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  • Sexual Fetishism Wikipedia
    . ^ "Common Misunderstandings of Fetishism" . K. M. Vekquin. Archived from the original on 5 January 2013 . ... CS1 maint: multiple names: authors list ( link ) ^ a b c d e f g h i j k Darcangelo, S., Hollings, A., Paladino, G. (2008). ... A., Roll, S., Englert, H., Willich, S. N., & Beier, K. M. (2011). "How unusual are the contents of paraphilias? ... PMC 7534020 . PMID 32605397 . ^ Freund, K., Seto, M. C., & Kuban, M. (1996). ... CS1 maint: multiple names: authors list ( link ) ^ Akins, C. K. (2004). "The role of Pavlovian conditioning in sexual behavior: A comparative analysis of human and nonhuman animals" .
  • Patellofemoral Pain Syndrome Wikipedia
    PMID 26616176 . ^ a b c d e f g h i j k l m n o p q r s t u Dixit S, DiFiori JP, Burton M, Mines B (January 2007). ... PMID 22513943 . ^ a b c d e f g h i j k l m n o p q Heintjes E, Berger MY, Bierma-Zeinstra SM, Bernsen RM, Verhaar JA, Koes BW (2004). ... PMID 29890402 . ^ de Oliveira Silva D, Barton C, Crossley K, Waiteman M, Taborda B, Ferreira AS, Azevedo FM (September 2018). ... British Journal of Sports Medicine . 52 (18): 1170–1178. doi : 10.1136/bjsports-2018-099397 . PMID 29925502 . ^ Crossley K, Bennell K, Green S, McConnell J (April 2001).
    • Patellofemoral Pain Syndrome Mayo_clinic
      Overview Patellofemoral (puh-tel-o-FEM-uh-rul) pain syndrome is pain at the front of the knee, around the kneecap. The kneecap also is known as the patella. Patellofemoral pain syndrome is sometimes called runner's knee. It's more common in people who run and who play sports that involve running and jumping. The knee pain often increases when running, walking up or down stairs, sitting for long periods, or squatting. Simple treatments, such as rest and ice, often help. But sometimes patellofemoral pain needs physical therapy.
  • Chytridiomycosis Wikipedia
    C.; Woeltjes, A.; Bosman, W.; Chiers, K.; Bossuyt, F.; Pasmans, F. (2013). ... PMID 17693553 . ^ a b c d Nichols D. K.; Lamirande E. W.; Pessier A. P.; Longcore J. ... S2CID 27149357 . ^ a b Harris R.; Brucker R.; Minbiole K.; Walke J.; Becker M.; Schwantes C.; et al. (2009). ... Retrieved 2017-05-15 . ^ Une Y.; Matsui K.; Tamukai K.; Goka K. (2012). "Eradication of the chytrid fungus Batrachochytrium dendrobatidis in the Japanese giant salamander Andrias japonicus" . ... PMID 22832723 . ^ a b Woodhams D. C.; Geiger C. C.; Reinert L. K.; Rollins-Smith L. A.; Lam B.; Harris R.
  • Rheumatic Fever Wikipedia
    PMID 27733282 . ^ a b Kumar, Vinay; Abbas, Abul K; Fausto, Nelson; Mitchell, Richard N (2007). ... PMID 1775859 . ^ " rheumatic fever " at Dorland's Medical Dictionary ^ Abbas, Abul K.; Lichtman, Andrew H.; Baker, David L.; et al. (2004). ... PMID 16622036 . ^ a b Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease . ... Archived from the original on 31 December 2005. ^ https://labtestsonline.org/tests/antistreptolysin-o-aso ^ https://labtestsonline.org/tests/anti-dnase-b ^ a b c d e f g h i j k Gewitz Michael H.; Baltimore Robert S.; Tani Lloyd Y.; Sable Craig A.; Shulman Stanford T.; Carapetis Jonathan; Remenyi Bo; Taubert Kathryn A.; Bolger Ann F.; Beerman Lee; Mayosi Bongani M. (19 May 2015). ... Retrieved 11 November 2009 . ^ Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. (2012).
    MYOM2, CDKN2A, TP53, TNF, HLA-DRB1, MDM2, BMI1, PAGR1, RBM45, GALNS, GAST, COMMD3-BMI1, NPM1, MBL2, TLR2, IL6, CDK4, PTEN, TGFB1, CTLA4, IL10, ATM, IL17A, HLA-A, RUNX1T1, TBX3, FCN2, MASP2, EGFR, CBX7, HNF1A, TBX2, TRIM21, TCF7, RHD, RARB, TRBV20OR9-2, PTH, CDK5RAP3, VIM, POTEF, TWIST1, VEGFA, CCDC6, RAB11A, PRC1, DMTF1, LINC01194, HAVCR2, HUWE1, POSTN, RASSF1, HARS2, SLC25A19, MBD2, ABL1, PIK3C3, E2F1, HARS1, GC, FOXM1, FGF1, FCN1, FCGR3B, FCGR2A, DMP1, NOTCH1, CRH, CLU, CDKN2B, RUNX1, BCR, PARP1, ACTB, HLA-DQA1, HLA-DQA2, HLA-DQB1, AGFG1, MYC, MUC1, MTTP, MNT, MEFV, ABO, CXCL10, IL2RG, IL1RN, IL1B, IGHG3, IGFBP2, IFNG, IDH1, ICAM1, H3P10
    • Rheumatic Fever-Related Antigen Omim
      Genetic predisposition to rheumatic fever has intrigued investigators since Cheadle (1889) first noted the familial aggregation of rheumatic fever. Wilson et al. (1943) suggested that susceptibility might be an autosomal recessive trait. Taranta et al. (1959) suggested reduced penetrance because of a low concordance in monozygotic twins. Patarroyo et al. (1979) found that a serum from a multiparous woman identified a novel B-cell alloantigen marker, 883, in persons previously identified as having had rheumatic fever with or without subsequent rheumatic heart disease. They found that 71% of patients typed in New York and 74% of patients typed in Bogota expressed this antigen on their B cells as compared with only 17% in the 2 disease-free control groups tested.
    • Rheumatic Fever Orphanet
      Rheumatic fever (RF) is a multisystem inflammatory disease occurring as a post-infectious, nonsuppurative sequela of untreated streptococcus pyogenes (Group A streptococcus [GAS]) pharyngitis, and mainly occurs in individuals aged 5 to 15 years. The most common presenting signs are fever, migratory polyarthritis and carditis. Epidemiology The incidence of RF in industrialized countries, due to sporadic outbreaks, is typically less than 1/20, 000 individuals. In the developing world, the annual incidence is at least 100 times higher with some reports of > 1/200 individuals in select subpopulations, such as Australian Aboriginals. RF remains a major cause of acquired cardiac morbidity and mortality among people under 50 years of age.
    • Rheumatic Fever Gard
      Rheumatic fever is an inflammatory condition that may develop after infection with group A Streptococcus bacteria, such as strep throat or scarlet fever . It is primarily diagnosed in children between the ages of 6 and 16 and can affect the heart, joints, nervous system and/or skin. Early signs and symptoms include sore throat; swollen red tonsils; fever; headache; and/or muscle and joint aches. Some affected people develop rheumatic heart disease, which can lead to serious inflammation and scarring of the heart valves. It is not clear why some people who are infected with group A Streptococcus bacteria go on to develop rheumatic fever, while others do not; however, it appears that some families may have a genetic susceptibility to develop the condition.
    • Rheumatic Fever Mayo_clinic
      Overview Rheumatic fever is an inflammatory disease that can develop when strep throat or scarlet fever isn't properly treated. Strep throat and scarlet fever are caused by an infection with streptococcus (strep-toe-KOK-us) bacteria. Rheumatic fever most often affects children ages 5 to 15. But it can develop in younger children and adults. Although strep throat is common, rheumatic fever is rare in the United States and other developed countries. Rheumatic fever can cause permanent damage to the heart, including damaged heart valves and heart failure.
  • Hellp Syndrome Wikipedia
    Louis Weinstein in 1982. [31] In a 2005 article, Weinstein wrote that the unexplained postpartum death of a woman who had haemolysis, abnormal liver function, thrombocytopenia, and hypoglycemia motivated him to review the medical literature and to compile information on similar women. [10] He noted that cases with features of HELLP had been reported as early as 1954. [10] [52] See also [ edit ] Acute fatty liver of pregnancy Hypertrophic decidual vasculopathy References [ edit ] ^ a b c d e f g h i j k l m n o p q "HELLP syndrome" . Genetic and Rare Diseases Information Center (GARD) – an NCATS Program . 2018 . Retrieved 5 October 2018 . ^ a b c d e f g h i j k l m Haram K, Svendsen E, and Abildgaard U (February 2009). ... PMID 14749644 . ^ a b Lachmeijer AM, Arngrimsson R, Bastiaans EJ, Frigge ML, Pals G, Sigurdardottir S, Stefansson H, Palsson B, Nicolae D, Kong A, Aarnoudse JG, Gulcher JR, Dekker GA, ten Kate LP, Stefansson K (October 2001). "A genome-wide scan for preeclampsia in the Netherlands" . ... PMID 22022598 . ^ Hulstein JJ, van Runnard Heimel PJ, Franx A, Lenting PJ, Bruinse HW, Silence K, de Groot PG, Fijnheer R (December 2006).
    CD46, CFH, CFI, HELLPAR, FASLG, FAS, PGF, F5, LEP, HADHA, F2, TNF, HPGDS, LGALS13, FLT1, VEGFA, MTHFR, MAPK14, TLR4, AIMP2, TLR2, MAPK3, TPBG, VEGFC, TGFB3, VWF, MAPK1, ABCG2, TFPI2, IL18R1, GRAP2, EBI3, AHSA1, ADAMTS13, SIRT4, RNF19A, POLDIP2, SLC17A5, ERVW-1, MBL3P, AHSP, NOD2, POTEF, SERPINE2, ACTB, SERPINE1, PAH, APC, CFB, CA9, CD40LG, CD59, CDKN1C, COX8A, CP, CRK, ENG, EPHX1, GAPDH, GNB3, GPT, NR3C1, GSTM1, GSTT1, HSPA4, HSPG2, IFNG, IL1B, IL1RN, CXCL8, IL10, LEPR, LNPEP, ADM, NOS3, PAEP, MBL2
    • Hellp Syndrome Orphanet
      A rare hemorrhagic disorder due to an acquired platelet anomaly characterized by hemolysis, elevated liver enzymes and thrombocytopenia that affects pregnant or post-partum women, and is frequently associated with severe preeclampsia. Symptoms are variable, typically including right upper quadrant or epigastric abdominal pain, nausea, vomiting, excessive weight gain, generalized edema, hypertension, general malaise, right shoulder pain, backache, and/or headache. Hepatic hemorrhage and rupture, renal failure, and pulmonary edema can result in maternal and/or fetal death.
    • Hellp Syndrome Gard
      HELLP syndrome is a life-threatening condition that can potentially complicate pregnancy. It is named for 3 features of the condition: H emolysis, E levated L iver enzyme levels, and L ow P latelet levels. It typically occurs in the last 3 months of pregnancy (the third trimester) but can also start soon after delivery. A wide range of non-specific symptoms may be present in women with HELLP syndrome. Symptoms may include fatigue; malaise; fluid retention and excess weight gain; headache; nausea and vomiting; pain in the upper right or middle of the abdomen; blurry vision; and rarely, nosebleed or seizures.
  • Cannabinoid Hyperemesis Syndrome Wikipedia
    The long-term outcomes of patients that have suffered from CHS is unknown. [10] 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 Chocron, Y; Zuber, JP; Vaucher, J (19 July 2019). ... PMID 19291829 . ^ a b c d e f g h i Ruffle, James K.; Bajgoric, Sanjin; Samra, Kiran; Chandrapalan, Subashini; Aziz, Qasim; Farmer, Adam D. ... S2CID 23685653 . ^ a b c d e f g h i j k l m n o p q r s Galli, JA; Sawaya, RA; Friedenberg, FK (December 2011). ... PMID 22150623 . ^ a b c d e f g h i j k l Sun, S; Zimmermann, AE (September 2013). ... PMID 26422191 . ^ a b c Hasler, William L.; Levinthal, David J.; Tarbell, Sally E.; Adams, Kathleen A.; Li, B U. K.; Issenman, Robert M.; Sarosiek, Irene; Jaradeh, Safwan S.; Sharaf, Ravi N.; Sultan, Shahnaz; Venkatesan, Thangam (26 June 2019).
  • Von Willebrand Disease Wikipedia
    . ^ Lavin M, Aguila S, Schneppenheim S, Dalton N, Jones KL, O'Sullivan JM, O'Connell NM, Ryan K, White B, Byrne M, Rafferty M, Doyle MM, Nolan M, Preston RJ, Budde U, James P, Di Paola J, O'Donnell JS (November 2017). ... Retrieved 4 April 2018 . ^ Lavin M, Aguila S, Dalton N, Nolan M, Byrne M, Ryan K, White B, O'Connell NM, O'Sullivan JM, Di Paola J, James PD, O'Donnell JS (July 2018). ... PMID 30042144 . ^ De Wee EM, Knol HM, Mauser-Bunschoten EP, van der Bom JG, Eikenboom JC, Fijnvandraat K, De Goede-Bolder A, Laros-van Gorkom B, Ypma PF, Zweegman S, Meijer K, Leebeek FW (November 2011). ... Kouides: Inherited Bleeding Disorders in Women P., ISBN 1-4051-6915-X ^ Favaloro EJ, Bonar R, Kershaw G, Sioufi J, Baker R, Hertzberg M, Street A, Marsden K (July 2006). "Reducing errors in identification of von Willebrand disease: the experience of the royal college of pathologists of australasia quality assurance program".
    VWF, P2RY12, F8, COX8A, ADAMTS13, GP1BA, F9, AK3, ABO, IL11, F11, ACTB, VWA8, ITIH1, TLR5, ITIH5, ANGPT2, POU2F3, CHRD, ALKBH1, CLEC4M, C20orf181, MUC5B, ATP6V0A2, SMPX, RABGEF1, CRISPLD2, SEC1P, PRB2, GP6, BMPER, TERF2IP, FAM20C, STXBP5, ANTXR1, ANO2, RAP1A, THPO, PDIA3, AGT, AVP, CANX, CD40, CLCA1, CSHL1, COCH, EPHA3, F2, F3, IFNA2, THBS1, RBPJ, ITGA2, ITGA2B, LRPAP1, MTHFR, CCN3, SERPINE1, PLG, POMC, SET, BOP
    • Von Willebrand Disease Orphanet
      A rare, inherited bleeding disorder characterized by defective platelet adhesion and secondary coagulation defect that manifests as abnormal bleeding of variable severity occurring either spontaneously or in association with an invasive procedure. Three main subtypes are defined based on the type of von Willebrand factor defect: partial (type 1) or total (type 3) deficiency, and qualitative/functional anomalies (type 2). Epidemiology The prevalence of Von Willebrand disease (VWD) in the general population is estimated at between 0.6 and 1.3% (including all forms) depending on the study, but the prevalence of symptomatic VWD that requires specific treatment is approximately 1/10 000. Type 3 VWD is much more rare (1/1 000 000). Clinical description Age of onset varies, with earlier onset being associated with more severe VWF deficiency. The disease manifests as abnormal bleeding of variable severity occurring either spontaneously or in association with an invasive procedure.
    • Von Willebrand Disease Mayo_clinic
      Overview Von Willebrand disease is a lifelong bleeding disorder in which your blood doesn't clot properly. People with the disease have low levels of von Willebrand factor, a protein that helps blood clot, or the protein doesn't perform as it should. Most people with the disease are born with it, having inherited it from one or both parents. However, warning signs, such as heavy bleeding after a dental procedure, might not show up for years. Von Willebrand disease can't be cured. But with treatment and self-care, most people with this disease can lead active lives.
    • Von Willebrand Disease, X-Linked Form Omim
      Holmberg and Nilsson (1973) used a monospecific precipitating rabbit antiserum against human antihemophilic factor-related protein to study 77 patients with von Willebrand disease (defined by low factor VIII, prolonged bleeding time and decreased platelet adhesiveness). They found two groups of patients. The larger group (57 patients) corresponded to classic von Willebrand disease and had low factor VIII protein. The other 20 patients had normal amounts of protein. Their disorder may be X-linked dominant. Infusion of human antihemophilic factor containing fraction I-O did not produce the delayed increase in antihemophilic factor characteristic of the first group. Various forms were suggested also by Koutts et al. (1975). Inheritance - ?
    • Von Willebrand Disease Gene_reviews
      Summary Clinical characteristics. Von Willebrand disease (VWD), a congenital bleeding disorder caused by deficient or defective plasma von Willebrand factor (VWF), may only become apparent on hemostatic challenge, and bleeding history may become more apparent with increasing age. Recent guidelines on VWD have recommended taking a VWF level of 30 or 40 IU/dL as a cutoff for those diagnosed with the disorder. Individuals with VWF levels greater than 30 IU/dL and lower than 50 IU/dL can be described as having a risk factor for bleeding. This change in guidelines significantly alters the proportion of individuals with each disease type. Type 1 VWD (~30% of VWD) typically manifests as mild mucocutaneous bleeding.
  • Werner Syndrome Wikipedia
    PMC 218746 . PMID 14527998 . ^ Kyng K, Croteau DL, Bohr VA (2009). "Werner syndrome resembles normal aging" . ... PMID 20075015 . ^ Goto M, Rubenstein M, Weber J, Woods K, Drayna D (Feb 1992). "Genetic linkage of Werner's syndrome to five markers on chromosome 8". ... PMID 18558713 . ^ Otterlei M, Bruheim P, Ahn B, Bussen W, Karmakar P, Baynton K, Bohr VA (2006). "Werner syndrome protein participates in a complex with RAD51, RAD54, RAD54B and ATR in response to ICL-induced replication arrest" (PDF) . ... Invest . 23 (1): 86–92. PMID 5431223 . ^ Salk D, Au K, Hoehn H, Martin GM (1981). "Cytogenetics of Werner's syndrome cultured skin fibroblasts: variegated translocation mosaicism". ... Cell Genet . 30 (2): 92–107. doi : 10.1159/000131596 . PMID 7273860 . ^ Fukuchi K, Martin GM, Monnat RJ (1989). "Mutator phenotype of Werner syndrome is characterized by extensive deletions" .
    WRN, BLM, HFM1, TP53, PARP1, RECQL4, LMNA, SERPINE1, FEN1, RAD51, POLB, XRCC6, IGFBP3, FN1, AHSA1, PRKAR1A, H2AX, GRAP2, PCNA, RECQL5, MRE11, XRCC5, EFEMP1, TGFB1, RECQL, MLH1, AIMP2, GYPA, MAPK1, ATR, WRNIP1, RNF19A, CRK, MAPK14, POLDIP2, SLC35G1, TAGLN, RAC1, MIR200C, CHD9, TFRC, APLF, BRIP1, TERT, GTF2IRD2, RPS3, PIWIL4, SSRP1, TOP3A, SLC20A1, SLC2A1, RPS6KA3, TIMP1, MON2, NEIL1, SIRT6, MMRN1, SAMHD1, RBPMS, PRPF19, DDX46, POLL, DESI1, EXD3, ENOSF1, ADIPOQ, PIWIL1, EXO1, CES2, DHX16, RAD54L, DDX19A, SUMO1, ABL1, PPP2CB, PPARG, GOLGA3, GCK, MTOR, FGFR1, FANCD2, EWSR1, ERCC4, ERCC1, DNA2, DKC1, DHX9, ACE, DCN, COL3A1, CKMT2, CDKN2A, CDC42, CAT, CASP1, CALCA, BRCA1, ATM, APOA1, APEX1, ANK1, HOXA@, HOXA1, HOXA3, KDR, POU1F1, POLD1, PLIN1, PLG, ACTB, OGG1, NBN, MYC, MECP2, MBNL1, LIG4, INSR, HOXA4, IL1B, IL1A, IGF2, ICAM1, HOXA13, HOXA11, HOXA10, HOXA9, HOXA7, HOXA6, HOXA5, H3P10
    • Werner Syndrome Gene_reviews
      Summary Clinical characteristics. Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. Individuals with Werner syndrome develop normally until the end of the first decade. The first sign is the lack of a growth spurt during the early teen years. Early findings (usually observed in the 20s) include loss and graying of hair, hoarseness, and scleroderma-like skin changes, followed by bilateral ocular cataracts, type 2 diabetes mellitus, hypogonadism, skin ulcers, and osteoporosis in the 30s. Myocardial infarction and cancer are the most common causes of death; the mean age of death in individuals with Werner syndrome is 54 years.
    • Werner Syndrome Omim
      A number sign (#) is used with this entry because Werner syndrome is caused by homozygous or compound heterozygous mutation in the RECQL2 gene (604611), which encodes a homolog of the E. coli RecQ DNA helicase, on chromosome 8p12. See also Hutchinson-Gilford progeria syndrome (HGPS; 176670), a more severe progeroid syndrome with earlier onset caused by mutation in the LMNA gene (150330). Clinical Features The features of Werner syndrome are scleroderma-like skin changes, especially in the extremities, cataract, subcutaneous calcification, premature arteriosclerosis, diabetes mellitus, and a wizened and prematurely aged facies. A particularly instructive pedigree was reported by McKusick (1963). The habitus is characteristic, with short stature, slender limbs, and stocky trunk. The nose is beaked. Epstein et al. (1966) studied a Japanese patient living in Seattle.
    • Werner Syndrome Orphanet
      Werner syndrome (WS) is a rare inherited syndrome characterized by premature aging with onset in the third decade of life and with cardinal clinical features including bilateral cataracts, short stature, graying and thinning of scalp hair, characteristic skin disorders and premature onset of additional age-related disorders. Epidemiology The prevalence among Japanese and Sardinian populations is estimated to be 1/50,000 due to the presence of founder mutations. Prevalence in other populations is unknown, but may be around 1/200,000. Clinical description WS patients are normal at birth and during childhood, apart from the absence of a pubertal growth spurt. WS presents between the ages of 20 and 30 with major symptoms of early onset bilateral cataracts, thinning and graying of the hair, short stature and skin changes (ankle ulceration, hyperkeratosis, tight skin, age spots, ''bird-like'' facies and subcutaneous atrophy).
    • Werner Syndrome Medlineplus
      Werner syndrome is characterized by the dramatic, rapid appearance of features associated with normal aging. Individuals with this disorder typically grow and develop normally until they reach puberty. Affected teenagers usually do not have a growth spurt, resulting in short stature. The characteristic aged appearance of individuals with Werner syndrome typically begins to develop when they are in their twenties and includes graying and loss of hair; a hoarse voice; and thin, hardened skin. They may also have a facial appearance described as "bird-like." Many people with Werner syndrome have thin arms and legs and a thick trunk due to abnormal fat deposition.
    • Werner Syndrome Gard
      Werner syndrome is a condition that causes premature aging. People with this syndrome will develop and grow normally until puberty. At puberty, growth stops and adults with Werner syndrome are typically shorter than average. By the early 20s-30s, people with this syndrome develop conditions usually associated with more advanced ages. In addition, people with Werner syndrome have an increased risk of developing cancer, especially thyroid and skin cancers. Heart attack and cancer are the most common causes of death. Werner syndrome is caused by mutations in the WRN gene and is inherited in an autosomal recessive manner.
  • Pulmonary Embolism Wikipedia
    Retrieved 12 March 2016 . ^ a b c d e f g h i j k Kearon C, Akl EA, Ornelas J, Blaivas A, Jimenez D, Bounameaux H, et al. ... Louis: Mosby's. ^ a b c d e f g h i j k l m n o p q r s Turetz M, Sideris AT, Friedman OA, Triphathi N, Horowitz JM (June 2018). ... PMID 10739372 . ^ a b van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW, et al. (January 2006). ... PMID 12928229 . ^ Crawford F, Andras A, Welch K, Sheares K, Keeling D, Chappell FM, et al. ... In Howard WA, Mistovich J, Karren K (eds.). Prehospital Emergency Care, 10e .
    FGA, MTHFR, EPO, PLAU, THBD, XDH, MERTK, TBXA2R, KLKB1, CAT, DAB2IP, PLAT, FGB, HP, MMP2, MMP9, CX3CL1, FGG, VCAM1, NOS3, CCL2, EDN1, TBXAS1, CX3CR1, CCN2, F13A1, F5, STAT4, TRNW, PLP1, PROC, PIGA, PTEN, PROS1, ABO, COX7A2L, TLR4, KLRC4, TRNS1, PROCR, TSPAN15, ERAP1, TET2, AGGF1, SLC44A2, SELENON, FUNDC2, TRIM8, IL23R, F11-AS1, UBAC2, TRNS2, ND5, TRNQ, ENG, TRNL1, HLA-B, HABP2, GNAQ, GDF2, F2, CD55, JAK2, CCR1, CBS, C4A, SERPINC1, FAS, AKT1, IL12A, IL10, KCNJ5, COX3, TRNH, TRNF, ND6, ACVRL1, ND4, ND1, IL12A-AS1, COX2, COX1, MPL, MEFV, SMAD4, CPB2, NPPB, TNNI3, SERPINF2, P2RY12, HGF, ALB, CRP
    • Pulmonary Embolism Mayo_clinic
      Overview A pulmonary embolism is a blood clot that blocks and stops blood flow to an artery in the lung. In most cases, the blood clot starts in a deep vein in the leg and travels to the lung. Rarely, the clot forms in a vein in another part of the body. When a blood clot forms in one or more of the deep veins in the body, it's called a deep vein thrombosis (DVT). Because one or more clots block blood flow to the lungs, pulmonary embolism can be life-threatening. However, prompt treatment greatly reduces the risk of death. Taking measures to prevent blood clots in your legs will help protect you against pulmonary embolism.
  • Treacher Collins Syndrome Wikipedia
    PMID 20640217 . ^ a b c d e f g h i j k l "Treacher Collins syndrome" . Genetics Home Reference . ... American Journal of Medical Genetics Part A, 179(12), 2365–2373. doi: 10.1002/ajmg.a.61359 ^ a b c d e f g h Katsanis SH, et al., Treacher Collins syndrome , 2004, GeneReviews ^ a b c d e f g h i j k l m n o "The Physician's Guide to Treacher Collins Syndrome" (PDF) . ... PMID 8218033 . ^ a b Marszałek, B; Wójcicki, P; Kobus, K; Trzeciak, WH (2002). "Clinical features, treatment and genetic background of Treacher Collins syndrome". ... Retrieved 2016-02-29 . ^ a b Dixon, Jill; Edwards, Sara J.; Gladwin, Amanda J.; Dixon, Michael J.; Loftus, Stacie K.; Bonner, Cynthia A.; Koprivnikar, Kathryn; Wasmuth, John J. (31 January 1996). ... S2CID 12500736 . ^ Isaac, C.; Marsh, K. L.; Paznekas, W. A.; Dixon, J.; Dixon, M.
    TCOF1
  • Onychomycosis Wikipedia
    ISBN 978-1-4160-2999-1 . ^ 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 Westerberg DP, Voyack MJ (December 2013). ... PMID 24364524 . ^ a b c d e f g h i j k l m n o p "Onychomycosis – Dermatologic Disorders" . ... PMID 11237081 . ^ Kreijkamp-Kaspers S, Hawke K, Guo L, Kerin G, Bell-Syer SE, Magin P, et al. ... S2CID 10079807 . ^ Loceryl (5% amorolfine) package labelling ^ "Drugs at FDA: JUBLIA" (PDF) . Retrieved 26 June 2014 . ^ Foley K, Gupta AK, Versteeg S, Mays R, Villanueva E, John D, et al. ... Superficial fungal infection: Dermatophytosis, onychomycosis, tinea nigra, piedra. In K Wolff et al., eds., Fitzpatrick's Dermatology in General Medicine, 7th ed., vol 2, pp. 1807–1821.
    CLEC7A, MMEL1, CARD9, DOCK8, CDH23, TNPO3, TRAF3IP2, USP8, STAT1, TNFSF15, IL17RC, POU2AF1, SDR9C7, IRF5, IL12RB1, IL12A, SPIB, LYST, VPS13B, RNA28SN5, ATR, TNMD, SLN, POLR2A, CYLD, COX8A, MFT2
    • Nail Fungus Mayo_clinic
      Overview Nail fungus is a common infection of the nail. It begins as a white or yellow-brown spot under the tip of your fingernail or toenail. As the fungal infection goes deeper, the nail may discolor, thicken and crumble at the edge. Nail fungus can affect several nails. If your condition is mild and not bothering you, you may not need treatment. If your nail fungus is painful and has caused thickened nails, self-care steps and medications may help. But even if treatment is successful, nail fungus often comes back. Nail fungus is also called onychomycosis (on-ih-koh-my-KOH-sis).
  • Chickenpox Wikipedia
    Retrieved 4 February 2015 . ^ a b c d e f g h i j k Atkinson, William (2011). Epidemiology and Prevention of Vaccine-Preventable Diseases (12 ed.). ... British Medical Bulletin . 103 (1): 115–127. doi : 10.1093/bmb/lds019 . PMID 22859715 . ^ a b Macartney, K; Heywood, A; McIntyre, P (23 June 2014). ... Retrieved 22 July 2009 . ^ Kanbayashi Y, Onishi K, Fukazawa K, Okamoto K, Ueno H, Takagi T, Hosokawa T (2012). ... PMID 8092915 . ^ Abro AH, Ustadi AM, Das K, Abdou AM, Hussaini HS, Chandra FS (December 2009). ... Retrieved 18 January 2008 . ^ Strangfeld A, Listing J, Herzer P, Liebhaber A, Rockwitz K, Richter C, Zink A (February 2009).
    • Chickenpox Mayo_clinic
      Overview Chickenpox is an illness caused by the varicella-zoster virus. It brings on an itchy rash with small, fluid-filled blisters. Chickenpox spreads very easily to people who haven't had the disease or haven't gotten the chickenpox vaccine. Chickenpox used to be a widespread problem, but today the vaccine protects children from it. The chickenpox vaccine is a safe way to prevent this illness and the other health problems that can happen during it. Symptoms The rash caused by chickenpox appears 10 to 21 days after you're exposed to the varicella-zoster virus.
  • Necrotizing Fasciitis Wikipedia
    The left leg shows extensive redness and tissue death . Pronunciation / ˈ n ɛ k r ə ˌ t aɪ z ɪ ŋ ˌ f æ ʃ i ˈ aɪ t ɪ s / or / ˌ f æ s -/ Specialty Infectious disease Symptoms Severe pain , fever , purple colored skin in the affected area [3] Usual onset Sudden, spreads rapidly [3] Causes Multiple types of bacteria , [4] occasional fungus [5] Risk factors Poor immune function such as from diabetes or cancer , obesity , alcoholism , intravenous drug use , peripheral artery disease [2] [3] Diagnostic method Based on symptoms, medical imaging [4] Differential diagnosis Cellulitis , pyomyositis , gas gangrene [6] Prevention Wound care , handwashing [3] Treatment Surgery to remove the infected tissue , intravenous antibiotics [2] [3] Prognosis ~30% mortality [2] Frequency 0.7 per 100,000 per year [4] Necrotizing fasciitis ( NF ), also known as flesh-eating disease , is an infection that results in the death of parts of the body's soft tissue . [3] It is a severe disease of sudden onset that spreads rapidly. [3] Symptoms usually include red or purple skin in the affected area, severe pain, fever , and vomiting. [3] The most commonly affected areas are the limbs and perineum . [2] Typically, the infection enters the body through a break in the skin such as a cut or burn . [3] Risk factors include poor immune function such as from diabetes or cancer , obesity , alcoholism , intravenous drug use , and peripheral artery disease . [2] [3] It is not typically spread between people. [3] The disease is classified into four types, depending on the infecting organism. [4] Between 55 and 80% of cases involve more than one type of bacteria . [4] Methicillin-resistant Staphylococcus aureus (MRSA) is involved in up to a third of cases. [4] Medical imaging is often helpful to confirm the diagnosis. [4] Necrotizing fasciitis may be prevented with proper wound care and handwashing . [3] It is usually treated with surgery to remove the infected tissue , and intravenous antibiotics . [2] [3] Often, a combination of antibiotics is used, such as penicillin G , clindamycin , vancomycin , and gentamicin . [2] Delays in surgery are associated with a much higher risk of death. [4] Despite high-quality treatment, the risk of death is between 25 and 35%. [2] Necrotizing fasciitis occurs in about 0.4 people per 100,000 per year in the US, and about 1 per 100,000 in Western Europe. [4] Both sexes are affected equally. [2] It becomes more common among older people and is rare in children. [4] It has been described at least since the time of Hippocrates . [2] The term "necrotizing fasciitis" first came into use in 1952. [4] [7] Contents 1 Signs and symptoms 2 Cause 2.1 Risk factors 2.2 Bacteria 3 Diagnosis 3.1 Medical imaging 3.2 Scoring system 4 Prevention 5 Treatment 5.1 Surgery 5.2 Antibiotics 5.3 Add on therapy 6 Epidemiology 7 History 7.1 Notable cases 8 See also 9 References 10 External links Signs and symptoms [ edit ] Symptoms may include fever, swelling, and complaints of excessive pain. ... Archived from the original on 2017-09-08. ^ 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 Hakkarainen, Timo W.; Kopari, Nicole M.; Pham, Tam N.; Evans, Heather L. (2014). ... PMID 25069713 . ^ a b c d e f g h i j k l m n o "Necrotizing Fasciitis: A Rare Disease, Especially for the Healthy" . ... Retrieved 13 August 2016 . ^ a b c d e f g h i j k l m n o p q r s t Paz Maya, S; Dualde Beltrán, D; Lemercier, P; Leiva-Salinas, C (May 2014). ... Archived from the original (PDF) on December 2, 2007. ^ Cartwright, K; Logan, M; McNulty, C; Harrison, S; George, R; Efstratiou, A; McEvoy, M; Begg, N (1995).
    PAGR1, GAST, GALNS, MYOM2, CD46, ALB, HAMP, FOXP3, AAK1, SLC9A6, RECK, LAP, RAB3IL1, CXCL8, C4BPA, HMGCR, HLA-DRB1, HLA-DQB2, HLA-DQB1, GNAO1, LRRC32, CRP, C4BPB, RBM45
    • Necrotizing Fasciitis Gard
      Necrotizing fasciitis is a serious infection of the skin, the tissue just beneath the skin (subcutaneous tissue), and the tissue that covers internal organs (fascia). Necrotizing fasciitis can be caused by several different types of bacteria, and the infection can arise suddenly and spread quickly. Early signs include flu-like symptoms and redness and pain around the infection site. A prompt diagnosis and treatment are essential. If the infection is not treated promptly, it can lead to multiple organ failure and death. Treatment typically includes intravenous (IV) antibiotics and surgery to remove infected and dead tissue.
  • Bronchiectasis Wikipedia
    Retrieved 10 August 2016 . ^ Bird, K; Memon, J (January 2019). "Bronchiectasis". ... ISSN 1600-0617 . PMID 29997246 . ^ a b Kwon, K. Y.; Myers, J. L.; Swensen, S. J.; Colby, T. ... ISSN 1349-3329 . PMID 21127394 . ^ Kim, C. K.; Chung, C. Y.; Kim, J. S.; Kim, W. ... PMID 27753690 . ^ Greenberger, Paul A.; Bush, Robert K.; Demain, Jeffrey G.; Luong, Amber; Slavin, Raymond G.; Knutsen, Alan P. ... PMID 27492829 . ^ Mishra, Mayank; Kumar, Naresh; Jaiswal, Ashish; Verma, Ajay K.; Kant, Surya (October 2012). "Kartagener's syndrome: A case series" .
    CFTR, SERPINA1, SCNN1B, SCNN1G, DNAH11, DNAI1, DNAH5, DNAAF1, PIK3R1, PIK3CD, NFKB2, NME8, CCDC40, SCNN1A, DNAI2, DNAL1, DNAAF2, RSPH9, RSPH4A, CCDC39, TNF, ICAM1, STAT1, TAP2, TAP1, TGFB1, TNFRSF13B, MUC5B, DNAAF3, ARHGEF1, TNFSF12, CCNO, FAM13A, ATP11A, LRRC6, DNAH1, RIPK1, CXCR4, DNAJB13, OFD1, USP11, BLNK, TERT, TERC, CCDC103, SFTPA1, TCF3, TAPBP, SPAG1, SFTPC, SFTPA2, STK36, PIH1D3, ICOS, STN1, CCDC151, TNFRSF13C, LRRC56, CCDC114, DNAAF4, DRC1, DPP9, RSPH1, CCDC65, CFAP300, ZNF341, RSPH3, TTC25, GAS2L2, CARMIL2, BACH2, CFAP298, LRRC8A, BTNL2, DNAH7, SLC29A3, COPD, ARMC4, DNAAF5, HYDIN, RTEL1, ZMYND10, MCIDAS, IL21R, ABCA3, RPGR, PRKCD, NFKB1, IGLL1, IGHM, IRF8, HLA-DRB1, PARN, GAS8, FCGR2A, ENG, PGM3, DSP, DNMT3B, CR2, LRBA, CD81, CD79B, CD79A, MS4A1, CD19, CD8A, BLM, B2M, ATM, NBN, MBL2, ELANE, CXCL8, MPO, IL17A, CALR, PLF, CRP, IL6, NTM, HLA-C, ELN, FOLH1, USO1, SEC14L2, ALB, MMP8, MMP9, NXF1, FLNB, MMP1, CTSB, SLC26A9, DIAPH1, G6PC3, PREP, PCBD1, PPARG, PDCD1, PRTN3, MUC2, PZP, CEL, STAT3, ADRB2, TRIM21, FCGRT, TNFRSF8, SGCA, SFTPD, RASA1, CAMP, CXCL12, CCL20, AVP, CCL17, TIMP3, RGMA, PARP9, RMRP, TRAF3IP2, SLC27A5, JMJD6, MUC5AC, LGALS9, PTPN22, LCN1, IL18, FLVCR1, IL13, IL10, MBL3P, FOXP3, ISYNA1, FCN2, IL23A, IL1B, IL1A, NHS, IFNG, CFI, NOS2, HOXB@, PAEP, HLA-B, RGS6, TLR2, FOXJ1, MICA
  • Acute Liver Failure Wikipedia
    Bacterial sepsis mostly due to gram positive organisms and fungal sepsis are observed in up to 80% and 30% patients, respectively. [6] Metabolic derangements [ edit ] Hyponatraemia is an almost universal finding due to water retention and a shift in intracellular sodium transport from inhibition of Na/K ATPase [ citation needed ] . Hypoglycaemia (due to depleted hepatic glycogen store and hyperinsulinaemia ), hypokalaemia , hypophosphataemia and metabolic alkalosis are often present, independent of renal function. ... Replacement therapy is recommended only in the setting of bleeding or prior to an invasive procedure. Vitamin K can be given to treat an abnormal prothrombin time, regardless of whether there is poor nutritional status. ... N Engl J Med . 336 (16): 1142–1148. doi : 10.1056/NEJM199704173361604 . PMID 9099658 . ^ Dierick K; et al. (2005). "Fatal family outbreak of Bacillus cereus-associated food poisoning" . ... CS1 maint: extra text: authors list ( link ) ^ Sood, Gagan K. "Acute Liver Failure" . Mescape . ... PMID 12606737 . ^ a b Farmer, DG; Anselmo, DM; Ghobrial, RM; Yersiz, H; McDiarmid, SV; Cao, C; Weaver, M; Figueroa, J; Khan, K; Vargas, J; Saab, S; Han, S; Durazo, F; Goldstein, L; Holt, C; Busuttil, RW (May 2003).
    TNF, ATP7B, HGF, FAS, ALB, IL1RN, GC, MAPK8, KRT8, KRT18, GFER, FASLG, CSF3, SERPINC1, CAST, GPNMB, PANX1, CD74, FST, POMC, SCO1, ALDOB, INHBA, INS, IL6, TLR4, CASP3, NOS3, PTGS2, ABCC2, NOS2, MET, CD14, CASP9, ATM, KCNJ10, PTAFR, CASP12, UCP2, COL1A2, HSPA8, FGA, BRIP1, THBD, INS-IGF2, LTC4S, NBAS, POLG, RINT1, TRMU, FAH, POLG2, JAK2, SCYL1, MST1, PORCN, HADH, GPT, GPR35, VPS13A, MPV17, ITCH, F5, CYC1, RYR1, GFM1, ACAD9, IKZF1, MEFV, CACNA1S, EIF2AK3, LARS1, TCF4, HLA-B, HMGB1, IL1B, F2, CCL4, IL10, MIR122, HMOX1, PPARA, STON1, AFM, GTF2A1L, MIR223, NLRP3, SLC1A2, HDAC2, STON1-GTF2A1L, HDAC6, MSC, IL1A, UGT1A, TP53, SLC17A5, ABCG2, SYT1, CXCL12, PEBP1, OTC, PRKAA1, RELA, WNK1, BCHE, AFP, IFNG, AHSG, GORASP1, GSK3B, PIM3, DDIT3, DGUOK, EXOSC3, BCL2L11, MIR17, MFN2, MIR155, ABCB6, AIM2, BTBD8, YAP1, IFNL3, PPARGC1B, APOA5, PIK3IP1, LMLN, MIR19A, LONP1, MIR210, ATG7, PPIG, MIR214, RGN, TIMELESS, SQSTM1, MIR375, MIR1224, TNFRSF10B, RIPK1, OCLN, BECN1, SOCS1, ARHGEF5, SHANK3, KHDRBS1, TXNIP, KCTD9, HAMP, ACKR3, NAT10, HAVCR1, SIGLEC9, PDLIM3, IGHV1-3, ATRNL1, TLR9, STX18, ERO1A, SCLC1, RRM2B, SLC25A37, CXCL16, NUP62, SERAC1, SLC27A5, DCTN4, CYSLTR1, CCL27, SLA2, EVA1A, TMPRSS13, SESN2, SIRT1, PARP9, ASRGL1, DHDDS, GSDMD, SIRT2, TBC1D9, TFEB, ACADM, VWF, GABPA, CYP2E1, CYP3A4, ESR1, FABP1, FABP7, FBP1, FCGR3A, FCGR3B, FOXO3, G6PD, GFAP, VIP, CXCR3, GTF2H1, HIF1A, HNF4A, HSPA5, HSPG2, ID1, IFNA1, IFNA13, IFNB1, CYP1A2, CX3CR1, CTNNB1, CTLA4, AHR, AKT1, ALAS1, ALPP, AMCN, AQP4, AR, ATHS, BCL2, OPN1SW, BID, BST2, CASP8, CD86, ENTPD1, CD40LG, CEL, CGA, CCR5, KLF6, CRP, IL1R1, IL2, CXCL8, S100A10, CCL2, SDC1, SLC6A12, SLC12A2, SLPI, SOAT1, STAR, STAT1, STAT3, MAP3K7, PPP1R11, TGFB1, TGFBR2, THBS1, THPO, TLR2, TLR3, TNFAIP3, TNFAIP6, TXN, UGT2B7, S100A12, RHD, IL18, ACP3, ITGAM, MARS1, KMT2A, MPO, MSMB, COX2, MYD88, NFE2L2, NT5E, SERPINE1, ABCB1, PIK3CA, PIK3CB, PIM1, PIK3CD, PIK3CG, SERPINF2, PPP2R5A, PRKAA2, PRKAB1, RBP4, MTCO2P12
    • Acute Liver Failure Mayo_clinic
      Overview Acute liver failure is loss of liver function that occurs quickly — in days or weeks — usually in a person who has no preexisting liver disease. It's most commonly caused by a hepatitis virus or drugs, such as acetaminophen. Acute liver failure is less common than chronic liver failure, which develops more slowly. Acute liver failure, also known as fulminant hepatic failure, can cause serious complications, including bleeding and increased pressure in the brain. It's a medical emergency that requires hospitalization. Depending on the cause, acute liver failure can sometimes be reversed with treatment.
    • Acute Liver Failure Orphanet
      A rare hepatic disease characterized by acute onset of severe liver dysfunction without evidence of underlying chronic liver disease. Patients present with nonspecific symptoms like jaundice, upper right abdominal pain, nausea, vomiting, pruritus, fatigue, and fever. The condition may rapidly progress to hepatic encephalopathy, coagulopathy, and life-threatening multiorgan failure. Liver biopsy typically shows massive hepatic necrosis.
  • Travelers' Diarrhea Wikipedia
    PMID 26900116 . ^ a b c d e f g h i j k l m n o p q r s t u Leder, K (2015). ... Archived from the original on 2016-03-10. ^ a b Ahmed, T; Bhuiyan, TR; Zaman, K; Sinclair, D; Qadri, F (5 July 2013). ... Traveler's diarrhea is sometimes called by its more colorful names: Montezuma's revenge, Delhi belly, and Turkey trots. ^ a b c d e f g h i j k l m n o p q r "Travelers' Diarrhea" . ... Archived from the original on April 3, 2008. ^ a b c d e f g h i j k l m n "Travelers' diarrhea" . safewateronline.com.
    SERPINA3, LTF, POTEKP, ACTBL2, ACOT7, FHL5, TBCA, SULT1E1, SLC9A3, TNFRSF11B, IL10, ACTG1, GUCY2C, GUCA2B, GUCA2A, GCY, EMD, MAP3K8, CD14, ACTG2, POTEM
    • Traveler's Diarrhea Mayo_clinic
      Overview Traveler's diarrhea is a digestive tract disorder that commonly causes loose stools and abdominal cramps. It's caused by eating contaminated food or drinking contaminated water. Fortunately, traveler's diarrhea usually isn't serious in most people — it's just unpleasant. When you visit a place where the climate or sanitary practices are different from yours at home, you have an increased risk of developing traveler's diarrhea. To reduce your risk of traveler's diarrhea, be careful about what you eat and drink while traveling.
  • Thrombosis Wikipedia
    Anticoagulation [ edit ] Main article: Anticoagulant Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reduce thromboembolic occurrence. ... PMID 16002765 . ^ eMedicine Article on Internal Jugular Vein Thrombosis by Dale K. Mueller| http://www.emedicine.com/med/topic2762c.htm [ permanent dead link ] ^ Creager, Mark A.; Kaufman, John A.; Conte, Michael S. (7 June 2012). ... (subscription required) ^ Bekker, J.; Ploem, S.; de Jong, K. P. (April 2009). "Early Hepatic Artery Thrombosis after Liver Transplantation: A Systematic Review of the Incidence, Outcome and Risk Factors" . ... PMID 19298450 . ^ a b c d e f g h i j k l m n o p q r s Hoffman , p. 960. sfn error: no target: CITEREFHoffman ( help ) ^ a b Moliterno , p. 306. sfn error: no target: CITEREFMoliterno ( help ) ^ Brunner , p. 874. sfn error: no target: CITEREFBrunner ( help ) ^ a b c d e f g h i j Copstead , p. 320. sfn error: no target: CITEREFCopstead ( help ) ^ a b c d e f g h i Moliterno , p. 307. sfn error: no target: CITEREFMoliterno ( help ) ^ a b Abele . sfn error: no target: CITEREFAbele ( help ) ^ a b c d e f g h i j k l m n o p q r s t u v w x Brunner , p. 875. sfn error: no target: CITEREFBrunner ( help ) ^ a b c d Copstead , p. 329. sfn error: no target: CITEREFCopstead ( help ) ^ "Pacing wire" .
    F2, SERPINC1, P2RY12, PLAU, FGA, F5, F3, PROC, VWF, SERPINE1, PROCR, SELP, PLAT, ADAMTS13, PROS1, TNF, PF4, FCGR2A, PTGS2, THBD, VHL, CRP, MERTK, GAS6, GP1BA, PDE3A, P2RY1, AGT, PTGER3, PODXL, HMOX1, TYRO3, KLF4, SIRT1, VKORC1, KLKB1, MAS1, HGF, FUT4, BDKRB2, CD2, CYP2C19, CYP3A5, EPO, F9, F10, FLT3, BCRP3, GUCY1A1, APOH, CD40LG, TBXAS1, C5AR1, PIK3CB, ACE2, JAK2, MTHFR, NOS3, ITGA2, ITGB3, CPB2, VASP, TFPI, F8, P2RX1, MPL, TNFSF14, SCUBE2, CD177, GP6, C1QBP, C4B, IL1B, SCUBE1, TUBB1, IL6, KLF2, MRVI1, CANT1, LPA, DCN, PLA2G6, F11, LEPR, LEP, FGG, PECAM1, FGB, F13A1, PTGS1, ITGA2B, ICAM4, EGR1, SLC19A1, TBXA2R, ANXA5, CD55, ENG
  • Vertigo Wikipedia
    Etymology [ edit ] Vertigo is from the Latin word, vertō , which means "a whirling or spinning movement". [48] See also [ edit ] Acrophobia – Extreme or irrational fear of heights Broken escalator phenomenon – The sensation of losing balance or dizziness when stepping onto an escalator which is not working Chronic subjective dizziness Fear of falling – natural fear typical of most mammals Head for heights Ideomotor phenomenon – Concept in hypnosis and psychological research Illusions of self-motion – Misperception of one's location or movement Proprioception – Sense of the relative position of one's own body parts and strength of effort employed in movement Motion sickness – Nausea caused by motion Sense of balance , also known as Equilibrioception – Physiological sense allowing animals to dynamically maintain an unstable posture Spatial disorientation – Inability of a person to correctly determine their body position in space References [ edit ] ^ a b c d e f g h i j k l m n Post, RE; Dickerson, LM (2010). ... Archived from the original on 2013-06-06. ^ a b c d e f g h i j k l m n Hogue, JD (June 2015). "Office Evaluation of Dizziness". ... Archived from the original on 2015-07-02. ^ a b c d e f g h i j k l m n o p q r Kerber, KA (2009). "Vertigo and dizziness in the emergency department" . ... PMID 19218018 . ^ a b c d e f g h i j k l m Neuhauser HK, Lempert T (November 2009). ... PMC 3169717 . PMID 21640178 . ^ a b Jahn, K; Dieterich, M (December 2011). "Recent advances in the diagnosis and treatment of balance disorders".
    CACNA1A, COCH, SLC26A4, STRC, SCN5A, PRKAR1A, RARA, RYR2, SCN1B, SCN2A, NAGA, SLC1A3, SLC12A3, SPG7, STAT3, STAT4, STAT5B, PML, NUMA1, PDGFB, TLR4, NPM1, NF2, MYO7A, MYL2, MYD88, MVK, MPL, MEN1, MEFV, KCNJ10, KCNA1, JUP, JAK2, THPO, TNFRSF1A, IL10, VHL, IRF2BP2, UBAC2, TECRL, IL23R, TUBB6, FIP1L1, TBL1XR1, FKRP, NABP1, CDH23, BCOR, CNNM2, TRPM4, TET2, ADA2, ERAP1, STRN4, TPK1, PTPN22, DKK1, AFG3L2, NOP56, TRDN, SH2B3, TMEM94, AIP, CACNA1G, KLRC4, ZBTB16, IL12A, IL12A-AS1, CALM1, DBH, CACNB4, C4A, FLI1, GATA2, BRAF, EPOR, GCDH, CCND1, B2M, CASQ2, ATP1A2, CTNNB1, NKX2-5, FAS, FOXI1, EGF, GLA, SLC25A4, COL3A1, CALM2, GYG1, CCR1, HFE, CLCNKB, HLA-B, CLCN1, CALM3, CKMT1B, S100B, CYP2D6, ABCB1, CHRNA4, CCT, CHRNA3, CHRNA7, CHRNB2, CHRNB3, ASIC3, LGI1, TES, IL1B, CASP9, PRIMA1, ZGLP1, GRXCR1, ADCY5, ADRA1A, COPD, ADRB1, ADRB2, APOE, CCHCR1, SPRTN, PANK2, EHMT1, AVP, HRH4, SPAG9, CAD, CHRNB4, CRY1, SELENBP1, OPRM1, NT5E, NPPA, GCG, NPY, GFAP, ACR, GFER, GJA1, GJB2, GLP1R, MME, GRM5, KCNJ13, HINT1, IFNA1, ITGB3, IFNA13, NTRK1, PAEP, CHRNA6, PFN2, PER2, TPM3, COMT, IGF1, TAC1, CUX1, SRY, CYP3A5, SHBG, SGSH, CCL2, DPP4, DSPP, S100A1, ERF, FES, PGR, ACHE
  • Abdominal Obesity Wikipedia
    .; Sandeep, S.; Deepa, R.; Vimaleswaran, K. S.; Farooq, S.; Mohan, V. (2004). ... PMID 14962997 . ^ Degawa-Yamauchi MBJE; Juliar BE; Watson W; Kerr K; Jones RM; Zhu Q; Considine RV (2003). ... PMID 15229336 . ^ Hirosumi J, Tuncman G, Chang L, Gorgun CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS (2002). ... G.; McTernan C. L.; Chetty R; Jenner K; Fisher FM; Lauer MN; Crocker J; Barnett AH; Kumar S. (2002). ... PMID 17261236 . S2CID 11796524 . ^ Knowles, K. M.; Paiva, L. L.; Sanchez, S. E.; Revilla, L.; Lopez, T.; Yasuda, M.
    EIF2S3, HSD11B1, USP8, PWRN1, SNORD115-1, PWAR1, RNPC3, MAGEL2, NPAP1, MKRN3-AS1, DYRK1B, AIP, HERC2, CUL4B, MKRN3, SNRPN, NDN, MTTP, LIPE, IPW, SNORD116-1
  • Catecholaminergic Polymorphic Ventricular Tachycardia Wikipedia
    OCLC 846445829 . ^ a b c d e f g h i j k l m Priori SG, Blomström-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J, Elliott PM, Fitzsimons D, Hatala R, Hindricks G, Kirchhof P, Kjeldsen K, Kuck KH, Hernandez-Madrid A, Nikolaou N, Norekvål TM, Spaulding C, Van Veldhuisen DJ (November 2015). "2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). ... S2CID 40499394 . ^ a b c d e f g h i j k l m n o p q r Lieve KV, van der Werf C, Wilde AA (May 2016). ... OCLC 47659382 . ^ a b Eisner DA, Caldwell JL, Kistamás K, Trafford AW (July 2017). "Calcium and Excitation-Contraction Coupling in the Heart" . ... Heart Rhythm . 4 (9): 1149–54. doi : 10.1016/j.hrthm.2007.05.017 . PMID 17765612 . ^ Shivkumar K, Ajijola OA, Anand I, Armour JA, Chen PS, Esler M, De Ferrari GM, Fishbein MC, Goldberger JJ, Harper RM, Joyner MJ, Khalsa SS, Kumar R, Lane R, Mahajan A, Po S, Schwartz PJ, Somers VK, Valderrabano M, Vaseghi M, Zipes DP (July 2016). ... CS1 maint: uses authors parameter ( link ) ^ Swan H, Piippo K, Viitasalo M, Heikkilä P, Paavonen T, Kainulainen K, Kere J, Keto P, Kontula K, Toivonen L (December 1999).
    RYR2, TRDN, CALM1, CASQ2, TECRL, KCNJ2, CALM2, CALM3, ANK2, KCNE1, FKBP1B, TRDN-AS1, KCNQ1, SCN5A, KCNH2, ARVD3, SNAP91, THEM5, CAVIN1, ASPH, CAMKMT, CACNA1S, KCNE2, FXN, AIP, SCN10A, KRIT1, RYR1, CNTN3, CTRL, PICALM
    • Catecholaminergic Polymorphic Ventricular Tachycardia Gene_reviews
      Summary Clinical characteristics. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by episodic syncope occurring during exercise or acute emotion in individuals without structural cardiac abnormalities. The underlying cause of these episodes is the onset of fast ventricular tachycardia (bidirectional or polymorphic). Spontaneous recovery may occur when these arrhythmias self-terminate. In other instances, ventricular tachycardia may degenerate into ventricular fibrillation and cause sudden death if cardiopulmonary resuscitation is not readily available. The mean age of onset of symptoms (usually a syncopal episode) is between age seven and twelve years; onset as late as the fourth decade of life has been reported.
    • Ventricular Tachycardia, Catecholaminergic Polymorphic, 1, With Or Without Atrial Dysfunction And/or Dilated Cardiomyopathy Omim
      A number sign (#) is used with this entry because catecholaminergic polymorphic ventricular tachycardia-1 (CPVT1) is caused by heterozygous mutation in the cardiac ryanodine receptor gene (RYR2; 180902) on chromosome 1q43. Description Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an arrhythmogenic disorder of the heart characterized by a reproducible form of polymorphic ventricular tachycardia induced by physical activity, stress, or catecholamine infusion, which can deteriorate into ventricular fibrillation. Patients present with recurrent syncope, seizures, or sudden death after physical activity or emotional stress. Typically, clinical cardiologic examinations, such as baseline ECG and echocardiogram, reveal mostly normal findings, and postmortem examinations, when carried out, have not disclosed any significant morphologic alterations in the fine structure of the heart, with the exception of mild fatty myocardial infiltration in a few patients. The hallmark of CPVT comprises ventricular arrhythmias of varying morphology not present under resting conditions but appearing only with physical exercise, excitement, or catecholamine administration.
    • Catecholaminergic Polymorphic Ventricular Tachycardia Orphanet
      A rare, severe genetic arrhythmogenic disorder of the structurally normal heart characterized by catecholamine-induced ventricular tachycardia (VT) manifesting as syncope and sudden death in young individuals. Epidemiology The prevalence of catecholaminergic polymorphic ventricular tachycardia (CPVT) is estimated to be 1/10,000. Both sexes are equally affected. Clinical description Typical age of onset of CPVT is between 7 and 15 years of age. Exercise- or emotion-induced syncopal spells are frequently the first symptom. In a subset of patients (10-20%), the disease is clinically silent, presenting only in the event of sudden death.
    • Catecholaminergic Polymorphic Ventricular Tachycardia Gard
      Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic disorder that causes an abnormally fast and irregular heart rhythm in response to physical activity or emotional stress. Signs and symptoms include light-headedness, dizziness, and fainting. Symptoms most often develop between 7 to 9 years of age. If untreated CPVT can cause a heart attack and death. CPVT is caused by mutations in the RYR2 or CASQ2 genes. When a RYR2 gene mutation is involved, the condition is passed through families in an autosomal dominant fashion. When CASQ2 gene mutations are involved, the condition is inherited in an autosomal recessive fashion.
    • Ventricular Tachycardia, Catecholaminergic Polymorphic, 2 Omim
      A number sign (#) is used with this entry because catecholaminergic polymorphic ventricular tachycardia-2 (CPVT2) is caused by homozygous or compound heterozygous mutation in the gene encoding calsequestrin-2 (CASQ2; 114251) on chromosome 1p13. For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772. Clinical Features Lahat et al. (2001) studied 41 members of 7 families from a highly inbred Bedouin tribe in northern Israel in which 9 children had unexplained sudden death, 7 during vigorous exercise and 2 during excitement. In addition, 12 other children had onset of recurrent syncope and seizures at around 6 years of age, with 70% of the episodes occurring during vigorous physical activity and 30% following sudden excitement. The parents of affected children were all related and were all asymptomatic.
    • Ventricular Tachycardia, Catecholaminergic Polymorphic, 4 Omim
      A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-4 (CPVT4) is caused by heterozygous mutation in the calmodulin gene (CALM1; 114180) on chromosome 14q32. For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772. Clinical Features Nyegaard et al. (2012) studied a large 4-generation Swedish family with a history of ventricular arrhythmias, syncope, and sudden death, predominantly in association with physical exercise or stress. The proband was a 42-year-old man who first developed syncope at 12 years of age while playing football; electrocardiogram (ECG) at that time showed bradycardia with a prominent U-wave in leads V2 and V3, without evidence of QT prolongation. He had a history of loss of consciousness on at least 4 occasions during physical activity and once in connection with a fire alarm.
    • Catecholaminergic Polymorphic Ventricular Tachycardia Medlineplus
      Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a condition characterized by an abnormal heart rhythm (arrhythmia). As the heart rate increases in response to physical activity or emotional stress, it can trigger an abnormally fast heartbeat called ventricular tachycardia. Episodes of ventricular tachycardia can cause light-headedness, dizziness, and fainting (syncope). In people with CPVT, these episodes typically begin in childhood. If CPVT is not recognized and treated, an episode of ventricular tachycardia may cause the heart to stop beating (cardiac arrest), leading to sudden death. Researchers suspect that CPVT may be a significant cause of sudden death in children and young adults without recognized heart abnormalities.
    • Ventricular Tachycardia, Catecholaminergic Polymorphic, 3 Omim
      A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-3 (CPVT3) is caused by homozygous mutation in the TECRL gene (617242) on chromosome 4q13. Description Catecholaminergic polymorphic ventricular tachycardia-3 (CPVT3) is characterized by overlapping features of long QT syndrome (see 192500) and CPVT. Affected individuals exhibit adrenergic ventricular tachycardia associated with a high prevalence of cardiac arrest and sudden cardiac death, with recurrent atrial tachycardia sometimes triggering the ventricular arrhythmias. In addition, affected individuals have a normal or mildly prolonged QTc on baseline electrocardiography, with a paradoxical QT increase during adrenergic simulation (summary by Devalla et al., 2016). For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772.
    • Ventricular Tachycardia, Catecholaminergic Polymorphic, 5, With Or Without Muscle Weakness Omim
      A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-5 with or without muscle weakness (CPVT5) is caused by homozygous or compound heterozygous mutation in the triadin gene (TRDN; 603283) on chromosome 6q22. For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772. Clinical Features Roux-Buisson et al. (2012) studied 2 families with cardiac arrhythmias. In the first family, which originated from the French West Indies, the 2-year-old proband experienced syncope followed by cardiac arrest after a shock while playing with his 7-year-old brother. Resting electrocardiogram (ECG) after resuscitation showed numerous polymorphic or bidirectional ventricular extra beats and runs of polymorphic ventricular tachycardia.
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