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Neurogenic Bladder Dysfunction Wikipedia

PMID 22847896 . ^ a b Ludwikowski, Barbara M.; Bieda, Jan-Christoph; Lingnau, Anja; González, Ricardo (2019).

CHRM2, NGF, GJA1, CISD2, TBCD, FBXO7, ATP13A2, VPS11, FARS2, COG5, ALG1, ARNT2, PEX3, WFS1, ELOVL1, FA2H, EHMT1, SNCA, ACER3, ATXN3, VANGL1, MNX1, COG7, GBE1, MTFMT, EEF1A2, COL6A1, EBF3, AMBP, VUR, C9orf72, ADRB3, WDHD1, BCL2L10, TWIST1, TGFB1, NTF3, LEP, HIF1A, ERBB3, CD38, BDNF, ZNF35
Childhood Disintegrative Disorder Wikipedia

. ^ Childhood Disintegrative Disorder - Causes Archived September 29, 2007, at the Wayback Machine ^ Myers, Scott M.; Johnson, Chris Plauché (1 November 2007).

TRRAP, SHANK3
- Childhood Disintegrative Disorder Orphanet
  
  Childhood disintergrative disorder is a rare pervasive developmental disorder with a disease onset before the age of three and characterized by a dramatic loss of behavioral and developmental functioning after atleast two years of normal development. Manifestations of the disease include loss of speech, incontinence, communication and social interaction problems, stereotypical autistic behaviors and dementia.
Anaplastic Thyroid Cancer Wikipedia

PMID 17098674 . [ permanent dead link ] ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab Chintakuntlawar, AV; Foote, RL; Kasperbauer, JL; Bible, KC (March 2019).

SOD2, TP53, RET, EGFR, AKT1, TERT, SLC5A5, PIK3CA, PIK3CB, PIK3CD, PIK3CG, CD274, BRAF, PPARG, TG, PTCH1, ALK, LOC110806263, CCDC6, TAS2R38, F9, PAX8, MYC, VEGFA, PTEN, EIF1AX, GOT2, CYP19A1, LGALS3, TNF, CDKN2A, TAF1, CTNNB1, STAT3, NOTCH1, ABCB1, ABCG2, KDR, ERBB2, MAP2K7, F11R, BCL2, PLK1, EPHB2, S100A4, FOXM1, MIR21, EZH2, MMP9, RASAL1, MAPK1, MADD, TGFB1, TNFSF10, TWIST1, FOXA1, TSHR, KIT, PRKAR1A, CXCL8, MALAT1, MIR126, MME, CXADRP1, TSTD1, MIR30A, MIR30D, LOX, NTRK1, MCM5, MIR17HG, MET, LCN2, FBLIM1, SPC24, DNER, CCNA1, TTF1, TSC2, TPO, NR1I3, TRIM13, NKX2-1, THY1, KATNB1, UBE2C, CCN1, SST, TBC1D9, SPG7, SOX2, LAT, SNAI2, SGSM3, CXCL12, CCL2, RAP1GAP, SLC7A5, GOPC, IL4, H3P10, ESRRG, CAV1, CASR, FOXO3, ARR3, CXADR, CASP3, CDKN1A, CCND1, CSF2, ELAVL2, PATZ1, CBX7, BRD4, HSPA9, TMEM158, RYBP, USP22, TSPO, KLRK1, ZHX2, TUSC2, BRMS1, BUB1, FOXD3, BUB1B, CAD, BSG, UHRF1, TFCP2L1, CDK12, SHC3, TPCN1, KRT20, INO80, BCKDHB, CEP55, IMPACT, ATF7IP, RASSF1, PPP1R13L, OGFR, SOCS3, BAG3, GDF15, KLF4, S1PR2, AURKB, SPAG9, HSPB3, GADD45G, CCK, IQGAP1, IL18R1, CCND2, SOCS1, CD1D, PCLAF, BMS1, PJA2, WDR1, CAT, EBI3, PSME3, GLYAT, YAP1, KAT5, ATG7, SPAG5, TXNIP, TRAF3IP2, NES, PARD3, HCP5, TMEM184C, CCL28, AXIN1, SLC12A9, MIR375, ANG, MIR99A, MIR34B, ANXA1, XIAP, MIR27B, MIR25, MIR222, APOE, MIR200A, MIR20A, MIR19A, MIR195, MIR191, MIR483, UCA1, AMFR, HOTAIRM1, AKT2, MTCO2P12, SIK1B, PTCSC3, MIR4516, KLRC4-KLRK1, APTR, MIR544A, ALDH1A1, ESRG, KRT8P3, MIR650, MIR599, MIR584, MIR182, MIR155, MIR148A, ULBP2, HAVCR2, ECRG4, MRO, FSD1L, ITCH, TRIM8, TCEAL4, SFXN1, FSD1, MAPKAP1, DUSP26, RXFP1, MRTFA, ATRX, ATM, RXFP2, MIR146A, NEAT1, MIR144, FAS, MIR10B, MIRLET7C, IYD, HMGA1P7, ASPM, DIS3L2, TIGIT, KLB, CCDC80, SIK1, ATF3, HT, CD27, CD68, CD44, MMP7, MUC1, COX2, MT1A, MSH2, MMP13, GLI1, MMP3, GDF1, MMP2, GLO1, GPI, MDM4, MCM7, HBB, MMUT, NEUROD1, EPCAM, PCNA, FOS, MTOR, PGD, PECAM1, PDGFRB, PDCD1, PAEP, NFATC1, PEBP1, FUCA1, NRAS, GAA, NME1, NFYB, SMAD7, TACSTD2, KMT2D, IGF1R, IL10, HRAS, IL4R, HSPA4, HSPA5, IGFBP7, IFNG, ILK, IFNB1, IDH2, IDH1, ICAM1, HTC2, HSPB2, IL11, IDO1, HDAC1, L1CAM, LIMK1, HDAC2, LDHA, HGF, STMN1, LAMC2, KRT8, CXCL10, HK2, HMGA1, KCNH2, CD82, JAK2, INSL3, FN1, FOXE1, PKD1, TFAP2A, TKT, CNR2, TIA1, COL1A1, CLDN7, CRABP2, CRYAB, CHRM3, TCP1, STRN, CTLA4, SSTR5, SSTR1, SSAV1, CLC, CDKN3, PKM, XPO1, NCOA4, HSPB1, TFPI2, MAFK, CXCR4, CD70, VIM, TRAF6, VEGFC, CDK1, VDR, CDH13, CDK2, CDK4, SRC, CYP24A1, CYP27B1, MAPK3, RAC1, PTHLH, PTGS2, ELAVL1, FDPS, MAP2K1, FES, DCT, FGF2, PPBP, MED1, FGFR1, FGFR4, PLAU, MOK, RAF1, EIF4E, RAP2A, AGER, RNH1, SNORA73A, ROS1, EGF, S100A8, S100A9, SCD, E2F1, DPP4, DOCK3, DECR1, SNAI1, ACACA
- Anaplastic Thyroid Carcinoma Orphanet
  
  A disorder that represents the ultimate dedifferentiation step of thyroid tumorigenesis and is one of the most severe cancers in humans. Epidemiology It accounts for less than 2% of thyroid cancers and affects older patients in their sixth to eighth decade. Clinical description Usual clinical presentation is a rapidly growing thyroid mass invading surrounding structures with compressive symptoms. Cervical lymph nodes enlargement and distant metastases occur frequently. Diagnostic methods Though cytological results obtained by fine needle aspiration may be suggestive of diagnosis, tissue biopsy for immunohistochemichal study can be necessary to exclude lymphoma and to validate aggressive therapies.
- Anaplastic Thyroid Cancer Gard
  
  Anaplastic thyroid cancer (ATC) accounts for less than 2% of all thyroid cancers and is the most aggressive type of thyroid cancer. Most cases of anaplastic thyroid cancer are diagnosed in the sixth to seventh decade of life. Women are more likely to be affected than men. ATC generally occurs in individuals with a history of goiter or thyroid cancer. A history of head and neck radiation or exposure to radioactive materials may also increase the risk for ATC. Patients with ATC generally present with a rapidly-growing neck mass which may cause trouble swallowing (dysphagia), coughing, neck pain, and trouble breathing (dyspnea).
Transvestism Wikipedia

Transvestites: The erotic drive to cross dress. (M. A. Lombardi-Nash, Trans.) Buffalo, NY: Prometheus Books. ^ Hirschfeld, Magnus.
Ptosis (Breasts) Wikipedia

. ^ a b c d e f g Rinker, B; Veneracion, M; Walsh, C (2008). "The Effect of Breastfeeding on Breast Aesthetics" .
Central Nervous System Tumor Wikipedia

Retrieved 2019-11-11 . ^ Jaiswal, Ritu; Sedger, Lisa M. (6 March 2019). "Intercellular Vesicular Transfer by Exosomes, Microparticles and Oncosomes - Implications for Cancer Biology and Treatments" .

TP53, APC, BAP1, MLH1, SMARCB1, EGFR, EWSR1, EPHB2, SMARCA4, RTEL1, STN1, LRIG1, ACOT11, ETFA, MAML2, SLC25A24, GOLGA3, LRRC31, POLR3B, KIF26B, SLC16A8, LMF1, SMYD3, IDH1, RHBDF1, RAVER2, HEATR3, MDM4, CCDC26, C2orf80, RNU6-1318P, MIR4300HG, RTEL1-TNFRSF6B, TRAF5, WT1, ZBTB16, CDKN2B-AS1, BRAF, SLC35A3, AKT3, AKAP6, POLR2A, PHLDB1, VTI1A, DBT, IDH2, NF2, GFAP, MYCN, NES, BCOR, VEGFA, MAP2K7, MRC1, MYC, NKX2-1, LAMC2, MIR34A, EPO, CSF2, BCL2, MIR200A, MVP, TCL1B, MIR21, F2RL3, KAT2B, PROM1, ULK1, TYR, GSTK1, XRCC6P5, MIR367, MIA, TCL1A, C20orf181, CD24, H3C9P, VHL, COMMD3-BMI1, OLIG2, PWAR4, YAP1, GOPC, KIAA1549, NT5C3A, LIN28A, GAL, PPP1R2C, CD274, SETD2, CD276, MINDY4, PYGO2, SGSM3, AZIN2, SLCO6A1, PRAME, FOXR2, ZHX2, RASSF1, GADL1, AGR2, PARP1, SDHB, TTF1, CTNNB1, DLG3, DRD4, EPHA2, ERCC1, FAP, FGFR1, KAT2A, GLS, H3-3A, H3-3B, HGF, HRG, HSPA4, IGFBP2, IL4, DES, CDKN2A, IL10, CDKN1A, ALK, AMBP, ANXA2, APOD, APOE, AQP1, ATRX, BMI1, BRCA2, DDR1, CALCR, CALR, CAPG, CDH1, CDK4, CXCL8, MAK, TPI1, PLG, MAPK1, PTGS2, PTPRC, RAF1, ROS1, S100A4, SAI1, CCL2, ALB, SLAMF1, SLC6A8, SMO, SOX10, AURKA, TF, PML, PLAU, CD46, PIK3CG, MEN1, MGMT, CD99, MNAT1, MSH2, MT1E, COX2, MTHFR, NRAS, PAWR, PDGFRA, PIK3C3, PIK3CA, PIK3CB, PIK3CD, MTCO2P12
Sleep Sex Wikipedia

Retrieved 15 November 2017 . ^ a b c Shapiro, Colin M; Trajanovic, Nikola N; Fedoroff, J Paul (29 November 2016).
Eagle Syndrome Wikipedia

. ^ a b c d e Kamal, A; Nazir, R; Usman, M; Salam, BU; Sana, F (November 2014).
- Eagle Syndrome Gard
  
  Eagle syndrome is characterized by recurrent pain in the middle part of the throat (oropharynx) and face. "Classic Eagle syndrome" is typically seen in patients after throat trauma or tonsillectomy. Symptoms include dull and persistent throat pain that may radiate to the ear and worsen with rotation of the head. Other symptoms may include difficulty swallowing, feeling of something stuck in the throat, tinnitus , and neck or facial pain. A second form of Eagle syndrome unrelated to tonsillectomy causes compression of the vessel that carries blood to the brain, neck, and face (carotid artery).
Thallium Poisoning Case Of Zhu Ling Wikipedia

Thus the matter serves as a vehicle for expression of public dissatisfaction with corruption and abuse of power by the political elite associated with the regime. [16] Notes [ edit ] ^ "Loonen J. (Rosas C&M, The Netherlands)Telemedicine--Telework in medicine and business" (PDF) .
Syndrome Of Subjective Doubles Wikipedia

. ^ a b c d e f g h i j Christodoulou, George N.; Margariti, M.; Kontaxakis, V. P.; Christodoulou, N.
Mirror-Touch Synesthesia Wikipedia

. ^ a b Baron-Cohen, S., Robson, E., Lai, M.-C., & Allison, C. (2016). Mirror-Touch Synaesthesia Is Not Associated with Heightened Empathy, and Can Occur with Autism.
Angiostrongyliasis Wikipedia

PMID 30070981 . ^ a b c d Baheti NN; Sreedharan M; et al. (2008). "Eosinophilic meningitis and an ocular worm in a patient from Kerala, south India" .

LGALS2, SIRT1
- Angiostrongyliasis Orphanet
  
  A foodborne zoonotic disease, endemic to Southeast Asia and the Pacific Islands, caused by the rat lungworm Angiostrongylus cantonensis and that is acquired by the ingestion of the infective larvae on vegetables or in raw or undercooked snails, slugs, land crabs, freshwater shrimps, frogs and lizards. The main feature is eosinophilic meningitis, with clinical manifestations including fever, headache, malaise, fatigue, vomiting, rhinorrhea, blurred vision, diplopia, cough, stiff neck, enteritis, constipation and paraesthesia due to the movement of the worms from the intestines to the lungs, central nervous system and eyes. In severe cases without treatment, coma and death can occur.
Coronary Vasospasm Wikipedia

. ^ a b c d e f Matta A, Bouisset F, Lhermusier T, Campelo-Parada F, Elbaz M, Carrié D, Roncalli J (2020-05-15).

NOS3, PON1, ARHGAP9, PLCD1, ALDH2, ABCC9, SGCD, DLL1, BCAR1, MED23, DLK1, SLC14A2, PLA2G7, XDH, CXCL12, OPA1, CAD, MMP3, IL6, HTR2A, HTR1B, UTS2R, EDN1, DECR1, ACE, CYBA, CTNND1, CSE1L, CAV1, TMX2-CTNND1
Pseudorabies Wikipedia

The Merck Veterinary Manual . 2006 . Retrieved 2007-03-31 . ^ Pensaert M, Labarque G, Favoreel H, Nauwynck H (2004).

ACKR1, NECTIN1, IFNB1, CALCA, GOSR1, USH2A, DNALI1, EOMES, IFITM1, TNFRSF14, SOCS3, CH25H, GSTO1, PCYT1B, ISG15, TNF, BCLAF1, BCL2L10, BCAP31, FASTK, TMED5, EXOSC3, IL27, COL6A4P1, MYMX, TPI1, PPP1R11, THBS1, CAT, CTBS, CYP1A2, CYP2C9, CYP2D6, CYP3A4, DUT, EGF, FOS, IL1A, IL1B, IL2, KLRD1, ENPP1, PSMD10, PVR, NECTIN2, S100A10, SST, STAT3, H3P24
Neurasthenia Wikipedia

Farmer A, Jones I, Hillier J, Llewelyn M, Borysiewicz L, Smith A (October 1995).

KRT7, TAL1, SCLY
Haemophilia In European Royalty Wikipedia

References and external links [ edit ] Potts, D. M. Queen Victoria's Gene . Sutton Publishing, 1999.
Seborrheic Keratosis Wikipedia

PMID 21965858 . ^ Yeatman JM, Kilkenny M, Marks R (Sep 1997). "The prevalence of seborrhoeic keratoses in an Australian population: does exposure to sunlight play a part in their frequency?".

PIK3CA, FGFR3, NTHL1, ERCC4, CDKN2A, IL9, H3P10, EGFR, EDN1, TP53, TEP1, PIK3CB, PIK3CD, PIK3CG, SLC2A1, NPS, STAT3, TP63, PTTG1, TNF, NOP53, PDPN, TYR, FOXN1, LINC00346, AKT1, NTRK1, NRAS, APC, APOA1, APOE, APP, AR, BCL2, CSF2, CSK, ERBB2, FGF3, H2AX, IL2, KCNE1, KRAS, ANXA1, LGALS3
- Seborrheic Keratosis Mayo_clinic
  
  Overview A seborrheic keratosis (seb-o-REE-ik ker-uh-TOE-sis) is a common noncancerous (benign) skin growth. People tend to get more of them as they get older. Seborrheic keratoses are usually brown, black or light tan. The growths (lesions) look waxy or scaly and slightly raised. They appear gradually, usually on the face, neck, chest or back. Seborrheic keratoses on the back Seborrheic keratoses are very common on the back. They appear as waxy light tan, brown or black growths that look as if they were dripped onto the skin by a candle.
- Keratosis, Seborrheic Omim
  
  A number sign (#) is used with this entry because of evidence that seborrheic keratosis can result from somatic mutations in the FGFR3 gene (134934) or the PIK3CA gene (171834). Description Seborrheic keratoses are common benign epidermal lesion that can develop on any part of the body. Clinical Features Reiches (1952) described 7 families in which seborrheic keratosis was transmitted through 2 or 3 generations. The keratoses were of late onset. The skin lesions of the basal cell nevus syndrome sometimes resemble seborrheic keratoses. Bedi (1977) observed congenital seborrheic verrucae in 11 members in 3 generations of a family.
White Band Disease Wikipedia

"Preferential carbon utilization by surface bacterial communities by water mass, normal, and white band diseased Acropora cervicornis" (PDF) . ^ a b c d e f g h i j k l m n o Gignoux-Wolfsohn, Marks, and Vollmer (2012).
Paternal Depression Wikipedia

. ^ Battle CL, Zlotnick C, Pearlstein T, Miller IW, Howard M, Salisbury A, Stroud L (2008–2010).
Jervell And Lange-Nielsen Syndrome Wikipedia

. ^ a b Giudicessi, John R.; Wilde, Arthur A. M.; Ackerman, Michael J. (October 2018).

KCNQ1, KCNE1, KCNE1B, RWS, GAST, KCNH2, HFE, NT5E, SCN5A, KCNQ4, KCNE2
- Jervell And Lange-Nielsen Syndrome Gene_reviews
  
  Summary Clinical characteristics. Jervell and Lange-Nielsen syndrome (JLNS) is characterized by congenital profound bilateral sensorineural hearing loss and long QTc, usually >500 msec. Prolongation of the QTc interval is associated with tachyarrhythmias, including ventricular tachycardia, episodes of torsade de pointes ventricular tachycardia, and ventricular fibrillation, which may culminate in syncope or sudden death. Iron-deficient anemia and elevated levels of gastrin are also frequent features of JLNS. The classic presentation of JLNS is a deaf child who experiences syncopal episodes during periods of stress, exercise, or fright. Fifty percent of individuals with JLNS had cardiac events before age three years.
- Jervell And Lange-Nielsen Syndrome 1 Omim
  
  A number sign (#) is used with this entry because of evidence that this form of Jervell and Lange-Nielsen syndrome (JLNS1) is caused by homozygous or compound heterozygous mutations in the KCNQ1 gene (607542) on chromosome 11p15. Long QT syndrome-1 (LQT1; 192500), also known as Ward-Romano syndrome, is caused by heterozygous mutation in the KCNQ1 gene. Description The Jervell and Lange-Nielsen syndrome is an autosomal recessive disorder characterized by congenital deafness, prolongation of the QT interval, syncopal attacks due to ventricular arrhythmias, and a high risk of sudden death (Jervell and Lange-Nielsen, 1957). Genetic Heterogeneity of Jervell and Lange-Nielsen Syndrome Also see JLNS2 (612347), caused by mutation in the KCNE1 gene (176261) on chromosome 21q22. Clinical Features Jervell and Lange-Nielsen (1957) reported a family in which 4 of 6 children, born to unrelated parents, had congenital deafness and prolonged QT interval and died suddenly in childhood.
- Jervell And Lange-Nielsen Syndrome Orphanet
  
  A rare, severe, familial long QT syndrome characterized by congenital profound bilateral sensorineural hearing loss, a long QT interval on electrocardiogram and life-threatening ventricular tachyarrhythmias. Epidemiology The disease is very rare. Prevalence is unknown and varies depending on the population studied (1/100,000-1/1,000,000) but is more common in countries in which consanguineous marriage is frequent. Clinical description Almost 50% of patients become symptomatic before age of 3 years. The typical presentation of Jervell and Lange-Nielsen syndrome (JLNS) is a congenitally deaf child who experiences syncopal episodes during periods of stress, exercise, or fright. Deafness is congenital, bilateral, profound and sensorineural. The QT interval is usually markedly prolonged (>500 ms) and associated with tachyarrhythmias (including ventricular tachycardia, episodes of Torsades de Pointes (TdP) ventricular tachycardia and ventricular fibrillation) that may cause syncope or sudden death.
- Jervell Lange-Nielsen Syndrome Gard
  
  Jervell Lange-Nielsen syndrome (JLNS) is an inherited disorder characterized by deafness present at birth and abnormalities of the electrical system of the heart. It is a form of long QT syndrome . This refers to the QT interval measurement seen on the electrocardiogram . The severity of cardiac symptoms seen in individuals varies from no apparent symptoms to increasing heartbeat ( tachycardia ), fainting, and cardiac arrest. There are two different types of JLNS type: 1, caused by mutations in the KCNQ1 gene, and type 2, caused by mutations in the KCNE1 gene. Both types are inherited in an autosomal recessive manner. The treatment of individuals with JLNS focuses on treating hearing loss utilizing devices such as cochlear implants and preventing other symptoms such as fainting and cardiac arrest.
- Jervell And Lange-Nielsen Syndrome 2 Omim
  
  A number sign (#) is used with this entry because of evidence that Jervell and Lange-Nielsen syndrome-2 (JLNS2) is caused by homozygous or compound heterozygous mutation in the KCNE1 gene (176261) on chromosome 21q22. Long QT syndrome-5 (LQT5; 613695) is caused by heterozygous mutation in the KCNE1 gene. Description The Jervell and Lange-Nielsen syndrome is an autosomal recessive syndrome of abnormal cardiac ventricular repolarization with prolonged QT interval and bilateral congenital deafness. For a general description and a discussion of genetic heterogeneity of Jervell and Lange-Nielsen syndrome, see 220400. Mapping In a small consanguineous British family with JLNS, Tyson et al. (1997) excluded linkage to KCNQ1 (607542), and found that the affected children were homozygous by descent for markers on chromosome 21, in a region containing the KCNE1 gene (176261).