1] Men [ edit ] Due to the vast scope of the HIV/AIDS epidemic, many Malawian men believe that HIV contraction and death from AIDS are inevitable. [3] Older men in particular often claim that the HIV/AIDS epidemic is a punishment issued by God or other supernatural forces. [3] Other men refer to their own irresponsible sexual behaviors when explaining why they believe that death from AIDS is inevitable. [3] These men sometimes claim that unprotected sex is natural (and therefore necessary and good) when justifying their lack of condom use during sex with extramarital partners. [3] Finally, some men identify as HIV-positive without having undergone testing for HIV, preferring to believe that they have already been infected so they can avoid adopting undesirable preventive measures such as condom use or strict fidelity . [3] Because of these fatalistic beliefs, many men continue engaging in extramarital sexual relations despite the prevalence of HIV/AIDS in Malawi. [8] However, despite these widespread feelings of fatalism, some men believe that they can avoid HIV contraction by modifying their personal behaviors. [3] Men who decide to change their behaviors to reduce their risk of infection are unlikely to use condoms consistently, particularly during marital intercourse; instead, they usually continue engaging in extramarital sexual relations, but alter the ways in which they choose their sexual partners. [3] For example, before selecting extramarital sexual partners, men sometimes survey their peers to determine whether their potential partners are likely to have exposed themselves to the virus. [10] Men who choose their sexual partners based on external appearances and peer recommendations often believe that women who violate traditional gender norms by, for example, wearing modern clothing are more likely to carry HIV, while young girls, who are perceived as sexually inexperienced, are considered "pure." [3] Because of this perception, many people are concerned that schoolchildren in Malawi, particularly girls, are becoming exposed to the virus through sexual harassment or abuse by their instructors. [6] Women [ edit ] According to traditional gender roles in Malawi, men operate primarily in the formal work sector and are responsible for supporting their families through paid labor, whereas women, who are valued for their domestic skills, are responsible for agricultural labor and care work ; this gender-based division of labor decreases women's autonomy , thereby increasing their vulnerability to HIV/AIDS. [9] Even within the home, women often lack bargaining power because they have limited access to education , formal employment , and other resources that could give them a sense of financial and personal independence. [9] Women who are able to work in the formal sector typically earn significantly less money than men , even when they are completing the same tasks, making it difficult for them to elevate their status. [9] Many women are convinced that their husbands are putting their lives at risk by engaging in extramarital sexual relations without using protection; however, because of their secondary status, they are often unwilling to initiate discussions about HIV/AIDS in the home. [9] Most women in Malawi do not view divorce as a viable option, even when their husbands are HIV-positive and refuse to protect them from the virus by wearing condoms during marital intercourse. [9] Because they lack the education and training needed to seek gainful employment , women are not usually able to support themselves and their children outside of marriage without resorting to commercial sex work for money. [9] However, despite their vulnerability, some women in rural Malawi believe that they do, to a certain extent, have control over their own health and well-being. [11] They tell their husbands that the HIV/AIDS epidemic has made sexual infidelity extremely dangerous and encourage them to refrain from engaging in extramarital sexual contact. [11] In addition, many women are convinced that, by appealing to the vulnerability of their children (who will probably be orphaned if their parents contract HIV), they can convince their husbands to use condoms consistently during extramarital sexual encounters. [11] Other women seek support from their friends and family members when they believe that their husbands' unsafe behaviors are putting their lives at risk. [11] Finally, as a last resort, women might warn their husbands that they will visit the ankhoswe , or traditional marriage counselor, and demand divorce if their husbands refuse to remain faithful and actively prevent the transmission of the disease. [11] Children [ edit ] AIDS orphans in Lilongwe, Malawi The number of orphaned children in Malawi has increased dramatically since the HIV/AIDS epidemic began in 1985, with certain surveys indicating that more than 35% of schoolchildren have experienced the death of at least one parent due to HIV/AIDS. [6] Because HIV is transmitted sexually, married couples who engage in unprotected sexual relations put their children at increased risk of becoming double orphans , or children who have lost both parents to HIV/AIDS. [6] Older children who have lost both parents to HIV/AIDS often become responsible for the care of their younger siblings, and many double orphans drop out of school or migrate to urban areas to try to support themselves and their siblings. [6] Girls who have been orphaned by HIV/AIDS have unusually high rates of school absenteeism in Malawi. [6] When parents die of HIV/AIDS, extended family members usually become the children's primary caregivers : in Malawi, 44% of double orphans are adopted by grandparents or other close relatives. [6] Extended family members often provide crucial support to HIV/AIDS orphans; [12] however, some sources indicate that extended family members mistreat orphans whose parents have died from HIV/AIDS. [6] For example, family members who are unable to support adopted children often arrange early marriages for female orphans, who may then become victims of domestic violence and sexual abuse . [6] Evidence suggests that schoolchildren in Malawi are at risk of being exposed to HIV by their teachers, who sometimes value them as sexual partners because they believe that children have not yet been exposed to the virus. [6] Children are particularly vulnerable to exploitation by adults who offer them money in exchange for sex; because they are often unable to afford basic necessities, they might feel compelled to accept gifts in exchange for sex out of desperation. [6] Interviews indicate that teachers and school administrators in Malawi often misinterpret the definition of sexual assault , as some believe that sexual relations between teachers and students are appropriate as long as the children have consented . [6] Although most schools have strict policies against sexual abuse , children are often hesitant to accuse adults of wrongdoing, and many administrators are unwilling or unable to investigate the truth behind the accusations. [6] Marriage and relationships [ edit ] Although couples are starting to use condoms during extramarital intercourse more frequently, condom use during marital sex is still viewed as inappropriate by many Malawians; in 2000, only 2.3% of people reported using condoms regularly during sexual intercourse with their spouses. [4] Some people believe that condoms are only necessary during sex with high-risk partners such as sex workers , and that condom use during marital sex implies infidelity . [4] Others believe that marital condom use violates the religious purposes of marriage: sexual pleasure and reproduction . [4] In a study published in 2007 by Agnes M. ... According to a 2003 study by Eliya Msiyaphazi Zulu and Gloria Chepngeno, although higher levels of education do correspond to greater knowledge about HIV/AIDS, education levels do not significantly impact the likelihood that couples will discuss HIV-related prevention strategies. [13] Economic impact [ edit ] Farmers with composting materials in Malawi A 2002 study conducted by CARE International across three districts in the Central Region of Malawi considers how HIV/AIDS has affected economic well-being in rural Malawi. [14] When skilled laborers are infected with HIV, they are usually unable to work; therefore, they often shift agricultural production on their land to less labor-intensive crops, sacrificing the opportunity to grow more profitable, labor-intensive crops such as tobacco . [15] When family members fall ill with HIV/AIDS, their relatives invest time in their treatment and care, further reducing household productivity. [14] In addition, when family members are infected with HIV, households often use the money they would normally invest in agriculture to cover medical expenses, further decreasing economic stability at the household level. [14] Finally, when adults contract HIV, their children often remain home from school to work in the fields, threatening long-term productivity and economic advancement in Malawi. [15] CARE International proposes several strategies that might reduce the destructive economic impact of HIV/AIDS on rural households . [14] They recommend introducing new technologies that improve productivity to allow households affected by HIV/AIDS to continue supporting themselves through agriculture. [14] Women in patrilineal / patrilocal villages are often unable to support themselves and their children when their husbands die of HIV/AIDS; therefore, helping women acquire traditionally masculine agricultural skills might decrease their vulnerability while improving agricultural productivity at the household and community levels. [14] CARE International recommends increasing cooperation at the community level by establishing labor and food banks in areas that have been devastated by the HIV/AIDS epidemic. [14] Finally, CARE International highlights the importance of increasing access to information about HIV/AIDS in Malawi to help families prepare for and cope with the economic burdens associated with the epidemic. [14] Impact on health services [ edit ] The HIV/AIDS epidemic in Malawi has been characterized by drastic declines in the number of health workers available to provide treatment and care and increasing strain on health services: more than half of all hospital admissions in Malawi are related to HIV/AIDS. [16] However, Malawi currently faces a significant deficit in human resources : only 159 doctors were practicing in Malawi in 2007. [17] The World Health Organization 's Essential Health Package recommends placing at least three health workers at every health facility in the country, but the vast majority of Malawi's health facilities fail to meet this standard. [17] While migration to more developed countries in search of better opportunities, also known as " brain drain ," is partially responsible for the shortage of health care workers in Malawi, many health care workers have been personally affected by the HIV/AIDS epidemic; in fact, an average of 48 nurses die of HIV/AIDS in Malawi every year. [1] The HIV/AIDS epidemic has resulted in high levels of absenteeism among health workers in Malawi, who often leave work to spend time with HIV-positive friends or relatives, and the Malawian government has failed to respond to the declining number of full-time employees working in the health sector. [16] Health workers who are not chronically absent frequently abandon their jobs because they are unable to cope with the heavy patient loads or because they are afraid that working in a medical environment will increase their risk of becoming infected with HIV. [16] Malawi has adopted task shifting strategies to overcome the shortage of workers available for HIV/AIDS treatment and care. [17] Task shifting, which has been successful in many other regions, involves training less specialized health workers to perform health-related tasks that do not require professional training, such as the initiation of antiretroviral therapy . [17] For example, at Thyolo District Hospital , health workers spend one week learning how to initiate antiretroviral therapy in a classroom setting and an additional two weeks practicing their knowledge in a supervised clinical setting; after completing this course, they are legally (under Ministry of Health guidelines) allowed to initiate antiretroviral therapy. [17] Another form of task shifting involves training health-oriented counselors in HIV testing and counseling , which relieves nurses of this additional task. [17] Interventions [ edit ] Malawi has taken many steps towards slowing the spread of HIV/AIDS, such as increasing access to condoms and improving testing services and treatment options. [1] Many of these efforts have been funded by international donors including the World Bank , the Global Fund , the World Health Organization , the President's Emergency Plan for AIDS Relief (PEPFAR), and the Joint United Nations Programme on HIV and AIDS (UNAIDS). [1] The World Bank has lent $407.9 million to Malawi, the Global Fund has agreed to give $390 million, and PEPFAR has donated $25 million for prevention and treatment campaigns. [1] Antiretroviral therapy [ edit ] The number of people using antiretroviral therapy in Malawi has increased dramatically in the past decade: between 2004 and 2011, an estimated 300,000 people gained access to antiretroviral treatment. [1] In addition to improving access to antiretroviral therapy, in 2008, Malawi introduced the World Health Organization 's treatment guidelines for antiretroviral therapy, which improved the quality of treatment available to Malawians. [1] However, Malawi's proposal for a new antiretroviral treatment plan in 2011, which would have cost $105 million per year, was rejected by the Global Fund , threatening Malawi's ability to continue expanding access to antiretroviral treatment. [1] In 2000, Malawi's Ministry of Health and Population began developing a plan to distribute antiretroviral drugs to the population, and, as of 2003, there were several sites providing antiretroviral drugs in Malawi. [16] The Lighthouse, a trust in Lilongwe that fights HIV/AIDS, provides antiretroviral drugs at a cost of 2,500 kwacha per month. [16] Queen Elizabeth Central Hospital in Blantyre provides antiretroviral therapy through its outpatient department, and Médecins Sans Frontières distributes antiretroviral drugs to patients for free in the Chiradzulu and Thyolo Districts. [16] Many different private providers sell antiretroviral drugs, particularly in cities; however, very few patients can afford to receive drugs from the private sector in Malawi. [16] In addition, private providers are not currently required to obtain certification before selling antiretroviral drugs, and, therefore, this practice is not closely monitored. [16] Finally, some employees receive access to antiretroviral drugs through the health insurance policies provided by their employers, but this practice is not widespread. [16] Due to the advent of antiretroviral drugs, HIV/AIDS has become a manageable disease for people who can access and afford treatment; however, antiretroviral therapy remains largely unaffordable and inaccessible to most people in Malawi. [16] For example, the South East region of Malawi has disproportionately low access to antiretroviral drugs. [1] In many rural areas, poor health infrastructure combined with widespread famine have made sustained, high-quality antiretroviral therapy difficult or impossible. [1] In addition, donations from the Global Fund to Fight AIDS, Tuberculosis, and Malaria were used to fund antiretroviral therapy programs that distributed medication on a "first-come, first-served" basis, making the drugs more accessible to the male, urban, educated population. [16] Because there are no explicit policies regarding the fair distribution of antiretroviral drugs in Malawi, individual health care workers often become responsible for deciding who will receive treatment, which inevitably leads to inequitable distribution. [16] Condom distribution [ edit ] Although condoms effectively prevent the sexual transmission of HIV, several factors have limited widespread condom distribution and uptake in Malawi. [1] People living in non-urban areas often have difficulty accessing condoms, and condoms are not typically available at bars and other social locations where they could have a significant impact on HIV prevention. [1] Many people oppose condoms because they believe that condoms make sex less enjoyable or because they question their ability to prevent the transmission of HIV. [1] However, despite these factors, many unmarried couples have started using condoms more consistently as concern and fear about the HIV/AIDS epidemic have increased. [4] Non-governmental organizations such as Population Services International (Malawi), an organization that strives to improve the health of Malawians, and Banja La Mtsogolo, an organization that distributes information and resources related to family planning , have conducted campaigns advertising condom use as an effective form of protection against HIV/AIDS. [1] Banja La Mtsogolo provides condoms to both men and women, and has significantly improved the availability of condoms for women in particular. [1] Because of efforts by Population Services International, Banja La Mtsogolo, and many other organizations, condoms have become more widely available to many people in Malawi. [1] Voluntary counseling and testing [ edit ] People living in areas with high rates of HIV/AIDS face several psychological barriers when deciding whether to undergo testing for HIV . [1] For example, people may prefer not to know if they are HIV-positive because, due to the obstacles they often face in gaining access to antiretroviral drugs, many view HIV/AIDS diagnoses as death sentences. [1] Others may simply believe that they are HIV-negative, either because they practice strict monogamy and consistently use condoms during sexual intercourse or because they are in denial about the prevalence of the disease. [1] However, despite these barriers, both mobile and static testing services have become more widely available in Malawi recently: 1,392 testing and counseling sites existed in 2011. [1] Certain non-governmental organization such as the Malawi AIDS Counseling and Resource Organisation (MACRO) provide door-to-door counseling and testing services, which have drastically improved the accessibility of HIV testing. [7] See also [ edit ] Malawi portal Viruses portal Sub-Saharan Africa HIV/AIDS in Africa Diseases of poverty Epidemiology of HIV/AIDS Misconceptions about HIV and AIDS AIDS orphan Healthcare in Malawi Sex for Fish References [ edit ] ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj "HIV & AIDS in Malawi" . ... "The Impact of the HIV/AIDS Epidemic on the Education Sector in Sub-Saharan Africa: A Synthesis of the Findings and Recommendations of Three Country Studies (review)". ... Review of Agricultural Economics . 28 (3): 429–39. doi : 10.1111/j.1467-9353.2006.00309.x . ^ a b c d e f g h i j k l Kemp, Julia; Jean Marion Aitken; Sarah LeGrand; Biziwick Mwale (2003). "Equity in health sector responses to HIV/AIDS in Malawi".
  • Endometriosis Mayo Clinic
    Overview Endometriosis (en-doe-me-tree-O-sis) is an often painful disorder in which tissue similar to the tissue that normally lines the inside of your uterus — the endometrium — grows outside your uterus. ... You may get a lot of information at your visit, and it can be difficult to remember everything. ... Use it to make notes of important information during your visit. Prepare a list of questions to ask your doctor. ... Is there a medication that can improve my symptoms? What side effects can I expect from medication use? ... Will I take a medication before or after surgery? Will endometriosis affect my ability to become pregnant? Can treatment of endometriosis improve my fertility?
    KRAS, CYP19A1, PGR, IL10, PTGS2, HDAC2, CCL11, GREB1, CDKN2B-AS1, ESR2, NR5A1, HSD17B1, IGF1, EGFR, HSD17B2, PRL, IGFBP1, IL15, SST, IL1R1, MIR21, AKR1C3, ARNT, TGFB2, PTGER4, IDO1, KLF9, FOS, PAPPA, NR3C1, NCOA1, ABCC4, NR2F2, NR4A1, RXFP1, LTF, TAGLN, KLF13, PLA2G2A, CXCL9, MTA1, MTA2, DICER1, ENPP1, CXCL14, NR3C2, ACTA2, TXNIP, PAX2, CXCL13, OLFM4, AKR1B1, TNC, HDAC1, ITGB1, HLA-DPB1, AKR1C1, AKR1C2, CCL1, RASGRP1, RGS4, CNR1, SLC16A6, CCNE2, NR2C2, MED14, NR2C1, PLXNC1, COPS2, MED17, SRD5A1, TOB1, TNF, NCOR1, CYP26A1, HS3ST3B1, NR1D2, MED16, DDX5, ABCC9, UST, RORB, CD55, SLC1A1, THRA, SRD5A2, TRH, NR2F6, PTGER2, CYB5A, FBLN1, FBN1, VEGFA, PRLR, HBEGF, VCAN, MED1, RARB, FKBP5, SPARCL1, DIO2, STC2, CFD, DUSP1, CCL22, FMO2, SUCLG2, NRP1, CPM, SELENOP, CLDN1, PTGFR, ELAVL1, MYLIP, ANKRD1, MED4, ITGA2, FAM180A, RASL11A, IL7R, SLC40A1, HERC5, CNIH3, BMP7, IMPA2, ERRFI1, MAOA, NTRK3, TACSTD2, SULF2, ANKH, AREG, ANO4, LAMB1, NDNF, ARHGAP28, LRRK2, DCSTAMP, OSR2, SCGB3A1, MAOB, ITGB8, SLC7A8, SMPDL3A, DKK1, BRD8, NCOA6, CD226, MMP2, C1R, NEDD4L, MMP9, IFNGR1, IGFBP6, ITGB3BP, DEPP1, LMOD1, METTL7A, GPX3, ABI3BP, SLC20A1, IFIT1, RBPJ, NEFM, IHH, CCL5, BCL2, KDR, SERPINF1, BIRC5, EGR1, HDAC3, RUNX1, LYN, VAV1, ESR1, BAX, WNT4, SELL, NFKBIA, BCL2L1, VEZT, BSG, FN1, CDC42, IL33, IGF1R, CCDC170, SYNE1, MAP3K4, PIK3CB, MME, PDE1C, GRIN2D, PIK3CA, IL1A, MEIS1, ICAM1, IL1B, PIK3CD, INHBA, IL6, PIK3CG, CXCL8, GSTM1, GSTT1, CCL2, HOXA10, MAPK1, PTEN, COX2, CYP17A1, COMT, CTNNB1, OR9Q1, LAMC3, CYP2B6, COL12A1, CYP1A1, RFLNA, SKAP1, ARID1A, CDC73, BEND5, CALHM3, MUC16, FOXP2, AGBL4, NAALADL2, CYP21A2, TP53, AKT1, CACNA1A, MTCO2P12, ARID3B, SYNJ2, LINC00861, C2, FGD6, TGFB1, CAPN14, GPNMB, THOC6, HSD17B7, HGF, ARTN, HIF1A, PPP1R2C, CXCR4, SERPINE1, AGRP, MIF, CXCL12, BDNF, CDH1, GALT, GSTM2, BRD2, STAT3, IFNG, MIR451A, IL1R2, BECN1, FSHR, EPHB2, HPGDS, IL4, MALAT1, TLR4, HP, PAEP, AMH, MAPK3, MMP1, STS, LEP, GSTP1, IL18, IL37, GPER1, MMP3, CD44, TAC1, FGF2, CYP2C19, KLF11, PPARG, HLA-DRB1, FCRL3, ANGPT2, VDR, HOXA11, VCAM1, UCN, CRK, RAF1, TNFRSF1B, MIRLET7B, S100A6, IL1RN, TIMP1, MIR145, MIR20A, MAPK14, AIMP2, CRH, NOTCH1, EGF, RNF19A, POLDIP2, PTPN22, AHSA1, CCR1, FOXP3, NOS3, SPP1, GRAP2, CDKN1B, POU5F1, SULT1E1, DHRS11, HNF1B, POU5F1P4, POU5F1P3, TERT, THBS1, MIR210, KLRK1, MIR17, MMP7, PLAU, MRC1, SLCO6A1, XRCC1, TIMP2, GSTK1, HSD17B13, PTGES, AHRR, IL13, FST, IL16, IL17A, NGF, HPSE, OGG1, MUC1, NAT2, BRCA2, GNRHR, CSF1, EZH2, CDKN2A, CRP, HLA-G, BRAF, BRCA1, HMGB1, DRD2, GC, AGTR1, NME1, AHR, SIRT1, GATA6, TNFRSF11B, PCNA, NFKB1, H3P10, GHRH, MPO, MTOR, MMP14, MIR126, CRHR1, MIR141, CREB1, MDK, SMAD3, LGALS3, LEPR, FSHB, CCN2, PGF, FOXO1, TACR1, CCND1, VPS11, STAR, ATM, ACKR3, SOD2, AR, TNFRSF1A, CCL25, ACE, FASLG, TWIST1, RNASE3, REN, CYP1B1, CTLA4, EZR, F3, MAPK8, ANXA1, PPARA, FGFR2, CCR9, PLG, CD36, ZEB1, ISG20, ITGAV, POSTN, ACTB, IL1RAP, CXCL10, KLRC4-KLRK1, CCN1, CD68, CFL1, CIB1, YAP1, ITGAM, SEMA6A, CSF2, HMGA1, ENPP3, CAPN7, CCR2, LINC00261, EMX2, SLC2A4, SKP2, FPR2, HMGA2, CKS1BP7, FPR1, FLT1, TIMP3, DNMT3A, HSD11B2, LINC00339, OPRM1, TCF21, P2RX3, THY1, NUP62, RELA, SLIT3, NTF4, SERPINB2, PAK1, CSF3, NTRK2, RMDN2, IL23A, IL7, FKBP4, FOXM1, PROK1, CDKN1A, DCTN4, APEX1, IL2RA, WNT7A, RMDN1, MANEA, PDCD4, CXCL5, IL2RB, VIM, EPO, TSLP, VEGFC, HSH2D, CCL21, HSPA4, MAP2K7, SRA1, CSF1R, ANXA2, MIR342, SEMA3C, TLR2, HOXA13, PAX8, ANG, PON1, CEBPA, C3, FGF1, ANGPT1, RB1, RNU1-1, USF2, ENO1, XRCC4, FGA, SOD1, PPIG, EMSLR, LTA, ERBB2, CD274, GTF2H1, SQSTM1, SMAD2, CDH3, MIR200C, STC1, ZHX2, NR1I2, STAT6, RNU1-4, MIR191, KIR2DS5, MIR183, CCNE1, IL22, USP10, LPA, AIF1, SYBU, ADIPOQ, RMDN3, S100B, PPARGC1A, CCR5, CKS1B, IL32, COL18A1, MIR31, FAS, ERVW-1, LHCGR, LIF, DUSP2, MIR29C, MS4A1, STIP1, KIR2DS1, CDK6, TNFSF10, LGR5, SOX9, MUC2, MUC4, AGT, SOX2, NCAM1, GH1, AGTR2, ACP1, ITGB3, IGFBP3, AHSG, NOS1, NOS2, MIR33B, CXCR2, MST1R, MST1, BCL6, MSI1, MIR143, MLH1, SSTR1, CXCR3, CXCR1, RETN, KHDRBS1, GLI1, ABCB6, DNMT3B, CRHR2, LINC02210-CRHR1, SRC, CD47, KRT20, GJA1, MSH2, MBL3P, BMP4, TMED7, HSPA14, SLC52A1, PAK4, CDC6, BNC2, RBFOX1, UGT1A1, DLL4, NOD1, ROBO4, RHOF, UGT2B28, TREM2, IL17D, BMPR1B, VTA1, NRN1, NDRG1, BRS3, CHD5, TBX21, SERPINH1, NUP210, PLCB1, CTCF, CXCR6, ASTN2, CD40LG, PDLIM5, DNMT3L, RUNX3, CAT, CD48, CASR, CASP3, HEY1, PLXND1, CCNB1, KIFAP3, CD14, PHB2, ENTPD1, SCN11A, GALNT6, AKAP13, NUDT6, CD19, UTS2, CD86, MMP24, DCTN6, LILRB1, TNFSF13B, SRRM2, CD74, AGR2, FOXP1, TMOD3, BTF3P11, MYL9, BTG1, REM1, CCDC22, BTK, CDK1, CD79A, RBMS3, TNFRSF21, TSPO, INTU, CACYBP, SERPING1, FAM215A, CARM1, FOXD3, GREM1, C5, ZNRD2, NECTIN3, C9, CA2, CALCA, CALD1, FJX1, CADM1, SH3BP4, DAPK2, LPAR3, CRISPLD2, ATAD3A, MIR205, MIR181C, MIR182, MIR195, MIR196A2, PARP1, MIR200A, MIR200B, MIR204, ADM, MIR33A, ADAR, MIR214, MIR216A, MIR22, MIR23B, MIR27B, MIR30A, MIR30C1, ADRA1A, MIR154, MIR148A, ADRA2B, IL27, CADM2, ALB, NCR3, CPP, TICAM2, USP17L2, TBPL2, HES5, MIRLET7D, MIR100, MIR106A, MIR10B, MIR122, MIR132, MIR139, MIR142, MIR30C2, MIR34A, VPS53, MIR3613, RGPD2, ACTN4, MIR543, MR1P1, DEFB4B, MIR1185-1, TMED7-TICAM2, MIR2861, LINC01541, MIR34B, LINC01672, MIR4634, PCAT1, PGR-AS1, LOC110386951, LOC110806263, LINC02605, H3P23, MIR629, MIR449B, MIR542, ACTN1, CCDC144NL-AS1, ADA, MIR135B, MIR370, MIR196B, MIR375, MIR378A, MIR381, H4C15, MIR363, ACVR2B, MIR488, MIR146B, MIR520G, MIR503, MIR483, ACVR1B, HOXA11-AS, ALOX15, TET3, STN1, RHOC, ARG1, ULBP3, NAA16, AQP9, AQP5, AQP2, NANOG, AQP1, ARX, RNF34, SPHKAP, TET1, ULBP2, SLC38A1, NECTIN4, CAB39L, MAP1LC3B, WNK1, GORASP1, ATG3, DCLRE1C, QRSL1, B2M, ST6GALNAC1, TRERF1, AXL, MYDGF, LTB4R2, PNO1, SALL4, ARSD, CXCL16, IL21, RHOG, AFAP1, SLC22A23, SRR, SMOC2, TMPRSS13, MAGT1, NLRC5, ANK1, H4-16, RBM45, SGPP2, CD200R1, ZFP42, AMHR2, DOCK11, MUC17, SIRPA, ALPP, IL34, ALPI, PDIK1L, GPBAR1, CCDC80, TTC39B, ZNF366, CYP2R1, ANTXR2, LOXL4, CTHRC1, CARD11, MAK16, KISS1R, AFAP1-AS1, APOE, GFM1, WNT3A, LMLN, UCN2, APOA2, CREB3L1, BIRC3, IGSF8, BIRC2, SFXN1, PRRT2, UCN3, LILRB2, IFNA13, EIF1, PDGFA, P2RX5, P2RY6, GATA3, GATA2, GALNT3, GABPA, PDCD1, NR5A2, PDGFRA, POLD1, PDGFRB, PF4, PF4V1, PHB, SERPINA1, FOXO3, PLCB4, PLK1, OXTR, CLDN11, GATM, NTF3, CD200, MSMB, GHRHR, MYB, MYC, NFE2L2, GDNF, MSTN, NGFR, NHS, NINJ1, GBA, NOTCH4, NPTX2, NRAS, YBX1, NT5E, PNN, POLE, MMP13, RBP1, PTPRC, PTPRD, PVR, NECTIN1, EXTL3, RARRES1, RARRES2, RASA1, ETS1, FGF9, ACACA, ROCK1, ESRRB, ROS1, RXRA, S100A1, S100A4, ERCC6, PTN, F2, F2R, F2RL1, PPP2R1A, PPP5C, PPT1, PRELP, PRKCA, PRKCB, FEN1, MAP2K1, FCGR3B, FCGR3A, HTRA1, PSEN1, PSMD2, PSMD9, PSMD10, PTBP1, FANCD2, MNAT1, MMP12, TSHZ1, JUN, HNF4A, FOXA2, INHA, INSR, EIF3E, ITGA5, HLA-DQB1, JAK1, CD82, KLRC1, KCNQ1, KCNQ2, HLA-C, KIR2DL1, KIR2DL3, KIR2DL4, KIR3DL1, KIR3DL2, ILK, HOXB4, HPGD, HPRT1, IFNA1, IGFBP7, IFI27, CFI, ID2, IAPP, HTC2, HSPD1, IL2, HSD17B3, HSD3B2, IL9, HSD3B1, IL11, IL12B, IL12RB1, AGFG2, KISS1, KNG1, GJB2, MECP2, SMAD4, MSH6, GSK3B, MAP2, MAS1, MAT2A, MBL2, MDM2, PDIA3, HLA-B, CXCL1, MET, KITLG, GRB2, GPX4, GPR42, GNRH1, GLI3, EPCAM, SH2D1A, H2AX, HAS1, L1CAM, HK1, LAMC2, STMN1, LBR, HCK, LGALS1, LGALS4, LGALS9, LHB, LIMK1, LIPC, LIPE, LMNB1, LOX, LOXL1, CYP4F3, SAG, SRL, ERCC2, DENR, H4C3, H4C8, H4C2, H4C5, H4C13, H4C14, BCAR3, NR0B2, CSE1L, IER3, CRMP1, IRS2, PEA15, HYAL2, TNFRSF6B, IL18R1, CRABP2, CLDN7, H4C11, H4C12, H4C6, H4C4, VWF, WT1, XBP1, CTH, XRCC3, YWHAZ, ZFP36, ZNF217, ZP3, CSK, BAG6, MIA, H3-4, H4C9, AXIN1, FZD7, H4C1, PROM1, CLDN3, ERCC1, BMS1, GDF3, CLOCK, RGS6, IPO13, CETP, SEMA3E, HDAC9, RASSF2, CDX1, BCL10, PDCD6, BCL2L11, CDKN3, DNM1L, KIF20A, CDK4, HNRNPA3P1, CDH15, BCAR1, CFTR, CHRM3, TECR, CLDN4, CPB2, COL1A1, LTB4R, CCR8, EBAG9, LPAR2, SLC33A1, CCR7, S1PR2, CLCN3, CD163, SLIT2, LIPG, CHUK, HAND2, CHST3, VTN, TRPV1, VIP, SRY, SMARCC1, SNAI1, SNCG, FSCN1, SOX15, EIF4EBP1, MEGF8, EDNRA, EDN1, CX3CR1, SSTR4, S1PR1, STAT4, DUSP6, STX5, SULT1A1, SULT2A1, SYP, SMARCA1, SNAI2, SLPI, ELAVL2, EPOR, CCL14, CCL16, CCL17, CCL19, CX3CL1, SDC1, SDC4, EPHB4, SELE, EPHA3, SFRP1, SFRP2, SHC1, SLC2A1, SLC2A3, SLC6A4, SYT1, ADAM17, DPYSL2, DLX3, DEFB4A, DECR1, TNS1, TPM3, TPT1, DCN, DAPK1, CYP11A1, TRO, TRPC6, TXN, TYK2, TYROBP, UCHL1, CYP3A4, UTRN, CYP1A2, CLDN5, TLR3, TCF3, TIMP4, TDGF1, TEK, TERF1, DPP6, DPP4, TFDP1, TFF3, DOK1, TGFB1I1, TGFB3, LEFTY2, TGFBI, TGFBR1, DNMT1, KLF10, SARDH, DLX5, UTF1
    • Extrapelvic Endometriosis Orphanet
      Rare endometriosis is a rare, non-malformative gynecologic disease characterized by the presence of functional endometrial glands and stroma in extrapelvic locations, such as lungs, pleura, kidneys, bladder, abdominal wall, umbilicus, and cesarean section scar among others. Clinical manifestations are menstrually-related and depend on the location of the ectopic tissue, but in general include pain, mass/nodule, swelling and/or bleeding in the involved area.
    • Endometriosis Wikipedia
      The amount of pain a person feels correlates weakly with the extent or stage (1 through 4) of endometriosis, with some individuals having little or no pain despite having extensive endometriosis or endometriosis with scarring, while others may have severe pain even though they have only a few small areas of endometriosis. [15] The most severe pain is typically associated with menstruation. ... Laparoscopy , a surgical procedure where a camera is used to look inside the abdominal cavity, is the only way to accurately diagnose the extent and severity of pelvic/abdominal endometriosis. [85] Laparoscopy is not an applicable test for extrapelvic sites such as umbilicus, hernia sacs, abdominal wall, lung, or kidneys. [85] Reviews in 2019 and 2020 concluded that 1) with advances in imaging, endometriosis diagnosis should no longer be considered synonymous with immediate laparoscopy for diagnosis, and 2) endometriosis should be classified a syndrome that requires confirmation of visible lesions seen at laparoscopy in addition to characteristic symptoms. [86] [87] Laparoscopy permits lesion visualization unless the lesion is visible externally (e.g., an endometriotic nodule in the vagina) or is extra-abdominal. [85] If the growths (lesions) are not visible, a biopsy must be taken to determine the diagnosis. [82] Surgery for diagnoses also allows for surgical treatment of endometriosis at the same time. ... In principle the various stages show these findings: [96] Stage I (Minimal) Findings restricted to only superficial lesions and possibly a few filmy adhesions . ... Because the incisions are very small, there will only be small scars on the skin after the procedure, and most individuals recover from surgery quickly and have a reduced risk of adhesions. [111] As for deep endometriosis, a segmental resection or shaving of nodules is effective but is associated with an important rate of complications which about 4,6% is major. [112] Historically, a hysterectomy (removal of the uterus) was thought to be a cure for endometriosis in individuals who do not wish to conceive. Removal of the uterus may be beneficial as part of the treatment, if the uterus itself is affected by adenomyosis. However, this should only be done in combination with removal of the endometriosis by excision.
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