-
Lymphatic Filariasis
Wikipedia
Specialty Infectious disease Symptoms None, severe swelling of the arms, legs, breasts, or genitals [2] Causes Filarial worms spread by mosquitos [3] Diagnostic method Microscopic examination of blood [4] Prevention Bed nets , mass deworming [2] Medication Albendazole with ivermectin or diethylcarbamazine [2] Frequency 38.5 million (2015) [5] Lymphatic filariasis is a human disease caused by parasitic worms known as filarial worms . [2] [3] Most cases of the disease have no symptoms . [2] Some people, however, develop a syndrome called elephantiasis , which is marked by severe swelling in the arms, legs, breasts , or genitals . [2] [6] The skin may become thicker as well, and the condition may become painful. [2] The changes to the body have the potential to harm the person's social and economic situation. [2] The worms are spread by the bites of infected mosquitoes . [2] Three types of worms are known to cause the disease: Wuchereria bancrofti , Brugia malayi , and Brugia timori , with Wuchereria bancrofti being the most common. [2] These worms damage the lymphatic system . [2] The disease is diagnosed by microscopic examination of blood collected during the night. [4] The blood is typically examined as a smear after being stained with Giemsa stain . [4] Testing the blood for antibodies against the disease may also permit diagnosis. [4] Other roundworms from the same family are responsible for river blindness . [7] Prevention can be achieved by treating entire groups in which the disease exists, known as mass deworming . [2] This is done every year for about six years, in an effort to rid a population of the disease entirely. [2] Medications used include antiparasitics such as albendazole with ivermectin , or albendazole with diethylcarbamazine . [2] The medications do not kill the adult worms but prevent further spread of the disease until the worms die on their own. [2] Efforts to prevent mosquito bites are also recommended, including reducing the number of mosquitoes and promoting the use of bed nets . [2] In 2015 about 38.5 million people were infected. [5] About 950 million people are at risk of the disease in 54 countries. [2] It is most common in tropical Africa and Asia. [2] Lymphatic filariasis is classified as a neglected tropical disease and one of the four main worm infections . [7] The impact of the disease results in economic losses of billions of dollars a year. [2] Contents 1 Signs and symptoms 2 Causes 3 Diagnosis 4 Prevention 5 Treatment 5.1 Anthelmintic 5.2 Antibiotics 5.3 Vaccine 5.4 Supportive treatments 6 Epidemiology 7 History 8 Research directions 9 References 10 External links Signs and symptoms [ edit ] The most spectacular symptom of lymphatic filariasis is elephantiasis , a stage 3 lymphedema with thickening of the skin and underlying tissues. ... Avoiding mosquito bites, such as by using insecticide -treated mosquito bed nets , also reduces the transmission of lymphatic filariasis. [19] [22] The Carter Center 's International Task Force for Disease Eradication declared lymphatic filariasis one of six potentially eradicable diseases. [19] According to medical experts, the worldwide effort to eliminate lymphatic filariasis is on track to potentially succeed by 2020. [23] For similar-looking but causally unrelated podoconiosis , international awareness of the disease will have to increase before elimination is possible.
-
Thrombophilia, Familial, Due To Decreased Release Of Tissue Plasminogen Activator
Omim
Individuals homozygous for the insertion had significantly increased net local release rates than those who were either heterozygous or homozygous for the deletion.
- Neonatal Bowel Obstruction Wikipedia
-
Money Disorder
Wikipedia
Retrieved 31 July 2011 . ^ Sullivan, Paul (6 May 2011). "Net Worth, Self-Worth and How We Look at Money" .
-
Aporophobia
Wikipedia
Part of a series on Discrimination General forms Age Class ( Caste ) Physical Disability Education Economic Employment Genetics Hair texture Height Housing Language Looks Race / Ethnicity / Nationality Rank Religion Sanity Sex Sexual orientation Size Skin color Specific forms Social Acephobia Adultism Amatonormativity Anti-albinism Anti-autism Anti-homelessness Anti-intellectualism Anti-intersex Anti-left handedness Anti-Masonry Antisemitism (Judeophobia) Aporophobia Audism Biphobia Clannism Cronyism Drug use Elitism Ephebiphobia Fatism Gerontophobia Heteronormativity Heterosexism HIV/AIDS stigma Homophobia Leprosy stigma Lesbophobia Misandry Misogyny Nepotism Pedophobia Perpetual foreigner Pregnancy Reverse Sectarianism Supremacism Black White Transphobia Non-binary Transmisogyny Vegaphobia Xenophobia Religious Ahmadiyya Atheism Baháʼí Faith Buddhism Catholicism Christianity post–Cold War era Druze Falun Gong Hinduism Persecution Islam Persecution Jehovah's Witnesses Judaism Persecution LDS or Mormon Neopaganism Eastern Orthodox Oriental Orthodox Copts Protestantism Rastafarianism Shi'ism Sufism Sunnism Zoroastrianism Ethnic/national African Albanian American Arab Armenian Australian Austrian Azerbaijani British Canadian Catalan Chechen Chilean Chinese Croat Dutch English Estonian European Filipino Finnish French Georgian German Greek Haitian Hazara Hispanic Hungarian Igbo Indian Indonesian Iranian Irish Israeli Italian Japanese Jewish Khmer Korean Kurdish Malay Manchu Mexican Middle Eastern Mongolian Montenegrin Pakistani Pashtun Polish Portuguese Quebec Romani Romanian Russian Scottish Serb Slavic Somali Soviet Tatar Thai Tibetan Turkish Ukrainian Venezuelan Vietnamese Western Manifestations Blood libel Bullying Compulsory sterilization Counter-jihad Cultural genocide Defamation Democide Disability hate crime Dog-whistle politics Eliminationism Ethnic cleansing Ethnic conflict Ethnic hatred Ethnic joke Ethnocide Forced conversion Freak show Gay bashing Gendercide Genital modification and mutilation Genocide examples Glass ceiling Hate crime Hate group Hate speech online Homeless dumping Indian rolling Lavender scare LGBT hate crimes Lynching Mortgage Murder music Occupational segregation Persecution Pogrom Purge Red Scare Religious persecution Religious terrorism Religious violence Religious war Scapegoating Segregation academy Sex-selective abortion Slavery Slut-shaming Trans bashing Victimisation Violence against women White flight White power music Wife selling Witch-hunt Policies Age of candidacy Blood purity Blood quantum Crime of apartheid Disabilities Catholic Jewish Ethnocracy Ethnopluralism Gender pay gap Gender roles Gerontocracy Gerrymandering Ghetto benches Internment Jewish quota Jim Crow laws Law for Protection of the Nation McCarthyism MSM blood donation restrictions Nonpersons Numerus clausus (as religious or racial quota) Nuremberg Laws One-drop rule Racial quota Racial steering Redlining Same-sex marriage (laws and issues prohibiting) Segregation age racial religious sexual Sodomy law State atheism State religion Ugly law Voter suppression Countermeasures Affirmative action Anti-discrimination law Cultural assimilation Cultural pluralism Diversity training Empowerment Feminism Fighting Discrimination Hate speech laws by country Human rights Intersex rights LGBT rights Masculism Multiculturalism Nonviolence Racial integration Reappropriation Self-determination Social integration Toleration Related topics Allophilia Anti-cultural, anti-national, and anti-ethnic terms Bias Christian privilege Civil liberties Cultural assimilation Dehumanization Diversity Ethnic penalty Eugenics Internalized oppression Intersectionality Male privilege Masculism Medical model of disability autism Multiculturalism Net bias Neurodiversity Oikophobia Oppression Police brutality Political correctness Polyculturalism Power distance Prejudice Prisoner abuse Racial bias in criminal news Racism by country Religious intolerance Second-generation gender bias Snobbery Social exclusion Social model of disability Social stigma Stereotype threat The talk White privilege v t e Aporophobia (from the Spanish aporofobia , and this from the Ancient Greek ἄπορος ( á-poros ), without resources, indigent, poor, and φόβος ( phobos ), fear) [1] [2] is fear of poverty and of poor people.
-
Velvet (Fish Disease)
Wikipedia
Finally, the adolescent tomite finds and enters the slime coat of a host fish, dissolving and consuming the host's cells, and needing only three days to reach full maturity before detaching to become a tomont once more. [2] Pathology [ edit ] A 15-day old Siamese fighting fish ( Betta splendens ) with velvet disease Velvet (in an aquarium environment) is usually spread by contaminated tanks, fish, and tools (such as nets or testing supplies). There are also rare reports of frozen live foods (such as bloodworms) containing dormant forms of the species.
-
Childhood Arthritis
Wikipedia
Retrieved 2020-10-29 . ^ Takken, Tim; van der Net, Janjaap J; Helders, Paul PJM (2001-10-23).SMAD3, JMJD1C, ADCY7, IL1RN, SLC11A1, CTLA4, LPP, NDEL1, BTG3, CD14, CXCL1, CXCR4, OSM, PLAUR, PLOD2, NRG1, ASAP1, MAPK1, SLC22A16, PGM5, RNF103, PROS1, TUBB2A, H2AC8, FOXP1, MIR22HG, SIPA1L1, TNFAIP8, ANKRD9, MAFF, KAT6B, GP1BB, GNG11, GMPR, BEND2, STAB1, FOSL2, FOSB, FOS, PER1, TNFRSF10C, AOPEP, H2BC8, HERPUD2, KRAS, MTSS1, KCNJ15, JUN, ITGB5, ITGA2B, ETNK1, FAM20A, MAP2, MAD1L1, RBM47, CXCR2, DYSF, HSPA6, WWOX, SH3BGRL2, MSN, NR4A3, MS4A4A, MEX3C, IGF1R, NR4A2, C2orf88, MAML2, ACRBP, OLR1, FCGR1A, AVL9, TTLL5, CMTM2, CALD1, BTG1, RHOBTB1, TFPI, LILRA5, C8B, TFDP1, TREML1, CREM, PACSIN2, CD8B, TCF7L2, STIM1, CLU, STAT3, CD83, THBS1, FAXDC2, RERE, KLF4, B4GALT5, AREG, FCHSD2, AQP9, PCYT1B, TNFAIP6, UBE3C, ALOX12, MYZAP, WASF3, PLK2, ACP3, R3HDM2, NEAT1, CAMSAP1, DUSP2, DDIT3, ZFC3H1, RASGEF1B, SIK1, HBEGF, DUSP1, DUSP4, DAPK1, EGF, EGR1, ELF2, CTTN, UHRF1BP1L, ETV6, GADD45A, ZFAND3, APOBEC3A, UBE2E1, TNIK, SLC2A3, C9orf72, HLA-DRB1, PTPN22, IL6, IL2RA, STAT4, VTCN1, MIF, LACC1, PTPN2, IL23R, CD247, ACP5, ANKRD55, REEP3, ZMIZ1, IL2RB, TIMMDC1, ATG16L1, CRB1, ADGRL2, SUOX, ATXN2L, ERAP2, TNF, IGF2-AS, NRBF2, FNBP1, LINC00993, CARD9, CTTNBP2, CACNA1I, ANGPTL5, HLA-A, DAG1, IL1B, IL1A, FUT2, TSBP1, CCDC26, RBM45, GPR35, NKD1, LRRK2, HLA-DPB1, FAM169B, ANKRD30A, LURAP1L, C1orf141, DCLRE1C, CSMD1, TSBP1-AS1, LINC01250, INS-IGF2, IL10, IRF1-AS1, TNFSF15, CCR5, FOXP3, IFNG, IL4, IL17A, HLA-DQA1, TRAF1, CRP, ESR1, IL2, S100A12, CXCR3, NLRP3, DEK, MEFV, IL18, TLR4, ERAL1, IL6R, ISG20, TNFRSF11B, CRYGD, GZMB, UNC13D, MTHFR, GH1, CXCL8, HSPD1, MIR146A, VDR, MMP9, TRBV20OR9-2, COMP, CD226, TNFSF11, TNFRSF1A, CCR4, MMP3, NLRP1, TAP1, IL6ST, TLR2, TIMP2, TNFAIP3, LINC01193, IRF1, USO1, MBL2, SPP1, CXCL10, MIR155, TIMP1, IRF5, HLA-C, HLA-B, CSF2, IL33, PSMA6, PSMB9, NXF1, PRKCQ, VIL1, HLA-DQB1, VEGFA, IL21, S100A8, HLA-DRB3, HMGB1, HSPA14, SEC14L2, CCL3, CCL5, TNFRSF11A, IGF1, FLNB, MTX1, CXCR6, ABCB6, POSTN, NR1I3, SH2B3, HMGB1P5, TRIM13, NAMPT, CARD14, CCL27, SUMO4, NT5C1A, EBPL, FCRL3, HT, PYDC1, FAM177A1, SERPINA2, CARD8, MIR125A, MIR204, MIR21, WG, CXADRP1, KIR2DS2, TLR10, NAA25, CXCL16, ZNF395, RSBN1, SIAE, TREM1, ERAP1, IL23A, TLR7, LINC00328, MBL3P, CD274, IL37, ACAD8, PADI4, CLEC16A, BMS1, ACACA, HDAC9, GSTT1, HMOX1, HLA-G, HLA-DRB5, HLA-DPA1, HIF1A, HFE, GSTP1, HYAL1, GSTM1, GHR, GEM, GATA3, GAS6, FCN2, HNF4A, ICAM1, ELK3, ITPA, KIR2DS4, KIR2DS1, KIR2DL3, KIR2DL2, KIR2DL1, KIF5A, IRAK1, IFN1@, IL13, IL7R, IL4R, IGHG3, IFNA13, IFNA1, FBN1, SLC26A2, KIR3DL2, ARR3, C2, BMP4, BGLAP, BCL2, ATM, ATIC, AR, C4BPA, FAS, ANXA11, AMH, ACAN, ADRB2, ADA, C4A, C5, ATN1, CCR7, DPP4, DHCR7, CXADR, CTNNB1, CSF3, CNR2, CHIT1, CALCR, CDK6, LRBA, ENTPD1, CD28, CAT, CASR, KIR3DL1, KIR3DS1, PRORP, SNAI1, TGFB1, PRDX2, TAP2, STXBP2, STAT1, SPG7, SLC19A1, TLR3, SELP, SELE, CXCL11, CXCL6, CCL21, CCL20, TGM2, TNFRSF1B, ATXN2, ABCC3, NCR2, IL32, PSTPIP1, SH2D2A, KSR1, CCN6, DGKZ, TP53, CDR3, VIM, VCAM1, TYK2, TWIST1, TTN, CCL19, SAG, AFF3, MME, NGF, NFKBIA, NCAM1, MMP8, MMP2, MMP1, CIITA, NOS3, MECP2, LYZ, LTA, LIG4, LEP, LBP, NM, NT5E, SAA1, PTX3, S100B, S100A9, S100A1, BRD2, RBP3, RAB27A, PTPRC, PDCD1, PSMC6, PSMA3, PRNP, PRKAR1A, PRF1, ABCB1, CCL2
-
Monomac
Wikipedia
Not to be confused with the .Net bindings MonoMac. monoMAC syndrome Other names MonoMAC/DCML, monocytopenia and mycobacterium avium complex/dendritic cell, monocyte, B and NK lymphocyte deficiency Specialty Medical genetics MonoMAC syndrome is a rare autosomal dominant syndrome associated with: monocytopenia , B and NK cell lymphopenia ; mycobacterial, viral, fungal, and bacterial opportunistic infections ; and virus infection-induced cancers .
-
Marfanoid–progeroid–lipodystrophy Syndrome
Wikipedia
Marfanoid–progeroid–lipodystrophy syndrome ( MPL ), also known as Marfan lipodystrophy syndrome ( MFLS ) or progeroid fibrillinopathy , is an extremely rare medical condition which manifests as a variety of symptoms including those usually associated with Marfan syndrome , an appearance resembling that seen in neonatal progeroid syndrome (NPS; also known as Wiedemann–Rautenstrauch syndrome), and severe partial lipodystrophy . [1] [2] [3] [4] [5] It is a genetic condition that is caused by mutations in the FBN1 gene , which encodes profibrillin , and affects the cleavage products of profibrillin, fibrillin-1 , a fibrous structural protein , and asprosin , a glucogenic protein hormone . [1] [6] As of 2016, fewer than 10 cases of the condition have been reported. [1] Lizzie Velásquez and Abby Solomon have become known publicly through the media for having the condition. [7] [8] In addition to severe lipodystrophy (loss of adipose tissue ), individuals with MPL show a concomitant marked loss of lean tissue mass , which also contributes to their "skinny" appearance. [3] Based on visual inspection, it was originally thought that the lipodystrophy associated with MPL was generalized . [3] However, it appears in fact to be partial, being confined to the face , distal extremities , and the paravertebral and lateral regions of the buttocks . [3] Normal amounts of subcutaneous fat are found in the torso over the chest and abdomen . [3] As such, the breasts are normal in females with MPL. [1] [2] Individuals with MPL have an appearance of being prematurely aged , but this is not due to actual early aging and is instead due to their paucity of subcutaneous fat . [1] As such, MPL is not truly a form of progeria . [1] In 2016, it was discovered that the partial lipodystrophy associated with MPL is caused by loss of the C-terminal domain cleavage product of profibrillin and novel glucogenic protein hormone, which has been named asprosin. [6] [8] Due to asprosin deficiency, individuals with MPL eat less, and do not gain weight or develop symptoms of diabetes like insulin resistance . [8] [3] [9] MPL patients burn less energy than normal individuals, but also consume less, and their net energy balance is moderately reduced. [10] In contrast to MPL patients, whose asprosin is undetectable in the blood, individuals with obesity and diabetes have elevated levels of asprosin. [6] As such, FBN1 has been nicknamed the "thin gene", and drug development for targeted inhibition of asprosin signaling is considered to be an "unusually promising" potential therapeutic route in the treatment of obesity and diabetes. [8] References [ edit ] ^ a b c d e f Passarge E, Robinson PN, Graul-Neumann LM (2016).
-
Fish Disease And Parasites
Wikipedia
Sea lice , particularly Lepeophtheirus salmonis and a variety of Caligus species, including Caligus clemensi and Caligus rogercresseyi , can cause deadly infestations of both farm-grown and wild salmon. [38] [39] Sea lice are ectoparasites which feed on mucous, blood, and skin, and migrate and latch onto the skin of wild salmon during free-swimming, planktonic naupli and copepodid larval stages, which can persist for several days. [40] [41] [42] Large numbers of highly populated, open-net salmon farms can create exceptionally large concentrations of sea lice; when exposed in river estuaries containing large numbers of open-net farms, many young wild salmon are infected, and do not survive as a result. [43] [44] Adult salmon may survive otherwise critical numbers of sea lice, but small, thin-skinned juvenile salmon migrating to sea are highly vulnerable. ... Management strategies include developing a vaccine and improving genetic resistance to the disease. [48] In the wild, diseases and parasites are normally at low levels, and kept in check by natural predation on weakened individuals. In crowded net pens they can become epidemics. Diseases and parasites also transfer from farmed to wild salmon populations. ... Fish farms drive wild salmon populations toward extinction Biology News Net. December 13, 2007. Salmonid parasites University of St Andrews Marine Ecology Research Group. ... Salmon lice Saprolegnia Schistocephalus solidus Sea louse Sphaerothecum destruens Swim bladder disease Tetracapsuloides bryosalmonae Velvet Xenoma Fish groups Diseases and parasites in cod Diseases and parasites in salmon Disease in ornamental fish List of aquarium diseases Related topics Amnesic shellfish poisoning Brevetoxin Ciguatera Diarrheal shellfish poisoning Fish kill Marine viruses Neurotoxic shellfish poisoning Paralytic shellfish poisoning Saxitoxin v t e Fisheries and fishing topic areas Fisheries Aquaculture Diversity of fish Fish diseases and parasites Fish farming Fisheries management Fisheries science Individual fishing quota Illegal, unreported and unregulated fishing Sustainable fishery Overfishing Wild fisheries Fishing Artisanal fishing Fisherman Fishing vessel History of fishing Industry List of harvested aquatic animals by weight By country Commercial fishing Marketing Markets Processing Products Seafood Recreation Angling Big-game fishing Catch and release Fishing tournaments Fly fishing Techniques Fish trap Fishfinder Fishing net Gathering seafood by hand Handline fishing Spearfishing Trawling Trolling Tackle Artificial flies Bait Bite indicators Hook Line Lures Rod Sinker Locations Fish ponds Fishing banks Fishing villages Marine habitats Glossary Index Outline Category
-
Kidney Disease
Wikipedia
Curtis (2002-12-01). "Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors" . ... PMID 24513954 . ^ Scialla, Julia J.; Appel, Lawrence J.; Astor, Brad C.; Miller, Edgar R.; Beddhu, Srinivasan; Woodward, Mark; Parekh, Rulan S.; Anderson, Cheryl A. M. (2011-07-01). "Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease" .UMOD, AGTR1, B2M, TTC21B, RPGRIP1L, TREX1, EDN1, ALB, KL, NFE2L2, FGA, AGT, REN, LCN2, EPO, TGFB1, MTHFR, ACE, CST3, IGF1, NPHS1, MPO, IL1RN, HAVCR1, PTGS2, SOD2, SPP1, COL4A1, WNK1, FGF2, SLC12A3, SPARC, NOS2, PPARA, LRP2, EGF, CASP1, ACKR3, MIR21, THG1L, ANXA1, IL33, GLIS2, WNT4, CYP2C8, SV2B, CYP3A5, FABP4, PYCARD, GSTP1, CYBB, CLU, SLC7A9, HNF1A, PARP1, MIR192, MXI1, LEPR, NQO1, RRM2B, CCL2, SLC22A2, RBP4, SMPD1, CALB1, TRPC6, ALAD, MT4, RASAL1, CNNM2, CTSD, SLC47A1, IFT122, PCSK5, NPR1, MMP9, HOXD11, HOXA11, SIX2, NR4A1, NEK8, POMC, TERT, TFAP2A, TFF3, CSF3, CDKN1A, ACTA2, THAS, CTF1, GATM, ADRA1B, RGN, ADRB2, CCL5, ABCB1, BMP7, CASP9, XYLT1, TGFBI, TGFBR2, MIF, G6PD, CASP3, RAMP2, CASP8, CFH, NLRP3, CYGB, SREBF2, ABCC3, SREBF1, RELB, MKI67, MYH9, PPP3CA, TGFBR1, LMX1B, PPARG, WT1, INS, GLA, TTR, APOA1, LYZ, MEFV, HNF4A, CD151, EIF2AK3, FOS, IFT140, TMEM67, SCNN1G, CEP290, WDR73, CLDN19, FAM20A, NPHP1, GCK, ABCC8, SCNN1A, SCARB2, CCND1, WFS1, BLK, PAFAH1B1, VPS33B, SIRT1, PAX4, FOXI1, INPP5E, SERPINE1, MAFB, ALG1, LAGE3, PRDX1, CISD2, WAS, ZNF423, NUP133, BSCL2, CFHR5, SAA1, VEGFA, IL6, SCNN1B, WDR34, IL10, WDR60, KLF11, DPP4, SLC26A4, OSGEP, TP53RK, DYNC2H1, MMACHC, ACE2, IGAN1, VIPAS39, HLA-DPB2, PKD2, WDR19, NOD2, NPHS2, PKD1, RAPGEF5, FGF23, HPRT1, APPL1, IFT80, CC2D2A, TMEM237, YWHAE, NUP107, WIPF1, IFT172, PRODH, PSMB8, GABPA, APOE, TMEM231, PTH, PDX1, HIC1, NOS3, TPRKB, SLC5A2, NEUROD1, TNF, ADA2, DYNC2LI1, AGPAT2, HORMAD2, TMEM138, MUC1, CCN2, CEP120, KCNJ10, WDR4, CEL, CAVIN1, HNF1B, COL7A1, COL4A5, COL4A3, ACTN4, SEC61A1, NR3C2, KCNJ11, TMEM216, CAV1, APOL1, AKR1B1, ADIPOQ, CRP, IL1B, ADM, POSTN, CNDP1, GCG, IL17A, GLP1R, LGALS3, AGER, EHMT1, ELMO1, ESR1, ACTB, VDR, TLR4, HIF1A, SLC2A1, STAT3, MTOR, HLA-DRB1, ZGLP1, RAC1, COL4A4, LEP, LPA, CAT, PLG, CABIN1, CCR5, EGFR, HMOX1, CTNNB1, FN1, DECR1, TNFRSF1A, PON1, PGR-AS1, CD2AP, TP53, TRPC5, KEAP1, GH1, INF2, PSMD9, CCR2, SOD1, FGF21, ANGPT2, ATP6AP2, BCL2, RENBP, NFKB1, COQ8B, IGHA1, TM7SF2, ANGPT1, VPS51, G6PC, GPBAR1, ABO, KLK1, IL4, HAMP, CXCL10, PKHD1, HGF, ACACB, IL1A, SMAD3, SLC33A1, MPV17, KLK4, GDF15, PAX2, HP, SMARCAL1, MBL2, IL18, NPPB, SMAD7, CXCL8, ADAM17, MMP2, PRKCB, SLC2A2, DCN, CYBA, IQCB1, DDR1, EDNRA, TXN, SCGB1A1, MOK, AVP, ATM, PCSK9, PRKD1, THBS1, GORASP1, TLR2, CYP24A1, TIMP1, RBM45, SLC4A1, RTN1, DIANPH, PODXL, MIR155, AHI1, MMP7, SGK1, GPX3, UTS2, EGR1, TSC2, SYNPO, GSTM1, TNFRSF12A, PPARGC1A, SYT1, SDC2, HLA-DQA1, SELL, COQ2, CCN3, KDR, SLC9C1, HSPG2, FABP1, GJA1, ACR, CUBN, CLDN16, COL4A6, MAPK8, MAP3K5, KLF15, CLCN5, TMSB4X, APOC3, ADD1, DKK3, ERAL1, FOXO1, OGA, HIPK2, IL22, TLR9, HMGB1, APOM, MYO1E, RELA, AGTR2, MYH2, ADAM19, KLF4, ARTN, CXCR6, LPAR2, COX1, SSTR4, COX2, TCF7L2, TGFA, NAGLU, ANGPTL3, XPR1, MTRR, HPSE, TIMP2, TNFSF13B, TNFSF13, SOAT1, GADD45G, PLA2G1B, NCF2, ANP32B, LOH19CR1, HDAC6, NR1H4, VWF, CNTN3, NEDD4L, SIRT3, MLYCD, ENPP1, SERPINF1, HMGA2, MAPK3, DDAH1, PRKAB1, PRKAA2, PRKAA1, CADM1, CXCR4, MANF, RNU1-4, SLC17A5, P2RX7, NPPA, SLC12A1, IRS2, SOCS1, NGF, NOTCH1, NOTCH3, TNFRSF1B, DGKE, TSC1, RPS6KA1, VCAM1, SLC11A2, CUL3, ULK1, SCN7A, SCD, NTRK1, RPS19, CXCL12, MAP3K14, SETD2, RETN, FAT1, MIR214, C3, FCGRT, BTK, FOXC1, FLI1, NOX5, BRS3, CRELD2, GATA3, AGXT2, GHR, HHIP, BDNF, CXCR3, UTS2R, GPR42, BDKRB1, HBA1, HFE, STS, ARSA, HSD11B2, PDSS2, CAD, CALD1, SLC19A3, NPHP4, CTLA4, CP, CTNS, COX8A, CTSL, CX3CR1, THSD7A, FRMD3, CYP2E1, CYP3A4, COPD, CLCNKB, MIR182, IFNL3, AQP11, CFTR, GOLGA6A, CDC42, ENO1, CD40, CD80, MS4A1, CD14, CASR, HSPA9, BGN, MAPK14, ADRA2B, AFM, IHG1, IL2, RCBTB1, AGRP, AHSG, ILK, IDO1, INSR, APEX1, SIRT6, AMBP, ITGAM, ALPL, NBAS, JAG1, ICAM1, KNG1, AKT1, KRT20, AHR, IGHG3, TREM1, ADRA1A, IGFBP7, MTCO2P12, NOX4, LINC01672, FAS, IFNG, ADAM10, MGP, NOG, MIR141, MTHFS, CCT2, H3P10, MIR10A, SLC19A2, MIR145, SLC22A6, PKD2L1, MIRLET7C, MASP2, CAPN9, PRSS55, MIR146A, MIR150, SLC7A7, SUMO4, AHSA1, STON1-GTF2A1L, IFNL1, H3P23, OR10A4, DCTN6, COX7A2L, PDPN, SPESP1, CRB2, TXNIP, CD163, HCAR2, FCGR2C, NRK, TBX18, SH2B2, TICAM2, GSTK1, CTCF, MIF-AS1, MIR1207, MIR191, BMS1, AIM2, MAGI2, HNP1, MIR146B, NPS, DELYQ11, ARHGEF11, NCF1, SPATA2, MIR618, KLRC4-KLRK1, RPL17-C18orf32, MIR377, MIR802, KTWS, SOD2-OT1, CD24, MFT2, TMED7-TICAM2, MIR1915, CLOCK, PTGES, TBPL1, MIR1249, COMMD3-BMI1, ARID2, UBD, GDF11, ZNRD2, UNC13B, NSA2, SIRT1-AS, MIR19B1, SLC22A8, GRAP2, CORO2B, KLF2, MIR216A, AD17, FADS2, MIR375, CELA3A, NAMPT, MIR99B, TRAP1, MIR148B, MIR4490, ABCB6, HDAC5, MIR151A, MIR373, NTN1, MIR200A, C1QTNF1, NES, SEMA3G, ZNF410, TRIB3, EPB41L5, USP36, GOPC, POLDIP2, C1GALT1, CHMP2B, PTPN22, CLEC4E, ANKS1B, SUCNR1, SLC2A9, CCL28, TP53INP2, SOSTDC1, BBS12, LY96, PSD4, DDAH2, COLEC11, SMURF2, DDX58, MPP5, ABCG8, RNF19A, IFIH1, XYLT2, TNMD, XPNPEP3, UBE2O, ELOVL5, ZC4H2, CNDP2, FAR2, SOST, SNX9, NOSIP, TMED7, SMPDL3B, DERL2, ASCC1, SGSM3, RNLS, TAS2R13, MBL3P, RGCC, COMMD5, NXPH1, ICOS, IL23A, GPRC5B, GNMT, IL17C, ANLN, IL37, CCHCR1, PALD1, INVS, FBLIM1, MKS1, NAT8, NOX1, TESC, FOXD3, MOCOS, BBS7, MMD, EFHD2, BHLHE41, CCDC114, STON1, SGF29, PRRT2, TREH, MYOCD, CHEK2, DNER, VASH1, RSAD2, GPR182, PHB2, LRSAM1, MCU, ABCC11, GTF2A1L, SORCS1, C1GALT1C1, VASN, KCNQ1OT1, IL17RE, MAPRE2, SLCO6A1, FERMT2, MAGED2, SIRPA, PTPRVP, PLB1, ZSWIM2, CFHR3, SDCCAG8, HFM1, TDGF1P6, HAVCR2, TNFRSF13B, STAB1, PDGFD, ITPKC, MCF2L2, DDN, KDM6B, TBC1D9, ALPK1, SPZ1, BICC1, JADE1, VTCN1, NLRX1, BRD4, CEP97, WNT10A, CMIP, MYO16, PALLD, APOL4, PLA2R1, MAPRE1, KLRK1, APOL3, SETD7, ARHGAP24, HMCN1, SACM1L, MINDY4, NLRP1, WDR83, NT5C1A, ABCA1, RSC1A1, SOCS3, FABP2, PTK2B, FCGR2A, FCGR2B, FGF13, FGG, FGL1, FOXC2, FLII, FLT1, FMOD, FOSB, FOSL2, GAST, SLC37A4, GAD1, GAD2, GAS1, GC, GCKR, GEM, GFPT1, ACSL1, F10, GLO1, F5, DUSP5, EDA, EDNRB, EFNB1, EFNB2, CELA1, ELAVL1, ENG, ENO2, STX2, ERBB4, ERCC1, ERCC4, ESRRA, ESRRG, ETFA, ETS1, EYA1, F2, F2R, F3, GCLC, GNAO1, INPP5D, HES1, HSPA1B, HSPA4, HSPA5, HSP90AA1, NDST1, HTC2, ID1, CFI, IFI27, IFN1@, IFNA1, IFNA13, IFNAR1, IFNB1, IGFBP1, IGFBP3, IL1R1, IL2RA, IL7R, IL9, CXCR2, HSPA1A, PRMT1, GNB3, HRES1, GOLGB1, GPT, GPX4, GRP, GSK3B, GSN, GSTT1, GUCA2A, GUCA2B, HAS2, HAS3, HDAC1, HDAC2, CFHR1, HLA-C, HLA-DPA1, HLA-DQB1, HLA-DQB2, HLA-E, HPS1, HPT, HBEGF, RCAN1, ATN1, SERPINC1, ATIC, ATR, BCL3, BGLAP, BLVRA, BMI1, DST, BRAF, BSG, BTF3P11, C3AR1, C5, C5AR1, CA1, CA2, CALR, CAMK4, CARS1, CAV2, RUNX2, CD5L, ATF4, ARSL, DRD3, ARRB1, ACACA, ADCYAP1, ADD3, ALOX12, ALOX5, AMH, SLC25A4, APOA4, APOB, APOC1, APRT, KLK3, AQP1, AQP2, AQP4, AQP5, AQP6, AREG, ARF6, ARG2, ARNTL, CD28, CD34, CD36, CD40LG, CSF1, CSH1, CSH2, VCAN, CTSB, CYLD, CYP2A6, CYP2B6, CYP2C19, CYP2C9, CYP19A1, CYP27B1, DAB2, DAO, DBH, DDIT3, DDOST, DES, DIAPH1, DMRT1, DNASE2, CRK, CR2, MAP3K8, CHGA, CDH5, CDH13, CDK4, CDK9, CDKN1C, CDKN2A, CEBPB, CETP, CFL1, CHI3L1, COL11A2, CHIT1, CISH, ERCC8, CLC, CMA1, CCR3, ABCC2, CNR1, COL4A2, INHBC, IRF5, HAP1, SRC, SSBP1, SST, ST2, STAT4, STATH, SULT1E1, TAC1, TAGLN, TBX3, TRBV20OR9-2, TFRC, TGFB2, THBD, THBS2, THY1, TIMP3, TLR3, NR2E1, TPM3, CRISP2, TRPC1, TRIM21, SP3, TWIST1, SOX2, SALL1, SCT, SRL, CCL7, CCL21, SDC1, SDC4, SELE, SFRP1, SFTPD, SHBG, SKP2, SLC5A1, SLC9A3, SLC15A2, SMARCB1, SIGLEC1, SNCA, SNRPD1, SOD3, SORD, TRPC3, TNFSF4, ITGA2, NR4A3, MKKS, PLA2G6, BBOX1, ITGA8, AP3B1, RUVBL1, AOC3, KCNK5, VAMP8, MBTPS1, TNFSF10, TNFRSF6B, NRP2, NRP1, KAT2B, PROZ, LDB1, PER2, ARHGEF7, SELENBP1, PGLYRP1, SLC25A16, AIMP2, TNFRSF4, RNF217-AS1, TYRO3, TYROBP, TYRP1, UCHL1, UGT2B17, KDM6A, VASP, VEGFC, VHL, EZR, VIM, TRPV1, VTN, WNT9A, XDH, YWHAZ, ZFP36, ZNF236, ALMS1, TFEB, PUJO, S100A8, RPL17, RPL10, LPL, LTF, SMAD2, MAS1, MCL1, CD46, SMCP, MDH2, MDM2, MFAP1, CXCL9, MLN, KMT2A, MME, MMP10, MMP14, MS, MST1R, ATP6, COX3, ND5, TRNT, LTA, LOXL2, ROS1, LMNA, ITGB1, ITGB2, JUN, JUNB, JUND, KCNE1, KCNQ1, KIR2DS1, KIR2DS3, KIR3DL1, KIR3DS1, KIT, KRAS, LAMA5, LAMB2, LCAT, LDLR, LECT2, LGALS1, LIMS1, LIPC, MYBPH, NCAM1, NDN, NFYA, PRKCA, MAPK1, MAP2K7, PROC, PSMA6, PTEN, PTGDS, PTGS1, PTK2, PTPRC, PTX3, PVR, RAB4A, RAG1, RARA, RARRES2, PLAAT4, REG1A, RFC1, RMRP, RNASE2, PRD, PPIA, PON2, PC, NGFR, NOS1, NPY, NOTCH2, NOTCH4, YBX1, TNFRSF11B, PAEP, PAH, PCBD1, PLXNA1, PCNA, PDCD1, PF4, CFP, PIK3CG, PLA2G2A, PLAT, PLAU, PLAUR, H3P40
-
Torsades De Pointes
Wikipedia
Please note that phase 0 leads to a net gain of Na + , while phases 1-3 lead to a net loss of K + .KCNH2, SCN5A, CYP3A4, KCNQ1, KCNE1, ANK2, KCNE2, NAA10, KCNJ5, SCN4B, SCN10A, SNTA1, ALG10B, CAV3, CALM2, CALM1, AKAP9, TRDN, C18orf21, NOS1AP, IL6, KCNK3, KCNA5, ATP12A, ATP4A, CYP19A1, KCNA4, ACE, SLC24A3, SLCO3A1, RAPGEF4, SLCO1B1, ATP5F1A, CRP, CYP2D6, NR1I2, TNF, SRL, SARDH, TLX2, HTR4, RYR2, RNPEP, ABCB1, ORM1, MSD, LBR, IL1A, ADRB1, IL1B, ADRA2C
-
Azotemia
Wikipedia
Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as urea (BUN), calcium, uric acid, and bicarbonate. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20 mEq/L).
-
Acrania
Wikipedia
The Fetus . ISSN 1057-137X . Archived from .net/page.php?id=77 the original Check |url= value ( help ) on 2009-08-27. ^ a b c Dennis, Jennifer F.; Kurosaka, Hiroshi; Iulianella, Angelo; Pace, Jennifer; Thomas, Nancy; Beckham, Sharon; Williams, Trevor; Trainor, Paul A. (2012).
-
Zika Fever
Wikipedia
Infectious disease caused by the Zika virus Zika fever Other names Zika virus disease, Zika, Zika virus infection Rash during Zika fever infection Pronunciation Zika / ˈ z iː k ə / Specialty Infectious disease Symptoms Fever , red eyes , joint pain , headache, maculopapular rash , Sometimes none [1] [2] [3] Complications Guillain–Barré syndrome , during pregnancy can cause microcephaly in the baby [4] [5] [6] Duration Short-term [2] Causes Zika virus mainly spread by mosquitoes , can also be sexually transmitted [2] Diagnostic method Testing blood, urine, or saliva for viral RNA or blood for antibodies [1] [2] Differential diagnosis Chikungunya , malaria , dengue , leptospirosis , measles [7] Prevention Decreasing mosquito bites, condoms [2] [8] Treatment Supportive care , Generally not needed in mild cases [2] Deaths None during initial infection [4] Zika fever , also known as Zika virus disease or simply Zika , is an infectious disease caused by the Zika virus . [1] Most cases have no symptoms, but when present they are usually mild and can resemble dengue fever . [1] [4] Symptoms may include fever , red eyes , joint pain , headache, and a maculopapular rash . [1] [2] [3] Symptoms generally last less than seven days. [2] It has not caused any reported deaths during the initial infection. [4] Mother-to-child transmission during pregnancy can cause microcephaly and other brain malformations in some babies. [5] [6] Infections in adults have been linked to Guillain–Barré syndrome (GBS). [4] Zika fever is mainly spread via the bite of mosquitoes of the Aedes type. [2] It can also be sexually transmitted and potentially spread by blood transfusions . [2] [8] Infections in pregnant women can spread to the baby. [5] [6] [9] Diagnosis is by testing the blood, urine, or saliva for the presence of the virus's RNA when the person is sick, or the blood for antibodies after symptoms are present more than a week. [1] [2] Prevention involves decreasing mosquito bites in areas where the disease occurs and proper use of condoms. [2] [8] Efforts to prevent bites include the use of insect repellent , covering much of the body with clothing, mosquito nets , and getting rid of standing water where mosquitoes reproduce. [1] There is no effective vaccine . [2] Health officials recommended that women in areas affected by the 2015–16 Zika outbreak consider putting off pregnancy and that pregnant women not travel to these areas. [2] [10] While there is no specific treatment, paracetamol (acetaminophen) may help with the symptoms. [2] Admission to hospital is rarely necessary. [4] The virus that causes the disease was first isolated in Africa in 1947. [11] The first documented outbreak among people occurred in 2007 in the Federated States of Micronesia . [2] An outbreak started in Brazil in 2015, and spread to the Americas, Pacific, Asia, and Africa. [12] This led to the World Health Organization declared it a Public Health Emergency of International Concern in February 2016. [12] The emergency was lifted in November 2016, but 84 countries still reported cases as of March 2017. [13] The last proven case of Zika spread in the Continental United States was in 2017. [14] Contents 1 Signs and symptoms 1.1 Guillain–Barré syndrome 1.2 Pregnancy 2 Cause 2.1 Reservoir 2.2 Transmission 3 Pathophysiology 4 Diagnosis 4.1 Screening in pregnancy 4.2 Infant testing 5 Prevention 5.1 CDC travel alert 5.2 WHO response 5.3 Vaccine 5.4 Mosquito control 6 Treatment 7 Outcomes 8 Epidemiology 8.1 Yap Islands 8.2 Oceania 8.3 Americas 8.4 Asia 9 History 9.1 Origin of the name 9.2 Microcephaly and other infant disorders 9.3 Guillain–Barré syndrome 10 Research 10.1 Mechanism 10.2 Mosquito control 11 References 12 External links Signs and symptoms [ edit ] Rash on an arm due to Zika fever Most people who are infected have no or few symptoms. [15] Otherwise the most common signs and symptoms of Zika fever are fever , rash , conjunctivitis (red eyes), muscle and joint pain , and headache, which are similar to signs and symptoms of dengue and chikungunya fever . [16] The time from a mosquito bite to developing symptoms is not yet known, but is probably a few days to a week. [17] The disease lasts for several days to a week and is usually mild enough that people do not have to go to a hospital. [1] [18] Due to being in the same family as dengue, there has been concern that it could cause similar bleeding disorders. ... Avoid applying repellent to their hands, eyes, or mouth Stay and sleep in screened-in or air-conditioned rooms Use a bed net if the area where you are sleeping is exposed to the outdoors Cover cribs, strollers and carriers with mosquito netting for babies under 2 months old.ERVK-32, RAF1, IVNS1ABP, PTPN11, ERVK-6, IFNA1, IFNA13, STAT2, IFNAR1, IFNAR2, AXL, IL1B, TNF, DDX58, PLAAT4, ROBO3, RSAD2, IFNL1, KRAS, TP53, IFNB1, HPR, IL6, ALB, IFNL2, NLRP3, STAT1, CD40LG, TAM, TLR3, CD14, CXCL10, STING1, SMPD3, HSPA4, G3BP1, IRF3, HMOX1, ITPA, PERCC1, ERVK-20, GAPDH, IFIH1, FGF2, ERVW-1, ISG15, ZBP1, CH25H, NTPCR, PARP1, WWTR1, PHGDH, KPNA6, CEP131, RASSF1, HAVCR1, TUBB3, RIPK3, IFITM3, HSP90B1, TXN, TYRO3, MOGS, RIPK1, GNE, SART3, B3GAT1, ALDH5A1, PPIP5K1, ARTN, NR1I2, FOXD3, PAF1, AGO2, APOBEC3C, EDC3, MAP1LC3B, TRIM56, MFSD2A, SLFN11, NEURL3, TWIST2, TRIM69, WIPF2, TICAM1, MIR34A, MIR34C, CD24, LINC01672, ERVK-18, ZC3H12A, PARP12, TRPV4, SMOX, C19orf53, F11R, CHCHD2, ISYNA1, PHAX, XRN1, DDIT4, MIB1, TFAP2A, ATG16L1, VAC14, PARD3, MAVS, NUFIP2, TFRC, ADAR, TAC3, EIF4G1, EIF5A, EPHB2, EZH2, F3, FCGR3A, FCGR3B, FMR1, GABPA, GDNF, CXCL2, PDIA3, HLA-E, HNRNPA2B1, HNRNPD, IFI16, IFIT1, IFNGR1, EIF4G2, SARDH, STAT5B, DHX9, AP2A1, AGRP, ATF4, ATM, BCL2, BMP6, CASP1, CASP3, CAT, CD48, CHML, COL11A2, CSF2, CUX1, DCX, DDX3X, DDX6, IFNR, IL1A, IDO1, INSR, PIK3CD, PIK3CG, MAPK1, UPF1, RPE, SAT1, SRL, CCL2, ADM, CCL8, CXCL11, SELP, SOAT1, SOD2, SOX2, STAT3, STAT5A, PIK3CB, PIK3CA, PDB1, MDM2, INSRR, IRF1, LAMP1, LAMC2, LCN2, LTBR, CAPRIN1, CXCL9, PCM1, MAP3K11, MS, MSI1, MSX1, NFE2L2, OAS3, PAX7, CCL5
-
Chagas Disease
Wikipedia
In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes , headaches, or swelling at the site of the bite. [1] After four to eight weeks, untreated individuals enter the chronic phase of disease, which in most cases does not result in further symptoms. [2] [5] Up to 45% of people with chronic infection develop heart disease 10–30 years after the initial illness, which can lead to heart failure . [2] Digestive complications, including an enlarged esophagus or an enlarged colon , may also occur in up to 21% of people, and up to 10% of people may experience nerve damage. [2] T. cruzi is commonly spread to humans and other mammals by the bite of a kissing bug. [6] The disease may also be spread through blood transfusion , organ transplantation , eating food contaminated with the parasites, and vertical transmission (from a mother to her baby). [1] Diagnosis of early disease is by finding the parasite in the blood using a microscope or detecting its DNA by polymerase chain reaction . [5] Chronic disease is diagnosed by finding antibodies for T. cruzi in the blood. [7] It affects more than 150 types of animals. [8] Prevention focuses on eliminating kissing bugs and avoiding their bites. [1] This may involve the use of insecticides or bed-nets . [9] Other preventive efforts include screening blood used for transfusions. [1] As of 2019 [update] , a vaccine has not been developed. [1] Early infections are treatable with the medications benznidazole or nifurtimox , which usually cure the disease if given shortly after the person is infected, but become less effective the longer a person has had Chagas disease. [1] When used in chronic disease, medication may delay or prevent the development of end–stage symptoms. [1] Benznidazole and nifurtimox often cause side effects, including skin disorders, digestive system irritation, and neurological symptoms, which can result in treatment being discontinued. [1] [2] As of 2019 [update] , new drugs for Chagas disease are under development, and experimental vaccines have been studied in animal models. [10] [11] It is estimated that 6.2 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2017, [1] [3] resulting in an estimated 7,900 deaths. [4] Most people with the disease are poor, [12] and most do not realize they are infected. [13] Large-scale population migrations have carried Chagas disease to new regions, which now include the United States and many European countries. [1] The disease was first described in 1909 by Brazilian physician Carlos Chagas , after whom it is named. [1] Chagas disease is classified as a neglected tropical disease . [14] Contents 1 Signs and symptoms 2 Cause 2.1 Transmission 3 Pathophysiology 4 Diagnosis 5 Prevention 6 Management 6.1 Complications 7 Epidemiology 7.1 Non-endemic countries 8 History 9 Research 9.1 Treatments 9.2 Diagnostic tests 10 See also 11 References 12 External links Signs and symptoms [ edit ] An acute Chagas disease infection with swelling of the right eye (Romaña's sign) Chagas disease occurs in two stages: an acute stage, which develops one to two weeks after the insect bite, and a chronic stage, which develops over many years. [2] [5] [15] The acute stage is often symptom-free. [2] When present, the symptoms are typically minor and not specific to any particular disease. [5] Signs and symptoms include fever, malaise , headache, and enlargement of the liver , spleen , and lymph nodes . [1] [2] [5] Rarely, people develop a swollen nodule at the site of infection, which is called "Romaña's sign" if it is on the eyelid, or a "chagoma" if it is elsewhere on the skin. [5] [16] In rare cases (less than 1–5%), infected individuals develop severe acute disease, which can cause life-threatening fluid accumulation around the heart , or inflammation of the heart or brain and surrounding tissues . [2] The acute phase typically lasts four to eight weeks and resolves without treatment. [2] Unless treated with antiparasitic drugs , individuals remain chronically infected with T. cruzi after recovering from the acute phase. [2] Most chronic infections are asymptomatic, which is referred to as indeterminate chronic Chagas disease. [2] However, over decades with chronic Chagas disease, 30–40% of people develop organ dysfunction ( determinate chronic Chagas disease), which most often affects the heart or digestive system . [2] [5] The most common manifestation is heart disease , which occurs in 14–45% of people with chronic Chagas disease. [2] People with Chagas heart disease often experience heart palpitations and sometimes fainting due to irregular heart function. [17] By electrocardiogram , people with Chagas heart disease most frequently have arrhythmias . [17] As the disease progresses, the heart's ventricles become enlarged ( dilated cardiomyopathy ), which reduces its ability to pump blood. [17] In many cases the first sign of Chagas heart disease is heart failure , thromboembolism , or chest pain associated with abnormalities in the microvasculature . [17] Also common in chronic Chagas disease is damage to the digestive system, particularly enlargement of the esophagus or colon , which affects 10–21% of people. [2] Those with enlarged esophagus often experience pain ( odynophagia ) or trouble swallowing ( dysphagia ), acid reflux , cough, and weight loss. [2] Individuals with enlarged colon often experience constipation , which can lead to severe blockage of the intestine or its blood supply . [2] Up to 10% of chronically infected individuals develop nerve damage that can result in numbness and altered reflexes or movement. [2] While chronic disease typically develops over decades, some individuals with Chagas disease (less than 10%) progress to heart damage directly after acute disease. [17] Signs and symptoms differ for people infected with T. cruzi through less common routes. ... Xenodiagnosis involves feeding the person's blood to triatomine insects, then examining their feces for the parasite 30 to 60 days later. [28] These methods are not routinely used, as they are slow and have low sensitivity. [27] [28] Prevention [ edit ] Bed nets can be used in endemic areas to prevent bites from triatomine bugs. [15] Efforts to prevent Chagas disease have largely focused on vector control to limit exposure to triatomine bugs. Insecticide-spraying programs have been the mainstay of vector control, consisting of spraying homes and the surrounding areas with residual insecticides. [30] This was originally done with organochlorine , organophosphate , and carbamate insecticides, which were supplanted in the 1980s with pyrethroids . [30] These programs have drastically reduced transmission in Brazil and Chile, [15] and eliminated major vectors from certain regions: Triatoma infestans from Brazil, Chile, Uruguay, and parts of Peru and Paraguay, as well as Rhodnius prolixus from Central America. [17] Vector control in some regions has been hindered by the development of insecticide resistance among triatomine bugs. [30] In response, vector control programs have implemented alternative insecticides (e.g. fenitrothion and bendiocarb in Argentina and Bolivia), treatment of domesticated animals (which are also fed on by triatomine bugs) with pesticides, pesticide-impregnated paints, and other experimental approaches. [30] In areas with triatomine bugs, transmission of T. cruzi can be prevented by sleeping under bed nets and by housing improvements that prevent triatomine bugs from colonizing houses. [15] Blood transfusion was formerly the second-most common mode of transmission for Chagas disease. [31] T. cruzi can survive in refrigerated stored blood, and can survive freezing and thawing, allowing it to persist in whole blood, packed red blood cells , granulocytes , cryoprecipitate , and platelets . [31] The development and implementation of blood bank screening tests has dramatically reduced the risk of infection during blood transfusion. [31] Nearly all blood donations in Latin American countries undergo Chagas screening. [31] Widespread screening is also common in non-endemic nations with significant populations of immigrants from endemic areas including the United Kingdom (implemented in 1999), Spain (2005), the United States (2007), France and Sweden (2009), Switzerland (2012), and Belgium (2013). [32] Blood is tested using serological tests , typically ELISAs , to detect antibodies against T. cruzi proteins. [31] Other modes of transmission have also been targeted by Chagas disease prevention programs.CYP51A1, TNF, IL10, IFNG, MMP2, LGALS3, CCR5, PPARG, MMP9, IL2, HLA-A, HLA-DRB1, HSPA4, MTCO2P12, IL6, IL17A, MBL2, TLR4, COX2, IL18, IL1B, PTGS2, RBM45, CALR, PPP1R2C, TLR2, NFE2L2, NDUFA5, TGFB1, MYD88, CYTB, REN, IL1RN, NLRP3, ACHE, APOA1, ATM, PRL, VIP, TP53, VDR, KNG1, HP, TPI1, FN1, TLR9, CTSL, TRIM33, CYP2B6, ACE, BACE1, EPGN, NPNT, CCL4, CCL3, SPN, AMZ1, CCL2, THBS1, RRAD, TNFRSF1B, MIR208A, CCR2, SPINK1, CX3CL1, SDC4, SKIL, SLC11A1, SMPD1, SOD2, TRBV20OR9-2, KIR2DS2, TCN2, TWIST1, RO60, TRIM21, SRM, ROS1, COLEC11, PPARGC1B, PANX1, MASP2, PPARGC1A, SBNO2, SIRT2, RPIA, PLCB1, SIRT1, PTPN22, EBI3, PYCARD, HSPA14, UBAP1, GGNBP2, SBNO1, OTUB1, RABEP2, HEXIM1, KNTC1, TYK2, TNFSF11, VIM, VIPR1, VPS11, FOSL1, CDR3, DYSF, DBA2, TP63, ARHGEF10, MCU, ADAM7, EIF2S2, LMLN, MBD2, SLC25A31, TMPRSS11D, VIPR2, ABO, RAD51, CSF3, CYBB, DECR1, DHODH, DMD, EIF2S1, EIF2S3, FBN1, FCN2, FDPS, FHIT, FOXO3, GAST, G6PD, GABPA, GCK, GEM, GLUL, CTSB, CR1, HLA-G, CDKN1A, ACTB, ADA, PARP1, AGT, ALB, ALOX5, ARG1, STS, ATP2A3, ATP2B1, BCHE, BDNF, C3, CACNA1C, CAMP, CD80, CD86, HLA-DPB1, HSPD1, PPBP, COX1, NGF, NHS, NOS2, PNP, NRF1, OCA2, P2RX7, PAEP, PCNA, PDE2A, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PLCB4, POLG, POMC, PPP1R12A, MIF, IGF1, MEF2D, IGHG3, IL2RA, IL4R, IL7, IL12B, IL13, IL15, ISG20, ITPR1, KIR2DL2, KIR3DL1, KRT8, LGALS9, LTA, LY6E, MAP6, MEF2A, NT5E
-
Pseudohypoaldosteronism, Type Iid
Omim
Description Familial hyperkalemic hypertension, also known as type II pseudohypoaldosteronism (PHAII) or Gordon syndrome, is a rare autosomal dominant disease in which a net positive sodium ion balance is associated with renal potassium ion retention, resulting in hypertension, hyperkalemia, and hyperchloremic metabolic acidosis (summary by Louis-Dit-Picard et al., 2012).
-
Coinfection
Wikipedia
Global prevalence or incidence of coinfection among humans is unknown, but it is thought to be commonplace, [1] sometimes more common than single infection. [2] Coinfection with helminths affects around 800 million people worldwide. [3] Coinfection is of particular human health importance because pathogen species can interact within the host. The net effect of coinfection on human health is thought to be negative. [4] Interactions can have either positive or negative effects on other parasites.GPT, IL10, TNF, IFNA1, IFNA13, IL1B, MBL2, ATAD1, IL6, TLR4, S100A8, NLRP3, IFNG, CRP, TLR2, TMPRSS13, MSMB, MPO, TCN1, MST1, LMLN, CRYL1, GLUD1, UGDH, MYD88, PTPN11, LPL, ALB, H6PD, TP53, CXCL10, UBE2B, STIL, IVNS1ABP, MMP1, TLR9, PMEL, IFNA2, IFNB1, IL2, CXCL8, IL17A, KLRC2, EXT1, SMOX, PDLIM7, ARG1, CACNA1B, BMPER, BRCA1, IL33, CCR5, LINC01194, CD14, MIR146A, CCL2, DEFB4A, AFP, LXN, DEFB4B, COPD, SOAT1, SNAP25, HACD1, SMARCB1, ST13, ST14, IL32, IL1RL1, FCGR2C, STXBP1, HSP90B1, SULT2A1, TAP1, TPO, TPI1, TLR3, UTRN, ZAP70, CXCR4, SLBP, NR4A3, BCAR3, TIMP4, DENR, TGM3, TGFB1, PRDX2, TNFSF10, PROM1, CD163, ARTN, NAT2, PPIG, TICAM1, HAMP, SRR, ERVK-6, MRPL41, RNF34, DNAJC5, UBASH3B, TSLP, HPS4, TRIM69, NLRP6, GDF15, IFNL3, VN1R2, VN1R4, VN1R5, TREML1, MIR20B, KLKP1, CCR2, TRAP, AD12, PGPEP1, RHOF, IER3IP1, HEBP1, TP53I3, APOBEC3B, STAM2, TRIM22, TACC3, SORBS1, C1QL1, METAP2, NT5C2, BRD4, SEC14L2, SUMF2, PARS2, IL17C, PRSS50, RMC1, OBP2A, ERVW-1, IL22, MBL3P, NTM, CAP1, PPARG, CXCL12, F12, DECR1, DHCR7, DHFR, DPP4, E2F1, EGR1, ELANE, ELAVL1, EPHA3, EPRS1, F8, FCGR3A, CXCL11, FCGR3B, FGF2, FGF9, FLNA, GAPDH, CBLIF, GJA1, GLB1, GRN, CXCL1, HDLBP, DAPK1, CYP26A1, CYP3A4, CYP2B6, ACTB, AGRP, AHR, AKT1, AMBP, ANXA6, AZU1, BCL2, OPN1SW, CFB, BMP1, CAV2, CD33, CD38, ENTPD1, CEACAM5, CEACAM3, CEACAM7, CHAT, CHML, COX8A, CRH, CTAA1, CFH, HLA-B, HLA-DQB1, OAS1, PCNA, PF4, SLC25A3, SERPINA1, SERPINB6, SERPINB9, PIK3CA, PIK3CB, PIK3CD, PIK3CG, ABCA1, PRCP, MAP2K1, EIF2AK2, PSEN1, PSG2, PSMB8, PTPN2, RAD51, RAG1, RTN2, SCD, CCL5, SERPINE1, NM, HLA-G, NFKB1, HMOX1, FOXA2, HSPA4, IFNA4, IFNAR2, IL1A, IL4, IL15, IL18, IRF3, ITGA2B, ITPA, KLKB1, KIF22, LNPEP, LTF, LYZ, MBP, CXCL9, MMP9, MUC2, NDUFS3, NFE2L2, ERVK-20
-
Diktyoma
Wikipedia
The chalky grayish-white particles within the tumor mass correspond to foci of cartilage on histology; the semi-translucent membrane covering the lens in some tumors corresponds to spreading neoplastic cells. [4] [6] Tumor cells form a characteristic diktyomatous pattern, with folded cords and sheets resembling a fisherman's net. [3] In early development of the retina, the medullary epithelial cells acquire polarity, such that a basement membrane associated with the vitreous forms the internal limiting membrane on one side, while terminal bars form the outer limiting membrane on the other side.
-
Root Rot
Wikipedia
Jr. (1976) Organic plant protection: a comprehensive reference on controlling insects and diseases in the garden, orchard and yard without using chemicals Rodale Press, Emmaus, PA, pp. 194, 208, 212–213, 226, 247, 260, 295, 321, 333, 337, 469, 488, 577, and 629, ISBN 0-87857-110-8 ; Ellis, Barbara W. and Bradley, Fern Marshall (eds.) (1992) The Organic gardener's handbook of natural insect and disease control: a complete problem-solving guide to keeping your garden & yard healthy without chemicals Rodale Press, Emmaus, PA, p. 401, ISBN 0-87596-124-X ; v t e Hydroculture Types Aeroponics Aquaponics Aquascaping Hydroponics passive Subtypes Aquatic garden Bottle garden Deep water culture Kratky method Ebb and flow Fogponics Microponics Nutrient film technique Organic hydroponics Organopónicos Sub-irrigated planter Top drip Substrates Charcoal Coco peat Diatomaceous earth Expanded clay aggregate Gravel Growstones Lava rock Mineral wool Perlite Pumice Rice hulls Sand Vermiculite Wood fibre Accessories Grow light Hydroponic dosers Irrigation sprinkler Leaf sensor Net-pot Spray nozzle Timers Ultrasonic hydroponic fogger Water chiller Related concepts Algaculture Aquaculture of coral Aquaculture of sea sponges Controlled-environment agriculture Historical hydroculture Hydroponicum Paludarium Plant nutrition Plant propagation Rhizosphere Root rot Vertical farming Water aeration Commons Wikibooks Wikiversity