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  • Dilation And Curettage Wikipedia
    WebMD. 2004-10-07. Archived from the original on 28 May 2008 . Retrieved 2007-04-29 . ^ a b "ACOG: FAQ: Dilation and Curettage" .
  • Clubroot Wikipedia
    Journal of Plant Growth and Regulation . 28 (3): 289–303. doi : 10.1007/s00344-009-9094-7 .
  • Nail Biting Wikipedia
    SteadyHealth. 30 December 2010 . Retrieved 28 April 2012 . ^ a b c d e f g h i j k l m n o p q r s Ghanizadeh, A (Jun 2011).
  • Hiv/aids In Yunnan Wikipedia
    Promoting condom use among female prostitutes in natural settings in Yunnan, China. 12th International AIDS Conference; Geneva, Switzerland; June 28–July 3, 1998. ^ Eldis gateway. HIV/AIDS: China's Titanic peril: 2001 update of the AIDS situation and needs assessment report.
  • Aberrations Of The Eye Wikipedia
    Contact Lens & Anterior Eye : The Journal of the British Contact Lens Association . 28 (2): 75–92. doi : 10.1016/j.clae.2005.02.003 .
  • Okamoto Syndrome Wikipedia
    "hnRNP K Is a Haploinsufficient Tumor Suppressor that Regulates Proliferation and Differentiation Programs in Hematologic Malignancies" . Cancer Cell . 28 (4): 486–499. doi : 10.1016/j.ccell.2015.09.001 .
    HNRNPK
    • Hydronephrosis, Congenital, With Cleft Palate, Characteristic Facies, Hypotonia, And Mental Retardation Omim
      Clinical Features Okamoto et al. (1997) reported what they believed to be a new MCA/MR syndrome in a 2-year-old Japanese girl and an unrelated 15-month-old Japanese boy. Manifestations included congenital hydronephrosis, severe mental retardation, growth failure, generalized floppiness, and cleft palate. The facies showed midface hypoplasia, hypertrichosis, long eyelashes, prominent eyes, epicanthus, low-set ears, long ear lobe, flat nasal bridge, short upturned nose, long philtrum, and webbed neck. The girl had mild aortic stenosis and regurgitation; ventricular septal defect, atrial septal defect, and patent ductus arteriosus (see 607411) had closed. The boy had endocardial cushion defect. In both patients, the karyotype was normal, the parents were nonconsanguineous and healthy, and sibs were normal.
    • Okamoto Syndrome Orphanet
      Okamoto syndrome is characterised by congenital hydronephrosis, intellectual deficit, growth retardation, cleft palate, generalised hypotonia and a characteristic face. Cardiac anomalies have also been reported. To date, 6 cases have been reported.
  • Fear Of Children Wikipedia
    Scharf, R. (2001) "Pedophobia, the gynarchy , and the androcracy ," Journal of Psychohistory 28 (3) (Winter 2001) p. 281-302. v t e Mental and behavioral disorders Adult personality and behavior Gender dysphoria Ego-dystonic sexual orientation Paraphilia Fetishism Voyeurism Sexual maturation disorder Sexual relationship disorder Other Factitious disorder Munchausen syndrome Intermittent explosive disorder Dermatillomania Kleptomania Pyromania Trichotillomania Personality disorder Childhood and learning Emotional and behavioral ADHD Conduct disorder ODD Emotional and behavioral disorders Separation anxiety disorder Movement disorders Stereotypic Social functioning DAD RAD Selective mutism Speech Stuttering Cluttering Tic disorder Tourette syndrome Intellectual disability X-linked intellectual disability Lujan–Fryns syndrome Psychological development ( developmental disabilities ) Pervasive Specific Mood (affective) Bipolar Bipolar I Bipolar II Bipolar NOS Cyclothymia Depression Atypical depression Dysthymia Major depressive disorder Melancholic depression Seasonal affective disorder Mania Neurological and symptomatic Autism spectrum Autism Asperger syndrome High-functioning autism PDD-NOS Savant syndrome Dementia AIDS dementia complex Alzheimer's disease Creutzfeldt–Jakob disease Frontotemporal dementia Huntington's disease Mild cognitive impairment Parkinson's disease Pick's disease Sundowning Vascular dementia Wandering Other Delirium Organic brain syndrome Post-concussion syndrome Neurotic , stress -related and somatoform Adjustment Adjustment disorder with depressed mood Anxiety Phobia Agoraphobia Social anxiety Social phobia Anthropophobia Specific social phobia Specific phobia Claustrophobia Other Generalized anxiety disorder OCD Panic attack Panic disorder Stress Acute stress reaction PTSD Dissociative Depersonalization disorder Dissociative identity disorder Fugue state Psychogenic amnesia Somatic symptom Body dysmorphic disorder Conversion disorder Ganser syndrome Globus pharyngis Psychogenic non-epileptic seizures False pregnancy Hypochondriasis Mass psychogenic illness Nosophobia Psychogenic pain Somatization disorder Physiological and physical behavior Eating Anorexia nervosa Bulimia nervosa Rumination syndrome Other specified feeding or eating disorder Nonorganic sleep Hypersomnia Insomnia Parasomnia Night terror Nightmare REM sleep behavior disorder Postnatal Postpartum depression Postpartum psychosis Sexual dysfunction Arousal Erectile dysfunction Female sexual arousal disorder Desire Hypersexuality Hypoactive sexual desire disorder Orgasm Anorgasmia Delayed ejaculation Premature ejaculation Sexual anhedonia Pain Nonorganic dyspareunia Nonorganic vaginismus Psychoactive substances, substance abuse and substance-related Drug overdose Intoxication Physical dependence Rebound effect Stimulant psychosis Substance dependence Withdrawal Schizophrenia , schizotypal and delusional Delusional Delusional disorder Folie à deux Psychosis and schizophrenia-like Brief reactive psychosis Schizoaffective disorder Schizophreniform disorder Schizophrenia Childhood schizophrenia Disorganized (hebephrenic) schizophrenia Paranoid schizophrenia Pseudoneurotic schizophrenia Simple-type schizophrenia Other Catatonia Symptoms and uncategorized Impulse control disorder Klüver–Bucy syndrome Psychomotor agitation Stereotypy v t e Youth empowerment Elements Evolving capacities Free-range parenting Intergenerational equity Leaving the nest Student voice Youth-adult partnership Youth mainstreaming Youth rights Youth voice Types Community youth development Popular education Anarchistic free school Democratic free school Positive youth development Student activism Student-centered learning Student rights Student voice Youth activism Youth council Youth court Youth engagement Youth leadership Youth-led media Youth movement Youth participation Youth philanthropy Youth service Youth suffrage Youth vote Youth voice Barriers Adultcentrism Adultism Age restrictions Ageism Control freak Fear of youth (ephebiphobia) Eleutherophobia Fear of children (pediaphobia) Gerontocracy Grounding Helicopter parent Infantilization Intrusiveness Narcissism Parental respect School-to-prison pipeline Vicariousness Paternalism Patriarchy Youth control complex Related articles The Catcher in the Rye Greaser Beatnik Teenage rebellion Beat Generation Subcultures of the 1950s Counterculture of the 1960s Defense of infancy Hippies Hungry generation International Youth Year The Teenage Liberation Handbook UK underground Index of youth rights-related articles v t e Discrimination General forms Age Caste Class Disability Education Economic Employment Genetic Hair texture Height Housing Language Looks Race / Ethnicity / Nationality Rank Sanity Sex Sexual orientation Size Skin color Social Acephobia Adultism Amatonormativity Anti-albinism Anti-autism Anti-homelessness Anti-intellectualism Anti-intersex Anti-left handedness Anti-Masonry Antisemitism (Judeophobia) Aporophobia Audism Biphobia Clannism Cronyism Drug use Elitism Ephebiphobia Fatism Gerontophobia Heteronormativity Heterosexism HIV/AIDS stigma Homophobia Leprosy stigma Lesbophobia Misandry Misogyny Nepotism Pedophobia Perpetual foreigner Pregnancy Reverse Sectarianism Supremacism Black White Transphobia Non-binary Transmisogyny Vegaphobia Xenophobia Religious Ahmadiyya Atheism Baháʼí Faith Buddhism Catholicism Christianity post–Cold War era Falun Gong Hinduism Persecution Islam Persecution Jehovah's Witnesses Judaism Persecution LDS or Mormon Neopaganism Eastern Orthodox Oriental Orthodox Protestantism Rastafarianism Shi'ism Sufism Zoroastrianism Ethnic/National African Albanian American Arab Armenian Australian Austrian British Canadian Catalan Chilean Chinese Croat Dutch English Estonian European Filipino Finnish French Georgian German Greek Haitian Hazara Hindu Hispanic Hungarian Igbo Indian Indonesian Iranian Irish Israeli Italian Japanese Jewish Khmer Korean Kurdish Malay Manchu Mexican Middle Eastern Mongolian Pakistani Pashtun Polish Portuguese Quebec Romani Romanian Russian Scottish Serb Slavic Somali Soviet Tatar Thai Turkish Ukrainian Venezuelan Vietnamese Western Manifestations Blood libel Bullying Compulsory sterilization Counter-jihad Cultural genocide Defamation Democide Disability hate crime Dog-whistle politics Eliminationism Enemy of the people Ethnic cleansing Ethnic conflict Ethnic hatred Ethnic joke Ethnocide Forced conversion Freak show Gay bashing Gendercide Genital modification and mutilation Genocide examples Glass ceiling Hate crime Hate group Hate speech Homeless dumping Indian rolling Lavender scare LGBT hate crimes Lynching Mortgage Murder music Native American sports mascots Occupational segregation Persecution Pogrom Purge Red Scare Religious persecution Religious terrorism Religious violence Religious war Scapegoating Segregation academy Sex-selective abortion Slavery Slut-shaming Trans bashing Victimisation 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  • Hyperekplexia Wikipedia
    "The Glycine Transporter GlyT2 Controls the Dynamics of Synaptic Vesicle Refilling in Inhibitory Spinal Cord Neurons" . Journal of Neuroscience . 28 (39): 9755–68. doi : 10.1523/JNEUROSCI.0509-08.2008 .
    GLRB, SLC6A5, GLRA1, GPHN, ATAD1, CSF1R, PRNP
    • Hyperekplexia 2 Omim
      A number sign (#) is used with this entry because of evidence that hyperekplexia-2 (HKPX2) is caused by compound heterozygous or homozygous mutation in the GLRB gene (138492) on chromosome 4q32. For a general phenotypic description and a discussion of genetic heterogeneity of hyperekplexia, see HKPX1 (149400). Clinical Features Rees et al. (2002) reported a male neonate who presented with generalized hypertonia and hyperreactivity 3 hours after birth. He had an exaggerated startle response and myoclonus elicited by testing the tendon reflexes or tapping on the back. Moro reflex was absent. Hyperreflexia and exaggerated startle response were noted until about 1 year of age, and then decreased somewhat.
    • Hyperekplexia 4 Omim
      A number sign (#) is used with this entry because of evidence that hyperekplexia-4 (HKPX4) is caused by homozygous mutation in the ATAD1 gene (614452) on chromosome 10q23. Description Hyperekplexia-4 is an autosomal recessive severe neurologic disorder apparent at birth. Affected infants have extreme hypertonia and appear stiff and rigid. They have little if any development, poor or absent visual contact, and no spontaneous movement, consistent with an encephalopathy. Some patients have early-onset refractory seizures, and many have inguinal or umbilical hernia. Most patients die in the first months of life due to respiratory failure or other complications (summary by Piard et al., 2018).
    • Hereditary Hyperekplexia Orphanet
      Hereditary hyperekplexia is a hereditary neurological disorder characterized by excessive startle responses. Epidemiology To date about 150 cases have been reported in the literature. Clinical description Hereditary hyperekplexia manifests shortly after birth with violent jerking to noise and touch, and massive and sustained stiffening of the trunk and limbs, clenching fists, and attacks of a high-frequency trembling. Newborns are at risk for sudden infant death due to laryngospasm and cardiorespiratory failure. Stiffness attacks may resemble epileptic seizures, although sleep can reduce or even abolish stiffness and jerking and EEG is normal.
    • Hereditary Hyperekplexia Gard
      Hereditary hyperekplexia is a nervous system disorder ( neurological disorder ), that is usually noticed shortly after birth. Symptoms in a newborn include generalized muscle stiffness while awake ( hypertonia ) and exaggerated startle reflex to unexpected loud noises, visual stimuli, or touch. Following the startle reaction, infants experience a brief period in which they are very rigid and are unable to move. During these rigid periods, some infants may stop breathing (apnea), which can be fatal and has been associated with sudden infant death syndrome (SIDS). Muscle stiffness usually fades completely during the first few years of life.
    • Hyperekplexia 3 Omim
      A number sign (#) is used with this entry because hyperekplexia-3 (HKPX3) is caused by homozygous or compound heterozygous mutation in the GLYT2 gene (SLC6A5; 604159) on chromosome 11p15. There is also evidence that a heterozygous mutation in the SLC6A5 gene can result in HKPX3. For a general description and a discussion of genetic heterogeneity of hyperekplexia, see HKPX1 (149400). Clinical Features Rees et al. (2006) reported 7 patients, including 2 sibs, with hyperekplexia. Affected individuals presented with neonatal hypertonia, an exaggerated startle response to tactile or acoustic stimuli, and life-threatening neonatal apnea episodes.
    • Hyperekplexia 1 Omim
      A number sign (#) is used with this entry because hyperekplexia-1 (HKPX1) is caused by heterozygous, homozygous, or compound heterozygous mutation in the GLRA1 gene (138491) on chromosome 5q32. Description Hyperekplexia is an early-onset neurologic disorder characterized by an exaggerated startle response to sudden, unexpected auditory or tactile stimuli. Affected individuals have brief episodes of intense, generalized hypertonia in response to stimulation. Neonates may have prolonged periods of rigidity and are at risk for sudden death from apnea or aspiration. Many affected infants have inguinal hernias. The symptoms tend to resolve after infancy, but adults may have increased startle-induced falls and/or experience nocturnal muscle jerks (summary by Ryan et al., 1992).
  • Flail Chest Wikipedia
    "Thoracic trauma: The deadly dozen". Critical Care Nursing Quarterly . 28 (1): 22–40. doi : 10.1097/00002727-200501000-00004 .
  • Expressive Language Disorder Wikipedia
    Int J Lang Commun Disord . 44 (4): 511–28. doi : 10.1080/13682820802708098 .
  • Communication Disorder Wikipedia
    "Relationship between speech-sound disorders and early literacy skills in preschool-age children: impact of comorbid language impairment" . J Dev Behav Pediatr . 28 (6): 438–47. doi : 10.1097/DBP.0b013e31811ff8ca .
    FOXP2, APOE, ARSD, AVPR1A, CALML3, DLD, DRD2, VEGFA, CSRP3, COTL1, SHANK3, AUTS5, CALHM1
  • Kyphosis Wikipedia
    "Prediction of osteoporotic spinal deformity". Spine . 28 (5): 455–62. doi : 10.1097/00007632-200303010-00009 .
    PLOD1, SLC26A2, PARP1, SLC39A13, LTBP3, FHL1, FGFR3, IDUA, HLA-B, TRIO, SYNE2, KLHL41, TGFB1, SEC23B, EBP, DLL3, CPLX1, TLK2, ERLIN2, RAB3GAP1, RAB18, DKK1, ACTA1, TBX5, MAPK8IP3, EXOC6B, UBA1, BICD2, SYNE1, OBSL1, TBX2, CLCF1, ATP6V0A2, NPAP1, RAB3GAP2, SH2B1, AUTS2, WIPI2, ZBTB20, TBL2, CCDC22, ZMPSTE24, MKRN3-AS1, MFN2, WASHC5, CLIP2, WHCR, NSD2, NELFA, WNT1, MKRN3, ALMS1, NAA10, ARID1A, CUL4B, TPM2, KCNAB2, MBTPS1, CCN6, HERC2, HERC1, BAZ1B, AIP, USP8, AIFM1, CTDP1, CRLF1, PLAA, EIF2AK3, GTF2IRD1, PTDSS1, TPI1, CUL7, SEC24D, FLVCR1, ACP5, NDUFAF4, GPR101, MGME1, WNT3A, HES7, GNPTG, PHF6, CCDC8, LAS1L, FKRP, ASXL3, PUS1, ALG9, SRD5A3, TMEM43, GNPTAB, SLC52A3, CANT1, B3GALT6, TBC1D20, RIPPLY2, VPS37A, PWAR1, MESP2, VPS13B, ARID2, KANSL1, SH3PXD2B, SNORD115-1, KY, FAM111B, PWRN1, SNORD116-1, FA2H, UPF3B, ANKRD11, FGFRL1, SETD5, BCOR, DYM, P4HTM, GTPBP2, MAGEL2, MBTPS2, KLC2, NDUFAF1, SEPSECS, YARS2, PDE11A, NSDHL, VAMP1, ASXL2, UFSP2, KMT2E, ZC4H2, LMOD3, SHROOM4, ARID1B, HACE1, TRPV4, SLC5A7, FKBP10, PIEZO2, PRDM16, P3H1, ROBO3, NXN, SIL1, TAF1, TFAP2A, KLLN, L1CAM, COL1A1, GNAS, GRIA3, GTF2I, HTT, HGD, HSPG2, IDS, ERCC8, SOX11, IPW, KIF22, CHRNG, NOTCH2, LETM1, CFL2, LFNG, LIMK1, LMNA, SCARB2, MECP2, MEIS2, NDN, NEB, NEU1, TONSL, GLI3, GLE1, GLB1, GJB1, CSF1R, CTBP1, CTSK, COL11A2, COL6A3, DCC, DHCR7, TOR1A, COL6A2, ELN, COL6A1, EMD, COL5A2, ERCC6, COL5A1, COL2A1, EXTL3, EZH2, COL1A2, FOXG1, FN1, FUCA1, GABRD, GALNS, GBA, COMP, NONO, NOTCH3, RET, NPR2, BGN, ATP7A, RERE, SDHB, SDHC, SDHD, TRAPPC2, ASAH1, SKI, SMARCA4, ABCC6, BIN1, SMARCB1, ALDH3A2, SMARCC2, SMARCE1, AKT1, AGA, SNRPB, SNRPN, SON, SOX4, ACTB, SOX9, RFC2, RPS6KA3, DPF2, POLD1, ROR2, NUP88, OCRL, TNFRSF11B, P4HB, CBS, RUNX2, PIK3CA, PLOD2, PMM2, PIK3R2, COL12A1, PTEN, PTCH1, PPIB, PRKAR1A, CTSA, PRPS1, MAP2K1, RSS, SMS, LGALS1, DMD, CD6, BMP2, MPEG1, CALR, DHDDS, ALDH2, CAPG, CD38, TRIM21, CRP, PGR, MAPK1, PKD2L1, PTPN11, DYSF, RPS27, UBL4A, SFPQ, SHOX, BEST1, UTRN, TTK, TSC2, CLEC3B, THBS1, MAP3K7, PLAT, PCNA, ASPSCR1, CTPP, CD55, DAO, EPHA2, NCOA5, SEMA6A, EPHB2, CHPT1, BBX, FBN1, APH1A, IGFBP7, LBP, ASF1A, SMAD3, CD46, IL6
    • Gibbus Deformity Wikipedia
      Gibbus deformity is a form of structural kyphosis typically found in the upper lumbar and lower thoracic vertebrae , where one or more adjacent vertebrae become wedged. Gibbus deformity most often develops in young children as a result of spinal tuberculosis and is the result of collapse of vertebral bodies. [1] [2] [3] This can in turn lead to spinal cord compression causing paraplegia . [4] [5] In addition to tuberculosis, other possible causes of gibbus deformity include pathological diseases, hereditary and congenital conditions, and physical trauma to the spine that results in injury. [6] [7] Gibbus deformity may result from the sail vertebrae associated with cretinism (the childhood form of hypothyroidism ), mucopolysaccharidosis (MPS) , and certain congenital syndromes, including achondroplasia . [8] Because most children with MPS I ( Hurler Syndrome ) also exhibit symptoms of a gibbus deformity, the latter can possibly be used to identify the former. [9] Gibbus deformity is included in a subset of structural kyphosis that is distinguished by a higher-degree angle in the spinal curve that is specific to these forms of kyphosis. Other conditions within this subset include Pott's disease and Scheuermann kyphosis , but gibbus deformity is marked by an especially sharp angle. Viewed from behind, the resulting hunchback is more easily seen when bending forward. [10] A kyphosis of >70° can be an indication of the need for surgery and these surgeries can be necessary for children as young as two years old, with a reported average of 8 years of age. [9] References [ edit ] ^ Kasper D.L. et al., Harrisons principles of internal medicine, 16.ed, 2005 p.958 ^ Batirel, A.; Erdem, H.; Sengoz, G.; Pehlivanoglu, F.; Ramosaco, E.; Gülsün, S.; Tekin, R.; Mete, B.; Balkan, İ.İ. (2015). "The course of spinal tuberculosis (Pott disease): results of the multinational, multicentre Backbone-2 study" .
    • Kyphosis Mayo_clinic
      Overview Kyphosis is an exaggerated, forward rounding of the upper back. In older people, kyphosis is often due to weakness in the spinal bones that causes them to compress or crack. Other types of kyphosis can appear in infants or teens due to malformation of the spine or wedging of the spinal bones over time. Mild kyphosis causes few problems. Severe kyphosis can cause pain and be disfiguring. Treatment for kyphosis depends on your age, and the cause and effects of the curvature.
  • Humerus Fracture Wikipedia
    Retrieved 25 August 2016 . Crosby, L.; Neviaser, R. (28 October 2014). Proximal Humerus Fractures: Evaluation and Management .
  • Medullary Thyroid Cancer Wikipedia
    Prognosis [ edit ] Depending on source, the overall 5-year survival rate for medullary thyroid cancer is 80%, [15] 83% [16] or 86%, [6] and the 10-year survival rate is 75%. [15] By overall cancer staging into stages I to IV, the 5-year survival rate is 100% at stage I, 98% at stage II, 81% at stage III and 28% at stage IV. [17] The prognosis of MTC is poorer than that of follicular and papillary thyroid cancer when it has metastasized (spread) beyond the thyroid gland.
    RET, NTRK1, KRAS, EGFR, FLCN, SST, TP53, CEACAM5, CALCA, BRAF, PSG2, CEACAM3, CEACAM7, POMC, MIR375, S100A12, CHGA, MT1A, VEGFA, SLC5A5, SMUG1, HRAS, CCKBR, MET, KDR, CDKN2C, MEN1, TG, MIR21, PTCH1, ASCL1, TSHR, EGF, HSPA4, F9, MAP1LC3B, SSTR2, FLT4, GDF1, GLP1R, SHC3, NKX2-1, IL2, CD274, PPP1R13L, SDHD, RNH1, CCDC6, PIK3CG, PIK3CD, PIK3CB, PIK3CA, TAS2R38, CALCR, HSP90AA1, PRL, CFL1, CALCB, PMPCA, MIR224, PTH, MAFK, PDCD4, PTGS2, PTPRF, RAF1, CXCR4, PAX8, HSPA9, LINC01194, PROX1, CDKN2A, MIR34A, CDKN1B, EEF1E1, NOTCH1, CDK5, PTTG1, ZNF197, PCNA, MYCN, COX2, YAP1, SCARB1, MOS, MIR183, CCK, CASR, PROM1, CTNNB1, NOTCH3, VHL, ATF4, MTCO2P12, AGBL2, FOLH1, ZMYND10, TGM2, STAT3, DOCK11, TPPP2, GFRA1, GFRA3, SSTR1, H3P12, TTF1, TSE2, SYP, ERBB2, ATRAID, MIR455, MTOR, ESR2, UBE2N, LAMTOR1, UBE2I, GRAP2, TGFB1, SQSTM1, CDK5R1, H3P9, TGFA, PDCD5, BECN1, LOC110806263, TK1, ZNF22, MIR31, ABCG2, UVRAG, ZGLP1, TWIST1, CND, UPK3B, TPO, MCS+9.7, ARID1A, TP63, TNFRSF10B, TMEM11, MIR222, CDCA5, MRPL28, PDE4DIP, XPO5, C17orf97, NTM, DERL2, DCTN4, MALAT1, P2RY13, KRT20, DGCR8, CHPT1, ACKR3, NANOS2, NDRG2, MIB1, SCO2, CTAG1A, RXFP1, SMYD3, MAPKAP1, FSD1, MCPH1, EHMT1, HNRNPA3, DHDDS, FSD1L, MAP1LC3A, MTDH, NXT1, GIT1, TFF1, MCAT, HNRNPA3P1, SPRY1, MIR182, MERTK, SEC23A, RXFP2, KHDRBS1, MIR17, BLCAP, SUB1, CKAP4, SDS, RNF139, DCTN3, CHP1, PHB2, ZHX2, MIR149, RPIA, TPX2, TBC1D9, MIR144, NUP62, LRIG1, MIR10A, EML4, NAT2, TERT, PRDX2, ESR1, EZH2, FCN2, FLT1, FOS, FOSB, GAST, FUT4, G6PD, GCG, GCHFR, GDNF, GLB1, GLI2, GOT2, GRB2, GRP, GSK3B, GSTP1, GTF2H1, HABP2, HIF1A, HK2, NR4A1, FOXA1, HPGD, HES1, HSPA5, TNC, EPHB2, TYMP, DPP4, CBR1, ALCAM, ALK, ANXA1, APC, APRT, AR, CCND1, BCL2, BDNF, BNIP3, KLF9, CA9, CASP3, TNFRSF8, DYNC1H1, CDK9, CDKN1A, CDKN2B, CLU, SLC31A2, CRH, CTAG1B, CTSK, CYP1A2, DBH, DCK, DCR, SARDH, ICAM1, ID1, IL1B, RNASE3, SLC26A4, ABCB1, PLK1, PPARG, PPP3CA, PPY, MAPK1, MAPK3, PSG5, AKT1, PTGS1, RASA2, RBP3, RPE65, PAX9, RPS6KA3, RREB1, CXCL12, SDHB, SDHC, SLC16A1, SOAT1, SORD, SPN, SPP1, SRC, SSTR5, STK11, PDGFRB, NRAS, IL12A, MEA1, INSL3, INSM1, JUN, JUNB, JUND, KIF5B, KIT, KRT19, LIF, LMNA, LUM, TACSTD2, MDM2, MFAP1, PNP, MIF, MME, MNAT1, MRC1, MSH2, MSN, COX1, NFKB1, NGF, NME1, NODAL, NOS2, NOTCH2, H3P10
    • Medullary Thyroid Carcinoma Orphanet
      Medullary thyroid carcinoma (MTC) is developed from thyroid C cells that secrete calcitonin (CT). Epidemiology MTC represents 5-10% of thyroid cancers with a 1-2% incidence in nodular thyroid diseases. Estimated prevalence in the general population is 1/14,300. Diagnostic methods Diagnosis is usually made in the presence of a solitary nodule often associated with nodal metastasis and confirmed by a high basal CT level which represents its biological marker. MTC may present as a sporadic form, and in about 30% of cases, as a familial form as a part of multiple endocrine neoplasia (see this term); a dominant inherited disease related to germline mutation of the protooncogene RET . Both biological (CT) and genetic ( RET ) markers allows optimal diagnosis and treatment of MTC; the former allowing screening and early diagnosis of MTC by routine CT measurements in nodular thyroid diseases that require adequate and complete surgery required to be performed.
  • Joubert Syndrome Wikipedia
    "Follow-Up in Children with Joubert Syndrome". Neuropediatrics . 28 (4): 204–211. doi : 10.1055/s-2007-973701 .
    INPP5E, AHI1, CPLANE1, TMEM67, KIAA0586, MKS1, PIBF1, TCTN1, TCTN2, CSPP1, CEP104, CEP41, ARMC9, TMEM237, HYLS1, ARL13B, RPGRIP1L, KIAA0753, KIAA0556, TMEM231, TMEM216, B9D2, B9D1, KIF7, CEP120, ARL3, TCTN3, FAM149B1, POC1B, TMEM138, ZIC1, CEP290, CC2D2A, OFD1, PDE6D, ITPR1, RCOR1, RNU4ATAC, ALX4, MVK, MEF2C, TFAP2A, IFT172, LRRCC1, C2CD3, NPHP1, LPO, CLUAP1, INVS, ARL13A, NPHP4, TMEM107, WNT1, CELSR2, BARHL1, BPIFA4P, ITFG1, TIPRL, PPP1R21, LCA5, METTL8, RPGRIP1, ANPEP, CHD7, SUFU, ATF4, CCND1, CSF2, TIMM8A, DVL1, FGF8, GYS2, INPP5B, JBS, LAMC2, RAC2, RASA1, RASGRF1, SMO, SOS1, TULP3, ZNF131, MKKS, MLRL, SYNJ1, SYNJ2, HAP1, ADGRG1, RGS6, KAT5, ZNF423, DMXL2, NXPH1, CEND1, LCA10
    • Joubert Syndrome Gene_reviews
      Fourteen (~3%) of 462 families with JS had pathogenic variants in TMEM216 [Valente et al 2010]. 28. Valente et al [2010], Lee et al [2012b] Table 1b. ... Genes Associated with JS by Phenotypic Features View in own window Gene Phenotypic Feature (in addition to the molar tooth sign) Allelic/Related Disorder 3 Retinal dystrophy Coloboma 1 Renal Oculorenal 2 Hepatic 1 Oral Polydactyly Other AHI1 ++ 4 (+) + 5 + (+) Polymicrogyria 6 CPLANE1 (+) + 7 + 7 Founder effects in French-Canadian 8 & Dutch populations 9 OFD VI CC2D2A + + + + + 10 Encephalocele, ventriculomegaly, seizures 11 ; milder phenotype in French-Canadian population 12 Meckel syndrome 13 CEP290 ++ + ++ ++ 14 + Encephalocele; cardiac; situs inversus; other 15 LCA, Meckel syndrome, BBS CSPP1 (+) (+) (+) (+) SNHL; corpus callosum hypoplasia; encephalocele; founder variant in Hutterite population 16 Meckel syndrome, JATD 17 INPP5E + + + (+) + MORM syndrome 18 KIAA0586 (+) + (+) (+) Broad range of phenotypes: severe HLS (& cleft palate) to JATD w/short ribs & narrow thorax to pure JS 19 HLS, JATD MKS1 (+) Kidney/liver findings & PD described in 1 individual 20 Meckel syndrome NPHP1 + ++ + "Mild molar tooth" sometimes described 21 Juvenile NPHP type 1, Cogan syndrome RPGRIP1L (+) (+) ++ + (+) (+) Encephalocele Meckel syndrome, retinal disease 22 TCTN2 21 Clubfoot 23 Meckel syndrome 24 TMEM67 + 25 + ++ 26, 27 (+) Encephalocele Meckel syndrome 28 TMEM216 29 (+) (+) ++ + (+) + + Cardiac findings; encephalocele Meckel syndrome (+) = feature is uncommon but has been described; + = feature is present in some cases; ++ = Major feature; HLS = hydrolethalus syndrome; NPHP = nephronophthisis; LCA = Leber congenital amaurosis; BBS = Bardet-Biedl syndrome; MORM = mental retardation, truncal obesity, retinal dystrophy, micropenis [Jacoby et al 2009]; OFD = oral-facial-digital syndrome; PD = polydactyly; JATD = jeune asphyxiating thoracic dystrophy; SNHL = sensorineural hearing loss 1. ... Baala et al [2007], Brancati et al [2009], Doherty et al [2010], Vilboux et al [2017] 28. More severe loss-of-function variants in TMEM67 have been identified in individuals with lethal forms of Meckel syndrome [Smith et al 2006], in comparison with variants with partial function causing JS with hepatic disease or nephronophthisis and liver fibrosis in the absence of the molar tooth sign and other neurologic symptoms [Otto et al 2009, Doherty et al 2010]. 29.
    • Joubert Syndrome Gard
      Joubert syndrome is disorder of brain development that may affect many parts of the body. It is characterized by the absence or underdevelopment of the cerebellar vermis (a part of the brain that controls balance and coordination) and a malformed brain stem (connection between the brain and spinal cord). Together, these cause the characteristic appearance of a molar tooth sign on MRI. Signs and symptoms can vary but commonly include weak muscle tone (hypotonia); abnormal breathing patterns; abnormal eye movements; ataxia; distinctive facial features; and intellectual disability. Various other abnormalities may also be present. Joubert syndrome may be caused by mutations in any of many genes.
  • Sunct Syndrome Wikipedia
    "Seasonal periodicity in SUNCT syndrome". Cephalalgia . 28 (1): 94–6. doi : 10.1111/j.1468-2982.2007.01434.x .
    • Sunct Syndrome Orphanet
      SUNCT syndrome (Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing) is a primary headache disorder characterized by unilateral trigeminal pain that occurs in association with ipsilateral cranial autonomic symptoms (conjunctival injection and tearing). Epidemiology The prevalence is estimated at approximately 1 in 15,000. It is slightly more predominant in males (male-to-female ratio of 1.5:1), with a mean age of onset of around 50 years. A few cases of SUNCT syndrome have been reported in children. Clinical description The disease manifests with strictly unilateral pain attacks of moderate-to-severe intensity. The pain is described as throbbing, sharp or stabbing. It usually involves the ophthalmic division of the trigeminal nerve but, rarely, it may involve any part of the head.
  • Epidermolysis Bullosa, Junctional, Non-Herlitz Type Omim
    There was no history of gastrointestinal symptoms or previous abdominal surgery. Revertant Mosaicism In a 28-year-old Dutch woman with a mosaic non-Herlitz JEB phenotype (Jonkman et al., 1995; Jonkman et al., 1996), Jonkman et al. (1997) identified compound heterozygosity for mutations in COL17A1 and demonstrated that the mosaic phenotype was caused by reversion of the maternally inherited 1-bp deletion (113811.0005) due to the nonreciprocal transfer of a part of 1 parental allele for the other by a mitotic gene conversion mechanism.
    LAMC2, ITGB4, LAMA3, LAMB3, LAMC1
    • Junctional Epidermolysis Bullosa Inversa Orphanet
      Junctional epidermolysis bullosa inversa is a rare severe subtype of junctional epidermolysis bullosa (JEB, see this term) characterized by blistering and erosions confined to intertriginous skin sites, the esophagus, and vagina. Epidemiology Prevalence is unknown. Four Scandinavian families and a case in England have been reported. Clinical description The condition is present at birth. Blistering is usually severe and lesions subsequently localize to folds especially axillae, groins, and perineum. Manifestations include atrophic scarring, nail dystrophy and sometimes milia formation. Extracutaneous manifestations include enamel hypoplasia and dental caries, oral, esophageal and vaginal blisters and erosions.
  • Whale Oil Wikipedia
    . ^ One or more of the preceding sentences incorporates text from a publication now in the public domain : Chisholm, Hugh, ed. (1911). " Whale-oil ". Encyclopædia Britannica . 28 (11th ed.). Cambridge University Press. pp. 573–574. ^ a b Tønnessen, Johan Nicolay; Johnsen, Arne Odd (1982-01-01).
  • Cadasil Wikipedia
    Lesnik Oberstein SA, Boon EM, Terwindt GM (June 28, 2012). CADASIL . University of Washington, Seattle.
    NOTCH3, HTRA1, EGF, COL4A1, COL18A1, NOTCH1, JAG1, APOE, APP, LPA, TREX1, GFAP, PLXNA2, CTSA, PROC, ACTB, SOD1, TGFB1, NOTCH2, LAP, MRS2, RNF213, NOX5, THBD, KDR, NEFL, ACTG2, RBPJ, FN1, FBN1, ELN, DVL1, DCN, CSF3, CSF1R, CLU, CACNA1A, BGN, APCS, LINC01191
    • Cadasil Gene_reviews
      Summary Clinical characteristics. CADASIL ( c erebral a utosomal d ominant a rteriopathy with s ubcortical i nfarcts and l eukoencephalopathy) is characterized by mid-adult onset of recurrent ischemic stroke, cognitive decline progressing to dementia, a history of migraine with aura, mood disturbance, apathy, and diffuse white matter lesions and subcortical infarcts on neuroimaging. Diagnosis/testing. The diagnosis of CADASIL is established in a proband either by identification of a heterozygous pathogenic variant in NOTCH3 by molecular genetic testing or, if molecular genetic testing is not definitive, by detection of characteristic findings by electron microscopy and immunohistochemistry of a skin biopsy. Management. Treatment of manifestations: There is no treatment of proven efficacy for CADASIL. Standard supportive treatment for stroke; the effect of thrombolytic therapy for the treatment of stroke remains unknown. Migraine should be treated symptomatically. Standard treatment for psychiatric disturbance.
    • Cerebral Autosomal Dominant Arteriopathy-Subcortical Infarcts-Leukoencephalopathy Orphanet
      CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a hereditary cerebrovascular disorder characterized by mid-adult onset of recurrent subcortical ischemic stroke and cognitive impairment progressing to dementia in addition to migraines with aura and mood disturbances seen in about a third of patients. Epidemiology In Europe, the prevalence of CADASIL has been estimated to range between 1/50 000- 1/25 000. Clinical description The first manifestation of the disease occurs at a mean age of 45-50, usually in the form of ischemic stroke or cognitive decline. The disease onset and course is variable, but more than two thirds of patients suffer from (recurrent) stroke or dementia. Migraine, usually with aura, occurs in about a third of patients and often precedes stroke and dementia symptoms, with a mean age of onset of about 30 years.
    • Cerebral Arteriopathy, Autosomal Dominant, With Subcortical Infarcts And Leukoencephalopathy, Type 1 Omim
      A number sign (#) is used with this entry because of evidence that autosomal dominant cerebral arteriopathy with subcortical infarcts and leukoencephalopathy type 1 (CADASIL1) is caused by heterozygous mutation in the NOTCH3 gene (600276) on chromosome 19p13. Description Autosomal dominant cerebral arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a progressive disorder of the small arterial vessels of the brain manifest by migraine, strokes, and white matter lesions, with resultant cognitive impairment in some patients (review by Kalimo et al., 1999). Clinical Features Stevens et al. (1977) reported an English family with onset of recurrent cerebral ischemic strokes between 39 and 57 years resulting in progressive neurologic dysfunction and eventual dementia. Affected individuals did not have hypertension, diabetes, or increased cholesterol, but neuropathologic investigation showed abnormalities of the cerebral vasculature; the authors suggested that it was a form of 'vascular encephalopathy.' Low et al. (2007) provided a follow-up of the family reported by Stevens et al. (1977), including confirmation of the CADASIL diagnosis by identification of a pathogenic mutation in the NOTCH3 gene (see MOLECULAR GENETICS).
    • Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts And Leukoencephalopathy Medlineplus
      Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, usually called CADASIL, is an inherited condition that causes stroke and other impairments. This condition affects blood flow in small blood vessels , particularly cerebral vessels within the brain. The muscle cells surrounding these blood vessels (vascular smooth muscle cells ) are abnormal and gradually die. In the brain, the resulting blood vessel damage (arteriopathy) can cause migraines, often with visual sensations or auras, or recurrent seizures (epilepsy). Damaged blood vessels reduce blood flow and can cause areas of tissue death (infarcts) throughout the body.
    • Cadasil Gard
      CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy) is an inherited disease of the blood vessels that occurs when the thickening of blood vessel walls blocks the flow of blood to the brain. The disease primarily affects the small blood vessels in the white matter of the brain. CADASIL is characterized by migraine headaches and multiple strokes , which progresses to dementia. Other symptoms include white matter lesions throughout the brain, cognitive deterioration, seizures, vision problems, and psychiatric problems such as severe depression and changes in behavior and personality. Individuals may also be at higher risk of heart attack. Symptoms and disease onset vary widely, with signs typically appearing in the mid-30s.
  • Hematuria Wikipedia
    . ^ a b c d e f g h i j k l m n o p "Medical Student Curriculum: Hematuria - American Urological Association" . www.auanet.org . Retrieved 2019-11-28 . ^ Izzo, Joseph L.; Sica, Domenic A.; Black, Henry Richard (2008).
    COL4A5, CFHR5, COL4A1, LMX1B, MYH9, ASPG, POMC, F7, PLAU, FOS, COL4A4, COL4A3, C3, B2M, NUMA1, NPM1, OCRL, NOTCH2, KIF1B, CD2AP, POU6F2, IL17RA, KANK2, PRDX1, MYO1E, SERPINF2, TMEM127, AGGF1, ITGA6, ITGA2, ITGA2B, ITGB3, ITGB4, SDHAF2, BCOR, LYZ, SMAD4, MAX, CD46, MDH2, PTPN22, MMACHC, PRTN3, PML, SPRY2, TSC1, TSC2, CLDN16, UMPS, YAP1, VHL, WT1, PRKAR1A, ZBTB16, TRIM28, SLC25A11, TRIP13, NUP93, GRHPR, TRAF3IP2, THBD, TGFB1, SRCAP, STAT5B, STAT4, STAT3, SPP1, SDHD, SDHC, SDHB, SDHA, RET, REST, RARA, CFI, TREX1, NUP133, IRAK1, DNASE1L3, IL17F, CLDN19, SCARB2, EFL1, GBA, GATA3, SLC37A4, TBL1XR1, FH, CD109, FGA, FIP1L1, F10, SLITRK6, IL17RC, DIS3L2, LMNB2, ENG, CCDC97, CLCNKB, DLST, HOGA1, GDF2, NABP1, H19, CLEC7A, HPRT1, HMOX1, HLA-DPB1, ACVRL1, HLA-DPA1, AGXT, CFH, HBB, MFF-DT, APOA1, C1R, APRT, CFB, GP1BB, IRF2BP2, GP1BA, GPC3, BRCA2, GLA, C1QA, CTLA4, IGAN1, CRP, TNF, KL, GPT, LAMC2, HPGDS, LAMA5, GSTP1, ALB, RAPGEF5, IGHA1, IQGAP3, AGT, ACE, CSF2, SFXN1, CX3CR1, INF2, TNFSF13B, ABCB6, MIR4511, GDF15, GSTK1, TLR9, RASSF1, ZMYND10, PCA3, PSAT1, FAM107A, RBM46, RNU1-1, SPAG8, CMIP, SLCO6A1, NID2, CFHR3, C1QL1, FCRLB, UBE2C, NPEPPS, ACAT1, GSTO1, CYP2C9, IL1RN, HSD11B2, HGF, PDIA3, GH1, GCH1, FN1, FGFR3, FCGR2B, FBN2, F3, F2, ESR1, DPYD, CYP1A1, IL17A, CRH, COL6A1, COL4A6, CLCN5, CISH, CDK5, CD14, CAT, CA9, BMP4, BCL2, KLK3, AMBP, ALCAM, IL6, KRT7, ADIPOQ, MAPK8, NRP1, IKBKG, FGF23, VIM, VEGFA, UBE2N, TWIST1, TLR4, TERT, SLC5A2, SGK1, CXCL12, PTGS2, PROS1, PLAG1, LASP1, PHEX, ACR, NOS3, NEUROG1, NEO1, MYBPH, MTHFR, COX2, MECP2, MCM5, MBL2, MB, MAT1A, LRPAP1, MTCO2P12
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