��-kok��-��700bet.net��-��-12��-��315bet.net��-��-��-��-��bet91.net��

Advanced

FindZebra Summary is loading...

Photoinhibition Wikipedia

3 Molecular mechanism(s) 3.1 Acceptor-side photoinhibition 3.2 Donor-side photoinhibition 3.3 Manganese mechanism 3.4 Singlet oxygen mechanisms 3.5 Low-light mechanism 4 Kinetics and action spectrum 5 PSII repair cycle 6 Protective mechanisms 6.1 The PsBs Protein 7 Measurement 7.1 Flashing light 8 Dynamic photoinhibition 9 Ecology of photoinhibition 10 See also 11 References 12 Further reading 13 External links History [ edit ] The first measurements of photoinhibition were published in 1956 by Bessel Kok. [1] Even in the very first studies, it was obvious that plants have a repair mechanism that continuously repairs photoinhibitory damage. In 1966, Jones and Kok measured the action spectrum of photoinhibition and found that ultraviolet light is highly photoinhibitory. [2] The visible-light part of the action spectrum was found to have a peak in the red-light region, suggesting that chlorophylls act as photoreceptors of photoinhibition. ... Thus, the redox state of Quinone A is no longer active and there is, again, no change in the concentration of carbon dioxide in the intracellular airspaces of the leaf. All these factors work to have a net decrease of stomatal conductance. ... Biochimica et Biophysica Acta . 21 (2): 234–244. doi : 10.1016/0006-3002(56)90003-8 . PMID 13363902 . ^ Jones LW, Kok B (1966). "Photoinhibition of Chloroplast Reactions. ... Photochemical & Photobiological Sciences . 4 (12): 950–956. doi : 10.1039/b507888c .
Deafness, X-Linked 2 OMIM

In their summary of the features of DFN3, de Kok et al. (1995) pointed out that this mixed type of deafness is characterized by both conductive hearing loss resulting from stapes fixation and progressive sensorineural deafness, and that sometimes a profound sensorineural deafness masks the conductive element. ... In 4 patients with X-linked mixed deafness, de Kok et al. (1995) demonstrated 2 missense mutations and 2 nonsense mutations, and in a fifth patient, classified as sensorineural deafness, a nonsense mutation was found (300039.0001-300039.0005). In addition, de Kok et al. (1995) found that 3 Xq21 microdeletions and 1 duplication that had been identified previously (Huber et al., 1994) in patients with DFN3 did not encompass the POU3F4 gene. ... In none of these patients, nor in 2 others with either a perilymphatic gusher during stapes surgery or a temporal bone defect, were point mutations detected within the POU3F4 gene. De Kok et al. (1995) concluded that these cases may be caused by mutations that affect 5-prime noncoding or regulatory sequences. ... From observations of DFN3 in association with a complex duplication/paracentric inversion, de Kok et al. (1995) concluded that there is a regulatory element located at least 400 kb upstream of the POU3F4 gene and that this was disconnected from the POU3F4 gene by the inversion.

POU3F4, GJB2, GJB6, PRPS1
- Deafness, Progressive, With Stapes Fixation OMIM
  
  Thies et al. (1996) described 4 adult sisters with bilateral conductive hearing loss, starting between the ages of 8 and 24 years. Tympanotomy showed ossification of the stapedial tendon or a bony bar from the neck of the stapes to the pyramidal eminence, leading to stapes fixation. After surgical removal of the bony tendon, hearing became normal in 3 sisters; in 1 sister, who had an additional deformity of the head of the stapes in the right ear, normal hearing was not restored after surgery. The parents of these sisters and 4 other sibs had normal hearing. This family showed an apparently autosomal recessive form of hearing loss due to stapes fixation. A similar type of hearing loss was reported by Grant and Grant (1991).
Neuropathy, Hereditary Sensory And Autonomic, Type I, With Cough And Gastroesophageal Reflux OMIM

Spring et al. (2005) reported detailed clinical features of the 2 unrelated affected families studied by Kok et al. (2003). Affected individuals had onset in early adulthood of paroxysmal cough and frequent throat clearing associated with gastroesophageal reflux, with later onset of an axonal neuropathy with distal sensory impairment of the upper and lower limb. ... Variable features included bilateral sensorineural hearing loss, lancinating pains, alacrima, and impotence. Mapping Kok et al. (2003) identified 2 families with HSN1 with cough and GER.
- Hereditary Sensory And Autonomic Neuropathy Type 1b Orphanet
  
  Hereditary sensory and autonomic neuropathy, type 1B (HSAN1B) is characterized by the association of type 1 HSAN with paroxysmal cough and gastroesophageal reflux (GOR). Epidemiology So far, it has been described in two families. Clinical description Onset occurs in adulthood with distal sensory loss due to an axonal neuropathy, GOR, and cough triggered by noxious odors or by pressure in the external auditory canal. The cough may be severe leading to syncope and retinal detachment. Additional features include throat clearing, a hoarse voice, and sensorineural hearing loss. Etiology Linkage to chromosome 3p22-p24 was found in both reported families. Genetic counseling Transmission is autosomal dominant.
Methemoglobinemia And Ambiguous Genitalia OMIM

Hegesh et al. (1986) had reported that the parents and 6 sibs had normal methemoglobin levels, whereas those in the patient varied between 12% and 19%. The patient's erythrocyte cytochrome b5 levels were about 25% of those found in other family members. ... Androgen deficiencies due to defects in 17-alpha-hydroxylase activity are a known cause of pseudohermaphroditism in males (202110), and cytochrome b5 has been shown to participate in 17-alpha hydroxylation in adrenal steroidogenesis by serving as an electron donor. Kok et al. (2010) reported a 46,XY infant, born to consanguineous parents, who had ambiguous genitalia at birth. ... In a 46,XY infant with elevated methemoglobin and ambiguous genitalia due to apparent isolated 17,20-lyase deficiency, Kok et al. (2010) sequenced the CYP17A1 and CYB5A genes and identified homozygosity for a nonsense mutation in the CYB5A gene (W27X; 613218.0002) for which his unaffected first-cousin parents were heterozygous. ... INHERITANCE - Autosomal recessive GENITOURINARY External Genitalia (Male) - Ambiguous genitalia - Micropenis - Hypospadias - Bifid scrotum - Undescended testicles - Male pseudohermaphroditism SKIN, NAILS, & HAIR Skin - Cyanosis due to methemoglobinemia ENDOCRINE FEATURES - Isolated 17,20-lyase deficiency - Elevated luteinizing hormone levels - Low testosterone levels - Subnormal response of testosterone to human chorionic gonadotropin stimulation - Elevated 17-hydroxyprogesterone levels - Normal glucocorticoid levels - Normal mineralocorticoid levels - Low urinary androgen metabolite excretion - Increased urinary pregnenetriol excretion - Increased ratio of 17-alpha-hydroxyprogesterone to androgen metabolites HEMATOLOGY - Decreased levels of erythrocyte cytochrome B5 LABORATORY ABNORMALITIES - Methemoglobin concentration 12 to 19% (in 1 patient) - Methemoglobinemia, mild (in some patients) MISCELLANEOUS - Onset in infancy - See the more common methemoglobinemia types I and II ( 250800 ) MOLECULAR BASIS - Caused by mutation in the cytochrome B5A gene (CYB5A, 613218.0001 ) ▲ Close

CYB5R3, CYB5A, DECR1, DLD, HBB, HBG2
- Hereditary Methemoglobinemia Orphanet
  
  A rare red cell disorder classified principally into two clinical phenotypes: autosomal recessive congenital (or hereditary) methemoglobinemia types I and II (RCM/RHM type 1; RCM/RHM type 2). Clinical description In RCM type 1, cyanosis from birth is the only symptom. It is well-tolerated and is associated with mild complaints of headaches, fatigue and shortness of breath upon exertion. RCM type 2 is much more severe; the cyanosis is accompanied by neurological dysfunction (with intellectual deficit, microcephaly, growth retardation, opisthotonus, strabismus and hypertonia), which usually becomes evident during the first four months of life. Two additional forms of RCM have also been reported. RCM type 3 was the term used to define a phenotype with cyanosis but without neurological abnormalities in which Cb5R deficiency was identified in leucocytes and platelets as well as erythrocytes.
- Methemoglobinemia Due To Deficiency Of Methemoglobin Reductase OMIM
  
  A number sign (#) is used with this entry because autosomal recessive methemoglobinemia due to deficiency of methemoglobin reductase is caused by homozygous or compound heterozygous mutation in the CYB5R3 gene (613213) on chromosome 22q13. See also autosomal recessive methemoglobinemia type IV (250790), which is caused by mutation in the cytochrome b5 gene (CYB5A; 613218). Type III has been withdrawn (see below and Nagai et al., 1993). Autosomal dominant methemoglobinemia, referred to as the 'M' type, is caused by variation in the hemoglobin A (HBA1; 141800) or hemoglobin B (HBB; 141900) genes; see 617973 and 617971, respectively. Description Methemoglobinemia due to NADH-cytochrome b5 reductase deficiency is an autosomal recessive disorder characterized clinically by decreased oxygen carrying capacity of the blood, with resultant cyanosis and hypoxia (review by Percy and Lappin, 2008). There are 2 types of methemoglobin reductase deficiency. In type I, the defect affects the soluble form of the enzyme, is restricted to red blood cells, and causes well-tolerated methemoglobinemia.
- Methemoglobin Reductase Deficiency OMIM
  
  Clinical Features Sass et al. (1967) found a black male with deficiency of NADPH (TPNH)-methemoglobin reductase, also known as NADPH-reductase and biliverdin reductase B (BLVRB; 600941). The case was detected when the patient's red cells were found to be abnormal with the methylene-blue screening test, which is ordinarily an indication of G6PD deficiency; by actual assay, G6PD activity was normal. Administration of primaquine for 30 days produced no hemolysis. Five close relatives including the mother had intermediate levels of NADPH-methemoglobin reductase consistent with heterozygous status. The father was dead. As one would predict from knowledge of the relative activities of the NADPH- and NADH (DPNH)-methemoglobin reductases, methemoglobinemia was not present in the presumed homozygote. Bloom and Zarkowsky (1970) also reported such a patient. Their patient, in comparison with methemoglobinemia cases, demonstrated that NADPH-reductase is separate from NADH-reductase.
Neuroendocrine Tumor Wikipedia

G1 and G2 neuroendocrine neoplasms are called neuroendocrine tumors (NETs) – formerly called carcinoid tumours. ... Unsourced material may be challenged and removed. ( November 2015 ) ( Learn how and when to remove this template message ) NETs from a particular anatomical origin often show similar behavior as a group, such as the foregut (which conceptually includes pancreas, and even thymus, airway and lung NETs), midgut and hindgut ; individual tumors within these sites can differ from these group benchmarks: Foregut NETs are argentaffin negative. ... Bone metastasis is uncommon. Hindgut NETs are argentaffin negative and rarely secrete 5-HT, 5-HTP, or any other vasoactive peptides. ... Not all cells are immediately killed; cell death can go on for up to two years. [ citation needed ] PRRT was initially used for low grade NETs. It is also very useful in more aggressive NETs such as Grade 2 and 3 NETs [83] [84] provided they demonstrate high uptake on SSTR imaging to suggest benefit. ... "The Pathologic Classification of Neuroendocrine Tumors" . Pancreas . 39 (6): 707–12. doi : 10.1097/MPA.0b013e3181ec124e .

MEN1, CDKN1B, SSTR2, DAXX, ATRX, BRAF, TYMS, PTHLH, SSTR3, SSTR1, BAP1, MTOR, SST, GAST, SLC6A2, INSM1, CTNNB1, RET, PIK3CA, DNMT3A, POMC, EPHB1, PIK3CG, PIK3CD, CHGA, ELK3, CHEK2, PIK3CB, GRN, CD274, SMUG1, AKT1, GNA12, TP53, SYP, VEGFA, CDKN2A, ASCL1, BCL2, ENO2, NCAM1, GCG, MYCN, EGFR, MGMT, KIT, RASSF1, VHL, SCLC1, SSTR5, FOLH1, NKX2-1, KRAS, CALCA, CCND1, TAC1, PTPRF, VIP, NTS, PAX5, RHBDF2, GRP, IGF1, SDHD, GOT1, MAP2K7, CCK, ERBB2, DLL3, PPY, CXCL12, TP63, SMAD4, MUC1, INS, GCGR, CKAP4, NEUROD1, ISL1, MYC, NGF, SATB2, GLP1R, HSP90AA1, H3P10, HRAS, CHGB, CALR, NTRK1, TEK, DLK1, CDK4, CDX2, TGFA, UCHL1, RPE65, PGR, PDGFRA, CARTPT, CRH, UVRAG, SLC5A5, CXCR4, IGF1R, OTP, IL6, PHLDA3, TTF1, PAX8, TACR1, STK11, TRIM21, PLA2G15, SCG2, SQLE, SLC18A2, TERT, HDAC9, SLC2A1, PROM1, BCL2L11, NTSR1, PAX6, NAMPT, NOCT, INA, PLCB3, CD200, MKI67, PDX1, MAPK1, NES, HPSE, PTEN, STMN1, ABO, RIPK1, RORC, RAF1, IL1B, TRPV1, GATA3, ANGPT2, FOXM1, PTK2B, SDHAF2, ACCS, BDNF, EPAS1, EGF, ACSS2, MIB1, DNMT1, CCN2, TRPM8, CLDN4, CPE, CD34, CD44, FLNA, CEACAM5, B3GAT1, GH1, GIP, GHSR, GIPR, ADCY2, ALB, H3P28, TPPP2, H4C5, GGH, MIR1290, TMEM209, ELOA3, H4C13, H4C14, GPR151, SRPX, LGR5, TNFSF11, PSMG1, DCBLD2, H4-16, NRP1, MRGPRX4, SOCS1, H4C2, MIR3137, MRGPRX3, TNFRSF25, H3P12, CYYR1, AZIN2, DNER, AK6, MLIP, LMLN, NRP2, GPR68, MIR1246, H4C8, MAFK, MIR150, MIR155, MBOAT4, H4C9, MIR21, POTEKP, VN1R17P, SNORD95, GPR166P, ARID1A, EID3, SLC7A5, MIR375, H4C15, FZD4, MIRLET7C, OXER1, H4C12, HMGA2, H4C3, ARX, ELOA3B, GPRC6A, H4C11, H4C6, C17orf97, POTEM, MRGPRX1, ARMH1, H4C1, GADL1, ACTBL2, H4C4, BRI3, SQSTM1, ISYNA1, GHRL, ACOT7, KLF12, KRT20, SLC27A4, TET2, BCOR, EBNA1BP2, RALBP1, PGRMC1, LAMTOR1, FBXW7, MEG3, MAML3, TMEM127, NTNG1, ATRAID, KHDRBS1, DCTN4, SNORD61, NUP62, SNORD48, NTSR2, LPAR3, MAPK8IP2, SRRM2, BRD4, TRAM1, SPINK4, XIST, PPWD1, RBMS3, SETD1B, ZHX2, TNFSF13B, USE1, MAK16, UBE2Z, ONECUT2, FHL5, GCM2, DCLK1, ZBED1, ARHGEF2, PALB2, ALG9, SNED1, TET1, PDCD1LG2, TMPRSS13, MTA1, RPAIN, H1-10, EEF1E1, LGR6, PRMT5, NEUROD4, YAP1, SCML2, LANCL1, PAK4, RABEPK, ZNF197, CTNNBL1, PNO1, INSL5, EPB41L5, HDAC5, AKT3, CD302, GBA3, DCAF1, ATAT1, SERPINA3, VCL, CGA, ESR1, ERBB4, EPHB2, E2F1, DUSP2, DSG3, DPT, DPP4, DMBT1, DDC, DAD1, VCAN, CREB1, CRABP1, KLF6, CLU, FOXN3, CEACAM7, CEACAM3, ESR2, ETFA, EZH2, GHRH, HSPA4, AGFG1, HMOX1, HMGA1, GTF2H1, GSN, GNAS, GNA15, GFRA1, F3, GDNF, FSHR, FLT4, FLII, FLI1, FOXO1, FHIT, FGFR4, CGB3, CFL1, UQCRFS1, CDKN2C, FAS, APRT, APLP1, XIAP, APC, SLC25A6, SLC25A4, ANGPT1, ALK, AKT2, AFP, PARP1, ADCYAP1R1, ADCYAP1, ACVRL1, ACTN4, ACTG2, ACTG1, ACR, AQP4, ARF1, ATM, CASP3, CDK6, CD40LG, CD36, CD33, CCNE1, CCKBR, SERPINA6, CAV1, CA9, ATOH1, VPS51, C5, BRS3, BRCA2, DST, BAX, AVP, ATP4A, HTC2, HTR2A, TNC, IAPP, SDC1, SCT, SORT1, RNASE3, RARB, PTPRZ1, PTPRM, PTBP1, PSMD7, PSG2, PRKAR1A, PPP4C, POU4F1, PNN, PKD2, PITX2, PCYT1A, SERPINA5, PAX4, SDCBP, SDHB, SDHC, ST2, UBE2I, TPM3, TPH1, TNF, TM7SF2, TERC, TAT, STAT3, SSTR4, SEMA3F, SSR2, SOX11, SOX4, SOX2, SLPI, SLC3A2, SLC1A5, SFRP1, PAK3, PAK1, TNFRSF11B, KIF11, MDK, MAOA, LCN2, RPSA, L1CAM, KRT19, KRT7, KRT5, IL12A, MET, IL9, CXCL8, IL2, IL1A, IGFBP1, IGF2, IFNA13, IFNA1, MDM2, MFAP1, ODC1, MUTYH, NTRK2, NT5E, NRAS, NOTCH3, NPY, NOTCH1, NFKB1, NEFM, MUC4, CD99, NUDT1, COX2, MTAP, MST1R, MST1, MSMB, MMP7, MLH1, PTPRC
- Neuroendocrine Tumors Mayo Clinic
  
  Overview Neuroendocrine tumors are cancers that begin in specialized cells called neuroendocrine cells. Neuroendocrine cells have traits similar to those of nerve cells and hormone-producing cells. Neuroendocrine tumors are rare and can occur anywhere in the body. Most neuroendocrine tumors occur in the lungs, appendix, small intestine, rectum and pancreas. There are many types of neuroendocrine tumors. Some grow slowly and some grow very quickly. Some neuroendocrine tumors produce excess hormones (functional neuroendocrine tumors).
Malaria Wikipedia

Symptoms of falciparum malaria arise 9–30 days after infection. [12] Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing , nystagmus , conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus , seizures , or coma . [12] Complications [ edit ] Malaria has several serious complications . ... The mosquitoes remain on the wall until they fall down dead on the floor. Insecticide treated nets [ edit ] A mosquito net in use. Mosquito nets help keep mosquitoes away from people and reduce infection rates and transmission of malaria. Nets are not a perfect barrier and are often treated with an insecticide designed to kill the mosquito before it has time to find a way past the net. Insecticide-treated nets are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net. [73] Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa. [74] About 13% of households in Sub-Saharan countries owned ITNs in 2007 [75] and 31% of African households were estimated to own at least one ITN in 2008. ... That number increased to 20.3 million (18.5%) African children using ITNs in 2007, leaving 89.6 million children unprotected [76] and to 68% African children using mosquito nets in 2015. [77] Most nets are impregnated with pyrethroids , a class of insecticides with low toxicity .

ICAM1, FCGR2B, HBB, CD36, NOS2, FCGR2A, TNF, CR1, G6PD, CRP, HP, ACKR1, GYPA, SLC4A1, GYPB, NCR3, TIRAP, GYPC, LTBR, CISH, IFNG, HMOX1, PKLR, ABO, ANK1, AQP4, ATP2B4, HBG2, CYTB, ENOSF1, MSMB, MST1, ZNF536, LINC00944, SMARCB1, DHODH, PDR, TREML4, ZNF804A, OR51F1, OR51B5, CDH13, PROCR, SPATA3, OR51N1P, DHFR, DDT, RECQL4, FAM155A, IGHG3, IL4, MMP26, IL6, IL10, TLR9, HLA-DRB1, CSMD1, HBE1, DNAJC5, TMPRSS13, KLHL3, HDGFL2, TLR4, ATAD1, LMLN, TENM3-AS1, MECP2, POMGNT2, MBL2, TFRC, TGFB1, MIF, HLA-B, HAMP, DHPS, SERPINA3, TLR2, IL1B, FOXP3, FHL5, ACOT7, POTEKP, POTEM, GEM, KIR3DL1, RN7SL263P, ACTG2, ACTG1, ACTB, ACTBL2, HBA2, CYP2B6, HSPA4, LSAMP, TRAP, FCGR3B, HSP90AA1, IL1A, LAMP3, CD81, OR10A4, CCL5, ABCB1, FAS, CD40LG, TEP1, CXCL8, IARS1, HLA-G, CTLA4, HBA1, INSRR, ANGPT2, TYMS, CFH, GSTP1, IFNAR1, AGT, GYPE, FCGR3A, TXN, IL13, HSPB3, APOE, MTCO2P12, ISYNA1, FCGR2C, FYB1, VDR, HLA-A, GSTM1, GSR, ATR, MBL3P, LAIR1, PNP, IL12B, MNAT1, IL1RN, CYP2D6, IGF1, CD55, ACHE, DECR1, COX2, IL3, CCL2, MAPK1, NLRP3, FBXW7, HAVCR2, THBD, VPS51, EMP1, ITGA2B, PTGS2, ANC, IL10RA, XPO1, VNN1, PLEK, UMPS, IL2, IL2RA, TPPP, VWF, ISG20, ADAMTS13, IRF1, IL7R, AIMP2, IL12RB1, CLEC11A, METAP2, CDK5R1, ING1, IL18R1, PGD, HAP1, H6PD, PRDX5, GRAP2, CXCL9, MMP9, MPO, TAP1, CCL4L2, COX1, EBI3, ITGAX, COX3, TLR6, CXCL11, MTHFR, NFKB2, NFYA, NOS1, TBC1D9, ORC1, MCF2, AKAP13, RNF19A, TLR7, NT5C3A, IRAK4, KIR2DS1, CCL4, KIR3DL2, ICOS, COQ2, PSIP1, PECAM1, TPT1, RNASE3, ARTN, TP53, POLDIP2, PDCD1, TLR1, AHSA1, UBL4A, AQP3, AGRP, H3C9P, CYP2C8, CYP2C19, GTF2H4, CRK, RNA18SN5, ANXA2, H3P37, CASP1, NANP, CCL4L1, MAPK14, CXCR3, GNAS, GLO1, FCN2, SMIM10L2B, FKBP4, CD27, FOXO3, RBM45, HM13, IL33, HK1, CCR5, IFNA13, IFNA1, H3P42, DNAJB1, CHIT1, CYP3A4, SMIM10L2A, EGF, CHI3L1, CAT, EPHA2, NSFL1C, ADRB2, MYMX, COX8A, GAPDH, ABCB6, NR1I3, TREML1, PUM3, FMN1, TICAM2, TRIM13, BMS1, FZD4, RABEPK, LANCL1, FUT9, TNFSF13B, DCTN6, CXCR6, ARL6IP5, MRGPRX1, ZNRD2, ASPM, KAT5, RAB7B, CIB1, SEMA3C, ARMH1, STING1, CFDP1, CPQ, MYLK4, DLC1, AKR1A1, PIEZO1, TMPRSS11D, HDAC9, CARTPT, DEFB4B, TIMELESS, SPHK1, TMED7-TICAM2, PSC, VNN2, PROM1, UPK3B, H3P23, H3P28, TNFRSF11A, TNFRSF18, TP63, PDXK, CNTNAP1, DHX16, STK24, H3P19, LOH19CR1, WASHC1, WASH6P, LPAR2, MIR146A, APOBEC3B, SPAG6, CLOCK, ATG5, MIR142, AIM2, ABCG2, PCSK9, MIR155, NCF1, PPIG, MIR29A, VN1R17P, GPR166P, CD163, MIR451A, CXADRP1, ARHGEF2, CERS1, SPINK5, MASP2, GEMIN4, ACD, TLR8, MPPE1, MCPH1, HSPA14, RNF34, TMED7, ARMC9, PPP1R2C, IL22, TRAF3IP2, A1CF, PDCD1LG2, SLC44A4, SGSM3, MCAT, HPGDS, B3GAT1, ROPN1L, PHGDH, RAB14, IL23A, ABCG4, IFIH1, CFC1, BTNL2, MARCHF1, POLE4, CMC2, TMED9, ACKR3, PDXP, RHOF, AICDA, POLD4, RBM25, TOLLIP, TREM1, LGR6, ADA2, BACH2, ERAP1, GOLPH3, PARS2, KRT88P, TRIM5, IL17RE, CHP1, GPR151, NRSN1, EIF5AL1, CD160, APCDD1, ERFE, OXER1, DNAJB1P1, DSTN, GPRC6A, CCNI, ADIRF, EBNA1BP2, TMED2, EHD1, RNPS1, HPSE, SEPTIN9, SCLT1, NT5C2, SLC25A21, LEO1, NLRP12, TIMD4, CDCA5, DBA2, CARD16, PTPMT1, CGAS, RAB39B, TADA1, MRGPRX3, MRGPRX4, PGLS, PANX1, SPO11, LPAR3, CBX5, POFUT2, SPPL3, NBEAL2, LUC7L, PTPRC, FGF23, EIF5, FLT3LG, FLT1, FECH, FBN2, FBN1, FANCD2, F3, EPO, ENO2, ADGRE1, ELK4, ELF4, EIF5A, EIF4G2, CXADR, EGR3, EDNRA, EDN1, S1PR3, RCAN1, ATN1, DNMT1, DEFB4A, DHX9, ACE, DBP, CYP1A2, CYC1, GABPA, GCHFR, GDF1, GPR42, IL4R, IL1R1, IGFBP1, IFNGR1, IFNB1, IFNA2, IFI27, IDE, HTN3, HSPA9, HSD11B1, HRES1, HPRT1, HPR, HPGD, HMGB1, HLA-DOA, UBE2K, HGF, SERPIND1, HBG1, GTF3A, GSTT1, GSN, GPX1, GPT, GRK5, CYBB, CTSL, IL9, ANXA1, C3, BSG, BRS3, BRCA2, PRDM1, BCL2, BAX, ASPA, ASIP, ARR3, NUDT2, ANXA7, ANXA4, ANPEP, CSH2, AMBP, ALOX5, ALB, AHR, AFP, ADSL, ADRA2B, ADRA1A, ADORA2A, ADH1B, ADA, ACP1, ACACA, CAST, CASR, CD1B, CD1C, CSH1, CSF1R, CSF1, CS, CRYZ, CREM, CR2, CLDN4, CPB1, CNTF, CCR4, CLU, ERCC8, CTSC, CEL, CDC25C, CD69, CD68, CD40, ENTPD1, CD34, CD28, CD19, CD14, CD9, CD1E, CD1D, IL5, IL12A, FOSL1, SELE, SPTA1, SPP1, SPINK1, SPG7, SOD3, SOD1, SMN1, SLC16A1, SLC11A1, SLC6A7, SLC2A1, SGCG, SET, SEA, ABCA1, SDC1, CXCL5, CCL22, CCL18, CCL3L1, CCL3, CCL1, SAFB, SORT1, RPS19, RBP2, RANBP2, PEX19, SSR2, SSTR4, DENND2B, STAT6, DDX39B, PRRC2A, PFBI, RAB7A, CXCR4, MOGS, ZBTB16, TRPV1, VCP, USP1, TYRP1, TTR, TTPA, TRPC1, TRP-AGG2-5, TPO, TPH1, TNFRSF1B, TLR3, TGFB2, TRBV20OR9-2, TCN2, HNF1A, TADA2A, ADAM17, TAC1, STK3, PTPRH, PTHLH, IL15, KIR3DS1, MAL, MAF, LTB, LTA, LMAN1, LEPR, LDLR, LCN2, LBR, RPSA, LAG3, KRT13, KNG1, KIR2DS5, PSMD9, KIR2DL3, KIR2DL2, KDR, KCNG1, KARS1, ITPA, ITGB2, ITGAM, ITGAL, CXCL10, IDO1, ILF3, IL18, MAP2, MAP6, MEFV, MVD, PSMD7, PSMD2, PSMB9, PSEN1, PSAP, PRSS1, PROC, MAP2K1, PRKG1, PRKAR1A, PPP1R1A, PPARG, SEPTIN4, PLP1, PGM1, PGAM1, P2RX7, SLC22A18, TNFRSF11B, OMD, ODC1, NOS3, NQO2, NFE2L2, NEK2, MYD88, MYC, H3P5
- Malaria, Susceptibility To OMIM
  
  Another polymorphism, consisting of 12 TG repeats in intron 3 (173510.0004), was strongly associated with reduction in the risk of cerebral malaria. Omi et al. (2003) demonstrated by RT-PCR amplification that this IVS3(TG)12 polymorphism is involved in the nonproduction of the variant CD36 transcript that lacks exons 4 and 5. Because exon 5 of the gene is known to encode the ligand-binding domain for P. falciparum-infected erythrocytes, IVS3(TG)12 itself or a primary variant on the haplotype with IVS3(TG)12 may be responsible for protection from cerebral malaria in Thailand. ... Although the relative strength of the protection is less than that of the sickle-cell variant, the greater frequency of the DQB1 (see HLA-DQB1; 604305) polymorphism makes the net effect on resistance to malaria comparable. ... Population Genetics Using data collected from 11,890 cases of severe malaria due to Plasmodium falciparum and 17,441 controls from 12 locations in Africa, Asia, and Oceania, the Malaria Genomic Epidemiology Network (2014) tested 55 SNPs in 27 loci previously reported to be associated with severe malaria.
- Malaria Orphanet
  
  A life-threatening parasitic disease caused by Plasmodium ( P. ) parasites that are transmitted by Anophles mosquito bites to humans and is typically clinically characterized by attacks of fever, headache, chills and vomiting.
- Malaria GARD
  
  Malaria is a serious and sometimes fatal disease caused by a parasite that commonly infects a certain type of mosquito which feeds on humans. Infection with malaria parasites may result in a wide variety of symptoms, ranging from absent or very mild symptoms to severe disease and even death. People who get malaria are typically very sick with high fevers, shaking chills, and flu-like illness. In general, malaria is a curable disease if diagnosed and treated promptly and correctly. Treatment depends on many factors including disease severity, the species of malaria parasite causing the infection and the part of the world in which the infection was acquired.
- Malaria Mayo Clinic
  
  To reduce malaria infections, world health programs distribute preventive drugs and insecticide-treated bed nets to protect people from mosquito bites. The World Health Organization has recommended a malaria vaccine for use in children who live in countries with high numbers of malaria cases. Protective clothing, bed nets and insecticides can protect you while traveling. ... Sprays containing permethrin are safe to apply to clothing. Sleep under a net. Bed nets, particularly those treated with insecticides, such as permethrin, help prevent mosquito bites while you are sleeping.
Pancreatic Neuroendocrine Tumor GARD

However in some cases, a pancreatic NET occurs outside of the pancreas. A NET arises from cells that produce hormones, so the tumor can also produce hormones. ... Pancreatic NETs are called either functional or nonfunctional. A functional pancreatic NET causes specific symptoms because it makes extra hormones, such as gastrin, insulin, or glucagon. ... Pancreatic NETs can be hard to diagnosis, often not identified until 5 to 10 years after they begin to grow. Most pancreatic NETs are not inherited and occur sporadically in people with no family history of NETs.

MEN1, PCSK1, ATM, BRCA2, C11orf65, IGF2, SST, TP53, CDKN2A, SLC6A2, MTOR, EPHB1, POMC, GH1, GCGR, DAXX, ELK3, KRT19, SSTR2, CHGA, SSTR5, UCHL1, FZD4, GCM2, DLGAP1, DCLK1, SSTR4, INA, STK11, EIF2AK3, TFE3, THBD, CXCR4, PAX8, TSC1, TTR, TYMS, VEGFA, ABO, CNPY2, MRGPRX4, GPR166P, VN1R17P, MIR196A1, GADL1, MRGPRX1, GPRC6A, OXER1, GPR119, GPR151, MRGPRX3, SEMA3A, AZIN2, ACCS, STK33, LGR6, ACSS2, MEG3, NEUROG3, LPAR3, LILRB1, PLA2G15, RET, SLC2A3, INSM1, GRN, FFAR1, GHRH, GAST, FGFR4, F3, EGFR, DHCR24, CSF1, CRH, CHGB, CD44, CCK, CALCA, VPS51, ATRX, ASS1, ASCL1, ANGPT2, HSF1, PDX1, SLC2A2, KIT, SLC2A1, SEA, SDHB, SDHA, AKT1, PYGM, PTH, PTEN, PPY, PTPA, PGR, PCYT1A, PCNA, NFKB1, NEUROD1, MUC1, SMAD4, STMN1, KRAS, H3P10
- Neuroendocrine Tumor Of Pancreas Orphanet
  
  Pancreatic endocrine tumor, also known as pancreatic neuroendocrine tumor (PNET), describes a group of endocrine tumors originating in the pancreas that are usually indolent and benign, but may have the potential to be malignant. They can be functional, exhibiting a hormonal hypersecretion syndrome, but can be non-functional presenting with non-specific symptoms and include insulinoma, glucagonoma, VIPoma, somatostatinoma (SSoma), PPoma and Zollinger-Ellison syndrome (ZES, or gastrinoma) and other ectopic hormone producing tumors (such as GRFoma) (see these terms). Epidemiology Prevalence in the U.S. is estimated at 1/4,000-1/3,300 and 1/37,000 in Japan, but this is likely an underestimate due to a low detection rate. Clinical description PNETs, when functional, usually present in the 5th decade of life as various hypersecretion syndromes. These include insulinoma presenting with hyperinsulinemic hypoglycemia; glucagonoma with necrolytic migratory erythema, diabetes mellitus, and thomboembolisms; VIPoma with watery diarrhea, hypokalemia and or hypo/achlorhydia; SSoma with diabetes mellitus, cholelithiasis, steatorrhea and hypochlorhydria; and ZES with severe peptic ulcer disease.
Neuroendocrine Tumor GARD

A neuroendocrine tumor (NET) is a rare type of tumor that arises from specialized body cells called neuroendocrine cells . ... Pancreatic neuroendocrine tumors (also called islet cell tumors) - NETs that typically arise in the pancreas, although they can occur outside the pancreas. A p heochromocytoma is another, rarer type of NET that usually develops in the adrenal gland , but can also arise in other parts of the body. ... Functional NETs produce a specific set of symptoms due to the production of excess hormones, while non-functional NETs generally do not cause specific symptoms. In many cases, a person has no symptoms until the tumor spreads to the liver and/or impairs the function of an organ or system. This can make NETs very hard to diagnose. The majority of NETs are not inherited and occur sporadically in people with no family history of NETs.

PRKAR1A, MEN1, CALCA, RUNX1T1, CDKN1B, CGA, CHGA, FN1, GAST, IGFBP3, PTH, RET, ADAM17, QRSL1, CDC73
- Endocrine Gland Neoplasm Wikipedia
  
  Archived from the original on 2007-12-20 . Retrieved 2007-12-22 . External links [ edit ] Classification D ICD - 10 : C73 - C75 D34 - D35 MeSH : D00470 v t e Overview of tumors , cancer and oncology Conditions Benign tumors Hyperplasia Cyst Pseudocyst Hamartoma Malignant progression Dysplasia Carcinoma in situ Cancer Metastasis Primary tumor Sentinel lymph node Topography Head and neck ( oral , nasopharyngeal ) Digestive system Respiratory system Bone Skin Blood Urogenital Nervous system Endocrine system Histology Carcinoma Sarcoma Blastoma Papilloma Adenoma Other Precancerous condition Paraneoplastic syndrome Staging / grading TNM Ann Arbor Prostate cancer staging Gleason grading system Dukes classification Carcinogenesis Cancer cell Carcinogen Tumor suppressor genes / oncogenes Clonally transmissible cancer Oncovirus Carcinogenic bacteria Misc.
Pancreatic Neuroendocrine Tumor Wikipedia

PanNETs are a type of neuroendocrine tumor , representing about one third of gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Many PanNETs are benign , while some are malignant . ... However, morphological imaging alone is not sufficient for a definite diagnosis [14] [16] On biopsy , immunohistochemistry is generally positive for chromogranin and synaptophysin . [17] Genetic testing thereof typically shows altered MEN1 and DAXX / ATRX . [17] Staging [ edit ] The 2010 WHO classification of tumors of the digestive system grades all the neuroendocrine tumors into three categories, based on their degree of cellular differentiation (from well-differentiated "NET G1" through to poorly-differentiated "NET G3"). ... Several agents have shown activity. [12] In well differentiated PanNETs, chemotherapy is generally reserved for when there are no other treatment options. ... "The pathologic classification of neuroendocrine tumors: a review of nomenclature, grading, and staging systems" (PDF) . Pancreas . 39 (6): 707–12. doi : 10.1097/MPA.0b013e3181ec124e . ... Archived from the original on 2013-01-17 . Retrieved 2014-12-25 . CS1 maint: archived copy as title ( link ) ^ a b http://www.pharma.us.novartis.com/product/pi/pdf/afinitor.pdf ^ National Cancer Institute.

MEN1, ATRX, DAXX, ELK3, TP53, EPHB1, SLC6A2, CEACAM5, CEACAM7, UQCRFS1, DHDDS, CHPT1, RALBP1, CIB1, SEMA4D, RIPK1, CXCR4, VEGFA, TTR, GNA12, TSC2, TFE3, CDKN1B, PSG2, POMC, MYCN, CEACAM3, GRN, MUC16
Intra-Abdominal Infection Wikipedia

They vary from appendicitis to fecal peritonitis . [1] Risk of death despite treatment is often high. [1] References [ edit ] ^ a b Sartelli, Massimo; Viale, Pierluigi; Catena, Fausto; Ansaloni, Luca; Moore, Ernest; Malangoni, Mark; Moore, Frederick A; Velmahos, George; Coimbra, Raul; Ivatury, Rao; Peitzman, Andrew; Koike, Kaoru; Leppaniemi, Ari; Biffl, Walter; Burlew, Clay Cothren; Balogh, Zsolt J; Boffard, Ken; Bendinelli, Cino; Gupta, Sanjay; Kluger, Yoram; Agresta, Ferdinando; Di Saverio, Salomone; Wani, Imtiaz; Escalona, Alex; Ordonez, Carlos; Fraga, Gustavo P; Junior, Gerson Alves Pereira; Bala, Miklosh; Cui, Yunfeng; Marwah, Sanjay; Sakakushev, Boris; Kong, Victor; Naidoo, Noel; Ahmed, Adamu; Abbas, Ashraf; Guercioni, Gianluca; Vettoretto, Nereo; Díaz-Nieto, Rafael; Gerych, Ihor; Tranà, Cristian; Faro, Mario Paulo; Yuan, Kuo-Ching; Kok, Kenneth Yuh Yen; Mefire, Alain Chichom; Lee, Jae Gil; Hong, Suk-Kyung; Ghnnam, Wagih; Siribumrungwong, Boonying; Sato, Norio; Murata, Kiyoshi; Irahara, Takayuki; Coccolini, Federico; Lohse, Helmut A Segovia; Verni, Alfredo; Shoko, Tomohisa (2013). "2013 WSES guidelines for management of intra-abdominal infections" .

CRP, FCGR1A, CORO7, TCF21, ALB, PTGS1, IL22, SLC17A5, CNPY2, PPP6R2, BRAP, TLR4, PIP, PTGER3, AMBP, NT5E, COX1, MTAP, MAP6, IMPA1, IL10, IL4, OCLN
Postural Orthostatic Tachycardia Syndrome Due To Net Deficiency Orphanet

A rare, genetic, primary orthostatic disorder characterized by dizziness, palpitations, fatigue, blurred vision and tachycardia following postural change from a supine to an upright position, in the absence of hypotension. A syncope with transient cognitive impairment and dyspnea may also occur. The norepinephrine transporter deficiency leads to abnormal uptake and high plasma concentrations of norepinephrine.

SLC6A2, SLC12A2
- Orthostatic Intolerance Wikipedia
  
  It was due to being diagnosed with this illness that Page left the group in 2006 and was replaced by his understudy Sam Moran . [8] [10] Two years later, he went on to create his own fund for OI to help fund research into this then little known disorder. [11] Page recovered sufficiently enough to temporarily return to The Wiggles in 2012 to help with the transition to the next generation of Wiggles, after which he again left the group and was replaced by Emma Watkins . [12] See also [ edit ] Orthostatic hypertension Orthostatic hypotension Postural orthostatic tachycardia syndrome (POTS) Vasovagal response References [ edit ] ^ a b c d Julian M.
- Postural Orthostatic Tachycardia Syndrome Wikipedia
  
  Ivabradine [83] [84] [99] [100] alpha-2 adrenergic receptor agonist Decreases blood pressure and sympathetic nerve traffic. Clonidine , [12] Methyldopa [12] Anticholinesterase inhibitors Splanchnic vasoconstriction. ... "Postural tachycardia syndrome: a heterogeneous and multifactorial disorder" . Mayo Clinic Proceedings . 87 (12): 1214–25. doi : 10.1016/j.mayocp.2012.08.013 . ... Journal of Cardiovascular Electrophysiology . 17 (1): 108–12. doi : 10.1111/j.1540-8167.2005.00318.x . ... "Ivabradine in Postural Orthostatic Tachycardia Syndrome: A Review of the Literature" . Cureus . 12 (4): e7868. doi : 10.7759/cureus.7868 . ... Zhonghua Er Ke Za Zhi = Chinese Journal of Pediatrics . 45 (12): 885–8. PMID 18339272 . ^ Moon J, Kim DY, Lee WJ, Lee HS, Lim JA, Kim TJ, et al.
- Orthostatic Intolerance OMIM
  
  A number sign (#) is used with this entry because of evidence that orthostatic intolerance is caused by heterozygous mutation in the gene encoding the norepinephrine transporter (SLC6A2; 163970) on chromosome 16q12. One such family has been reported. Clinical Features Orthostatic intolerance is a syndrome characterized by adrenergic symptoms that occur when an upright posture is assumed: the heart rate increases by at least 30 beats per minute, without orthostatic hypotension (Jacob et al., 1997). Most patients with orthostatic intolerance are women between the ages of 20 and 50 years (Low et al., 1995). This syndrome, first described by Da Costa (1871), has been called soldiers heart (Fraser and Wilson, 1918), neurocirculatory asthenia (Wooley, 1976), and mitral valve prolapse syndrome (Boudoulas et al., 1980). It is similar in many respects to chronic fatigue syndrome (Schondorf and Freeman, 1999).
Neuroendocrine Neoplasm Of Esophagus Orphanet

A group of esophageal epithelial neoplasms characterized by neuroendocrine differentiation, comprising well-differentiated neuroendocrine tumors (NETs), poorly differentiated neuroendocrine carcinomas (NECs), and mixed neuroendocrine-non-neuroendocrine neoplasms, an umbrella category including mixed adenoneuroendocrine carcinoma. ... NECs may also arise in other parts of the esophagus. On endoscopy, NETs usually appear as small polypoid or nodular submucosal masses, while NECs are large, infiltrative, and ulcerated. Patients most commonly present with dysphagia, pain, weight loss, and sometimes melena. Metastatic NETs may be associated with carcinoid syndrome.
Hyperekplexia 1 OMIM

Barbiturate medication resulted in improvement. See also Kok and Bruyn (1962) (Kok and Suhren are the same person Went, 1974). ... The neurologic features could be controlled with clonazepam. Markand et al. (1984) examined 12 of 15 affected members of the family reported by Morley et al. (1982).

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.
- Hyperekplexia Wikipedia
  
  In comparison to the GlyT1 transporter, found mostly in glial cells , GlyT2 helps maintain a high concentration of glycine within the axon terminal of glycinergic neurons. [12] Mutations of the SLC6A5 gene have been associated with hyperekplexia in an autosomal recessive manner. [13] Defects within this gene are hypothesized either to affect the incorporation of the transporter into the cellular membrane or to its affinity for the molecules it transports: sodium ions, chloride ions and glycine. [13] Any of these actions would drastically reduce the pre-synaptic cell's ability to produce the high vesicular concentrations of glycine necessary for proper glycine neurotransmission. ... This is named the Vigevano maneuver after the doctor who invented it. [19] History [ edit ] The disorder was first described in 1958 by Kirstein and Silfverskiold, who reported a family with 'drop seizures'. [20] In 1962 Drs. Kok and Bruyn reported an unidentified hereditary syndrome, initially started as hypertonia in infants. [21] Genetic analysis within this large Dutch pedigree was later found to carry a mutation within the GLRA1 gene, which was the first gene implicated in hyperekplexia. [6] See also [ edit ] Jumping Frenchmen of Maine Latah Stiff person syndrome References [ edit ] ^ Beers, Mark H. ... "Residues within transmembrane segment M2 determine chloride conductance of glycine receptor homo- and hetero-oligomers" . EMBO Journal . 12 (10): 3729–37. doi : 10.1002/j.1460-2075.1993.tb06050.x . ... PMID 13594585 . S2CID 143799581 . ^ Kok, O.; G. W. Bruyn (1962). "An Unidentified Hereditary Disease".
- 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.
Familial Gastric Type 1 Neuroendocrine Tumor Orphanet

A rare neoplastic disease characterized by occurrence of atypical and aggressive gastric type 1 neuroendocrine tumors (NET) in early adulthood. The tumors often show nodal infiltration requiring total gastrectomy. ... Patients present high serum gastrin concentrations and iron-deficiency anemia (rather than megaloblastic anemia, which is a typical feature in patients with sporadic gastric type 1 NET, where the tumor usually arises on the background of autoimmune atrophic gastritis).
Immature Personality Disorder Wikipedia

Find sources: "Immature personality disorder" – news · newspapers · books · scholar · JSTOR ( October 2020 ) Immature personality disorder Specialty Psychiatry Symptoms -Lack of stamina [1] -Poor adaptation capabilities [1] -Inability to deal with stress [2] Diagnostic method Based on reported symptoms Differential diagnosis Bipolar [3] Personality disorders Cluster A (odd) Paranoid Schizoid Schizotypal Cluster B (dramatic) Antisocial Borderline Histrionic Narcissistic Cluster C (anxious) Avoidant Dependent Obsessive–compulsive Not specified Depressive Haltlose Immature Passive–aggressive Cyclothymic Psychopathy v t e Immature personality disorder (IPD [4] ) is an ICD-10 diagnosis characterized by lack of emotional development, low tolerance of stress and anxiety, inability to accept personal responsibility, and reliance on age-inappropriate defense mechanisms . [4] The disorder has been "gaining prominence" [5] [ better source needed ] in the 21st century. [6] It is listed under "F60.8 Other specific personality disorders". [7] A study in Denmark found that together, these 6 "Other" types constituted 2.4% of all personality disorder diagnoses. [8] While borderline personality disorder is the most common personality disorder among those who commit non-suicidal self-harm, the overall rate of deliberate self-harm is highest among those with immature personality disorder. [9] It has been noted for displaying "an absence of mental disability", [4] and demonstrating "ineffectual responses to social, psychological and physical demands." [10] Mechanics [ edit ] IPD involves a weakness of the ego , which limits the ability to restrain impulses or properly model anxiety . [4] They fail to integrate the aggressive and libidinal factors at play in other people, and thus are not able to parse their own experiences. [4] It can be caused by a neurobiological immaturity of brain functioning, or through a childhood trauma, or other means. [4] In law and custom [ edit ] In the 1980s, it was noted that immature personality disorder was one of the most common illnesses invoked by the Roman Catholic Church in order to facilitate annulment of undesired marriages. [11] In 1978, David Augustine Walton was tried in Barbados for killing two passersby who had offered his mother and girlfriend a ride following an argument, and pleaded diminished capacity resulting from his immature personality disorder; he was nevertheless convicted of murder. [12] In 1989, a former employee of the Wisconsin Department of Transportation had his claim of discrimination dismissed, after alleging that his employment had been terminated due to his Immature Personality Disorder alongside a sexual fetish in which he placed chocolate bars under the posteriors of women whose driving capabilities he was testing. [13] A 1994 Australian case regarding unemployment benefits noted that while "mere personal distaste for certain work is not relevant, but a condition (such as immature personality disorder) may foreclose otherwise suitable prospects". [14] In 2017, an individual whose sole diagnosis was Immature Personality Disorder was allowed to die through Belgian euthanasia laws that require a medical diagnosis of a life-long condition that could impair well-being. [15] References [ edit ] ^ a b "Personality disorders" . medicineworld.org . Retrieved November 26, 2020 . ^ "Peter Pan Syndrome: The Science Behind It, What It Is & How To Treat It | Betterhelp" . www.betterhelp.com . ^ Department of Veterans Affairs Regional Office in Winston-Salem, NC, Docket No 04-12 158A ^ a b c d e f Almeida, Fernando; Ribeiro, Patrícia; Moreira, Diana (September 16, 2019). ... Bloomfield, Illinois: American Academy of Psychiatry and the Law . 12 (1): 49–66. doi : 10.1177/009318538401200106 . S2CID 158806167 . ^ Kok, Lee Peng; Cheang, Molly; Chee, Kuan Tsee (1990).
Dogger Bank Itch Wikipedia

In Dogger Bank itch, sensitivity is acquired after repeated handling of the sea chervils that become entangled in fishing nets. [ citation needed ] The specific toxin responsible for the rash was determined to be the sulfur -bearing salt (2-hydroxyethyl) dimethylsulfoxonium chloride. [3] This salt is also found in some sea sponges and has potent in vitro activity against leukemia cells. [4] Treatment [ edit ] A study of two cases in 2001 suggests that the rash responds to oral ciclosporin . ... A. diaphanum is a gelatinous, smooth, sponge-like colony up to 15–30 cm (6–12 in) long, growing on rocks and shells from lower shore down to approximately 100 m (330 ft); superficially, they resemble seaweed. [5] The distribution of this animal is from the North Sea to the Mediterranean. [ citation needed ] The disease is especially prevalent among trawlermen working in the Dogger Bank , an important fishing bank in the North Sea . [6] It has also been reported from the Baie de la Seine in France. [6] History [ edit ] A medical case reported in 1957 tells of a fishing captain who worked in the Dogger Bank in the North Sea. The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water. ... Journal of Dermatological Treatment . 12 (1): 23–24. doi : 10.1080/095466301750163536 .
Epileptic Encephalopathy, Early Infantile, 45 OMIM

The patient had onset of seizures at age 12 months and showed developmental regression at age 35 months. ... In vitro functional studies in HEK293 cells showed that the mutation altered the kinetic properties of the channel, resulting in the net loss of GABAergic inhibition. In a boy with EIEE45, Lien et al. (2016) identified a de novo heterozygous missense mutation in the GABRB1 gene (T287I; 137190.0002).

GABRB1
Esophageal Food Bolus Obstruction Wikipedia

This may be encouraged by giving carbonated drinks that release gas such as Coca-Cola , which may dislodge the food. [12] While glucagon has been used in those with esophageal food bolus obstruction, evidence as of 2019 does not support its effectiveness, and its use may result in more side effects. [2] Older reviews considered it an acceptable option as long it does not lead to delays in arranging other treatments. [5] [13] Other medications ( hyoscine butylbromide , benzodiazepines and opioids ) have been studied but the evidence is limited. [12] Hyoscine butylbromide (also known as Buscopan) is used intravenously as a treatment in some cases, although there is a small risk of serious side effects in people who may have underlying cardiac issues such as high blood pressure , tachycardia , or heart disease . [14] Historical treatment of food bolus obstruction included administration of proteolytic enzymes (such as meat tenderizers ) with the purpose of degrading the meat that was blocked; however, it is possible that these methods may increase the risk of perforation of the esophagus. [15] Other modalities rarely used now include removal of boluses using catheters , [16] [ unreliable medical source? ] and the use of large-bore tubes inserted into the esophagus to forcefully lavage it. [17] [ unreliable medical source? ] Endoscopic [ edit ] The Roth net can be inserted through the endoscope to remove pieces of the obstructed food. ... Traditional endoscopic techniques involved the use of an overtube, a plastic tube inserted into the esophagus prior to the removal of the food bolus, in order to reduce the risk of aspiration into the lungs at the time of endoscopy. [7] However, the "push technique", which involves insufflating air into the esophagus, and gently pushing the bolus toward the stomach instead, has emerged as a common and safe way of removing the obstruction. [7] [18] Other tools may be used to remove food boluses. The Roth Net is a mesh net that can be inserted through the endoscope, and opened and closed from the outside; it can be used to retrieve pieces of obstructed food.
Coxalgia Wikipedia

Find sources: "Coxalgia" – news · newspapers · books · scholar · JSTOR ( February 2017 ) ( Learn how and when to remove this template message ) Coxalgia [kok sáljə] also known as coxodynia (koks'ō-din'ē-ă) from coxa – hip (L) and -algia / odyne (G) pain and is defined as pain in the hip or disease-related pain of the hip.

TRPV4, COL2A1, COL9A1, HNRNPA1, HNRNPA2B1, BSCL2, MATN3, VCP, DMD, ACR, CCL22, SLC45A2, AIM2, AURKB, BEST1, NGF, RHAG, PDGFRA, CRYBG1, ADAM11, IFNG, COMP, ATF3, FIP1L1
West Nile Fever Wikipedia

West-Nile reversible paralysis, Like WNP, the weakness or paralysis is asymmetric. [12] Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement. [12] Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms. [12] The prognosis for recovery is excellent. ... Retrieved 28 October 2017 . ^ Gompf, Sandra. "West Nile Virus" . Medicine Net . MedicineNet Inc . Retrieved 15 January 2019 . ^ "Symptoms, Diagnosis, & Treatment" . Centers for Disease Control and Prevention . USA.gov. 2018-12-10 . Retrieved 15 January 2019 . ^ "West Nile virus" . ... "West Nile virus chorioretinitis" . Br J Ophthalmol . 88 (12): 1599–60. doi : 10.1136/bjo.2004.049460 . ... "Risk factors for West Nile virus neuroinvasive disease, California, 2005" . Emerging Infect. Dis . 13 (12): 1918–20. doi : 10.3201/eid1312.061265 .

CCR5, ERVK-32, ROBO3, MAVS, DDX58, PLAAT4, IFIT2, ERVK-6, STAT1, SPP1, OAS1, IL1B, IFNB1, RNASEL, CASP8, HLA-DRB1, PELI1, SELENBP1, ARHGEF2, LRRFIP1, NAMPT, TRAIP, RIPK3, SEC14L2, CSF1R, LAMP3, ERVW-1, FOXP3, ZMYND10, DDX56, CCR7, VCP, CDKN2A, IFIH1, DHX58, ZBP1, HAVCR2, PIK3IP1, NLRP3, TNFRSF13C, TRIM6, RBM45, CCR2, ERVK-20, ERVK-18, VAMP8, TNFRSF1A, IFNA1, TNF, IFNA13, HLA-DQA1, IL1A, HLA-C, IL10, IL17A, IL18, IRF3, IRF5, KIR2DL2, KIR3DL1, KIR3DS1, LSAMP, CD180, SMAD4, MMP9, HLA-A, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PZP, GLS, CASP1, SNCA, GEM, DDX3X, TAP1, TLR3, ATF4