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Acute Respiratory Distress Syndrome
Wikipedia
Corticosteroids may increase the number of ventilator-free days during the first 28 days of hospitalization. [24] One study found that dexamethasone may help. [25] The combination of hydrocortisone, ascorbic acid, and thiamine also requires further study as of 2018. [26] Inhaled nitric oxide (NO) selectively widens the lung's arteries which allows for more blood flow to open alveoli for gas exchange . Despite evidence of increased oxygenation status, there is no evidence that inhaled nitric oxide decreases morbidity and mortality in people with ARDS. [27] Furthermore, nitric oxide may cause kidney damage and is not recommended as therapy for ARDS regardless of severity. [28] Extracorporeal membrane oxygenation [ edit ] Extracorporeal membrane oxygenation (ECMO) is mechanically applied prolonged cardiopulmonary support. ... Traumakine (FP-1201-lyo) is a recombinant human IFN beta-1a drug, developed by the Finnish company Faron Pharmaceuticals , which is undergoing international phase-III clinical trials after an open-label, early-phase trial showed an 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. [48] The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced. [49] Aspirin has been studied in those who are at high risk and was not found to be useful. [1] An intravenous ascorbic acid treatment was tested in the 2019 RCT , in people with ARDS due to sepsis and there was no change in primary endpoints. [50] See also [ edit ] Respiratory monitoring References [ edit ] ^ a b c d e f g h i j k l m n o p q r s t Fan, E; Brodie, D; Slutsky, AS (20 February 2018). ... "Diabetic patients have a decreased incidence of acute respiratory distress syndrome". Crit Care Med . 28 (7): 2187–92. doi : 10.1097/00003246-200007000-00001 . ... "Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute respiratory distress syndrome: Time for a reevaluation". Critical Care Medicine . 28 (1): 232–235. doi : 10.1097/00003246-200001000-00039 .THBD, EDN1, RAMP2, SOD2, CCL2, ALB, MT3, CHPT1, MIR30B, ACAA2, MIR30A, MIR99A, MIR135B, MIR337, IGFBP6, IFRD1, MIR346, GNRH1, MIR380, TIMP1, GABRB1, MIRLET7B, MIR215, FGFR4, CYB5A, MIR210, MIR19A, MIR18A, TSPAN8, MIR128-2, MIR127, MIR126, PRDX6, MIRLET7D, FBLN5, EBF1, SERPINH1, LIM2, SLC25A11, CES3, ACO2, PLA2G4A, PROS1, PSMA4, EIF2AK1, ALAD, AKR1B1, MT2A, APC, S100A4, S100A9, MDH1, LCT, LCN2, SERPINC1, IL10, AGER, IL1RN, CXCL10, HSPA4, PDPN, TBXA2R, C3AR1, MIR26A1, MFN1, C5AR1, C5, CXCL8, SFTPB, TNF, BTBD8, IL6, ABCA3, TGFB1, ACE, VEGFA, ANGPT2, SFTPD, IL17A, ACE2, SFTPC, SFTPA2, IL1B, MMP9, NFE2L2, SFTPA1, HMOX1, HMGB1, NAMPT, TLR4, IL18, MPO, NLRP3, AGT, IL1A, FGF7, REN, NR3C1, VPS51, GABPA, SCGB1A1, AGTR1, PI3, MIR155, ELANE, STAT3, SARS2, IFNG, ANGPT1, IGF1, LINC01672, MIF, PLA2G7, SARS1, MAPK1, CRP, HP, YWHAZ, PLA2G1B, SMUG1, F3, PLB1, CFTR, POLDIP2, MAPK14, IL33, FAS, VWF, NFKB1, FASLG, CXCL5, MBL2, MYLK, AIMP2, IL17D, SIRT3, SIRT1, PLA2G2A, PIK3CB, SERPINA1, SERPINE1, RNF19A, PTGS2, NT5E, NOS3, HPGDS, ABCA4, AHSA1, MOK, RELA, LTA, SLC12A2, HABP2, STAT5A, IL27, TLR3, CBLIF, TM7SF2, UCN3, GZMB, DCN, MYDGF, TFPI, HGF, TEK, CRK, SYT1, MIR223, STAT5B, ICAM1, GORASP1, ARSD, ELAVL1, TSPO, EPAS1, PROCR, MIR34A, PLF, CHRM3, WNK1, GRAP2, CCN2, HAP1, KCNQ1OT1, PIEZO1, LATS1, ATG5, SLC27A5, IFI44L, PCYT1B, MAPKAPK2, BMS1, AKT3, HCST, ITM2B, ARID5A, CCNB2, HPSE, EBI3, CELF2, KLF2, ADIPOQ, ISG15, SH2B2, KL, RIPK3, AKR1B10, CNMD, RAMAC, LINC01194, NPSR1, H3P44, TREML1, OR10A4, HCA1, ANKS4B, XKR3, SERPINA12, CCDC26, INO80C, IL17RC, MINDY4, KAT8, TAS1R3, MIR122, MIR150, MIR211, MIR615, RN7SL263P, RNU6-392P, LARP1BP2, THRIL, AD14, MIR802, MIR506, MIR216A, MIR494, MIR146B, MIR381, MIR27B, MIR27A, MIR221, PARP9, SLC2A10, POLG2, PANK2, ANLN, TREM1, TLR8, CLEC1B, ANGPTL4, NOX4, SMARCAL1, NAAA, NOX1, HAVCR1, SPATS2L, IL17RA, LY96, KPNA6, ANGPTL2, EGLN1, UGT1A1, PPP6R3, POLD4, DOK3, LPCAT1, GSDMD, CORO7, POPDC3, ZNF335, PELI2, CARMIL1, HDAC3, POLE4, IL36G, NSMCE3, SLC50A1, CENPJ, TIMELESS, RAB27A, PIK3R3, ETS2, FOS, FN1, FOXM1, FER, FAAH, F5, F2, ERG, IL2, EPHX2, EPHB2, EGF, S1PR3, DPP4, DNASE1, NQO1, FUSE, GAD1, GJA5, CXCR3, IKBKB, IGFBP3, IFNB1, IFIT1, TNC, HSPA1B, HSPA1A, HSD11B2, HRG, HNRNPA1, FOXA2, HIF1A, HADHA, GZMA, GPT, CFD, DEFB1, DAPK1, CD40, CCNB1, CAV1, SERPING1, BTK, BMP7, AQP5, AQP1, KLK3, BIRC3, APCS, ANXA2, AGTR2, ADCY9, ACACA, ABO, CD14, CD40LG, CYP3A5, CD44, CYP3A7, CYP1B1, CYP1A1, CTSG, CTNNB1, CST3, CRYGD, COL4A5, CCR4, CIRBP, CEL, CDKN3, CDH5, CD68, CD59, IL1R1, IL2RA, PLA2G10, PTK2, SMPD1, SLC22A4, SELPLG, CCL7, RENBP, PRPH2, PTN, PSMD12, IL4, PROS2P, PROC, MAP2K1, MAPK8, PPARA, POMC, FXYD1, FSCN1, ST2, TAPBP, TCF21, FGF23, ARHGEF5, CXCR4, XDH, VIP, UGT8, TXNRD1, TXN, TST, TPI1, TOP2A, TNFRSF1A, NKX2-1, TIA1, TERT, PLD1, PLCL1, PLAUR, MMP3, CXCL9, MAP3K1, MDK, MCL1, SMAD3, SH2D1A, LY6E, LHCGR, LGALS3, KRT19, KDR, ITGB2, ITGAM, IL13, IL7R, MMP2, MPP1, PIK3CG, MUC1, PIK3CD, PIK3CA, CFP, PRDX1, PAFAH1B1, P4HB, P2RX7, OPRM1, OAS3, NM, NFYA, NFKBIA, MYD88, MYC, MUC5AC, H3P5
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Anismus
Wikipedia
Rectal cooling test [ edit ] The rectal cooling test is suggested to differentiate between rectal inertia and impaired relaxation/paradoxical contraction [24] Other techniques include manometry , balloon expulsion test , evacuation proctography (see defecating proctogram ), and MRI defecography. [25] Diagnostic criteria are: fulfillment of criteria for functional constipation , manometric and/or EMG and/or radiological evidence (2 out of 3), evidence of adequate expulsion force, and evidence of incomplete evacuation. [25] Recent dynamic imaging studies have shown that in persons diagnosed with anismus the anorectal angle during attempted defecation is abnormal, and this is due to abnormal (paradoxical) movement of the puborectalis muscle . [26] [27] [28] Treatment [ edit ] Initial steps to alleviate anismus include dietary adjustments and simple adjustments when attempting to defecate. ... CS1 maint: extra text: authors list ( link ) ^ Shafik, A; Mostafa, RM; Shafik, I; Ei-Sibai, O; Shafik, AA (2006-07-28). "Functional activity of the rectum: A conduit organ or a storage organ or both?" ... World Journal of Gastroenterology . 12 (28): 4549–52. doi : 10.3748/wjg.v12.i28.4549 .
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Werner Syndrome
Wikipedia
WRNp also physically interacts with p53 , a tumor suppressor gene that stops the formation of tumors and the progression of cancers, [27] which inhibits the exonuclease activity of the WRNp. [28] Since WRNp's function depends on DNA, it is only functional when localized to the nucleus. ... This process likely involves the helicase and exonuclease activities of WRN protein that operate together with DNA polymerase beta in long patch base excision repair . [33] Effects on cell structure and function [ edit ] Mutations which cause Werner syndrome all occur at the regions of the gene which encode for protein, and not at non-coding regions. [34] There are 35 different known mutations of WRN, which correspond to stop codons , insertions , or deletions that result in a frameshift mutation. [28] These mutations can have a range of effects. ... "Werner protein cooperates with the XRCC4-DNA ligase IV complex in end-processing" . Biochemistry . 47 (28): 7548–56. doi : 10.1021/bi702325t .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
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Sinusitis
Wikipedia
If the infection is of bacterial origin, the most common three causative agents are Streptococcus pneumoniae (38%) , Haemophilus influenzae (36%) , and Moraxella catarrhalis (16%) . [12] [28] Until recently, H. influenzae was the most common bacterial agent to cause sinus infections. ... This method, similar to balloon angioplasty used to "unclog" arteries of the heart, utilizes balloons in an attempt to expand the openings of the sinuses in a less invasive manner. [31] The effectiveness of the functional endoscopic balloon dilation approach compared to conventional FESS is not known. [31] Treatments directed to rhinovirus infection [ edit ] A study has shown that patients given spray formulation of 0.73 mg of Tremacamra (a soluble intercellular adhesion molecule 1 [ICAM-1] receptor) reduced the severity of illness. [28] Prognosis [ edit ] A 2018 review has found that without the use of antibiotics, about 46% were cured after one week and 64% after two weeks. [57] Epidemiology [ edit ] Sinusitis is a common condition, with between 24 and 31 million cases occurring in the United States annually. [78] [79] Chronic sinusitis affects approximately 12.5% of people. [8] Research [ edit ] Based on recent theories on the role that fungus may play in the development of chronic sinusitis, antifungal treatments have been used, on a trial basis. ... "The pathogenesis of orbital complications in acute sinusitis". The Laryngoscope . 80 (9): 1414–28. doi : 10.1288/00005537-197009000-00007 . ... Archived from the original on 2007-11-01 . Retrieved 2007-10-28 . ^ Rimmer J, Fokkens W, Chong LY, Hopkins C (1 December 2014).CFTR, IL13, RSPH4A, AZGP1, MET, PIP, PPP1R9B, PRTN3, PNP, PTPN22, CXCR4, MGP, CIITA, NBN, NCF2, NCF4, PIK3R1, CYBC1, TCF3, WIPF1, PSMB4, PSMB9, WAS, LRRC8A, CCDC40, RFX5, RFXAP, DNAI1, NME8, DNAAF1, BLNK, CYBB, BLM, RUNX2, RFXANK, CD79A, CD79B, NCF1, DNAAF3, CTLA4, CYBA, IL2RG, DNMT3B, FMR1, HLA-DPA1, HLA-DPB1, ATM, IRF8, CFI, IGHM, IGLL1, IKBKB, ADA, BTK, CCL5, IL6, HIF1A, MUC5AC, IL5, DICER1, IL33, IL22, ASCC1, SMOX, GORASP1, WNK1, PDPN, AP5B1, CLEC4D, MUC5B, POSTN, AAVS1, SLC9A6, ACR, CD40, CLU, CSF2, IL1A, IL1B, CXCL8, IL17A, LTC4S, NFKB1, SERPINE1, PTGDS, ARHGEF7, RAG2, RELA, CCL7, CCL11, SLC5A5, SYT1, TNF, VEGFA, ST8SIA4, EPX, H3P40
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Childhood Leukemia
Wikipedia
Generally prognostic factors are more meaningful in ALL than in AML. [28] ALL [ edit ] The 5-year survival rate for children and adolescents under the age of 15 years diagnosed with ALL was 91.8% in the USA between 2007 and 2013. ... Initial treatment response: Children who respond to treatment quickly initially have a better prognosis. [5] [28] AML [ edit ] The survival rate for children under the age of 15 years with AML was 66.4% in the USA between 2007 and 2013. ... Children who are a normal weight usually have a better prognosis than those who are overweight or underweight. [4] [17] [28] After effects [ edit ] Main article: Cancer survivor As treatments for childhood leukemias have gotten better, there are more children surviving and living into adulthood.CSF2, CDKN2B, CXCR4, BMI1, CCR7, RARA, BCR, CSF3, CSF3R, PTPN11, PTEN, CTNNB1, MLLT10, BCL2, CXADR, PRKAR1A, PML, TCL1A, NQO1, PIK3CG, PIK3CD, PIM1, PIK3CB, DNMT1, CASP3, CEBPA, CDKN2A, ATN1, CDKN1B, BRD4, CASR, RUNX1, RUNX1T1, CBFB, TRBV20OR9-2, TAL1, CD6, TP53, CD19, STAT5B, CXADRP1, TBC1D9, STAT5A, CD33, CD34, STAT3, CD38, VEGFA, CD44, WT1, SPG7, ABL1, ABCB1, PIK3CA, PBX1, MLLT1, ARR3, MEIS1, MDM2, MCL1, AKT1, LMO2, FLT3, KIT, KIR3DL1, JAK2, TCL1B, PRMT5, TMEM132D, GATA1, IKZF1, GEM, NR1I3, IL2, ASRGL1, TRIM13, HOXA9, DOT1L, HOXA@, KMT2A, MEN1, MME, EPO, ALL1, NUP98, NRAS, NPM1, NOTCH1, NCAM1, MYH11, MYC, MTTP, EZH2, MBD2, MTHFR, ERG, MPO, COMMD3-BMI1, ETV6, MECOM, TNF, IL15, ABCC1, CYP1A1, CD40LG, IL3, TCF3, ETS1, RAF1, PAX5, CEBPZ, LONP1, CALM1, SNAP91, SETD2, ERVW-1, EIF4E, MIR155, CREBBP, GATA2, CDKN1A, KRAS, IL6, CALM2, HLA-A, CALM3, MAPK8, FANCB, IFNG, PICALM, IFNA13, MYB, CCNA1, PROM1, IFNA1, CXCL12, CD274, IL1B, IDH2, PBX3, PARP1, OPN1SW, KDM1A, MDM4, NUP214, MAPK1, MLLT3, DNMT3A, ELANE, TNFSF10, SPI1, MTOR, IDH1, HOXA10, TOP1, IRF8, PRAME, CD22, BTK, KRT20, KDR, ERVK-20, EVPL, HSP90AA1, MIR21, TGFB1, DHFR, PRDM16, CBFA2T3, FN1, SALL4, MIR150, GSTT1, HFE, HLA-C, CCND1, HIF1A, FLT1, MLH1, LEP, KAT6A, HDAC9, FUT4, KLRC4-KLRK1, TPMT, GSTM1, MSH3, DNER, CD80, GFI1, CDK6, SOAT1, DNMT3B, BRAF, IL7, MS4A1, GSTP1, KLRK1, ATM, IGH, HLA-B, PRTN3, ABL2, XIAP, RUNX2, MAP2K7, NFE2L2, GRAP2, AHSA1, ABO, IL24, MSH2, ESR1, AFDN, PTPA, ASPG, GSTK1, MPL, TET2, PSIP1, SLC12A9, ANPEP, MIR126, PHF6, SLCO6A1, SLC9A1, JAK3, TET1, FTO, CCR5, DEK, LEF1, PIM3, ITGAM, AIMP2, RAG2, CRK, NCOA2, MIR17HG, MAPK14, CIB1, POLDIP2, CD47, CD27, XRCC1, RNF19A, IL2RA, IL2RG, TRIB1, HLF, ALDH1A1, HTC2, GSK3B, INPP4B, NM, NME1, HMGB1, TLX1, IL7R, IRF4, ARHGEF1, IL10, FHIT, ABCG2, CD99, MLF1, STMN1, FLI1, FLT3LG, MNX1, TRIM5, PCBP4, PRAM1, ITGB2, LGALS3, IRF1, IGF2BP1, ILK, ASXL1, PAG1, SIRT1, GLIS2, PTPRC, PPARG, BCL11A, RTEL1, MAPK3, BAX, WWOX, MAP2K1, AURKA, HOTAIR, ZHX2, HPGDS, MIR29B2, MIR29B1, POU5F1, BRCA2, HMOX1, RAC1, CRYZ, CDK2, OPN1LW, MACROD1, MIR223, RNASE3, SET, TLX3, ATXN1, POU5F1P4, SCT, MIR196B, LETMD1, PECAM1, TOP2A, DOK1, POU5F1P3, TAT, ADAM17, WDR5, QRSL1, CALR, FAS, ROR1, ABI1, SH2B3, WLS, SMARCA4, NXT1, HOXA5, KMT2B, SMARCA1, THPO, SRSF2, TRIB2, DPY30, THBS1, TERT, ZAP70, IL3RA, IL4, DICER1, SLC22A1, SYT1, IGF1, TP73, HOXB4, ARHGAP24, HES1, HSF1, HOXB3, HOXB@, FIP1L1, TCHP, SYK, CCL2, TCF4, TCF7, TYMS, COL18A1, ICAM1, TYR, UBE2I, KDM6A, IFI27, AFF4, EBI3, HP, ZNF521, SEPTIN9, ZBTB16, IL18, GDE1, EIF2AK2, KMT2D, MMP2, MMP9, TLR9, CIAPIN1, CD200, AHI1, PLK1, PDCD5, LAMTOR1, CDR3, ELL, ASH2L, PIM2, NR0B2, DCTN6, SOCS3, RALBP1, MUC1, PDGFRA, PCNA, SF3B1, NBN, SUB1, TNFSF13, FBXW7, HEMGN, PSMD9, MRPL28, MEF2C, ATRAID, S100A8, TMED7, ROS1, ROCK1, MERTK, SBDS, IL18R1, WNK1, RARG, MARCKSL1, WT1-AS, EEF1E1, RAG1, DDX41, PTPN2, KRT7, DCDC2, MAFK, GORASP1, SCLY, ZNRD2, CRLF2, ZNF197, NR4A3, LYZ, SMAD4, ATG5, PTPN6, RELA, ERVK-6, CD28, EPHB2, CD14, GLB1, EPS15, COL11A2, FPGS, CDKN2C, TMED7-TICAM2, EPOR, CRKL, KAT2A, GPT, CSF1R, FASLG, FLT4, FLII, NR3C1, BMP4, FOXO3, MIR16-1, EWSR1, APEX1, BRCA1, MIR22, TPPP2, PTK2B, CES1, BCL6, CDKN2B-AS1, FUT1, BCL2A1, CFL1, ZNF384, OSCP1, AXL, ATR, GABPA, CHEK1, BSG, RERE, GATA3, CDA, EP300, MSI2, RUNX3, HDAC1, EGR1, ERVK-18, H3P12, AHR, ALB, GADD45A, CBL, DCK, H3P9, ALK, DCC, ERVK-32, PDIK1L, TICAM2, FGFR1, HLA-G, H3P10, CYP2B6, TSLP, CAV1, CYBB, LINC01194, EBF1, E2F1, H3P23, SRC, SPIB, SPP1, SRPK2, SRPK1, STAT1, CD40, SETBP1, CEBPB, MIR34B, CD70, MIR221, GNL3, IGHV1-12, SON, DLL1, CDK1, CDC42, CDH1, MIR34A, TRBC1, CDK4, HIPK2, CDK9, CDKN1C, CDKN2D, SNAP25, CDX2, SOX4, CCL3, SELE, HMMR, S100B, IL23A, PTGS2, CCN2, PSMB6, CTNNA1, CYP1B1, LIN28B, KDM3B, DDX4, PLAT, PLAGL2, PKM, NSD3, PIP4K2A, PIN1, DNASE1, DNTT, PHB, PF4, PDGFRB, PDGFB, DUSP1, PTK7, SIRT6, TRPM5, MIR125A, S100A9, S100A4, A1CF, FOXP3, MIR183, RNF6, REN, CCR6, KDM5A, MIR15A, RAP1GAP, RANGAP1, CREB1, RAD51, RAC2, CSF1, PVT1, MIR143, PTPRO, ETV7, PTPN4, REG1A, H4C15, SAMHD1, KLK3, EBP, HSPB3, BCL10, NR1I2, DLEU2, KDM5B, ZNF268, NRP1, APP, APRT, TNFRSF10B, TNFSF9, H4C2, RIPK1, ABCC3, BECN1, ASIP, ASNS, SOCS1, AKR1C3, CNTNAP1, ASPA, H4C14, H4C13, GPRC5A, ANXA2, AURKB, XPR1, NAMPT, LRPPRC, OLIG2, H3P13, PRG4, ACP3, ACTB, GPHN, MVP, TELO2, ABCC4, ZEB2, DLEU1, HERPUD1, ESPL1, NCOR1, NCR1, AKR1B1, ARL6IP5, ALOX5, RECQL4, ADIPOQ, KLF4, H4C5, H4C8, CD9, THY1, BUB1, KDM4C, UGCG, SEPTIN6, C3, TWIST1, BCRP3, CASP2, TLR4, ASPM, TIMP2, CASP9, H4C3, TGFBI, TEK, TEAD1, SH3BP4, HNF1A, CNTN2, CD1D, CD3G, CD5, CD8A, CD8B, VAV1, VCAM1, BTG1, VDR, H4C11, H4C12, H4C6, H4C4, H4C1, GFI1B, DUX4, H4C9, CHAF1B, TAF15, B2M, CHEK2, BCL2L1, TFPI2, RGPD2, ST8SIA4, PRDM2, ZFP36, YY1, XRCC3, PLA2R1, NT5C2, MIR638, NUDT15, COX8A, MYOD1, MTRR, H4-16, ERCC2, CXCL10, GSN, POGLUT1, KMT2C, SLC52A2, HTN3, SMAD2, FUS, EXOSC5, MTR, FGF2, EPHA3, DCLRE1C, LYL1, HSPB2, HSPB1, ISG20, MYCN, BACH2, FGF4, SLC29A1, JMJD1C, HSPA5, ITGAL, ENG, NFKB1, MRC1, ID1, TNFRSF9, ACKR3, FCGR3B, MEIS2, GH1, FCGRT, BAALC, FCGR3A, IL1A, MFAP1, RBPJ, MECP2, IL6ST, IGFBP7, CLEC12A, GPR180, AICDA, FANCD2, FDXR, CXCL8, MRTFA, F9, IFNAR1, GPX3, CIP2A, GRB2, IL11, F2R, G6PD, ITGB3, MEF2D, FOXM1, H2AX, LIG4, RPSA, ROPN1L, LIFR, LCK, NOTCH3, HGF, EMB, LIF, KCNH2, HDC, NGF, LEPR, KIR2DS1, EGFR, HDAC2, ARID5B, PWAR1, NTRK1, HLA-DPB1, EGR3, LDLR, PAFAH1B1, HOXA1, ATG3, JAK1, GZMB, AGFG2, ENOSF1, HAVCR2, KIR3DL2, HPRT1, HMBS, MYCBP2, SETD1B, SETX, ANXA8, ACD, FAM168A, MRGPRX4, MIR563, EHMT1, ADRM1, DIP, KDM6B, LIN28A, ABHD2, NUDT21, RTN4R, TWIST2, BRI3BP, LRRK2, GPR151, PHF8, GATA5, MIR600, ESM1, MLXIP, SUV39H2, MIR663A, PHB2, SACM1L, SPANXB1, MRGPRX3, PDAP1, CDC73, ANXA8L1, TUSC2, IKZF3, HSPA4L, ANKRD26, CILK1, B4GALNT2, MAGED4, NOX5, ECD, CCR2, CD24, UHMK1, BMI1P1, CCDC51, INTS3, VTCN1, MUL1, PVRIG, CEMP1, CEP152, AKAP13, CD200R1, DKK1, PACSIN2, SNF8, PARK7, FSD1, MRGPRX1, SLC46A1, ARAP1, SOX7, HAX1, GATD3B, HOXB13, ERVK-11, MAGT1, FSD1L, CRISPLD2, ANP32B, JAM3, DYNLRB2, PARTICL, IGF2BP2, ERVK-22, SLC22A16, SLCO1B1, SH2B2, TXNIP, PDPN, POSTN, TCF7L1, CAB39L, ERVK-12, EAF1, ARIH2, CBSL, BGLT3, CBX2, KDM2B, TNK2, ZNF382, NT5C1A, ZFYVE19, RHOXF2, MSLN, NUDCD1, MIR22HG, ABCC11, LOC110806263, ZMPSTE24, STUB1, KAT8, SMYD5, MTCO2P12, HMGB1P5, LUNAR1, USP42, KLF2, IGF2BP3, ERVK-2, UBA5, DTX2, SLFN11, ZNF300, RUVBL2, MRPS30, PAPOLA, ULBP1, LINC01672, EHMT2, ULBP2, COBL, MIR155HG, KHDRBS1, ZC3H12A, SERINC3, MLLT11, RAB40B, CGAS, COPS5, RIPK3, CMTM5, NANOG, MRGPRF, MTHFD2, TSGA10, ESAM, HOTAIRM1, KLF1, CXCR6, CTCF, BCL2L2-PABPN1, WNT3A, CD226, DEL11P13, TNFSF13B, TMX2-CTNND1, SIGLEC10, GADD45GIP1, MICA, USP39, NFAT5, NUDC, PLK4, STAG2, GIPC1, NES, MAGED4B, LRSAM1, MLC1, TNPO3, WWC1, HDAC7, MARCHF8, CHMP5, MIR142, METTL3, MIR130A, MIR128-2, MIR127, TRPV5, KYAT3, RNF20, MYDGF, TRPV2, MIR122, WSB2, MED15, MIR10A, GINS2, MIR107, CMPK1, SPINK6, UOX, CD244, LTB4R2, UNC13D, ASH1L, TLR7, DDX53, MLXIPL, MIR182, KMT5B, MIR17, EGFL7, ARID2, CRTC2, DCTN4, APOBEC3A, TNFRSF12A, MIR144, DACT1, KLRF1, SMYD2, C19orf48, PMEPA1, LXN, MIR149, MIR146A, UBR5, GPR137, PBK, GPRC6A, OXER1, RCBTB1, ATF7IP, TESC, GOLGA6A, ABCB5, VSTM1, PGP, SERINC5, NLRP2, MTPAP, THUMPD1, HECTD4, BCOR, TRIM62, ASXL2, NEAT1, SOX6, CSNK2A3, TRPV6, MEG3, NCR3, LARP6, COPD, NUTM1, ZFP64, SERP2, ROBO4, MAP3K20, IL27, MALAT1, IL17D, MBD3, GJB7, ZBTB38, WNT4, TMEM30A, GEN1, DDIT4, SWT1, DLL4, UGT1A1, PDP1, FBLIM1, SEPTIN11, PWAR4, ARSH, CXorf66, TRPM7, CNDP2, MIR193A, ASAP1, UCA1, QPCT, SMPX, SGK3, RBMXL1, MIR345, GPR166P, NSD1, NOD2, LAMP5, ZFAS1, TFIP11, LYPD4, NUP62, VN1R17P, SLC39A8, MAGEF1, PRDM14, BCORL1, L3MBTL1, CHD5, NRARP, MIR98, LGR6, MIR375, SSBP2, EPC2, MIR511, FBXW11, SYNE1, SCFV, SMCHD1, LINC00273, CDCP1, MIR486-1, ARHGEF12, MIR495, MIR146B, RBM15, MKRN2, CBX7, SMYD3, TNFRSF13B, APCDD1, KAT6B, PI4K2B, RBFOX2, MIR378A, LPAR3, CASP14, SIGIRR, TES, MBL3P, NKX2-3, RGCC, MIR23A, CBX8, ZC3H7A, VANGL2, ZMIZ1, MYLIP, MIR222, VPS13B, CBLL2, UHRF1, TRBV7-9, BLNK, ZNF296, TFPT, GOPC, ZNF695, LEXM, TIGAR, KNL1, MIR203A, IL22, FLVCR1, TRBV16, PAQR3, DNAJC2, PHGDH, IL21, FBXO9, MYCBP, PLEKHB1, MIR93, TRIB3, HSPB8, METTL14, RNU1-1, B3GAT1, MIR29A, PPM1K, MIR29C, STIM2, SGSM3, POLM, PCDH10, MARVELD2, TRDJ1, TRDD3, TRDC, NAT2, SNCA, TRIM28, GRM3, GYPE, GYPB, GYPA, GTF2H1, MSH6, GSTA1, GRIA3, HCL2, GRB10, GPR42, GPI, GNB2, GNB1, GLS, H2AZ1, HIP1, GLI1, HNRNPA1, HOXA13, HOXA11, HOXA7, HOXA6, HOXA4, HOXA3, SLC29A2, HK1, NR4A1, HMGCR, HMGB3, HMGB2, HLA-DQB1, HK2, GLI2, GJA1, ETS2, FCGR2A, FGFR2, FGFR3, FGF1, FES, FEN1, FCGR2B, FCER2, FOXO1, FAT1, FANCF, FABP4, F8, F3, EZH1, FH, FLNC, B4GALT1, NR5A1, GATA6, GATA4, GAS6, XRCC6, FUT3, GAST, NR5A2, FMOD, FRA7G, FRA6F, FXN, FPR1, FOS, FOLH1, HOXB1, HOXB2, HOXB5, LDHA, LOX, LMO1, LMNA, LLGL1, LIMS1, LGALS1, LCN2, LRP6, LAMB3, LAG3, KIR2DS5, KIR2DS4, KIR2DL1, KCNH1, LRP1, LTA, HOXB6, MAGEA1, MDK, MCM7, MCM3, MBP, MBL2, MATK, SMAD7, LTB, SMAD5, EPCAM, LYN, LY9, LTK, LTF, CD82, JUN, JARID2, PRMT1, MRPL58, IAPP, TNC, HSPA9, HSPA4, HSD11B2, HRAS, EIF6, HOXD13, HOXD@, HOXC10, HOXB9, HOXB8, HOXB7, IFIT3, IFNB1, IGF1R, IGF2, IGFBP2, IGFBP4, IGL, IL1R1, IL1RN, IL5, IL9, IL15RA, IL17A, INPP5D, IRAK1, ITGA6, ITGA2B, EXT1, ERN1, RAD50, C1QC, SLC25A20, DDR1, CA2, FMNL1, VPS51, C4BPA, BST2, CAMK4, BRS3, ZFP36L2, BPHL, BMP2, PRDM1, BDNF, CALCA, CAMLG, BCL3, CCND2, TNFRSF8, MS4A3, CD247, CD2, CD1A, CCNG2, CCNB1, CAMP, CCNA2, CBS, CASP8, CASP7, CASP5, CAPS, TNFRSF17, BCL2L2, ERCC5, ADCY7, AIC, ADRA2B, ADRA1A, PARP4, ADD1, ADCYAP1, ADAM10, ALPI, ADA, ACVRL1, ACTG1, ACP1, ACHE, ABR, ALOX15, ALPP, BAK1, AQP8, BAG1, ATP7A, ATIC, ATF4, ARNTL, AR, APOBEC1, ANG, APCS, APAF1, AOX1, ANXA7, ANK1, ANGPT2, CD36, CD37, CD48, DAPK1, DLD, DHODH, DES, DEFB1, DECR1, ACE, DGKA, DNA2, DAG1, DACH1, CYP3A5, CYP2E1, CYP2D6, CUX1, DMBT1, DPP4, CD58, EIF4EBP1, ERBB3, EPHA1, EPAS1, ENO2, MARK2, EMD, EGF, DPYD, EFNB2, EFNB1, PHC1, EDNRB, EDNRA, TSC22D3, CTSL, CTSG, CTSB, CDR1, CHGB, AKR1C4, CHD1, CFTR, CEBPE, CDX4, CDK8, CTNND1, CDK5, CDC34, CD79B, CD79A, CD68, CD59, CHI3L1, CHRNA4, CKB, LTB4R, CNTF, CR1, CR2, CRP, CSE1L, CSF2RB, CSHL1, CSNK2A1, CSNK2A2, CSPG4, CTBP2, CTF1, CTLA4, ME2, RAB8A, MET, UQCRFS1, WNT5A, WEE1, VWF, VIM, VDAC1, USP1, UNG, XIST, UMOD, UGT1A, UFD1, UBE2E2, TYK2, TTN, WNT7A, XPC, HSP90B2P, USP7, HMGA2, ANC, HRX, RNF217-AS1, LAP, CP20, BRPF1, XRCC4, LEPQTL1, ZYX, ZNF224, TRIM25, MZF1, ZFX, TSG101, TRAF1, MGMT, TAC1, TRB, TCN2, TCF7L2, TALDO1, MAP3K7, TACR1, SUV39H1, TEF, ABCC8, SULT2A1, STC1, STAT6, SSTR4, SST, TRD, TMBIM6, TPM3, TLE1, TPD52, TP53BP2, TNR, TNFAIP3, TLR3, TLR2, TK1, TERF1, THOP1, TFRC, TFR2, TFCP2, TF, TERF2, MIA, TAM, GATD3A, LPXN, BAG3, TBPL1, LITAF, ADAMTS1, GSTO1, TJP2, RAB9A, APOBEC3B, PDLIM7, UBE2L6, MSC, NOG, PTTG1, DCLK1, BCAR1, NCOR2, USP9X, FCHSD2, ABCB6, SMC4, HDAC6, SCO2, HNRNPDL, SLC23A2, SETDB1, IKBKE, GAB2, PCLAF, TOX, HDAC4, SETD1A, SOCS5, IL1RL1, LPAR2, CBFA2T2, PIAS1, TNFRSF10D, TNFRSF11A, TNFRSF18, TNK1, EIF3D, EIF3A, DGKZ, INA, GAS7, PARG, PPM1D, SMARCA5, FZD9, FZD4, TNFRSF10C, TNFRSF10A, GGH, KSR1, ASAP2, LDB1, PER2, IER3, SQSTM1, FUBP1, SLC5A6, F2RL3, CH25H, SPAG9, DOK2, USP10, FCGR2C, SSRP1, TRIM21, SRI, PFDN5, PITX2, PIK3R2, PIK3R1, SERPINA4, ABCB4, PGD, PAX6, PKNOX1, PAWR, PRKN, REG3A, PAK1, PAEP, P2RY1, PKD2, PLAU, PRKAA2, POU4F1, PRF1, PPP5C, PPP2R5C, PPIB, PPBP, PPARA, POU3F1, PMAIP1, POU2F1, PON2, PON1, POMC, SEPTIN5, PRRX1, P2RX7, P2RX5, OPRK1, MOV10, CYTB, COX2, COX1, MSX1, MSR1, MRE11, MNDA, ODC1, MNAT1, MMP8, MMP7, MMP1, NR3C2, AFF1, MTX1, MYBL2, MYD88, NCL, NDN, NEDD8, NF1, NFATC3, NGFR, NNAT, NOS3, NPY, NOTCH4, YBX1, NT5E, ROR2, OAZ1, PRKAA1, PRKAB1, SPTBN1, SEMG1, STIL, PMEL, SHMT1, SHB, SH3GL1, SFRP5, SELPLG, SLC19A1, SELP, SELL, CLEC11A, SAI1, S100A11, S100A10, SIX1, SLC22A4, MAPK7, SOX2, SPN, SPARC, SP100, SP1, SOX11, SOX10, SOS1, SMARCA2, SOD2, SOD1, SIGLEC1, SMPD2, SMPD1, SMARCD2, RXRA, RRAS, RPS19, PTPN1, NECTIN2, PVR, PVALB, PTX3, PTPRA, PTPN13, PTN, RPS6KB1, PTGS1, PSMA7, PSEN1, PRL, MAP2K5, MAPK9, RAB27A, RAD52, RALA, RARS1, RARRES1, RASGRF1, RB1, ARID4A, RBL1, RFC1, RHEBP1, RMRP, BRD2, RPL15, RPL22, RPN1, RPS6KA3, MIR223HG
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Devil Facial Tumour Disease
Wikipedia
The tetraploid form has been linked to lower mortality rates. [25] The cell type origin of this strain of DFTD is unknown. [26] Increased levels of tetraploidy have been shown to exist in the oldest strain of DFTD as of 2014, which correlates with the point at which devils became involved in a DFTD removal programme. [ citation needed ] Because ploidy slows the tumour growth rate, the DFTD removal programme has been suggested as a selective pressure favouring slower-growing tumours, and more generally that disease eradication programmes aimed at DFTD may encourage the evolution of DFTD. [27] The existence of multiple strains may complicate attempts to develop a vaccine, and there are reports of concerns that the evolution of the cancer may allow it to spread to related species such as the quoll . [28] Preservation response [ edit ] Wild Tasmanian devil populations are being monitored to track the spread of the disease and to identify changes in disease prevalence. ... Archived from the original (PDF) on 2016-05-28 . Retrieved 2010-10-23 . ^ "Frequently Asked Questions About Devil Facial Tumour Disease" (PDF) . ^ Conservation Breeding Specialist Group (2008). ... PMID 27575253 . ^ "Healthy Tasmanian devils found in mission to save species from extinction" . ABC News . 28 April 2018 . Retrieved 30 April 2018 . ^ "BBC NEWS - World - Asia-Pacific - Fence hope for Tasmanian Devils" . bbc.co.uk .
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Voyeurism
Wikipedia
In the United Kingdom , for example, non-consensual voyeurism became a criminal offence on May 1, 2004. [27] In the English case of R v Turner (2006), [28] the manager of a sports centre filmed four women taking showers. ... "Compulsive voyeurism and exhibitionism: A clinical response to paroxetine". Archives of Sexual Behavior . 28 (1): 23–30. doi : 10.1023/A:1018737504537 . ... London. ^ a b (2020) Court of Appeal, R v Richards. ^ a b Bowcott, Owen (2020-01-28). "Filming partner without their consent during sex ruled a criminal offence" .
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Treacher Collins Syndrome
Wikipedia
Causes may be a variable expressivity, an incomplete penetrance [27] or germline mosaicism . [28] Only 40% of the mutations are inherited. ... Archived from the original (PDF) on 2017-01-28. ^ a b c Posnick, Jeffrey C (1 October 1997). ... Retrieved 2020-01-15 . ^ Vento AR, et al., The O.M.E.N.S classification of hemifacial microsomia , 1991, Cleft Palate Craniofac, J 28 , p. 68-76 ^ a b Posnick JC; et al. (2000). ... Archived from the original on 2020-02-18 . Retrieved December 28, 2020 . External links [ edit ] Classification D ICD - 10 : Q75.4 ICD - 9-CM : 756.0 OMIM : 154500 MeSH : D008342 DiseasesDB : 13267 External resources MedlinePlus : 001659 eMedicine : plastic/183 Orphanet : 861 v t e Congenital malformations and deformations of musculoskeletal system / musculoskeletal abnormality Appendicular limb / dysmelia Arms clavicle / shoulder Cleidocranial dysostosis Sprengel's deformity Wallis–Zieff–Goldblatt syndrome hand deformity Madelung's deformity Clinodactyly Oligodactyly Polydactyly Leg hip Hip dislocation / Hip dysplasia Upington disease Coxa valga Coxa vara knee Genu valgum Genu varum Genu recurvatum Discoid meniscus Congenital patellar dislocation Congenital knee dislocation foot deformity varus Club foot Pigeon toe valgus Flat feet Pes cavus Rocker bottom foot Hammer toe Either / both fingers and toes Polydactyly / Syndactyly Webbed toes Arachnodactyly Cenani–Lenz syndactylism Ectrodactyly Brachydactyly Stub thumb reduction deficits / limb Acheiropodia Ectromelia Phocomelia Amelia Hemimelia multiple joints Arthrogryposis Larsen syndrome RAPADILINO syndrome Axial Skull and face Craniosynostosis Scaphocephaly Oxycephaly Trigonocephaly Craniofacial dysostosis Crouzon syndrome Hypertelorism Hallermann–Streiff syndrome Treacher Collins syndrome other Macrocephaly Platybasia Craniodiaphyseal dysplasia Dolichocephaly Greig cephalopolysyndactyly syndrome Plagiocephaly Saddle nose Vertebral column Spinal curvature Scoliosis Klippel–Feil syndrome Spondylolisthesis Spina bifida occulta Sacralization Thoracic skeleton ribs : Cervical Bifid sternum : Pectus excavatum Pectus carinatum v t e Nucleus diseases Telomere Revesz syndrome Nucleolus Treacher Collins syndrome Spinocerebellar ataxia 7 Cajal body : Spinal muscular atrophy Centromere CENPJ Seckel syndrome 4 Other AAAS Triple-A syndrome Laminopathy SMC1A / SMC3 Cornelia de Lange Syndrome SETBP1 Schinzel–Giedion syndrome see also nucleus
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Erectile Dysfunction
Wikipedia
In general, exercise , particularly of the aerobic type, is effective for preventing ED during midlife. [26] : 6, 18–19 Counseling can be used if the underlying cause is psychological, including how to lower stress or anxiety related to sex. [27] Medications by mouth and vacuum erection devices are first-line treatments, [26] : 20, 24 followed by injections of drugs into the penis, as well as penile implants. [26] : 25–26 Vascular reconstructive surgeries are beneficial in certain groups. [28] Treatments, other than surgery, do not fix the underlying physiological problem, but are used as needed before sex. [29] Medications The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken by mouth. [26] : 20–21 As of 2018, sildenafil is available in the UK without a prescription. [30] Additionally, a cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for ED. [31] Penile injections, on the other hand, can involve one of the following medications: papaverine , phentolamine , and prostaglandin E1 , also known as alprostadil . [26] In addition to injections, there is an alprostadil suppository that can be inserted into the urethra. ... More drastically, inflatable or rigid penile implants may be fitted surgically. [ citation needed ] Surgery Main article: Penile implant Often, as a last resort, if other treatments have failed, the most common procedure is prosthetic implants which involves the insertion of artificial rods into the penis. [26] : 26 Some sources show that vascular reconstructive surgeries are viable options for some people. [28] Alternative medicine The Food and Drug Administration (FDA) does not recommend alternative therapies to treat sexual dysfunction. [34] Many products are advertised as " herbal viagra " or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of ED, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products. [35] [36] [37] [38] [39] The FDA has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant. [40] History An unhappy wife is complaining to the qadi about her husband's impotence. ... Retrieved 2019-08-05 . ^ "Viagra can be sold over the counter" . BBC News . 28 November 2017 . Retrieved 5 April 2018 . ^ Bujdos, Brian.NOS3, EDN1, BCL2, EDNRA, BCL2L1, VEGFA, SHBG, PRL, GRIN3A, PDE5A, VIP, NOS1, TNF, NOS2, IL6, GJA1, AKT1, AGT, CASP3, DYNLL1, GRK2, TGFB1, IGFBP3, BAD, BAX, P2RY2, CFL1, P2RY1, SIRT1, CCND2, HDAC3, PRKG1, KDR, FABP4, MCAM, AGER, CCND1, CNR1, FSHR, LMNB1, SUFU, TTC7A, ACOXL, CHD7, WDR11, KISS1, ANOS1, IRF8, GRAMD1B, HFE, HEXB, MATN2, NSMF, MEN1, SLC40A1, TTR, FGF17, TFR2, TACR3, TAC3, CACNA1G, SMARCB1, AIP, ATXN8OS, HS6ST1, PTGFRN, SP140, PDGFB, GUCY1A1, SACS, NF2, COQ2, HAMP, IRF4, ACE, FMR1, HJV, ABCD1, DUSP6, PROKR2, CDH13, SLC5A12, FGF8, FGFR1, GPR101, KISS1R, DRAIC, MIR4435-2HG, BMP2, SPRY4, ATXN8, CDH23, PROK2, GNRH1, GNRHR, CRP, ARG2, IGF1, GNB3, NGF, DECR1, BDNF, ALDH7A1, TLR4, ROCK2, ROCK1, SHH, CXCL12, TWIST2, AR, ADIPOQ, GPT, NECTIN1, MIAT, NFE2L2, MYOCD, ADRB3, MTHFR, TERT, FGF2, ALB, PTK2B, LOX, MBTPS1, TBPL1, PEA15, PCSK9, S1PR2, MIR155, MIR328, MIR146A, MIR205, MSC, MIR141, SELENBP1, CES2, CLOCK, MIR200A, PLA2G15, WASF2, ABCC4, TRPM8, PNPLA2, TP63, ACSS2, MEG3, DDIT4, CCHCR1, COA8, MCHR2, NT5C1A, SCLY, EBPL, MYLIP, ACCS, NUS1, DKK2, DKK3, SMR3A, PART1, OPRPN, DDAH1, DDAH2, NT5C2, MLXIP, CIT, MARCHF8, ESM1, IL27, NUS1P3, ACHE, POMC, VWF, MSTN, EGF, ELK3, ENG, ENO2, EPO, FLNA, FSHMD1A, GABPA, GH1, VHL, CXCR3, GUCY1B1, HMGCS2, IL7R, ILK, KCNMA1, KLK1, KRT7, DRD4, DRD2, CYP19A1, COMP, ADRA1A, AHSG, ALCAM, AMBP, ANGPT1, ANGPT2, KLK3, ARG1, ATM, BGLAP, VPS51, CAMP, CASP1, CD37, CD40, CDH5, CFTR, LBP, LEP, LIMK1, MAPK8, PTAFR, PTX3, RAC1, REG1A, ROS1, S100A1, S100A8, SDC1, SIM1, SLC2A1, SLC5A2, SOAT1, SRC, TAL1, THPO, TNNI3, TYRP1, PSMB9, PON1, LIMK2, ACTB, LPL, MBP, COX2, MYD88, NEUROD1, NPR1, OCA2, OXTR, PAEP, PCYT1A, PDE3A, SERPINF1, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PITX3, CERNA3
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List Of Mass Hysteria Cases
Wikipedia
This conclusion was supported by a Palestinian health official, who said that while 20% of the early cases may have been caused by the inhalation of some kind of gas, the remaining 80% were psychosomatic . [28] Day-care sex-abuse hysteria was a moral panic that occurred primarily in the 1980s and early 1990s featuring charges against day-care providers of several forms of child abuse , including Satanic ritual abuse . [29] [30] San Diego (1988) – The US Navy evacuated 600 men from barracks; 119 were sent to San Diego hospitals with complaints of breathing difficulty. ... Journal of Practical Nursing and Mental Health Services 14: 23–28. ^ Bartholomew, Robert E. (2001). ... University of California, Berkeley: Blackwell Publishing. 15 (1): 28–42. doi : 10.1525/ae.1988.15.1.02a00030 .
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Acute Radiation Syndrome
Wikipedia
These symptoms are common to many illnesses, and may not, by themselves, indicate acute radiation sickness. [3] Dose effects [ edit ] Phase Symptom Whole-body absorbed dose ( Gy ) 1–2 Gy 2–6 Gy 6–8 Gy 8–30 Gy > 30 Gy Immediate Nausea and vomiting 5–50% 50–100% 75–100% 90–100% 100% Time of onset 2–6 h 1–2 h 10–60 min < 10 min Minutes Duration < 24 h 24–48 h < 48 h < 48 h N/A (patients die in < 48 h) Diarrhea None None to mild (< 10%) Heavy (> 10%) Heavy (> 95%) Heavy (100%) Time of onset — 3–8 h 1–3 h < 1 h < 1 h Headache Slight Mild to moderate (50%) Moderate (80%) Severe (80–90%) Severe (100%) Time of onset — 4–24 h 3–4 h 1–2 h < 1 h Fever None Moderate increase (10–100%) Moderate to severe (100%) Severe (100%) Severe (100%) Time of onset — 1–3 h < 1 h < 1 h < 1 h CNS function No impairment Cognitive impairment 6–20 h Cognitive impairment > 24 h Rapid incapacitation Seizures , tremor , ataxia , lethargy Latent period 28–31 days 7–28 days < 7 days None None Illness Mild to moderate Leukopenia Fatigue Weakness Moderate to severe Leukopenia Purpura Hemorrhage Infections Alopecia after 3 Gy Severe leukopenia High fever Diarrhea Vomiting Dizziness and disorientation Hypotension Electrolyte disturbance Nausea Vomiting Severe diarrhea High fever Electrolyte disturbance Shock N/A (patients die in < 48h) Mortality Without care 0–5% 5–95% 95–100% 100% 100% With care 0–5% 5–50% 50–100% 99–100% 100% Death 6–8 weeks 4–6 weeks 2–4 weeks 2 days – 2 weeks 1–2 days Table source [11] A person who happened to be less than 1 mile (1.6 km) from the atomic bomb Little Boy ' s hypocenter at Hiroshima, Japan was found to absorb about 9.46 grays (Gy). [12] [13] [14] [15] The doses at the hypocenters of the Hiroshima and Nagasaki atomic bombings were 240 and 290 Gy, respectively. [16] Skin changes [ edit ] Main article: Radiation burn Harry K. ... The 50% chance of death from the blast extends out to ~8 km from a 1 megaton atmospheric explosion. [28] Scientific testing on humans done without consent has been prohibited since 1997 in the United States. ... Japan Epidemiological Association. 28 (4): 162–169. doi : 10.2188/jea.je20170321 . ... Archived from the original on 2010-03-28. ^ "Nuclear Bomb Effects" . The Atomic Archive . solcomhouse.com .
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Chronic Wasting Disease
Wikipedia
The MFFP ministry in Quebec practiced 9500 tests in the period between 2007 and autumn 2018 before they detected a seropositive case in September 2018. [28] The September 2018 discovery of CWD on a managed operation in Grenville-sur-la-Rouge Quebec prompted a wholesale slaughter of 3500 animals in two months before the enterprise shut its doors for good. [29] The CFIA ordered the cull, as well as the decontamination of 10 inches of soil in certain places on the 1000-acre operation. [28] Post-discovery, each animal was tested for CWD by the CFIA before it was released onto the market. ... By April 2016, CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported from Canada for farming in the late 1990s. [2] [46] In the summer of 2018, cases were discovered in the Harpur Farm herd in Grenville-sur-la-Rouge , Quebec . [28] Over the course of 2018 fully 12% of the mule deer that were tested in Alberta , had a positive result.
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Side Effects Of Bicalutamide
Wikipedia
Breast changes [ edit ] Gynecomastia in a 60-year-old man treated with 150 mg/day bicalutamide for prostate cancer. [26] The most common side effects of bicalutamide monotherapy in men are breast pain/tenderness and gynecomastia. [11] These side effects may occur in as many as 90% of men treated with bicalutamide monotherapy, [27] but gynecomastia is generally reported to occur in 70 to 80% of patients. [28] In the EPC trial, at a median follow-up of 7.4 years, breast pain and gynecomastia respectively occurred in 73.6% and 68.8% of men treated with 150 mg/day bicalutamide monotherapy. [8] [9] Gynecomastia associated with NSAA monotherapy usually develops within the first 6 to 9 months following initiation of treatment. [26] In more than 90% of affected men, bicalutamide-related breast changes are mild-to-moderate in severity. [9] [29] It is only rarely and in severe and extreme cases of gynecomastia that the proportions of the male breasts become so marked that they are comparable to those of women. [30] In addition, bicalutamide-associated breast changes improve or resolve in most men upon discontinuation of therapy. [9] In the EPC trial, 16.8% of bicalutamide patients relative to 0.7% of controls withdrew from the study due to breast pain and/or gynecomastia. [29] The incidence and severity of gynecomastia are reportedly higher with estrogens (e.g., diethylstilbestrol ) than with NSAAs like bicalutamide in the treatment of men with prostate cancer. [31] Management of breast changes [ edit ] Severe gynecomastia with 150 mg/day bicalutamide monotherapy in a 64-year-old man with prostate cancer. ... Eventually, the symptoms disappeared and did not recur. [61] Flutamide is also associated with photosensitivity, but much more frequently in comparison to bicalutamide. [61] [63] Fat distribution [ edit ] Antiandrogen therapy and estrogen therapy are known to produce demasculinizing and feminizing effects on fat distribution in people assigned male at birth . [60] Bone density and fractures [ edit ] Bicalutamide monotherapy preserves bone mineral density in men with prostate cancer relative to surgical or medical castration. [7] [64] [65] [66] [67] This is considered to be due to preservation of gonadal estradiol production with bicalutamide monotherapy, in contrast to castration which greatly reduces estradiol levels. [7] The risk of osteoporosis and serious bone fractures with bicalutamide monotherapy appears to be no different than with non-use in men with prostate cancer. [68] Gastrointestinal system [ edit ] The incidence of diarrhea with bicalutamide monotherapy in the EPC trial was comparable to placebo (6.3% vs. 6.4%, respectively). [9] In phase III studies of bicalutamide monotherapy for LAPC , the rates of diarrhea for bicalutamide and castration were 6.4% and 12.5%, respectively, the rates of constipation were 13.7% and 14.4%, respectively, and the rates of abdominal pain were 10.5% and 5.6%, respectively. [69] Heart, liver, kidneys, and lungs [ edit ] Cardiovascular system [ edit ] See also: Testosterone and the cardiovascular system In the LPC group of the EPC study, although 150 mg/day bicalutamide monotherapy had reduced mortality due to prostate cancer relative to placebo, there was a trend toward significantly increased overall mortality for bicalutamide relative to placebo at 5.4-year follow-up (25.2% vs. 20.5%). [19] [70] [71] This was because more bicalutamide than placebo recipients had died due to causes unrelated to prostate cancer in this group (16.8% vs. 9.5% at 5.4-year follow-up; 10.2% vs. 9.2% at 7.4-year follow-up). [19] [71] [8] At 7.4-year follow-up, there were numerically more deaths from heart failure (1.2% vs. 0.6%; 49 vs. 25 patients) and gastrointestinal cancer (1.3% vs. 0.9%) in the bicalutamide group relative to placebo recipients, although cardiovascular morbidity was similar between the two groups and there was no consistent pattern suggestive of drug-related toxicity for bicalutamide. [8] [72] In any case, although the reason for the increased overall mortality with 150 mg/day bicalutamide monotherapy has not been fully elucidated, [28] it has been said that the finding that heart failure was twice as frequent in the bicalutamide group warrants further investigation. [73] In this regard, it is notable that low testosterone levels in men have been associated in epidemiological studies with cardiovascular disease as well as with a variety of other disease states (including hypertension , hypercholesterolemia , diabetes , obesity , Alzheimer's disease , osteoporosis, and frailty ). [74] According to Iversen et al. (2006), the increased non-prostate cancer mortality with bicalutamide monotherapy in LPC patients has also been seen with castration (via orchiectomy or GnRH analogue monotherapy) and is likely a consequence of androgen deprivation in men rather than a specific drug toxicity of bicalutamide: [75] The increased number of deaths in patients with localized disease receiving bicalutamide was meticulously investigated and they appeared to be due to a number of small imbalances rather than a specific cause. ... The increased number of non-prostate cancer deaths in the early castration therapy arm [(via orchiectomy or GnRH monotherapy)] in the [Medical Research Council] study suggests that the trend towards an increased number of deaths in patients with localized disease in the present study is a reflection of early endocrine therapy as a concept rather than a bicalutamide-related phenomenon. [75] A study of 300 to 600 mg/day bicalutamide monotherapy in 248 men with LAPC or metastatic prostate cancer found that there were no effects of bicalutamide on heart rate , blood pressure , or electrocardiogram parameters. [76] [77] In addition, at 5-year follow-up, the incidence of cardiovascular events was low, with no differences between the bicalutamide and castration groups. [76] [77] There were also no differences in the incidences of arrhythmia , myocardial infarction , or other ischemic cardiac or cerebrovascular conditions . [76] [77] These findings suggest that bicalutamide does not cause an excess in cardiovascular events or conditions. [76] [77] A meta-analysis of prospective randomized clinical trials of GnRH agonist-based ADT for the treatment of non-metastatic prostate cancer that included over 4,000 patients found no evidence of increased cardiovascular mortality or overall mortality. [78] Non-prostate cancer mortality was not specifically assessed. [78] A case report in which bicalutamide was described as a probable cause of heart failure in an elderly man with prostate cancer has been published. [79] Cardiovascular risks have been reviewed and subjected to meta-analysis . [80] [81] Coagulation [ edit ] NSAA monotherapy is associated with a greater risk of venous thromboembolism (VTE) than non-use, although not to the same extent as surgical or medical castration or particularly high-dose estrogen therapy . [82] [83] [84] [85] [86] Kidney function [ edit ] Androgens and anabolic steroids , including testosterone, have trophic and anabolic effects in the kidneys . [87] [88] [89] [90] Androgen deprivation therapy, including with GnRH agonists and bicalutamide monotherapy, may increase the risk of kidney failure in men. [91] [92] [93] A large randomized controlled trial in men with prostate cancer found that the incidence of kidney failure was 1 to 2% with combined androgen blockade using bicalutamide or flutamide . [94] [95] [96] Anemia [ edit ] Androgens including testosterone are known to stimulate erythropoiesis (formation of red blood cells ) and increase hematocrit (red blood cell levels). [97] [98] These effects are mediated by increasing production and secretion of erythropoietin from the kidneys . [98] Erythropoietin in turn stimulates erythropoiesis in hematopoietic tissues such as bone marrow . [99] The high levels of testosterone in males are why hematocrit and hemoglobin levels are higher in men than in women. [100] Due to stimulation of erythropoiesis, anabolic–androgenic steroids (AAS) such as oxymetholone and nandrolone decanoate are effective for and used in the treatment of severe anemia (very low hematocrit). [98] [101] High doses or levels of AAS, including testosterone , can cause polycythemia —high red blood cell and/or hemoglobin levels that increase the risk of stroke —as an adverse effect. [97] [98] Conversely, whether via castration, NSAA monotherapy, or CAB , decreased erythropoiesis resulting in mild anemia is a common side effect of ADT in men. [53] [102] The incidence of anemia with bicalutamide as a monotherapy or with castration was about 7.4% in clinical trials. [53] A decrease of hemoglobin levels of 1 to 2 g/dL after approximately six months of treatment may be observed. [102] Liver toxicity [ edit ] Bicalutamide may cause liver changes rarely, such as elevated transaminases and jaundice. [103] In the EPC study of 4,052 prostate cancer patients who received 150 mg/day bicalutamide as a monotherapy, the incidence of abnormal liver function tests was 3.4% for bicalutamide and 1.9% for standard care (a 1.5% difference potentially attributable to bicalutamide) at 3-year median follow-up. [8] [104] For comparison, the incidences of abnormal liver function tests are 42 to 62% for flutamide, 2 to 3% for nilutamide, [103] [105] and (dose-dependently) between 10% and 28% for CPA , [106] [107] [108] whereas there appears to be no risk with enzalutamide. [109] [110] In the EPC trial, bicalutamide-induced liver changes were usually transient and rarely severe. [8] The medication was discontinued due to liver changes (manifested as hepatitis or marked increases in liver enzymes) in approximately 0.3% to 1% of patients treated with it for prostate cancer in clinical trials. [59] [111] The risk of liver changes with bicalutamide is considered to be small but significant, and monitoring of liver function is recommended. [8] [112] Elevation of transaminases above twice the normal range or jaundice may be an indication that bicalutamide should be discontinued. [113] Liver changes with bicalutamide usually occur within the first 3 or 4 months of treatment, and it is recommended that liver function be monitored regularly for the first 4 months of treatment and periodically thereafter. [59] Symptoms that may indicate liver dysfunction include nausea, vomiting, abdominal pain, fatigue, anorexia, "flu-like" symptoms, dark urine, and jaundice. [59] A total of 7 case reports of bicalutamide-associated hepatotoxicity or liver failure, two of which were fatal, have been published in the literature as of 2018. [114] [103] [115] One of these cases occurred after two doses of bicalutamide, and has been said to more likely to have been caused by prolonged prior exposure of the patient to flutamide and CPA . [103] [105] [116] [117] [118] In the reported cases of bicalutamide-associated hepatotoxicity, the dosages of the drug were 50 mg/day (three), 80 mg/day (one), 100 mg/day (one), and 150 mg/day (two). [114] [115] Relative to flutamide (which has an estimated incidence rate of 0.03% or 3 per 10,000), hepatotoxicity is far rarer with bicalutamide and nilutamide, and bicalutamide is regarded as having the lowest risk of the three medications. [119] [116] [120] For comparison, by 1996, 46 cases of severe cholestatic hepatitis associated with flutamide had been reported, with 20 of the cases resulting in death. [106] Moreover, a 2002 review reported that there were 18 reports of hepatotoxicity associated with CPA in the medical literature, with 6 of the reported cases resulting in death, and the review also cited a report of an additional 96 instances of hepatotoxicity that were attributed to CPA , 33 of which resulted in death. [106] The clinical studies that have found elevated liver enzymes and the case reports of hepatotoxicity with bicalutamide have all specifically pertained to men of advanced age with prostate cancer. [8] [104] [103] [115] It is notable that older age, for a variety of reasons, appears to be an important risk factor for drug-induced hepatotoxicity. [121] [122] As such, the risk of liver changes with bicalutamide may be less in younger patients, for instance young hirsute women and transgender women. [121] [122] However, it has been reported on the basis of very limited evidence that this may not be the case with flutamide. [123] There is no evidence of greater liver function changes with higher doses of bicalutamide. [124] From a theoretical standpoint (on the basis of structure–activity relationships ), it has been suggested that flutamide, bicalutamide, and nilutamide, to varying extents, all have the potential to cause liver toxicity . [125] However, in contrast to flutamide, hydroxyflutamide , and nilutamide, bicalutamide exhibits much less or no mitochondrial toxicity and inhibition of enzymes in the electron transport chain such as respiratory complex I ( NADH ubiquinone oxidoreductase ), and this may be the reason for its much lower risk of hepatotoxicity in comparison. [126] [127] [128] [129] The activity difference may be related to the fact that flutamide, hydroxyflutamide, and nilutamide all possess a nitroaromatic group , whereas in bicalutamide, a cyano group is present in place of this nitro group, potentially reducing toxicity. [116] [126] [129] [130] v t e Published case reports of bicalutamide-associated liver injury # Age Sex Dosage Use Onset Outcome Source 1 60 years Male 50 mg/day Prostate cancer 2 days Survived Dawson et al. (1997) 2 79 years Male 80 mg/day Prostate cancer 1.5 months Survived Ikemoto et al. (2000) 3 59 years Male 50 mg/day Prostate cancer 4 days Death O'Bryant et al. (2008) 4 61 years Male 50 mg/day Prostate cancer 3.5 months Death Castro Beza et al. (2008) 5 81 years Male 150 mg/day Prostate cancer 3 weeks Survived Hussain et al. (2014) 6 62 years Male 100 mg/day Prostate cancer 4.5 months Survived Yun et al. (2016) 7 67 years Male 150 mg/day Prostate cancer 3 weeks Survived Gretarsdottir et al. (2018) 8 74 years Male 80 mg/day Prostate cancer 1.5 months Survived Kotoh et al. (2018) 9 79 years Male ? ... Archived (PDF) from the original on 28 August 2016. ^ a b c d e f g Anderson J (March 2003). ... A preliminary report". Scand. J. Urol. Nephrol . 28 (1): 67–70. doi : 10.3109/00365599409180473 .
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Nocturnal Enuresis
Wikipedia
The following causes are less common, but are easier to prove and more clearly treated: In some bed wetting children this increase in ADH production does not occur, while other children may produce an increased amount of ADH but their response is insufficient. [20] [23] Attention deficit hyperactivity disorder patients are 2.7 times more likely to have bedwetting issues. [24] Caffeine increases urine production. [25] Chronic constipation can cause bed wetting. [26] When the bowels are full, it can put pressure on the bladder . [27] Often such children defecate normally, yet they retain a significant mass of material in the bowel which causes bed wetting. [28] Infections and disease are more strongly connected with secondary nocturnal enuresis and with daytime wetting . ... Archived from the original on 2010-05-30 . Retrieved 2010-05-28 . ^ "Nocturnal Enuresis" . UCLA Urology. Archived from the original on 2010-07-07 . Retrieved 2010-05-28 . ^ Butler RJ, Holland P (August 2000). ... Archived from the original (PDF) on 2007-06-28 . Retrieved 2008-02-03 . ^ Jindal V, Ge A, Mansky PJ (June 2008).AQP2, AVPR2, RNF168, FA2H, BNC2, AVP, CRH, DRD4, NGF, SULT1E1, MIXL1, IGAN1, SCLY, TAL1, AMY1A, NOS1, KRT7, AMY1B, MAP3K8, BDNF, STS, AMY1C, HTR2A
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Specific Language Impairment
Wikipedia
Differences in the brains of children with SLI vs typically developing children are subtle and may overlap with atypical patterns seen in other neurodevelopmental disorders . [26] [27] Genetic [ edit ] It is now generally accepted that SLI is a strongly genetic disorder . [28] The best evidence comes from studies of twins. ... Journal of Communication Disorders . 35 (4): 311–28. doi : 10.1016/S0021-9924(02)00087-4 . ... Assessment of Communication and Language (Communication and Language Intervention Series) . Brookes Publishing Company. pp. 1–28 . ISBN 978-1-55766-193-7 . OCLC 34772171 . ^ Ingram TT, Reid JF (June 1956).PLAT, L1CAM, GRN, ACTB, CFHR3, TCF4, TCOF1, HIRA, UBTF, UFD1, VCP, SQSTM1, ADAMTS2, POLR1C, SEC24C, RAI1, CHMP2B, SMARCA2, NSDHL, POLR1D, TREM2, NDUFB11, TMEM106B, ALG1, EHMT1, L2HGDH, PRRT2, AMER1, CKAP2L, FLCN, C9orf72, TBX1, SCN8A, ACTG1, SCN2A, STS, ARVCF, ATP1A2, ATRX, CACNA1A, COL1A1, COL1A2, COMT, COX7B, FGFR1, GP1BB, GRIN2A, HCCS, CFH, CFHR1, KCNQ2, KCNQ3, KRAS, MAPT, MECP2, OCRL, PLEC, PSEN1, RREB1, SCN1A, JMJD1C, TARDBP, IARS2
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Gender Dysphoria
Wikipedia
The creation of a specific diagnosis for children reflects the lesser ability of children to have insight into what they are experiencing, or ability to express it in the event that they have insight. [23] Other specified gender dysphoria or unspecified gender dysphoria can be diagnosed if a person does not meet the criteria for gender dysphoria but still has clinically significant distress or impairment. [17] Intersex people are now included in the diagnosis of GD. [24] The International Classification of Diseases ( ICD-10 ) lists several disorders related to gender identity: [25] [26] Transsexualism (F64.0): Desire to live and be accepted as a member of the opposite sex, usually accompanied by a desire for surgery and hormonal treatment Gender identity disorder of childhood (F64.2): Persistent and intense distress about one's assigned gender, manifested prior to puberty Other gender identity disorders (F64.8) Gender identity disorder, unspecified (F64.9) Sexual maturation disorder (F66.0): Uncertainty about one's gender identity or sexual orientation, causing anxiety or distress The ICD-11 , which will come into effect on 1 January 2022, significantly revises classification of gender identity-related conditions. [27] Under "conditions related to sexual health", the ICD-11 lists "gender incongruence", which is coded into three conditions: [28] Gender incongruence of adolescence or adulthood (HA60): replaces F64.0 Gender incongruence of childhood (HA61): replaces F64.2 Gender incongruence, unspecified (HA6Z): replaces F64.9 In addition, sexual maturation disorder has been removed, along with dual-role transvestism . [29] ICD-11 defines gender incongruence as "a marked and persistent incongruence between an individual’s experienced gender and the assigned sex", with presentations similar to the DSM-5 definition, but does not require significant distress or impairment. ... It is not a mental illness." [71] In May 2009, the government of France declared that a transsexual gender identity will no longer be classified as a psychiatric condition, [72] but according to French trans rights organizations, beyond the impact of the announcement itself, nothing changed. [73] Denmark made a similar statement in 2016. [74] In the ICD-11, GID is reclassified as "gender incongruence", a condition related to sexual health. [28] The working group responsible for this recategorization recommended keeping such a diagnosis in ICD-11 to preserve access to health services. [29] See also [ edit ] List of transgender-related topics Transmedicalism References [ edit ] ^ a b c d "Gender Dysphoria" (PDF) . ... Retrieved August 11, 2018 . ^ a b "Gender incongruence (ICD-11)" . icd.who.int . WHO . Retrieved August 28, 2018 . ^ a b Reed GM, Drescher J, Krueger RB, Atalla E, Cochran SD, First MB, Cohen-Kettenis PT, Arango-de Montis I, Parish SJ, Cottler S, Briken P, Saxena S (October 2016). ... International Review of Psychiatry . 28 (1): 13–20. doi : 10.3109/09540261.2015.1115754 . ... ISSN 1448-5028 . ^ Conron, KJ; Scott, G; Stowell, GS; Landers, S (January 2012), "Transgender Health in Massachusetts: Results from a Household Probability Sample of Adults", American Journal of Public Health , American Public Health Association , 102 (1): 118–222, doi : 10.2105/AJPH.2011.300315 , ISSN 1541-0048 , OCLC 01642844 , PMC 3490554 , PMID 22095354 , Between 2007 and 2009, survey participants aged 18 to 64 years in the Massachusetts Behavioral Risk Factor Surveillance System (MA-BRFSS; N = 28 662) were asked: "Some people describe themselves as transgender when they experience a different gender identity from their sex at birth.
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Helminthiasis
Wikipedia
Soil is eaten, for example, by children or pregnant women to counteract a real or perceived deficiency of minerals in their diet. [28] Diagnosis [ edit ] Identification and quantification of helminth eggs at UNAM university in Mexico City, Mexico Specific helminths can be identified through microscopic examination of their eggs (ova) found in faecal samples. ... The maximum worm burden is at five to ten years of age, declining rapidly thereafter. [65] Individual predisposition to helminthiasis for people with the same sanitation infrastructure and hygiene behavior is thought to result from differing immunocompetence , nutritional status , and genetic factors . [64] Because individuals are predisposed to a high or a low worm burden, the burden reacquired after successful treatment is proportional to that before treatment. [64] Disability-adjusted life years [ edit ] It is estimated that intestinal nematode infections cause 5 million disability-adjusted life years (DALYS) to be lost, of which hookworm infections account for more than 3 million DALYS and ascaris infections more than 1 million. [66] There are also signs of progress: The Global Burden of Disease Study published in 2015 estimates a 46 percent (59 percent when age standardised) reduction in years lived with disability (YLD) for the 13-year time period from 1990 to 2013 for all intestinal/nematode infections, and even a 74 percent (80 percent when age standardised) reduction in YLD from ascariasis. [67] Deaths [ edit ] As many as 135,000 die annually from soil transmitted helminthiasis. [3] [68] [69] The 1990–2013 Global Burden of Disease Study estimated 5,500 direct deaths from schistosomiasis, [70] while more than 200,000 people were estimated in 2013 to die annually from causes related to schistosomiasis. [71] Another 20 million have severe consequences from the disease. [72] It is the most deadly of the neglected tropical diseases. [73] Helminth genera Common name Infections (million per year) Direct deaths per year Regions where common Soil transmitted helminthiasis (STH) (classified as neglected tropical disease ): Ascaris lumbricoides Roundworm 1000 to 1450 807 to 1,121 [74] 20,000 Many regions of South-east Asia, Africa, and Central and South America [75] [76] [77] [78] [79] [80] Trichuris trichiura Whipworm 500 604–795 [74] In moist, warm, tropical regions of Asia, Africa, Central and South America, and the Caribbean islands. [77] [78] [79] [80] [81] Ancylostoma duodenale Hookworm 900 to 1300 576–740 (hookworm in general) [82] In tropical and subtropical countries (Sub-Saharan Africa) [78] [81] Necator americanus Strongyloides stercoralis Hookworm , pinworm 50 to 100 Thousands In moist rainy areas of the tropics and subtropics, in some areas of southern and eastern Europe and of the United States of America [78] [79] All STH together 1500 to 2000 [6] 135,000 [3] [68] [69] Tropical and subtropical areas, in particular sub-Saharan Africa, the Americas, China and east Asia. [6] Not transmitted via soil but classified as neglected tropical disease: Schistosoma mansoni Blood fluke All types of Schistosoma together: 160 to 200 (210 "affected" [83] ) 12,000 [84] 150,000 deaths from kidney failure [85] 200,000 indirect deaths from "causes related to" Schistosomiasis [71] In tropical and subtropical regions [77] [78] [79] [80] [81] Schistosoma haematobium 112 (in Sub-Saharan Africa alone) [85] Echinococcus granulosus 3 [86] Developing countries Not transmitted via soil and not classified as neglected tropical disease: Toxocara canis Dog roundworm 50 Many regions of South-east Asia, Africa, and Central and South America [75] [76] [77] [78] [79] [80] Taenia solium Pork tapeworm 50 South America, Southeast Asia, West Africa and East Africa [77] [78] [79] [80] Taenia saginata Beef tapeworm 50 (all types of Taenia : 40 to 60 [87] ) Hymenolepis nana Dwarf tapeworm 100 Hymenolepis diminuta Rat tapeworm Fasciola hepatica , Fascioloides magna Liver fluke 50 Largely in southern and eastern Asia but also in central and eastern Europe [78] [79] Fasciolopsis buski Giant intestinal fluke Dracunculus medinensis Guinea worm Nowadays negligible thanks to eradication program [88] Formerly widespread in India, west Africa and southern Sudan [78] [79] Trichostrongylus orientalis Roundworm 1–3 ("several") Rural communities in Asia [78] [79] Other 100 Worldwide [78] [79] Total (number of infections) Approx. 3.5 billion Worldwide See also [ edit ] Kato technique References [ edit ] ^ a b "Neglected Tropical Diseases" . cdc.gov . 6 June 2011 . Retrieved 28 November 2014 . ^ London Declaration (30 January 2012). ... "Status of medical parasitology in South Africa: new challenges and missed opportunities". Trends in Parasitology . 28 (6): 217–219. doi : 10.1016/j.pt.2012.03.005 . ... PMID 10072156 . ^ "Neglected Tropical Diseases" . cdc.gov . 6 June 2011 . Retrieved 28 November 2014 . ^ a b "Parasites – Soil-transmitted Helminths (STHs)" .IL4, IL13, IL5, IL10, IL33, IL9, IFNG, IL25, IL17A, FOXP3, MYDGF, CCL11, BCL11B, NELFCD, GREM1, PRDX5, NMUR1, ADIPOQ, IL1RL1, ABO, FBXW7, EOMES, SUCNR1, RETN, CYSLTR2, CLEC7A, NBEAL1, FUZ, SETD7, NLRP3, LINGO2, SERPINA13P, SUCLA2, STAT6, TYROBP, FCER2, AGXT, ARNTL, TNFRSF8, TNFSF8, CD38, CRP, CSF2, CTSB, EGFR, MS4A2, GAMT, TNFRSF4, GLB1, IL1A, IL1B, IL4R, ITGAX, LTBR, SERPINA1, ADCY9, TGFB1, TNFSF4, MIR155
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Trichotillomania
Wikipedia
The hair pulling may resolve when other conditions are treated. [8] Psychotherapy [ edit ] Habit reversal training (HRT) has the highest rate of success in treating trichotillomania. [8] HRT has also been shown to be a successful adjunct to medication as a way to treat trichotillomania. [7] [28] With HRT, the individual is trained to learn to recognize their impulse to pull and also teach them to redirect this impulse. ... Archived from the original on 2013-02-28 . Retrieved 2013-02-22 . ^ Chamberlain, Samuel. ... Retrieved November 27, 2009 . ^ "Hannah Sussman's Art Imitates Life Join Her For a Screening October 3rd" . Century City News. September 28, 2009. Archived from the original on December 16, 2009 .
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Tularemia
Wikipedia
For a time, Martha's Vineyard was identified as the only place in the world where documented cases of tularemia resulted from lawn mowing . [28] However, in May 2015 [29] a resident of Lafayette, Colorado , died from aerosolised F. tularensis , which was also connected to lawn mowing, highlighting this new vector of risk. ... ISBN 978-0-8493-3205-0 . Retrieved 28 October 2010 . ^ Mörner T (December 1992). ... PMID 11757506 . ^ a b Byars, Mitchell (May 28, 2015). "Lafayette resident contracts tularemia after mowing lawn, dies of other medical complications" .
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Pachydermoperiostosis
Wikipedia
However, further investigation is needed to confirm this use of disease monitoring. [3] Prostaglandin E2 may also be raised in patients with lung cancer and finger clubbing. [26] This may be related to raised levels of cyclooxygenase -2, an enzyme involved in the metabolism of prostaglandins. [27] A similar association has been noted in cystic fibrosis . [28] Classification [ edit ] PDP is one of the two types of hypertrophic osteoarthropathy . ... "Prostaglandin E2 and bone turnover markers in the evaluation of primary hypertrophic osteoarthropathy (pachydermoperiostosis): a case report". Rheumatol. Clin . 28 (10): 1229–1233. doi : 10.1007/s10067-009-1197-9 . ... "A novel homozygous splice site mutation in the HPGD gene causes mild primary hypertrophic osteoarthropathy". Clin Exp Rheumatol . 28 (2): 153–157. PMID 20406614 . ^ a b Silver F, et al. (1996).
