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  • Ciguatera Fish Poisoning Wikipedia
    ., Ciguatera fish poisoning , retrieved 6 April 2015 ^ a b Schep LJ, Slaughter RJ, Temple WA, Beasley DM (2010). "Ciguatera poisoning: an increasing occurrence in New Zealand".
  • List Of Periodontal Diseases Wikipedia
    Res . 10 (3): 115–27. doi : 10.1111/j.1600-0765.1975.tb00016.x . PMID 126310 . ^ a b c d e Payne WA, Page RC, Ogilvie AL, Hall WB (May 1975).
    CTSC, PON1, IL17A, IL16, IL15, CD80, CD40LG, IL24, IL19, IL7, IL21, TNF, MMP8, IL10, IL6, IL1A, IL1B, NLRP3, VDR, TNFSF11, IL4, CRP, TLR4, VEGFA, IFNG, TNFRSF11B, FN1, PTGS2, CD14, IL1RN, COX2, MMP9, MTCO2P12, GCFC2, CAMP, TREM1, MPO, STAT1, SQSTM1, F2RL1, ALOX5, LRWD1, DEFB1, TGFB1, ADRB3, TLR2, IL18, CXCL10, GOPC, TREM2, TLR9, FBLIM1, WNT5A, PWAR1, CXCL8, SLC52A2, IL2RA, MIR146A, CDKN2B-AS1, IFI16, ICAM1, IBSP, ISG20, MMP3, LTA, LTF, VCAM1, SOCS1, DLK1, CCN6, TIMP3, HPD, SMPD1, CXCL12, CCL2, RARRES2, ADM, NR1I2, PLG, NOS3, AGO2, IL37, VSX1, TRIM25, MMP1, HSPD1, NAT2, PTX3, FOXO1, CD28, CASP9, COX8A, CTLA4, APOE, EGF, F2R, FGF2, CAT, HIF1A, MIR15A, PES1, DHS, SDS, BTF3P11, SLC7A9, WDHD1, PADI2, KDM4B, JMJD6, CAMTA1, SIRT1, ANGPTL2, MAPK8IP2, SEMA4D, PADI4, BSG, BPI, TRBV16, TRBV7-9, TRBC1, SETD2, PKN3, BDNF, DPP7, BCHE, PDPN, CRTAP, AHSG, AIM2, PEA15, MIR1226, IL18R1, CASP8, HDAC3, CASP3, CASP1, MSC, VAMP3, AGTR1, NTN1, CYTIP, GPNMB, PLPPR4, HDAC6, EDIL3, ARPC5, CTDSP2, EBI3, DDX39A, CTDSPL, EDS8, TLR6, NOD1, IL22, TRAT1, FOXP3, UNC5B, IL33, DNER, IL17F, ALPL, MRGPRX2, RBM45, ALOX15, IL34, ESCO2, MIR30E, TMPRSS6, ALDH2, CRACR2A, MIR22, IL27, PCSK9, COPD, FDCSP, IFNL1, BRINP3, SERPINA13P, RTL1, SMIM10L2A, MIR106B, SMIM10L2B, PPP1R2C, GAL, DRAM1, ANGPTL4, HSPA14, IL23A, CD19, AZU1, AR, KLK3, DEFA1B, FAM20A, ODAM, SLC52A1, ATF7IP, TET1, AMY1C, SLAMF7, CXCL16, NLRC4, MIR646, AMY1B, ACE2, TRPV4, NOD2, AMY1A, DHX40, IL17D, HLA-DRB1, RECK, FBN1, KIR3DL1, LBP, LGALS9, ESR1, LYZ, MBL2, MFGE8, MAP3K11, MARK2, MMP2, ELN, EGFR, MMP13, EDN1, MT2A, ECE1, MTNR1B, NFATC1, NFKB1, NFKBIL1, NHS, NOS2, RCAN1, NOTCH1, PNP, ITGB2, IRF1, OCA2, FCGR3A, HLA-DQB1, TNC, HGF, CFH, IRF8, HBB, GSTP1, IGFBP2, IGFBP3, IGHA1, GSR, GRN, GOT1, IL2, GIP, GHSR, GEM, FPR1, FOLR1, CXCR1, IL12RB2, IL13, FGF7, FGB, FCGR3B, NRAS, DMBT1, DDX39B, SLC6A4, CTSB, SNAP25, SOD2, SPG7, SPP1, STAT3, SYK, ADAM17, CST2, TRB, TRBV20OR9-2, CSF1, TGFB3, TH, THRB, CRYGD, CCR5, CCR1, TNFRSF1A, TNFRSF1B, CLU, CFTR, CD81, TLX2, CXCR4, SLIT3, SLC2A4, OTC, SLC2A1, P2RX7, SERPINE1, PECAM1, PIN1, PLAU, DEFB4A, PLTP, DEFA1, PPARG, HTRA1, ACE, CUX1, CTSS, REN, S100A2, S100A12, CTSK, CCL3, CCL7, CCL20, CTSD, SELE, SELL, SETMAR, SH3BP2, CD34
  • Alexithymia Wikipedia
    S2CID 20228527 . ^ Shipko S, Alvarez WA, Noviello N (1983). "Towards a teleological model of alexithymia: alexithymia and post-traumatic stress disorder".
    THAS, SLC6A4, COMT, SCLY, KRT7, TAL1, ANKK1, BDNF, DRD2, OXTR, YWHAE, CHST3, BAG3, ARSD, ARHGAP32, SF3B1, TET2, ATF7IP, TP53AIP1, GOLPH3, ASXL1, TMEM88B, TNF, ACSM3, TBCA, REN, TAS2R38, PAFAH1B1, IL18, IL6, IL1B, IL1A, HTR1A, ESR1, ACE, CASP8, CAST, SERPING1, LOC110806262
  • Non-Hodgkin Lymphoma Wikipedia
    . ^ Patte C, Bleyer A, Cairo MS (2007). "Non-Hodgkin Lymphoma". In Bleyer WA, Barr RD (eds.). Cancer in Adolescents and Young Adults (Pediatric Oncology) .
    RAD54L, RAD54B, BCL2, BCL6, FAS, CASP10, CSF3, MTHFR, HLA-DRB1, NPM1, TYMS, NBN, SHMT1, CBS, CD79B, BRAF, CYP2E1, PAX5, TFRC, IFNA2, BCL10, CSF2, CD79A, CHEK2, FPGS, PRF1, BHMT, SPEN, TBL1XR1, EPHX1, IKBKB, CREBBP, S1PR2, MTSS1, ATM, TET2, KIT, ASXL1, NTHL1, LTA, MS4A1, IL10, SRSF2, CD19, TNFRSF8, ABCB1, CCND1, IGH, IL2, KRT20, RTEL1, ALK, SMUG1, EZH2, CDKN2A, PDLIM7, MYC, VEGFA, TP53, TNF, NAT2, IL6, LEP, IL4, GSTP1, NLRP2, CD37, IL2RA, IRF4, CXADR, NAT1, PIK3CD, TRBV20OR9-2, SPG7, ARR3, CXCL12, NR1I3, PRKAR1A, TRIM13, CDR3, CASR, CD274, CXADRP1, FGF2, FCGR3A, ERCC2, GSTT1, RBM45, GSTM1, MTR, STAT3, CD70, LEPR, CD40LG, CD34, CXCL8, TNFSF10, NCAM1, NOS2, AICDA, MDM2, PIK3CA, TBC1D9, FCGR2A, MTRR, PIK3CB, TNFSF13B, TLR2, DLC1, PIK3CG, MAPK1, XRCC1, VDR, H3P10, AKT1, CD22, BCR, CASP8, CD44, CD40, CDKN2B, IL12A, CASP3, CD47, IFI27, ALDH1L1, HPGDS, CASP9, IL13, CXCR4, FOXP3, GPX1, CALM3, DCTN6, TLR9, ZNRD2, CALM2, FOXO1, PLK1, BCL2L11, CLLS2, IL1RN, DLEC1, HDAC9, PON1, CALM1, IGL, CDK2, TMED7, PSMD9, CD28, TP73, H3P23, HLA-DQB1, CTLA4, TMED7-TICAM2, SELL, CD38, MIR21, MRE11, RNASE3, CCR5, LINC01194, MSH2, TICAM2, KRIT1, AHR, NPAS2, NFKB1, CAMKMT, H2AX, SERPING1, RAF1, TNFRSF13C, MYD88, CCL21, BTK, RIT1, PTPN6, PTEN, TSPO, BRCA1, BRD2, PDCD1, PLXNA2, CCND3, MCL1, MGMT, MKI67, MMP2, MMP9, MOS, MPO, ABCC1, MTX1, PIM1, MUC1, MYOD1, NME1, NPR2, CAT, PCNA, SOD2, CASP1, SLC16A1, WRN, CXCR5, AURKA, POLDIP2, MCAT, MCTS1, NXT1, POLE3, MIB1, BACH2, MARCKSL1, WLS, ARHGAP24, TXLNA, IFNL3, CLEC4D, SLC35B2, ASPG, MIR150, MIR155, MIR203A, MIR34A, FAM72B, CCR2, FAM72A, MEF2B, KLRC4-KLRK1, ERVK-32, H3P9, H3P11, RNF19A, TNFAIP8, TOGARAM1, TP63, SYK, TGFB1, TIMP1, TIMP2, TLR1, BCL3, TRAF1, TRAF3, BAX, GPANK1, AIMP2, NR0B2, DYNLL1, ANXA5, TNFRSF10B, SOCS3, GRAP2, KLK3, HDAC6, RAD50, CIB1, MRPL28, AHSA1, SUB1, XIAP, KLRK1, LTB, CRK, FH, CCR7, ERBB2, CYBA, KDR, HLA-G, FN1, ISG20, CYP2B6, CYP2C9, CDKN1B, IL18, HLA-B, HLA-A, CDC25A, CEBPA, FGFR4, EPO, CYP1A1, DDIT3, MAPK14, GBA, CMA1, IRF8, LGALS1, LYVE1, TPX2, GOLGA7, LEF1, CCR9, ACSBG1, HSPH1, ANXA1, FCGR1A, CES1, PLEKHO1, WT1-AS, FCGR2B, FCN2, SF3B1, CCL27, RASSF1, UBE2C, EBNA1BP2, FCGR3B, C1RL, ALPP, ANPEP, ERCC5, GPR132, PSAT1, ERVW-1, DLL1, IGHV1-12, SMARCAL1, IGHV3-69-1, IGHV3OR16-7, CHEK1, PDLIM3, ICOS, EPHX2, ESR1, MASP2, ATRNL1, ETS1, PART1, DERL2, CFL1, ANG, CADM1, LMNA, BIRC5, FRA16B, FASLG, BCLAF1, CDKN2C, RGS6, TCL1B, NCOR2, CYTIP, CLOCK, BAG5, EEF1E1, NPEPPS, ADIPOQ, CD52, KLF4, AR, ARG1, ARHGEF2, FCGR2C, ARTN, MTOR, LIMD1, MBD2, RHOA, PER3, BMS1, SLC23A2, SLC23A1, FLT4, KHDRBS1, SLCO1B1, FGFR1, GDE1, FOXM1, CRTAP, APOH, TUBA1B, TLR6, AKR1A1, TNIP1, LANCL1, DLEU1, SPRY2, RABEPK, APRT, ZNF197, FLT1, EDIL3, SMC4, FLT3, FLT3LG, TANK, ATRAID, TMEM260, ALDH1A1, EPHB2, MIR28, MIR26B, CYP1B1, MIR200B, MIR152, CYP17A1, MIR143, MIR124-1, MIRLET7B, CYP24A1, LOC390714, KMT5A, CYP27B1, GSTK1, CD55, DAPK1, ARMH1, DCC, H19, ACE, CTAG1A, TIGIT, AKR1C1, ACACA, RMDN2, MIR17HG, XRCC6P5, MIR148B, ERVK-20, H3P5, H3P28, CR2, COMT, CSF3R, LOC105379528, UPK3B, LOC102724971, LOC102723407, ERVK-18, H3P12, CTAG1B, KIR2DL5B, CTNNB1, CUX1, CX3CR1, MIR618, OCM, LGALS7B, ACAA1, SCFV, MIR502, MIR202, H4C15, SLCO6A1, PARP1, TPPP2, DHX33, E2F1, IL21, CXCL16, C6orf47, POLD4, CFAP97, EEF2, SCYL1, EIF4A2, KIR2DL5A, GOPC, POLE4, ERVK-6, PCDHGB7, CFC1, CCAR1, AIF1, NAT10, LAMTOR1, GGH, EIF4E, FBLIM1, ALB, EIF4G1, IGAN1, PLEKHG2, H4-16, CARD11, MIR155HG, TIRAP, NLRP3, CDCA5, PRRT2, MUC16, MTDH, TSLP, DIXDC1, PWWP3A, HAVCR2, MIXL1, RAPH1, DDT, TLR10, DEFB126, RNF34, ASRGL1, DECR1, DNMT1, AGRP, VTCN1, BIRC7, DPP4, CDK5R1, RHOH, NRP1, P2RX7, PRKCB, PRKCA, FMNL1, CDH13, IL1B, PMS1, PML, CDC6, PLAG1, IL2RG, CDK11B, IL5, CD59, IL7R, IL9, PDGFRB, PDGFRA, PDE6H, IL10RA, IL12B, SERPINA5, PC, IL12RB1, PAFAH1B1, PAEP, IFNGR2, MAPK3, MAPK8, PTPRC, ICAM1, RMD1, ID4, RING1, RFC1, RCD1, RB1, IDH1, RAC2, NECTIN2, PTPRJ, PTPN13, MAP2K1, PTPN11, IDH2, PTGS2, CDK4, IFNG, PSMD7, PSMB9, PSMB6, RELN, PROS1, PRL, PEBP1, ORC4, RORB, OGG1, MSMB, MSH5, KIR2DS1, KIR3DS1, KRAS, KRT81, MNAT1, LAIR1, MMP3, RPSA, MMP1, MME, KMT2A, LBR, CD33, MFAP1, MDM4, TNFSF8, MDK, MBP, EPCAM, SH2D1A, LTK, LGALS3, LGALS7, MTAP, MTHFD1, CD14, NFKBIL1, NTRK1, IL15, IL16, CAV3, TNFRSF9, NOTCH4, NPY, NOS3, SERPINA6, NOS1, NGF, IDO1, CD5, NEDD9, NCF4, CCK, INSL3, INSR, MYCN, MYCL, CCND2, ISL1, ITGB3, JAK2, RORA, RPS6, CES2, GZMB, ADAM12, MAFK, GPT, GSTM3, PRRC2A, IL1R2, ZMYM2, ZBTB16, ZAP70, YWHAE, YY1, XRCC4, B2M, XPO1, CDKN1A, VIPR1, VIP, MSH6, BCHE, VCAM1, UCP1, UBE2I, TYRO3, BCL2L1, TRAF6, KMT2D, GPR34, TCL1A, H4C14, TNFRSF10A, G6PD, TNFRSF14, LSP1, TNFSF13, NCOA1, AKR1C3, GCHFR, DYRK2, ATHS, GNA15, H4C13, ATIC, H4C5, H4C2, H4C8, H4C3, H4C11, H4C12, H4C6, H4C4, H4C1, H4C9, NCOA3, GUCY2D, TPM3, RRM1, HBB, SRC, SPP1, SPN, HOXC5, HOXC6, SOAT1, SLPI, SLC19A1, HRAS, STIL, PMEL, SHMT2, HSPA1L, BRCA2, SEMG1, HSPA4, SELE, HSPD1, TNC, CCL5, CCL1, SAI1, S100A4, RYR3, RXRB, SST, BLM, STAT6, THY1, HGF, TNFRSF1B, TNFRSF1A, TNFAIP3, BCL7A, TSPAN7, TNFRSF17, HIC1, TJP1, HIF1A, TIA1, TGFBR3, HMGB1, TGFBR2, TGFBR1, CDK6, TFDP1, TERT, TERC, CRY2, TCN1, TCF3, TAT, TAP2, BDNF
    • Lymphoma, Non-Hodgkin, Familial OMIM
      A number sign (#) is used with this entry because non-Hodgkin lymphoma is associated with somatic mutations in a number of genes, including CASP10 (601762), ATM (607585), RAD54L (603615), BRAF (164757), CARD11 (607210), and RAD54B (604289). Inheritance Wiernik et al. (2000) analyzed 11 published reports of multigenerational familial non-Hodgkin lymphoma (NHL) and 18 previously unreported families with familial NHL for evidence of anticipation. They determined the difference in disease-free survival between generations and the difference in the age of onset for each affected parent-child pair. To avoid ascertainment bias, the analyses were also performed separately using only parent-child pairs with age of onset greater than 25 years. In addition, the age-of-onset distribution of the studied cases was compared with that of the Surveillance Epidemiology and End Results (SEER) program using data for 1973 to 1998.
    • Non-Hodgkin Lymphoma Orphanet
      Non-Hodgkin malignant lymphomas(NHL) is a heterogeneous group of malignant tumors of the lymphoid system.
    • Non-Hodgkin's Lymphoma Mayo Clinic
      Overview Non-Hodgkin's lymphoma is a type of cancer that begins in your lymphatic system, which is part of the body's germ-fighting immune system. In non-Hodgkin's lymphoma, white blood cells called lymphocytes grow abnormally and can form growths (tumors) throughout the body. Non-Hodgkin's lymphoma is a general category of lymphoma. There are many subtypes that fall in this category. Diffuse large B-cell lymphoma and follicular lymphoma are among the most common subtypes. The other general category of lymphoma is Hodgkin's lymphoma. Advances in diagnosis and treatment of non-Hodgkin's lymphoma have helped improve the prognosis for people with this disease.
  • Hyperkalemia Wikipedia
    ISBN 9780470090558 . ^ a b Mahoney, BA; Smith, WA; Lo, DS; Tsoi, K; Tonelli, M; Clase, CM (18 April 2005). ... Retrieved 25 March 2016 . ^ Parham WA, Mehdirad AA, Biermann KM, et al. (2006).
    CYP17A1, INS, WNK4, CA12, NNT, CUL3, ABCB6, SLC30A9, TXNRD2, LPIN1, KLHL3, SLC2A1, INVS, SAMD9, MRAP, WNK1, STAR, SCNN1G, CACNA1S, SCNN1B, SCNN1A, SCN4A, RYR1, NR3C2, MC2R, HSD3B2, GABRA3, CYP11B2, CYP11B1, CYP11A1, CLCN5, KCNJ18
  • Meconium Aspiration Syndrome Wikipedia
    . ^ Carson, BS; Losey, RW; Bowes Jr, WA; Simmons, MA (1976). "Combined Obstetric and Pediatric Approach to Prevent Meconium Aspiration Syndrome".
    ATF2, AGT, AGTR2, NAP1L1, OPTN, NRP1, PTGS2, NOS2, GNAS, LINC01672, CPOX, DMBT1, NANOS2, ACE2, TLR8, TLR7, AMY1A, COX5A, AMY1B, SCGB1A1, TLR4, TLR1, REN, AMY1C, PTGS1, NT5E, NOS3, C5, NOS1, CD14, NR3C2, MAS1, KCNJ13, CXCL8, COX8A, GH1, GDNF, AFP
    • Meconium Aspiration Syndrome Orphanet
      Meconium aspiration syndrome is a pulmonary complication appearing in newborns with a meconium-stained amniotic fluid. Aspirated meconium can interfere with normal breathing by several mechanisms including airway obstruction, chemical irritation, infection and surfactant inactivation and induces more or less severe signs of respiratory distress at birth.
    • Meconium Aspiration Syndrome GARD
      Meconium aspiration syndrome is a serious condition in which a newborn breathes a mixture of meconium and amniotic fluid into the lungs around the time of delivery. This can cause breathing difficulties due to swelling (inflammation) in the baby's lungs after birth. Treatment may include suctioning the newborn's mouth as soon as the head emerges during delivery, deep suctioning of the windpipe, antibiotics to treat infection, oxygen to keep blood levels normal, and radiant heat to maintain body temperature. In severe cases, the baby may need assistance breathing (ventilator).
  • L1 Syndrome Wikipedia
    . ^ Miller DT, Adam MP, Aradhya S, Biesecker LG, Brothman AR, Carter NP, Church DM, Crolla JA, Eichler EE, Epstein CJ, Faucett WA, Feuk L, Friedman JM, Hamosh A, Jackson L, Kaminsky EB, Kok K, Krantz ID, Kuhn RM, Lee C, Ostell JM, Rosenberg C, Scherer SW, Spinner NB, Stavropoulos DJ, Tepperberg JH, Thorland EC, Vermeesch JR, Waggoner DJ, Watson MS, Martin CL, Ledbetter DH (May 2010).
    L1CAM, PLP1, PTHLH, PRDX5, PDXP, ENOPH1, CALM1, CALM2, CALM3, CANX, KRIT1, F7, F8, RNF6, CAMKMT, ASRGL1
    • X-Linked Complicated Spastic Paraplegia Type 1 Orphanet
      A congenital, X-linked, clinical subtype of L1 syndrome, characterized by spastic paraplegia, mild to moderate intellectual disability and normal brain morphology. This subtype represents the milder end of the L1 syndrome spectrum.
    • L1 Syndrome Orphanet
      A rare, congenital X-linked developmental disorder characterized by hydrocephalus of varying degrees of severity, intellectual deficit, spasticity of the legs, and adducted thumbs. The syndrome represents a spectrum of disorders including: X-linked hydrocephalus with stenosis of the aqueduct of Sylvius (HSAS), MASA syndrome, X-linked complicated hereditary spastic paraplegia type 1, and X-linked complicated corpus callosum agenesis. Epidemiology L1 syndrome primarily affects males. HSAS is the most common genetic form of congenital hydrocephalus, with a prevalence of approximately 1/30,000. The prevalence and incidence of the other disorders in the spectrum are not known. Clinical description Presentation is commonly in the antenatal or neonatal period but, depending on the severity of condition, may present later in life with developmental delay and other neurological features such as spasticity.
    • Masa Syndrome Wikipedia
      MASA syndrome Other names Mental retardation-aphasia-shuffling gait-adducted thumbs syndrome This condition is inherited in an X-linked recessive manner. Specialty Neurology MASA syndrome is a rare X-linked recessive neurological disorder on the L1 disorder spectrum belonging in the group of hereditary spastic paraplegias [1] a paraplegia known to increase stiffness spasticity in the lower limbs. [2] This syndrome also has two other names, CRASH [3] syndrome and Gareis-Mason syndrome. Contents 1 Signs and symptoms 2 Genetics 3 Previous Cases 4 Diagnosis 5 Treatment 6 References 7 External links Signs and symptoms [ edit ] The acronym "MASA" stands for the four main signs and symptoms associated with the syndrome: (1) mental retardation (mild to moderate intellectual disability), (2) aphasia (delayed onset of speech), (3) shuffling gait , and (4) adducted thumbs [4] characterized by cleft palate, microcephaly, and dysmyelination. [5] Affected males may also have a variable dilatation (widening) of the third heart ventricle. [4] MASA has five other factors including hydrocephalus . The build-up is often caused by an obstruction that prevents proper fluid drainage. [6] Spasticity of the lower limbs, causing the muscles to stiffen or tighten, preventing normal fluid movement. [7] Aphasia , which is when someone loses the ability to understand or express speech, due to brain damage. Seizures, an abrupt, uncontrolled [8] disturbance in the brain. Lastly, agenesis of the corpus callosum , a rare congenital disorder.
    • Masa Syndrome Orphanet
      A X-linked, clinical subtype of L1 syndrome, characterized by mild to moderate intellectual disability, delayed development of speech, hypotonia progressing to spasticity or spastic paraplegia, adducted thumbs, and mild to moderate distension of the cerebral ventricles.
    • L1 Syndrome GARD
      L1 syndrome is a mild to severe congenital disorder with hydrocephalus of varying degrees of severity, intellectual disability, spasticity of the legs, and adducted thumbs. It includes several conditions, some more severe than others: X-linked hydrocephalus with stenosis of the aqueduct of Sylvius (HSAS) - the most severe of all; MASA syndrome (intellectual disability, aphasia (delayed speech), spastic paraplegia (shuffling gait), adducted thumbs); SPG1 (X-linked complicated hereditary spastic paraplegia type 1) X-linked complicated corpus callosum agenesis . It is inherited in an X-linked manner; therefore, it only affects males. It is caused by alterations (mutations) in L1CAM gene. The diagnosis is made in males who have the clinical and neurologic findings and a family history consistent with X-linked inheritance and is confirmed by a genetic test showing the L1CAM gene mutation. The treatment involves doing a surgery for the hydrocephalus.
    • L1 Syndrome GeneReviews
      Summary Clinical characteristics. L1 syndrome involves a phenotypic spectrum ranging from severe to mild and includes three clinical phenotypes: X-linked hydrocephalus with stenosis of the aqueduct of Sylvius (HSAS) MASA ( m ental retardation [intellectual disability], a phasia [delayed speech], s pastic paraplegia [shuffling gait], a dducted thumbs) syndrome including X-linked complicated hereditary spastic paraplegia type 1 X-linked complicated corpus callosum agenesis Males with HSAS are born with severe hydrocephalus, adducted thumbs, and spasticity; intellectual disability is severe. In less severely affected males, hydrocephalus may be subclinically present and documented only because of developmental delay; intellectual disability ranges from mild (IQ: 50-70) to moderate (IQ: 30-50). It is important to note that all phenotypes can be observed in affected individuals within the same family. Diagnosis/testing. The diagnosis of L1 syndrome is established in a male proband with suggestive findings and a hemizygous pathogenic variant in L1CAM identified by molecular genetic testing. The diagnosis of L1 syndrome in a female is unusual but not impossible (most likely in the setting of general delay and/or hydrocephalus) and is established with the identification of a heterozygous pathogenic variant in L1CAM by molecular genetic testing.
    • Masa Syndrome OMIM
      A number sign (#) is used with this entry because MASA syndrome, also known as spastic paraplegia-1 (SPG1), is caused by mutation in the gene encoding the L1 cell adhesion molecule (L1CAM; 308840). X-linked aqueductal stenosis or hydrocephalus (HSAS; 307000) is an allelic disorder. Description The hereditary spastic paraplegias (SPG) are a group of clinically and genetically diverse disorders characterized by progressive, usually severe, lower extremity spasticity; see reviews of Fink et al. (1996) and Fink (1997). Some forms of SPG are considered 'uncomplicated,' i.e., progressive spasticity occurs in isolation; others are considered 'complicated,' i.e., progressive spasticity occurs with other neurologic features. X-linked, autosomal dominant (see 182600), and autosomal recessive (see 270800) forms of SPG have been described.
  • Hereditary Spastic Paraplegia Wikipedia
    Zhonghua Yi Xue Yi Chuan Xue Za Zhi 26(3):298-301 ^ Helbig KL, Hedrich UB, Shinde DN, Krey I, Teichmann AC, Hentschel J, Schubert J, Chamberlin AC, Huether R, Lu HM4, Alcaraz WA, Tang S, Jungbluth C, Dugan SL, Vainionpää L, Karle KN, Synofzik M, Schöls L, Schüle R, Lehesjoki AE, Helbig I, Lerche H, Lemke JR (2016) A recurrent mutation in KCNA2 as a novel cause of hereditary spastic paraplegia and ataxia.
    ATL1, SPAST, REEP1
    • Spastic Paraplegia 3a GeneReviews
      Summary Clinical characteristics. Spastic paraplegia 3A (SPG3A; also known as ATL1 -HSP) is characterized by progressive bilateral and mostly symmetric spasticity and weakness of the legs. Compared to other forms of autosomal dominant hereditary spastic paraplegia (HSP), in which diminished vibration sense (caused by degeneration of the corticospinal tracts and dorsal columns) and urinary bladder hyperactivity are present in all affected individuals, these findings occur in a minority of individuals with SPG3A. The average age of onset is four years. More than 80% of reported individuals manifest spastic gait before the end of the first decade of life. Most persons with early-onset ATL1 -HSP have a "pure" ("uncomplicated") HSP; however, complicated HSP with axonal motor neuropathy and/or distal amyotrophy with lower motor neuron involvement (Silver syndrome phenotype) have been observed. The rate of progression in ATL1 -HSP is slow, and wheelchair dependency or need for a walking aid (cane, walker, or wheelchair) is relatively rare.
    • Hereditary Spastic Paraplegia GARD
      Hereditary spastic paraplegia (HSP) is a group of hereditary, degenerative, neurological disorders that primarily affect the upper motor neurons. Upper motor neurons in the brain and spinal cord deliver signals to the lower motor neurons, which in turn, carry messages to the muscles. In hereditary spastic paraplegia, upper motor neurons slowly degenerate so the muscles do not receive the correct messages, causing progressive spasticity (increased muscle tone/stiffness) and weakness of the legs. This leads to difficulty walking. As degeneration continues, symptoms worsen. If only the lower body is affected, HSP is classified as uncomplicated or pure.
    • Spastic Paraplegia Type 3a MedlinePlus
      Spastic paraplegia type 3A is one of a group of genetic disorders known as hereditary spastic paraplegias. These disorders are characterized by muscle stiffness (spasticity) and weakness in the lower limbs (paraplegia). Hereditary spastic paraplegias are often divided into two types: pure and complex. The pure types involve only the lower limbs, while the complex types also involve other areas of the body; additional features can include changes in vision, changes in intellectual functioning, difficulty walking, and disturbances in nerve function (neuropathy). Spastic paraplegia type 3A is usually a pure hereditary spastic paraplegia, although a few complex cases have been reported.
    • Spastic Paraplegia 3, Autosomal Dominant OMIM
      A number sign (#) is used with this entry because autosomal dominant spastic paraplegia-3A (SPG3A) is caused by heterozygous mutation in the ATL1 gene (606439) on chromosome 14q22. See also autosomal dominant hereditary sensory neuropathy type 1D (HSN1D; 613708), an allelic disorder with a different phenotype. Description The hereditary spastic paraplegias are a group of clinically and genetically diverse disorders characterized by progressive, usually severe, lower extremity spasticity; see reviews of Fink et al. (1996) and Fink (1997). SPG is classified according to both the mode of inheritance (autosomal dominant, autosomal recessive (see 270800), and X-linked (see 303350)) and whether progressive spasticity occurs in isolation ('uncomplicated SPG') or with other neurologic abnormalities ('complicated SPG'), including optic neuropathy, retinopathy, extrapyramidal disturbance, dementia, ataxia, ichthyosis, mental retardation, and deafness. The major neuropathologic feature of autosomal dominant, uncomplicated SPG is axonal degeneration that is maximal in the terminal portions of the longest descending and ascending tracts (crossed and uncrossed corticospinal tracts to the legs and fasciculus gracilis, respectively).
    • Autosomal Dominant Spastic Paraplegia Type 3 Orphanet
      A rare, pure or complex subtype of hereditary spastic paraplegia, with highly variable phenotype, typically characterized by childhood-onset of minimally progressive, bilateral, mainly symmetric lower limb spasticity and weakness, associated with pes cavus, diminished vibration sense, sphincter disturbances and/or urinary bladder hyperactivity. Additional associated manifestations may include scoliosis, mild intellectual disability, optic atrophy, axonal motor neuropathy and/or distal amyotrophy.
  • Aneurysm Wikipedia
    ., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2020.
    MMP1, NOX4, TIMP1, COL3A1, SLC2A10, TGFBR2, COL5A1, COL5A2, FBN1, FARSB, SMAD3, COL1A1, MYH11, MYLK, NF1, MMP9, PRF1, CXCL8, TNF, IL6, GZMB, CHI3L1
    • Aneurysms Mayo Clinic
      Overview An aneurysm is an abnormal bulge or ballooning in the wall of a blood vessel. An aneurysm can burst. This is called a rupture. A ruptured aneurysm causes bleeding inside the body and often leads to death. Some aneurysms may not cause symptoms. You might not know you have an aneurysm even if it is large. Aneurysms can develop in several parts of the body, including: The body's main artery, called the aorta ( aortic aneurysm ). The part of the aorta that passes through the belly area ( abdominal aortic aneurysm ).
  • Insulin Resistance Wikipedia
    . ^ "Science daily" . Jun 2009. ^ Schinner S, Scherbaum WA, Bornstein SR, Barthel A (June 2005).
    ADRB3, SERPINE1, ADIPOQ, LPL, FABP2, PPARG, PLG, MTTP, LMNA, LEP, TNF, APOB, INSR, AGT, IRS1, ACE, ENPP1, RETN, CD59, ADIPOR2, ADIPOR1, SHBG, LPAL2, ACSM3, PTEN, TPD52, PNPLA3, VWF, NR0B2, PPARGC1A, SLC27A4, SIRT1, TM6SF2, CHDH, ABCG5, ABCG8, PPARA, PDE3B, PKD1, PIK3CG, APOA2, APOA4, APOC4, BCHE, CD36, CETP, CP, CRP, GCG, GYS1, IGF2, IGFBP3, INS, KRT16, LIPA, TRIM37, NOS3, PCSK1, PIK3CA, PIK3CB, PIK3CD, LOC102723407
  • Premature Ejaculation Wikipedia
    Med . 92 (2 Pt 2): 329–31. doi : 10.7326/0003-4819-92-2-329 . PMID 7356224 . ^ Truitt WA, Coolen LM (2002). "Identification of a potential ejaculation generator in the spinal cord".
    SLC6A4, OXTR, APP, PRL, SLC6A3, MMS, PART1, PKD2L1, PDE5A, VIP, SHBG, AR, HTR2C, FLT4, COMT, AVP, STIN2-VNTR
    • Premature Ejaculation Mayo Clinic
      Overview Premature ejaculation occurs in men when semen leave the body (ejaculate) sooner than wanted during sex. Premature ejaculation is a common sexual complaint. As many as 1 out of 3 people say they have it at some time. Premature ejaculation isn't cause for concern if it doesn't happen often. But you might be diagnosed with premature ejaculation if you: Always or nearly always ejaculate within 1 to 3 minutes of penetration Are not able to delay ejaculation during sex all or nearly all the time Feel distressed and frustrated, and tend to avoid sexual intimacy as a result Premature ejaculation is a treatable condition. Medications, counseling and techniques that delay ejaculation can help improve sex for you and your partner.
  • Pregnancy-Associated Malaria Wikipedia
    . ^ a b Mordmüller B, Sulyok M, Egger-Adam D, Resende M, de Jongh WA, Jensen MH, et al. (October 2019).
  • Pectus Excavatum Wikipedia
    Retrieved 7 September 2016 . ^ Fokin AA, Steuerwald NM, Ahrens WA, Allen KE (2009). "Anatomical, histologic, and genetic characteristics of congenital chest wall deformities".
    ABL1, IFT52, ATP6V0A2, LRRC6, RAB3GAP2, NIPBL, COG4, DNAH1, TCTN3, ZBTB20, TBL2, DNAI1, STK36, BBS9, PGAP2, EFEMP2, ZDHHC9, DNAH11, NME8, MBTPS2, ZMYND10, PIGT, MAP3K20, MAGEL2, HYDIN, BCOR, NSUN2, DNAAF5, CCDC40, ARMC4, MSTO1, DNAAF2, KAT6B, TGDS, SIK3, SPECC1L, SMC3, ACTA1, NOG, TRIP4, PIGL, GTF2IRD1, ADAMTSL2, TMEM94, PIEZO1, CUL7, ZEB2, SEC24D, TELO2, MED12, HUWE1, PQBP1, CD96, CCNO, KLHL41, SLC9A6, SEC23B, CRTAP, FBLN5, MRAS, PUF60, MORC2, KDM6B, SYNE2, SYNE1, SETD5, PIGV, PACS1, PGAP3, IFT43, NACC1, CHST14, LRRC56, CCDC151, DNAAF1, PROKR2, DNAJC21, PIH1D3, AMER1, A2ML1, B3GLCT, CCBE1, VPS13B, FAM120AOS, DNAAF4, RSPH9, GAS2L2, PIGW, SH3PXD2B, CCDC39, FREM2, MCIDAS, RSPH4A, DNAAF3, DNAJB13, KIF7, CCDC103, KLLN, CCDC114, DRC1, IFT122, SCARF2, HDAC8, LMOD3, CFAP298, NUP107, SELENON, WDR35, WDR19, PIEZO2, NXN, DNAI2, VPS33A, UPF3B, TMEM43, TMEM231, PALB2, FRAS1, SLC2A10, TTC25, DNAL1, RSPH3, SPRTN, MEGF10, MYPN, PIGO, PPP1R15B, PIGY, CFAP300, CCDC65, RSPH1, BAZ1B, HACD1, SMAD3, KMT2A, FGD1, FGFR3, FHL1, FOXG1, FLNA, FLNB, FMR1, FZD2, GAS8, GPC3, GNB1, GTF2I, HNRNPK, HPGD, HSD17B4, HSPG2, IGBP1, IGF1R, IHH, INPPL1, ITGA7, KRAS, LIG4, LIMK1, LMNA, LMX1B, OFD1, MATN3, MECP2, GPC4, FKTN, FBN1, COL3A1, ACTB, AKT1, ATP7A, BMP2, BRAF, CBL, CBS, CDH11, CFL2, CHRM3, CHRNG, COL1A2, COL2A1, COL11A2, ERF, CREBBP, DHODH, DMD, DNAH5, DVL1, DVL3, DYRK1A, EFNB1, MEGF8, ELN, EMD, EP300, ERCC5, MGAT2, BIVM-ERCC5, MYF5, TGFBR2, SDHC, MYH3, SKI, SLC16A2, SMS, SOS1, SOS2, SOX10, SPAG1, SRY, TBCD, TBX5, TCF20, TGFBR1, TP53, RRAS, TPM2, TPM3, TRIO, CLIP2, WNT5A, PCGF2, SHOC2, PDHX, MFAP5, LZTR1, RBM10, KDM5C, SMC1A, NAA10, SDHB, SDHD, RPS6KA3, MAP2K1, MYL2, NEB, NF1, NFIX, NOTCH3, NRAS, ROR2, DDR2, PIK3CA, CTSA, RPGR, PPP1CB, PPP2R1A, PPIB, MAP2K2, RASA2, RIT1, PTCH1, PTEN, RFC2, PTPN11, ALDH18A1, RET, RAD21, RAF1, PLF, AR, ASD1, EYA1, KRT7, GAL3ST4, ADGRG6, IS1, SCLY, TSPYL2, CDAN1, TAL1, TP63
    • Pectus Excavatum OMIM
      Nowak (1936) traced pectus excavatum in 2 to 4 generations in 12 families; a generation was skipped in 5 families. Stoddard (1939) reported an extensively affected family with a pattern consistent with autosomal dominant inheritance. This deformity also occurs in the Marfan syndrome and some other hereditary disorders. Leung and Hoo (1987) reported 3 Chinese families in each of which there were several instances of pectus excavatum. Male-to-male transmission was seen. Thorax - Pectus excavatum Inheritance - Autosomal dominant form ▲ Close
    • Pectus Excavatum Mayo Clinic
      Overview Pectus excavatum is a condition in which the person's breastbone is sunken into the chest. In severe cases, pectus excavatum can look as if the center of the chest has been scooped out, leaving a deep dent. While the sunken breastbone is often noticeable shortly after birth, the severity of pectus excavatum typically worsens during the adolescent growth spurt. Also called funnel chest, pectus excavatum is more common in boys than in girls. Severe cases of pectus excavatum can eventually interfere with the function of the heart and lungs.
  • Niemann–pick Disease, Type C Wikipedia
    Niemann–Pick Disease Type C . GeneReviews™ [Internet] . Seattle WA: University of Washington, Seattle.
    NPC1, LIPA, NPC2, PDLIM7, APP, SMPD1, PSMB9, ABCA1, RASSF1, CDKN2A, TNF, CHIT1, LINC01193, ERCC2, FCER2, IFNG, LAMP1, LDLR, CD274, MAPT, VEGFA, BACE1, PTCH1, CCL2, SOX2, TP53, ERCC1, H3P10, ATM, CKS1B, SRRM2, APOE, POSTN, APOD, WIF1, CUL9, NBEAL2, SIRT1, TARDBP, SEZ6L, SCO2, ARL2BP, DDX58, APC, TRIM29, DKK3, PDCD4, TMEM97, ANXA6, HDAC6, RAB9A, ATP7B, CD163, TRAF1, UBE2N, UGCG, VHL, VIM, VIP, ZNF154, BSND, ARID1A, ULK1, NR0B2, BECN1, CDK5R1, PER2, ST3GAL5, SPHK1, ARF6, FOXP3, ZMYND10, GDE1, MIR185, NEGR1, NPCA1, H19, STPG4, CELIAC2, ANXA1, MIR10B, MIR130A, MIR203A, RTRAF, MIR31, POU5F1P3, POU5F1P4, UCA1, MIR663A, APOBEC3A_B, UPK3B, CNE-2, NPB, APOBEC3A, ARHGAP42, CKS1BP7, NLK, OTUD4, NLRP2, LPAR5, GBA2, OVOL2, NEUROG2, ROBO3, GORASP1, WNK1, SPNS1, HAVCR2, FATE1, SCGB3A1, CDCA5, SEZ6, OSCP1, TP73, B2M, CP, CD58, GCHFR, GFAP, HCRT, HDAC2, HLA-A, HOXC6, HSPB1, HSP90AA1, IGFBP6, XRCC6, IL1A, IL1B, IL12A, IL17A, JAK2, JUN, JUNB, JUND, GBA, FOSB, THBS1, EGR1, CPT1A, CRP, CTLA4, CTNNB1, DAP, DAPK1, TYMP, S1PR3, EPHA2, FOS, EIF4E, CDKN2B, CDK5, FASN, CDH1, FCN2, FGF2, FOXM1, CD40, SCARB1, LGALS9, SLC6A8, RBM3, RELA, REST, SATB1, BSG, ALB, CCL18, SFRP1, SLPI, CCK, BMP2, BCL2, STAR, STAT3, SYT1, TRBV20OR9-2, TERT, TGFBR1, PLAAT4, PVALB, PTPN12, PTPN6, CAV1, MGMT, MLH1, MMP1, MNAT1, MYC, NBN, CASP8, OSM, OTC, PAK1, ABCB1, PIK3CA, POU5F1, CALR, CALCR, PTK2, CCL5
    • Niemann-Pick Disease Type C GeneReviews
      Summary Clinical characteristics. Niemann-Pick disease type C (NPC) is a slowly progressive lysosomal disorder whose principal manifestations are age dependent. The manifestations in the perinatal period and infancy are predominantly visceral, with hepatosplenomegaly, jaundice, and (in some instances) pulmonary infiltrates. From late infancy onward, the presentation is dominated by neurologic manifestations. The youngest children may present with hypotonia and developmental delay, with the subsequent emergence of ataxia, dysarthria, dysphagia, and, in some individuals, epileptic seizures, dystonia, and gelastic cataplexy. Although cognitive impairment may be subtle at first, it eventually becomes apparent that affected individuals have a progressive dementia.
    • Niemann-Pick Disease, Type C2 OMIM
      A number sign (#) is used with this entry because Niemann-Pick disease type C2 (NPC2) is caused by homozygous mutation in the NPC2 gene (601015) on chromosome 14q24. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene (607623), referred to as type C1 (257220); 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2. The clinical manifestations of types C1 (257220) and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Clinical Features Vanier et al. (1996) reported 5 patients with NPC2.
    • Niemann-Pick Disease Type C Orphanet
      Niemann-Pick disease type C (NP-C) is a lysosomal lipid storage disease (see this term) characterized by variable clinical signs, depending on the age of onset, such as prolonged unexplained neonatal jaundice or cholestasis, isolated unexplained splenomegaly, and progressive, often severe neurological symptoms such as cognitive decline, cerebellar ataxia, vertical supranuclear gaze palsy (VSPG), dysarthria, dysphagia, dystonia, seizures, gelastic cataplexy, and psychiatric disorders.
    • Niemann-Pick Disease, Type C1 OMIM
      A number sign (#) is used with this entry because Niemann-Pick disease type C1 and Niemann-Pick disease type D, also known as the Nova Scotian type, are caused by homozygous or compound heterozygous mutation in the NPC1 gene (607623) on chromosome 18q11. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene, referred to as type C1; 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2 (607625). The clinical manifestations of types C1 and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Historically, Crocker (1961) delineated 4 types of Niemann-Pick disease: the classic infantile form (type A; 257200), the visceral form (type B; 607616), the subacute or juvenile form (type C), and the Nova Scotian variant (type D).
  • Sprained Ankle Wikipedia
    Kerkhoffs GM, van den Bekerom M, Elders LA, van Beek PA, Hullegie WA, Bloemers GM, de Heus EM, Loogman MC, Rosenbrand KC, Kuipers T, Hoogstraten JW, Dekker R, Ten Duis HJ, van Dijk CN, van Tulder MW, van der Wees PJ, de Bie RA (September 2012).
    • Sprained Ankle Mayo Clinic
      Overview A sprained ankle is an injury that occurs when you roll, twist or turn your ankle in an awkward way. This can stretch or tear the tough bands of tissue (ligaments) that help hold your ankle bones together. Ligaments help stabilize joints, preventing excessive movement. A sprained ankle occurs when the ligaments are forced beyond their normal range of motion. Most sprained ankles involve injuries to the ligaments on the outer side of the ankle. Treatment for a sprained ankle depends on the severity of the injury.
  • Benzodiazepine Overdose Wikipedia
    Veterinary and Human Toxicology . 34 (2): 141–3. PMID 1354907 . ^ Wolf BC, Lavezzi WA, Sullivan LM, Middleberg RA, Flannagan LM (March 2005).
  • Alcohol Withdrawal Syndrome Wikipedia
    Ceylon Med J . 54 (2): 63–5. doi : 10.4038/cmj.v54i2.877 . PMID 19670554 . ^ Hunt, WA. (November–December 1993). "Are binge drinkers more at risk of developing brain damage?"
    AR, LEP, MPDZ, CCK, NGF, CYP19A1, KDM4C, GSTM1, NQO1, MALAT1, GLUL, SORCS2, SLC6A3, BDNF, CRH, SLC6A4, DRD2, FKBP5, DBH, GRIN1, GRIN2B, NPY, CCL2, APOE, POMC, PPARA, PPARD, PPARG, SORT1, SLC6A2, COMT, KCNQ4, SLC18A1, SNCA, PIK3CG, ADIPOQ, BMS1, C1D, PPARGC1A, AKT1, TMEM97, PNPLA3, PNOC, NPY5R, PIK3CD, HTR2C, CCKAR, CAT, GAD1, GATA4, GH1, NR3C1, GRM5, TSPO, HDAC2, IL6, PIK3CB, KRT18, LBP, MAOA, ADH1B, NQO2, NPY1R, NPY2R, CFP, PIK3CA, ACACA
  • Dysentery Wikipedia
    Retrieved 15 November 2019 . ^ a b c d Marie, C; Petri WA, Jr (30 August 2013). "Amoebic dysentery" .
    LCT, MME, SLC26A3, IL6, LEP, MPO, TNF
    • Diarrhea Wikipedia
      For other uses, see Diarrhea (disambiguation) . Loose or liquid bowel movements Diarrhea Other names Diarrhoea An electron micrograph of rotavirus , the cause of nearly 40% of hospitalizations from diarrhea in children under five [1] Specialty Infectious disease , gastroenterology Symptoms Loose frequent bowel movements, dehydration [2] Causes Usually infection (viral, bacterial, parasitic) [2] Risk factors Contaminated food or water [2] Prevention Handwashing , rotavirus vaccination , breastfeeding [2] Treatment Oral rehydration solution , zinc supplementation [2] Frequency ≈2.4 billion (2015) [3] Deaths 1.3 million (2015) [4] Diarrhea , also spelled diarrhoea , is the condition of having at least three loose, liquid, or watery bowel movements each day. [2] It often lasts for a few days and can result in dehydration due to fluid loss. [2] Signs of dehydration often begin with loss of the normal stretchiness of the skin and irritable behaviour. [2] This can progress to decreased urination , loss of skin color , a fast heart rate , and a decrease in responsiveness as it becomes more severe. [2] Loose but non-watery stools in babies who are exclusively breastfed , however, are normal. [2] The most common cause is an infection of the intestines due to either a virus , bacterium , or parasite —a condition also known as gastroenteritis . [2] These infections are often acquired from food or water that has been contaminated by feces , or directly from another person who is infected. [2] The three types of diarrhea are: short duration watery diarrhea, short duration bloody diarrhea, and persistent diarrhea (lasting more than two weeks, which can be either watery or bloody). [2] The short duration watery diarrhea may be due to cholera , although this is rare in the developed world. [2] If blood is present, it is also known as dysentery . [2] A number of non-infectious causes can result in diarrhea. [5] These include lactose intolerance , irritable bowel syndrome , non-celiac gluten sensitivity , celiac disease , inflammatory bowel disease such as ulcerative colitis , hyperthyroidism , bile acid diarrhea , and a number of medications. [5] [6] [7] In most cases, stool cultures to confirm the exact cause are not required. [8] Diarrhea can be prevented by improved sanitation , clean drinking water , and hand washing with soap. [2] Breastfeeding for at least six months and vaccination against rotavirus is also recommended. [2] Oral rehydration solution (ORS)—clean water with modest amounts of salts and sugar —is the treatment of choice. [2] Zinc tablets are also recommended. [2] These treatments have been estimated to have saved 50 million children in the past 25 years. [1] When people have diarrhea it is recommended that they continue to eat healthy food and babies continue to be breastfed. [2] If commercial ORS is not available, homemade solutions may be used. [9] In those with severe dehydration, intravenous fluids may be required. [2] Most cases; however, can be managed well with fluids by mouth. [10] Antibiotics , while rarely used, may be recommended in a few cases such as those who have bloody diarrhea and a high fever, those with severe diarrhea following travelling , and those who grow specific bacteria or parasites in their stool. [8] Loperamide may help decrease the number of bowel movements but is not recommended in those with severe disease. [8] About 1.7 to 5 billion cases of diarrhea occur per year. [2] [5] [11] It is most common in developing countries , where young children get diarrhea on average three times a year. [2] Total deaths from diarrhea are estimated at 1.26 million in 2013—down from 2.58 million in 1990. [12] In 2012, it was the second most common cause of deaths in children younger than five (0.76 million or 11%). [2] [13] Frequent episodes of diarrhea are also a common cause of malnutrition and the most common cause in those younger than five years of age. [2] Other long term problems that can result include stunted growth and poor intellectual development. [13] Play media Video explanation ( script ) Contents 1 Definition 1.1 Secretory 1.2 Osmotic 1.3 Exudative 1.4 Inflammatory 1.5 Dysentery 2 Health effects 3 Causes 3.1 Infections 3.1.1 Sanitation 3.1.2 Nutrition 3.2 Malabsorption 3.3 Inflammatory bowel disease 3.4 Irritable bowel syndrome 3.5 Other diseases 3.6 Medications 4 Pathophysiology 4.1 Evolution 5 Diagnostic approach 5.1 Chronic diarrhea 6 Prevention 6.1 Sanitation 6.1.1 Hand washing 6.1.2 Water 6.2 Vaccination 6.3 Nutrition 6.3.1 Breastfeeding 6.4 Others 7 Management 7.1 Fluids 7.2 Eating 7.3 Medications 7.4 Alternative therapies 8 Epidemiology 9 Terminology 10 See also 11 References 12 External links Definition Bristol stool chart Diarrhea is defined by the World Health Organization as having three or more loose or liquid stools per day, or as having more stools than is normal for that person. [2] Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days, by World Gastroenterology Organization . [14] Secretory Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a cholera toxin that stimulates the secretion of anions , especially chloride ions (Cl – ). Therefore, to maintain a charge balance in the gastrointestinal tract , sodium (Na + ) is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is isotonic with plasma even during fasting. [15] [16] It continues even when there is no oral food intake. Osmotic Osmotic diarrhea occurs when too much water is drawn into the bowels.
  • Medical Abortion Wikipedia
    Medical abortion Background Abortion type Medical First use United States 1979 ( carboprost ), West Germany 1981 ( sulprostone ), Japan 1984 ( gemeprost ), France 1988 ( mifepristone ), United States 1988 ( misoprostol ) Gestation 3–24+ weeks Usage Medical abortions as a percentage of all abortions France 64% (2016) Sweden 92% (2016) UK: Eng. & Wales 62% (2016) UK: Scotland 83% (2016) United States 39% (2017) Infobox references A medical abortion , also known as medication abortion , occurs when pills are used to bring about an abortion . The recommended regimen consists of a combination of medications, starting with mifepristone followed by misoprostol . [1] Mifepristone followed by misoprostol for abortion is considered both safe and effective throughout a range of gestational ages. [2] When mifepristone is not available, misoprostol alone may be used. Contents 1 Medical use 1.1 Through 12 weeks gestation 1.2 After 12 weeks gestation 1.3 Self-administered medical abortion 1.4 Telehealth 1.4.1 Clinic-to-clinic 1.4.2 Direct-to-patient 2 Contraindications 3 Adverse effects 3.1 Management of bleeding 3.2 Complications 4 Pharmacology 5 Frequency 6 History 7 Society and culture 7.1 "Reversal" controversy 7.2 Cost 8 References 9 External links Medical use [ edit ] 200 mg mifepristone and 800 mcg misoprostol, the typical regimen for early medical abortion. Through 12 weeks gestation [ edit ] For medical abortion prior to 12 weeks gestation, the World Heath Organization recommends mifepristone 200 mg by mouth followed 1–2 days later by misoprostol 800 mcg inside the cheek, vaginally, or under the tongue; misoprostol may be repeated to maximize success. [3] The success rate of mifepristone followed by one dose of misoprostol through 10 weeks pregnancy is 96.6%. [4] Those who took misoprostol less than 24 hours after mifepristone had higher failures rates compared to women who waited 1–2 days. [5] The National Abortion Federation (NAF) also recommends a mifepristone and misoprostol combination regimen. For medication abortion up to 10 weeks of pregnancy, 200 mg mifepristone is taken followed in 24 to 48 hours by 800 mcg misoprostol.
  • Meningioma Wikipedia
    PMID 17695387 . ^ Taylor BW, Marcus RB, Friedman WA, Ballinger WE, Million RR (August 1988).
    NF2, AKT1, BAP1, SMARCB1, PDGFB, SMARCE1, PTEN, SUFU, MLLT10, WRN, PGR, SMO, TRAF7, KLF4, HES1, CST3, CSTB, CTSL, ALAD, PIK3CA, ARMC5, DNMT1, CHEK2, NF1, KRIT1, CCM2, MIB1, SEC23B, TERT, MN1, MKI67, SDHD, MMP9, VEGFA, CDKN2A, GNAS, TP53, PDCD10, NTHL1, EPB41L3, KLLN, ESR1, EGFR, SDHB, SST, SDHC, LMNA, ERBB2, LOC110806263, SSTR2, EGF, MMP2, STAT3, PIK3CB, CTNNB1, IGF2, PIK3CD, PIK3CG, CD274, AZIN2, MEN1, PLAU, TP73, GADL1, CTSB, CASP3, MTHFR, TIMP1, PTGS2, ARHGAP24, IL6, FGF2, MGMT, MTOR, NDRG2, MIA2, MB, HTC2, GSTT1, MDM2, H3P10, MAPK1, TGFA, TIMP3, ABCB1, CCND1, CD44, BCL2, MAPK3, S100B, AQP4, CASP8, APC, ACKR3, MEG3, BCR, MCM7, PRDM2, XRCC1, TOP2A, HOXA9, CDKN2C, EDN1, SPP1, ATM, IGF1, ASL, PTPRJ, AQP1, LEPR, HPGDS, MIR29C, TNC, TGFB1, S100A1, PLAUR, ODC1, PCNA, SFRP1, ACTB, CDH1, FOS, AP1B1, PDGFRB, MYC, MTRR, CD34, EPHB2, PLG, TGM2, GSTP1, TIMP2, SPARC, HIF1A, TXNIP, IL1B, CCL2, IGFBP5, GNRH1, EEF1E1, GSTM1, CXCL12, PTTG1, YAP1, SLC9A3R1, DLC1, RAD54L, RPS6KB1, RB1, NR3C1, MAFK, KDR, MYCN, PON1, POLR2A, MSH2, VIM, COX2, MUC1, IGF2BP1, RAC1, UBE2I, UBE2D1, PDCD1, NOS2, NOTCH1, NOTCH2, THBS1, KMT2A, MLH1, MIF, PTGDS, TAT, XRCC3, STAT6, YWHAZ, CXCR4, MCM2, PTN, SMAD4, PTX3, LGALS3, STMN1, LAMC2, GJA1, ZNF197, GFAP, ATRAID, CADM1, BSG, ERBB3, CA9, CTAG1A, CAV1, CCK, CCND2, TPPP2, EIF4A2, CD68, PRAP1, EDNRB, LAMTOR1, MIR200A, TCHP, DCC, CDKN2B, CYP2D6, CXCL16, MINDY4, CFL1, CKS2, CTAG1B, CXCR6, WNK2, CSF2, CD276, BRCA1, EPB41, H3P12, AHR, FOXM1, FAS, FGF9, AP2B1, AR, ALPL, BIRC5, ANPEP, MIR224, FGFR3, ETV6, MIR219A1, RASSF1, MTCO2P12, DOT1L, TNF, MIR205, CLDN5, MAK16, TRP-AGG2-6, SLC25A21, TLR4, DPP9, PGR-AS1, BRIP1, LINC02210-CRHR1, TYMS, CAMKMT, H3P47, KCNH6, MAP1LC3B, SMARCA1, H3P9, TYK2, TTR, MNS16A, TXNRD1, SESN2, TXN, HIRA, TLE3, FSCN1, MTDH, NEK9, TCF12, TUBB, MIR34A, C10orf53, H19, TDO2, TCN2, ZEB1, ZBTB7C, TCEA1, ZAR1, LINC01194, MIR145, MIR21, MIR190A, TGFB3, MIR335, TJP1, SOX10, SOAT1, FAT3, SOD3, RBM45, NKX2-1, PLB1, CBLL2, THY1, TMEM30B, TRPV3, SP100, IDO2, DHFR2, RHBDF2, UCHL1, VHL, MUL1, PART1, CD163, SRRM2, TSPAN12, SMUG1, SRSF11, SNHG1, LARGE1, KIF4A, CLDN1, AIP, PPM1D, PROM1, CFLAR, EGFL6, IL18R1, ADAM23, TNKS, TP63, PSMG1, LGR5, RPL13A, ADIPOQ, SYNM, SEC31A, MRPL28, OGA, NES, SUB1, RALBP1, MSLN, PMEL, UBE2C, EBI3, CORO1A, KIF20A, PPIF, TSPAN2, DNM1L, ABCC5, HNRNPDL, KIF14, PIEZO1, AKAP12, LMO4, TIPARP, UCN, VSIR, NDC1, DIABLO, PNO1, XDH, ADAMTSL3, TXNDC16, WT1, TRPV4, LRRC4, TRPV1, RASAL1, PDLIM2, VIP, MMP25, EZR, NDRG4, MLPH, HMGN5, VDR, VDAC2, SMG8, YY1, DPP8, ARID4B, TAGLN2, PLA2G6, DKK3, RBMS3, TMEM97, AXIN1, SETD2, ARID1A, NXT1, RACGAP1, CLTCL1, TCL1A, PSCA, BICRA, TFPI2, KCNIP3, EXOSC3, PLA2G7, WWOX, SIX1, A1BG, SGK1, GH1, EIF4A1, EDNRA, DVL3, DUSP2, DSP, DRD1, DPP4, DMD, DHCR24, DEFB1, DEFA5, DDX3X, GADD45A, DCX, DCT, CD55, DAB2, CYP19A1, CYP1B1, CYP1A1, CYC1, CXADR, CX3CR1, CTLA4, CCN2, VCAN, CSF3, EIF4E, EIF4G1, EIF5A, F13A1, GAPDH, GABPA, FOLR1, FLT1, FGFR1, FGF13, FCGR3B, FCGR3A, FCER1G, FASN, FBLN1, FAP, F3, ELAVL1, ETS1, ETFA, ERCC5, ERCC4, ERCC2, ERBB4, EPO, EPHA1, EPAS1, ENO2, ENG, ELAVL4, CRYAB, CRHR1, CLDN7, ARNT, CALM3, CALM2, CALM1, CALCA, CAPN5, C1QBP, BRCA2, BRAF, BMP4, BCL6, ATP5F1B, STS, AREG, RUNX3, AQP5, KLK3, APOE, APOA1, ANG, ALOX5, ALDH1A3, ALDH1A1, AGTR2, JAG1, ADCYAP1R1, ABCA2, CAPN1, CBS, CPA1, CDK6, COX8A, KLF6, COL5A1, COL1A2, CNR1, CMM, CCR6, CETN3, CETN2, CENPF, CDKN1C, CDKN1A, CDK4, CCKAR, CDK2, CDC25A, CDK1, CD81, CD70, CD69, CD63, CD33, CD9, CD8A, CCNB1, CCKBR, GCG, GJB2, SFRP4, GLI1, PLA2G2A, PLA2G1B, PGF, PDGFRA, PDGFA, PAX5, PRKN, PAK1, SERPINE1, NAT2, OGN, OMD, NT5E, NPY2R, NOS3, NOS1, NME1, NFKB1, NFE2L2, NBN, MUTYH, MMUT, MUC4, MTR, COX1, MSN, MSH3, PODXL, POLD1, PPARA, PTK2, SET, CX3CL1, SAI1, S100A10, S100A6, S100A4, ROS1, RFC1, RDX, RANBP2, RAC3, PTPRC, PTHLH, PPID, PTGS1, PTGER4, PTCH1, PTBP1, KLK6, PROP1, PRLR, PRL, MAPK8, PRKCD, PRELP, PTPA, ABCC1, MMP11, MMP1, HOXA3, IGFBP7, IGFBP6, IGFBP2, IGF1R, IFNB1, IFNA2, HSF1, HRAS, HPRT1, HOXD@, HOXA10, HOXA7, HOXA@, IL13, HNRNPC, HLA-DRB1, HLA-DQB1, HLA-A, HGF, HFE, GSTM3, GSC2, GRB2, GPX1, GOT2, GNRHR, IL2, IDO1, MME, LTBP2, CD99, MET, MEIS1, MDM4, MDK, MCM6, MCM5, MCM4, MCM3, MAPT, SMAD2, SMAD1, CYP4F3, ING2, LGALS1, LEP, KRAS, KIFC1, KIF11, KCNMA1, JAK3, JAK2, JAK1, ITGB1, ITGA3, INS, OPHN1
    • Meningioma GARD
      Meningioma s are tumors that originate in the meninges , the membranes that surround the brain and spinal cord. Most meningiomas are not cancerous ( benign ), though a minority of meningiomas can be classified as atypical or cancerous ( malignant ). Though rare, malignant meningiomas can be highly aggressive. However, even benign meningiomas can cause problems if their growth affects neighboring areas of the brain. Though most meningiomas grow slowly, there is no way to predict the rate of growth for a particular meningioma or to know how long a specific meningioma was growing before it was diagnosed. Signs and symptoms can vary but may include seizures, headaches, weakness in the arms and legs, and vision loss.
    • Meningioma Orphanet
      A rare, mostly benign, neoplastic disease characterized by a primary tumor of the meninges, usually located intracranially (~90%) but spinal meningiomas occur as well. Clinical symptoms relate to the location of the tumor and may include seizures, focal neurological deficits (sensory-motor or visual symptoms, cranial nerve dysfunction), vascular complications (occlusion of cerebral blood vessels, deep venous thrombosis, pulmonary embolism), chronically increased intracranial pressure neurocognitive impairment and/or loss of bladder/anus sphincter control. Epidemiology In adults, intracranial meningiomas represent approximately 30% of central nervous system tumors. The male to female ratio is 1:3.5. Clinical description Whilst meningioma may appear at any age, it is predominantly diagnosed between the third and sixth decade of life. Meningiomas typically appear as broad-based dural hemispheric or oval lesions, attached to the dura mater.
    • Meningioma Mayo Clinic
      Overview A meningioma is a tumor that arises from the meninges — the membranes that surround the brain and spinal cord. Although not technically a brain tumor, it is included in this category because it may compress or squeeze the adjacent brain, nerves and vessels. Meningioma is the most common type of tumor that forms in the head. Most meningiomas grow very slowly, often over many years without causing symptoms. But sometimes, their effects on nearby brain tissue, nerves or vessels may cause serious disability. Meningiomas occur more commonly in women and are often discovered at older ages, but they may occur at any age.
    • Meningioma, Radiation-Induced OMIM
      Following radiotherapy, secondary cancer may occur after a long latent period. Zattara-Cannoni et al. (2001) reported cytogenetic studies of 6 cases of radiation-induced meningiomas. Two of the cases occurred after radiation for tinea capitis, after an interval of 17 and 54 years, respectively; in the first of these cases, local recurrence occurred after an additional period of 29 years. Using spectral karyotyping (SKY) and comparative genomic hybridization (CGH), Zattara-Cannoni et al. (2001) found that all 6 cases had the same chromosome abnormality, t(1;22)(p11;q12). They suggested that a gene on chromosome 1p11 is involved in radiation-induced meningiomas.
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