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Cognitive Deficit Wikipedia

Discovering Psychology . Worth Publishers. ISBN 0-7167-5704-4 . [ page needed ] ^ Fried, Yehuda; Joseph Agassi (1976). ... Needham Heights, MA, USA: Allyn & Bacon. ISBN 0-205-14164-1 . Das, J.P. (2002). A better look at intelligence. ... Cambridge: Cambridge University Press. pp. 445–476. ISBN 978-0-521-59648-0 . Lay summary (22 July 2013). ... Essentials of Psychological Testing . John Wiley & Sons. ISBN 978-0-471-41978-5 . Lay summary (10 October 2013). ... Cambridge: Cambridge University Press. pp. 20–38. ISBN 978-0-521-73911-5 . Lay summary (9 February 2012).

PSEN1, MAPT, APP, APOE, COMT, FMR1, GSK3B, BCHE, PTGS2, DRD2, EPO, CDK5R1, VIP, FGF14, MAOA, EIF2S1, SLC1A1, SLC10A2, MET, DRD3, SMAD4, LAMB2, TSC1, AGT, ZNF41, RAB40AL, SLC51A, NR0B2, IGF2, OTC, SLC51B, CRH, ABCC4, FOSB, OXTR, SLC4A10, AFF4, SLC6A4, CYP2D6, ACHE, DYRK1A, BDNF, PVALB, DISC1, NFE2L2, CHRNA4, BACE1, PIK3CB, PIK3CA, PIK3CD, PIK3CG, SIRT1, GABPA, SNCA, TNF, MTOR, HTT, RELN, DTNBP1, CFP, CDK9, KL, AKT1, NUFIP2, VEGFA, GBA, GRN, GRM5, ACTB, CNR1, CSF2, DLG4, MME, IL6, SYP, LAMC2, DMD, IL4, IL1B, NGF, PREP, PERCC1, MIR34A, PDE4A, PDE2A, EPHB2, FOXP1, MAPK1, TARDBP, SNAP25, ADIPOQ, FUS, HTR2A, NRG1, TCF4, TGFB1, HDAC6, GRM2, GRM3, SUCLA2, ABCA1, CREB1, CDK5, CASP6, CACNA1C, ADAM10, CRP, H3P40, NUBP1, NFKB1, RUNX1T1, NGFR, DCTN4, ASCC1, NOTCH3, MECP2, NTS, UBQLN2, AGTR1, POLDIP2, CD36, CD40, CASP1, AKR1C4, HMGB1, LRRK2, CHRNA7, NLRP3, IGF1, CHRNA5, COASY, SHROOM4, IL10, EHMT1, INSR, CIP2A, CDR1, LEP, RNF19A, PLA2G1B, NUP62, HDAC2, SPP1, SPTBN1, GRAP2, LGI1, TM7SF2, SQSTM1, ARHGEF7, SYNJ1, APLN, UBE3A, BECN1, VCAM1, TP63, VSNL1, YWHAZ, GTF2IRD1, SLC6A8, ANGPT1, PTPN11, PTPA, CALB1, MAPK8, SYNM, PTEN, HRH3, REST, SLC1A2, S100B, NRG3, SCN1A, KHDRBS1, AHSA1, SIGMAR1, TAAR1, TREM2, AIMP2, GAD1, GTF2H1, DAB1, GRIA1, CRK, GH1, MIR132, GFAP, FGFR3, ADCYAP1, CREBBP, CUX1, DBH, CX3CR1, CYBB, ERBB4, DBN1, NR3C1, PLB1, MAPK14, CHL1, MIR361, NPS, SNORD116@, CXCR6, SPAG11A, SFTPA1, PDE10A, TXNRD2, BAIAP2, SPAG11B, TUBA1B, RTN3, MIR574, GJB6, ADAMTS13, PPARGC1A, MIR342, ALDH2, SIRT3, ADNP, MED13L, CRTC1, MIR21, AGTPBP1, ASTN2, MDD1, ARC, PHF8, NMNAT2, VN1R17P, GPR166P, FAM107A, PSIP1, IL1RAPL1, OLIG2, SDS, EHMT2, GADD45G, AMPH, SETD1A, OPN1MW2, PSME3, OCLN, FPGT-TNNI3K, OPN1MW3, CBSL, ANXA1, HDAC3, SYNGAP1, ADA, APOA1, UPK3B, MTCO2P12, PDE5A, NCOA1, H3P45, PSMG1, KHSRP, NCK2, APOB, FZD4, ANP32A, AP3B2, EIF2S2, NOL3, CDKL2, NTN1, KEAP1, NCS1, HDAC9, ABCG1, CCR2, PTGES, HOMER2, AD10, GS1-600G8.3, C20orf181, SEMA5A, NRXN1, ANK3, ANPEP, TGM5, SRSF11, NOG, ECT, LPAR2, USP2, MIR188, OR2AG1, MIR181C, ALB, CALHM1, SPG11, PCSK9, TNFAIP8L2, PLEKHF1, LYNX1, DCLRE1C, LGR6, ACE2, NGB, PCDH10, SEMA6A, MRGPRX1, ADRA2B, PCDH19, KIDINS220, COPD, ADRB1, PCBP4, ACKR3, NPAS4, GPRC6A, DIPK2A, SRCIN1, ADCYAP1R1, GPR151, VPS13B, HSPB6, ADRA1A, DEGS2, OXER1, MRGPRX4, MRGPRX3, OMA1, KLHDC8B, TRAPPC9, CDCA5, FOXP2, CHRDL1, SLC39A13, CHRFAM7A, PTPN5, C9orf72, ADRA2A, KLF16, PAG1, NSUN5, CCDC141, AUTS2, IRF2BP2, RTL1, IGHD4-11, TMEM97, SRPX2, AGER, AHR, SIGLEC7, HES5, NECTIN3, DNAAF3, MIR137, TPSG1, SLC24A2, BRD1, FRRS1L, PDIK1L, AIF1, LPAR3, MAPK8IP2, HDGFL3, TNNI3K, CHD7, FAM3B, SMPD3, CCDC91, RCBTB1, CC2D1A, PGPEP1, AHI1, TMEM106B, EPM2A, NANS, SETD4, GEN1, GOLGA6A, CINP, HOOK1, ZDHHC3, MCIDAS, NRN1, CD320, CRBN, TUBB2B, MIR181A2, DCX, LRP8, IFIT1, IL18, IL13, IL12A, CHAT, IL2RB, CHI3L1, IKBKB, IGFALS, IFNG, IFNA13, IFNA1, IAPP, IRS1, HTR4, HTR2C, HTR1A, HSPA4, PRMT2, AGFG1, HPRT1, HOXA1, HMOX1, HIF1A, CLCN3, IDO1, ITGAM, CLU, MDM2, RNR2, COX2, COX1, MS, MPO, CD200, MNAT1, MMP9, MMP2, CBS, MAP3K5, MAOB, ITPR1, CDH1, CAPRIN1, LIMK1, LGALS9, LGALS3, LCN2, CEACAM4, KCNQ2, KCNJ6, JAK2, ITPR3, HDAC1, HCRT, FAS, CYP1A2, FGFR1, CXADR, FES, FDPS, FCN2, FAT1, PTK2B, FABP5, FABP3, ETS2, ESR1, EPHA4, FOXO3, ENO2, EIF4E, EIF2S3, EGR1, EDNRA, EDN1, TOR1A, DAO, DUSP2, DUSP1, DRD4, FOXO1, AFF2, HCLS1, GLUL, HCFC1, HARS1, GZMH, GTF2I, KLF6, GRPR, GRP, CORT, GRIN2B, GRIA2, GPR42, GLI3, FOLR1, GJB2, GIP, MSTN, GDF2, OPN1MW, GCHFR, GCG, FYN, FUT1, CST3, CTRL, MTRR, CEACAM6, NEUROD1, BRCA1, BMI1, STAT3, SSTR4, SST, SREBF1, SOX4, SOD1, SOAT1, BMP1, BMP2, SMARCA4, BRAF, ATP5F1A, SLC2A3, BRS3, SFRP1, SETMAR, SET, SELP, CX3CL1, CCL11, CCL2, SCN8A, SCN2A, TAT, TCF3, NF1, UBC, XPNPEP1, CLIP2, WAS, TRPV1, VLDLR, AQP4, AR, VDR, VCP, UFD1, SUMO1, TXN, TCN2, ARSD, TPT1, TPM2, TNFRSF1B, ASL, TLR4, TLR2, TJP1, THY1, DRD1, TDO2, ATXN1, TSPAN31, S100A1, PAFAH1B1, CALB2, CAMK4, CAPN1, CAST, PEPD, PDE9A, PDE4D, CASP2, CASP3, PAK3, SERPINE1, CAT, RXRA, ORM1, OPRL1, OPHN1, NTRK1, NRGN, NOVA2, NOTCH1, NOS2, NOS1, NMB, CBR1, PITX2, PLAT, PLD2, PNOC, RPS27A, RPS6KB1, OPN1LW, RBM3, RARB, MOK, RAC1, BUB1B, PTPRG, ACAT1, PTGS1, PTGER3, PTGER2, PSMC1, PSEN2, C5AR1, PRNP, MAPK10, MAPK3, CAD, PRKCA, PRCP, PPARA, ATP1A3
Isolated Atrial Amyloidosis Wikipedia

Lippincott Williams & Wilkins. pp. 433–. ISBN 978-0-7817-7012-5 . Retrieved 17 November 2010 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2
African Trypanosomiasis Wikipedia

The World Health Organization plans to eradicate sleeping sickness by the year 2030. [37] [38] Trypanosoma brucei gambiense [39] 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 Angola 1498 2094 2406 1796 1274 2441 6726 8275 6610 5351 4546 4577 3621 3115 2280 1727 1105 648 517 247 211 154 70 69 36 35 19 18 79 30 Benin 0 0 2 1 0 0 0 0 0 20 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Burkina Faso 27 27 20 17 18 13 12 1 15 15 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 Cameroon 86 69 21 3 20 21 17 10 54 32 27 14 32 33 17 3 15 7 13 24 16 15 7 6 7 6 6 5 7 17 Central African Republic 308 197 362 262 368 676 492 730 1068 869 988 718 572 539 738 666 460 654 1194 1054 395 132 381 59 194 147 124 76 57 86 Chad 20 221 149 65 214 315 178 122 134 187 153 138 715 222 483 190 276 97 196 510 232 276 197 195 95 67 53 28 12 16 Congo 580 703 727 829 418 475 474 142 201 91 111 894 1005 717 873 398 300 189 182 87 87 61 39 20 21 36 18 15 24 17 Côte d'Ivoire 365 349 456 260 206 326 240 185 121 104 188 92 97 68 74 42 29 13 14 8 8 10 9 7 6 3 0 3 2 1 Democratic Republic of the Congo 7515 5825 7757 11384 19021 18182 19342 25094 26318 18684 16951 17300 13816 11459 10339 10249 8013 8155 7318 7178 5624 5590 5968 5647 3205 2351 1769 1110 660 604 Equatorial Guinea 63 36 45 30 85 37 46 67 62 28 16 17 32 23 22 17 13 15 11 7 8 1 2 3 0 0 3 4 4 3 Gabon 80 45 33 80 61 20 32 11 6 38 45 30 26 26 49 53 31 30 24 14 22 17 9 17 10 9 10 9 16 8 Ghana 3 6 16 0 0 0 1 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 Guinea 52 29 24 27 26 33 38 88 99 68 52 72 132 130 95 94 48 69 90 79 68 57 70 78 33 29 107 140 74 69 Mali 0 0 0 27 17 11 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Nigeria 24 0 0 0 0 0 0 0 0 27 14 14 26 31 10 21 3 0 0 0 2 3 2 0 0 0 1 0 0 0 South Sudan 67 58 28 62 69 56 157 737 1726 1312 1801 1919 3121 3061 1742 1853 789 469 623 373 199 272 317 117 63 45 17 12 17 11 Togo 2 0 0 0 0 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Uganda 2066 1328 2042 1764 1469 1062 981 1123 971 1036 948 310 604 517 378 311 290 120 198 99 101 44 20 9 9 4 4 0 1 2 Total 12756 10987 14088 16607 23266 23671 28736 36585 37385 27862 25841 26095 23799 19941 17100 15624 11372 10466 10380 9680 6973 6632 7091 6228 3679 2733 2131 1420 953 864 Trypanosoma brucei rhodesiense [40] 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 Kenya 91 8 4 2 1 0 2 5 14 22 15 10 11 0 0 0 1 0 0 1 0 0 2 0 0 0 0 0 0 0 Malawi 228 195 143 53 31 15 8 7 10 11 35 38 43 70 48 41 58 50 49 39 29 23 18 35 32 30 37 7 15 91 Mozambique 3 7 24 10 16 No data No data No data No data No data No data No data 1 No data 1 No data No data No data No data No data No data No data No data No data No data No data No data No data No data No data Uganda 1417 832 606 503 342 497 178 217 283 283 300 426 329 338 335 473 261 119 138 129 112 84 71 43 70 28 10 13 4 5 United Republic of Tanzania 187 177 366 262 319 422 400 354 299 288 350 277 228 113 159 186 127 126 59 14 5 1 4 1 1 2 3 3 0 3 Zambia 7 No data 4 1 1 1 3 No data No data 15 9 4 5 15 9 7 6 10 13 4 8 3 6 6 12 8 2 3 5 15 Zimbabwe No data No data No data No data 1 No data No data 9 No data No data No data No data No data No data No data 3 No data No data 0 3 2 4 9 1 3 3 1 1 0 2 Total 1933 1219 1147 831 710 935 591 583 606 619 709 755 617 536 552 707 453 305 259 187 154 111 101 85 115 68 52 27 24 116 History [ edit ] In 1903, David Bruce recognized the tsetse fly as the arthropod vector. ... Lancet . 380 (9859): 2095–128. doi : 10.1016/S0140-6736(12)61728-0 . hdl : 10536/DRO/DU:30050819 . PMID 23245604 . ... Parasites & Vectors . 8 : 236. doi : 10.1186/s13071-015-0851-0 . PMC 4436790 . PMID 25928366 . ^ a b Brun R, Blum J, Chappuis F, Burri C (January 2010). ... Cambridge University Press. p. 748. ISBN 978-0-521-22803-9 . Archived from the original on 18 March 2015. ^ Steverding D (March 2010).

NOS2, APOL1, TMPRSS11D, APBB3, SRA1, MSR1, IL10, LSAMP, LAMP3, HPR, NXT1, SERPINA1, IL6, ODC1, RMDN1, SMUG1, VSX2, MRPL28, STT3B, SUB1, MCF2L, SEC14L2, DNAJB1P1, TIMM10, CMTR2, RMDN3, SYBU, PAQR7, RMDN2, TUT1, TIMM9, NXF1, CDKN2B, GMPS, SLC9A6, DNAJB1, SARDH, DNAH8, FLNB, GAPDH, UTS2R, HLA-G, HP, PRMT1, IL1A, PEX16, IL1RN, CXCL10, STT3A, SRL, TNF, USO1, DDOST, NR1I2, H3P9
- African Trypanosomiasis Orphanet
  
  Human African Trypanosomiasis (HAT), also called sleeping sickness, is a vector-borne parasitic disease caused by a protozoa of the Trypanosoma genus transmitted by the bite of a tsetse fly (genus Glossina ), that is found under its chronic form (average duration of 3 years) in western and central Africa (in case of the T. brucei gambiense sub-species), and under its acute form (lasting from few weeks to 6 months) in eastern and southern Africa (in case of the T. brucei rhodesiense sub-species). HAT comprises an initial hemo-lymphatic stage characterized by fever, weakness, musculoskeletal pain, anemia, and lymphadenopathy, along with dermatologic, cardiac and endocrine complications or hepatosplenomegaly, followed by a meningo-encephalitic stage characterized by neurologic involvement (sleep disturbances, psychiatric disorders, seizures) that progresses, in the absence of treatment, towards a fatal meningoencephalitis.
Glycogen Storage Disease Type 0 Medlineplus

Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired. The signs and symptoms of muscle GSD 0 typically begin in early childhood. ... Because some people with muscle GSD 0 die from sudden cardiac arrest early in life before a diagnosis is made and many with liver GSD 0 have mild signs and symptoms, it is thought that GSD 0 may be underdiagnosed. Causes Mutations in the GYS1 gene cause muscle GSD 0, and mutations in the GYS2 gene cause liver GSD 0.

GYS2
- Glycogen Storage Disease 0, Liver Omim
  
  A number sign (#) is used with this entry because of evidence that liver glycogen storage disease-0 (GSD0A) is caused by homozygous or compound heterozygous mutation in the GYS2 gene (138571), which encodes glycogen synthase-2, on chromosome 12p12. ... Mapping Orho et al. (1998) established linkage of glycogen storage disease 0 to intragenic and flanking polymorphic markers of the GYS2 gene on chromosome 12p12.2. Molecular Genetics In affected members of 5 families with liver glycogen storage disease 0, Orho et al. (1998) identified homozygous or compound heterozygous mutations in the GYS2 gene (138571.0001-138571.0008) Inheritance - Autosomal recessive Neuro - Seizures Lab - Glycogen synthetase deficiency Metabolic - Neonatal hypoglycemia - Fasting hypoglycemia - Fasting hyperketonemia - Hyperglycemia and hyperlactatemia with feeding ▲ Close
- Glycogen Storage Disease Due To Hepatic Glycogen Synthase Deficiency Orphanet
  
  A genetically inherited anomaly of glycogen metabolism and a form of glycogen storage disease (GSD) characterized by fasting hypoglycemia. This is not a glycogenosis, strictly speaking, as the enzyme deficiency decreases glycogen reserves. Epidemiology It is an extremely rare disease; about 20 cases have been reported in the literature so far. Clinical description It commonly appears in infancy or in early childhood. Patients present with morning fatigue and fasting hypoglycemia (without hepatomegaly) associated with hyperketonemia but without hyperalaninemia or hyperlactacidemia.
- Glycogen Storage Disease Type 0, Liver Gard
  
  Glycogen storage disease type 0, liver (liver GSD 0), a form of glycogen storage disease (GSD), is a rare abnormality of glycogen metabolism (how the body uses and stores glycogen, the storage form of glucose). Unlike other types of GSD, liver GSD 0 does not involve excessive or abnormal glycogen storage, and causes moderately decreased glycogen stores in the liver. ... This condition differs from another form of GSD 0 which chiefly affects the muscles and heart ( Glycogen storage disease type 0, muscle ) and is thought to be caused by mutations in the GYS1 gene.
Heredofamilial Amyloidosis Wikipedia

Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .

TTR, FGA, RET, GSN, APOA1, LYZ, ITM2B, EPO, CST3, FAP, ACTB, NLRP3, GGTLC1, HAMP, FURIN, PRNP, PMP22, APOA2, LOC102724197
- Hereditary Amyloidosis Gard
  
  Hereditary amyloidosis refers to a group of inherited conditions that make up one of the subtypes of amyloidosis . Hereditary amyloidosis is characterized by the deposit of an abnormal protein called amyloid in multiple organs of the body where it should not be, which causes disruption of organ tissue structure and function. In hereditary amyloidosis, amyloid deposits most often occur in tissues of the heart, kidneys, and nervous system. While symptoms of hereditary amyloidosis may appear in childhood, most individuals do not experience symptoms until adulthood. There are many types of hereditary amyloidosis associated with different gene mutations and abnormal proteins.
Secondary Systemic Amyloidosis Wikipedia

Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .
Secondary Cutaneous Amyloidosis Wikipedia

Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .
Glycogen Storage Disease Type 0 Wikipedia

Glycogen storage disease type 0 Glycogen storage disease type 0 has defect in glycogen synthase Specialty Medical genetics Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). ... Serum electrolytes calculate the anion gap to determine presence of metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an anion gap in the reference range and no acidosis. ... In patients with glycogen-storage disease type 0, hyperlipidemia is absent or mild and proportional to the degree of fasting. ... In patients with glycogen-storage disease type 0, urine ketones findings are positive, and urine-reducing substance findings are negative. ... The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [2] Mortality/Morbidity [ edit ] The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency.

GYS2, CPLANE1
Estrogen-Dependent Condition Wikipedia

Jaypee Brothers Publishers. 2007. pp. 347–. ISBN 978-81-8061-996-0 . ^ Leonard J. Deftos (1 January 1998). ... Rowman & Littlefield Publishers. pp. 73–. ISBN 978-0-7591-2332-8 . ^ Vasan; R.S. (1 January 1998). ... Biochemistry and Function of Sterols . CRC Press. pp. 26–27. ISBN 978-0-8493-7674-0 . ^ Michael Crocetti; Michael A. ... Lippincott Williams & Wilkins. pp. 564–. ISBN 978-0-7817-3770-8 . ^ W. Steven Pray (2006). ... Elsevier Health Sciences. pp. 1281–. ISBN 978-0-323-08678-3 . ^ Guy I. Benrubi (28 March 2012).
Androgen-Dependent Condition Wikipedia

Neonatal Skin: Structure and Function . CRC Press. pp. 67–. ISBN 978-0-8247-0887-0 . ^ Mariagrazia Stracquadanio; Lilliana Ciotta (20 April 2015). ... A Woman Doctor's Guide to Skin Care: Essential Facts and Information on Keeping Skin Healthy . Hyperion. ISBN 978-0-7868-8100-0 . ^ Sarah Bekaert (2007). ... CUP Archive. pp. 321–. ISBN 978-0-521-22673-8 . ^ Raphael Rubin; David S. ... Lippincott Williams & Wilkins. pp. 816–. ISBN 978-0-7817-9516-6 . ^ Andrea Dunaif; R. ... Academic Press. 3 October 1994. pp. 1994–. ISBN 978-0-08-058373-0 . Further reading [ edit ] Shukla, G.
Laryngotracheoesophageal Cleft Type 0 Orphanet

Laryngo-tracheo-esophageal cleft (LC) type 0 is a congenital respiratory tract anomaly characterized by a submucosal laryngo-tracheo-esophageal cleft with minor symptoms or an asymptomatic course. ... Clinical description Subjects with type 0 LC may have no obvious symptoms or mild symptoms such as occasional aspirations.
Nevus Comedonicus Wikipedia

Louis: Mosby. p. 1673. ISBN 1-4160-2999-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . This Epidermal nevi, neoplasms, cysts article is a stub .

NEK9, IL6, AKT1, SRD5A2, MIR511, PCSK9, ASXL1, ABCA12, MCF2L, JMJD6, PRSS21, VEGFA, TOP2A, TOP1, TNFAIP6, TNF, SKP2, BAX, CCL4, PTH, POMC, PECAM1, OPRL1, LRP2, KRT15, KRT10, IL7R, CYP21A2, CASP3, BCL2, MIR146B
- Nevus Comedonicus Omim
  
  A number sign (#) is used with this entry because of evidence that nevus comedonicus (NC) is caused by somatic mutation in the NEK9 gene (609798) on chromosome 14q24. Description Nevus comedonicus (NC) is a rare type of epidermal nevus with predilection for the face and neck area. The condition develops within the first decade of life in most patients. NC is characterized by dilated, plugged follicular ostia containing lamellar keratinaceous material and grouped in a honeycomb pattern; the distribution of lesions may be unilateral, bilateral, linear, interrupted, segmental, or along the lines of Blaschko. NC may be nonpyogenic with an acne-like appearance or associated with the formation of cysts, papules, pustules, and abscesses.
- Nevus Comedonicus Syndrome Orphanet
  
  A rare, syndromic nevus characterized by the association of typically unilateral, closely arranged, linear, slightly elevated, multiple, nevus comedonicus lesions located usually on the face, neck, trunk or limbs (with or without a central, dark, firm, hyperkeratotic plug and secondary acneiform lesions) with extracutaneous ocular, skeletal, and/or central nervous system abnormalities, such as ipsilateral cataract, corneal erosion, poly-/syndactyly, absent fifth finger, scoliosis, vertebral defects, corpus callosum agenesis, seizures, interhemispheric cyst, intellectual deficiency, and/or developmental delay.
- Nevus Comedonicus Syndrome Wikipedia
  
  Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . External links [ edit ] Classification D ICD - 10 : Q82.5 OMIM : 617025 External resources Orphanet : 64754 This Epidermal nevi, neoplasms, cysts article is a stub .
Acephalgic Migraine Wikipedia

Lippincott Williams & Wilkins. p. 1152. ISBN 0-7817-7513-2 . ^ Pryse-Phillips, William (2003). ... Oxford University Press US. p. 587. ISBN 0-19-515938-1 . ^ Bradley, Walter George (2004). ... Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... Lippincott Williams & Wilkins. p. 1289. ISBN 0-7817-4811-9 . ^ a b Loder, Elizabeth; Dawn A. ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007).
Neurosis Wikipedia

State University of New York Press. ISBN 0-7914-5754-0 . ^ Jacobson, Kirsten. 2006. ... The Loss of Sadness . Oxford. ISBN 978-0-19-531304-8 . ^ Wilson, Mitchell. 1993. ... New York: Anchor Books / Doubleday . ISBN 0-385-05221-9 . Ladell, R. M., and T. ... Albany: State University of New York Press. ISBN 0-7914-5754-0 Winokur, Jon . 2005. Encyclopedia Neurotica. ISBN 0-312-32501-0 . External links [ edit ] Classification D ICD - 10 : F40 - F40.8 Library resources about Neurosis Resources in your library Resources in other libraries Janov, Arthur (1991).

GPC6, NKAIN2, MDGA2, ABO, COMT, CRP, NHS
Pili Pseudoannulati Wikipedia

Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . This condition of the skin appendages article is a stub .
- Pseudopili Annulati Omim
  
  Description Pseudopili annulati is an unusual variant of normal hair characterized by a banded appearance of the hair under reflective light, as observed in pili annulati (180600), but resulting from a distinct underlying physical defect. There is no increased hair fragility (Price et al., 1970). Clinical Features Price et al. (1970) reported a 9-year-old girl with blond hair whose scalp hair showed light and dark banding since infancy. Light microscopy showed that the banding appeared only if the light struck the hair at right angles to the long axis of the hair, which was distinct from that observed with pili annulati. Polarizing light indicated variability in the thickness of the hair shaft, and illuminating light did not show bands, 2 additional features that distinguished it from pili annulati. Further examination of the hair shaft showed that the pseudopili annulati hairs had periodic widening and narrowing, that the fiber cross-section was roughly elliptical, and that a periodic twisting of the hair (30 to 40 degrees in 2 alternating directions) was superimposed on the ellipticity.
Pigmented Hairy Epidermal Nevus Syndrome Wikipedia

Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . This Epidermal nevi, neoplasms, cysts article is a stub .
Cutaneous Diphtheria Infection Wikipedia

Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Geoffrey V. Gill; Nick Beeching (1 March 2004). ... Wiley-Blackwell. pp. 33–. ISBN 978-0-632-06496-0 . Retrieved 14 May 2010 .
Pterygium Unguis Wikipedia

Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . This condition of the skin appendages article is a stub .

COL17A1, DKC1, NOP10, NHP2
Pili Annulati Wikipedia

St. Louis: Mosby. ISBN 1-4160-2999-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ http://www.omim.org/entry/180600 External links [ edit ] Hair Transplant Classification D ICD - 10 : Q84.1 ( ILDS Q84.110) ICD - 9-CM : 757.4 MeSH : C537187 v t e Congenital malformations and deformations of skin appendages Nail disease Anonychia Leukonychia Pachyonychia congenita / Onychauxis Koilonychia Hair disease hypotrichosis /abnormalities: keratin disease Monilethrix IBIDS syndrome Sabinas brittle hair syndrome Pili annulati Pili torti Uncombable hair syndrome Björnstad syndrome Giant axonal neuropathy with curly hair hypertrichosis : Zimmermann–Laband syndrome This condition of the skin appendages article is a stub .

FZD10
- Ringed Hair Omim
  
  Description Pili annulati, or 'ringed hair,' is a disorder in which scalp hairs show alternating light and dark bands. It is often an incidental finding, and the hair usually does not show increased fragility (Green et al., 2004). See also pseudopili annulati (613241), a distinct entity. Clinical Features Cady and Trotter (1920) reported 3 unrelated families with ringed hair. The condition was restricted to hairs on the scalp. Based on refractive patterns under transmitted and reflective light, Cady and Trotter (1920) concluded that the light areas were caused by the presence of gas in the interstices of the medulla and cortex of the hair shaft, and not by lack of pigmentation. Ashley and Jacques (1950) reported a 4-generation pedigree with ringed hair inherited in an autosomal dominant pattern.
- Pili Annulati Gard
  
  Pili annulati is a hair disorder. In pili annulati, affected hair has a pattern of light and dark banding. People with pili annulati may describe their hair as "striped" or as having silvery beads. Pili annulati typically involves 20-80% of scalp hair, however it can involve facial and body hair as well. Affected hairs may be more prone to breakage. Pili annulati can present in infancy, childhood, or later in life. It can be seen with the naked eye, however it may be more difficult to see in people with dark hair.
- Ringed Hair Disease Orphanet
  
  Pili annulati is an isolated, benign hair shaft abnormality, usually presenting after the age of 2 and affecting the hair of the scalp or very rarely beard, axillary, or pubic hair, that is characterized by a banded or speckled appearance due to alternating light bands (corresponding to air-filled cavities within the cortex of the affected hair shafts) and dark bands. The bands have a lifelong duration, may only be detectable under light microscopy, are more apparent in fair-colored hair or with age-related graying, and have no effect on hair growth or fragility in the vast majority of cases.
Pili Torti Wikipedia

Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . External links [ edit ] Classification D ICD - 10 : Q84.1 ( ILDS Q84.120) MeSH : C562485 C562485, C562485 DiseasesDB : 29682 v t e Congenital malformations and deformations of skin appendages Nail disease Anonychia Leukonychia Pachyonychia congenita / Onychauxis Koilonychia Hair disease hypotrichosis /abnormalities: keratin disease Monilethrix IBIDS syndrome Sabinas brittle hair syndrome Pili annulati Pili torti Uncombable hair syndrome Björnstad syndrome Giant axonal neuropathy with curly hair hypertrichosis : Zimmermann–Laband syndrome This condition of the skin appendages article is a stub .

BCS1L, CDH3, KRT85, LMNA, PEX1, PEX6, NECTIN1, ST14, WRN, HR, NECTIN4, HEPHL1
- Pili Torti Orphanet
  
  Pili torti is a hair shaft abnormality characterized by flat hair that is twisted at irregular intervals. Hair is normal at birth but progressively stops growing long and becomes fragile. Pili torti can be isolated or occur in association with syndromes such as Menkes disease or Bazex syndrome (see these terms).
- Pili Torti, Early-Onset Omim
  
  Description Pili torti, or twisted hair, is a condition in which the hair shafts are flattened and rotated along their long axis. Hairs are fragile and break at short length. Some patients may have associated dental or nail findings, and many have resolution of the fragile hair at puberty (review by Dawber, 1996). Pili torti is also a feature in several disorders, including Bjornstad syndrome (BJS; 262000), Bazex syndrome (BZX; 301845), and Menkes disease (309400). Clinical Features Pili torti was first described and named by Ronchese (1932), who observed 2 affected Italian sisters. The proband had dull blonde scalp hair that was 'lank and frizzy, with a wild, bushy appearance.'
- Pili Torti Gard
  
  Pili torti is a rare hair condition characterized by fragile hair. In pili torti hair has a flattened shaft with clusters of narrow twists at irregular intervals. Some cases may be inherited in autosomal dominant or autosomal recessive patterns, while others are acquired. In the inherited form, symptoms tend to be present from early childhood. It can occur alone or as part of other diseases like ectodermal dysplasias , Menke disease , Bjornstand syndrome , or Bazex syndrome . Acquired cases of pili torti may be associated with anorexia nervosa , malnutrition, oral retinoid treatment, or inflammatory scalp conditions (e.g., cutaneous lupus erythematousus ).