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  • Premature Ejaculation Wikipedia
    Med . 92 (2 Pt 2): 329–31. doi : 10.7326/0003-4819-92-2-329 . PMID 7356224 . ^ Truitt WA, Coolen LM (2002). "Identification of a potential ejaculation generator in the spinal cord".
    SLC6A4, OXTR, APP, PRL, SLC6A3, MMS, PART1, PKD2L1, PDE5A, VIP, SHBG, AR, HTR2C, FLT4, COMT, AVP, STIN2-VNTR
    • Premature Ejaculation Mayo Clinic
      Overview Premature ejaculation occurs in men when semen leave the body (ejaculate) sooner than wanted during sex. Premature ejaculation is a common sexual complaint. As many as 1 out of 3 people say they have it at some time. Premature ejaculation isn't cause for concern if it doesn't happen often. But you might be diagnosed with premature ejaculation if you: Always or nearly always ejaculate within 1 to 3 minutes of penetration Are not able to delay ejaculation during sex all or nearly all the time Feel distressed and frustrated, and tend to avoid sexual intimacy as a result Premature ejaculation is a treatable condition. Medications, counseling and techniques that delay ejaculation can help improve sex for you and your partner.
  • Pregnancy-Associated Malaria Wikipedia
    . ^ a b Mordmüller B, Sulyok M, Egger-Adam D, Resende M, de Jongh WA, Jensen MH, et al. (October 2019).
  • Pectus Excavatum Wikipedia
    Retrieved 7 September 2016 . ^ Fokin AA, Steuerwald NM, Ahrens WA, Allen KE (2009). "Anatomical, histologic, and genetic characteristics of congenital chest wall deformities".
    ABL1, IFT52, ATP6V0A2, LRRC6, RAB3GAP2, NIPBL, COG4, DNAH1, TCTN3, ZBTB20, TBL2, DNAI1, STK36, BBS9, PGAP2, EFEMP2, ZDHHC9, DNAH11, NME8, MBTPS2, ZMYND10, PIGT, MAP3K20, MAGEL2, HYDIN, BCOR, NSUN2, DNAAF5, CCDC40, ARMC4, MSTO1, DNAAF2, KAT6B, TGDS, SIK3, SPECC1L, SMC3, ACTA1, NOG, TRIP4, PIGL, GTF2IRD1, ADAMTSL2, TMEM94, PIEZO1, CUL7, ZEB2, SEC24D, TELO2, MED12, HUWE1, PQBP1, CD96, CCNO, KLHL41, SLC9A6, SEC23B, CRTAP, FBLN5, MRAS, PUF60, MORC2, KDM6B, SYNE2, SYNE1, SETD5, PIGV, PACS1, PGAP3, IFT43, NACC1, CHST14, LRRC56, CCDC151, DNAAF1, PROKR2, DNAJC21, PIH1D3, AMER1, A2ML1, B3GLCT, CCBE1, VPS13B, FAM120AOS, DNAAF4, RSPH9, GAS2L2, PIGW, SH3PXD2B, CCDC39, FREM2, MCIDAS, RSPH4A, DNAAF3, DNAJB13, KIF7, CCDC103, KLLN, CCDC114, DRC1, IFT122, SCARF2, HDAC8, LMOD3, CFAP298, NUP107, SELENON, WDR35, WDR19, PIEZO2, NXN, DNAI2, VPS33A, UPF3B, TMEM43, TMEM231, PALB2, FRAS1, SLC2A10, TTC25, DNAL1, RSPH3, SPRTN, MEGF10, MYPN, PIGO, PPP1R15B, PIGY, CFAP300, CCDC65, RSPH1, BAZ1B, HACD1, SMAD3, KMT2A, FGD1, FGFR3, FHL1, FOXG1, FLNA, FLNB, FMR1, FZD2, GAS8, GPC3, GNB1, GTF2I, HNRNPK, HPGD, HSD17B4, HSPG2, IGBP1, IGF1R, IHH, INPPL1, ITGA7, KRAS, LIG4, LIMK1, LMNA, LMX1B, OFD1, MATN3, MECP2, GPC4, FKTN, FBN1, COL3A1, ACTB, AKT1, ATP7A, BMP2, BRAF, CBL, CBS, CDH11, CFL2, CHRM3, CHRNG, COL1A2, COL2A1, COL11A2, ERF, CREBBP, DHODH, DMD, DNAH5, DVL1, DVL3, DYRK1A, EFNB1, MEGF8, ELN, EMD, EP300, ERCC5, MGAT2, BIVM-ERCC5, MYF5, TGFBR2, SDHC, MYH3, SKI, SLC16A2, SMS, SOS1, SOS2, SOX10, SPAG1, SRY, TBCD, TBX5, TCF20, TGFBR1, TP53, RRAS, TPM2, TPM3, TRIO, CLIP2, WNT5A, PCGF2, SHOC2, PDHX, MFAP5, LZTR1, RBM10, KDM5C, SMC1A, NAA10, SDHB, SDHD, RPS6KA3, MAP2K1, MYL2, NEB, NF1, NFIX, NOTCH3, NRAS, ROR2, DDR2, PIK3CA, CTSA, RPGR, PPP1CB, PPP2R1A, PPIB, MAP2K2, RASA2, RIT1, PTCH1, PTEN, RFC2, PTPN11, ALDH18A1, RET, RAD21, RAF1, PLF, AR, ASD1, EYA1, KRT7, GAL3ST4, ADGRG6, IS1, SCLY, TSPYL2, CDAN1, TAL1, TP63
    • Pectus Excavatum OMIM
      Nowak (1936) traced pectus excavatum in 2 to 4 generations in 12 families; a generation was skipped in 5 families. Stoddard (1939) reported an extensively affected family with a pattern consistent with autosomal dominant inheritance. This deformity also occurs in the Marfan syndrome and some other hereditary disorders. Leung and Hoo (1987) reported 3 Chinese families in each of which there were several instances of pectus excavatum. Male-to-male transmission was seen. Thorax - Pectus excavatum Inheritance - Autosomal dominant form ▲ Close
    • Pectus Excavatum Mayo Clinic
      Overview Pectus excavatum is a condition in which the person's breastbone is sunken into the chest. In severe cases, pectus excavatum can look as if the center of the chest has been scooped out, leaving a deep dent. While the sunken breastbone is often noticeable shortly after birth, the severity of pectus excavatum typically worsens during the adolescent growth spurt. Also called funnel chest, pectus excavatum is more common in boys than in girls. Severe cases of pectus excavatum can eventually interfere with the function of the heart and lungs.
  • Niemann–pick Disease, Type C Wikipedia
    Niemann–Pick Disease Type C . GeneReviews™ [Internet] . Seattle WA: University of Washington, Seattle.
    NPC1, LIPA, NPC2, PDLIM7, APP, SMPD1, PSMB9, ABCA1, RASSF1, CDKN2A, TNF, CHIT1, LINC01193, ERCC2, FCER2, IFNG, LAMP1, LDLR, CD274, MAPT, VEGFA, BACE1, PTCH1, CCL2, SOX2, TP53, ERCC1, H3P10, ATM, CKS1B, SRRM2, APOE, POSTN, APOD, WIF1, CUL9, NBEAL2, SIRT1, TARDBP, SEZ6L, SCO2, ARL2BP, DDX58, APC, TRIM29, DKK3, PDCD4, TMEM97, ANXA6, HDAC6, RAB9A, ATP7B, CD163, TRAF1, UBE2N, UGCG, VHL, VIM, VIP, ZNF154, BSND, ARID1A, ULK1, NR0B2, BECN1, CDK5R1, PER2, ST3GAL5, SPHK1, ARF6, FOXP3, ZMYND10, GDE1, MIR185, NEGR1, NPCA1, H19, STPG4, CELIAC2, ANXA1, MIR10B, MIR130A, MIR203A, RTRAF, MIR31, POU5F1P3, POU5F1P4, UCA1, MIR663A, APOBEC3A_B, UPK3B, CNE-2, NPB, APOBEC3A, ARHGAP42, CKS1BP7, NLK, OTUD4, NLRP2, LPAR5, GBA2, OVOL2, NEUROG2, ROBO3, GORASP1, WNK1, SPNS1, HAVCR2, FATE1, SCGB3A1, CDCA5, SEZ6, OSCP1, TP73, B2M, CP, CD58, GCHFR, GFAP, HCRT, HDAC2, HLA-A, HOXC6, HSPB1, HSP90AA1, IGFBP6, XRCC6, IL1A, IL1B, IL12A, IL17A, JAK2, JUN, JUNB, JUND, GBA, FOSB, THBS1, EGR1, CPT1A, CRP, CTLA4, CTNNB1, DAP, DAPK1, TYMP, S1PR3, EPHA2, FOS, EIF4E, CDKN2B, CDK5, FASN, CDH1, FCN2, FGF2, FOXM1, CD40, SCARB1, LGALS9, SLC6A8, RBM3, RELA, REST, SATB1, BSG, ALB, CCL18, SFRP1, SLPI, CCK, BMP2, BCL2, STAR, STAT3, SYT1, TRBV20OR9-2, TERT, TGFBR1, PLAAT4, PVALB, PTPN12, PTPN6, CAV1, MGMT, MLH1, MMP1, MNAT1, MYC, NBN, CASP8, OSM, OTC, PAK1, ABCB1, PIK3CA, POU5F1, CALR, CALCR, PTK2, CCL5
    • Niemann-Pick Disease Type C GeneReviews
      Summary Clinical characteristics. Niemann-Pick disease type C (NPC) is a slowly progressive lysosomal disorder whose principal manifestations are age dependent. The manifestations in the perinatal period and infancy are predominantly visceral, with hepatosplenomegaly, jaundice, and (in some instances) pulmonary infiltrates. From late infancy onward, the presentation is dominated by neurologic manifestations. The youngest children may present with hypotonia and developmental delay, with the subsequent emergence of ataxia, dysarthria, dysphagia, and, in some individuals, epileptic seizures, dystonia, and gelastic cataplexy. Although cognitive impairment may be subtle at first, it eventually becomes apparent that affected individuals have a progressive dementia.
    • Niemann-Pick Disease, Type C2 OMIM
      A number sign (#) is used with this entry because Niemann-Pick disease type C2 (NPC2) is caused by homozygous mutation in the NPC2 gene (601015) on chromosome 14q24. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene (607623), referred to as type C1 (257220); 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2. The clinical manifestations of types C1 (257220) and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Clinical Features Vanier et al. (1996) reported 5 patients with NPC2.
    • Niemann-Pick Disease Type C Orphanet
      Niemann-Pick disease type C (NP-C) is a lysosomal lipid storage disease (see this term) characterized by variable clinical signs, depending on the age of onset, such as prolonged unexplained neonatal jaundice or cholestasis, isolated unexplained splenomegaly, and progressive, often severe neurological symptoms such as cognitive decline, cerebellar ataxia, vertical supranuclear gaze palsy (VSPG), dysarthria, dysphagia, dystonia, seizures, gelastic cataplexy, and psychiatric disorders.
    • Niemann-Pick Disease, Type C1 OMIM
      A number sign (#) is used with this entry because Niemann-Pick disease type C1 and Niemann-Pick disease type D, also known as the Nova Scotian type, are caused by homozygous or compound heterozygous mutation in the NPC1 gene (607623) on chromosome 18q11. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene, referred to as type C1; 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2 (607625). The clinical manifestations of types C1 and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Historically, Crocker (1961) delineated 4 types of Niemann-Pick disease: the classic infantile form (type A; 257200), the visceral form (type B; 607616), the subacute or juvenile form (type C), and the Nova Scotian variant (type D).
  • Sprained Ankle Wikipedia
    Kerkhoffs GM, van den Bekerom M, Elders LA, van Beek PA, Hullegie WA, Bloemers GM, de Heus EM, Loogman MC, Rosenbrand KC, Kuipers T, Hoogstraten JW, Dekker R, Ten Duis HJ, van Dijk CN, van Tulder MW, van der Wees PJ, de Bie RA (September 2012).
    • Sprained Ankle Mayo Clinic
      Overview A sprained ankle is an injury that occurs when you roll, twist or turn your ankle in an awkward way. This can stretch or tear the tough bands of tissue (ligaments) that help hold your ankle bones together. Ligaments help stabilize joints, preventing excessive movement. A sprained ankle occurs when the ligaments are forced beyond their normal range of motion. Most sprained ankles involve injuries to the ligaments on the outer side of the ankle. Treatment for a sprained ankle depends on the severity of the injury.
  • Benzodiazepine Overdose Wikipedia
    Veterinary and Human Toxicology . 34 (2): 141–3. PMID 1354907 . ^ Wolf BC, Lavezzi WA, Sullivan LM, Middleberg RA, Flannagan LM (March 2005).
  • Alcohol Withdrawal Syndrome Wikipedia
    Ceylon Med J . 54 (2): 63–5. doi : 10.4038/cmj.v54i2.877 . PMID 19670554 . ^ Hunt, WA. (November–December 1993). "Are binge drinkers more at risk of developing brain damage?"
    AR, LEP, MPDZ, CCK, NGF, CYP19A1, KDM4C, GSTM1, NQO1, MALAT1, GLUL, SORCS2, SLC6A3, BDNF, CRH, SLC6A4, DRD2, FKBP5, DBH, GRIN1, GRIN2B, NPY, CCL2, APOE, POMC, PPARA, PPARD, PPARG, SORT1, SLC6A2, COMT, KCNQ4, SLC18A1, SNCA, PIK3CG, ADIPOQ, BMS1, C1D, PPARGC1A, AKT1, TMEM97, PNPLA3, PNOC, NPY5R, PIK3CD, HTR2C, CCKAR, CAT, GAD1, GATA4, GH1, NR3C1, GRM5, TSPO, HDAC2, IL6, PIK3CB, KRT18, LBP, MAOA, ADH1B, NQO2, NPY1R, NPY2R, CFP, PIK3CA, ACACA
  • Dysentery Wikipedia
    Retrieved 15 November 2019 . ^ a b c d Marie, C; Petri WA, Jr (30 August 2013). "Amoebic dysentery" .
    LCT, MME, SLC26A3, IL6, LEP, MPO, TNF
    • Diarrhea Wikipedia
      For other uses, see Diarrhea (disambiguation) . Loose or liquid bowel movements Diarrhea Other names Diarrhoea An electron micrograph of rotavirus , the cause of nearly 40% of hospitalizations from diarrhea in children under five [1] Specialty Infectious disease , gastroenterology Symptoms Loose frequent bowel movements, dehydration [2] Causes Usually infection (viral, bacterial, parasitic) [2] Risk factors Contaminated food or water [2] Prevention Handwashing , rotavirus vaccination , breastfeeding [2] Treatment Oral rehydration solution , zinc supplementation [2] Frequency ≈2.4 billion (2015) [3] Deaths 1.3 million (2015) [4] Diarrhea , also spelled diarrhoea , is the condition of having at least three loose, liquid, or watery bowel movements each day. [2] It often lasts for a few days and can result in dehydration due to fluid loss. [2] Signs of dehydration often begin with loss of the normal stretchiness of the skin and irritable behaviour. [2] This can progress to decreased urination , loss of skin color , a fast heart rate , and a decrease in responsiveness as it becomes more severe. [2] Loose but non-watery stools in babies who are exclusively breastfed , however, are normal. [2] The most common cause is an infection of the intestines due to either a virus , bacterium , or parasite —a condition also known as gastroenteritis . [2] These infections are often acquired from food or water that has been contaminated by feces , or directly from another person who is infected. [2] The three types of diarrhea are: short duration watery diarrhea, short duration bloody diarrhea, and persistent diarrhea (lasting more than two weeks, which can be either watery or bloody). [2] The short duration watery diarrhea may be due to cholera , although this is rare in the developed world. [2] If blood is present, it is also known as dysentery . [2] A number of non-infectious causes can result in diarrhea. [5] These include lactose intolerance , irritable bowel syndrome , non-celiac gluten sensitivity , celiac disease , inflammatory bowel disease such as ulcerative colitis , hyperthyroidism , bile acid diarrhea , and a number of medications. [5] [6] [7] In most cases, stool cultures to confirm the exact cause are not required. [8] Diarrhea can be prevented by improved sanitation , clean drinking water , and hand washing with soap. [2] Breastfeeding for at least six months and vaccination against rotavirus is also recommended. [2] Oral rehydration solution (ORS)—clean water with modest amounts of salts and sugar —is the treatment of choice. [2] Zinc tablets are also recommended. [2] These treatments have been estimated to have saved 50 million children in the past 25 years. [1] When people have diarrhea it is recommended that they continue to eat healthy food and babies continue to be breastfed. [2] If commercial ORS is not available, homemade solutions may be used. [9] In those with severe dehydration, intravenous fluids may be required. [2] Most cases; however, can be managed well with fluids by mouth. [10] Antibiotics , while rarely used, may be recommended in a few cases such as those who have bloody diarrhea and a high fever, those with severe diarrhea following travelling , and those who grow specific bacteria or parasites in their stool. [8] Loperamide may help decrease the number of bowel movements but is not recommended in those with severe disease. [8] About 1.7 to 5 billion cases of diarrhea occur per year. [2] [5] [11] It is most common in developing countries , where young children get diarrhea on average three times a year. [2] Total deaths from diarrhea are estimated at 1.26 million in 2013—down from 2.58 million in 1990. [12] In 2012, it was the second most common cause of deaths in children younger than five (0.76 million or 11%). [2] [13] Frequent episodes of diarrhea are also a common cause of malnutrition and the most common cause in those younger than five years of age. [2] Other long term problems that can result include stunted growth and poor intellectual development. [13] Play media Video explanation ( script ) Contents 1 Definition 1.1 Secretory 1.2 Osmotic 1.3 Exudative 1.4 Inflammatory 1.5 Dysentery 2 Health effects 3 Causes 3.1 Infections 3.1.1 Sanitation 3.1.2 Nutrition 3.2 Malabsorption 3.3 Inflammatory bowel disease 3.4 Irritable bowel syndrome 3.5 Other diseases 3.6 Medications 4 Pathophysiology 4.1 Evolution 5 Diagnostic approach 5.1 Chronic diarrhea 6 Prevention 6.1 Sanitation 6.1.1 Hand washing 6.1.2 Water 6.2 Vaccination 6.3 Nutrition 6.3.1 Breastfeeding 6.4 Others 7 Management 7.1 Fluids 7.2 Eating 7.3 Medications 7.4 Alternative therapies 8 Epidemiology 9 Terminology 10 See also 11 References 12 External links Definition Bristol stool chart Diarrhea is defined by the World Health Organization as having three or more loose or liquid stools per day, or as having more stools than is normal for that person. [2] Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days, by World Gastroenterology Organization . [14] Secretory Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a cholera toxin that stimulates the secretion of anions , especially chloride ions (Cl – ). Therefore, to maintain a charge balance in the gastrointestinal tract , sodium (Na + ) is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is isotonic with plasma even during fasting. [15] [16] It continues even when there is no oral food intake. Osmotic Osmotic diarrhea occurs when too much water is drawn into the bowels.
  • Medical Abortion Wikipedia
    Medical abortion Background Abortion type Medical First use United States 1979 ( carboprost ), West Germany 1981 ( sulprostone ), Japan 1984 ( gemeprost ), France 1988 ( mifepristone ), United States 1988 ( misoprostol ) Gestation 3–24+ weeks Usage Medical abortions as a percentage of all abortions France 64% (2016) Sweden 92% (2016) UK: Eng. & Wales 62% (2016) UK: Scotland 83% (2016) United States 39% (2017) Infobox references A medical abortion , also known as medication abortion , occurs when pills are used to bring about an abortion . The recommended regimen consists of a combination of medications, starting with mifepristone followed by misoprostol . [1] Mifepristone followed by misoprostol for abortion is considered both safe and effective throughout a range of gestational ages. [2] When mifepristone is not available, misoprostol alone may be used. Contents 1 Medical use 1.1 Through 12 weeks gestation 1.2 After 12 weeks gestation 1.3 Self-administered medical abortion 1.4 Telehealth 1.4.1 Clinic-to-clinic 1.4.2 Direct-to-patient 2 Contraindications 3 Adverse effects 3.1 Management of bleeding 3.2 Complications 4 Pharmacology 5 Frequency 6 History 7 Society and culture 7.1 "Reversal" controversy 7.2 Cost 8 References 9 External links Medical use [ edit ] 200 mg mifepristone and 800 mcg misoprostol, the typical regimen for early medical abortion. Through 12 weeks gestation [ edit ] For medical abortion prior to 12 weeks gestation, the World Heath Organization recommends mifepristone 200 mg by mouth followed 1–2 days later by misoprostol 800 mcg inside the cheek, vaginally, or under the tongue; misoprostol may be repeated to maximize success. [3] The success rate of mifepristone followed by one dose of misoprostol through 10 weeks pregnancy is 96.6%. [4] Those who took misoprostol less than 24 hours after mifepristone had higher failures rates compared to women who waited 1–2 days. [5] The National Abortion Federation (NAF) also recommends a mifepristone and misoprostol combination regimen. For medication abortion up to 10 weeks of pregnancy, 200 mg mifepristone is taken followed in 24 to 48 hours by 800 mcg misoprostol.
  • Meningioma Wikipedia
    PMID 17695387 . ^ Taylor BW, Marcus RB, Friedman WA, Ballinger WE, Million RR (August 1988).
    NF2, AKT1, BAP1, SMARCB1, PDGFB, SMARCE1, PTEN, SUFU, MLLT10, WRN, PGR, SMO, TRAF7, KLF4, HES1, CST3, CSTB, CTSL, ALAD, PIK3CA, ARMC5, DNMT1, CHEK2, NF1, KRIT1, CCM2, MIB1, SEC23B, TERT, MN1, MKI67, SDHD, MMP9, VEGFA, CDKN2A, GNAS, TP53, PDCD10, NTHL1, EPB41L3, KLLN, ESR1, EGFR, SDHB, SST, SDHC, LMNA, ERBB2, LOC110806263, SSTR2, EGF, MMP2, STAT3, PIK3CB, CTNNB1, IGF2, PIK3CD, PIK3CG, CD274, AZIN2, MEN1, PLAU, TP73, GADL1, CTSB, CASP3, MTHFR, TIMP1, PTGS2, ARHGAP24, IL6, FGF2, MGMT, MTOR, NDRG2, MIA2, MB, HTC2, GSTT1, MDM2, H3P10, MAPK1, TGFA, TIMP3, ABCB1, CCND1, CD44, BCL2, MAPK3, S100B, AQP4, CASP8, APC, ACKR3, MEG3, BCR, MCM7, PRDM2, XRCC1, TOP2A, HOXA9, CDKN2C, EDN1, SPP1, ATM, IGF1, ASL, PTPRJ, AQP1, LEPR, HPGDS, MIR29C, TNC, TGFB1, S100A1, PLAUR, ODC1, PCNA, SFRP1, ACTB, CDH1, FOS, AP1B1, PDGFRB, MYC, MTRR, CD34, EPHB2, PLG, TGM2, GSTP1, TIMP2, SPARC, HIF1A, TXNIP, IL1B, CCL2, IGFBP5, GNRH1, EEF1E1, GSTM1, CXCL12, PTTG1, YAP1, SLC9A3R1, DLC1, RAD54L, RPS6KB1, RB1, NR3C1, MAFK, KDR, MYCN, PON1, POLR2A, MSH2, VIM, COX2, MUC1, IGF2BP1, RAC1, UBE2I, UBE2D1, PDCD1, NOS2, NOTCH1, NOTCH2, THBS1, KMT2A, MLH1, MIF, PTGDS, TAT, XRCC3, STAT6, YWHAZ, CXCR4, MCM2, PTN, SMAD4, PTX3, LGALS3, STMN1, LAMC2, GJA1, ZNF197, GFAP, ATRAID, CADM1, BSG, ERBB3, CA9, CTAG1A, CAV1, CCK, CCND2, TPPP2, EIF4A2, CD68, PRAP1, EDNRB, LAMTOR1, MIR200A, TCHP, DCC, CDKN2B, CYP2D6, CXCL16, MINDY4, CFL1, CKS2, CTAG1B, CXCR6, WNK2, CSF2, CD276, BRCA1, EPB41, H3P12, AHR, FOXM1, FAS, FGF9, AP2B1, AR, ALPL, BIRC5, ANPEP, MIR224, FGFR3, ETV6, MIR219A1, RASSF1, MTCO2P12, DOT1L, TNF, MIR205, CLDN5, MAK16, TRP-AGG2-6, SLC25A21, TLR4, DPP9, PGR-AS1, BRIP1, LINC02210-CRHR1, TYMS, CAMKMT, H3P47, KCNH6, MAP1LC3B, SMARCA1, H3P9, TYK2, TTR, MNS16A, TXNRD1, SESN2, TXN, HIRA, TLE3, FSCN1, MTDH, NEK9, TCF12, TUBB, MIR34A, C10orf53, H19, TDO2, TCN2, ZEB1, ZBTB7C, TCEA1, ZAR1, LINC01194, MIR145, MIR21, MIR190A, TGFB3, MIR335, TJP1, SOX10, SOAT1, FAT3, SOD3, RBM45, NKX2-1, PLB1, CBLL2, THY1, TMEM30B, TRPV3, SP100, IDO2, DHFR2, RHBDF2, UCHL1, VHL, MUL1, PART1, CD163, SRRM2, TSPAN12, SMUG1, SRSF11, SNHG1, LARGE1, KIF4A, CLDN1, AIP, PPM1D, PROM1, CFLAR, EGFL6, IL18R1, ADAM23, TNKS, TP63, PSMG1, LGR5, RPL13A, ADIPOQ, SYNM, SEC31A, MRPL28, OGA, NES, SUB1, RALBP1, MSLN, PMEL, UBE2C, EBI3, CORO1A, KIF20A, PPIF, TSPAN2, DNM1L, ABCC5, HNRNPDL, KIF14, PIEZO1, AKAP12, LMO4, TIPARP, UCN, VSIR, NDC1, DIABLO, PNO1, XDH, ADAMTSL3, TXNDC16, WT1, TRPV4, LRRC4, TRPV1, RASAL1, PDLIM2, VIP, MMP25, EZR, NDRG4, MLPH, HMGN5, VDR, VDAC2, SMG8, YY1, DPP8, ARID4B, TAGLN2, PLA2G6, DKK3, RBMS3, TMEM97, AXIN1, SETD2, ARID1A, NXT1, RACGAP1, CLTCL1, TCL1A, PSCA, BICRA, TFPI2, KCNIP3, EXOSC3, PLA2G7, WWOX, SIX1, A1BG, SGK1, GH1, EIF4A1, EDNRA, DVL3, DUSP2, DSP, DRD1, DPP4, DMD, DHCR24, DEFB1, DEFA5, DDX3X, GADD45A, DCX, DCT, CD55, DAB2, CYP19A1, CYP1B1, CYP1A1, CYC1, CXADR, CX3CR1, CTLA4, CCN2, VCAN, CSF3, EIF4E, EIF4G1, EIF5A, F13A1, GAPDH, GABPA, FOLR1, FLT1, FGFR1, FGF13, FCGR3B, FCGR3A, FCER1G, FASN, FBLN1, FAP, F3, ELAVL1, ETS1, ETFA, ERCC5, ERCC4, ERCC2, ERBB4, EPO, EPHA1, EPAS1, ENO2, ENG, ELAVL4, CRYAB, CRHR1, CLDN7, ARNT, CALM3, CALM2, CALM1, CALCA, CAPN5, C1QBP, BRCA2, BRAF, BMP4, BCL6, ATP5F1B, STS, AREG, RUNX3, AQP5, KLK3, APOE, APOA1, ANG, ALOX5, ALDH1A3, ALDH1A1, AGTR2, JAG1, ADCYAP1R1, ABCA2, CAPN1, CBS, CPA1, CDK6, COX8A, KLF6, COL5A1, COL1A2, CNR1, CMM, CCR6, CETN3, CETN2, CENPF, CDKN1C, CDKN1A, CDK4, CCKAR, CDK2, CDC25A, CDK1, CD81, CD70, CD69, CD63, CD33, CD9, CD8A, CCNB1, CCKBR, GCG, GJB2, SFRP4, GLI1, PLA2G2A, PLA2G1B, PGF, PDGFRA, PDGFA, PAX5, PRKN, PAK1, SERPINE1, NAT2, OGN, OMD, NT5E, NPY2R, NOS3, NOS1, NME1, NFKB1, NFE2L2, NBN, MUTYH, MMUT, MUC4, MTR, COX1, MSN, MSH3, PODXL, POLD1, PPARA, PTK2, SET, CX3CL1, SAI1, S100A10, S100A6, S100A4, ROS1, RFC1, RDX, RANBP2, RAC3, PTPRC, PTHLH, PPID, PTGS1, PTGER4, PTCH1, PTBP1, KLK6, PROP1, PRLR, PRL, MAPK8, PRKCD, PRELP, PTPA, ABCC1, MMP11, MMP1, HOXA3, IGFBP7, IGFBP6, IGFBP2, IGF1R, IFNB1, IFNA2, HSF1, HRAS, HPRT1, HOXD@, HOXA10, HOXA7, HOXA@, IL13, HNRNPC, HLA-DRB1, HLA-DQB1, HLA-A, HGF, HFE, GSTM3, GSC2, GRB2, GPX1, GOT2, GNRHR, IL2, IDO1, MME, LTBP2, CD99, MET, MEIS1, MDM4, MDK, MCM6, MCM5, MCM4, MCM3, MAPT, SMAD2, SMAD1, CYP4F3, ING2, LGALS1, LEP, KRAS, KIFC1, KIF11, KCNMA1, JAK3, JAK2, JAK1, ITGB1, ITGA3, INS, OPHN1
    • Meningioma GARD
      Meningioma s are tumors that originate in the meninges , the membranes that surround the brain and spinal cord. Most meningiomas are not cancerous ( benign ), though a minority of meningiomas can be classified as atypical or cancerous ( malignant ). Though rare, malignant meningiomas can be highly aggressive. However, even benign meningiomas can cause problems if their growth affects neighboring areas of the brain. Though most meningiomas grow slowly, there is no way to predict the rate of growth for a particular meningioma or to know how long a specific meningioma was growing before it was diagnosed. Signs and symptoms can vary but may include seizures, headaches, weakness in the arms and legs, and vision loss.
    • Meningioma Orphanet
      A rare, mostly benign, neoplastic disease characterized by a primary tumor of the meninges, usually located intracranially (~90%) but spinal meningiomas occur as well. Clinical symptoms relate to the location of the tumor and may include seizures, focal neurological deficits (sensory-motor or visual symptoms, cranial nerve dysfunction), vascular complications (occlusion of cerebral blood vessels, deep venous thrombosis, pulmonary embolism), chronically increased intracranial pressure neurocognitive impairment and/or loss of bladder/anus sphincter control. Epidemiology In adults, intracranial meningiomas represent approximately 30% of central nervous system tumors. The male to female ratio is 1:3.5. Clinical description Whilst meningioma may appear at any age, it is predominantly diagnosed between the third and sixth decade of life. Meningiomas typically appear as broad-based dural hemispheric or oval lesions, attached to the dura mater.
    • Meningioma Mayo Clinic
      Overview A meningioma is a tumor that arises from the meninges — the membranes that surround the brain and spinal cord. Although not technically a brain tumor, it is included in this category because it may compress or squeeze the adjacent brain, nerves and vessels. Meningioma is the most common type of tumor that forms in the head. Most meningiomas grow very slowly, often over many years without causing symptoms. But sometimes, their effects on nearby brain tissue, nerves or vessels may cause serious disability. Meningiomas occur more commonly in women and are often discovered at older ages, but they may occur at any age.
    • Meningioma, Radiation-Induced OMIM
      Following radiotherapy, secondary cancer may occur after a long latent period. Zattara-Cannoni et al. (2001) reported cytogenetic studies of 6 cases of radiation-induced meningiomas. Two of the cases occurred after radiation for tinea capitis, after an interval of 17 and 54 years, respectively; in the first of these cases, local recurrence occurred after an additional period of 29 years. Using spectral karyotyping (SKY) and comparative genomic hybridization (CGH), Zattara-Cannoni et al. (2001) found that all 6 cases had the same chromosome abnormality, t(1;22)(p11;q12). They suggested that a gene on chromosome 1p11 is involved in radiation-induced meningiomas.
  • Sunburn Wikipedia
    Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). GeneReviews® . Seattle (WA): University of Washington, Seattle.
    • Sunburn Mayo Clinic
      Overview Sunburn is inflamed, painful skin that feels hot to the touch. It often appears within a few hours of being in the sun too long. You can get sunburn relief with simple self-care measures such as taking pain relievers and cooling the skin. But it may take days for the sunburn to fade. Preventing sunburn year-round by wearing sunscreen or using other skin-protection habits is important for everyone. It is especially important when you're outdoors, even on cool or cloudy days. Symptoms Sunburn symptoms can include: Inflamed skin, which looks pink or red on white skin and may be harder to see on brown or Black skin Skin that feels warm or hot to the touch Pain, tenderness and itching Swelling Small, fluid-filled blisters, which may break Headache, fever, nausea and fatigue, if the sunburn is severe Eyes that feel painful or gritty Any exposed part of the body — including the earlobes, scalp and lips — can burn.
    • Solar Erythema Wikipedia
      Solar erythema Specialty Dermatology Solar erythema is a skin condition characterized by redness of the skin following exposure to ultraviolet light , not to be confused with sunburn . [ further explanation needed ] [1] : 27 See also [ edit ] Skin lesion References [ edit ] ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . v t e Radiation-related disorders / Photodermatoses Ultraviolet / ionizing Sunburn Phytophotodermatitis Solar urticaria Polymorphous light eruption Benign summer light eruption Juvenile spring eruption Acne aestivalis Hydroa vacciniforme Solar erythema Non-ionizing Actinic rays Actinic keratosis Atrophic actinic keratosis Hyperkeratotic actinic keratosis Lichenoid actinic keratosis Pigmented actinic keratosis Actinic cheilitis Actinic granuloma Actinic prurigo Chronic actinic dermatitis Infrared / heat Erythema ab igne ( Kangri ulcer Kairo cancer Kang cancer Peat fire cancer ) Cutis rhomboidalis nuchae Poikiloderma of Civatte Other Radiation dermatitis Acute Chronic radiodermatitis ) Favre–Racouchot syndrome Photoaging Photosensitivity with HIV infection Phototoxic tar dermatitis This cutaneous condition article is a stub . You can help Wikipedia by expanding it . v t e
  • Diseases Of Affluence Wikipedia
    Ethnicity & Health . 2 (4): 287–295. doi : 10.1080/13557858.1997.9961837 . PMID 9526691 . ^ Filate WA, Johansen HL, Kennedy CC, Tu JV (2003).
  • Valvular Heart Disease Wikipedia
    . ^ Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. Zoghbi WA , Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ, American Society of Echocardiography.
    HTR2B, IL1B, FGFR1, CCL2, PYCARD, JAK2, LY86, ADAMTSL2, PCDHA9, LCN2, RIPK3, TIMP1, LSP1, ITGB2, FCGR1A, IL18, SPP1, SPN, COL1A2, COL1A1, PTPN6, CASP3, BGLAP, COL18A1, NOTCH1, C6, TNF, GALNT1, VWF, CALR, FLNA, TGFB1, TRIM21, TH, ACACA, MYOM2, BMS1, PDLIM5, SLC6A8, CNMD, MMRN1, KCNIP2, IL23A, CXCL16, IFIH1, VKORC1, GATA5, ADAMTS19, POSTN, LPA, SLC6A4, GATA4, APOE, HCN2, BMP2, CALCR, CAPN2, CRP, ACE, F2, F10, FDPS, FN1, GAP43, HTR1B, RYR2, TNC, IDS, IL1R1, IL13, IL17A, KCNK1, LGALS3BP, APLNR, NOS3, PITX1, PON1, PTH, TRIM72
    • Heart Valve Disease Mayo Clinic
      Overview In heart valve disease, one or more of the valves in your heart doesn't work properly. Your heart has four valves that keep blood flowing in the correct direction. In some cases, one or more of the valves don't open or close properly. This can cause the blood flow through your heart to your body to be disrupted. Your heart valve disease treatment depends on the heart valve affected and the type and severity of the disease.
  • Serotonin Syndrome Wikipedia
    . ^ a b c Ener RA, Meglathery SB, Van Decker WA, Gallagher RM (March 2003). "Serotonin syndrome and other serotonergic disorders" .
    • Serotonin Syndrome Mayo Clinic
      Overview Serotonin syndrome is a serious drug reaction. It is caused by medications that build up high levels of serotonin in the body. Serotonin is a chemical that the body produces naturally. It's needed for the nerve cells and brain to function. But too much serotonin causes signs and symptoms that can range from mild (shivering and diarrhea) to severe (muscle rigidity, fever and seizures). Severe serotonin syndrome can cause death if not treated. Serotonin syndrome can occur when you increase the dose of certain medications or start taking a new drug. It's most often caused by combining medications that contain serotonin, such as a migraine medication and an antidepressant.
    • Serotonin Syndrome Orphanet
      Serotoninergic syndrome is characterised by an excess of serotonin in the central nervous system, associated with the use of various agents, including selective serotonin reuptake inhibitors (SSRIs). Epidemiology Data regarding prevalence in Europe are not available. Clinical description Serotoninergic syndrome may result in muscle rigidity, myoclonus, agitation, confusion, hyperthermia, hyperreflexia as well as dysautonomic symptoms, with a risk of shock with low peripheral vascular resistance, seizures, coma, rhabdomyolysis and/or disseminated intravascular coagulation (DIC). Etiology SSRIs and monoamine oxidase inhibitors (MAOIs) may be responsible for this syndrome at toxic but also at therapeutic concentrations. The syndrome may appear: -a few hours to a few days after the initiation of the treatment ; - following simultaneous combination (counter-indication) of MAOIs-A (toloxatone, moclobemide) and SSRIs or successive combination with an excessively short pill-free interval ; - as the result of drug-drug interactions ; - or in some cases of acute poisoning. Individual susceptibility and severity of clinical effects may be explained by interindividual pharmacokinetic and pharmacodynamic differences.
  • Acute Coronary Syndrome Wikipedia
    PMID 19932401 . ^ Achar SA, Kundu S, Norcross WA (2005). "Diagnosis of acute coronary syndrome" .
    CRP, IL6, TNNI3, MMP9, PAPPA, TNF, PON1, TLR4, ITGB3, HSPD1, FASN, TNNT2, TUBB1, SERPINC1, PSMB1, ARHGDIB, HSPA8, SOD2, CAPZB, LDHB, CKM, RAB7B, CKB, VCL, GSN, TUBA1C, ACTG1, GAPDH, TPM4, VIM, GSTP1, PDIA3, ENO1, PLA2G7, CST3, APOE, LPA, TMEM231, CELSR2, GABRB1, ACE, TOMM5, GLCCI1, FAM114A1, PCSK9, CYP2C19, FRMD5, CASTOR3, CYP3A7, CYP3A51P, P2RY12, ACCS, MPO, FHIT, SERPINA5, PLA2G15, ADCY9, GDF15, ACSS2, CATSPER2P1, SCARB1, NOS3, BTD, UGT2B7, CYP3A7-CYP3A51P, TP53BP1, ARPC1A, ALB, NPPB, CD40, F3, CETP, ABCB1, APOA1, OLR1, CAD, MMP2, CD40LG, LDLR, FOXP3, IL18, BDNF, TGFB1, IL37, IL10, SERPINE1, PTX3, VASP, CXCL16, VWF, IL1B, ADIPOQ, PLA2G2A, PPIG, ITGA2B, PPARG, EDN1, F10, ADRB2, THBD, PCYT1A, DPP4, MTHFR, HLA-DRB1, SPP1, BSG, VEGFA, CIITA, ST2, MMRN1, P2RY1, CCN1, PLA2G1B, F2R, PLA2G6, TNFSF4, S100A9, TNFRSF4, PTGS2, PTGS1, CCL2, CX3CR1, MMP1, MMP3, PPARA, SELP, PLXNA2, MIR146A, IL1RN, COX1, MSR1, SELENBP1, MIR499A, ACSL5, IL17D, SH2D1A, RCBTB1, CHGA, TIMP2, TLR2, LGALS3, COX2, TNFRSF11B, FSTL1, NFKB1, S100A12, SMUG1, ACSL6, CXCL12, MTHFD1L, PLAT, SELPLG, GREM1, VPS51, FOXD3, APCS, MIR223, NRDC, CD14, CD28, MIR21, NPPA, ANGPTL2, APOB, MIR122, IL27, GOLGA6A, CYP2B6, LCN2, IFNA13, IFNA1, BPIFA4P, CYP3A4, AGTR1, AGT, EHMT1, F2, ALDH2, ADRB1, GPT, GLP1R, NLRP3, LIPG, CERNA3, MTCO2P12, ZNF746, APLN, FABP3, IL2RA, IGF1, ENHO, TTR, LCAT, CPB2, KDR, MAPK14, ISG20, ALOX5AP, REN, BET1, CXCL8, IL17A, TNFRSF9, SIRT1, MIR3149, MPRIP, MIR208B, CLEC16A, KLF2, RIPK3, FADS2, SLC23A2, MIR605, TFG, SLC33A1, TBC1D9, CARM1, ADAMTS4, UGT2A1, MIR486-1, MRAS, WDTC1, ADAMTS7, HDAC9, FCMTE2, DKK1, PGR-AS1, AKR1A1, EMSLR, HPSE, MVP, ABCB6, SCA9, MIR330, APOO, NLRC4, CARD18, ACE2, UBL5, F2RL3, LGR6, PEAR1, HPSE2, VSIR, C16orf58, CRTC3, VKORC1, FTO, TREML4, STARD7, DHX40, ECHDC3, MRGPRX1, GPRC6A, ABCC11, KIF6, DNER, CARD16, FCRL3, MRGPRX3, OXER1, MRGPRX4, GPR151, HAMP, MIR126, LPAR3, MIR224, PADI4, GPR166P, AMACR, KCNE5, VN1R17P, SULT4A1, POU2F3, CARD17, PTPN22, MIR29B2, MIR29B1, HAVCR1, FETUB, PLB1, RETN, MBL3P, MIR19B1, GP6, MIR186, MIR15A, CLEC1B, MIR150, TERF2IP, DGCR8, CCHCR1, ELOVL2, APOM, MYDGF, TBX21, ABO, PER2, FAP, GEM, GCK, GAS6, FLT1, FGB, FBLN1, FABP4, GJA4, F12, F7, EPHX2, EGR1, EGFR, DBP, CBLIF, GLS, CYP2D6, HRH2, IL2, IL1A, IGFBP4, ICAM1, HSPA4, HSPA1A, HMOX1, GNB3, HMGB1, HLA-B, HLA-A, HGF, NR3C1, GPX1, CYP3A5, CYP2C9, IL7R, ANXA5, AVP, ATM, ARSA, FASLG, FAS, APOC3, ANXA1, BCL2, ANGPT2, ALOX5, ALCAM, AKT1, ADRA2B, ADAM10, B2M, BGN, CYP1A1, CDH6, CYBA, CTSD, CTSB, CP, CCR5, CLU, CD70, BRCA1, CD68, CD36, CD34, CD80, CD247, CASP1, IL7, IL9, PROZ, SELL, STAT5B, STAT5A, STAT3, SREBF2, SRI, SHBG, SELE, TRA, CXCL5, CCL21, CCL19, S100A8, PTPRA, PTH, ABCC8, TERC, MAPK8, VCAM1, TNFRSF11A, SOCS1, FZD4, FGF23, CUBN, LAP, UMOD, TFPI, UCP2, TYR, TRAF1, TNNI1, TIMP1, TGM2, PTGER2, PRG2, IL15, LEP, MAZ, CYP4F3, LRP2, LRP1, FADS1, LGALS3BP, RPSA, MBL2, KLK1, KIR3DL1, JUP, JAK2, IRS1, IRF5, MB, MIF, PPBP, PECAM1, ACADS, POR, PLG, PLA2G4A, PI3, SERPINF1, SERPINB2, NR3C2, NPR3, NPR2, NPR1, NPPC, NDUFC2, MMP8, LINC02605
    • Acute Coronary Syndrome Mayo Clinic
      Overview Acute coronary syndrome is a term that describes a range of conditions related to sudden, reduced blood flow to the heart. These conditions include a heart attack and unstable angina. A heart attack happens when cell death damages or destroys heart tissue. A heart attack also is known as a myocardial infarction. Unstable angina occurs when blood flow to the heart decreases. It's not severe enough to cause cell death or a heart attack. But the reduced blood flow may increase your risk of a heart attack. Acute coronary syndrome often causes severe chest pain or discomfort.
  • Transient Myeloproliferative Disease Wikipedia
    . ^ a b Marshall GM, Carter DR, Cheung BB, Liu T, Mateos MK, Meyerowitz JG, Weiss WA (April 2014). "The prenatal origins of cancer" .
    GATA1, TTN, TAM, GAS6, ESR1, CAPN3, CCL2, TGFB1, MSTO1, CTNNB1, NFKB1, MPST, VEGFA, MAP3K10, KISS1R, WT1, AURKB, CCNE2, SQSTM1, ARHGEF7, CMYA5, NRIP1, YY1, VCP, VIM, SEMA3A, TYRO3, KANSL1, TP53, TNF, THPO, MIR100, SH2B3, MERTK, NDC80, NUP62, ORAI1, QRSL1, GOLM1, DCTN4, ASCC1, DLL1, DESI1, INTU, BBC3, UCN3, MAP1LC3B, PRAME, SIRT3, SIRT4, CTCF, SLC35G1, ZEB1, KHDRBS1, LAMTOR5, CLEC10A, ABL1, PCNA, CCL5, CDK1, FANCD2, EZH2, ERG, EGFR, CYP19A1, CYP2D6, CUX1, COMT, COL4A3, CD40, NR5A1, CASP3, FOXL2, BCL2, CCND1, AXL, ARHGDIA, APP, APOE, APC, FOXM1, GHR, PTPN11, JAK3, PSMB6, AKT1, OVGP1, MYCN, MPL, MMP9, MDM2, KIT, KISS1, ITGAL, GPER1, ITGA2B, CXCR2, CXCL8, IL6, IL3, IGFBP1, IGF1, HSPA5, GTF2H1, H3P40
    • Myeloproliferative Syndrome, Transient OMIM
      Transient myeloproliferative syndrome is a leukemoid reaction that occurs in some newborn infants with Down syndrome and rarely in phenotypically normal infants (Seibel et al., 1984). In 9 Down syndrome patients with transient myeloproliferative syndrome, Niikawa et al. (1991) found that the mode of inheritance of centromeric chromosomal markers was compatible with duplication of one parental chromosome 21. Therefore, they proposed a hypothesis of 'disomic homozygosity' of a mutant gene on chromosome 21 as the causative mechanism (Abe et al., 1989). Niikawa et al. (1991) observed a Down syndrome patient who had an inversion of one chromosome 21; by studies with DNA polymorphic markers in 5 other patients, they obtained results suggesting that the putative gene (which they symbolized TMS) was located at 21q11.2. Cytogenetic and molecular studies demonstrated that in Down syndrome associated with transient abnormal myelopoiesis, trisomy 21 had arisen much more frequently through mitotic (or meiosis II) nondisjunctions than through meiosis I errors (Shen et al., 1995).
    • Transient Myeloproliferative Syndrome Orphanet
      A rare hematologic disease characterized by clinical and morphological findings indistinguishable from those of acute myeloid leukemia, typically occurring in newborns with Down syndrome. Peripheral blood and bone marrow blasts display features suggestive of megakaryoblasts. In addition to trisomy 21, acquired GATA1 mutations are present in blast cells. Patients may be asymptomatic or present with thrombocytopenia, less commonly other cytopenias, leukocytosis, hepatosplenomegaly, jaundice, ascites, respiratory distress, bleeding, and pericardial or pleural effusions. Most patients undergo spontaneous remission within the first three months of life, although some may develop life-threatening hepatic, renal, or cardiac complications.
  • Epilepsy-Intellectual Disability In Females Wikipedia
    SCN1A-Related Seizure Disorders . Seattle (WA): University of Washington, Seattle.
    PCDH19, TSPAN6
    • Epileptic Encephalopathy, Early Infantile, 9 OMIM
      A number sign (#) is used with this entry because early infantile epileptic encephalopathy-9 (EIEE9), also known as epilepsy and mental retardation restricted to females (EFMR), is caused by mutation in the gene encoding protocadherin-19 (PCDH19; 300460) on chromosome Xq22. Description Epileptic encephalopathy-9 is an X-linked disorder characterized by seizure onset in infancy and mild to severe intellectual impairment. Autistic and psychiatric features have been reported in some individuals. The disorder affects heterozygous females only; transmitting males are unaffected (summary by Jamal et al., 2010). For a general phenotypic description and a discussion of genetic heterogeneity of EIEE, see EIEE1 (308350).
    • Female Restricted Epilepsy With Intellectual Disability Orphanet
      Female restricted epilepsy with intellectual disability is a rare X-linked epilepsy syndrome characterized by febrile or afebrile seizures (mainly tonic-clonic, but also absence, myoclonic, and atonic) starting in the first years of life and, in most cases, developmental delay and intellectual disability of variable severity. Behavioral disturbances (e.g. autistic features, hyperactivity, and aggressiveness) are also frequently associated. This disease affects exclusively females, with male carriers being unaffected, despite an X-linked inheritance.
  • Restless Legs Syndrome Wikipedia
    . ^ a b c Allen, R; Picchietti, D; Hening, WA; Trenkwalder, C; Walters, AS; Montplaisi, J; Restless Legs Syndrome Diagnosis Epidemiology workshop at the National Institutes of Health; International Restless Legs Syndrome Study Group (2003).
    BTBD9, MEIS1, PTPRD, TF, POMC, DRD3, MAP2K5, SNCA, PRKN, MFN2, LRRK2, PARK7, FTL, HTRA2, VPS13C, DNAJC6, ATXN7, LINC02086, PINK1, UCHL1, RLS1, CASC16, PODXL, MYT1, LINC02520, LINC01478, CCDC148, SKOR1, HMOX1, TOX3, DRD2, VDR, MAOA, RLS3, CHM, FXYD1, TH, CHMP2B, SLC11A2, ATXN1, HAMP, GABRR3, RLS4, RLS6, NTS, ADH1B, HMOX2, CRP, GABRA4, FXN, EEF1A2, DMRT1, KNG1, IL1B, HFE, MPZ, MAOB, NOS1, ATXN3, ZC4H2, MIXL1, REEP1, AVP, PCDHA3, MOCOS, FAT2, GABRR2, NANS, SLC25A37, ATL1, PYCARD, GCH1, FMR1, C3, TRAPPC6B, CAD, TMPRSS6, DRD4, GLO1, C9orf72, DBP, MIR122, LINC00423, MIR330, RLS2, CPT1B, CHKB, RLS5, KCTD18, NPAS2, SPATS2L, MCF2L, NKX2-1, TFRC, IL17A, TRA, AFP, SLC6A3, SLC1A2, L1CAM, ATXN2, LRP2, TSPAN31, REN, LY6E, SMCP, SERPINA1, TNF, TYMS, IGLC2, SCAF11, CNTN3, HNMT, ZEB2, IGHA1, LITAF, SLC9A3R2, APLN, UTRN, RNMT, GEMIN2, ATRN, FGF23, NR4A3, IGKC, TBP
    • Restless Legs Syndrome Mayo Clinic
      Overview Restless legs syndrome (RLS) is a condition that causes an uncontrollable urge to move the legs, usually because of an uncomfortable sensation. It typically happens in the evening or nighttime hours when you're sitting or lying down. Moving eases the unpleasant feeling temporarily. Restless legs syndrome, also known as Willis-Ekbom disease, can begin at any age and generally worsens as you age. It can disrupt sleep, which interferes with daily activities. Simple self-care steps and lifestyle changes may help relieve symptoms. Medications also help many people with RLS . Symptoms The chief symptom is an urge to move the legs.
  • Transmissible Spongiform Encephalopathy Wikipedia
    This was confirmed with the identification of a Kuru-like disease, called new variant Creutzfeldt–Jakob disease , in humans exposed to BSE . [45] Although the infectious disease model of TSE has been questioned in favour of a prion transplantation model that explains why cannibalism favours transmission, [46] the search for a viral agent is being continued in some laboratories. [47] [48] References ^ Bastian FO, Sanders DE, Forbes WA, Hagius SD, Walker JV, Henk WG, Enright FM, Elzer PH; Sanders; Forbes; Hagius; Walker; Henk; Enright; Elzer (2007). " Spiroplasma spp. from transmissible spongiform encephalopathy brains or ticks induce spongiform encephalopathy in ruminants" .
    PRNP, CX3CL1, CX3CR1, SNCA, CLU, MARK4, LINC02210-CRHR1, TOMM40, CARD14, MS4A4A, CHN2, ABCB6, ABCA7, RPS4XP2, PRDX2, PPP1R12B, CCDC62, CD2AP, SLC2A13, C4BPA, BST1, LINC02210, MS4A4E, BLOC1S3, C9orf72, ANK3, EPHA1-AS1, GH1, MAPT, CSF2, LAMC2, PRKN, APP, APOE, SOD1, HECTD2, CBLL2, MUL1, PDIK1L, NEFL, LINC01672, IGFALS, HSPA4, TNF, SPRN, MGRN1, GSS, AHSP, IL6, IL1B, IAPP, SERPINA3, GPI, ADAM10, FXN, SMUG1, MMRN1, SARM1, CHN1, SIRT3, CABIN1, CFH, CHI3L1, PRND, SEC61A1, CFL1, CD44, GDE1, TPPP, STMN2, XAF1, YWHAQ, STIP1, HPSE, CHRM1, PLK3, RABEPK, EDIL3, DNM1L, CR1, CST7, BAG6, CR2, EGLN1, FKBP10, CD40LG, CXCR5, ACHE, SNORD3A, ACTB, MIR342, MIR21, AKT1, PLCXD3, APCS, NEGR1, CALHM1, AQP1, AQP4, BRCA2, THY1, LRFN5, CPNE8, C5AR1, SIRPA, NLRP3, CASP1, CD9, CD14, AKT1S1, MINDY4, CD28, CD40, TLR2, TGFB2, TGFB3, HIF1A, P4HB, OGG1, NGF, NFKB1, NFE2L2, EGFR, ERBB2, MTR, MKLN1, MFGE8, MBP, FANCD2, LGALS1, LAMA3, LAG3, KARS1, IRF3, CXCL8, GFAP, GLS, IL1A, IFNAR1, IFN1@, PDIA3, HSPD1, HSPA5, GSN, DECR1, PDCD1, PDK1, RARB, CRYAB, ADAM17, HSPA13, SP1, SOD2, CSF1R, SNCG, CTSD, SNCB, SLC1A3, CYBB, RYR2, PVALB, PIK3CA, PTGS2, PSEN1, RELN, DAB1, PRKAB1, PRKAA2, PRKAA1, PPIA, PIN1, PIK3CG, PIK3CD, ABCA1, PIK3CB
    • Human Prion Disease Orphanet
      Prion diseases are a group of rare transmissible disorders characterized by progressive debilitating neurological manifestations due to spongiform changes with an invariably fatal course. The disorders all involve accumulation of an abnormal prion protein in the central nervous system with no specific immunological response. Sporadic Creutzfeldt-Jakob disease (CJD; see this term) is the most frequent form accounting for about 85% of prion disease cases. The other forms of prion disease are genetic (5-15%) and include inherited CJD, fatal familial insomnia (FFI), and Familial Alzheimer-like prion disease (see these terms). Acquired forms (< 5%) include iatrogenic CJD and variant CJD (vCDJ).
  • Neonatal Diabetes Wikipedia
    .; Stephens, Karen; Amemiya, Anne; Ledbetter, Nikki (eds.). GeneReviews . Seattle (WA): University of Washington, Seattle.
    ABCC8, INS, KCNJ11, GLIS3, GCK, EIF2AK3, GATA6, RFX6, ZFP57, PDX1, NEUROD1, SLC2A2, MNX1, NEUROG3, HNF1B, PTF1A, STAT3, FOXP3, IER3IP1, SLC19A2, NKX2-2, GATA4, INSR, IL2RA, AGPAT2, INS-IGF2, HNF4A, HNF1A, GLIS2, PHPT1, ZACN, ASAH1, KLF11, PDHX, BCL2A1, POMC, PLAGL1, PAX4, HLA-DRB1, GCG, FOXM1, SOX3
    • Neonatal Diabetes Mellitus Orphanet
      Neonatal diabetes mellitus presents as hyperglycemia, failure to thrive and, in some cases, dehydration and ketoacidosis which may be severe with coma, in a child within the first months of life. Epidemiology Transient (TNDM) and Permanent (PNDM) neonatal diabetes are rare conditions occurring in 1:300,000-400,000 live births. Clinical description TNDM infants develop diabetes in the first few weeks of life but go into remission in a few months, with possible relapse to a permanent diabetes state usually around adolescence or as adults. The pancreatic dysfunction may be maintained throughout life, with relapse initiated at times of metabolic stress such as puberty or pregnancy. Patients with TNDM are more likely to have intrauterine growth retardation and less likely to develop ketoacidosis than patients with PNDM.
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