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Abortion In Francoist Spain And The Transition Period
Wikipedia
Italy made abortion legal in May 1981 as a result of a referendum, while in Portugal abortion was legalized by the Parliament in November 1982. [17] Marí Carmen [28] Marí Carmen La Mari Carmen quiere abortar La Mari Carmen busca un hospital A Mari Carmen le dicen que no Ay Mari Carmen, tienes un marrón. ... This was likely a result of an increased number of illegal abortions taking place in Spain in newly opened women's health clinics. [18] In 1985, shortly before abortion became legal, Mari Carmen Talavera died in Madrid as the result of an illegal abortion. [29] [30] Her death led to several feminist and pro-legalized abortion chants. [28] [31] Anti-abortion activists made it difficult for non-governmental family planning clinics to offer and perform legal abortions, as they harassed medical staff.
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Health Effects Of Wine
Wikipedia
When alcohol is mixed with food, it can slow the stomach's emptying time and potentially decrease the amount of food consumed at the meal. [21] A 150-millilitre (5-US-fluid-ounce) serving of red or white wine provides about 500 to 540 kilojoules (120 to 130 kilocalories) of food energy , while dessert wines provide more. [28] Most wines have an alcohol by volume (ABV) percentage of about 11%; the higher the ABV, the higher the energy content of a wine. [28] Psychological and social [ edit ] Danish epidemiological studies suggest that a number of psychological health benefits are associated with drinking wine. ... ISBN 978-92-832-1244-7 . ^ a b Hydes, Theresa J.; Burton, Robyn; Inskip, Hazel; Bellis, Mark A.; Sheron, Nick (28 March 2019). "A comparison of gender-linked population cancer risks between alcohol and tobacco: how many cigarettes are there in a bottle of wine?" ... "Moderate alcohol consumption lowers the risk of type 2 diabetes: a meta-analysis of prospective observational studies" . Diabetes Care . 28 (3): 719–25. doi : 10.2337/diacare.28.3.719 . ... The Science of the Total Environment . 350 (1–3): 28–37. doi : 10.1016/j.scitotenv.2004.09.044 .
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Extranodal Nk/t-Cell Lymphoma, Nasal Type
Wikipedia
Overall 3 year survival in these 3 respective groups were 81, 55, and 28%. [23] Patients, particularly those in the advanced poor risk groups may develop hemophagocytic lymphohistiocytosis or have their disease progress to aggressive NK-cell leukemia. ... The following regimens are recommended by many studies and the European Society for Medical Oncology Clinical Practice guidelines [14] or National Comprehensive Cancer Network : [28] Localized stage I and 2 diseases are treated with a combination of local radiation followed by DeVIC ( dexamethasone , etopoxide , ifosfamide , and carboplatin ). ... Pathogens (Basel, Switzerland) . 7 (1): 28. doi : 10.3390/pathogens7010028 .JAK3, STAT5B, CFLAR, ASRGL1, NCAM1, PDLIM7, TNFRSF8, PRDM1, SOAT1, TRBV20OR9-2, ASPG, TMTC3, CREBZF, CD274, STAT3, ABO, GNLY, TP53, KRT20, PDCD1, ABCB1, MS4A1, EZH2, MYC, MME, BCL2, HAVCR2, ELF4, ETS1, BCOR, FCGR3A, TBC1D9, PLK2, FCGR3B, GZMH, GZMB, EOMES, IL2, TNFAIP3, TIA1, IL4, KIT, KLRD1, LAG3, SLC22A2, PTPRC, POU2F2, PLOD2, ADM, MEFV, NOS2, NOS1, MIR223
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Sensory Processing Disorder
Wikipedia
Damage in any part of the brain involved in multisensory processing can cause difficulties in adequately processing stimuli in a functional way. [ citation needed ] Mechanism [ edit ] Current research in sensory processing is focused on finding the genetic and neurological causes of SPD. EEG , [28] measuring event-related potential (ERP) and magnetoencephalography (MEG) are traditionally used to explore the causes behind the behaviors observed in SPD . ... PMID 25075609 . ^ a b Palmer B (2014-02-28). "Get Ready for the Next Big Medical Fight Is sensory processing disorder a real disease?"
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Hypoglycemia
Wikipedia
Overnight fasting glucose levels are below 3.9 mmol/l (70 mg/dl) in 5% of healthy adults, but up to 5% of children can be below 3.3 mmol/l (60 mg/dl) in the morning fasting state. [28] As the duration of fasting is extended, a higher percentage of infants and children will have mildly low plasma glucose levels, typically without symptoms. ... Archived from the original on 1 July 2015 . Retrieved 28 June 2015 . ^ a b c Yanai H, Adachi H, Katsuyama H, Moriyama S, Hamasaki H, Sako A (February 2015). ... Clin. Endocrinol. Metab . 94 (3): 709–28. doi : 10.1210/jc.2008-1410 . PMID 19088155 . ^ "FDA approves first treatment for severe hypoglycemia that can be administered without an injection" . ... "Characterizing sudden death and dead-in-bed syndrome in Type 1 diabetes: analysis from two childhood-onset Type 1 diabetes registries" . Diabetic Medicine . 28 (3): 293–300. doi : 10.1111/j.1464-5491.2010.03154.x .ABCC8, IGF2, SERAC1, HNF1A, INS, IL1B, TNF, SOD2, CACNA1C, GSR, SERPINA1, PPARA, CRH, PNMT, TH, GH1, GRIN2B, IGF1, G6PC, INSR, KCNJ11, HNF4A, ACADM, CPT1A, HADHA, GHSR, TANGO2, PGM1, HADH, PC, SETD2, AGL, PCK1, NR3C1, MEN1, MPI, TFAM, DBH, EIF2AK3, EIF2S3, ETFDH, NDUFS2, PTEN, FBP1, UQCRC2, GHR, SLC22A5, SLC37A4, HMGCL, UQCRB, NFKB2, PURA, GLI2, GLP1R, MPC1, NBAS, HSD17B10, NR1H4, PYGL, NDUFAF1, ROBO1, HMGCS2, TIMMDC1, HRAS, MRPS2, SEPSECS, RARB, WARS2, KCNMA1, NDUFS3, NDUFS4, NDUFS6, NDUFS8, NDUFV2, PPP2R5D, NOTCH3, OTC, OTX2, PPM1B, PCCA, PCCB, PCK2, NNT, GPR161, PHKA2, POU1F1, MLYCD, NDUFV1, NDUFS1, MRPS7, NDUFB10, CDON, PROP1, NDUFAF4, ACAD9, LRPPRC, APC2, NDUFB11, NDUFAF3, MPV17, MTO1, ND1, ND2, ND3, NDUFA1, NDUFA6, NDUFB3, NDUFB9, GPC3, GJA1, GK, PROKR2, SLC35A2, CA5A, SLC25A20, MICOS13, COG7, NDUFAF2, LHX4, COG8, NUBPL, CAMKMT, EHMT1, CYB561, NDUFAF5, DBT, CTDP1, DGUOK, DLD, NDUFA11, SGPL1, NSD1, BCS1L, ACADSB, KCNMA1-AS1, ACAT1, SUCLG1, ZGLP1, UQCC3, HESX1, ALDOB, NDUFS7, GOLGA6A, PTF1A, ACSF3, ATP5F1D, ATP7A, AUH, BCKDHA, BCKDHB, DPP4, CYP21A2, MTOR, GALT, FAH, RCBTB1, GPC4, PNPO, SLC52A1, MCCC2, PREPL, GCDH, WDR11, GCG, RNF125, GCK, SLC5A2, SAMD9, SLC3A1, DMXL2, FOXRED1, POMC, SOX3, MCCC1, ETFA, ETFB, TMEM126B, CYP2C9, ALB, SLC2A4, ACE, DSPP, FFAR1, SI, MGAM, SLC2A1, AKT2, GLUD1, HIF1A, NPY, SST, VEGFA, PRL, PIK3CA, ADRB2, TXN, KCNH2, GPR119, SLC5A1, UCP2, SLC2A2, IGFBP3, NFE2L2, SELENBP1, MAPK8, PPP1R13L, SHBG, ADIPOQ, TXNIP, SLC2A3, RNH1, PRKAA1, REN, AKT3, PIK3CG, PIK3CD, KDR, APRT, BDNF, ANTXR2, CPT2, CHPT1, GABPA, GDF1, CCHCR1, SHC3, GPT, HK1, IAPP, IL6, GIP, ARFIP2, PIK3CB, MFAP1, DNM1L, KCNH6, ARID1B, KL, MTA2, SEMA6A, SLC16A7, LPAR2, PDIA2, FTO, DHDDS, SOCS3, DAPK2, RPAIN, TIGAR, SLC52A3, SORCS1, CXCR6, CPT1C, SLC39A14, TBPL2, MIR155, MIR665, EMSLR, RIPK1, IRS2, KHSRP, TMPRSS11D, ACKR3, SOCS7, SH3BP1, GAL, ERO1A, PIAS1, HNRNPDL, CRYL1, PADI1, HGH1, FGF19, SIRT6, GLS2, KEAP1, RAPGEF5, WWOX, UQCRQ, KMT2B, DCAF1, FGF21, ROBO4, BNC2, DEPP1, VPS13C, TUBB3, H6PD, TMEM132A, MARCHF1, DENR, ACADL, MLRL, AAAS, TIMM8A, DNMT1, ARID3A, DSC3, EDNRA, EGFR, ELAVL1, ENO1, ENO2, ERBB4, ESRRA, F2R, F3, FBN1, FGF1, FGF2, FOS, NR5A1, GCGR, GHRH, GHRHR, GIPR, GLA, GCLC, GPER1, GPR42, GRIN1, GSK3B, GYS1, CYP2C8, CTNNB1, CRMP1, BID, ACADVL, ADCY5, ADRA1A, ADRA2B, AHR, AIF1, AKT1, APOE, APP, AQP4, AQP7, ARNT, AVP, BRS3, CRIP1, C3, CALD1, CCND2, CD34, CD36, CD59, LRBA, CDH15, CEBPA, CHAT, CHGA, CKB, CREM, FOXA2, HNRNPC, HNRNPL, SSTR4, PRKAR1A, PSMB9, PTHLH, RAD21, RB1, RIT2, RORC, SELP, SIAH2, ST3GAL4, SLC16A1, SLC22A1, SREBF1, STAR, PRKAA2, STAT5A, STAT5B, SYK, TAP1, TCF7L2, TGM2, TP53, TRH, UGDH, UTRN, VCAM1, CNBP, KMT2D, PRKAB1, PPY, AGFG1, MC4R, HTC2, IFNG, IGFBP6, KCNQ1, KHK, KIT, LEP, LEPR, LGALS1, LIPE, LPL, SMAD3, MAFD2, MET, PTPA, NR3C2, MTHFR, NHS, NUCB2, P4HB, PECAM1, PFKFB3, ABCB1, PIK3R2, POR, POU2F1, PPARD, PPARG, LOC102723407
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Jaundice
Wikipedia
Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT). [28] No single test can differentiate between various classifications of jaundice. ... Pathologic causes of neonatal jaundice include the following: breastmilk jaundice formula jaundice [45] hereditary spherocytosis glucose-6-phosphate dehydrogenase deficiency pyruvate kinase deficiency ABO / Rh blood type autoantibodies alpha 1-antitrypsin deficiency Alagille syndrome (genetic defect resulting in hypoplastic intrahepatic bile ducts) Progressive familial intrahepatic cholestasis pyknocytosis (due to vitamin deficiency) cretinism (congenital hypothyroidism) sepsis or other infectious causes Pathophysiology [ edit ] Transient neonatal jaundice is one of the most common conditions occurring in newborns (children under 28 days of age) with more than eighty percent affected during their first week of life. [46] Jaundice in infants, like adults, is characterized by increased bilirubin levels (total serum bilirubin greater than 5 mg/dL).ICAM1, CYP1A1, CCL25, UGT1A1, CYP1A2, ABCB11, SERPINA1, ABCC2, PRKAR1A, SPTB, SPTA1, CASR, BRCA2, NBAS, DGUOK, ATP8B1, HNF1B, PRSS1, PTPN3, SLCO1B3, PEX19, ABCD3, DUOX2, PEX2, PEX5, RAB27A, PRSS2, ACADVL, PRF1, PROP1, PEX14, SLC26A4, PEX1, PEX6, PEX10, PEX12, PEX13, PFKM, IER3IP1, ABCB4, PKLR, DCDC2, POU1F1, POU2AF1, GLRX5, VPS33B, RHAG, SLC2A1, SLC4A1, TP53, TPI1, TPO, TSHB, TSHR, PAX8, TNFSF15, LHX3, TTC37, PEX3, PEX11B, HESX1, EIF2AK3, CYP7B1, CLDN1, NR1H4, SLC25A13, SEC23B, SPIB, SLC5A5, TNPO3, PALLD, MST1, POLG2, ADAMTS13, SPINK1, SLCO1B1, AKR1D1, TCF4, TFAM, TG, THRA, THRB, CTRC, TBX19, F5, NKX2-5, GALE, ATP11C, VIPAS39, FLI1, ATP7A, CPLANE1, ETFDH, ETFB, ETFA, EPB42, EPB41, DHFR, MMEL1, PALB2, HSD3B7, TRMU, C15orf41, COX4I2, CPOX, CPA1, LYST, SERAC1, LHX4, COG7, CFTR, ATP7B, CDKN2A, TBCK, BRCA1, BPGM, GALT, ANK1, IL12RB1, GCLC, PEX16, OCLN, SMAD4, DUOXA2, LPL, LIPA, IYD, LBR, KRT18, KRT8, KRAS, KCNN4, JAK2, IRF5, UNC80, IL12A, HMGCL, PEX26, GPI, GPR35, GPT, HBB, HK1, SLC30A10, HNF4A, ALDOB, SP110, IL2RG, ALDOA, G6PD, IFNL3, UGT1A, ALB, UGT1A7, SLC35A2, UGT1A8, UGT1A4, UGT1A10, UGT1A6, NR1I3, GGTLC1, SLC17A5, UGGT1, UGT1A3, UGT1A9, UGT1A5, NELFCD, LOC102724197, UBL4A, CTSZ, CRP, PER3, CHAT, CRYGEP, NUDT10, CAT, CEACAM5, CEACAM3, CEACAM7, CRY2, BCL2, CRYGC, CXADR, F2, MMS19, GAST, BTD, ARR3, OPN1MW, GGTLC5P, OPN1MW3, ACP1, GGTLC4P, OPN1MW2, GGT2, GGTLC3, CXADRP1, ASPG, POU5F1P4, SMIM10L2B, POU5F1P3, AFP, SMIM10L2A, AHR, HAMP, GGT1, NR1I2, SPG7, RRAS, CCL5, SLC10A1, SLC22A3, SMN1, SMN2, TIMP1, PSG2, TLR1, TRIM13, TLR2, TNF, UGDH, NR4A3, PVALB, PRL, GOT1, MMP7, HMOX1, HSPA4, CXCL8, CXCR2, IL15, LGALS3BP, MMP9, POU5F1, MPV17, MVD, ADA2, NBN, PC, PKM, ABO
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Female Foeticide In India
Wikipedia
Thus, some scholars argue that disparities in access to resources such as healthcare, education, and nutrition play at least a small role in the high sex ratios seen in some parts of the world. [11] Public goods provisions by female leaders (majority vs. minority spillover goods) [ edit ] Minority goods provided by female leaders in India help to alleviate some of the problems of disparate gendered access to resources for women. [27] Public goods are defined as non-excludable and non-rival, but India lacks a system of public goods and has many problems with access to clean water or roads. [28] Additionally, many of the "public goods" exclude females because families choose to prioritize their male children's access to those resources. ... In Rajasthan, where women complain more often about drinking water, women politicians invest more in water and less in roads. [28] Dowry system [ edit ] Even though the Dowry System legally ended with the Dowry Prohibition Act of 1961 , the impossibility of monitoring families and the prevalence of corruption have led to its continuance all over India. [30] A dowry is a payment from the bride's family to the groom's family at the time of marriage. ... "Culture, ecology, and beliefs about gender in son preference caste groups". Evolution and Human Behavior . 28 (5): 319–329. doi : 10.1016/j.evolhumbehav.2007.01.004 . ^ a b c Beaman, Lori; Duflo, Esther; Pande, Rohini; Topalova, Petia (2012-02-03). ... PMID 12769123 . ^ "Government scheme to save girls in womb a flop: Study" . India Today . 2011-12-28 . Retrieved 2018-03-05 . ^ Brody, Samuel (2010).
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Genetic Disorder
Wikipedia
These diseases most often follow autosomal recessive inheritance. [28] Multifactorial disorder [ edit ] Genetic disorders may also be complex, multifactorial, or polygenic, meaning they are likely associated with the effects of multiple genes in combination with lifestyles and environmental factors. ... "Huntington's disease". Lancet . 369 (9557): 218–28 [221]. doi : 10.1016/S0140-6736(07)60111-1 .
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Testicular Cancer
Wikipedia
A pregnancy test may be used to detect high levels of chorionic gonadotropin; however, the first sign of testicular cancer is usually a painless lump. [24] Note that only about 25% of seminomas have elevated chorionic gonadotropin, so a pregnancy test is not very sensitive for making out testicular cancer. [25] Screening [ edit ] The American Academy of Family Physicians recommends against screening males without symptoms for testicular cancer. [26] Staging [ edit ] After removal, the testicle is fixed with Bouin's solution [27] [28] because it better conserves some morphological details such as nuclear conformation. ... Retrieved 5 August 2010 . ^ Forman, D; M C Pike; G Davey; S Dawson; K Baker; C E D Chilvers; R T D Oliver; C A C Coupland (28 May 1994). "Aetiology of testicular cancer: association with congenital abnormalities, age at puberty, infertility, and exercise.KITLG, STK11, DMRT1, ERCC1, ERCC4, ATF7IP, BAP1, KIT, FGFR3, CTAG1A, MAGEC2, TP53, BCL10, ITGA4, CTAG1B, PCDH11X, MAGEA3, SSX2, MAGEA1, LINC00328, ANKRD36B, ZNF654, CERNA3, CCDC54, MAGEA4, SPA17, PCYT1A, PRAME, SSX2B, SPAG9, CTCFL, MAGED4, MAGED4B, SSX1, XAGE1A, SYCP1, SSX4, AKAP3, AR, XAGE1B, ESR1, AFP, STK31, PLAC1, PANX1, ACRBP, INSL3, POU5F1, SPANXC, SCPEP1, SEMG1, L1CAM, SLC12A9, CTDSP1, THEG, AZF1, DNMT1, CYP1A1, POU5F1P3, CTAG2, KLK14, CT45A1, GPT, CDKN1A, POU5F1P4, FMR1NB, SSX4B, XIST, HLA-C, MIR371A, UGT1A1, HPGDS, RASSF1, LY6K, TFDP3, DKK3, PIWIL2, DCAF12, VCX, CABYR, CT55, IGHV1-12, SULF1, SLCO1B3, KRT20, LUZP4, CD274, SMUG1, SPANXA1, LARP6, NUP62, SHC3, KLK13, DCTN4, PDE11A, TSGA10, DDX43, CT83, CCDC83, MEIOB, FAM133A, POTED, FAM71F2, GSTK1, RTL1, CSAG3, MIR142, MIR155, MIR17, MIR199A1, MIR199A2, TSPY3, SPANXB1, SPANXA2, LIN28B-AS1, LOC100288966, TSPY10, PCAT6, CSAG2, TMEM31, SPAG17, SULF2, DDX53, NXF2, RNF17, TDRD1, DNAH7, EXOSC5, EXO5, GGCT, NANOG, PPP1R13L, ACTL8, NUF2, RHOXF2, CCDC62, SCGB3A1, LEMD1, RXFP2, SPACA3, SLCO6A1, PASD1, TEKT5, TDRD5, KLK11, AADAC, KDM5B, EWSR1, FLI1, MLANA, FRZB, FSHR, ADAM2, GDF1, GJA1, GSTM1, GSTP1, GTF2H1, HDAC1, CFHR2, HLA-A, HOXA10, HSPA1A, HSPA1B, HSPA2, HSP90AA1, ICAM1, IFNG, IL2, INHA, ITGA5, FEN1, ERCC2, KIFC1, ERBB2, ACTB, AGRP, APEX1, STS, ARSL, ATM, BCL2, OPN1SW, BRAF, CACNA1F, MS4A1, CD63, CD69, CETN1, CHGB, CLU, CYP3A7, CYP3A5, DNMT3A, DRD1, ATN1, EGF, EGFR, JUNB, LHCGR, KHDRBS1, TRO, TYR, UQCRC2, WT1, TFPI2, YARS1, TMEFF1, TNFSF10, DLK1, CCNK, HDAC3, ACACA, AKAP4, SQSTM1, CCNA1, MBD2, ARTN, SLC16A5, PPIG, EIF2AK3, BAG3, KLK4, BMS1, POSTN, TSPY1, TEAD1, SMAD4, TAF9, MAGEA10, MDM2, MECP2, MGMT, MIF, ATXN3, MLH1, MMP9, MMP14, MRC1, MSH2, MYCN, MYO5A, NDN, NDUFS1, SERPINE1, PLEC, PODXL, PTPRC, RNH1, SHBG, FBXW4, PMEL, PROM1
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Beta Thalassemia
Wikipedia
These tests include complete blood count ; hemoglobin electrophoresis ; serum transferrin , ferritin , total iron-binding capacity ; urine urobilin and urobilogen; peripheral blood smear , which may show codocytes , or target cells; [26] hematocrit ; and serum bilirubin. [27] [28] The expected pattern on hemoglobin electrophoresis in people with beta-thalassemia is an increased level of hemoglobin A2 and slightly increased hemoglobin F . [ citation needed ] Skeletal changes associated with expansion of the bone marrow: Chipmunk facies : bossing of the skull, prominent malar eminence, depression of the bridge of the nose, tendency to a mongoloid slant of the eye, and exposure of the upper teeth due to hypertrophy of the maxillae. [29] Hair-on-end (or "crew cut") on skull X-ray: new bone formation due to the inner table. [ citation needed ] DNA analysis [ edit ] All beta thalassemias may exhibit abnormal red blood cells, a family history is followed by DNA analysis. [3] This test is used to investigate deletions and mutations in the alpha- and beta-globin-producing genes. ... PMID 21119108 . ^ "Gene Therapy Shows Promise for Treating Beta-Thalassemia and Sickle Cell Disease" . 2012-03-28 . Retrieved 2015-10-15 . ^ Uranüs, Selman.HBB, HBA2, HAMP, EPO, LCN2, TFR2, CACNA1H, DHODH, TFRC, UMPS, CAD, HBB-LCR, HBG2, HBG1, HBA1, VDR, HFE, CD34, GH1, APOE, GSTM1, PROS1, BCL11A, UGT1A1, F2, UGT1A6, GATA1, IFNL3, UGT1A, PTH, CD38, CD19, UGT1A10, UGT1A8, HSPA4, KLF1, ALB, HPGDS, MTHFR, CSF3, UGT1A7, UGT1A5, PGD, KLF10, SLC35A2, UGGT1, F5, PC, UGT1A3, GPT, UGT1A4, UGT1A9, IQCB1, HBFQTL2, H6PD, TNFSF11, OGA, HCST, FHL5, TNFRSF11A, ACOT7, ZHX2, PPRC1, LPCAT3, SERPINA3, CUL9, CADM1, RN7SL263P, PSC, CD24, POTEM, POTEKP, MIR223, LINC01194, GSTK1, ACTBL2, ERFE, HJV, SLCO6A1, CHPT1, SOX6, XPO1, PRRX2, AHSP, CRYL1, SOST, DLL1, PRDX5, YY1, PSMB6, TRPV1, CYP2E1, GYPB, GYPA, GSTT1, GSTA1, GLUD1, GHRH, FOXO3, ESR1, ELANE, CD55, CYP3A4, CRP, VEGFA, CR1, CPT2, CPT1A, CPB2, CP, CHIT1, CD59, ENTPD1, CAPS, FAS, ACTG2, GYPE, HNRNPA1, HPT, IFNA1, UGDH, TNF, TGFB1, TERT, PRDX2, CCL18, SCD, ACTG1, PRS, PRH2, PRH1, POMC, PRRX1, PMCH, PRDX1, TNFRSF11B, NOS3, LPA, LMO2, IL7, IL6R, IL3, IFNA13, LINC02605
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Carbon Monoxide Poisoning
Wikipedia
Acute poisoning [ edit ] CO toxicity symptoms The main manifestations of carbon monoxide poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart . [16] The initial symptoms of acute carbon monoxide poisoning include headache , nausea , malaise , and fatigue . [25] These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis . [26] Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous. [27] Increasing exposure produces cardiac abnormalities including fast heart rate , low blood pressure , and cardiac arrhythmia ; [28] [29] central nervous system symptoms include delirium , hallucinations , dizziness , unsteady gait , confusion , seizures , central nervous system depression , unconsciousness , respiratory arrest , and death . [30] [31] Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia , atrial fibrillation , pneumonia , pulmonary edema , high blood sugar , lactic acidosis , muscle necrosis , acute kidney failure , skin lesions , and visual and auditory problems. [28] [32] [33] [34] One of the major concerns following acute carbon monoxide poisoning is the severe delayed neurological manifestations that may occur. ... "Carbon monoxide poisoning" . Critical Care Clinics . 28 (4): 537–48. doi : 10.1016/j.ccc.2012.07.007 . ... Ferri's Clinical Advisor 2017 E-Book: 5 Books in 1 . Elsevier Health Sciences. pp. 227–28. ISBN 978-0323448383 . Archived from the original on 10 September 2017 . ... Archived from the original on 2008-05-28 . Retrieved 2009-09-14 . ^ Lipman GS (2006). ... Reidel Publishing Company. p. 90. ^ a b Gosink T (1983-01-28). "What Do Carbon Monoxide Levels Mean?"
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Peanut Allergy
Wikipedia
Peanut allergies are uncommon in children of undeveloped countries [3] where peanut products have been used to relieve malnutrition . [25] The hygiene hypothesis proposes that the relatively low incidence of childhood peanut allergies in undeveloped countries is a result of exposure to diverse food sources early in life, increasing immune capability, whereas food selection by children in developed countries is more limited, reducing immune capability. [3] [4] A possibility of cross-reaction to soy was dismissed by an analysis finding no linkage to consumption of soy protein, and indicated that appearance of any linkage is likely due to preference to using soy milk among families with known milk allergies . [26] Timing of exposure [ edit ] In infants with a family history of peanut allergy, consuming peanut proteins at 4 to 11 months old has been shown to reduce the risk of developing an allergic response by 11-25% [27] From these results, the American Academy of Pediatrics rescinded their recommendation to delay exposure to peanuts in children, also stating there is no reason to avoid peanuts during pregnancy or breastfeeding. [28] [29] Diet during pregnancy [ edit ] There is conflicting evidence on whether maternal diet during pregnancy has any effect on development of allergies due to a lack of good studies. [30] A 2010 systematic review of clinical research indicated that there is insufficient evidence for whether maternal peanut exposure, or early consumption of peanuts by children, affects sensitivity for peanut allergy. [31] Routes of exposure [ edit ] Peanuts While the most obvious route for an allergic exposure is unintentional ingestion, some reactions are possible through external exposure. ... The contact along with the release of the cytokine IL-4 induces their differentiation into CD4+ Th2 cells . [35] The Th2 cells proliferate and release pro-inflammatory cytokines , such as IL-4 , IL-5 , and IL-13 , which can be bound to receptors on undifferentiated B cells or B cells of the IgM subtype. [35] The receptor-cytokine binding causes their differentiation into IgE which can then be bound onto FcεRI on mast cells , eosinophils and basophils . [35] This elicits degranulation of the aforementioned cells which release potent cytokines and chemokines , thus triggering inflammation and causing the symptoms characteristic of allergy. [35] Diagnosis [ edit ] Diagnosis of food allergies, including peanut allergy, begins with a medical history and physical examination. [2] [5] National Institute of Allergy and Infectious Diseases guidelines recommend that parent and patient reports of food allergy be confirmed by a doctor because "multiple studies demonstrate 50% to 90% of presumed food allergies are not allergies." [5] Skin prick testing [ edit ] Skin prick tests can be used to confirm specific food allergies. [1] [2] [5] Skin prick tests are designed to identify specific IgE bound to cutaneous mast cells. [1] During the test, a glycerinated allergen extract drop is placed on the patient's skin. [2] The patient's skin is then pricked through the drop. [2] This procedure is repeated with two controls: a histamine drop designed to elicit an allergic response, and a saline drop designed to elicit no allergic response. [2] The wheal that develops from the glycerinated extract drop is compared against the saline control. [2] A positive allergic test is one in which the extract wheal is 3mm larger than the saline wheal. [2] A positive skin prick test is about 50% accurate, so a positive skin prick test alone is not diagnostic of food allergies. [1] [2] [5] Oral food challenge [ edit ] The "gold standard" of diagnostic tests is a double-blind placebo-controlled oral food challenge. [2] [5] At least two weeks prior to an oral food challenge, the person is placed on an elimination diet where the suspected allergen is avoided. [36] During the oral food challenge, they are administered a full age-appropriate serving of a suspected allergen in escalating size increments. [36] They are continuously monitored for allergic reaction during the test, and the challenge is stopped and treatment administered at the first objective sign of allergic reaction. [36] Oral food challenges pose risks. [37] In a study of 584 oral food challenges administered to 382 patients, 48% (253) of challenges resulted in allergic reactions. [37] 28% (72) of these challenges resulted in "severe" reactions, which were defined by the study as a patient having: lower respiratory symptoms; cardiovascular symptoms; or any four other, more minor, symptoms. [37] Double-blind placebo-controlled oral food challenges are also time-consuming and require close medical supervision. [2] Because of these drawbacks to the double-blind placebo-controlled oral food challenge, open food challenges are the most commonly used form of food challenge. [36] Open food challenges are those in which a patient is fed an age-appropriate serving of a suspected food allergen in its natural form. [36] The observation of objective symptoms resulting from ingestion of the food, such as vomiting or wheezing, is considered diagnostic of food allergy if the symptoms correlate with findings from the patient's medical history and laboratory testing such as the skin prick test. [5] Prevention [ edit ] In 2017, the US National Institute of Allergy and Infectious Diseases (NIAID) published revised guidelines for lowering the risk or preventing peanut allergies by creating separate ways to assess childhood allergies and guide parents with infants at high, moderate or low risk. [13] [38] [7] The guidelines discussed how to introduce peanut foods to infants as early as 4 to 6 months of age, with the goal of preventing peanut allergy. [6] [3] [7] For high-risk children, the guide recommended that an allergy specialist assess a child's susceptibility, possibly involving peanut allergy testing , followed by gradual introduction of peanut foods under the supervision of an allergy specialist. [6] [7] Peanut allergy is confirmed only if there is a history of reactions to peanut consumption and by a positive allergy test. [7] Moderate-risk children – who display an allergic reaction to peanut products with mild to moderate eczema – are typically not assessed in a clinic, but rather have peanut foods gradually provided to them at home by their parents, beginning at around age 6 months. [6] [15] [7] The Learning Early About Peanut Allergy (LEAP) study supported by NIAID established that early introduction of peanut products into a child's diet can prevent – rather than only delay – the development of childhood peanut allergies, and that the effect is beneficial and lifelong. [6] [15] [3] Treatment [ edit ] As of 2020, there is no cure for peanut allergy other than strict avoidance of peanuts and peanut-containing foods.
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Criminal Transmission Of Hiv
Wikipedia
Retrieved 27 November 2019 . ^ "U=U | United States | Prevention Access Campaign" . prevention . Retrieved 28 November 2019 . ^ a b Global Network of People Living with HIV/AIDS Europe, Terrence Higgins Trust (2005). ... Retrieved 20 November 2019 . ^ a b "Committee Report No. 28 - JUST (42-1) - House of Commons of Canada" . www.ourcommons.ca . Retrieved 28 November 2019 . ^ Kaida, Angela; Spencer, Sarah. ... NZ Herald . 6 October 2005. ISSN 1170-0777 . Retrieved 28 July 2020 . ^ "HIV 'predator' may be bisexual" . ... Retrieved 19 May 2009 . ^ "Man in court accused of infecting men with HIV" . The New Zealand Herald . 28 May 2009. ^ "HIV accused Glenn Mills found dead in cell" .
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Death Anxiety (Psychology)
Wikipedia
Depending on the certain meaning one has associated with death, positive or negative, the consequences will vary accordingly. [26] Religiosity [ edit ] A 2012 study involving Christian and Muslim college -students from the US, Turkey, and Malaysia found that their religiosity correlated positively with an increased fear of death. [27] A 2017 review of the literature found that in the US, both the very religious and the not-at-all religious enjoy a lower level of death anxiety and that a reduction is common with old age. [28] A 2019 study further examined the aspect of religiosity and how it relates to death and existential anxiety through the application of supernatural agency. [29] According to this particular study, existential anxiety relates to death anxiety through a mild level of preoccupation that is experienced concerning the impact of one’s own life or existence in relation to its unforeseen end. [29] It is mentioned how supernatural anxiety exists independently on a different dimensional plane than the individual and, as a result, is seen as something that cannot be directly controlled. [29] Often times supernatural agency is equated with the desires of a higher power such as God or other major cosmic forces. [30] The inability for one to control supernatural agency triggers various psychological aspects that induce intense periods of experienced death or existential anxiety. ... New York: McGraw-Hill Education. pp. 27–28. ISBN 9780078035463 . OCLC 842883173 . ^ a b c d e http://www.escp.org/death_anxiety.html ^ a b c d e f Langs, Robert (2004).
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Osteitis Fibrosa Cystica
Wikipedia
If muscular symptoms appear upon the onset of hyperparathyroidism, they are generally sluggish contraction and relaxation of the muscles. [24] Deviation of the trachea (a condition in which the trachea shifts from its position at the midline of the neck), in conjunction with other known symptoms of OFC can point to a diagnosis of parathyroid carcinoma. [23] Blood tests on patients with OFC generally show high levels of calcium (normal levels are considered to range between 8.5 and 10.2 mg/dL, [25] parathyroid hormone (levels generally above 250 pg /mL, as opposed to the "normal" upper-range value of 65 pg/mL [26] ), [27] and alkaline phosphatase [2] (normal range is 20 to 140 IU /L [28] ). X-rays may also be used to diagnose the disease. ... Archived from the original on 2009-05-27 . Retrieved 2009-01-28 . ^ a b Arabi, A. (2006). "Regression of Skeletal Manifestations of Hyperparathyroidism with Oral Vitamin D" .
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Wolff–parkinson–white Syndrome
Wikipedia
Wedd (1887–1967) was the next to describe the condition in 1921. [28] Cardiologists Louis Wolff (1898–1972), John Parkinson (1885–1976) and Paul Dudley White (1886–1973) are credited with the definitive description of the disorder in 1930. [29] Notable cases [ edit ] LaMarcus Aldridge , American basketball player [30] Michael Cera , Canadian actor [31] Nathan Eagleton , former Australian rules football player [32] Jeff Garlin , American actor, writer, and comedian [33] Quentin Groves , American football player who died of a heart attack at age 32 [34] Dan Hardy , British UFC welterweight fighter, [35] turned analyst and commentator Mitch Hurwitz , American television writer and producer, creator of Arrested Development [33] Jessie J , British musician [36] Marilyn Manson , American musician, painter, and actor [37] Meat Loaf , American musician [38] Michael Rupp , American ice hockey player [39] Montel Vontavious Porter , professional wrestler [40] Michael Montgomery , American football player [41] Claire Dunphy , Modern Family Character [42] See also [ edit ] Re-entry ventricular arrhythmia References [ edit ] ^ a b c d e f g h i j k Reference, Genetics Home (March 2017). ... CS1 maint: archived copy as title ( link ) ^ "Meat Loaf recalls stage collapse" . BBC News . 2003-11-28. Archived from the original on 2009-01-11 .
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Duchenne Muscular Dystrophy
Wikipedia
Treatment [ edit ] Salbutamol (albuterol) — a β 2 agonist No cure for DMD is known, and an ongoing medical need has been recognized by regulatory authorities . [27] Gene therapy has shown some success. [28] Treatment is generally aimed at controlling the onset of symptoms to maximize the quality of life which can be measured using specific questionnaires, [29] and include: Corticosteroids such as prednisolone and deflazacort lead to short-term improvements in muscle strength and function up to 2 years. [30] Corticosteroids have also been reported to help prolong walking, though the evidence for this is not robust. [31] Randomised control trials have shown that β 2 agonists increase muscle strength, but do not modify disease progression. ... PMID 22292807 . ^ "University of Utah Muscular Dystrophy" . Genome.utah.edu. 2009-11-28 . Retrieved 2013-02-16 . ^ a b Bushby K, Finkel R, Birnkrant DJ, Case LE, Clemens PR, Cripe L, et al.DMD, LTBP4, TGFB1, CD4, POSTN, CCL2, CTSS, LINC02694, ADCY8, SPP1, DOCK1, XYLT1, SHKBP1, RGS6, DAG1, ADCY1, UTRN, OTC, MSTN, PTPN1, GK, ACE, BEST1, MB, TTN, MMP9, MMP2, SSPN, CCN2, ADIPOQ, TNF, MIR206, GH1, LAMA2, NOS1, PLF, NR3C2, NR0B1, MIR21, TNFRSF11B, G6PD, ACTB, PROM1, DCN, SGCA, TIMP1, SMN1, SLN, GJA1, AAVS1, FSD1L, PPARD, FSD1, FN1, ELP1, AR, NEB, IL6, BGN, HPX, AQP4, BMI1, IL1B, CD38, PART1, FST, CAPN2, P2RX7, MFAP1, NFE2L2, GABPA, DYSF, IGF1, NOS2, KL, HLA-B, PIK3C2A, PDGFRA, TPPP3, HTC2, ST8SIA4, NR3C1, LGALS1, SLMAP, PLA1A, HLA-A, VEGFA, SMN2, PLAU, MIR31, RELA, CAV3, CAPN3, CAPN1, CA3, BTF3P11, BRCA1, BMP4, MIR29C, SYT1, CLK1, APRT, APC, ANGPT1, MIR483, SRY, SGCG, CCR2, LINC01672, H3P14, CFTR, DTNBP1, TLR4, FAM168B, CMYA5, GORASP1, WNK1, TM7SF2, NLRP3, CYBB, TUBB6, TIMP2, CSF3, PDE5A, TIMP3, ST14, TGM2, TNFRSF11A, TIMP4, HAP1, LARGE1, IL1RL1, TNNI3, TNFSF11, TRBV20OR9-2, DENR, AIMP2, TGFBR2, TGFA, THAS, VIM, TERT, VCAM1, DYNLT3, WNT7A, CCDC6, THBS1, THBS4, VCP, CMAHP, VCL, TERF1, SERPINA3, NOG, PANX3, RAB40AL, RMDN2, HJV, MAGEB16, RBM45, B4GALNT2, PRRT2, CPP, ATAD1, TNFAIP8L2, MMEL1, SCAF1, RAB40C, RNF213, H19, ACTBL2, CCL28, TRIM72, COMMD3-BMI1, MUPP, MIR675, POTEM, MIR486-1, MIR499A, POTEKP, FAM111B, MIR30C2, MIR30C1, MIR200C, MIR150, MIR146A, MIRLET7C, NLN, ASH1L, LIPG, ADAMTS5, SYNE1, SYNM, KDM6B, TRIM32, ACOT7, CORO1A, AHSA1, PANX1, CARM1, PPIF, HDAC9, SDC3, FHL5, GRAP2, SUN1, SUN2, SYBU, EFEMP2, RMDN3, SNTG1, PTRH2, TRPV2, TLR7, RMDN1, KLF15, PAMR1, SGSM3, SOX9, HPGDS, FGF21, POLDIP2, RNF19A, EIF3K, PITPNA, SNTA1, FKTN, FABP5, F9, F8, EZH2, ETFA, ERG, ERBB2, ENO1, EMD, ELAVL2, E2F1, DTNB, DPP4, DPEP1, DNAH8, ACSL4, FHL1, DHFR, GDNF, HSPG2, DNAJB2, HPRT1, HP, HMOX1, HLA-E, HLA-DRB1, HLA-DQA1, HLA-C, HIVEP1, HIF1A, GPX3, GPC1, GLP1R, GLB1, SEPTIN1, DFNX3, SHOX, CEACAM1, BCL2, ATP2A2, AQP1, APP, BIRC2, AGT, JAG1, AGER, ADRB2, PARP1, ADM, ACVR2B, ACTN3, ACTG2, ACTG1, BGLAP, BRCA2, CTSL, CAPNS1, CTSB, VCAN, MAPK14, CRK, CNR1, CCR5, CHI3L1, CTSC, CDKN3, CDKN1C, CD68, CD40, CASQ1, CASP4, CASP3, TNC, IFNA1, IFNA13, PRKAA1, PPID, PMP22, PLXNB1, PLN, PKD1, PITX2, PDE4A, PAX7, PAX3, SERPINE1, PAH, P2RX4, NPC1, NOTCH1, NGF, PRG2, PRKAA2, IFNG, PRKAB1, SGCD, SELENOP, CXCL11, S100B, RYR1, RGS12, RET, MOK, PTH, PTCH1, TAS2R38, MAPK1, PRKCQ, PRKCB, PRKCA, NFKB1, NF2, NCAM1, MYOD1, LRPAP1, LGALS3, LEP, KDR, ITPR3, ITPR1, ITGA7, ITGA5, ITGA4, ITGA6, INSR, IDO1, IL17A, IL10, IGF2R, MAFD2, MAOA, MAOB, MMP10, MYD88, MYCL, MYC, MUC1, MS, MRC1, MMP7, MAS1, MMP1, MIF, KITLG, MAP3K5, CD46, MBL2, H3P47
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Glucose-6-Phosphate Dehydrogenase Deficiency
Wikipedia
This is the basis for another theory, that is that the genetic defect confers resistance due to the fact that the G6PD-deficient host has a higher level of oxidative agents that, while generally tolerable by the host, are deadly to the parasite. [28] History [ edit ] The modern understanding of the condition began with the analysis of patients who exhibited sensitivity to primaquine . [29] The discovery of G6PD deficiency relied heavily upon the testing of prisoner volunteers at Illinois State Penitentiary , a type of study which today is considered unethical and cannot be performed. ... S2CID 30959794 . ^ "Favism | genetic disorder" . ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009-05-28). Robbins and Cotran Pathologic Basis of Disease, Professional Edition: Expert Consult - Online (Robbins Pathology) (Kindle Locations 33351-33354).G6PD, UBL4A, MPDU1, UGT1A1, ABO, DECR1, TNF, HP, UGT1A7, SLCO1B1, UGT1A, UGT1A10, UGT1A8, UGT1A6, UGT1A4, PON1, PDR, TKT, SLC35A2, ST14, VCAM1, PRB1, FOSL1, PAH, PLXNA2, HPGDS, PIEZO1, C5AR2, NDUFAB1, NOX4, CASZ1, CA10, FSD1, RABEP2, FSD1L, TMPRSS13, ATAD1, LMLN, NOS2, MTHFR, MTM1, GLA, GYPE, GYPB, GYPA, GSTM1, GSR, GPI, FLNA, HBA2, F5, F2, CYP2D6, CR1, COX8A, CDKN2A, HBA1, HBG2, ACP1, ITGB2, MST1, MSMB, MBP, MAFD2, CYP4F3, LDLR, IRS1, HK1, IL10, IL6, ICAM1, HMOX1, HMGCR, HLA-B, OR10A4
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Metastasis
Wikipedia
According to the "seed and soil" theory, it is difficult for cancer cells to survive outside their region of origin, so in order to metastasize they must find a location with similar characteristics. [28] For example, breast tumor cells, which gather calcium ions from breast milk, metastasize to bone tissue, where they can gather calcium ions from bone. ... National Cancer Institute . Retrieved 2008-08-28 . ^ Olteanu G-E, Mihai I-M, Bojin F, Gavriliuc O, Paunescu V.
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Listeriosis
Wikipedia
Between June 2015 and July 2018, nine people had reportedly died as a result of Listeriosis, of a total of forty seven confirmed cases. [28] In an update on the EFSA website, it was stated that the contamination had supposedly been present since at least 2015, and as a result the Hungarian Food Chain Safety Office had prohibited the marketing of all affected frozen vegetables and frozen vegetable packs produced by the plant in Baja between August 2016 and June 2018. [29] This followed a previous abstract study that found the majority of L. monocytogenes isolates had been found in a 2017 sample of various frozen vegetables, with a minority found in a 2016 sample, and a miniscurity found in a 2018 sample. ... Retrieved June 21, 2013 . ^ "Colorado cantaloupes kill up to 16 in listeria outbreak" . BBC News . September 28, 2011. ^ "Listeria Found in Lettuce, Too" .TNF, CYLD, IL15, IFNG, HSP90B1, NOD2, SUMF2, DECR1, IL10, IL37, ISG15, STIP1, BAHD1, FAF1, ABCG2, CPQ, SIRT2, LGI1, SQSTM1, SOCS2, BECN1, PTP4A2, ARHGEF5, CARD8, ACTA1, NT5C2, CLEC5A, TP53, SENP1, NOP53, DUOX2, HSPA14, LGI2, LXN, BCL11B, CASD1, TNIP3, HAVCR2, ZNRF4, MIR146A, EIF2AK1, ADAM17, TNFRSF1A, GRIN1, IL6, IL4, IFNB1, IFIT3, HSPG2, HSPD1, GRN, ACTB, XCR1, GFAP, CCR5, CD44, CAT, CASP1, IL12A, ISG20, ITGAM, ITGB2, LIPE, MET, MYH9, NEDD4, NFATC1, OCRL, PML, PPIA, S100A1, S100B, SELE, SLC5A1, SPP1, H3P7