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Neuroendocrine Tumor Wikipedia

G Mitotic count (per 10 HPF ) Ki-67 index (%) GX Grade cannot be assessed G1 < 2 < 3% G2 2 to 20 3–20% G3 > 20 > 20% If mitotic count and Ki-67 are discordant, the figure which gives the highest grade is used. ... 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. ... World Journal of Clinical Oncology . 2 (1): 28–43. doi : 10.5306/wjco.v2.i1.28 . ... World Journal of Gastrointestinal Surgery . 2 (5): 153–56. doi : 10.4240/wjgs.v2.i5.153 . ... Archived from the original on January 2, 2010. ^ Walsh, Bryan (January 1, 2010).

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

Malaria Wikipedia

Malaria Malaria parasite connecting to a red blood cell Pronunciation / m ə ˈ l ɛər i ə / Specialty Infectious disease Symptoms Fever, vomiting, headache, yellow skin [1] Complications Seizures , coma [1] Usual onset 10–15 days post exposure [2] Causes Plasmodium spread by mosquitoes [1] Diagnostic method Examination of the blood, antigen detection tests [1] Prevention Mosquito nets , insect repellent , mosquito control , medications [1] Medication Antimalarial medication [2] Frequency 228 million (2018) [3] Deaths 405,000 in 2018 [3] Malaria is a mosquito-borne infectious disease that affects humans and other animals. [2] Malaria causes symptoms that typically include fever , tiredness , vomiting , and headaches . [1] In severe cases, it can cause yellow skin , seizures , coma , or death . [1] Symptoms usually begin ten to fifteen days after being bitten by an infected mosquito . [2] If not properly treated, people may have recurrences of the disease months later. [2] In those who have recently survived an infection , reinfection usually causes milder symptoms. [1] This partial resistance disappears over months to years if the person has no continuing exposure to malaria. [1] Malaria is caused by single-celled microorganisms of the Plasmodium group. [2] The disease is most commonly spread by an infected female Anopheles mosquito. [2] The mosquito bite introduces the parasites from the mosquito's saliva into a person's blood . [2] The parasites travel to the liver where they mature and reproduce . [1] Five species of Plasmodium can infect and be spread by humans. [1] Most deaths are caused by P. falciparum , whereas P. vivax , P. ovale , and P. malariae generally cause a milder form of malaria. [1] [2] The species P. knowlesi rarely causes disease in humans. [2] Malaria is typically diagnosed by the microscopic examination of blood using blood films , or with antigen-based rapid diagnostic tests . [1] Methods that use the polymerase chain reaction to detect the parasite's DNA have been developed, but are not widely used in areas where malaria is common due to their cost and complexity. [4] The risk of disease can be reduced by preventing mosquito bites through the use of mosquito nets and insect repellents or with mosquito-control measures such as spraying insecticides and draining standing water . [1] Several medications are available to prevent malaria in travellers to areas where the disease is common. [2] Occasional doses of the combination medication sulfadoxine/pyrimethamine are recommended in infants and after the first trimester of pregnancy in areas with high rates of malaria. [2] As of 2020, there is one vaccine which has been shown to reduce the risk of malaria by about 40% in children in Africa. [5] [6] Efforts to develop more effective vaccines are ongoing. [6] The recommended treatment for malaria is a combination of antimalarial medications that includes artemisinin . [1] [2] The second medication may be either mefloquine , lumefantrine , or sulfadoxine/pyrimethamine. [7] Quinine , along with doxycycline , may be used if artemisinin is not available. [7] It is recommended that in areas where the disease is common, malaria is confirmed if possible before treatment is started due to concerns of increasing drug resistance . [2] Resistance among the parasites has developed to several antimalarial medications; for example, chloroquine -resistant P. falciparum has spread to most malarial areas, and resistance to artemisinin has become a problem in some parts of Southeast Asia. [2] The disease is widespread in the tropical and subtropical regions that exist in a broad band around the equator . [1] This includes much of sub-Saharan Africa , Asia , and Latin America . [2] In 2018 there were 228 million cases of malaria worldwide resulting in an estimated 405,000 deaths. [3] Approximately 93% of the cases and 94% of deaths occurred in Africa. [3] Rates of disease have decreased from 2010 to 2014 but increased from 2015 to 2017, during which there were 231 million cases. [3] Malaria is commonly associated with poverty and has a significant negative effect on economic development . [8] [9] In Africa, it is estimated to result in losses of US$12 billion a year due to increased healthcare costs, lost ability to work, and adverse effects on tourism. [10] Play media Video summary ( script ) Contents 1 Signs and symptoms 1.1 Complications 2 Cause 2.1 Life cycle 2.2 Recurrent malaria 2.3 Climate change 3 Pathophysiology 3.1 Genetic resistance 3.2 Liver dysfunction 4 Diagnosis 4.1 Classification 5 Prevention 5.1 Mosquito control 5.1.1 Insecticide treated nets 5.1.2 Indoor residual spraying 5.1.3 Housing modifications 5.1.4 Other mosquito control methods 5.2 Medications 5.3 Others 6 Treatment 6.1 Uncomplicated malaria 6.2 Severe and complicated malaria 6.3 Resistance 7 Prognosis 8 Epidemiology 9 History 10 Society and culture 10.1 Economic impact 10.2 Counterfeit and substandard drugs 10.3 War 10.4 Eradication efforts 11 Research 11.1 Vaccine 11.2 Medications 11.3 New targets 11.4 Other 12 Other animals 13 References 13.1 Citations 13.2 Sources 14 Further reading 15 External links Signs and symptoms [ edit ] Main symptoms of malaria [11] The signs and symptoms of malaria typically begin 8–25 days following infection, [11] but may occur later in those who have taken antimalarial medications as prevention . [4] Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms , [12] and can resemble other conditions such as sepsis , gastroenteritis , and viral diseases . [4] The presentation may include headache , fever , shivering , joint pain , vomiting , hemolytic anemia , jaundice , hemoglobin in the urine , retinal damage , and convulsions . [13] The classic symptom of malaria is paroxysm —a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days ( tertian fever ) in P. vivax and P. ovale infections, and every three days ( quartan fever ) for P. malariae . ... 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

Several SNPs within the ATP2B4 gene showed significant association, with rs10900585 within intron 2 showing strongest association (odds ratio = 0.65; P = 6.1 x 10(-9)). ATP2B4 encodes the major Ca(2+) pump in erythrocytes, the host cells of the pathogenic stage of malaria, and Timmann et al. (2012) hypothesized that variants in ATP2B4 may disturb homeostasis of intraerythrocytic Ca(2+) concentrations and impact parasite reproduction and maturation. ... 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. ... Compared to patients with a wildtype allele, who had a median of 189,667 parasites/microliter, Q248H patients had 28,000 parasites/microliter (2-sided Fisher's test and chi-square test, p = 0.025). ... Resistance Versus Tolerance Hosts can in principle employ 2 different strategies to defend themselves against parasites: resistance and tolerance.
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. ... These include repellents that contain DEET, picaridin, IR3535, oil of lemon eucalyptus (OLE), para-menthane-3,8-diol (PMD) or 2-undecanone. Do not use a spray directly on your face. ... 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 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 . ... Contents 1 Types 2 Signs and symptoms 3 Diagnosis 4 Staging 5 Treatment 6 Genetics 7 References 8 External links Types [ edit ] The majority of PanNETs are benign , while some are malignant . ... The ASCO Post. May 15, 2011, Volume 2, Issue 8 "Archived copy" . Archived from the original on 2013-01-17 . ... id=607 ^ "Pfizer Scores New Approval for Sutent in Europe" . 2 Dec 2010. ^ Raymond E, Dahan L, Raoul JL, Bang YJ, Borbath I, Lombard-Bohas C, et al. ... "Genome-wide analysis of pancreatic cancer using microarray-based techniques". Pancreatology . 9 (1–2): 13–24. doi : 10.1159/000178871 .

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

Afterdepolarization Wikipedia

Abnormal depolarizations of cardiac myocytes Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart . ... Early afterdepolarizations [ edit ] Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed. Phase 2 may be interrupted due to augmented opening of calcium channels , while phase 3 interruptions are due to the opening of sodium channels . ... They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. [3] [4] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia .

Adenosine Deaminase 2 Deficiency Medlineplus

Adenosine deaminase 2 (ADA2) deficiency is a disorder characterized by abnormal inflammation of various tissues. ... Signs and symptoms that can occur with ADA2 deficiency include fevers that are intermittent, meaning they come and go; areas of net-like, mottled skin discoloration called livedo racemosa; an enlarged liver and spleen (hepatosplenomegaly); and recurrent strokes affecting structures deep in the brain that can start in the first few years of life. ... This gene provides instructions for making an enzyme called adenosine deaminase 2. Studies suggest that this enzyme plays an essential role in the growth and development of certain immune system cells, including macrophages , which are a type of white blood cell that plays a critical role in inflammation. ... Mutations in the ADA2 gene severely reduce or eliminate the activity of adenosine deaminase 2. Researchers do not fully understand how a shortage (deficiency) of this enzyme's activity leads to vasculitis and immune system abnormalities. ... Learn more about the gene associated with Adenosine deaminase 2 deficiency ADA2 Inheritance Pattern This condition is inherited in an autosomal recessive pattern , which means both copies of the gene in each cell have mutations.

ADA2, ADA, ARSA

Sneddon Syndrome Omim

Rebollo et al. (1983) concluded that the Sneddon syndrome is a genetic progressive arteriopathy, occlusive and noninflammatory, involving medium-sized vessels. Scott and Boyle (1986) reported 2 sibs with the disorder. The 24-year-old proposita had generalized livedo reticularis and progressive intellectual decline. ... Pettee et al. (1994) presented the clinical, hematologic, and radiographic findings in 2 brothers with Sneddon syndrome associated with antiphospholipid antibodies. ... Two patients developed hypertension associated with renal dysfunction thought to result from thickened renal vessels. Skin biopsy of 2 patients showed the classic findings of Sneddon syndrome, with small arteries showing intimal proliferation, thickened walls, and occasional occlusion.
Sneddon's Syndrome Wikipedia

Sneddon syndrome Other names Ehrmann-Sneddon syndrome, Livedo racemosa-cerebrovascular accident syndrome, Livedo reticularis-cerebrovascular accident syndrome [1] This condition is inherited in an autosomal recessive manner [2] Specialty Rheumatology Sneddon's syndrome [1] is a form of arteriopathy characterized by several symptoms, including: Severe, transient neurological symptoms or stroke Livedo reticularis , or livedo racemosa Contents 1 Signs and symptoms 2 Pathogenesis 3 Diagnosis 4 Treatment 5 Epidemiology 6 History 7 See also 8 References 9 Further reading 10 External links Signs and symptoms [ edit ] Sneddon's syndrome generally manifests with stroke or severe, transient neurological symptoms, and a skin rash ( livedo reticularis ).
Sneddon Syndrome Gard

It is primarily characterized by livedo reticularis (net-like patterns of discoloration on the skin) and neurological abnormalities.
Sneddon Syndrome Orphanet

Clinical description The mean age of onset of neurological symptoms is 39 years, though the livedo is generally observed up to 10 years earlier and sometimes since childhood. Livedo racemosa is a persistent net-like violaceous-cyanotic, mottled discoloration of the skin affecting primarily the legs and arms, but also involving the buttocks and the trunk, and that is exacerbated by cold or pregnancy. ... Loss-of-function mutations in cat eye syndrome chromosome region candidate 1 CECR1 (22q11.2) encoding adenosine deaminase 2 have been found. Diagnostic methods SS is suspected on the basis of the clinical picture.

Clanging Wikipedia

This is associated with the irregular thinking apparent in psychotic mental illnesses (e.g. mania and schizophrenia ). [1] Gustav Aschaffenburg found that manic individuals generated these "clang-associations" roughly 10–50 times more than non-manic individuals. [2] Aschaffenburg also found that the frequency of these associations increased for all individuals as they became more fatigued. [3] Clanging refers specifically to behavior that is situationally inappropriate. ... "Formal thought disorder in schizophrenia: A factor analytic study". Comprehensive Psychiatry . 33 (2): 105–110. doi : 10.1016/0010-440X(92)90005-B . ... Livingstone. p. 32 . ^ Spitzer, Manfred (1999). The mind within the net: Models of learning, thinking, and acting .

Retiform Parapsoriasis Wikipedia

Retiform parapsoriasis Specialty Dermatology Retiform parapsoriasis is a cutaneous condition, considered to be a type of large-plaque parapsoriasis . [1] It is characterized by widespread, ill-defined plaques on the skin, that have a net-like or zebra-striped pattern. [2] Skin atrophy , a wasting away of the cutaneous tissue , usually occurs within the area of these plaques. [1] See also [ edit ] Parapsoriasis Poikiloderma vasculare atrophicans List of cutaneous conditions References [ edit ] ^ a b Lambert WC, Everett MA (Oct 1981). ... Dermatol . 5 (4): 373–95. doi : 10.1016/S0190-9622(81)70100-2 . PMID 7026622 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . St. Louis: Mosby. ISBN 1-4160-2999-0 .

Poikiloderma Vasculare Atrophicans Wikipedia

Poikiloderma vasculare atrophicans Other names Parapsoriasis variegata [1] or Parapsoriasis lichenoides [2] Typical skin changes and discoloration described as poikiloderma vasculare atrophicans Specialty Dermatology Poikiloderma vasculare atrophicans ( PVA ), is a cutaneous condition ( skin disease ) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation , respectively), telangiectasia and skin atrophy . [3] [4] [5] Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis . [6] The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. [7] PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". [3] On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin). [3] [6] Mycosis fungoides, a type of skin lymphoma , may be a cause of PVA. ... PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis ; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis . [5] Contents 1 Presentation 2 Cause 3 Diagnosis 3.1 Classification 4 Management 5 See also 6 References 7 External links Presentation [ edit ] The layers of the epidermis (left). ... Seminars in Cutaneous Medicine and Surgery . 19 (2): 91–99. doi : 10.1016/S1085-5629(00)80005-X . ... PMID 1103107 . ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . St. Louis: Mosby. ISBN 978-1-4160-2999-1 . ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad Lambert WC, Everett MA (Oct 1981). ... Dermatol . 5 (4): 373–395. doi : 10.1016/S0190-9622(81)70100-2 . PMID 7026622 . ^ a b Bonvalet, D.; Colau-Gohm, K.; Belaïch, S.; Civatte, J.; Degos, R.

Dogger Bank Itch Wikipedia

Dogger Bank itch Specialty Dermatology Dogger Bank itch is a cutaneous condition characterized by a long-lasting dermatitis caused by exposure to the sea chervil , Alcyonidium diaphanum , a bryozoan . [1] The disease, common in fishermen who work in the North Sea , has been recognized by the Danish Workman's Compensation Act since 1939. [2] Contents 1 Pathogenesis 2 Treatment 3 Epidemiology 4 History 5 See also 6 References Pathogenesis [ edit ] The structural formula of the toxin responsible for Dogger Bank itch The rash is caused by a type of cell-mediated hypersensitivity reaction; this type of hypersensitivity normally occurs in people who become sensitized to volatile organic compounds . ... 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 . ... The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water. ... Allergy . 1 : 40–46. doi : 10.1111/j.1398-9995.1948.tb03301.x . ^ Carle JS, Christophersen C (1980). "Dogger Bank itch the allergen is 2-hydroxyethyldimethyl sulfonium ion". ... "Dogger Bank Itch revisited: isolation of (2-hydroxyethyl) dimethylsulfoxonium chloride as a cytotoxic constituent from the marine sponge Theonella aff. mirabilis ".

Chelonitoxism Wikipedia

This last region has recorded 89 deaths from (primarily hawksbill and green) sea turtle poisoning from 1840 to 1983, mainly in Tamil Nadu and northern and western Sri Lanka. [2] Chelonitoxism can be deadly, and supportive treatment is the only treatment available; there is no known antidote . [4] [5] Sea turtle is a traditional food in the region of the Western Pacific and Indian Oceans. [2] Symptoms of chelonitoxism begin to show up within hours to a week following ingestion of turtle meat which has not been repeatedly parboiled . [2] Children are especially susceptible, and the toxins have been reported to transfer readily via breastfeeding, even when the mother experiences no illness. [1] [2] Digestive system signs include nausea , vomiting, diarrhea , abdominal pain, dysphagia , tongue abnormalities and a firm, nontender liver . ... Other organs found to be abnormal on autopsy include swollen gall bladder, congested kidneys and enlarged spleen. [2] Cardiovascular signs include variable slight tachycardia and a moderate drop in systolic blood pressure , pallor and, on autopsy, a flabby heart with hemorrhagic petechiae . ... On autopsy, cerebral cortical edema was found, along with hemorrhagic petechiae. [2] Low fever, thirst, constipation and spontaneous abortion have also been reported, while typical signs of allergic reaction are absent. ... It has been speculated by Silas and Bastian that chelonitoxism may involve a neurotoxin. [2] Research on the biochemistry of both poisonous turtle tissues and tissues of turtle poisoning patients is scant, and local medical practitioners have minimal treatment protocols for chelonitoxism at their disposal. [2] Currently, with loggerheads (and other turtles under pressure from hunting) under legal protection against hunting, researchers hope that programs to discourage turtle consumption on health grounds may both increase turtle numbers and prevent human morbidity and mortality. [2] References [ edit ] ^ a b Multiple fatalities following ingestion of sea turtle meat Archived 2014-04-13 at the Wayback Machine NACCT Congress – September 23–26, 2011 Washington DC POSTER SESSION III 169 ^ a b c d e f g h i j Silas, E. ... PMID 17250862 . ^ Chelontoxism Food Safety Net ^ Pacific Islanders die after feasting on poisonous turtle meat Telegraph v t e Turtle terminology Carapace Chelonitoxism Fibropapillomatosis Gular scute Jackson ratio Plastron Pyramiding Shell Tortoiseshell

Steroid Diabetes Wikipedia

It is usually, but not always, a transient condition. Contents 1 Cause 2 Mechanism 3 Diagnosis 3.1 Criteria 4 Treatment 5 References Cause [ edit ] The most common glucocorticoids which cause steroid diabetes are prednisolone and dexamethasone given systemically in "pharmacologic doses" for days or weeks. ... Mechanism [ edit ] Glucocorticoids oppose insulin action and stimulate gluconeogenesis , especially in the liver , resulting in a net increase in hepatic glucose output. ... Because it is not unusual for steroid treatment to precipitate type 1 or type 2 diabetes in a person who is already in the process of developing it, it is not always possible to determine whether apparent steroid diabetes will be permanent or will go away when the steroids are finished. More commonly undiagnosed cases of type 2 diabetes are brought to clinical attention with corticosteroid treatment because subclinical hyperglycemia worsens and becomes symptomatic. Generally, steroid diabetes without preexisting type 2 diabetes will resolve upon termination of corticosteroid administration.

Maple Syrup Urine Disease Gene_reviews

Genes are listed in alphabetic order. 2. See Table A. Genes and Databases for chromosome locus and protein. 3. ... Plasma leucine levels rise predictably as a result of net protein catabolism provoked by a variety of physiologic stresses, including (more...) Each episode of acute leucinosis is associated with a risk for cerebral edema (see Figure 2) [Levin et al 1993] and death [Strauss et al 2020]. ... Establish euvolemia using isotonic sodium chloride solutions Measure serum osmolality & electrolytes every 6-12 hours Prevent serum osmolality from decreasing >5 mOsm/kg H 2 O per day (0.20 mOsm/kg H 2 O per hour) Monitor for other laboratory abnormalities. ... Acute neuroimaging may be indicated in some circumstances. 10 Treat symptomatic hypo-osmolality or worsening signs of intracranial hypertension using the following agents alone or in sequence: mannitol 0.5-1 mg/kg per dose; hypertonic (3%) saline 2-3 mEq/kg per dose; furosemide 0.5-1.0 mg/kg per dose In those w/moderate-to-severe encephalopathy, consider administration of hypertonic (3%) saline drip: 5-15 mEq/kg per day sodium chloride titrated to serum osmolality 290-300 mOsm/kg H 2 O, serum sodium 138-145 mEq/L, & serum osmolality change <0.2 mOsm/kg H 2 O per hr (5 mOsm/kg H 2 O per day) General measures Identify & treat precipitating catabolic stress (e.g., infection, dehydration, trauma).

DBT, BCKDHB, BCKDHA, BCAT2, PPM1K, DLD, ARID4B, BDNF, CTSD, SERPINE1, TNS3, CACNA2D2, MKRN3, UMOD, SPN, NME1, PAH, NBN, MEA1, IL1B, GPR4, GLI2, F2, MECP2

Maple Syrup Urine Disease Wikipedia

It is one type of organic acidemia.[2] The condition gets its name from the distinctive sweet odor of affected infants' urine Maple syrup urine disease Other names Branched-chain ketoaciduria Isoleucine (pictured above), leucine , and valine are the branched-chain amino acids that build up in MSUD. ... The BCKAD complex consists of four subunits designated E 1 α, E 1 β, E 2 , and E 3 . The E 3 subunit is also a component of pyruvate dehydrogenase complex and oxoglutarate dehydrogenase complex . [7] MSUD can result from mutations in any of the genes that code for these enzyme subunits, E 1 α, E 1 β, E 2 , and E 3 . ... The blood concentration of leucine and isoleucine is measured relative to other amino acids to determine if the newborn has a high level of branched-chain amino acids . Once the newborn is 2–3 days old the blood concentration of branched-chain amino acids like leucine is greater than 1000 µmol/L and alternative screening methods are used. ... Journal of Inherited Metabolic Disease . 22 (2): 107–114. doi : 10.1023/A:1005433516026 . ... "Genetic conditions among Canadian Mennonites: evidence for a founder effect among the old country (Chortitza) Mennonites". Clin Invest Med . 12 (2): 127–141. PMID 2706837 . ^ Mary Kugler, R.N.
Maple Syrup Urine Disease, Mild Variant Omim

In addition, patient cells showed a 2-fold increase in reactive oxygen species compared to control, suggesting an increase in metabolic stress.
Maple Syrup Urine Disease Orphanet

Etiology MSUD is due to mutations in the genes encoding subunits E1a, E1b, and E2 of the branched chain 2-ketoacid dehydrogenase (BCKAD) complex, involved in the second enzymatic step in the degradation of the branched chain amino acids (BCAAs): leucine, isoleucine and valine.
Maple Syrup Urine Disease Gard

Maple syrup urine disease (MSUD) occurs when the body is unable to breakdown certain parts of proteins. This leads to the build-up of toxic substances that can cause organ and brain damage. There are several forms of MSUD. The most common is the classic or infantile form. Symptoms of the classic form of MSUD start in early infancy and include poor feeding, irritability, extra sleepiness, and muscle spasms. If untreated, respiratory failure (lack of oxygen getting to the blood) may occur.

Esophageal Food Bolus Obstruction Wikipedia

The use of glucagon , while common, has not been found to be useful. [2] Contents 1 Signs and symptoms 2 Risk factors 3 Treatment 3.1 Conservative 3.2 Endoscopic 4 References 5 External links Signs and symptoms [ edit ] Many foods can lodge themselves in the esophagus , but the most common are meats such as steak , poultry , or pork [3] leading to the colourful description of the phenomenon as steakhouse syndrome. [1] People with food bolus obstruction typically display acute dysphagia (difficulty swallowing), often to the point that they cannot even swallow their saliva , leading to drooling. ... ] 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. ... A retrospective, observational study". Gastrointestinal Endoscopy . 53 (2): 193–8. doi : 10.1067/mge.2001.112709 . ... Digestive Diseases and Sciences . 25 (2): 100–3. doi : 10.1007/bf01308305 .

Epileptic Encephalopathy, Early Infantile, 45 Omim

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). ... INHERITANCE - Autosomal dominant HEAD & NECK Eyes - Cortical visual impairment (in 1 of 2 patients) MUSCLE, SOFT TISSUES - Hypotonia NEUROLOGIC Central Nervous System - Epileptic encephalopathy - Delayed psychomotor development - Psychomotor regression - Seizures - Hypsarrhythmia - Ataxia - Thin corpus callosum (in 1 of 2 patients) MISCELLANEOUS - Onset in infancy - Seizures are refractory - Two unrelated patients have been reported (last curated October 2016) MOLECULAR BASIS - Caused by mutation in the gamma-aminobutyric acid receptor, beta-1 gene (GABRB1, 137190.0001 ) ▲ Close

GABRB1

Leishmaniasis Wikipedia

Leishmaniasis Other names Leishmaniosis Cutaneous leishmaniasis in the hand of a Central American adult Pronunciation Leishmaniasis / ˌ l iː ʃ m ə ˈ n aɪ ə s ɪ s / leishmaniosis / l iː ʃ ˌ m eɪ n i ˈ oʊ s ɪ s , - ˌ m æ n i -/ [1] Specialty Infectious disease Symptoms Skin ulcers , fever , low red blood cells , enlarged liver [2] [3] Causes Leishmania parasites spread by sandflies [2] Prevention Bug nets , insecticide [2] Frequency 4–12 million [4] [5] Deaths 24,200 (2015) [6] Leishmaniasis is a disease caused by parasites of the Leishmania type. [2] It is spread by the bite of certain types of sandflies , and occurs most frequently in the tropics and sub-tropics of Africa, Asia, the Americas, and southern Europe. [2] The disease can present in three main ways: cutaneous , mucocutaneous, or visceral . [2] The cutaneous form presents with skin ulcers, while the mucocutaneous form presents with ulcers of the skin, mouth, and nose. The visceral form starts with skin ulcers and later presents with fever, low count of red blood cells, and enlarged spleen and liver. [2] [3] Infections in humans are caused by more than 20 species of Leishmania . [2] Risk factors include poverty , malnutrition , deforestation , and urbanization . [2] All three types can be diagnosed by seeing the parasites under microscopy. [2] Additionally, visceral disease can be diagnosed by blood tests. [3] Leishmaniasis can be partly prevented by sleeping under nets treated with insecticide . [2] Other measures include spraying insecticides to kill sandflies and treating people with the disease early to prevent further spread. [2] The treatment needed is determined by where the disease is acquired, the species of Leishmania , and the type of infection. [2] Some possible medications used for visceral disease include liposomal amphotericin B , [7] a combination of pentavalent antimonials and paromomycin , [7] and miltefosine . [8] For cutaneous disease, paromomycin, fluconazole , or pentamidine may be effective. [9] About 4 to 12 million people are currently infected [4] [5] in some 98 countries. [3] About 2 million new cases [3] and between 20 and 50 thousand deaths occur each year. [2] [10] About 200 million people in Asia, Africa, South and Central America, and southern Europe live in areas where the disease is common. [3] [11] The World Health Organization has obtained discounts on some medications to treat the disease. [3] It is classified as a neglected tropical disease . [12] The disease may occur in a number of other animals, including dogs and rodents . [2] Contents 1 Signs and symptoms 2 Cause 2.1 Vector 2.2 Organisms 2.3 Risk factors 3 Diagnosis 4 Prevention 5 Treatment 6 Epidemiology 7 History 8 Society and culture 9 Research 10 See also 11 References 12 External links Signs and symptoms [ edit ] Cutaneous leishmaniasis ulcer The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person is bitten by infected sand flies. ... Prevention [ edit ] Using insecticide can reduce phlebotomine sandfly numbers which in turn reduces the risk of cutaneous leishmaniasis infection. [18] Leishmaniasis can be partly prevented by using nets treated with insecticide while sleeping. [2] To provide good protection against sandflies, fine mesh sizes of 0.6 mm or less are required, but a mosquito net with 1.2mm mesh will provide a limited reduction in the number of sandfly bites. [19] Finer mesh sizes have the downside of higher cost and reduced air circulation which can cause overheating. ... "Further Notes on Leishman's Bodies" . British Medical Journal . 2 (2239): 1401. doi : 10.1136/bmj.2.2239.1401 . ... Social Sciences and Missions . 30 (1–2): 30–43. doi : 10.1163/18748945-03001001 .

TNF, IFNG, IL10, IL6, ARG1, IL18, CRP, TNFRSF18, MCL1, HSPA4, IL1B, SLC11A1, CXCL10, NLRP3, IL17A, TLR2, CCR5, TLR4, IL32, PRDX2, LEP, TGFB1, CD274, FCN2, CD163, MTOR, HM13, IL4, BCL2, BAX, LMLN, IGF1, HIF1A, ANXA1, VDR, UNG, TAM, NR0B2, EZR, ADA, TLR3, STAT1, MAPK3, MAPK4, EIF2AK2, PSG5, PSMD7, PTHLH, PTPN1, PTPN2, PTPN6, RPA1, RPS6, CCL2, CCL8, CXCL11, SLC1A5, SLC1A7, SNAP25, SOAT1, SPP1, TP63, EIF2S2, CDK5R1, GOPC, FOXP3, HSPA14, CD244, TOLLIP, FBLIM1, MSTO1, FBXW7, ACSS2, PDXP, SLC52A2, ALDH1A2, TMPRSS13, DCLK3, IL33, CDCA5, PWAR1, ARMH1, HNP1, CCR2, UPK3B, DLL1, SGSM3, NOX1, PABPC1, NR1I2, SPHK1, EIF2B4, EIF2B2, PRKAB1, HSPB3, SLC7A6, ARHGEF2, AIM2, H6PD, RABEPK, LANCL1, TNFSF13B, EBNA1BP2, CD160, GABARAPL2, GABARAPL1, PRDX5, POLR1A, MAPK1, NOS2, PRKAA2, PRKAA1, CST3, CTLA4, CTSB, CTSL, CYP51A1, DDT, DHFR, DPAGT1, DPP4, DSPP, DUSP4, EEF1B2, EEF2, EGFR, EIF2B1, F2R, FCGR2A, FECH, FLI1, CPB1, CCR7, LRBA, ATR, AKT1, ALDH1A1, APEX1, APRT, AQP1, ATM, ATP2A3, ATP2B4, PRDM1, CD69, BRCA1, CAPN1, CD1A, CD28, CD86, CD40, CD40LG, CD44, FPR2, G6PD, GAPDH, CYTB, MNAT1, CD200, MPG, MPL, MPST, MRC1, MSMB, MST1, AHR, MFAP1, PAEP, PHB, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PLP1, PNOC, MAP3K10, MBL2, GCHFR, IFNB1, GCK, GTF3C1, HLA-C, HMOX1, HSPD1, IFN1@, IFNA1, IFNA13, IL1A, LTA, IL9, IL12A, IL12RB1, IL13, ITGA4, ITGAL, JAK2, RPSA, H3P28

Kala-Azar, Susceptibility To, 1 Omim

Bucheton et al. (2003) suggested the interleukin-2 receptor beta-chain gene (IL2RB; 146710) as a candidate gene for susceptibility to kala-azar on chromosome 22q12. ... To identify susceptibility loci for visceral leishmaniasis in Indian and Brazilian populations, the LeishGEN Consortium and Wellcome Trust Case Control Consortium 2 (2013) used genomewide association studies and variance components methodology (i.e., a mixed model) to avoid confounding due to population structure and relatedness. ... The LeishGEN Consortium and Wellcome Trust Case Control Consortium 2 (2013) concluded that the HLA-DRB1-HLA-DQA1 region contributes to susceptibility to visceral leishmaniasis, regardless of geographic region and parasite species.
Leishmaniasis Gard

Leishmaniasis is a parasitic disease spread by the bite of infected sand flies. There are several different forms of leishmaniasis. The most common are cutaneous and visceral. The cutaneous type causes skin sores. The visceral type affects internal organs such as the spleen, liver and bone marrow. People with this form usually have fever, weight loss, and an enlarged spleen and liver. Visceral disease can be deadly without proper treatment. Leishmaniasis is found in parts of the Middle East, Central America, South American, Asia, Africa, and southern Europe.
Leishmaniasis Orphanet

A parasitic disease caused by different species of the genus Leishmania , transmitted through the bite of hematophagous female phlebotomine sand flies. The clinical spectrum ranges from asymptomatic to clinically overt disease which can remain localized to the skin or disseminate to the upper oral and respiratory mucous membranes or throughout the reticulo-endothelial system. Three main clinical syndromes have been described: visceral (or Kala-Azar; with fever, weight loss, hepatosplenomegaly), cutaneous, and mucocutaneous leishmaniasis (cutaneous or mucocutaneous ulceration).

Lichen Spinulosus Wikipedia

Lichen spinulosus Other names Keratosis spinulosa [1] : 776 Specialty Dermatology Lichen spinulosus is a rare skin disorder characterized by follicular keratotic papules that are grouped into large patches. [2] It is a variant of keratosis pilaris named for its resemblance to a patch of lichen . Contents 1 See also 2 Notes 3 References 4 External links See also [ edit ] Hook nail List of cutaneous conditions Notes [ edit ] ^ James, William; Berger, Timothy; Elston, Dirk (2005). ... ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . St. Louis: Mosby. ISBN 1-4160-2999-0 . ... Clinicopathologic review of thirty-five cases". J Am Acad Dermatol . 22 (2 Pt 1): 261–4. doi : 10.1016/0190-9622(90)70035-G . PMID 2179296 . External links [ edit ] Derm Net NZ Emedicine Thehinhso v t e Diseases of the skin and appendages by morphology Growths Epidermal Wart Callus Seborrheic keratosis Acrochordon Molluscum contagiosum Actinic keratosis Squamous-cell carcinoma Basal-cell carcinoma Merkel-cell carcinoma Nevus sebaceous Trichoepithelioma Pigmented Freckles Lentigo Melasma Nevus Melanoma Dermal and subcutaneous Epidermal inclusion cyst Hemangioma Dermatofibroma (benign fibrous histiocytoma) Keloid Lipoma Neurofibroma Xanthoma Kaposi's sarcoma Infantile digital fibromatosis Granular cell tumor Leiomyoma Lymphangioma circumscriptum Myxoid cyst Rashes With epidermal involvement Eczematous Contact dermatitis Atopic dermatitis Seborrheic dermatitis Stasis dermatitis Lichen simplex chronicus Darier's disease Glucagonoma syndrome Langerhans cell histiocytosis Lichen sclerosus Pemphigus foliaceus Wiskott–Aldrich syndrome Zinc deficiency Scaling Psoriasis Tinea ( Corporis Cruris Pedis Manuum Faciei ) Pityriasis rosea Secondary syphilis Mycosis fungoides Systemic lupus erythematosus Pityriasis rubra pilaris Parapsoriasis Ichthyosis Blistering Herpes simplex Herpes zoster Varicella Bullous impetigo Acute contact dermatitis Pemphigus vulgaris Bullous pemphigoid Dermatitis herpetiformis Porphyria cutanea tarda Epidermolysis bullosa simplex Papular Scabies Insect bite reactions Lichen planus Miliaria Keratosis pilaris Lichen spinulosus Transient acantholytic dermatosis Lichen nitidus Pityriasis lichenoides et varioliformis acuta Pustular Acne vulgaris Acne rosacea Folliculitis Impetigo Candidiasis Gonococcemia Dermatophyte Coccidioidomycosis Subcorneal pustular dermatosis Hypopigmented Tinea versicolor Vitiligo Pityriasis alba Postinflammatory hyperpigmentation Tuberous sclerosis Idiopathic guttate hypomelanosis Leprosy Hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized Drug eruptions Viral exanthems Toxic erythema Systemic lupus erythematosus Localized Cellulitis Abscess Boil Erythema nodosum Carcinoid syndrome Fixed drug eruption Specialized Urticaria Erythema ( Multiforme Migrans Gyratum repens Annulare centrifugum Ab igne ) Nonblanchable Purpura Macular Thrombocytopenic purpura Actinic/solar purpura Papular Disseminated intravascular coagulation Vasculitis Indurated Scleroderma / morphea Granuloma annulare Lichen sclerosis et atrophicus Necrobiosis lipoidica Miscellaneous disorders Ulcers Hair Telogen effluvium Androgenic alopecia Alopecia areata Systemic lupus erythematosus Tinea capitis Loose anagen syndrome Lichen planopilaris Folliculitis decalvans Acne keloidalis nuchae Nail Onychomycosis Psoriasis Paronychia Ingrown nail Mucous membrane Aphthous stomatitis Oral candidiasis Lichen planus Leukoplakia Pemphigus vulgaris Mucous membrane pemphigoid Cicatricial pemphigoid Herpesvirus Coxsackievirus Syphilis Systemic histoplasmosis Squamous-cell carcinoma This condition of the skin appendages article is a stub .

Feline Hyperaldosteronism Wikipedia

Contents 1 Causes 1.1 Primary hyperaldosteronism 1.2 Secondary hyperaldosteronism 2 Mechanism 3 Symptoms 4 Diagnosis 5 Treatment 6 Epidemiology 7 References Causes [ edit ] Primary hyperaldosteronism [ edit ] Primary hyperaldosteronism (PHA) is a disorder of the adrenal cortex that causes increased circulating aldosterone levels. ... This causes a lower total body concentration of potassium and potentially, hypokalemia . [1] Hypokalemia affects polarization of nerve and muscle membranes, which causes episodic muscle weakness . [2] Symptoms [ edit ] Most affected cats present with muscular weakness and/or ocular signs of hypertension . ... Ocular signs of arterial hypertension include mydriasis , hyphema , or blindness due to retinal detachment and/or intraocular hemorrhages . [1] A palpable mass in the cranial abdomen is another potential finding. [2] Diagnosis [ edit ] Persistently increased blood pressure may also be due to kidney disease or hyperthyroidism . ... Specific therapy for treating high blood pressure (e.g., amlodipine ), should be added if necessary. [2] Epidemiology [ edit ] Most affected cats are over 10 years old. ... "Primary Hyperaldosteronism: Expanding the diagnostic net". Journal of Feline Medicine and Surgery . 13 (9): 641–650. doi : 10.1016/j.jfms.2011.07.017 . ^ a b c d e Kooistra, Hans S. (2006).

Mutyh Polyposis Gene_reviews

Genes and Databases for chromosome locus and protein. 2. See Molecular Genetics for information on allelic variants detected in this gene. 3. ... A deletion of exon 15 has also been reported [Ricci et al 2017]. Table 2. Detection Frequency of Biallelic Germline MUTYH Pathogenic Variants by Number of Polyps in Individuals with APC Mutation-Negative Polyposis View in own window Number of Polyps Detection Frequency of Biallelic Germline MUYTH Pathogenic Variants 1-19 2% (25/1,430) 10-19 2% (58/2,634) 20-49 11% (60/540) 20-99 7% (306/4,425) 50-99 21% (22/107) 100-999 16% (133/809) >1,000 8% (2/24) Based on Grover et al [2012], Stanich et al [2019], Terlouw et al [2020] Tumor tissue testing prior to germline molecular genetic testing of a proband is generally not required; however, it may be required in certain circumstances (e.g., by third-party payer policy). ... Two of 15 probands with familial NET of the small intestine and four of 215 individuals with nonfamilial NET of the small intestine were heterozygous for MUTYH pathogenic variant p.Gly396Asp [Dumanski et al 2017]. It is unclear if a heterozygous MUTYH pathogenic variant is a risk factor for NET or ACC, as the risk of NET or ACC in individuals with biallelic MUTYH pathogenic variants appears to be quite low. ... Weren et al [2015], Grolleman et al [2019] 2. Leads to overexpression of GREM1 3.

Diabetic Angiopathy Wikipedia

Contents 1 Presentation 1.1 Complications 2 Pathophysiology 3 Diagnosis 4 Treatment 5 Prognosis 6 References 7 External links Presentation [ edit ] Complications [ edit ] Diabetes mellitus is the most common cause of adult kidney failure worldwide. ... Pathophysiology [ edit ] As insulin is required for glucose uptake, hyperglycemia in diabetes mellitus does not result in a net increase in intracellular glucose in most cells. ... There is also neuropathy ; also associated with diabetes mellitus; type 1 and 2. References [ edit ] ^ Holt, Richard I. ... External links [ edit ] Classification D ICD - 10 : E10.5, E11.5, E12.5, E13.5, E14.5 ICD - 9-CM : 250.7 MeSH : D003925 v t e Diabetes Types Type 1 Type 2 LADA Gestational diabetes Diabetes and pregnancy Prediabetes Impaired fasting glucose Impaired glucose tolerance Insulin resistance KPD MODY Neonatal Transient Permanent Type 3c (pancreatogenic) Type 3 Blood tests Blood sugar level Glycosylated hemoglobin Glucose tolerance test Postprandial glucose test Fructosamine Glucose test C-peptide Noninvasive glucose monitor Insulin tolerance test Management Diabetic diet Anti-diabetic drugs Insulin therapy intensive conventional pulsatile Cure Embryonic stem cells Artificial pancreas Other Gastric bypass surgery Complications Diabetic comas Hypoglycemia Ketoacidosis Hyperosmolar hyperglycemic state Diabetic foot ulcer Neuropathic arthropathy Organs in diabetes Blood vessels Muscle Kidney Nerves Retina Heart Diabetic skin disease Diabetic dermopathy Diabetic bulla Diabetic cheiroarthropathy Neuropathic ulcer Hyperglycemia Hypoglycemia Other Glossary of diabetes History of diabetes Notable people with type 1 diabetes

NOS3, AGER, HP, THBS1, SERPINF1, MTHFR, ADCY3, HMOX1, CREM, CASP3, ASS1, FASLG, ADCY8, THBS2, ALB, RELA, VEGFA, FN1, PTK2B, NOS2, CCL2, SPARC, ICAM1, BDKRB1, MOK, EDN1, MPO, ADM, RENBP, AKR1B1, PPARG, PON1, SERPINE1, SMPD1, DPP4, SOD1, TFRC, STIP1, TLR2, ADAMTS13, MIR185, TGFBI, CIP2A, JTB, MIR200C, TCF7L2, SERP1, MIR216B, NOX4, SOD2, MIR146A, TNF, RNF10, MIR130A, TNFRSF1A, TRIB3, MIR126, NOP53, TRAF6, HPSE, VDR, CCDC8, FZD5, ARHGEF5, AOC3, SQSTM1, KLF4, OR10A4, PON2, SGK1, IAPP, GLP1R, GCG, FGF2, EGFR, E2F1, DUSP6, ACE, CMA1, CAT, CANX, ATF3, APOE, AKT1, AHR, AGT, HMGB1, IFIT3, SELL, IGF1, REN, PTEN, MAPK7, MAPK3, PRKCB, PPIA, PLG, TNFRSF11B, MSX2, LGALS3, KLK1, KDR, ITGAM, IRAK1, IGFBP7, H3P7

Pancreatic Cancer Wikipedia

NETs can start in most organs of the body, including the pancreas, where the various malignant types are all considered to be rare . ... More than 90% of cases at all grades carry a faulty KRAS gene, while in grades 2 and 3, damage to three further genes – CDKN2A ( p16 ), p53 , and SMAD4 – are increasingly often found. [2] A second type is the intraductal papillary mucinous neoplasm (IPMN). These are macroscopic lesions, which are found in about 2% of all adults. This rate rises to about 10% by age 70. ... Typical sites for metastatic spread (stage IV disease) are the liver, peritoneal cavity and lungs , all of which occur in 50% or more of fully advanced cases. [58] PanNETs [ edit ] The 2010 WHO classification of tumors of the digestive system grades all the pancreatic neuroendocrine tumors (PanNETs) into three categories, based on their degree of cellular differentiation (from "NET G1" through to the poorly differentiated "NET G3"). [19] The U.S. ... Cancers of the tail of the pancreas can be resected using a procedure known as a distal pancreatectomy , which often also entails removal of the spleen . [2] [3] Nowadays, this can often be done using minimally invasive surgery . [2] [3] Although curative surgery no longer entails the very high death rates that occurred until the 1980s, a high proportion of people (about 30–45%) still have to be treated for a post-operative sickness that is not caused by the cancer itself.

BRCA2, TP53, CDKN2A, STK11, KRAS, BRCA1, SMAD4, EP300, PALB2, ABO, NR5A2, MYC, CTNNB1, TNF, MMP2, AKT2, APC, PDX1, PTEN, PTGS2, STAT3, ATM, KDR, CXCL8, TYMS, SST, TNFSF10, TERT, EGFR, TGFB1, HIF1A, MSLN, CD44, SPINK1, MMP9, PPARG, CD24, LDHA, PLAU, SOD2, PALLD, SSTR2, SLC29A1, MAP2K4, DPYD, TGM2, AXL, IL24, IFNA1, PTCH1, EPCAM, NR4A1, TFPI2, CDH1, LINC00673, NRP1, RAP1GAP, MEN1, RB1, VHL, WT1, KLF5, TYMP, PTHLH, GADD45A, FGF13, CCL20, EFEMP1, CFLAR, AHR, TNFRSF10B, SSTR1, FXYD3, TP63, BAP1, FOXP1, ANXA10, DAXX, NFKBIA, TSC2, RNF43, BUB1, VEGFB, MIR1179, SSTR3, IFNA2, RABL3, SUGCT, CNR1, IFNA5, CNR2, ETAA1, CLPTM1, SYCP1, RBBP8, GAGE1, CCAT1, BCL2L1, BCAR1, LY6E, ZNRF3, ATRX, COL18A1, CLPTM1L, DAB2, SBF2, HSPB2, ERBB2, CCKBR, HRAS, HSPB1, HSP90AA1, LINC01829, PPFIBP1, EPHB2, PIK3CA, CCK, HGF, ERBB3, MIA, PDHX, PSCA, SIRT1, HSPB3, H3P10, PIM3, NOTCH1, CEACAM5, EGF, SMUG1, PIK3CB, PARP1, MAPK1, MAPK8, MTCO2P12, GPC1, CDK4, HDAC9, CEACAM3, ABCG2, ACTB, CEACAM7, LINC01088, MAPK3, NDRG1, PSG2, YAP1, PIK3CG, TAFA5, SLC19A1, SPARC, PRSS1, PROM1, PIK3CD, HP, GLI1, MAP2K7, F3, NGF, ZEB1, FBXW7, NFE2L2, TEX11, ITGB1, VEGFA, GABPA, BICD1, ANXA2, CD82, GAST, DCLK1, COX2, CCND1, XIAP, MET, BACH1, S100A4, LGALS1, MDM2, DPP6, MUC16, FOXM1, MIR21, SLC39A4, MIR221, IFNG, EZH2, LINC00964, AKT1, ALB, LDLRAD4, C9, MUC5AC, SETD2, CXCR4, VIM, MUC4, CD274, LEPQTL1, XRCC1, IGF1, MUC1, IGF1R, CXCL12, IL1B, IL6, BCL2, HNF1A, SCT, TWIST1, CCN2, TLR4, DNMT1, AURKA, CAV1, PLK1, CASP3, PKM, MTHFR, LGALS3, MTOR, BRAF, PRKAA1, MIR301A, AGER, HOTAIR, EPHA2, MCL1, VTCN1, COL11A2, RAC1, DUSP6, CDKN2B, CRP, MAPK14, RUNX3, MALAT1, FN1, MIR155, MIR210, ERCC2, DCK, AGR2, CFTR, GDF15, CDKN1A, ADIPOQ, PRKN, MIR200C, TIMP1, KIF20A, PTF1A, PSMD9, TGFBR2, TICAM2, RRM1, MIR137, MIR142, ALOX5, MLH1, MIR29A, SOCS3, IFI27, SRC, GLP1R, PRKAA2, SP1, SOX2, TMED7-TICAM2, HMGA1, SOAT1, H3P23, PAK4, CHEK1, ZNRD2, BMI1, HMGA2, RALBP1, PALD1, TMED7, TLR7, BSG, DCTN6, WNT5A, EPAS1, WEE1, POSTN, BNIP3, MST1, FGFR1, ATN1, MST1R, GSK3B, PRKAB1, CD47, NFATC2, HSPA5, FANCG, PVT1, SHH, MBD1, ETS1, NPTX2, ABCB1, SLC2A1, MUC2, IFNA13, MMP7, MRC1, IGF2, CCN1, NQO1, LUM, MDK, IL10, PTPA, ELAVL2, POU5F1, FLT1, CXCR2, GSTT1, AIMP2, DKK3, MIR23A, KLF10, CRK, MIR214, MUL1, MIR203A, MIR200B, MIR195, APEX1, GRAP2, MIR145, CDKN1B, MIR141, RIPK1, TNFRSF6B, NR1I2, LINC01194, TGFA, THBS1, ALDH1A1, POLDIP2, MICA, NES, HOTTIP, UCA1, POU5F1P4, MIR34A, POU5F1P3, RNF19A, CASP8, CBLL2, CTLA4, AHSA1, RUNX2, ERCC1, OGG1, FANCC, ZG16B, DNER, NTRK1, FGF2, F2RL1, MMP14, FOXO3, CD276, NUPR1, RMC1, MSH2, AFAP1-AS1, DCC, LIF, MIR10B, HDAC1, HDAC2, HMGB1, ACTN4, HMOX1, ADM, ADRB2, IAPP, ICAM1, GDNF, MIR96, MIR25, IL1A, IL2, MIR223, MIR212, MIR205, ANXA1, MIR148A, MMRN1, MIR143, LCN2, MIR132, REG3A, TMEM97, UQCRFS1, STAT1, RET, TGFBI, CDC42, DPP4, CDK2, KLF4, CTNND1, IL32, DSPP, BAG3, CUX1, VDR, TAZ, PIM1, PCNA, SOX9, SEMA5A, XPO1, MAP2K1, SUB1, PRKD1, SPP1, JUN, TOP2A, MLRL, XIST, RAF1, IL4, IL4R, VEGFC, MIR222, MIR216A, NAT2, IL13, 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TRPM7, ISG15, CLOCK, MIR345, SET, CDK7, MIR200A, MIR216B, JUNB, JUND, ADAMTS1, KL, ITGAM, SERPINF1, SFTPD, SHC1, SELE, ITGA2, HDAC3, ARNTL, PBK, TUG1, SLC16A1, PDGFRB, DCN, RGN, KISS1, CHI3L1, SREBF1, IQGAP1, BSND, FGF7, ZNF35, VASH2, YY1, ESR1, AGT, PEAK1, TFF1, TFRC, NOTCH3, EZR, COX8A, FBP1, CLDN4, HAVCR2, VAV1, CRYZ, FASN, TIMP2, MUC6, TSPAN8, MYB, MIR196B, TXN, MIR330, ATF2, MIR31, IL33, AGTR1, VSIR, CES2, LOXL2, TNFRSF10C, PGK1, SSTR4, ABCC3, PEBP1, CEMIP, CLIC1, EGLN3, ADRA1A, PRDM14, HHIP, SLC52A2, MIR29B1, CDCP1, ADRA2B, MIR29B2, TAM, KLK7, MAP3K1, CCR7, ALCAM, MAP3K7, MGMT, MIF, CXCL10, EDNRA, NEK2, RASA1, TPX2, NEAT1, EEF1B2P2, PRMT1, GJB2, KDM1A, APLP2, CXCR6, RBM14-RBM4, MIR146A, GJA1, KANK2, NOX4, REG1A, USP22, MIR150, CA9, HTC2, MAP2K2, CD40, GGT1, GPR42, DKK1, MIR15B, E2F1, PDCD4, FAS, AREG, HHLA2, GOLGA6A, HPGDS, BHLHE22, HNRNPA2B1, MCAT, GOT1, SLCO1B3, RGCC, EIF4E, LILRB1, MIR106B, NRG1, PTK2, PHGDH, PWAR1, CCKAR, ARF6, GSTP1, MSH6, MARK2, EBI3, IGFBP1, S100A8, CDK1, S100A9, RBPJ, S100A11, CAT, GATA4, MIR191, SATB1, CDA, MIR1247, ENO1, CBX7, DNM1L, ABCC5, SERPINA1, SCO2, ARL2BP, BRS3, CHST15, CHEK2, GRP, AKR1A1, GSTM1, PLG, ECT2, PRNP, RPL10, SDF4, MIR17, RBM14, MIRLET7B, PLAC8, ADH1A, TRIM29, THY1, NAF1, C17orf97, ASPH, PTPN1, TCF7L2, TWF1, TPD52, PTPN11, TP53BP1, LPAR1, MTDH, TK1, LMLN, TLR1, TNS4, TGFBR1, TFF3, CRY2, CRMP1, AR, FAM83A, PTK6, PTBP1, TFAP2A, E2F3, KISS1R, TGFB2, MAK16, TIAM1, CCL21, TBX2, IDO2, CYP24A1, RFXAP, CASC2, ROBO1, DNM2, ROS1, SMARCA2, RBM45, RPS6KA2, RPS6KB1, RPS27A, ABHD11-AS1, S100A2, RELA, SIX1, TRIM69, SFRP4, ARHGAP4, LDLRAD3, SEL1L, SARDH, RMDN2, CCL2, PDIK1L, TICAM1, CCL18, DNMT3A, LRG1, TAT, DLX6-AS1, TACR1, PTPN14, TAC1, PTPRC, SOX2-OT, RAB5A, SYT1, STING1, GADL1, PRRT2, CDCA5, DUSP1, STK4, CYP2B6, STAT5B, SNHG15, CYP1A1, DPYSL3, DNMT3B, CYP1A2, CYP1B1, OSBPL5, SSAV1, RECQL, SRY, SRF, AZIN2, BHLHE23, TPM3, CD68, IL23A, PRMT3, PSME3, ABCC4, B3GALT5, GOLM1, TUBB3, ING4, PRMT5, WASF2, VAV3, RMDN1, SEMA4D, DESI2, ATG7, ANP32B, CD40LG, FOXP3, GDE1, ZFR, SLIT2, DLL4, MEG3, COX5A, RMDN3, CDH17, HEATR1, SLC52A1, CDH3, PAF1, IQSEC1, NAMPT, MFN2, KRT20, TLR9, BCL2L11, PTPRU, CDC25B, WWOX, CDC20, ASAP1, TXNIP, BTK, PRPF31, KLF8, DDR1, CTRC, BBC3, CILK1, MYOF, ZHX2, NOC2L, SMG1, CD36, SULF1, CASP9, TFIP11, SLC7A8, ANGPTL2, SNHG1, SRRM2, DAPK2, RASSF1, MAP4K1, FSTL1, SRPX2, DELEC1, CELF2, CTCF, CD86, ERO1A, SLC39A3, AP4B1, EEF2K, GIPC1, CD80, UHRF1, TBK1, MCTS1, CD14, SGSM3, RBMS3, WDR5, CDK8, CDK9, TPT1, COL4A2, COL11A1, WNT10B, DHDDS, XPC, XRCC3, XRCC4, BAX, ZFP36, COL1A2, ULBP2, LIN28A, MANF, MCPH1, TUSC3, TCTN1, BHLHE41, CMM, FOSL1, LAT2, VIP, SYBU, UBC, NR2C2, TRAF2, TRAF6, TMPRSS13, CPOX, TTK, ITCH, TYRO3, NUF2, BAG1, ARHGAP24, ATR, AVP, CLDN3, UTRN, KDM6A, UVRAG, VCL, USP5, LTB4R, WNK1, HAP1, KSR1, CDK5R1, PER3, PER2, PNO1, SQSTM1, BNC1, DIABLO, METTL3, USP9X, TM4SF5, ARTN, AIP, DMAP1, SLC16A4, SLC16A3, DYRK1B, BUB3, CES1, CCN5, CFL1, CHPT1, CMA1, GORASP1, ROBO3, CUL4B, IL21, CIP2A, DENR, CLU, DANCR, TP73-AS1, SMURF1, TNFSF13, AKR1B10, CEACAM1, TNFRSF10D, TNFRSF10A, IL18R1, CCR5, PADI4, MIR629, LINC01672, HSPD1, PAWR, HSPG2, PARN, ITGAV, C20orf181, MME, EPS8, ERBB4, FGF10, ITGA3, GFRA2, PRDX1, SNHG16, MIR451A, PAEP, AKR1B1, MMP11, ALDOA, P2RX7, P2RX5, ALDH1B1, GRK2, MIR296, OLR1, MNAT1, MAP3K10, ITGB2, NTS, MIR204, EPHB4, PFN1, MIR483, KCNJ11, KCNH2, MIR509-1, PER1, PDPK1, MIR497, HOXB7, MIR193B, MIR885, MIR373, HSPA4, ITK, HOXD13, GLI3, PDK1, FGFR4, MICOS10-NBL1, PDCD1, ANGPT1, MITF, TMX2-CTNND1, HSPA2, ANG, IFIT3, ROR2, PHB, TMEM238L, FBN2, MIR1231, IL6ST, IL17A, TNFRSF9, MIR135B, GAPDH, MIR1246, IL9, MTRR, FAT1, MIR148B, FAP, MIR424, MIR375, IL12A, CISD2, NEDD9, IL15, NEDD4, NCL, NBN, NBL1, MUTYH, IL13RA2, MIR374A, MTAP, IL2RA, ADAM8, NPY, NTRK2, NTF3, IRF2, FDPS, MIR1290, FCN2, FBL, GCHFR, PNP, IGF2R, ILK, MSMB, ESRRB, NGFR, NOS2, MIR1291, MSN, MIR1181, FCGR3B, MIR99B, AFP, IL18, NME1, MIR1271, FCGR3A, IKBKB, MIR744, MAP3K5, PRRX1, ELAVL1, POTEF, PPIA, GGT2, APOA2, FOXL1, EIF4EBP1, LASP1, RPSA, CCR2, EIF5A, CXCR3, FOXC1, GGTLC4P, MIR144, BIRC5, PODXL, HFE, UPK3B, HIC1, SNHG14, CDKN2B-AS1, PMS1, SMAD7, MIR15A, MR1, MIR139, LDHB, LTB, GSN, RELN, GRB7, PRSS2, AQP3, EEF1A2, MUC5B, CXCL1, GSK3A, FADS1, MIR601, MIR10A, PRKCB, MIR130B, MIR122, ANXA8L1, PRKAR1A, MIR126, GGTLC3, LRP2, GGTLC5P, ANXA8, EIF4A1, FOLR1, LTA, MAGEA3, CEACAM6, KCNN4, MCC, HNF4G, PCAT1, MCAM, GLO1, HNRNPK, KCNQ1, ENG, MIR196A1, MIR192, MIR185, PLAUR, SLC25A3, PLAT, MAP1A, LINC-ROR, MIR455, FKBP4, MIR181C, MIR183, MIR486-1, FOXA1, BMP8B, PIMREG, MTPAP, ZNF654, RHOF, NLRP2, CCL28, LTB4R2, MRGBP, PRPF40A, MIR874, ERO1B, MIR940, EIF5A2, STYK1, MIR646, MIR92B, IL17RB, LXN, MAML3, FERMT1, SMARCAD1, RIPK4, MIR652, TRPV6, ETNK1, TREM1, TERF2IP, KCMF1, SPHK2, BMP3, CHD7, ANLN, GPR137, MIR374B, MIR935, RETN, STK31, BNIP3L, GACAT2, ADPGK-AS1, OGDHL, CEP55, SNHG9, SARS2, CNDP2, OCIAD1, AGAP2-AS1, INTS11, MIR675, NKRF, ZGLP1, MSTO1, SLC35F6, LINC00462, MIR891B, MIR365A, BOK, PSENEN, ANO1, PIWIL2, KDM3A, PRR11, EXOC2, MIR876, CDKAL1, SULF2, SOX6, NSUN5, MIR1225, SLC38A7, BMP2, DIP, PARP14, KDM7A-DT, UGT1A1, MIR760, UGT1A3, PBRM1, ASPN, LOC729970, BPHL, CC2D1A, RADIL, ST7L, ALKBH5, HHAT, SLC25A36, SYCE1L, DST, MYDGF, MED29, KPNA7, PCBP3, GLS2, ERVK-11, MYB-AS1, LSM1, BANCR, LINC01111, HCAR1, GHET1, CA2, AGO2, SERPING1, LOC102723407, GATD3B, DKK4, SIK1B, CDR1-AS, CAD, CALCR, ANKRD1, SPINK4, MIR5100, UBE2S, RABGEF1, ATAD2, HIPK2, MACROD1, NOB1, ERVK-22, MIR2682, MIR4656, LAMTOR2, REM1, DLL1, SPRY4-IT1, SLCO3A1, SLCO4A1, HTRA2, DESI1, PSC, C3, DNAI1, USP21, SNORA74A, LETMD1, LOC112694756, MOB4, ZEBTR, PRPF40B, LNCRNA-ATB, EML2, CADM1, RAB38, SH3BP4, TMEFF2, ACADS, H3P13, H3P8, ABCA4, FAM215A, DDX58, SERPINA3, USP49, CASP7, IRAIN, LOC110806263, EHF, PERCC1, FGF21, PTPN22, CERNA3, KCNK15-AS1, LINC00976, CAPN1, NUTF2P3, CHD5, SIRT1-AS, ACO1, NECTIN3, CAST, CLIC4, MYRIP, TMEM158, C1GALT1C1, LINC00339, DUOX1, ADAM10, PRKAG2, CRLF3, ZMYND10, MIR1301, MIR1180, MIR634, TLR8, BTC, KLF9, C1QBP, CLDN18, CKLF, ZEB2-AS1, HSPA14, LEF1, MIR663B, MIR4306, ACVR2A, YTHDF2, SIRT6, RAB14, NT5DC3, GPR87, LOXL1-AS1, MBD3, IL17D, LINC00994, BCL11A, ADA2, MAP3K20, CDK12, CMPK1, CAB39, RAB23, SF3B6, MIR1297, PIAS4, MIR1243, MIR1266, MIR3686, A4GNT, INSIG2, IL20, DUOX2, ERVW-1, ACTA2, VSX1, KLRC4-KLRK1, ACP3, UBQLN1, BUB1B, ERVK-2, STRN4, NPC1L1, MIR3064, TSPO, BRD7, MYLIP, ERVK-12, PYCARD, ACVR1, IL21R, IRAK4, PXN-AS1, ANGPTL4, MIR642B, MIR3923, APIP, GMNN, MIR3679, ISOC1, LINC01133, BTF3, ASCC1, SMIM31, TRAT1, LINC00958, F11R, TAS2R10, LINC01006, ARHGEF4, SLC25A37, DIO3OS, EMSY, PROKR2, CD109, ADAT2, GPR151, SLCO6A1, EMB, REG3G, ANPEP, MIR208A, ANGPT2, FATE1, MIR211, TMIGD2, SPNS2, MSI2, ARR3, JDP2, SPPL3, H4-16, CCDC26, MUC17, GATA5, ANXA5, LINC00052, MIR198, MIR199A1, PTGR2, PRIMA1, FBXL14, MIR199A2, MIR19A, MIR19B1, SYT9, MIR20A, CACUL1, ANXA11, ANXA6, TMEM37, BRI3BP, SLC32A1, CYP2R1, TMEM45B, PRAP1, MAL2, MCM3AP-AS1, ALDH1A3, IL17F, MIR28, EGLN2, AGTR2, PPP1R14A, MIR302A, ART1, FOXQ1, ASAH1, DMKN, ASNS, MIR30C1, MARVELD3, LRP5L, MIR30C2, NLRP3, MIR155HG, ALPG, MIR224, MIR215, TWIST2, MRGPRX4, MRGPRX3, DCD, ANIB1, TM4SF18, CMTM5, CTHRC1, MIR219A1, NOSTRIN, MIR22, UHRF2, ALOX15, FBXO32, ALK, CSMD2, MIR197, SIK1, APAF1, MIR127, MCIDAS, MIR129-2, RSPO2, KLK3, ANO9, APRT, CHSY3, TRIM59, APOC1, ARG1, LYPD5, LINC00346, LINC01559, OR10A4, BCL9L, APOA1, SLC25A45, MACC1, PWAR4, SBF2-AS1, DNAAF3, CCSER1, PAIP2B, LINC01121, C16orf74, HRNR, MIRLET7C, SERPINA13P, CEP85L, MIRLET7D, LINC-PINT, MIR100, MIR106A, FASLG, ENTPD8, GSTK1, TMPRSS9, MIR125A, H19, ASPM, MIR193A, MUC20, ARID2, B3GNT6, MIR182, ADAMTS18, OIT3, BHLHA15, OXER1, IFNLR1, SLFN5, EML5, CLEC14A, MIR186, SLC5A8, RHOB, FEZF1-AS1, NKAIN2, DAB2IP, MIR181A2, CENPX, MRGPRX1, MED19, MIR149, SGMS1, NPCA1, FAM133B, ARG2, MIR152, RICTOR, IL27, SEMA3D, BIRC2, GPRC6A, FOXK1, KDM1B, MIR18A, ALKBH3, MARCHF8, VWCE, LINC00473, MIR32, SMYD2, SMURF2, NIBAN2, YTHDC2, PORCN, IL25, DEPTOR, ILRUN, S100PBP, SMYD3, TMPRSS3, PNPT1, HIF3A, COP1, RHBDF1, MMS19, LINC01060, BGLAP, MIIP, SAV1, MIR520H, PINK1, MIR519D, MIR181D, BCL6, DHX40, DYNC2H1, TMEM204, MIR489, MIR146B, BCR, MIR202, PLEKHF1, MIR492, BDNF, MIR493, CFB, GGCT, STK33, ADRB3, CDK15, AFAP1, LGR6, ACE2, SLURP1, ADH4, PNPLA2, CXADRP1, CIAPIN1, ADAMTS9, PRDM1, H3P38, MIR539, SNORA25, MIR421, MIR584, KIF15, OTUD7B, MIR607, MIR608, MIR613, MIR623, CD248, NORAD, IL22RA1, ADH6, SNX6, SINHCAF, HAMP, ANKRD36B, KLHL1, MRTFA, CFAP97, PCDH10, CERNA2, CRNDE, MIB1, RPTOR, ARID1B, PPM1H, BGN, AICDA, PARP4, MIR485, MIR410, BCKDHB, VN1R17P, EBPL, GPR166P, FOXB2, XRCC6P5, ZGPAT, NT5C1A, MCHR2, HOPX, MCM8, RAB11FIP4, PROK1, RPAIN, MIR331, AP2A1, MIR340, USP44, MIR367, TRIM63, KDM2B, MIR370, MIAT, TSLP, NKD1, MIR320A, MIR34B, SNHG7, MIR93, JAG1, RAB2B, ATAD1, PARP10, MIR99A, RIOX2, KMT5C, PSRC1, CRISP1, ASTL, HINT2, MYCBPAP, ATF3, SH3D21, PPP1R2C, GRHL2, DUXAP8, JADE1, DUXAP10, NANOG, UBA5, NBDY, MFSD13A, KDM8, MIR448, MIR449A, H4C15, MIR431, MMRN2, MYH14, BCHE, MIR452, NAA25, CEP70, MIR371A, MIR425, RERE, IMMP2L, HASPIN, SUMO1P3, SESN2, VANGL1, NETO2, MIR377, MIR381, MIR384, NECTIN4, AZGP1, ZFP91, ITIH5, SLC44A4, SRCIN1, BAK1, GPX2, HS3ST3B1, LPAR3, PLOD2, EFNB2, PKN1, EGR1, PRKAR2A, PRKACG, EGR3, EIF4A2, PRELP, PPP5C, PPP1R1A, PPID, PPIB, MED1, PPARA, PON2, PON1, POLE, POLD1, PNMT, PNLIP, PMS2, PMS2P3, PMAIP1, PRKCZ, PRKDC, EFNA2, PTAFR, PTPRJ, PTPRG, PTPRA, PTPN13, QSOX1, PTN, E2F2, PTGS1, PTH, PTGER4, PSMD10, EEF1G, PYY, PRTN3, KLK10, HTRA1, KLK6, PRSS3, EDNRB, PROX1, EEF1A1, MAPK9, PLXNA1, CELA1, DYRK1A, PLEK, CDK16, PCBP1, PCBD1, PBX3, PAX6, PAX5, PAK3, PAK2, EREG, SERPINB2, ERCC4, PAFAH1B2, PCSK6, P2RY6, P2RY2, OSM, OSBP, ORM1, OPRM1, OPRD1, TNFRSF11B, ERCC5, ODC1, PCYT1A, PDE8A, PDGFA, PIGR, ELK3, PLCB3, EMD, PLA2G4A, PKLR, PKD1, PIN1, EPHA1, EPHA4, EPHB1, EPHB3, PDGFB, PGR, PFKP, PFKM, PFKFB4, PFDN5, PEG3, PECAM1, PDZK1, ENPP1, PDK4, PVR, RGL2, PSD4, SAFB, SLC1A2, DCX, SKIL, SKI, SIM2, ST3GAL4, ST6GAL1, DDB2, SFRP1, DDT, SELP, CX3CL1, XCL1, CXCL5, DLD, CCL8, CCL7, DMD, SRL, SCTR, SCN10A, SCN9A, SARS1, ACE, SLC5A1, DCTD, DAG1, SPP2, CYP2C19, SPG7, CYP3A4, SOX12, SOX15, CYP51A1, SOS1, SOD3, DACH1, SNCG, SLC6A8, DAP, SMO, SMN2, SMN1, SMARCC1, DAPK1, SLPI, DAPK3, SLC9A1, SLC8A1, SAI1, S100B, RAB27A, S100A10, RGS16, TRIM27, REST, REN, RDX, RBP4, RBP1, RBM3, KDM5A, DPEP1, RASGRF1, PLAAT4, RARB, RAP1B, RAP1A, RALA, RAG2, DRD2, HBEGF, RAD17, DVL2, RABIF, RAB27B, RNASE1, RNASE3, RNASEL, RPS8, S100A7, S100A6, DNA2, SORT1, S100A1, RXRA, DNAH5, DNASE1, DYNC1H1, RPS15A, RPS6KA3, RNF2, RPS6KA1, RPL39, RPL34, RPL29, RPL26, RPE65, RORB, RORA, SNORA73A, BRD2, ERG, NTRK3, ERN1, IARS1, GAS6, GATA1, GATA2, GATA3, IGSF1, GC, IGFBP7, IGFBP2, GCK, GCKR, GCNT1, IFNB1, IFNAR1, IFNA17, GCY, GDF2, GDF10, IFN1@, GFPT1, IDH1, ID2, IRF8, ICAM2, CXCR1, GALNT3, GAD2, ITGB4, KRT8, FRZB, FUS, KCNK2, FUT3, FUT4, GABBR1, JAK1, JAG2, EIF6, GABRA3, GAD1, ITGA5, ITGA1, ISG20, IRS1, IRF1, ITGA6, GABRP, INSR, INPP4A, IDO1, GFRA1, HYAL1, NT5E, HTR1D, HLA-DRB1, HLA-DOA, HLA-C, HLA-B, GOT2, GP2, HGFAC, GPI, HDGF, HCRTR1, HCRT, H2AX, H1-5, H1-4, GUSB, GUCY2C, GPT, GSTM3, GPX1, GRM1, GRIA3, GRB10, GRB2, GNRHR, HMGB2, HMGCR, HPD, HTR1B, HSPE1, GHR, GHRH, HSPA9, GJB1, HES1, AGFG1, GPC3, HPGD, HOXB9, GLUL, HOXB8, HOXB6, HOXB2, HOXA1, HNRNPU, HNRNPC, ONECUT1, HNF4A, GLUD1, HMMR, KRT17, KRT18, KRT19, FPR2, NEDD8, MYH9, MYD88, FANCD2, MMUT, TRIM37, PTK2B, MTR, ND2, FBLN2, MT1M, MRE11, MPST, MPO, MPL, MMP16, MMP15, GPC4, MMP13, MMP12, FER, MMP3, GPC5, NELL1, NEO1, NEU2, NQO2, YBX1, NRTN, NPY2R, NPM1, NPC1, CCN3, NOTCH2, NOS1, NOP2, NNMT, NM, NEUROD1, NHS, ETV4, NFYA, ETV5, EWSR1, EYA2, NFE2, F9, F10, NEUROG1, KMT2A, MAP3K9, MKI67, FLNA, LMO2, LMNB1, LLGL1, LIPE, LIMS1, LIMK2, LIMK1, LIG4, LIG3, LIFR, FLNB, LPA, LGALS3BP, FOLH1, LFNG, LEPR, FOLR2, LBR, LAMC2, LAMP1, LAMB3, LAG3, LOX, LRP1, MICB, VEGFD, MFAP1, FH, MAP3K4, MAP3K3, MEF2D, MEF2A, MECP2, ME2, FHL2, MDH1, MATK, LRP6, MAT1A, MAP2, SMAD6, SMAD3, SMAD1, FOXD1, TACSTD2, FLI1, BCAM, LTA4H, SPOCK1, CYP2B7P, SREBF2, MVP, GDF11, TRIM13, RBM5, RBM6, TRIM28, G3BP1, ARFRP1, FRY, LRPPRC, RAD50, PPIF, ACTR2, ARPC4, EDIL3, IL18BP, ABCB6, GNE, HDAC6, AKT3, HNRNPDL, NUP153, NR1H4, NR1I3, TRIB1, CNKSR1, SF3B4, CD74, DDX17, CD63, SEMA3C, CARM1, CAP1, MERTK, TACC3, GPNMB, BASP1, RACK1, DLC1, CDK2AP2, IRF9, TUBA1B, MICU1, KLF2, WARS2, TLR6, TNIP1, RTN3, SF3A1, STUB1, MED12, USP15, MSC, GPX4, LITAF, MAGED1, ROCK2, ATG5, RASAL2, MAP4K4, AIM2, GSTO1, QKI, NTN1, RECQL5, CD101, KIF3B, SLC9A3R1, SLC9A3R2, CD163, SOCS6, SNORD22, ADGRG1, BCL7B, PIWIL1, MAPKAPK2, AIMP1, SCAMP1, BAG5, CDH13, SDC3, DLEC1, KIF14, NUAK1, TLK1, CDC25C, MTSS1, SETD1A, USP34, CDH5, DCAF1, MDC1, PTGES, SOCS5, TTLL4, WTAP, PRDX6, APOBEC3B, SPAG6, CDH11, CHD1L, CXCL14, EI24, NEBL, CD59, ARPC1A, HTATIP2, KLRK1, ARHGEF15, MLXIP, FASTKD2, NLRP1, VASH1, CCNA2, ITGA11, CBX3, TUSC2, PDAP1, PHB2, GPR182, SLCO2B1, KLF12, FILIP1L, SLC6A14, GALNT5, CCNB1, WIF1, MAP4K5, RPP14, ADAMTS8, KIFAP3, SIRT2, STK38L, NCAPH, ZNF281, PES1, ICMT, CELA3B, GPR161, TPSD1, CAV2, RUNX1, SIRT4, DICER1, NCSTN, CBR1, SATB2, SIN3B, BICD2, MPRIP, CBL, KDM6B, PEG10, KDM4C, PDS5B, TNIK, RER1, TRIM31, TOPBP1, KHDRBS1, PLK2, KDM5B, RBBP9, PLK4, NFAT5, POLQ, USP39, CCT8, DLL3, TNFSF13B, SPINT2, WASF3, SCGB1D2, IGF2BP2, CD34, IGF2BP1, ENTPD1, PDLIM5, SLCO1B1, ENTPD2, SMC2, OLFM4, SEPTIN9, FRS2, UBE2C, STIP1, OGFR, RIPK3, DSTN, RAB31, CCND2, CCND3, KCNQ1OT1, COPS6, FERMT2, CKAP4, CCNG1, CD28, EHMT2, PAPOLA, GADD45G, BRD8, MALT1, PPARGC1A, MRPS30, NMU, ME3, ADAM28, GCNT3, CDKN1C, SRPK2, TNFAIP1, COMP, COMT, SLC31A1, CPE, NR1H2, UCK2, UGT1A, UGP2, UCHL3, UCHL1, UBE2N, CPN1, TULP3, TUFT1, TTR, TRH, HSP90B1, TPO, TPD52L2, CREBBP, CREM, TOP1, TNFRSF1B, BEST1, TRPV1, VTN, XRCC2, NELFE, DEK, SCLC1, PAX8, BTG2, ZNF154, ZBTB16, CNBP, ZFX, YES1, COL5A2, WARS1, COL6A1, XPA, XK, COL6A2, COL6A3, WNT7B, WNT2, WNT1, COL17A1, WAS, TNFRSF1A, CRKL, PTTG1, CLDN5, CTPS1, HNF1B, CTRL, TBX3, TCEA3, TCEA2, TCEA1, CTSB, TAGLN, ADAM17, CTSD, SULT1A1, CTSE, CTSH, STIM1, CX3CR1, STAT2, CXADR, ST13, CYP2A6, CYP2A13, SSR2, TRIM21, CST1, PPP1R11, TDG, CS, TMSB4X, TMPRSS2, TM7SF2, TLR3, TLR2, TLE1, CRY1, THBS2, THBD, THAS, TGIF1, PRDX2, CSF1R, TGFB1I1, CSF3, CSN2, TFF2, TFCP2, TF, CSNK2A2, TERC, VCAN, TFEB, COL1A1, CNC2, ABCC2, SPHK1, ARHGEF7, IER3, ASAP2, DLEU2, CCN6, NRP2, INPP4B, CHGA, RAB11A, CHKA, ADAM15, CHRM3, CHRNA7, TNK1, BECN1, EIF3F, IRS2, DYNLL1, CLCA1, NUMB, PTCH2, RUVBL1, FUBP1, NAE1, MBD2, ATP6V0D1, MTA2, AURKB, CDKN2D, ARHGEF2, SCAF11, TMSB10, EBAG9, EXO1, ATG12, CCNE2, CDO1, WASF1, DIRAS3, CLDN8, CDX1, BRSK2, CLIC3, MAP3K14, F2RL3, CEBPB, P4HA2, CDK5R2, NOP14, AKR7A2, MADD, UBL4A, H4C11, H4C12, H4C6, H4C4, H4C1, FZD6, FZD4, CDC7, H4C9, ARID1A, GATD3A, H4C8, SLC7A5, ANP32A, GPR68, YEATS4, KMT2D, MFAP5, RASSF7, ADAM12, SLC25A16, CUBN, H4C3, H4C2, LMO4, TTF2, HAT1, PARG, PIK3R3, PPFIA4, CLTC, GEMIN2, SEMA7A, OGT, SORBS2, KLF11, DOC2A, H4C5, RAD54L, STK24, TAGLN2, SPARCL1, PIP4K2B, PIP5K1B, PIP5K1A, NME5, H4C14, H4C13, H3P40

Mosquito Bites Mayo_clinic

Avoid and exclude mosquitoes Limit exposure to mosquitoes by: Repairing any tears in the screens on windows, doors and camping gear Using mosquito netting over strollers and cribs Using mosquito netting when sleeping outdoors Selecting self-care products that don't have scents Use insect repellent Use insect repellent when mosquitoes are active. The most effective insect repellents in the United States include one of these active ingredients: DEET Icaridin, also called picaridin Oil of lemon eucalyptus IR3535 Para-menthane-diol (PMD) 2-Undecanone These ingredients temporarily repel mosquitoes and ticks. ... Used according to package directions, these products are generally safe for children and adults, with a few exceptions: Don't use DEET-containing products on infants younger than 2 months. Don't use icaridin on infants younger than 6 months Check the labels of products with oil of lemon eucalyptus — some aren't suitable for children under 3 years old. ... Some sporting goods stores sell clothing pretreated with permethrin. Don't wash bed nets or set them in sunlight, as this breaks down permethrin.