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  • Mixed Connective Tissue Disease Wikipedia
    In some studies these patients become reclassified over time with other diseases, such as rheumatoid arthritis in 9%, SLE in 15%, and scleroderma in 21% of cases. [27] Such progression is, in part, determined genetically, thus SLE is more likely in patients with HLA-DR3 and scleroderma in patients with HLA-DR5. [24] Epidemiology [ edit ] The prevalence of MCTD is higher than that of dermatomyositis and lower than that of SLE. [28] In a 2011 Norwegian study, the prevalence of MCTD was 3.8 per 100,000 adults, with an incidence of 2.1 per million per year. [29] MCTD is much more frequent in women than in men at between a 3:1 to 16:1 ratio, and in women younger than 50. [10] The general age at onset is around 15–25 years old. [ citation needed ] See also [ edit ] Autoimmunity Overlap syndrome Rheumatoid arthritis Autoimmune disease Scleroderma Systemic lupus erythematosus Polymyositis Rheumatology References [ edit ] ^ a b Rapini RP, Bolognia JL, Jorizzo JL (2007).
    RNPC3, LSM2, HLA-DRB1, SNRNP70, HLA-DRB4, RBM45, TRBV20OR9-2, FSCN1, SNRPA, HNRNPDL, RO60, TRB, TNF, SFTPD, TNFRSF1A, CDR3, PIK3R3, CD40LG, CDK2AP2, SUB1, PTBP1, BTG3, RPP14, POLG2, LAMTOR2, SF3B6, ENAH, NT5C1A, IL17F, H3P44, S100A9, PON1, PSMD12, HNRNPAB, COL17A1, CRP, DSG3, ERG, F8, FOS, CBLIF, HLA-DOA, HLA-DPB1, HLA-DQA1, HLA-DQB1, HLA-DRB3, HNRNPC, CDKN2A, IFNA1, IFNA13, IL2RA, IL6, IL10, IL12B, IL17A, IRF7, MPP1, MUC1, NCAM1, P4HB, H3P8
    • Mixed Connective Tissue Disease Mayo_clinic
      Overview Mixed connective tissue disease (MCTD) has signs and symptoms of a combination of disorders — primarily lupus, scleroderma, and polymyositis. Many people with this uncommon disease also have Sjogren's syndrome. For this reason, mixed connective tissue disease (MCTD) is sometimes called an overlap disease. In mixed connective tissue disease, the symptoms of the separate diseases usually don't appear all at once. Instead, they tend to occur over a number of years, which can complicate diagnosis. Early signs and symptoms often involve the hands. Fingers might get puffy, and the fingertips become white and numb, often in response to cold exposure.
    • Mixed Connective Tissue Disease Orphanet
      Mixed connective tissue disease (MCTD) is a rare connective tissue disorder combining clinical features of systemic lupus erythematosus (SLE), systemic sclerosis (SSc), polymyositis (PM) (see these terms) and/or rheumatoid arthritis (RA). Epidemiology The exact prevalence of MCTD is unknown, except in Japan where it is estimated at 1/37,000. MCTD is found in all ethnic groups with a female-to-male ratio of approximately 10:1. Clinical description Onset usually occurs between 15 and 35 years old. Common clinical signs include Raynaud's phenomenon (see this term), arthralgia/arthritis, swollen hands/puffy fingers, sclerodactyly, and myositis.
    • Mixed Connective Tissue Disease Gard
      Mixed connective tissue disease (MCTD) is a rare autoimmune disorder that is characterized by features commonly seen in three different connective tissue disorders: systemic lupus erythematosus , scleroderma , and polymyositis . Some affected people may also have symptoms of rheumatoid arthritis . Although MCTD can affect people of all ages, it appears to be most common in women under age 30. Signs and symptoms vary but may include Raynaud's phenomenon ; arthritis; heart, lung and skin abnormalities; kidney disease; muscle weakness, and dysfunction of the esophagus. The cause of MCTD is currently unknown. Treatment may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) , corticosteroids and immune-suppressing drugs to help manage symptoms.
  • Glycogen Storage Disease Type Iv Gene_reviews
    Of 42 affected individuals, 37 had at least one identifiable variant detected by sequencing analysis; 28 individuals had biallelic pathogenic variants, and six had one identifiable pathogenic variant, implying that the second causative variant was not identified. 6.
    GBE1, RBCK1, COL1A2, G6PC, GAA, KCNJ3, KCNJ6, KCNJ12, RNF31, SEMA6A
    • Glycogen Storage Disease Due To Glycogen Branching Enzyme Deficiency Orphanet
      Glycogen branching enzyme (GBE) deficiency (Andersen's disease or amylopectinosis), or glycogen storage disease type 4 (GSD4), is a rare and severe form of glycogen storage disease which accounts for approximately 3% of all the glycogen storage diseases (see these terms). Clinical description Clinical presentation is extremely heterogeneous and involves the liver or the neuromuscular system. In the classical form, children are normal at birth, but develop hepatomegaly, hypotonia, and developmental delay during their first months. The disease then rapidly progresses to cirrhosis with portal hypertension and ascites, ultimately causing death in early childhood. A non-progressing hepatic form has been reported in a few cases. In the neuromuscular presentation, the age of onset ranges from fetal to adult age.
    • Glycogen Storage Disease Type Iv Wikipedia
      Human disease Glycogen storage disease type IV Other names Andersen's triad , Andersen’s Disease [1] Glycogen Specialty Endocrinology , medical genetics , hepatology Glycogen storage disease type IV is a form of glycogen storage disease , which is caused by an inborn error of metabolism . It is the result of a mutation in the GBE1 gene, which causes a defect in the glycogen branching enzyme. Therefore, glycogen is not made properly and abnormal glycogen molecules accumulate in cells; most severely in cardiac and muscle cells. The severity of this disease varies on the amount of enzyme produced. Glycogen Storage Disease Type IV is autosomal recessive, which means each parent has a mutant copy of the gene but show no symptoms of the disease.
    • Glycogen Storage Disease Type 4 Gard
      Glycogen storage disease type 4 (GSD 4) is part of a group of disorders which lead to abnormal accumulation of glycogen (a storage form of glucose) in various parts of the body. Symptoms of GSD 4 usually begin in infancy and typically include failure to thrive ; enlarged liver and spleen (hepatosplenomegaly); and in many cases, progressive liver cirrhosis and liver failure. In rare cases individuals may have a form with non-progressive liver disease, or a severe neuromuscular form. GSD 4 is caused by mutations in the GBE1 gene and is inherited in an autosomal recessive manner. Treatment typically focuses on the specific symptoms that are present in each individual.
  • Liver Disease Wikipedia
    Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and oxidative stress. [27] [28] [29] In addition, activation of neutrophils in alcoholic liver disease contributes to the pathogenesis of hepatocellular damage by releasing reactive oxygen species (which can damage DNA). [30] The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis. [30] However, as reviewed by Nishida et al., [24] alcohol exposure, causing oxidative DNA damage (which is repairable), can result in epigenetic alterations at the sites of DNA repair.
    ABCB4, SERPINA1, AFP, GPT, TNF, GGT1, NR1H4, ATP7B, NPC1, CCL2, MMP9, HMOX1, NOS2, NFKB1, CCR2, MTHFR, SCO1, CSF3, HSPA1A, SORT1, SRSF5, TIMP3, NQO1, CRISPLD2, ALPL, HPGDS, COL3A1, CYP7B1, SC5D, IL1RAP, LTB4R, ENO3, MRPS23, TYROBP, CD86, TXN, CD3D, RNASE6, CCK, SOD1, IL1R2, DDAH1, TM4SF4, ACTA2, SOCS1, IL11, HK3, TREM1, IL9R, BCL2L1, INS, GNG8, GABRR2, CD79B, AHR, JUP, ALAD, CYP2E1, GRK5, NRP1, RAC1, TGM1, ALOX5AP, SOCS3, AMACR, ASAH2, ITGB6, SULT1E1, SERPINE1, CCR1, ST8SIA1, CYP1A2, LAT, FAS, TRMU, DPYD, MDM2, HLA-DOA, DNAJA2, FASLG, ARG1, TM6SF2, IFNA1, GOLM1, ALB, IL10, MIR122, PNPLA3, KRT18, SPP1, NFE2L2, HLA-DRB1, IL18, HAMP, FBL, ABCB11, IL6, IFNL3, HFE, IFNA13, TGFB1, SLC17A5, IL17A, UGT1A1, TP53, IFNG, HGF, TLR4, ADIPOQ, GGTLC4P, ATP8B1, GGTLC5P, GGT2, GGTLC3, FECH, GABPA, APOE, IL33, CXCL10, IL1B, PPIG, F2, KRT8, ALDH2, LOC102724197, GGTLC1, LEP, REN, RBM45, LGALS3BP, CCL4, CYP2B6, GCG, STAT4, FAH, IL22, PPARA, CFTR, ADH1C, CD14, MBL2, CDKN2A, ABCD1, XPR1, NLRP3, TIMP1, GPBAR1, HAVCR2, ADH1B, CXCL12, GOLPH3, CYP2C19, CHI3L1, TLR3, IGF1, CCR5, BCL2, TERT, CTNNB1, PTEN, CCN2, FGF21, VIPR1, ABCC2, IL2, IGFBP1, IL1RN, IL4, APLN, TNFRSF1B, CXCL8, TLR2, CP, IGF2, SIRT1, CD1D, CD40, EXT1, IL1A, MMRN1, IL37, IFNA2, GFER, AKT1, LIPA, ACTB, AKR1B10, IL21, PTGS2, GSTP1, PRKCSH, VDR, MTTP, GNMT, NAT10, GDF2, HLA-DQA1, ATHS, H3P10, VWF, VTN, MBOAT7, ANGPT1, SLPI, PDCD1, AKR1A1, MIR34A, HADHA, CCL27, ADAMTS13, ACE2, CX3CL1, PIK3CA, ALPP, PIK3CG, NOS3, PIK3CD, ASRGL1, PIK3CB, PF4, TNFRSF11B, VEGFA, LTA, MIR223, CYP3A4, THPO, CEACAM5, DGUOK, SERPINA3, FGF19, ACE, CYP7A1, PDLIM3, STAT3, CYP2D6, SMAD3, MAPK1, CST3, LGALS3, MAPK14, CR1, NR1I2, DDC, ESR1, PON1, SST, TMBIM4, ATRNL1, IL23A, PPARG, LBP, PTPN1, LCN2, POLDIP2, FST, RETN, POSTN, CD274, MPI, RDX, HLA-DPB1, RNF19A, PSG2, SLCO1B1, HLA-DRB3, LMNA, ABCB6, KRAS, PAEP, HNF4A, KDR, MGMT, LARS1, PRKAB1, TNFRSF12A, CXCL9, ATP6AP2, RIPK3, SLC25A13, COX2, RBP4, UGT1A7, PGF, HP, GDF15, PTPN2, MMP2, PKHD1, DEPDC5, SLC5A2, AHSA1, CCL5, REXO1L1P, CTLA4, RIPK1, HNF1B, STS, TAP2, CYP1A1, TAP1, CYP2A6, CYP2C9, TNFSF10, IL23R, TXNRD1, TAC1, DECR1, DLAT, APOC3, TFEB, DNASE1, DPP4, APOA1, MICOS13, UBE2B, EGF, MIR200A, ENG, HIF1A, PCSK9, UCP2, CRP, MIR192, TM7SF2, CASP1, TNFAIP6, CASP3, CD19, MIR146A, OPN1SW, BCHE, CDKN1A, MIR221, ATP6AP1, CEBPA, THBS1, CEACAM3, CEACAM7, CLU, TNFSF11, CCR6, HSD17B6, AIMP2, TERC, SERPINC1, BTBD8, CRK, SRY, ST2, MICA, GNAS, ERN1, MSC, ADH1A, GHR, SHBG, GPC3, PSC, IFNL4, CD163, GLI2, GLO1, MTCO2P12, GAPDH, SDC1, CXCL2, LOC110806263, ERVK-6, GSTM1, CXCL16, CXCL11, GRAP2, CCL21, CCL20, ABCG2, DCLK1, BPI, YY1, ANXA2, ANXA1, SOD2, FABP4, AGRP, LCS1, SMPD1, FLT1, F10, CXCR4, ARTN, WNT3A, ALDH1B1, COL18A1, ALDH1A1, AGT, F3, APEX1, FAT1, KMT2D, ST8SIA4, ABCC4, SLC7A5, ARHGEF5, PEMT, CPQ, C1orf61, TRIM22, TFPI2, XRCC1, PAK4, MERTK, CNBP, TFG, XRCC4, WARS2, ABCC3, SLC25A15, TAM, MGAM, SELENBP1, RAPGEF5, TM4SF5, PPP6R2, MRPL28, ISG15, AIP, RGN, PRDX6, HGS, APOBEC3B, IL32, H6PD, S1PR2, CCL4L2, CXCL14, CIR1, TBPL1, SLC9A3R1, FHL5, WASF1, TIMELESS, SQSTM1, IL18BP, KDM5D, WASF2, NR0B2, SOAT2, IKBKG, LGR5, NAMPT, KHSRP, LRPPRC, NR1H3, ARHGEF7, AOC3, BECN1, TNFSF13, NR1I3, TNFRSF10B, SLC23A1, GGH, SLC23A2, MFN2, NAT2, UGT1A6, IVNS1ABP, NLRP6, BHLHE23, CMPK2, REG3G, SLCO6A1, KLF14, TMEM199, IFNLR1, DDX53, BMPER, IMMP1L, EHMT1, MLKL, SPDYA, COPD, IFNL1, MIR7-3HG, STPG4, ATP11C, CELIAC2, HSD17B13, CLNK, CTHRC1, C1QTNF1, CYGB, CPEB4, PDCD1LG2, HM13, TRAPPC9, NBPF3, CCDC115, IL1F10, GPT2, PPP1R15B, KRT90P, TRIM5, GFM1, TSLP, DPP9, TMEM67, DNER, MUC16, SFXN1, IL17F, ACTBL2, ARSH, GSTK1, MIR25, MIR29A, MIR93, POTEKP, MIR338, MIR451A, DELYQ11, POTEM, MSMP, KRT8P3, ZGLP1, SYCE1L, MIR1224, LINC01672, KLRC4-KLRK1, MIR4717, ERVK-20, TP53COR1, ERVK-32, H3P9, MIR27A, MIR224, LRRC37A3, MIR22, ZNF699, SERPINA13P, CCL4L1, MIRLET7C, MIRLET7G, MIR101-2, MIR125A, MIR126, MIR136, MIR148A, MIR149, MIR155, MIR17, MIR18A, MIR191, MIR20A, MIR21, MIR212, MIR219A1, HSD3B7, LIN28A, IGF2BP1, SLC40A1, VPS33B, HAVCR1, NPHP3, SIGLEC7, GLS2, IL17B, ANGPTL3, SLCO1B3, NXT1, ERVW-1, MANEA, CD209, IL20, IL21R, NTM, ASCC1, SEPSECS, SBDS, DCTN4, ZDHHC2, KRT23, CHMP2B, BRD1, NUP62, KHDRBS1, CXCR6, TNFSF13B, FGL2, SUB1, CIT, PSIP1, RASSF1, SEC63, MAN1B1, ACOT7, NID2, KLRK1, PEG10, STAB1, GANAB, RPGRIP1L, POFUT1, SMUG1, CLEC1B, TLR7, CYP39A1, SPHK2, AICDA, BIRC6, CC2D2A, KLHL1, IGDCC4, ZNF410, RBPJP4, CIDEC, NOD2, XYLT2, CARD9, HIF3A, DCLRE1C, CPEB1, CDCP1, MPPE1, AHNAK, ADIPOR2, NEIL1, UGGT1, CFC1, ISYNA1, WDR11, SIRT6, NBAS, DNAJB11, CMPK1, TLR9, ANLN, CCHCR1, UGT1A10, UGT1A8, WT1, UGT1A5, UGT1A9, UGT1A4, UGT1A3, MARCHF5, DPP8, CHDH, IMPACT, RNPC3, XBP1, PTPRO, WNT2B, FUT1, FOXC1, FOXM1, FOXO3, FLNA, FMR1, FN1, MTOR, NR5A2, FUSE, FUT2, IL6ST, G6PC, GALT, GBE1, GC, GCK, GCKR, MSTN, GEM, GH1, FGFR3, FGF7, FGF2, FANCA, DSC3, DSPP, DUSP5, EDN1, EGFR, EGR1, EHHADH, ELN, EPAS1, EPHB2, EPHX1, ERBB4, ESR2, ETV3, EZH2, F5, F8, F9, FABP3, GIP, GJB2, GCLM, HMGB3, FOXA2, FOXA3, ONECUT1, HOXD13, HRC, HSD11B1, HSPA1B, HSPA4, HSPB1, HSPG2, HTR2A, ICAM1, IFNAR2, IGF2R, IGFBP2, IGFBP3, IGFBP6, CCN1, IKBKB, HMGCS2, HMGB1, GLP1R, HMBS, CXCR3, GRB2, GRN, CXCL1, GSPT1, GSTA1, GTF2H1, GUSB, HADH, HARS1, HAS1, HAS3, SERPIND1, HCLS1, HDAC1, CFH, HGFAC, HLA-A, HLA-DRB4, ATN1, SLC26A3, DOK1, ANPEP, XIAP, BIRC5, APLP2, APOB, AQP6, ABCC6, AREG, ASS1, ATD, RERE, ATP12A, ATP4A, AVP, BAGE, BCS1L, CEACAM1, BMP2, BMP4, BMP8B, AIRE, ANGPT2, BUB1, AMBP, ACACA, ACADM, ACADVL, ACHE, ACTG1, ACTG2, ACVRL1, ADAM8, ADAM10, ADAR, ADCYAP1, PLIN2, ADH5, AFM, AGER, JAG1, AGTR1, ALAS2, AKR1B1, BRCA2, SERPING1, DMRT1, COMT, CLDN3, CPOX, CREB1, CREBBP, CRYGD, CSF2, CSF3R, SLC25A10, CTSL, CTSS, CTSZ, CUX1, CYP1B1, CYP17A1, CYP51A1, DCX, AKR1C1, DDX3X, DMBT1, COX8A, COL1A2, VPS51, CNR2, CALR, CASP2, RUNX3, CD34, CD36, CD40LG, CD68, CD151, CDA, CDC25A, CDK4, CDKN2B, CDO1, CDSN, CES1, CFL1, CHUK, CLTC, CNR1, IL2RB, IL7R, WARS1, CCL22, ROS1, S100A4, S100A9, S100B, SERPINB3, SERPINB4, SCN2A, CCL17, CCL19, SELE, IL10RB, SELP, SELENOP, SRSF4, SI, ST6GAL1, ST3GAL4, SKIV2L, SLC2A1, SLC3A2, RORA, ABCE1, RNASE1, RIT2, SEPTIN4, POLG, PPARD, PRF1, PRKAA1, PRKAA2, PRKACA, PRKCZ, MAPK3, MAPK8, MASP1, RELN, PTPN6, PTPN11, PVR, RAD51, RARRES2, RENBP, REST, SLC4A1, SLC4A2, SLC10A1, TGFBR1, TIMP2, TKT, TLE1, TLL1, TLR5, TMSB4X, TNFAIP3, TNFRSF1A, TPMT, TPO, TRPC5, TYRP1, SLC35A2, UGT1A, UGT2B7, UMOD, UROD, VCAM1, VIP, THAS, TGFB2, SOX9, TEP1, SPINK1, SPINT1, SPRR2A, SPTBN1, SRD5A2, AKR1D1, SREBF2, STAT5A, STAT5B, SULT2A1, SYK, ADAM17, TALDO1, TBX1, TCF3, TCF7L2, ZEB1, TEAD1, TMBIM6, PMM2, PLA2G5, PKM, LIG4, CYP4F3, LTBP3, BCAM, SH2D1A, LYZ, EPCAM, SMAD7, MAGEA3, MAT2A, MDM4, MAP3K5, MET, MFGE8, MIA2, ATXN3, MLH1, NR3C2, MMP1, MMP3, LTB, LGALS9, MMP10, LEPR, IL13, IL15, IMPA1, IDO1, INSR, ITGA6, IRF6, IRF7, ISG20, ITPA, ITPR3, JAK2, JUN, KCNJ5, KIR3DL1, KNG1, KIF22, LCAT, LDLR, MMP7, MMP13, PKD1, NTS, OAS1, OAS2, OGG1, OLR1, OPRM1, OSM, OTC, PAH, PAK2, PAK3, PDGFRA, PDGFRB, ENPP2, SERPINF1, PEX1, ABCB1, PHB, PHKG2, PIM1, NUP88, YBX1, MOS, SLC11A2, MPL, ABCC1, MSH3, MT1B, MTAP, MUC2, MUC4, MVK, MYC, MYD88, MYO5B, NAGA, NCAM1, NGF, NGFR, NHS, NM, NOS1, CCN3, H3P40
    • Liver Disease Mayo_clinic
      Overview The liver is an organ about the size of a football. It sits just under your rib cage on the right side of your abdomen. The liver is essential for digesting food and ridding your body of toxic substances. Liver disease can be inherited (genetic). Liver problems can also be caused by a variety of factors that damage the liver, such as viruses, alcohol use and obesity. Over time, conditions that damage the liver can lead to scarring (cirrhosis), which can lead to liver failure, a life-threatening condition. But early treatment may give the liver time to heal. Symptoms Liver disease doesn't always cause noticeable signs and symptoms.
  • Raynaud Syndrome Wikipedia
    People with severe disease prone to ulceration or large artery thrombotic events may be prescribed aspirin. [22] Sympatholytic agents, such as the alpha-adrenergic blocker prazosin , may provide temporary relief to secondary Raynaud's phenomenon. [22] [26] Losartan can, and topical nitrates may, reduce the severity and frequency of attacks, and the phosphodiesterase inhibitors sildenafil and tadalafil may reduce their severity. [22] Angiotensin receptor blockers or ACE inhibitors may aid blood flow to the fingers, [22] and some evidence shows that angiotensin receptor blockers (often losartan ) reduce frequency and severity of attacks, [27] and possibly better than nifedipine. [28] [29] The prostaglandin iloprost is used to manage critical ischemia and pulmonary hypertension in Raynaud's phenomenon, and the endothelin receptor antagonist bosentan is used to manage severe pulmonary hypertension and prevent finger ulcers in scleroderma . [22] Statins have a protective effect on blood vessels, and SSRIs such as fluoxetine may help symptoms, but the data is weak. [22] PDE5 inhibitors are used off-label to treat severe ischemia and ulcers in fingers and toes for people with secondary Raynaud's phenomenon; as of 2016, their role more generally in Raynaud's was not clear. [30] Surgery [ edit ] In severe cases, an endoscopic thoracic sympathectomy procedure can be performed. [31] Here, the nerves that signal the blood vessels of the fingertips to constrict are surgically cut.
    GSTM1, GSTT1, IFNA2, GUCY1A1, IRAK1, AGXT, SLC12A3, SPP1, STAT4, ADAR, TREX1, SAMHD1, COQ2, ADA2, RNF125, IFIH1, RNASEH2B, RNASEH2A, LBR, RNASEH2C, COL4A1, C1QA, C1R, CLCNKB, CRP, TNF, RNPC3, PDE5A, EDN1, CALCA, VWF, F8, TRPM8, SLC29A3, HIF1A, VEGFA, CALCB, CDH5, CDH11, BTG3, HLA-DPB1, TRPA1, TNFRSF14, ANXA5, HMOX1, HTR1B, HLA-DRB1, ESR1, IL6, EGF, KRT10, NOS1, PTGIR, PTX3, S100A12, SAFB, CXCL6, SDHC, ACE, SPARC, GAD1, SSB, GSTM2
  • Vaginitis Wikipedia
    There is no firm evidence to suggest that eating live yogurt or taking probiotic supplements will prevent candidiasis. [24] Studies have suggested a possible clinical role for the use of standardized oral or vaginal probiotics in the treatment of bacterial vaginosis, either in addition to [26] or in place of [27] the typical antibiotic regimens. However, recent articles [28] [29] question their efficacy in preventing recurrence compared with other means, or conclude that there is insufficient evidence for or against recommending probiotics for the treatment of bacterial vaginosis.
    PLG, SOD1, CDR1, GLA, IGFALS, IL2, IVD, MBL2, ABCB1, SLC5A2, TBC1D9, MIR1976
    • Vaginitis Mayo_clinic
      Overview Vaginitis is an inflammation of the vagina that can result in discharge, itching and pain. The cause is usually a change in the balance of vaginal bacteria or an infection. Reduced estrogen levels after menopause and some skin disorders also can cause vaginitis. The most common types of vaginitis are: Bacterial vaginosis. This results from an overgrowth of the bacteria naturally found in your vagina, which upsets the natural balance. Yeast infections. These are usually caused by a naturally occurring fungus called Candida albicans.
  • Vitamin A Deficiency Wikipedia
    However, high-dose supplementation of pregnant women should be avoided because it can cause miscarriage and birth defects . [28] Food fortification is also useful for improving VAD.
    RBP4, PARP1, BMP4, LRAT, TGM1, CYP26A1, HAMP, VCAM1, DGAT1, IREB2, CRP, PIK3CD, PIK3CB, PIK3CA, PIK3CG, BCO2, ALDH1A2, XPR1, ABCB11, IKBKG, ADAM10, FOXP3, SLC40A1, RDH11, BCO1, CHD7, CYBRD1, ABCC11, STRA8, TYR, S100A8, TFRC, ABCC8, APP, TNFRSF17, BDNF, CD14, G6PD, HSD11B1, IL1B, LYZ, FOXO4, NDUFA2, PVALB, RARA, RXRA, ADCYAP1, SCD, SOX9, ST13, MIR363
  • Benign Tumor Wikipedia
    However, undifferentiated benign tumors and differentiated malignant tumors can occur. [26] [27] Although benign tumors generally grow slowly, cases of fast-growing benign tumors have also been documented. [28] Some malignant tumors are mostly non-metastatic such as in the case of basal cell carcinoma . [4] CT and chest radiography can be a useful diagnostic exam in visualizing a benign tumor and differentiating it from a malignant tumor.
    HMGA2, CDKN2A, VEGFA, MYC, AKR1B10, TOP1, SST, MSLN, PTGS2, BRCA1, ERCC1, ABCB1, FASN, LCN2, NQO1, GLP1R, CSF1R, PDIA3, GSTT1, HSF1, TERT, SRF, ID1, SOD2, SLC5A5, SKP2, KRAS, IL1B, IL2, E2F1, PPARA, PLAUR, KDM6A, NOS3, EPHA2, IL18, KCNH2, LTF, NAT1, ATF2, VDR, PLEKHS1, ATM, SNORD50A, DNAJC10, WDR74, BIRC6, LIN28A, NACC1, ENOX2, AHR, APOBEC3A, LIN28B, MIR129-2, SNORD50B, OCLN, ARHGAP45, GPX3, CAT, YY1, APOBEC3B, GPR55, TNFRSF10A, CAPN1, CITED2, GSTO1, TRPV1, DLC1, ASIP, TP53, TSC2, NF2, NME1, BRAF, MUC16, EGFR, CCND1, ERBB2, COX8A, IGF2, PTEN, SMARCB1, IGF1, MDM2, TSC1, SMUG1, H3P10, ESR2, FOLH1, RET, MGMT, CTSB, MIB1, HSP90AA1, HNF1A, NF1, TAS2R38, F9, SSX2, PTCH1, HP, CYP19A1, IL6, CXCL8, MMP13, DAPK1, MMP9, KRT20, CEACAM5, TOP2A, COPS5, CDKN2B, PLAG1, PAX8, SERPINE1, GH1, CCDC6, ADAM12, RASSF1, SSX2B, CTNNB1, MIR21, EGF, MTOR, HMGA1, MIR106B, NPY, STIP1, SEMA4F, DICER1, HPSE, SEMA4D, VSIG4, BCL2, BSG, TUBB3, BTG1, BTG3, AKR1A1, CCNG1, FLOT1, SIRT1, PDLIM7, ABI1, KLK4, PCAP, SCG2, REEP5, TFPI2, NCOA4, FGF23, CUL1, RGS5, CBX4, AKR7A2, RIPK1, ADAM9, TNFRSF6B, TNFRSF11A, CDKN1C, KAT2B, SOCS3, CLDN1, USP6, P2RX6, KIF1A, CDH1, NTN1, CD68, GDF15, NPEPPS, BAG3, BCAR1, CD44, BAK1, CD274, TRIM29, MIR17, AKT1, HT, RAB40A, CNTN4, ZNF367, AFP, THSD7A, RAB40AL, ADH6, C17orf97, LINC01194, MIR10B, ADH4, MIR15A, MIR187, CLIC4, MIR200A, MIR211, MIR23B, MIR17HG, MIR372, MIR373, MIR375, NME1-NME2, ADH1C, SYCE1L, CD24, ADH1B, TMX2-CTNND1, MTCO2P12, HTRA3, AKR1B1, TBRG1, ING5, AQP6, DKK2, RPS6KA6, RABGEF1, HTRA2, IGHV1-12, PSAT1, STOML2, LEF1, IGF2-AS, GDE1, MED15, AQP5, AQP1, SYTL2, BCOR, ANO1, FBXW7, KLK15, KLK3, BIRC5, KLHL1, CPAT1, ELAC2, GAS5, SOX17, RHBDF2, APC, ANXA2, PRDM2, FOSB, WNT5A, CENPF, EXT2, ILK, INSRR, MECOM, KDR, KIT, ETV4, KRT19, ETS1, LGALS3BP, LMNA, LMX1A, LPP, LTBP2, MCAM, ESR1, MEN1, MET, MELTF, MIF, MKI67, MLH1, MMP7, MMP14, COX2, ERG, NDUFAB1, EPHB3, NFE2L2, IL17A, IL16, EZH2, HIF1A, FUS, GABPA, KAT2A, GFAP, GLI1, GLI2, FOS, CXCR3, FN1, FOXM1, HDAC1, HDC, HGF, HLA-DRB1, F3, HOXA7, HOXD8, HPR, HPT, HPV18I2, HRAS, FGFR2, TNC, ICAM1, FBLN1, FAP, IGFBP2, IGFBP3, EIF4E, NME2, NOS1, TGFB1, DNMT3A, SLC2A1, DDIT3, DCN, SNAI1, SOX1, SPP1, SRD5A2, CTSL, SS18, STAT3, TCF7, TG, THBD, SRSF3, TIMP1, TIMP2, CTNND1, TPO, CSE1L, CLDN4, TSHR, TTR, ABCC2, CCR7, CCR5, VIM, VIPR1, SGTA, SFRP1, NOTCH3, PPP2R1B, NRAS, TNFRSF11B, PAX1, PAX3, PCNA, PDGFRB, SERPINF1, EDNRB, PLAU, EDNRA, PLXNA2, POMC, EDN1, ADH1A, SEMG2, PROS1, LPAR1, PTH, DUSP6, PTPRC, RAD51B, RAP1GAP, S100A4, S100A6, S100A12, CCL2, CCL18, SEMA3F, PRKCD
  • Medulloblastoma Wikipedia
    Despite intensive treatment, only four of 66 patients were still alive 5 years after a relapse. [28] A US study involved 161 patients between the ages of three and 21 with a high-risk profile .
    PTCH1, SMO, EWSR1, PMS2, HES1, HEY1, PON1, NOTCH2, IFNG, CD99, TP53, FLI1, MYC, MYCN, CCK, FLII, MGMT, CHGA, CDKN2A, NGFR, EGFR, SMARCB1, IGF1, ABCB1, CDK4, SCG2, ZIC1, RHOV, PIK3CG, PIK3CD, PIK3CB, STK11, PIK3CA, SMS, ENO2, NPY, PDGFRA, BCOR, VIM, VHL, CHP1, CTNNB1, TBC1D9, NGF, SGSM3, SYP, GFAP, TCF3, SSTR2, SST, TIMP1, ABO, SSR2, SSR1, SRC, SPARC, SOX10, SNAI2, SLC6A2, SHH, SFRP1, S100A4, REN, PVT1, PTGS2, TNFRSF1B, ZBTB16, TPM3, UCHL1, AMACR, SIGLEC7, HPGDS, BHLHE22, DNAJC15, NOSIP, NT5C3A, PINX1, MARCKSL1, STK33, WLS, CD276, PHF5A, SLCO6A1, ADGRF3, GSTK1, HOTAIR, DICER1, CHEK2, RASSF1, BTRC, UGCG, VEGFA, VIP, XRCC5, SMARCA5, KHSRP, ABCC3, CLDN10, PSIP1, CLDN6, INA, DCLK1, HDAC9, HDAC5, TUBB3, NDRG1, PTEN, NTRK1, MAP2K1, E2F1, CDK9, CDKN2C, CHGB, COL1A2, CUX1, DCC, DMBT1, EEF1B2P2, POMC, ELK3, EPHB1, ERG, F3, FGFR4, FOXO1, FLT3, CDK6, CDK2, CDH2, CD38, ALB, ANXA2, APC, ASCL1, ASMT, ASPH, ATRX, CCND1, BCL2, BDNF, BRCA2, BRS3, CAPS, CASP3, CD6, FLT3LG, MTOR, GCGR, STMN1, MAP2, MCF2, MDK, MELTF, MNAT1, MRC1, ABCC1, NEUROD2, NEUROG1, NF1, ABR, OPRK1, PAWR, PCSK2, SERPINF1, LIF, KRT19, GH1, KRAS, GIPR, GCLC, GRM1, HCLS1, HCRT, NRG1, HMMR, TLX1, HRAS, IGF1R, IL1B, IL2RB, INSM1, KDR, KIT, H3C9P
    • Primitive Neuroectodermal Tumor Wikipedia
      Not to be confused with pancreatic neuroendocrine tumor , which is also abbreviated as PNET. Primitive neuroectodermal tumor Other names PNET Micrograph of an H&E stained section of a peripheral PNET. Specialty Oncology Primitive neuroectodermal tumor is a malignant (cancerous) neural crest tumor. [1] It is a rare tumor , usually occurring in children and young adults under 25 years of age. The overall 5 year survival rate is about 53%. [2] It gets its name because the majority of the cells in the tumor are derived from neuroectoderm , but have not developed and differentiated in the way a normal neuron would, and so the cells appear "primitive". PNET belongs to the Ewing family of tumors . Contents 1 Genetics 2 Diagnosis 2.1 Classification 2.1.1 Peripheral PNET 2.1.2 PNET of the CNS 3 Treatment 4 See also 5 References Genetics [ edit ] This section needs more medical references for verification or relies too heavily on primary sources .
  • Hereditary Gingival Fibromatosis Wikipedia
    Leblebicioglu, “Hereditary gingival fibromatosis—a review,” Compendium of Continuing Education in Dentistry, vol. 28, no. 3, pp. 138–143, 2007. View at Scopus ^ a b c R.
    SOS1, GINGF2, REST, HGF, TGFB1, MET, IL6, TIMP1, SERPINH1, FN1, VEGFA, IL1B, HPSE, MMP1, EGFR, MMP2, CCN2, CAV1, TGFBR2, TGFB3, THAS, TGFB2, TIMP2, SMN2, SMN1, SHH, TNF, TP53, ACTB, SOCS1, SLC52A2, LINC02605, COMETT, GINGF3, MIR335, MIR93, NRK, PWAR1, ASH1L, NR1I2, SLC25A37, UNC50, PAK4, ENAM, SEMA3E, CD163, MAPK8, MSC, PIK3CA, MAPK1, HBG1, GPT, FGF1, F2R, EZH2, EPHB2, MARK2, EGF, CTNNB1, CDKN2A, CDK9, CDK2, BMP7, BMP2, ASCL1, XIAP, HAS3, HBG2, PIK3R1, HPN, PIK3CG, PIK3CD, PIK3CB, ALB, PCNA, NGF, MMP9, KISS1, IL13, CXCL8, IL7, IGF1, IFNG, ICAM1, HES1, H3P10
    • Fibromatosis, Gingival, 1 Omim
      A number sign (#) is used with this entry because of evidence that gingival fibromatosis-1 (GINGF1) is caused by heterozygous mutation in the SOS1 gene (182530) on chromosome 2p22. One such family has been reported. Description Gingival fibromatosis is a rare overgrowth condition characterized by a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of maxillary and mandibular keratinized gingiva (summary by Hart et al., 2002). Genetic Heterogeneity of Hereditary Gingival Fibromatosis Other loci for gingival fibromatosis have been mapped to chromosome 5q (GINGF2; 605544), chromosome 2p23.3-p22.3 (GINGF3; 609955), and chromosome 11p15 (GINGF4; 611010). GINGF5 (617626) is caused by mutation in the REST gene (600571) on chromosome 4q12. There is some evidence for a locus on chromosome 2p16-p13 (see MAPPING).
    • Fibromatosis, Gingival, 4 Omim
      Description Hereditary gingival fibromatosis is a benign disorder manifested by a slowly progressive overgrowth of the oral gingival tissues, which results in the teeth being partially or totally engulfed by keratinized gingiva (summary by Zhu et al., 2007). For general phenotypic information and a discussion of genetic heterogeneity of hereditary gingival fibromatosis, see GINGF1 (135300). Clinical Features Zhu et al. (2007) reported 2 large unrelated Chinese families with maternally inherited gingival fibromatosis. The disease phenotype was only manifested in the offspring of affected or carrier females, suggesting an imprinting effect. The families could be traced for 5 and 4 generations, respectively. Age at onset was within the first year of life.
    • Fibromatosis, Gingival, 5 Omim
      A number sign (#) is used with this entry because of evidence that gingival fibromatosis-5 (GINGF5) is caused by heterozygous mutation in the REST gene (600571) on chromosome 4q12. Description Gingival fibromatosis-5 is an autosomal dominant benign overgrowth disorder characterized by slowly progressive fibrous enlargement of the keratinized gingival tissues. Affected individuals may have diastema, malposition of the teeth, and prolonged retention of primary teeth. Onset is in the first decade. Treatment by surgical resection is generally followed by regrowth of the gingival tissues (summary by Pehlivan et al., 2009). Clinical Features Pehlivan et al. (2009) reported a large 3-generation Turkish family in which 6 individuals had severe generalized gingival hyperplasia involving both the mandibular and maxillary arches with onset around age 3 years.
    • Fibromatosis, Gingival, 2 Omim
      Description Hereditary gingival fibromatosis is a benign disorder manifested by a slowly progressive enlargement of the oral gingival tissues (summary by Xiao et al., 2001). For general phenotypic information and a discussion of genetic heterogeneity of hereditary gingival fibromatosis, see GINGF (135300). Clinical Features Xiao et al. (2001) reported a 4-generation Chinese family in which gingival fibromatosis manifested in the first year of life. Mapping In a 4-generation Chinese family segregating gingival fibromatosis, Xiao et al. (2001) identified a locus for the condition on chromosome 5q13-q22. A maximum 2-point lod score of 4.31 at D5S1721 (theta = 0.00) was observed.
    • Fibromatosis, Gingival, 3 Omim
      For phenotypic information and a discussion of genetic heterogeneity of hereditary gingival fibromatosis, see GINGF (135300). Clinical Features Ye et al. (2005) ascertained a 5-generation Chinese family with autosomal dominant nonsyndromic hereditary gingival fibromatosis, with onset between 2 to 6 years of age, around the time of tooth eruption. The 12 individuals examined all had typical findings, but gingival involvement was variable, ranging from mild to severe. Mapping By haplotype construction and analysis in a 5-generation Chinese family segregating autosomal dominant hereditary gingival fibromatosis, Ye et al. (2005) identified a novel locus for this disorder, which they designated GINGF3, in an 11.4-cM interval between markers D2S2221 and D2S1788 on chromosome 2p23.3-p22.3. Maximum 2-point and multipoint lod scores of 3.45 and 5.00, respectively, were achieved for this region.
    • Hereditary Gingival Fibromatosis Orphanet
      Hereditary gingival fibromatosis (HGF) is a rare benign, slowly progressive, non-inflammatory fibrous hyperplasia of the maxillary and mandibular gingivae that generally occurs with the eruption of the permanent (or more rarely the primary) dentition or even at birth. It presents as a localized or generalized, smooth or nodular overgrowth of the gingival tissues of varying severity. It can be isolated, with autosomal dominant inheritance, or as part of a syndrome.
  • Pain Management During Childbirth Wikipedia
    . ^ a b c Smith, Caroline A; Levett, Kate M; Collins, Carmel T; Armour, Mike; Dahlen, Hannah G; Suganuma, Machiko (2018-03-28). "Relaxation techniques for pain management in labour" .
    ADRB2, CRK, MAPK14, GCH1, LEP, OPRM1, MAPK1, AIMP2, GRAP2, AHSA1, RNF19A, POLDIP2
  • Tree Nut Allergy Wikipedia
    Neither the identification of the source of a specific ingredient in a parenthetical statement nor the use of statements to alert for the presence of specific ingredients, like "Contains: milk", are mandatory according to FSIS. [25] [26] FALCPA also does not apply to food prepared in restaurants. [27] [28] The EU Food Information for Consumers Regulation 1169/2011 – requires food businesses to provide allergy information on food sold unpackaged, for example, in catering outlets, deli counters, bakeries and sandwich bars. [29] In the United States, there is no federal mandate to address the presence of allergens in drug products.
    HLA-DRB1, CCR1, HLA-A, STAT6, RBM45, NUTM1
  • Toxic Shock Syndrome Wikipedia
    The sole exception was Rely, for which the risk for TSS was still higher when corrected for its absorbency. [25] The ability of carboxymethylcellulose to filter the S. aureus toxin that causes TSS may account for the increased risk associated with Rely. [18] Notable cases [ edit ] Clive Barker , fully recovered, contracted the syndrome after visiting the dentist. [26] Lana Coc-Kroft , fully recovered, contracted the syndrome due to group A streptococcal infection . [27] Jim Henson , d. 1990, contracted the syndrome due to group A streptococcal infection and subsequently died from it. [28] [29] Nan C. Robertson , d. 2009, the 1983 winner of the Pulitzer Prize for Feature Writing for her medically detailed account of her struggle with toxic shock syndrome, a cover story for The New York Times Magazine which at that time became the most widely syndicated article in Times history. [30] Mike Von Erich , d. 1987, developed the syndrome after shoulder surgery: he made an apparent recovery but suffered brain damage and weight loss as a result of the condition; he died by suicide later. [31] References [ edit ] ^ a b c d e f g h i j k l m n o p q r s t u v w x y z Low, DE (July 2013).
    TNF, NOS2, GC, AQP1, C5AR1, HLA-DRA, TBXA2R, SELL, ADM, MIF, MC2R, HMOX1, A2M, CCKBR, ENO2, ELANE, TST, SETBP1, SEA, SLC9A6, IL10, IL17A, TRBV20OR9-2, MYD88, CXCL8, RAB7B, RAB7A, PCSK9, VEGFA, MYOM2, GSTO1, TREM1, GSTO2, CCL28, AGR2, SUMF2, TRBV28, TRBV3-1, MAVS, IL23A, RAB1B, OXA1L, TLR2, HLA-A, ALB, CASR, CD40, EDNRB, EPHB2, FN1, FUT2, HSPG2, SYN1, IFNG, IL1B, IL6, LAMA2, MAPK1, SAG, CCL20, TST1
    • Toxic Shock Syndrome Mayo_clinic
      Overview Toxic shock syndrome is a rare, life-threatening complication of certain types of bacterial infections. Often toxic shock syndrome results from toxins produced by Staphylococcus aureus (staph) bacteria, but the condition may also be caused by toxins produced by group A streptococcus (strep) bacteria. Toxic shock syndrome can affect anyone, including men, children and postmenopausal women. Risk factors for toxic shock syndrome include skin wounds, surgery, and the use of tampons and other devices, such as menstrual cups, contraceptive sponges or diaphragms. Symptoms Possible signs and symptoms of toxic shock syndrome include: A sudden high fever Low blood pressure Vomiting or diarrhea A rash resembling a sunburn, particularly on your palms and soles Confusion Muscle aches Redness of your eyes, mouth and throat Seizures Headaches When to see a doctor Call your doctor immediately if you have signs or symptoms of toxic shock syndrome.
  • Posterior Ischemic Optic Neuropathy Wikipedia
    Progress in Retinal and Eye Research . 28 (1): 34–62. doi : 10.1016/j.preteyeres.2008.11.002 .
    IFNA2
  • Neurodevelopmental Disorder Wikipedia
    The most common nutritional cause of neural tube defects is folic acid deficiency in the mother, a B vitamin usually found in fruits, vegetables, whole grains, and milk products. [26] [27] (Neural tube defects are also caused by medications and other environmental causes, many of which interfere with folate metabolism, thus they are considered to have multifactorial causes.) [28] [29] Another deficiency, iodine deficiency , produces a spectrum of neurodevelopmental disorders ranging from mild emotional disturbance to severe mental retardation.
    TANC2, TBR1, CDKL5, MECP2, STXBP1, SCN2A, CHD2, PTEN, FOXG1, FOXP1, TCF4, GRIN2B, MEF2C, POGZ, SYNGAP1, SCN1A, EEF1A2, SCN8A, DHX30, DDX3X, GABRB3, ZNF292, ARID1B, TRIO, GABRB2, KCNQ2, DLG4, CTNNB1, DYRK1A, MYT1L, ANKRD11, CASK, WDFY3, KCNH1, TCF7L2, BRSK2, HNRNPU, PPM1D, GNAO1, TRIP12, NEXMIF, SETD5, KMT2E, ASH1L, DOCK8, HIVEP3, ALG13, GIGYF2, ASXL3, PAK1, SNAP25, KMT2C, PURA, PHF2, PLXNB1, PAX5, PPP2R5D, CACNA2D3, PTK7, PTPN11, KMT2A, SETD2, LMX1B, WAC, ITPR1, ILF2, SLC6A1, KMT5B, SPAST, KATNAL2, TBL1XR1, RIMS1, CDC42BPB, MED13L, PARD3B, TNRC6B, IQSEC2, SMC3, ADNP, DLGAP1, DNM1, CUL3, WDR45, SETBP1, SMC1A, SRCAP, NCKAP1, SRGAP3, DSCAM, ANK2, CERT1, ADCY5, ZC3H4, EBF3, NRXN1, NKX2-1, CNTNAP2, UBE3A, BRPF1, SHANK3, FMR1, SMARCA1, MBD5, ARSD, MTOR, PRKN, BDNF, PTCHD1, EHMT1, CBLL2, BANF1, ARX, MUL1, FOXP2, GPHN, PVALB, ANK3, CTCF, USP9X, KCNB1, MCPH1, CNTN6, CSNK2A1, L1CAM, AUTS2, DTNBP1, CACNA1C, ARHGEF2, RBFOX1, RELN, GRIN2A, MAGEL2, SATB2, MET, DISC1, ACTL6B, KDM5C, USP7, KDM5B, SNRPN, HUWE1, PHF8, HNF1B, PRS, NRG3, AHDC1, KAT6A, PSMD12, CNTN5, SETD1A, SOX5, SMARCA4, SMARCA2, SOX11, SLC6A3, HERC2, SLC2A1, TRIM32, SHANK2, SLC1A4, TSC2, GREM1, CYFIP2, VEGFA, TLK2, RPL10, BCL11A, ZBTB20, NSUN2, DEAF1, DHPS, SLC2A4RG, WDR62, GRM5, NPAS4, GATAD2B, ZMIZ1, HTR7, HTT, GNB1, MIR137, ATP1A3, ASTN1, HTC2, BCL11B, STRADA, HES1, HECW2, DPP6, KIRREL3, CSNK2B, EIF5A, ELN, CNTN4, NTNG2, DLG2, BPTF, GRM7, CACNA1A, KDM6B, KANK1, TPH2, H4-16, PIK3AP1, FBXW7, ZNF804A, TANC1, RHOBTB2, ARHGEF9, ASTN2, ADGRL3, WWC1, DMXL2, CAPS2, CUX2, NEDD4L, TNPO3, SH2B1, UPF2, NFASC, MICU2, NAXE, WASH6P, ALDH1L1, CCDC88C, MIR379, BDNF-AS, RAI1, H4C15, SNORD116@, MACROD2, PTLS, WASHC1, GNB5, PTCHD1-AS, CXCR6, SLU7, PDE10A, MDD1, MIR219A1, PNKP, DLGAP4, ZNF507, AGMO, NTNG1, TRAK1, LRRTM1, RAB40AL, KCTD13, PHACTR1, SCAMP5, RLS1, VPS13B, RBFOX3, PHF6, NAA15, IMMP2L, CPA6, UGT1A1, ACKR3, NLGN3, RARS2, PCBP4, WWOX, TBC1D24, DPYSL5, FZR1, SLC12A5, SHROOM4, PRR12, KIDINS220, NLGN4X, ANKS1B, FMN2, KLF16, AHI1, ULK4, MEG3, KIF21A, UHRF1BP1, CC2D1A, NDE1, ATG7, GTPBP2, FBLIM1, PPP1R9A, AMBRA1, CHD7, PAG1, MEPCE, PHF21A, PCDH19, SEPSECS, GTDC1, TSPYL2, NPAS3, UPF3B, SECISBP2, MSANTD2, ELP4, PHGDH, HACE1, INTS1, FAM124B, DARS2, FBXO11, NDEL1, APH1B, PRUNE1, EPG5, LRRC4C, ZSWIM6, SRPX2, HPGDS, DLL1, GIT1, CHD8, UNC79, NLGN2, LRRC7, TAOK1, EJM2, EXOSC3, NUFIP2, ATL1, AAVS1, H4C2, ZBTB18, YAP1, GSTP1, GRM2, GRIK2, GRIA4, GRIA2, GPR42, GNAI2, GFAP, GDI1, GABRG3, GABRG2, GABRA1, GAST, FRAXE, FRAXA, FGF2, EZH2, ESR2, ERBB4, ENPEP, EN2, EIF4G1, EIF4EBP2, GUK1, H2AZ1, HCFC1, KIF5C, NCAM2, MTRR, MTR, MRC1, MEF2A, MAPT, MAB21L1, LIMK1, LAMB1, AFF3, KCNQ3, NRG1, KCNMA1, KCNA2, INSR, IL10, IL6, ICAM1, HPRT1, HNRNPH2, HMGN1, UBE2K, EIF4E, EIF4A1, EFNB2, ATP7A, CAPN1, CALR, CALCR, CALB2, CACNA1E, CACNA1D, DAGLA, BRS3, BRAF, AVP, ASNS, CD38, STS, ARNTL, APP, APOE, NUDT2, ADRA2B, ADRA1A, ADCYAP1R1, ADCYAP1, ADAM10, SERPINH1, CDH2, EEF1D, DARS1, EEF1B2, EDNRA, DUSP2, DPH1, DOCK3, DMD, DIO3, DIAPH1, DDX6, BRINP1, CYP2C9, CDH13, CYP2C19, CX3CR1, CTLA4, CRP, CREBBP, KLF6, COL9A3, CHRNA7, CHRNA4, CHD4, NDP, NFIC, CNOT3, H4C5, HDAC3, CCNK, RAB11A, EIF3A, PSMG1, CNTNAP1, SMARCA5, GNPAT, H4C14, H4C13, ACTB, AP1S2, H4C8, H4C3, H4C11, H4C12, H4C6, H4C4, H4C1, FZD9, H4C9, KMT2D, EIF2B2, SNURF, ZNF142, GTF2IRD1, CPQ, RACK1, WARS2, FEM1B, DGCR2, MED13, TLK1, SETDB1, ZEB2, TMEM94, GABBR2, PHOX2B, ATG5, CDYL, NRXN2, NRXN3, LHX2, TAOK2, AP4M1, LPAR2, TOP3B, MBD2, AIMP2, ZNF711, NTRK1, POMC, RNF2, OPN1LW, RARS1, RAC3, PTPN4, PSD, PPP3CA, PTPA, PPP2CA, POU3F3, PLK1, RORB, PIK3CG, PIK3CD, PIK3CB, PIK3CA, PIK3C3, PC, PAFAH1B1, OXTR, ODC1, NR4A2, ROBO1, RYR2, ZFX, SYT1, VIP, VDR, VARS1, NR1H2, SLC35A2, TSC1, HSP90B2P, TLR3, TFE3, TAF1, SYP, SCN3A, VAMP2, SSTR4, SRY, SOX4, SOX3, SNCA, SMARCC2, SMARCB1, SLC6A8, ST3GAL3, ERICD
    • Mental Disorders Diagnosed In Childhood Wikipedia
      April 16, 2013, from http://www.gomentor.com/articles/feeding-and-eating-disorders-of-infancy-or-early-childhood.aspx Archived 2015-05-29 at the Wayback Machine ^ Tic Disorders. Encyclopedia of Mental Disorders. 28 Mar. 2013. http://www.minddisorders.com/Py-Z/Tic-disorders.html ^ "Tic Disorders Treatment." ... Archived from the original on 2013-06-28 . Retrieved 2013-04-04 . CS1 maint: archived copy as title ( link ) ^ "Elimination Disorders and Encopresis in Children."
  • Parkinson Disease 8, Autosomal Dominant Omim
    Saunders-Pullman et al. (2011) examined olfaction in 31 individuals with G2019S-related PD, 30 with non-LRRK2 PD, 28 nonmanifesting G2019S carriers, and 46 controls.
    LRRK2
  • Gingivitis Wikipedia
    Journal of Periodontology . 78 (7): 1218–28. doi : 10.1902/jop.2007.060269 . PMID 17608576 . ^ WebMD Treatments for Gum Disease External links [ edit ] Classification D ICD - 10 : K05.0 - K05.1 ICD - 9-CM : 523.0 - 523.1 MeSH : D005891 DiseasesDB : 34517 SNOMED CT : 66383009 External resources MedlinePlus : 001056 eMedicine : article/763801 v t e Dentistry involving supporting structures of teeth ( Periodontology ) Anatomy Periodontium Alveolar bone Biologic width Bundle bone Cementum Free gingival margin Gingiva Gingival fibers Gingival sulcus Junctional epithelium Mucogingival junction Periodontal ligament Sulcular epithelium Stippling Disease Diagnoses Chronic periodontitis Localized aggressive periodontitis Generalized aggressive periodontitis Periodontitis as a manifestation of systemic disease Periodontosis Necrotizing periodontal diseases Abscesses of the periodontium Combined periodontic-endodontic lesions Infection A. actinomycetemcomitans Capnocytophaga sp.
    ELANE, ITGB2, CTSC, CYBB, TCIRG1, GFI1, B4GALT7, ALMS1, KRT6A, PLG, SRP54, SLC6A19, CYBA, STAT3, OCRL, SAMD9, COL3A1, TSC2, NCF1, LYST, TSC1, CD40LG, TNF, FERMT1, IL1B, NCF4, NCF2, CYBC1, IL6, MMP8, IL17A, MPO, TNFSF11, CRP, BOP, MMP9, IL10, PI3, IL11, IL18, HIF1A, DEFB1, IL1RN, IL1A, TGFB1, TLR4, HMGB1, AHSG, ANXA1, CSF1, NLRP3, PADI4, JMJD6, NT5C2, BMS1, PDLIM7, VEGFA, BHLHE40, PADI2, OGA, KLHDC2, CDK5R1, SMC3, VDR, ACACA, PART1, GORASP1, UPK3B, OPN1MW3, DEFB4B, OPN1MW2, DEFB103A, AMTN, IL34, CDCA5, IL17F, SHCBP1, USB1, WNK1, RETN, LRIT1, DEFB103B, NLRP2, TIMP1, CRCT1, HSPA14, FOXP3, DELEC1, TRBC1, TRBV7-9, TRBV16, APOBEC3C, SMR3A, TLR2, PTHLH, TGM2, KRT19, ITGAL, ISG20, IL13, IL12A, IL4, IL2RA, IFNG, HSPD1, HGF, GOLGB1, OPN1MW, GCHFR, FOLR1, FCN2, ESR1, ECE1, DEFB4A, CST3, CCR6, CCR4, CGA, CBS, CASP1, AHR, AGTR1, ITGAM, LPO, TRBV20OR9-2, LTA, TRB, ADAM17, SYT1, SPIB, SLC2A1, SELE, CCL3, CCL2, S100A12, S100A9, S100A2, RELA, ADAM8, PTGS2, HTRA1, PROS1, PF4, PAM, NOS2, COX2, MNAT1, MMP13, MMP1, CXCL9, LYZ, MTCO2P12
    • Gingivitis Mayo_clinic
      Overview Gingivitis is a common and mild form of gum disease (periodontal disease) that causes irritation, redness and swelling (inflammation) of your gingiva, the part of your gum around the base of your teeth. It's important to take gingivitis seriously and treat it promptly. Gingivitis can lead to much more serious gum disease called periodontitis and tooth loss. The most common cause of gingivitis is poor oral hygiene. Good oral health habits, such as brushing at least twice a day, flossing daily and getting regular dental checkups, can help prevent and reverse gingivitis. Symptoms Healthy gums are firm and pale pink and fitted tightly around the teeth. Signs and symptoms of gingivitis include: Swollen or puffy gums Dusky red or dark red gums Gums that bleed easily when you brush or floss Bad breath Receding gums Tender gums When to see a dentist If you notice any signs and symptoms of gingivitis, schedule an appointment with your dentist.
  • Acanthamoeba Keratitis Wikipedia
    However, these agents have shown limited efficacy against the cystic forms. [12] [24] Due to the efficacy of these drugs against the Acanthamoeba, as well as their low toxicity to the cornea, they are commonly used as the first line medications in the treatment of AK. [12] [21] Biguanides have also been found to act synergistically when used in combination with diamidines, with propamidine isethionate and hexamidine being the most commonly used. [25] A limitation of diamidine use is relative corneal toxicity with long term use. [12] A combined regimen of propamidine , miconazole nitrate, and neomycin has also been suggested. [26] [27] [28] Due to the potential for negative longterm visual outcomes with AK, therapy is usually started with a combination of a biguanide and a diamidine.
    TLR4, ARSA, ERVK-7, ERVK-24, ERVK-25, ERVK-18, ERVK-21, ERVK-9, ERVK-10, DEFB109B, ERVK-8, DEFB103A, BAK1, DEFB103B, IL22, TLR2, IL10, CXCL8, TNC, CXCL2, FN1, ERVK-19
    • Amoebic Keratitis Orphanet
      A rare corneal infection due to the protozoan Acanthamoeba that generally occurs in contact lens wearers and that is characterized by severe ocular pain, blepharospasm, photophobia, eye tearing, blurred vision and foreign body sensation. It can lead to impaired visual acuity if not treated promptly.
  • Cystinosis, Nephropathic Omim
    Of 82 alleles bearing the 65-kb deletion, 38 derived from Germany, 28 from the British Isles, and 4 from Iceland.
    CTNS
    • Infantile Nephropathic Cystinosis Orphanet
      A subtype of cystinosis characterized by an accumulation of cystine in the organs and tissues, particularly in the kidneys and eyes, and that clinically manifests from infancy with renal Fanconi syndrome, photophobia, hypothyroidism, impaired growth and rickets, in addition to various other systemic effects. Progressive extra-renal manifestations include hypothyroidism, hypogonadism and male infertility, insulin-dependent diabetes, hepatosplenomegaly with portal hypertension, muscle involvement with distal muscle weakness and atrophy, pharyngeal and oral dysfunction, swallowing difficulties, cerebral involvement with hypotonia, speech and walking difficulties, and cerebellar syndrome.
  • Eosinophilic Esophagitis Wikipedia
    Current Opinion in Gastroenterology . 28 (4): 382–388. doi : 10.1097/MOG.0b013e328352b5ef .
    TSLP, CAPN14, TRIM8, TNK2, STAT6, JAZF1, EMSY, CCL26, IL13, IFFO2, HSF2BP, LINC02588, ANKRD27, CCDC81, MEAK7, SHROOM3, KIF17, IL5, CLEC16A, DCC, TIMP2, P2RX6, LINC02240, XKR6, CAPN5, CEP295NL, TGFB1, POSTN, FLG, TNF, DSG1, IL33, CCL11, FOXP3, ATP12A, ATP4A, IL4, IL6, IL15, EPC2, SPINK7, WDR36, CLDN7, CPA3, SIGLEC8, MID1, IL18, TNFSF10, SOAT1, EPX, CLDN1, DHTKD1, RNASE2, IL9, FFAR3, ALOX15, BDNF, IL18R1, COPD, LOC283710, IL32, IL1RL1, SLC9C2, SERPINA13P, MIR223, SPAG9, NR1I2, OGDHL, DEFB103A, FST, TNFRSF14, MIR375, EMBP1, BECN1, ABCB11, DEFB4B, BANCR, EOS, CBLL2, RSAD2, TRPV1, HBS1L, DEFB103B, CRLF2, ANO1, OXR1, SLC52A1, RHOF, TLR9, BCL11A, KLF13, CPA4, MUL1, LRRC31, CHIA, ACAD8, PANK2, MAPK8IP2, FIP1L1, SYNPO, PTGDR2, SERPINB12, SPINK5, REEP5, AGA, VCAM1, GFER, ESR2, F2RL1, FGF9, FKBP4, FKBP5, GABPA, LRRC32, GJA1, DNM1, GRM5, HIF1A, ICAM1, IFNG, IL1A, IL1B, IL5RA, ESR1, DEFB4A, TYK2, CD1D, ALOX5, ANXA5, CCND1, BID, BNIP3, CALB2, CAMP, CD44, CYP2C19, CEACAM8, CLC, CCR3, CCR8, ABCC2, COL8A2, CSF2, IL9R, IL15RA, ITGAM, CCL18, KLK6, PTGDR, PTGS2, RNASE3, S100A7, SAFB, CCL2, SGSH, KCNJ2, AGXT, SPRR3, STAT1, STC1, TFDP1, TLR3, TNFRSF4, KLK7, PRG2, PTPA, PLG, LALBA, LCT, LOX, LTC4S, SMAD2, KITLG, MIF, MMP2, MMP14, MPG, MYB, NFE2L2, SLC22A18, OSM, PRKN, SLC9A3
    • Esophagitis, Eosinophilic, 2 Omim
      For a general phenotypic description and a discussion of genetic heterogeneity of eosinophilic esophagitis, see EOE1 (610247). Mapping Rothenberg et al. (2010) genotyped approximately 550,000 genomewide SNPs in a discovery cohort of 181 eosinophilic esophagitis (EOE) cases and 1,974 controls and a replication cohort of 170 EOE cases and 1,130 controls. Significant association was found with variants at a region on chromosome 5q22 encompassing the TSLP (607003) and WDR36 (609669) genes (combined p = 3.19 x 10(-9) for rs3806932). Analysis of esophageal biopsies revealed that TSLP was significantly overexpressed in EOE cases compared to controls (p less than 0.0001 for TSLP isoform 2), whereas WDR36 was unchanged. TSLP expression levels were also significantly correlated with the rs3806932 genotype in EOE cases, with homozygote carriers of the protective minor G allele showing less TSLP expression than heterozygotes or homozygotes for the ancestral allele.
    • Eosinophilic Esophagitis Mayo_clinic
      Overview Eosinophilic esophagitis (e-o-sin-o-FILL-ik uh-sof-uh-JIE-tis) is a chronic immune system disease. With this disease, a type of white blood cell, called an eosinophil, builds up in the lining of the tube that connects your mouth to your stomach. This tube is also called the esophagus. This buildup, which is a reaction to foods, allergens or acid reflux, can inflame or injure the esophageal tissue. Damaged esophageal tissue can lead to difficulty swallowing or cause food to get stuck when you swallow. Eosinophilic esophagitis has been identified only since the early '90s, but is now considered a major cause of digestive system illness.
    • Eosinophilic Esophagitis Orphanet
      A rare chronic, local immune-mediated disease of the esophagus characterized clinically by symptoms of esophageal dysfunction (including, dysphagia, feeding disorders, food impaction, vomiting and abdominal pain) and histologically by eosinophil-predominant inflammation in esophageal biopsies. Epidemiology Prevalence in adults is estimated at 1/2,370 and in children 1/2,900 in Europe and North America; however, a steady rise in incidence and prevalence is observed. Males are predominantly affected (male/female ratio being 2.5). Clinical description Most cases of eosinophilic esophagitis (EoE) present in children and young adults, but it may occur at any age. Infants and toddlers manifest with food refusal, vomiting, choking with meals and in rare cases, failure to thrive. School-aged children most commonly present with dysphagia, choking/gagging with meals, food impactions and, less commonly, regurgitation, vomiting, and chest/abdominal pain.
    • Esophagitis, Eosinophilic, 1 Omim
      Description Eosinophilic esophagitis (EOE) has an incidence of approximately 1 per 10,000 people. Symptoms include difficulty feeding, failure to thrive, vomiting, epigastric or chest pain, dysphagia, and food impaction. Individuals with EOE are predominantly young males with a high rate of atopic disease, and the diagnosis is made by endoscopy and biopsy findings of isolated eosinophils in the esophagus (summary by Rothenberg et al., 2010). Genetic Heterogeneity of Eosinophilic Esophagitis Eosinophilic esophagitis-1 (EOE1) is associated with variation at chromosome 7q11.2. Another locus (EOE2; 613412) has been been associated with variation in the TSLP gene (607003) on chromosome 5q22.
  • Optic Atrophy 1 Omim
    To analyze the influence of OPA1 gene mutations on optic nerve head morphology in patients with dominant optic atrophy, Barboni et al. (2010) studied the optic nerve head of 28 OPA1 mutation-positive patients from 11 pedigrees and 56 age-matched controls by optical coherence tomography (OCT).
    OPA1, DNM1L, OPA3, MFN2, MFN1, DENR, DAPK2, OMA1, FIS1, UTRN, CRMP1, SIRT3, IMMT, MFF, MED12, YME1L1, SSBP1, PRKAB1, NFE2L2, PPARGC1A, PPARG, PRKAA1, KIF1B, OPA5, PRKAA2, GSTM1, FXN, WFS1, SLC14A1, LEP, TOMM70, TOMM40, SQSTM1, YAP1, OPTN, COX5A, MRPS30, MAD2L1BP, KEAP1, PAPOLA, ACO2, TPPP, PACC1, PGAM5, CCDC50, MCU, MAP1LC3B, MUL1, PINK1, TFB2M, OPA4, SEMA6A, ADCK1, MTPAP, TREH, APTX, TMED9, ASAP1, CD274, FGF21, GABARAPL1, TUSC2, CDK5R1, PDAP1, PHB2, ASAP2, TP53BP1, BECN1, CNR2, GABPA, ERG, EPHB2, ELAVL1, DGKG, CYP1B1, CYC1, CTRL, CPOX, COX8A, CDKN1A, AKAP1, CDH1, CAV1, CAST, CAPN1, BNIP3L, BNIP3, CEACAM1, BGLAP, BCL2, AFM, GSTT1, H2AX, HRES1, HES1, VEGFA, PHLDA2, ACP3, CLDN5, SPG7, SOD1, SLC5A1, SDHA, MAPK1, PRKCA, PLXNA2, PLIN1, PKLR, REG3A, NRF1, NOS3, NFE2L1, NDUFV2, MYC, LCN2, LAMP1, OPA8
    • Optic Atrophy Type 1 Gene_reviews
      Summary Clinical characteristics. Optic atrophy type 1 (OPA1, or Kjer type optic atrophy) is characterized by bilateral and symmetric optic nerve pallor associated with insidious decrease in visual acuity (usually between ages 4 and 6 years), visual field defects, and color vision defects. Visual impairment is usually moderate (6/10 to 2/10), but ranges from mild or even insignificant to severe (legal blindness with acuity <1/20). The visual field defect is typically centrocecal, central, or paracentral; it is often large in those with severe disease. The color vision defect is often described as acquired blue-yellow loss (tritanopia). Other findings can include auditory neuropathy resulting in sensorineural hearing loss that ranges from severe and congenital to subclinical (i.e., identified by specific audiologic testing only).
    • Optic Atrophy 1 Gard
      Optic atrophy 1 , also known as optic atrophy type 1 is a disease that affects the optic nerve . The optic nerve carries signals from the eye to the brain about what is seen. People with optic atrophy type 1 have an optic nerve that has lost some tissue ( atrophy ). This atrophy causes the optic nerve not to work as well as it should, which affects the vision. Signs and symptoms of optic atrophy type 1 include vision loss , difficulty distinguishing colors, and an abnormally pale appearance (pallor) of the optic nerve.
    • Dominant Optic Atrophy Gard
      Dominant optic atrophy (DOA) is an inherited optic nerve disorder characterized by degeneration of the optic nerves. It typically starts during the first decade of life. Affected people usually develop moderate visual loss and color vision defects. The severity varies and visual acuity can range from normal to legal blindness. About 20% of people with DOA have non-ocular features, such as sensorineural hearing loss; myopathy ; peripheral neuropathy; multiple sclerosis-like illness; and spastic paraplegia (impaired function of the legs). These cases may be referred to as 'DOA plus.' DOA is inherited in an autosomal dominant manner and may be caused by a mutation in any of several genes, some of which have not been identified.
    • Optic Atrophy 5 Omim
      A number sign (#) is used with this entry because of evidence that optic atrophy-5 (OPA5) is caused by heterozygous mutation in the DNM1L gene (603850) on chromosome 12p11. Description OPA5 is an autosomal dominant form of nonsyndromic optic atrophy, manifest as slowly progressive visual loss with variable onset from the first to third decades. Additional ocular abnormalities may include central scotoma and color vision defects. The pathogenesis is related to defective mitochondrial fission (summary by Gerber et al., 2017). For a discussion of genetic heterogeneity of optic atrophy, see OPA1 (165500).
    • Kjer's Optic Neuropathy Wikipedia
      This article includes a list of general references , but it remains largely unverified because it lacks sufficient corresponding inline citations . Please help to improve this article by introducing more precise citations. ( October 2009 ) ( Learn how and when to remove this template message ) Kjer's optic neuropathy Other names Autosomal dominant optic atrophy, Kjer type; Kjer optic atrophy; or, Kjer's autosomal dominant optic atrophy. Specialty Neurology Dominant optic atrophy , or dominant optic atrophy, Kjer's type , is an autosomally inherited disease that affects the optic nerves , causing reduced visual acuity and blindness beginning in childhood. This condition is due to mitochondrial dysfunction mediating the death of optic nerve fibers. Dominant optic atrophy was first described clinically by Batten in 1896 and named Kjer’s optic neuropathy in 1959 after Danish ophthalmologist Poul Kjer, who studied 19 families with the disease. [1] Although dominant optic atrophy is the most common autosomally inherited optic neuropathy (i.e., disease of the optic nerves) aside from glaucoma , it is often misdiagnosed.
    • Optic Atrophy Type 1 Medlineplus
      Optic atrophy type 1 is a condition that often causes slowly worsening vision, usually beginning in childhood. People with optic atrophy type 1 typically experience a narrowing of their field of vision (tunnel vision). Affected individuals gradually lose their sight as their field of vision becomes smaller. Both eyes are usually affected equally, but the severity of the vision loss varies widely, even among affected members of the same family, ranging from nearly normal vision to complete blindness. In addition to vision loss, people with optic atrophy type 1 frequently have problems with color vision (color vision deficiency) that make it difficult or impossible to distinguish between shades of blue and green.
    • Optic Atrophy 4 Omim
      For a discussion of genetic heterogeneity of optic atrophy, see OPA1 (165500). Mapping In a family of German descent living in western Maryland, Kivlin et al. (1983, 1984) found possible linkage of autosomal dominant optic atrophy to Kidd blood group (111000) (maximum lod score of 2.0 at theta 0.18), then thought to be on chromosome 2, but later mapped to chromosome 18q. By genetic linkage studies in the same family, Kerrison et al. (1999) mapped the locus to 18q12.2-q12.3. Delettre et al. (2000) suggested that a mitochondrial protein may be involved in OPA4 inasmuch as OPA1 and Leber hereditary optic neuropathy (LHON; 535000) are caused by defects in mitochondrial proteins.
    • Autosomal Dominant Optic Atrophy, Classic Form Orphanet
      A rare neuro-ophthalmological disease which is one of the most common forms of hereditary optic neuropathy characterized by progressive bilateral visual loss with an onset during the first decade of life, associated with optic disc pallor, visual acuity loss, visual field deficits and color vision defects. Epidemiology The prevalence of Autosomal dominant optic atrophy (ADOA) is variable, commonly varying between 1/10,000 in Denmark (due to a founder effect) to 1/35,000 in the UK and probably worldwide. Clinical description ADOA is usually detected during the first decade of life, often by vision screening in school but later onset is possible. Visual impairment is usually moderate (visual acuity ranges from 20/80 to 20/120) but may range from mild to severe. Visual field defect is typically centrocecal, central, or paracentral.
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