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Dermatitis
Wikipedia
Different dendritic cells sub types, such as Langerhans cells, inflammatory dendritic epidermal cells and plasmacytoid dendritic cells have a role to play. [26] [27] Diagnosis [ edit ] Diagnosis of eczema is based mostly on the history and physical examination . [4] In uncertain cases, skin biopsy may be taken for a histopathologic diagnosis of dermatitis . [28] Those with eczema may be especially prone to misdiagnosis of food allergies . [29] Patch tests are used in the diagnosis of allergic contact dermatitis. [30] [31] Classification [ edit ] The term eczema refers to a set of clinical characteristics. ... Archived from the original on 2 February 2017 . Retrieved 28 January 2017 . Cite journal requires |journal= ( help ) ^ "Eczema" . ... Retrieved 4 May 2010 . ^ Atopic Dermatitis National Eczema Association. ^ "Balsam of Peru contact allergy" . Dermnetnz.org. 28 December 2013. Archived from the original on 5 March 2014 . ... Primary Care Respiratory Journal . 16 (1): 28–35. doi : 10.3132/pcrj.2007.00006 . ... ISBN 9780203091449 . Archived from the original on 28 May 2016. ^ "Definition of ECZEMA" . www.merriam-webster.com .FLG, IL4, SHARPIN, IL13, NOD2, DSG1, ITGB2, EGFR, HLA-B, ZFP36, EGF, VCAM1, PARP1, HLA-DQA1, CXCL12, PLA2G4A, HCN2, IL17A, IL31, TNF, IL6, IL1B, IL1A, IL22, IL23A, IL33, TSLP, IFNG, AHR, STAT3, IL10, IL17C, CCL2, MPO, CXCL8, MMP9, NLRP3, PTGS2, SOD3, MYD88, GORASP1, STAT6, F2RL1, MAPK14, RELA, TLR7, WNK1, NFE2L2, IL18, CAMP, TLR4, IL5, SYT1, CARD14, MYDGF, IL9, IL1F10, S100A8, IL25, CTLA4, CCL17, MIR146A, IL24, TLR2, CCL27, MMP2, TNFRSF1A, TLR3, GABPA, NR1I2, TRPV3, PPARA, CD274, STAT5B, RABGEF1, IFNA13, TAC1, CD207, TRBV20OR9-2, IL1RN, IFNA1, ICAM1, TXN, HMOX1, FOXP3, TNFRSF12A, GRB2, STAT5A, MAPK1, TRPV1, STAT1, IL1RL2, PLG, TRPA1, COX2, TNFSF14, KLK6, CCL26, GADD45G, TDGF1P6, ZDHHC13, LGALS3, IL17RA, KLK5, ITGAX, S100A9, ITGAM, CCL11, CCL20, CCL22, PPARG, CXCR2, IL7R, TRIM21, GPER1, IL1R1, DSP, MTOR, CX3CR1, CASP1, PBK, IL26, IL22RA2, CAT, ALOX15, FN1, CCR10, BRAF, FAT1, CTNND1, RNF31, GATA3, BSG, SLC52A1, GH1, MIR31, CCR3, TMX2-CTNND1, MTCO2P12, CERS3, TNFSF10, PARP14, TNFSF12, OPN5, RIPK1, IL27, AKR1C3, NPNT, TP63, IKBKG, TAM, MBTPS1, HDAC3, MPZL3, GALR2, GRAP2, COX5A, ADIPOQ, VAMP3, S1PR2, MSC, IL32, ARHGEF2, PSTPIP1, SOCS3, GPBAR1, BTLA, EIF2B5, ZNF746, NRIP1, CFLAR, CLEC4C, CXCL17, MCIDAS, CDR3, TYK2, VDR, TNFSF12-TNFSF13, MIR485, SCART1, TYRP1, CCR2, TYR, HMGA1P6, S100A7A, TNFRSF4, TRPM2, TRAF6, TRAF5, TRAF2, TP53, DEFB4B, VEGFC, MIR17HG, MIR26B, MIR210, HCAR2, SLC7A5, AIMP2, ARMH1, PCLAF, ARSH, SLC30A4, GSTK1, XRCC1, C10orf99, XBP1, VTN, MIR145, MIR155, MIR21, TBPL1, CD109, TNFSF15, GDF11, PIEZO2, HPGDS, ADAMDEC1, ATOD1, C5AR2, CRLF2, IFIH1, ROBO3, ELOVL1, BCL11B, ELOVL6, IL37, NAAA, LAT, CLMP, ZC3H12A, ATP2C1, IL21, NLRC4, STIM2, MEG3, KRT20, TLR9, IL17RD, IL17D, RTRAF, SLC25A37, SDF4, SLC39A4, MAVS, IL21R, DUOX2, VAC14, SLURP1, IL19, S100A14, BLNK, NPTN, IL36RN, SLC17A5, AP1S3, HPSE, MRGPRX2, TRAF3IP2, POSTN, RBCK1, AHSA1, CLEC10A, IL17RE, EBNA1BP2, SLCO6A1, TNIP1, LANCL1, CARMIL2, RABEPK, CD300LF, IL23R, MALT1, MRGPRF, ARMC9, DMKN, TMEM79, PTPN22, ORAI1, POLDIP2, RTTN, RNF19A, UBASH3B, SMPX, CD160, DDX58, CASP14, RBFOX2, POFUT1, NLRP1, IL17F, KLK8, NAT1, REN, TNFAIP3, DECR1, EREG, EPAS1, EDN1, S1PR1, DUSP1, TSC22D3, DLX3, CFD, DEFB4A, DEFB1, ACE, COL17A1, CYP2D6, CTNNB1, CCN2, CSHL1, CSF3, CSF2, CRP, CRK, CPOX, COX8A, ESR2, ETS1, FDFT1, FGF2, HLA-DMB, HLA-DMA, HIF1A, GZMB, GSK3B, CXCL1, NR3C1, GRN, GPT, FFAR2, GPR15, CXCR3, GLI3, GCH1, FUT7, FOSB, FOS, FLT4, FLT3, FLNA, FGF7, COMP, COL9A3, TLE1, BIRC3, BLMH, BDNF, ALDH7A1, ATM, ASTN1, ASGR1, ARG1, FASLG, APRT, APOE, BIRC2, COL9A2, ANXA6, ANXA1, ALOX5, ALDH3A2, ALB, AGXT, AGER, AP2A1, ACHE, ABCA1, TSPO, C4A, C4B, C5, COL9A1, LTB4R, ACKR2, CCR6, CHRM3, CHI3L1, CETN1, CD74, CD44, CD40LG, TNFRSF8, CD28, CD27, MS4A1, CD19, CD1B, CD1A, CBS, CASP8, CALR, CALCR, HPR, HSPA1A, HSPA1B, PLAU, PTGDS, PSMD7, KLK7, MAPK8, MAPK3, PREP, POMC, PMS1, PLCB3, PLAUR, PLAT, IFNAR2, PLA2G1B, PIK3CG, PIK3CD, PIK3CB, PIK3CA, CFP, PECAM1, PDCD1, PCSK2, PAPPA, PTPN2, RAC2, PLAAT4, NAT2, TIMP2, THBS1, THBD, TGM3, TGM2, TGFB1, TFAP2A, TEK, TAP1, ADAM17, STK10, STIM1, STAT4, SOD2, SLC6A8, SDC1, CX3CL1, CXCL11, CCL5, SCN8A, S100A7, REG3A, PAEP, OSM, KRT17, JUND, JUNB, JUN, JAK2, JAK1, ITGB1, ITGAE, ISG20, IRF2, IRAK1, IL16, IL15RA, IL15, IL12RB2, IL4R, IL2RA, IL2, IKBKB, RBPJ, CCN1, IFNB1, KRT10, LAMA3, NOTCH1, RPSA, NOS2, CYTB, MRC1, CD200, MMP3, MME, NR3C2, MAP3K11, MIF, MFAP1, MDM2, MCC, MC5R, MC1R, MBL2, SMAD7, LTB, LTA, LGALS9, LEP, LDLR, H3P28
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Lyme Disease
Wikipedia
The incubation period from infection to the onset of symptoms is usually one to two weeks, but can be much shorter (days), or much longer (months to years). [26] Lyme symptoms most often occur from May to September, because the nymphal stage of the tick is responsible for most cases. [26] Asymptomatic infection exists, but occurs in less than 7% of infected individuals in the United States. [27] Asymptomatic infection may be much more common among those infected in Europe. [28] Early localized infection [ edit ] Early localized infection can occur when the infection has not yet spread throughout the body. ... The pain is often described as unlike any other previously felt, excruciating, migrating, worse at night, rarely symmetrical, and often accompanied by extreme sleep disturbance. [31] [33] Mononeuritis multiplex is an inflammation causing similar symptoms in one or more unrelated peripheral nerves. [30] [29] Rarely, early neuroborreliosis may involve inflammation of the brain or spinal cord , with symptoms such as confusion, abnormal gait, ocular movements, or speech , impaired movement , impaired motor planning , or shaking . [29] [31] In North America, facial palsy is the typical early neuroborreliosis presentation, occurring in 5-10% of untreated people, in about 75% of cases accompanied by lymphocytic meningitis. [29] [34] Lyme radiculopathy is reported half as frequently, but many cases may be unrecognized. [35] In European adults, the most common presentation is a combination of lymphocytic meningitis and radiculopathy known as Bannwarth syndrome , accompanied in 36-89% of cases by facial palsy. [31] [33] In this syndrome, radicular pain tends to start in the same body region as the initial erythema migrans rash, if there was one, and precedes possible facial palsy and other impaired movement . [33] In extreme cases, permanent impairment of motor or sensory function of the lower limbs may occur. [28] In European children, the most common manifestations are facial palsy (in 55%), other cranial neuritis, and lymphocytic meningitis (in 27%). [31] In about 4-10% of untreated cases in the U.S. and 0.3-4% of untreated cases in Europe, typically between June and December, about one month (range 4 days-7 months) after the tick bite, the infection may cause heart complications known as Lyme carditis . [36] [37] Symptoms may include heart palpitations (in 69% of people), dizziness , fainting , shortness of breath , and chest pain . [36] Other symptoms of Lyme disease may also be present, such as EM rash, joint aches , facial palsy , headaches , or radicular pain . [36] In some people, however, carditis may be the first manifestation of Lyme disease. [36] Lyme carditis in 19-87% of people adversely impacts the heart's electrical conduction system, causing atrioventricular block that often manifests as heart rhythms that alternate within minutes between abnormally slow and abnormally fast. [36] [37] In 10-15% of people, Lyme causes myocardial complications such as cardiomegaly , left ventricular dysfunction, or congestive heart failure . [36] Another skin condition, found in Europe but not in North America, is borrelial lymphocytoma , a purplish lump that develops on the ear lobe, nipple, or scrotum . [38] Late disseminated infection [ edit ] After several months, untreated or inadequately treated people may go on to develop chronic symptoms that affect many parts of the body, including the joints, nerves, brain, eyes, and heart. ... The abnormalities seen in the SPECT images are very similar to those seen in people with cerebral vacuities and Creutzfeldt–Jakob disease , which makes them questionable. [121] Differential diagnosis [ edit ] Community clinics have been reported to misdiagnose 23–28% of Erythema migrans (EM) rashes and 83% of other objective manifestations of early Lyme disease. [105] EM rashes are often misdiagnosed as spider bites , cellulitis , or shingles . [105] Many misdiagnoses are credited to the widespread misconception that EM rashes should look like a bull's eye. [2] Actually, the key distinguishing features of the EM rash are the speed and extent to which it expands, respectively up to 2–3 cm/day and a diameter of at least 5 cm, and in 50% of cases more than 16 cm.CFH, TLR2, FHL1, HPLH1, CXCL13, POLD3, DCN, HLA-DRB1, PLG, HNRNPD, IFNG, EBPL, ELK3, NUP37, UBXN2B, CDK5R1, HSPD1, CCNH, NT5C2, CD8B, TNF, CDK5R2, CDCA5, ATP6V0D1, MLIP, IL6, CXCL8, IL10, PRH1, CPVL, IL17A, JUN, TLR1, LAMC2, RMRP, RHBDL2, PRH2, MNAT1, IL12A, ANXA1, NRSN1, FCN2, ERVK-19, CD14, UPK3B, AK6, ERVK-9, CSF2, ENO2, EPHA5, KARS1, FN1, VHLL, GCHFR, ABCC11, DCTN3, SENP6, SRRM2, BRD4, RHOBTB2, ERVK-24, PHB2, CD300A, CHP1, ERVK-11, TMED10P1, PPP1R14A, ERVK-25, TMED10, STIP1, PTGES3, IFNL1, SORBS1, IL23R, CAP1, PDLIM7, HACD1, H3P7, H3P17, IL37, R3HCC1L, ERVK-18, LINC01672, SQSTM1, ERVK-7, MAK16, ERVK-8, GOLPH3, SELENOK, RAB22A, FAM20C, PNO1, HLP, ERVK-10, H3P6, NELFCD, TLR8, TLR7, EXOSC1, ERVK-21, RBM45, IL22, NOP53, SGSM3, RBMS3, FOXP3, TGFB1, RNMT, IFNB1, HK1, HLA-A, HMGB1, IFIT3, IFNA1, IFNA13, IGH, FGF1, IL1B, IRF7, KRT10, LNPEP, CD180, MAZ, HIF1A, ENO1, MIP, CD48, CALR, CANX, CD1B, CD28, CD38, CD40, CD68, EEF1A1, CCR7, CRP, MAPK14, CTAA1, DAG1, DYNC1H1, MBL2, MMP1, AOC3, TPT1, ABCC8, TRBV20OR9-2, TFPI, BGN, TLR5, TNFRSF1A, TTN, CXCL11, TUFM, VCAM1, ARHGEF5, YBX3, BLZF1, RRP1, SRI, CCL19, MMP9, MAPK1, MMP13, MPZ, COX1, NFKB1, SERPINB6, PRF1, PTBP1, CCL2, PTGS1, PTGS2, RAB5A, RAD51, RRAS, S100A8, H3P29
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Trapeziometacarpal Osteoarthritis
Wikipedia
Intervention techniques: Kaltenborn Mobilization Technique [24] Maitland's Mobilization [25] Neurodynamic Techniques [26] [27] [28] Kaltenborn mobilization technique [ edit ] The specific Kaltenborn mobilization of posterior-anterior gliding with distraction in grade 3 of the CMC joint; the Convex/Concave Rule was applied in each case. ... At each session, the technique can be applied 3 times for 3 min separated by 1-min rest periods. [28] Surgery [ edit ] If conservative treatment does not reduce the complaints of patients, surgical treatment is indicated. [8] This might be the case when pain persists or when functional disability remains present after conservative treatment.
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Pressure Ulcer
Wikipedia
Guttmann had learned the technique from the work of Boston physician Donald Munro. [28] There is lack of evidence on prevention of pressure ulcer whether the patient is put in 30 degrees position or at the standard 90 degrees position. [29] Nursing homes and hospitals usually set programs in place to avoid the development of pressure ulcers in those who are bedridden, such as using a routine time frame for turning and repositioning to reduce pressure. ... Similarly, there is wide variation in prevalence : 10% to 18% in acute care, 2.3% to 28% in long-term care, and 0% to 29% in home care.IL10, FGF2, VEGFA, HIF1A, ALB, CSF2, PPP1R2C, LAMC2, NHS, IL6, VEGFC, BTBD8, TMSB4X, MMP9, ASIC3, PKD2L1, GIT2, PER2, PLA2G15, ADM, ACSS2, GKN1, CHPT1, NBEAL1, DHDDS, ACCS, HCA1, MIR491, TRPV5, PTGS2, VDR, IL1A, CAMP, CBR1, CD6, CRP, ELN, FLT4, GH1, IL1B, TNF, IL15, JAK2, MMP19, NGF, AGTR1, SLC7A2, TGFB1, MIR885
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Motion Sickness
Wikipedia
Army Research Institute for the Behavioral and Social Sciences in a report published May 1995 titled "Technical Report 1027 – Simulator Sickness in Virtual Environments", out of 742 pilot exposures from 11 military flight simulators, "approximately half of the pilots (334) reported post-effects of some kind: 250 (34%) reported that symptoms dissipated in less than one hour, 44 (6%) reported that symptoms lasted longer than four hours, and 28 (4%) reported that symptoms lasted longer than six hours. ... This technology has been implemented in both standalone devices [26] and Google Glass . [27] [28] In two NIH -backed studies, greater than 90% of people experienced a reduction in the symptoms of motion sickness while using this technology. [25] One promising looking treatment is for to wear LCD shutter glasses that create a stroboscopic vision of 4 Hz with a dwell of 10 milliseconds. [29] Medication [ edit ] Three types of medications are useful: antimuscarinics such as scopolamine , H 1 antihistamines such as dimenhydrinate , and amphetamines such as dexamphetamine . [2] Benefits are greater if used before the onset of symptoms or shortly after symptoms begin. [1] Side effects, however, may limit the use of medications. [2] A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness. [2] [1] Scopolamine is the most effective medication. [1] Evidence is best for when it is used preventatively. [30] It is available as a skin patch . [1] Side effects may include blurry vision. [1] Other effective first generation antihistamines include meclizine , promethazine , cyclizine , and cinnarizine . [1] In pregnancy meclizine and dimenhydrinate are generally felt to be safe. [1] Side effects include sleepiness. [1] Second generation antihistamines have not been found to be useful. [1] Dextroamphetamine may be used together with an antihistamine or an antimuscarinic. [1] Concerns include their addictive potential. [1] Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications. [31] [32] [33] [34] [35] Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail". [36] Alternative medicine [ edit ] Acupuncture has not been found to be useful. [2] Ginger root is commonly thought to be an effective anti-emetic , but it is ineffective in treating motion sickness. [37] Providing smells does not appear to have a significant effect on the rate of motion sickness. [2] Epidemiology [ edit ] Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions.LINC02641, LINC00924, LRP1B, PDZRN4, AUTS2, NLGN1, CPNE4, POU6F2, CELF2, ST18, SDK1, MAP2K5, HOXB-AS3, LINC02607, HOXD3, HOXB3, LINC01241, GPD2, LINC01243, LINC01440, PRDM16, EFHD2, CNR1, CNR2, TRPV1, SMS, MAPK3, HRH1, HNMT, GHSR, CREB1, COPE
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Non-Specific Effect Of Vaccines
Wikipedia
Albert Sabin and is made from live attenuated polioviruses of three serotypes . [22] The first evidence of non-specific effects of OPV was protection by vaccination with OPV of serotype 2 against disease caused by serotype 1 poliovirus without any evidence of cross-neutralization . [23] Vaccination with trivalent OPV helped to stop outbreak of paralytic disease caused by Enterovirus 71 in Bulgaria . [24] In large prospective clinical trials OPV was shown to protect against seasonal influenza and other acute respiratory diseases . [25] [26] Immunization with OPV was also shown to lead to a faster healing of genital herpes lesions. [27] Immunization with OPV was found to reduce all-cause childhood mortality [28] [29] even in the absence of wild poliovirus circulation, hospital admission rate, [30] incidence of bacterial diarrhea , [31] and otitis media . [32] Vaccination with OPV results in Interferon induction that is believed to be the main mediator of the non-specific protective effects of OPV. [33] Measles vaccine [ edit ] Standard titer measles vaccine is recommended at 9 months of age in low-income countries where measles infection is endemic and often fatal. ... PMID 1449986 . ^ Aaby, Peter; Jensen, Henrik; Samb, Badara; Cisse, Badara; Sodemann, Morten; Jakobsen, Marianne; Poulsen, Anja; Rodrigues, Amabelia; Lisse, Ida Marie; Simondon, Francois; Whittle, Hilton (28 June 2003). "Differences in female-male mortality after high-titre measles vaccine and association with subsequent vaccination with diphtheria-tetanus-pertussis and inactivated poliovirus: reanalysis of West African studies" .
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2009 Swine Flu Pandemic
Wikipedia
Officials in Taiwan suggested use of the names "H1N1 flu" or "new flu". [28] The World Organization for Animal Health , an IGO based in Europe, proposed the name "North American influenza". [29] The European Commission adopted the term "novel flu virus". ... In 2011, a study from the US Flu Vaccine Effectiveness Network estimated the overall effectiveness of all pandemic H1N1 vaccines at 56%. A CDC study released 28 January 2013, estimated that the Pandemic H1N1 vaccine saved roughly 300 lives and prevented about a million illnesses in the US. ... King Jr. suggested that every county should create an "influenza action team" to be run by the local health department , parents, and school administrators. [128] By 28 October 2009, about 600 schools in the United States had been temporarily closed, affecting over 126,000 students in 19 states. [129] Workplace [ edit ] Fearing a worst-case scenario, the U.S. ... The patient in the first confirmed case had flu symptoms including fever and cough upon clinical examination on 30 March and the second on 28 March. [175] The first confirmed H1N1/09 pandemic flu death, which occurred at Texas Children's Hospital in Houston, Texas, was of a toddler from Mexico City who was visiting family in Brownsville, Texas , before being air-lifted to Houston for treatment. [176] The Infectious Diseases Society of America estimated that the total number of deaths in the U.S. was 12,469. [177] Data reporting and accuracy [ edit ] See also: GISAID , National Influenza Centers , Disease surveillance , and Clinical surveillance Influenza surveillance information "answers the questions of where, when, and what influenza viruses are circulating.
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Myocarditis
Wikipedia
In young adults, up to 20% of all cases of sudden death are due to myocarditis. [10] Among patients with HIV, myocarditis is the most common cardiac pathological finding at autopsy , with a prevalence of 50% or more. [28] Myocarditis is the third most common cause of death among young adults with a cumulative incidence rate globally of 1.5 cases per 100,000 persons annually. [29] Myocarditis accounts for approximately 20% of sudden cardiac death in a variety of populations. [10] Populations that experience this increased mortality rate include: adults under 40, young athletes, U.S. ... "Viral myocarditis" . Current Opinion in Rheumatology . 28 (4): 383–9. doi : 10.1097/BOR.0000000000000303 .IL6, TNF, CRP, SLC22A3, SLC22A5, SLC22A4, IL10, IL17A, CTLA4, CXCL10, ACE, SPP1, CXCR3, LCN2, IL22, CX3CL1, TNFRSF11B, ICOS, MIF, ADRB2, CYP11B1, STAT6, TNFSF11, TNFRSF11A, PPA2, IL1B, SLC2A10, GPX4, ABCD1, IFNG, SMUG1, LGALS3, CD274, TLR4, IL4, IL1A, NLRP3, STAT3, NOS2, TNNI3, IFNA1, IFNB1, CXADR, TLR3, IFNA13, ATN1, LGALS9, COX2, ITGAL, ITGB2, IL13, IL1RN, HMGB1, NR1I2, MMP9, MMP2, IL37, GJA1, TLR7, NFE2L2, RAG1, IL33, MTCO2P12, MIR98, TSPO, CCL2, MIR155, CD68, CHRNA4, REN, ISYNA1, PTGS2, MAPK1, ITGAM, ESR1, PDCD1, TXN, GABPA, SST, ISG15, AIM2, GRAP2, STAT4, WNT5A, F2RL3, ADAM17, APLN, TACR3, VDR, MAP3K7, UTRN, TLR5, TEAD1, TFPI2, AIMP2, KEAP1, TFPI, TTN, TGFB3, THBS2, THM, ADAM9, TRAF6, THY1, DENR, TNFAIP3, WNT1, ADRB1, NR1I3, TMBIM1, SLC52A2, HDAC11, BCL2L12, PRRT2, EMB, TRIM69, PWAR1, TICAM1, DDX53, IL27, PPP1R42, PWAR4, MALAT1, MIR10A, MIR148A, MIR203A, MIR21, MIR214, MIR215, MIR30A, DEFB103A, MIR146B, MIR181D, CXADRP1, CCR2, MIR208B, KLRC4-KLRK1, NOD2, MYDGF, DNM1L, DEFB103B, EBI3, TRIM13, KLF2, CXCL13, AHSA1, FGL2, MORF4, RIPK3, RASSF1, KLRK1, DAPK2, RNF19A, POLDIP2, SLC17A5, PDCD4, RABGEF1, NOX4, IL21R, FOXP3, SCARA3, GDE1, GPRC5B, IL17D, TLR9, TREM1, TERF2IP, SLC52A1, TRIM21, PRKCA, SPG7, CYP11B2, DSC2, HBEGF, EDN1, EIF4EBP1, MARK2, EPHB2, EPO, ERBB4, ESR2, F2R, F2RL1, F3, F5, FOXO3, FUT4, CBLIF, GJA5, GCLC, GLS, GNAO1, GPX1, GRN, GSR, GZMB, NRG1, DMD, CX3CR1, HLA-DQB1, CTSB, AGT, AKT1, AKT2, APC, APEX1, FAS, FASLG, AQP4, ARR3, ARRB2, ARSB, CXCR5, CA4, CASP3, CASR, CD40, CLU, CREBBP, CRK, CRMP1, MAPK14, CSF1, CSF2, CSF3, CTH, HLA-DQA1, HLA-DQB2, SPARC, CXCL9, MST1, MYBPC3, MYD88, MYH6, NCAM1, NUP98, PAWR, PI3, PPARA, PRKAR1A, PRKCB, MAPK3, MAPK8, MAP2K7, PTPRC, RAP1A, RASGRF1, S100A8, S100A9, SLC2A1, SMN1, SMN2, SNRNP70, SOD1, SOS1, MSN, MEFV, HMGA1, MDK, HMOX1, HSPA4, HSPB1, IDS, IFNA2, IFNGR1, IFNGR2, IGHMBP2, IL3, CXCL8, TNFRSF9, ILK, INS, IRF1, IRF3, IRF5, ITGAX, ITK, JAK2, KIT, KLRB1, LAG3, MAS1, MB, MBP, ORI6
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Havana Syndrome
Wikipedia
The fact that, as of February 2019 [update] , there was no knowledge of the cause of “Havana syndrome” had made it challenging for the RCMP to investigate. [28] In 2019, the government of Canada announced that it was reducing its embassy staff in Havana after a 14th Canadian diplomat reported symptoms of Havana syndrome in late December 2018. [29] In February 2019, several Canadian diplomats sued the Canadian government, arguing that it failed to protect them or promptly address serious health concerns. [30] [31] The government has sought to dismiss the suit, arguing in November 2019 that it was not negligent and did not breach its duties to its employees. ... Retrieved October 1, 2017 . ^ "U.S. says another American suffers illness at its Cuba embassy" . Reuters . June 28, 2018 . Retrieved July 3, 2018 . ^ Hurley, Dan (March 22, 2018). ... June 6, 2018. ^ Dorsey, Steve (November 28, 2017). "Uzbekistan incident raises suspicions of Russian involvement in Cuba attacks" .
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Myotonic Dystrophy
Wikipedia
History [ edit ] Myotonic dystrophy was first described by a German physician, Hans Gustav Wilhelm Steinert , who first published a series of 6 cases of the condition in 1909. [27] Isolated case reports of myotonia had been published previously, including reports by Frederick Eustace Batten and Hans Curschmann, and Type 1 myotonic dystrophy is therefore sometimes known as Curschmann-Batten-Steinert syndrome. [28] The underlying cause of type 1 Myotonic dystrophy was determined in 1992. [2] References [ edit ] ^ a b c d e f g h i j k l m n o p q r s t u v w x "myotonic dystrophy" . ... Archived from the original on 2017-01-28. updated 2013 ^ Liquori CL, Ricker K, Moseley ML, Jacobsen JF, Kress W, Naylor SL, Day JW, Ranum LP (August 2001).DMPK, CNBP, NKX2-5, CELF1, MBNL1, CCT3, APOC2, INSR, SIX5, CKM, ERCC1, CLCN1, FXN, RANGAP1, PRKCA, HCRT, PRRT2, DMD, BUB1, PRKCB, POMC, NEK6, DMWD, MAPT, ACTB, CEBPD, MBNL2, SCN4A, TNF, QPCT, KCNN3, TNNI3, IGHD1-7, MSH3, UGT8, OXA1L, PLCB1, PGD, SCN5A, CDC42BPB, ALB, RAN, REM1, TNNT1, GH1, FSD1L, FSD1, BCL3, APOC1, MIR206, BIN1, GSK3B, CLIP2, MAK16, GGTLC1, RIDA, BPIFA2, OPN1MW3, OPN1MW2, SLC35G1, ROCK2, WASL, MTMR1, C9orf72, CTCF, CDC42BPA, DYSF, ST8SIA4, MIR29C, CELF2, RAB6B, FAM107B, ASB2, TNFRSF12A, TP53, RBFOX1, NAT10, IGHD1-14, DESI1, RBMS3, PDLIM3, FGF21, PNO1, ATRNL1, JPH3, MMD, CELF6, SRRM2, GGCT, ASRGL1, SPEN, LDB3, RSPH6A, RAB1B, CCL27, RAP2B, TCF4, CYP2B6, KCNQ1, IL6, IGLC3, GPR4, GHRH, OPN1MW, GC, FRAXE, FEN1, F5, DDX6, DDX5, CYP2A13, MEF2A, CYP2A7, CYP2A6, CDC42, CD59, CCND3, ATP1A3, ATHS, ARF3, APOE, AMPH, AMH, ALPP, LDLR, MEF2C, SYN1, PSPH, STXBP3, SRF, SLPI, SLC1A2, SRSF2, ATXN1, CLIP1, RRAS, ROCK1, REG1A, RAP1B, PTBP1, PSPN, ATXN3, PRNP, PRKCG, PRKAB1, PRKAA2, PRKAA1, PEPD, MYOG, MTM1, MSMB, MSH2, MRC1, MLH1, LOC102724197
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Hypersexuality
Wikipedia
Persons suffering from injuries to this part of the brain are at increased risk for aggressive behavior and other behavioral problems including personality changes and socially inappropriate sexual behavior such as hypersexuality. [26] The same symptom can occur after unilateral temporal lobotomy . [27] There are other biological factors that are associated with hypersexuality such as premenstrual changes, and the exposure to virilising hormones in childhood or in utero. [28] In research involving the use of antiandrogens to reduce undesirable sexual behaviour such as hypersexuality, testosterone has been found to be necessary, but not sufficient, for sexual drive. [28] Other proposed factors include a lack of physical closeness and forgetfulness of the recent past. [29] Pathogenic overactivity of the dopaminergic mesolimbic pathway in the brain—forming either psychiatrically, during mania , [30] or pharmacologically, as a side effect of dopamine agonists , specifically D 3 -preferring agonists [31] [32] —is associated with various addictions [33] [34] and has been shown to result among some in overindulgent, sometimes hypersexual, behavior. [30] [31] [32] HPA axis dysregulation has been associated with hypersexual disorder. [35] The American Association for Sex Addiction Therapy acknowledges biological factors as contributing causes of sex addiction.
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Scabies
Wikipedia
Less commonly, scabies infestation can happen through the sharing of clothes, towels, and bedding, but this is not a major mode of transmission; individual mites can survive for only two to three days, at most, away from human skin at room temperature. [25] [26] As with lice, a latex condom is ineffective against scabies transmission during intercourse, because mites typically migrate from one individual to the next at sites other than the sex organs. [27] Healthcare workers are at risk of contracting scabies from patients, because they may be in extended contact with them. [28] Pathophysiology [ edit ] The symptoms are caused by an allergic reaction of the host's body to mite proteins, though exactly which proteins remains a topic of study. ... November 2, 2010. Archived from the original on 28 April 2015 . Retrieved 18 May 2015 . ^ a b c d e f g h i j k l m n o p q r Andrews RM, McCarthy J, Carapetis JR, Currie BJ (December 2009). ... Archived from the original on 2010-02-26 . Retrieved 2009-07-28 . ^ "Uganda: Out of the Wild" . Frontline .
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Psoriasis
Wikipedia
This can result in a sausage-shaped swelling of the fingers and toes known as dactylitis . [26] Psoriatic arthritis can also affect the hips, knees, spine ( spondylitis ), and sacroiliac joint ( sacroiliitis ). [28] About 30% of individuals with psoriasis will develop psoriatic arthritis. [12] Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases. [27] Nail changes [ edit ] Psoriasis of a fingernail, with visible pitting A photograph showing the effects of psoriasis on the toenails Psoriasis can affect the nails and produces a variety of changes in the appearance of finger and toe nails. ... Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy. [43] In those with long-term, well-controlled psoriasis, new HIV infection can trigger a severe flare-up of psoriasis and/or psoriatic arthritis. [ medical citation needed ] Microbes [ edit ] Psoriasis has been described as occurring after strep throat , and may be worsened by skin or gut colonization with Staphylococcus aureus , Malassezia spp., and Candida albicans . [44] Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection (tonsillitis or pharyngitis). [17] Medications [ edit ] Drug-induced psoriasis may occur with beta blockers , [10] lithium , [10] antimalarial medications , [10] nonsteroidal anti-inflammatory drugs , [10] terbinafine , calcium channel blockers , captopril , glyburide , granulocyte colony-stimulating factor , [10] interleukins , interferons , [10] lipid-lowering medications , [14] : 197 and paradoxically TNF inhibitors such as infliximab or adalimumab . [45] Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect . [46] Mechanism [ edit ] Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin . [47] Abnormal production of skin cells (especially during wound repair ) and an overabundance of skin cells result from the sequence of pathological events in psoriasis. [16] The sequence of pathological events in psoriasis is thought to start with an initiation phase in which an event (skin trauma, infection, or drugs) leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease. [31] [17] Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days. [48] These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells , macrophages , and T cells (three subtypes of white blood cells ). [12] [39] These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as interleukin-36γ , tumor necrosis factor-α , interleukin-1β , interleukin-6 , and interleukin-22 . [31] [49] These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate. [31] One hypothesis is that psoriasis involves a defect in regulatory T cells , and in the regulatory cytokine interleukin-10 . [31] The inflammatory cytokines found in psoriatic nails and joints (in the case of psoriatic arthritis) are similar to those of psoriatic skin lesions, suggesting a common inflammatory mechanism. [17] Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of psoriasis. [50] [51] Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis [52] and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α. [52] In response to these chemical messages from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signal downstream inflammatory cells to arrive and stimulate additional inflammation. [31] Dendritic cells bridge the innate immune system and adaptive immune system .CARD14, STAT3, VEGFA, ERAP1, TYK2, IL12B, IL23R, TRAF3IP2, TNFAIP3, TNIP1, IL13, RNF114, NOS2, IFIH1, GJB2, DDX58, FBXL19, CSMD1, SERPINB8, HLA-C, LCE3B, LCE3C, IL23A, TNF, IL1B, IL4, IL6, TP53, CRP, S100A7, IL36RN, TGFA, APOE, REL, CSF2, PPARG, ZNF816, CAT, IFNLR1, PCNA, NFKBIA, PTTG1, RUNX3, MKI67, REN, VNN3, LCE3D, VNN1, SOD2, HCAR2, TAGAP, VNN2, CYP2S1, CARM1, AP1S3, ZC3H12C, CP, ITGB2, TTC7A, IL19, SPTLC2, HLA-B, IL10, ARPC4, CCHCR1, PDE4A, PTPN22, NFKB1, NOD2, TLR4, RUNX1, TNFSF15, IL2RA, COG6, IL27, HCP5, ITGAL, CDKAL1, GATD3A, AHR, NOTCH1, TNFRSF1A, CD40, NFATC1, FUT2, ERAP2, AIM2, ZMIZ1, CD226, SPATA2, ANKRD55, SMAD3, CD6, JAZF1, IL1R1, STAT2, FNDC3A, BTD, BANK1, ZGLP1, PRKRA, PTPN2, TNFRSF6B, ZNF365, GLYAT, F9, KLRC1, FNBP1, SBNO2, SYNE2, PLCL2, FLG, ESR2, RAD50, PSORS4, ERN1, PKIG, ADGRL2, MYT1L, CLEC16A, PARK7, SLC9A8, ATXN2L, CRB1, UBBP4, SP140, DNAJB4, FGFR1OP, POLI, USP49, IL17RA, BPTF, ETS1, ELOA, SH2B3, PTPRN2, SUOX, STK11, SON, SLIT3, ATXN2, RPS26, RPS6KB1, REV3L, REG1A, IFNG, IFNGR2, RDX, IL1A, HLA-DRB1, IL6R, MAPK1, CXCL8, PRKCQ, PRKCB, PLAU, IL15, IL17A, IL18, NPPA, MST1, MGMT, ICAM5, HLA-DQA1, ELMO1, ATG5, NR5A2, KEAP1, SCRN1, ZFYVE16, SETD1A, PRORP, GART, IKBKE, GBAP1, RGS6, NPEPPS, GCKR, GNA12, HLA-A, OSMR, FIBP, SKAP2, GPR35, BSN, ACAD8, ASAP2, KSR1, IL18R1, TNFRSF14, VDR, UBE2L3, GPR183, GPR160, DENND1B, LRRC43, SLC39A11, TMEM258, MYRF, TRIM65, HIPK1, ITPRID1, BLOC1S2, CAMK2G, FAM177A1, CAVIN1, LURAP1L, PUDPP2, PRDM1, UBAC2, IL37, CAMP, FLG-AS1, ZNF831, ANTXR2, NXPE1, LRRK2, NRAD1, ZPBP2, RAVER1, RBM45, RNF145, LINC01620, CASR, PUS10, CMC1, LINC02085, CAST, C17orf67, IRGM, STX1B, ADCY7, TH2LCRR, LINC00824, LINC01147, LINC00993, LINC02863, CCR5AS, ADCY3, CHROMR, LINC01714, LINC02571, ACTA2, LINC01932, ACO1, H3P13, LINC01250, IFNG-AS1, LINC02213, TRAF3IP2-AS1, C1orf141, LINC01185, TEX41, MIR146A, IRF1-AS1, KPRP, LINC00598, RTEL1-TNFRSF6B, INS-IGF2, C1orf68, SPATA48, ELOA-AS1, ALDH2, ZNF816-ZNF321P, RMI2, KRT17, IL17F, UBASH3A, ELOVL6, CHST8, DAP, CARD9, DAG1, FOXP3, IGF2-AS, TLR7, HDAC7, KLF13, GAL3ST2, THADA, CPEB4, BACH2, IL21, CREM, GIPC2, RASIP1, FAM118A, PPP2R3C, ATG16L1, RIC8B, INAVA, EXOC2, CS, CLCN6, IL22, DELEC1, MFSD4B, IL17B, ANKRD30A, AP5B1, DNMT3A, KCNH7, UQCR10, NKD1, MYPN, CFL1, DONSON, PAK5, IL20, KIAA1109, QTRT1, CDKN2A, TSPAN14, CDKN2D, CDSN, NDFIP1, ACE, PIK3CG, MTHFR, IL9, PIK3CD, IL17C, LEP, EGF, EIF2AK1, CCL2, CCRL2, S100A9, TGFB1, PIK3CA, IL2, PIK3CB, CCR6, DEFB4A, HT, TLR2, ADIPOQ, TRBV20OR9-2, TP63, CCL27, PRL, IL1RL2, MIR21, MIR31, JAK1, TEK, AREG, PI3, DEFB4B, TAP1, EGFR, MICA, PSORS1C1, IFNA13, ADAM33, TSLP, IFNA1, IL33, S100B, IL1RN, S100A8, CCL20, IGF1, NLRP3, IL24, SIRT1, RPSA, SLCO6A1, LCN2, NGF, IL1F10, H3P28, EBNA1BP2, RABEPK, TAC1, ARHGEF2, GSTK1, ARMH1, RETN, MIR155, MIR203A, PSMD7, MAPK3, CCL17, SLC2A1, TLR9, PSORS6, STAT4, PON1, PSORS9, LANCL1, H3P10, GOT2, CHI3L1, AKT1, EDN1, GSTM1, CXCL10, MAPK14, TIMP3, NXF1, PLAAT4, CSTA, HMOX1, FLNB, HLA-DPB1, TNFRSF1B, POLDIP2, AHSA1, ADAM17, HMGB1, S100A1, MTX1, MAPK8, SOAT1, FCGR3A, SLC22A4, MYDGF, FGF7, SELE, CRK, CCL22, CCL5, CCND1, S100A7A, ADAMTSL5, SERPINB3, CD79A, GRAP2, ACR, CXCL1, GRN, KIR2DS1, USO1, KRT16, NFKBIZ, CCR5, GSTT1, MIR223, MIR99A, LOC102724971, PPARD, JUN, AIMP2, KYNU, RNF19A, PSORS5, WNT5A, SEC14L2, LOC102723407, DEFB103A, DEFB104B, ANXA6, SERPINA1, CXCR2, IFI27, IFN1@, CSF3, DEFB103B, APOB, POU5F1, RARRES2, CCL4L1, APOA1, TREX2, KLK7, HP, IL36G, CD1D, ZNF750, SOCS3, SLC9A3R1, GATA3, RIPK1, MBTPS1, GSTM2, CDR3, ACKR2, FOSL1, FZD5, TRPV1, FN1, HIF1A, SLURP1, CD1A, DEFB104A, TGM1, CASP1, CALCA, TAP2, PSORS1C2, CA2, HES1, CRH, C4B, C4A, HSP90AA1, PECAM1, CAV1, DUSP1, LTA, JUNB, TLR8, LGALS3, IL17D, LOXL2, OPRM1, CCR2, HPGDS, KDR, MMP2, AGER, IVL, GATD3B, PSORS1C3, CXCL9, MIF, ITGAX, LORICRIN, KIR3DL1, ITGAE, ISG20, NFE2L2, NF1, PIPOX, FLT4, SLC22A5, HLA-DOA, ACE2, HRH4, NLN, OR2AG1, CLDN3, SEMA3A, CPQ, S100A14, TIMP1, HAX1, TGM3, TGM2, HBEGF, MMP9, PDPN, TFPI, SYT1, HNRNPA1, ITGAM, MUC1, RPTOR, ALB, C5AR1, ABCC1, MRC1, STAT1, TRIM21, TSC22D3, SPP1, SOX9, MIB1, GNLY, FOXO1, AGT, DUT, TNFRSF4, ISYNA1, JAK2, CD14, GABPA, JUND, TNFSF10, GCG, SLC12A8, GORASP1, DEFB1, IL25, CCL4L2, ACD, GEM, CYP24A1, NR1I2, WNK1, ABCG2, KRT14, BCL10, CYP27A1, TGM5, IL32, CYP27B1, MYOM2, CCR10, CCR4, PCLAF, CD69, NR1H3, UBE2N, UVRAG, CD27, SHBG, FOS, VIP, CD274, MC1R, IL22RA2, TNFSF8, FOSB, LPA, CD34, MBL2, AKT3, CMKLR1, DPP4, OPN4, CCR7, ACTB, CD40LG, ROBO3, SLC6A4, S100A4, COPD, IFI16, ETFA, TRIM32, TNFRSF11B, KLK6, DKK1, CTNNB1, F2RL1, SLC52A1, PTEN, MIR126, CTLA4, FABP4, CCN1, OLR1, ANGPT2, RBP1, WDHD1, IL26, NT5E, RELA, ANGPT1, FCGR2A, RPE65, IL4R, IL7, ESR1, SLCO1C1, PDE3A, PDCD1, MIR424, CYP1A1, ABCB1, ELANE, REG3A, CX3CR1, IL12RB2, CTSS, PLAT, CXCR1, MIR17HG, QPCT, PLG, POMC, KLK5, EPAS1, IL20RB, MIR210, ORM1, CTSG, NOTCH4, OAS2, LCE3A, BDNF, SELP, SAA1, FGF2, SAA2, CX3CL1, CKAP4, FCGR3B, S1PR1, SELPLG, CXCL11, SERPINB4, HTR2A, IRF5, CCL4, C4B_2, MALT1, NAT9, CCL19, IRF2, NOTCH2, NOS3, BSG, BTNL2, BCL2, IFNL1, IRF1, CTSL, MUL1, CRHR2, CLEC7A, TREM1, MAVS, NAA16, NBAS, DUOX1, SLC12A9, DGCR8, CCR1, AKR1B10, CKLF, FYCO1, MED15, CLU, CYBB, RIPK4, IL17RD, PSORS7, TET2, KIR2DL5A, LYNX1, MARCKSL1, PGLYRP4, PIAS4, CYLD, CLC, CTSV, CRHR1, TNFRSF12A, IL20RA, CYP2E1, CYP3A4, CYP2D6, COX8A, CST6, TRMO, CYP2B6, PROK2, SUGP1, SCLY, ACOT13, CRABP1, IL22RA1, TNFAIP8L2, JAM2, ZC4H2, SULF2, CXCL16, WDR11, TRIB3, SPHK2, ITLN1, CTSB, AZI2, CD244, CYP2C19, GRHL3, CALML5, POMP, SUCO, MOCOS, CNR1, ATOD1, COMT, SEMA6A, NCOA5, CCN2, PRO2268, MSX2P1, NANS, KIR3DL2, CHRNA4, MIR193B, APP, MIR17, MIR187, MIR197, MIR19A, MIR20A, MIR221, BIRC2, TNFSF12-TNFSF13, SLURP2, MXRA7, MIR330, MIR340, MIR369, ANXA2, PLF, WG, PRR9, MIR146B, APRT, MIR145, MIR143, C10orf99, ATP5F1A, ASIP, TICAM2, STS, ARG1, IL31, SUMO4, NPSR1, RTL1, MIR130A, AQP3, AQP1, FASLG, FAS, MIRLET7B, MIR122, MIR125A, MIR125B1, MIR492, MIR486-1, CLMN, POU5F1P3, MIR4516, AHCY, AGTR1, JAG1, ADRA1B, PARP1, MIR6731, ADH1B, ADCYAP1, ADA, LINC02210-CRHR1, UPK3B, LOC110806262, LYNX1-SLURP2, LINC02605, H3P9, ACACA, H3P23, AOC1, COMMD3-BMI1, ALOX12, PWAR6, MIR744, ANXA1, POU5F1P4, SLC25A5, NME1-NME2, HNRNPA1P10, ANPEP, POTEF, MIR876, C20orf181, ALOX15, AMH, CD24, KLLN, PRINS, ALOX15B, MIR320B1, TMED7-TICAM2, AAA1, HCP5B, LINC01193, BCL3, LINC02693, IL17RC, CDC6, CD68, CD59, CD47, ENTPD1, DMKN, MUC16, CD38, SCARB1, CDCA5, PIK3IP1, TXNRD3, PGLYRP3, TNFRSF13C, TNFRSF8, CD86, CD28, CD19, CDH13, RNASE7, SPINK7, CEBPD, VASH2, EHMT1, WLS, GRHL2, NAA25, ZC3H12A, SCUBE1, CETN1, SLC38A1, CDK2, CDKN2B, SHARPIN, CDKN1A, TLCD3B, ANGPTL6, STK40, CDK5, CDK4, CD1C, OSCP1, CD1B, BMX, KIAA1324L, VAMAS6, C3, IPMK, CADM2, BST2, PCSK9, TAB3, BMP6, CACNA1A, CXCL17, SLC9C2, TCAIM, HCG22, BMP4, BMI1, CFB, TNFRSF17, VPS51, OLIG3, CCNB1, YDJC, CCKBR, PSORS8, CCKAR, CCK, TEPSIN, B3GNTL1, GLIS1, SDF4, CASP5, SLC25A20, PLB1, CASP3, FGD5, CAPN1, AMOT, CBLL2, SPRED1, C16orf82, HSPA14, NES, TMED7, SEA, RPA1, RYR1, S100A2, ID4, ID1, ICAM1, S100A12, IARS1, TSPAN31, MSMO1, HTR3A, SCN7A, CCL3, CCL7, HTR1A, HTC2, CCL21, CXCL5, SDC1, TRIM27, RENBP, IFNAR1, PTPN11, PSMB9, IL1RAP, PSMD9, PTH, PTGS1, PTPN1, IGH, PTPN6, PTPRC, IFNB1, PTX3, PZP, MOK, RARA, RARRES1, RBP4, IGF2, IGF1R, CXCL12, SETMAR, SOST, SFRP4, TCF3, TCF7L2, TCF19, TRGV5, HLA-G, HLA-E, THBS1, TIMP4, HLA-DRB5, TLE1, TLR1, HLA-DQB1, HLA-DQA2, HLA-DMB, TNNT1, TNXB, HLA-DMA, TPM1, TPM2, NAT2, TBCC, TAZ, SOD3, SFTPD, ST6GAL1, HSPD1, SLC22A1, SLPI, SNAI1, SNRNP70, HSPB2, HSPB1, TAT, SRF, HSPA1B, HSPA1A, STAT6, AURKA, HOXA5, TAL1, FOXA1, PSMB8, PSAP, IL3, MAPK9, MMP10, MMP12, MMP19, MNAT1, CD200, COX2, MYD88, NAGLU, NAP1L1, NCAM1, NEDD8, NFATC2, NFATC4, NFKBIL1, IRF3, NHS, NM, NME1, NME2, MMP8, MME, MGST2, LRP6, KLK1, KLRC2, KRT7, KRT10, LAG3, LAMP1, LGALS1, LNPEP, LRP5, MGAT5, LYN, LYZ, SMAD2, SMAD7, MCAM, SMCP, MDM2, MFAP1, IRAK1, NRTN, NTRK1, PLCD1, IL16, IL15RA, IL13RA2, IL13RA1, PKD1, PLA2G1B, PLA2G2A, IL12RB1, POLR2G, PHB, IL12A, PPARA, IL9R, PPBP, PPP3R1, PPP6C, PRELP, PRKCZ, TNFRSF9, PGR, NTS, SERPINB2, NTSR1, NR4A2, OPRK1, OSM, OXA1L, P2RX7, FURIN, SERPINE1, CNTN3, PGF, PRKN, INSRR, PDC, PDE4B, PDE4D, PDE7A, SERPINF1, PF4, TPO, TRAF6, TRPC6, DDX39A, LYVE1, SUB1, RAB40B, COPS5, SPINK5, KLK11, LILRA3, EFEMP1, SLC7A9, PWP1, FANCE, FABP7, KLK8, FABP1, TREX1, F13A1, COPE, IKZF3, NLRP1, FCN2, HPSE, NCKAP1, TACC2, SPRY2, TRAIP, FLT1, TLR6, FOXO3, SEMA4D, ZNRD2, MRPL28, SLCO1B1, KIR3DS1, POSTN, KHDRBS3, FOXC1, DCTN6, TNFSF13B, B3GNT2, PTTG2, MASP2, F3, EZH2, CD93, NXT1, EHF, SLC17A5, EDA, ECM1, IL36B, ATN1, R3HCC1L, TRAJ23, TBK1, OPTC, DNASE1, DLAT, DHFR, CRNN, AKR1C1, IL21R, DBH, TAS2R13, FGF21, TES, STAB1, TNFRSF13B, EPHB2, ENG, EMP1, DMXL2, SATB2, ELN, SERPINB1, BRD4, SMUG1, PCDHGA12, EIF4E, PLXNB2, EGR1, SH3BP4, TFIP11, PRDX5, LPAR1, PNISR, FLT3, LHFPL6, TXK, PDZK1IP1, NR0B2, GALR3, HAT1, LMO4, GSTP1, TNFSF11, AOC3, AKR1C3, SOCS1, TNFSF12, GSK3B, TNFRSF11A, TNFRSF10B, CXCL2, NRP1, CD84, GGH, GRIN1, CDK5R1, PLA2G10, FZD8, NRIP1, WT1, TYR, CFH, UGT8, VCAM1, GZMB, GZMA, WNT7B, WNT10B, XBP1, FGF23, YWHAZ, ZFP36, ZNF148, CXCR4, PSORS3, DDX39B, PLA2G7, NR4A3, APLN, GPX4, GPX1, MTOR, RNF7, AATK, ISG15, GAPDH, IFI6, BMS1, FZD2, ACKR1, FPR2, NAPSA, FAM20B, FGF19, FOSL2, ACOT8, TANK, EDIL3, BCAP31, EBI3, GCHFR, GH1, SPHK1, USP2, FFAR2, MCHR1, BAIAP3, BTRC, HSPB3, PGLYRP1, GPR15, GPRC5A, SYNGR1, CBLIF, CXCR3, LRRFIP1, GLP1R, RPS6KA5, MAPKAPK2, CD163, PPIG, GJA1, NAT1
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Hyponatremia
Wikipedia
These two act in concert to raise the serum sodium to the normal range. [26] [27] [28] Hyponatremia [ edit ] Hyponatremia occurs 1) when the hypothalamic-kidney feedback loop is overwhelmed by increased fluid intake, 2) the feedback loop malfunctions such that ADH is always "turned on", 3) the receptors in the kidney are always "open" regardless of there being no signal from ADH to be open; or 4) there is an increased ADH even though there is no normal stimulus (elevated serum sodium) for ADH to be increased. ... Nephrology Dialysis Transplantation . 28 (9): 2277–83. doi : 10.1093/ndt/gft023 .AVP, TRPV4, OXT, IFNG, AVPR2, CA12, SCNN1G, NR3C2, CYP11B2, SCNN1A, TBX19, SARS2, SAMD9, TDP2, ELP1, HMBS, HSD3B2, BSND, MC2R, STAR, SCNN1B, NFKB2, NNT, OCRL, SLC26A3, REN, TXNRD2, MAGED2, SCN4A, PRF1, NUP214, CLCNKA, NR0B1, CLCNKB, MRAP, PLVAP, ALB, CPOX, CTNS, CYP11A1, CYP11B1, AQP2, CRP, POMC, AGT, CYP2D6, RAPGEF5, ACE, LGI1, APLN, GH1, IL6, EMP1, HCRT, CSF2, LAMC2, CORO7, MALAT1, PGR-AS1, SGSM3, SLC33A1, SLC17A5, NPS, ERAL1, CPP, COPD, CLDN16, KLHL40, FOXP2, TBC1D9, ACCS, CNTNAP2, NBEAL2, PLA2G15, ACSS2, ADD1, TYMS, ESR1, AGTR1, AQP1, AQP4, ATM, BDNF, BRAF, CD19, CFTR, CMM, COMT, CORT, CSF3, DMBT1, ERCC2, FGA, TCF21, GPT, HCRTR1, HSD11B2, HSP90AA1, KCNJ1, NPPB, ABCB1, MAP2K7, RORC, RYR1, SCT, SLC2A1, SLC6A2, SLC6A3, LOC107987479
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Tumefactive Multiple Sclerosis
Wikipedia
In particular, it has been found that switching from standard MS therapies to fingolimod can trigger tumefactive lesions in some MS patients [27] [28] [29] [30] While standard multiple sclerosis process has an autoimmune response after the breach of the blood-brain barrier , in tumefactive MS things do not process in the same way, and demyelinating lesions do not always show antibody damage. ... "Managing the Symptoms of Multiple Sclerosis: A Multimodal Approach". Clinical Therapeutics . 28 (4): 445–460. doi : 10.1016/j.clinthera.2006.04.005 .
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Sick Building Syndrome
Wikipedia
For example, higher light intensity was significantly related to skin dryness, eye pain, and malaise. [21] Higher temperature has also been found to correlate with symptoms such as sneezing, skin redness, itchy eyes and headache, while higher relative humidity has been associated with sneezing, skin redness, and pain of the eyes. [21] In 1973, in response to the oil crisis and conservation concerns, ASHRAE Standards 62-73 and 62-81 reduced required ventilation from 10 cubic feet per minute (4.7 L/s) per person to 5 cubic feet per minute (2.4 L/s) per person, but this was found to be a contributing factor to sick building syndrome. [27] As of the 2016 revision, ASHRAE ventilation standards call for 5 to 10 cubic feet per minute of ventilation per occupant (depending on the occupancy type) in addition to ventilation based on the zone floor area delivered to the breathing zone. [28] Psychological factors [ edit ] One study looked at commercial buildings and their employees, comparing some environmental factors suspected of inducing SBS to a self-reported survey of the occupants, [29] finding that the measured psycho-social circumstances appeared more influential than the tested environmental factors. [30] Limitations of the study include that it only measured the indoor environment of commercial buildings, which have different building codes than residential buildings, and that the assessment of building environment was based on layman observation of a limited number of factors. [ citation needed ] Research has shown that SBS shares several symptoms common in other conditions thought to be at least partially caused by psychosomatic tendencies. ... "Norovirus" . Clinical Microbiology Reviews . 28 (1): 134–164. doi : 10.1128/CMR.00075-14 .
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Abortion In The United States
Wikipedia
It also prohibited producing or publishing information pertaining to the procurement of abortion or the prevention of conception or venereal disease , even to medical students. [28] The production, publication, importation, and distribution of such materials was suppressed under the Comstock Law as being obscene, and similar prohibitions were passed by 24 of the 37 states. [29] In 1900, abortion was a felony in every state. ... Viability is usually placed at about seven months (28 weeks) but may occur earlier, even at 24 weeks". ... According to the Guttmacher Institute, "more than 7 in 10 U.S. women obtaining an abortion report a religious affiliation (37% protestant, 28% Catholic, and 7% other), and 25% attend religious services at least once a month. ... (Data source: Centers for Disease Control and Prevention) Safety of abortions [ edit ] See also: Abortion § Safety In the US, the risk of death from carrying a child to term is approximately 14 times greater than the risk of death from a legal abortion. [125] The risk of abortion-related mortality increases with gestational age, but remains lower than that of childbirth through at least 21 weeks' gestation. [126] [127] [128] Public opinion [ edit ] See also: Societal attitudes towards abortion , United States abortion-rights movement , and United States anti-abortion movement Trend percent of Americans self-identifying as either "pro-life" or "pro-choice" Americans have been equally divided on the issue; a May 2018 Gallup poll indicated that 48% of Americans described themselves as "pro-choice" and 48% described themselves as "pro-life". [ citation needed ] A July 2018 poll indicated that 64% of Americans did not want the Supreme Court to overturn Roe vs. Wade, while 28% did. [129] The same poll found that support for abortion being generally legal was 60% during the first trimester, dropping to 28% in the second trimester, and 13% in the third trimester. [130] Support for the legalization of abortion has been consistently higher among more educated adults than less educated, [131] and in 2019, 70% of college graduates support abortion being legal in all or most cases, compared to 60% of those with some college, and 54% of those with a high school degree or less. [132] In January 2013, a majority of Americans believed abortion should be legal in all or most cases, according to a poll by NBC News and The Wall Street Journal . [133] Approximately 70% of respondents in the same poll opposed Roe v. ... Since the 2011 poll, support for legal abortion during the first trimester has declined. 2018 Poll 2012 Poll 2011 Poll 2003 Poll 2000 Poll 1996 Poll Legal Illegal Legal Illegal Legal Illegal Legal Illegal Legal Illegal Legal Illegal First trimester 60% 34% 61% 31% 62% 29% 66% 35% 66% 31% 64% 30% Second trimester 28% 65% 27% 64% 24% 71% 25% 68% 24% 69% 26% 65% Third trimester 13% 81% 14% 80% 10% 86% 10% 84% 8% 86% 13% 82% By circumstance or reasons [ edit ] According to Gallup's long-time polling on abortion, the majority of Americans are neither strictly "pro-life" or "pro-choice"; it depends upon the circumstances of the pregnancy.
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Foot Binding
Wikipedia
Women, their families and their husbands took great pride in tiny feet, with the ideal length, called the "Golden Lotus", being about 3 Chinese inches ( 寸 ) long, around 11 centimetres (4 in) in Western measurement. [25] [26] This pride was reflected in the elegantly embroidered silk slippers and wrappings girls and women wore to cover their feet; these shoes also served as support, as some women with bound feet might not have been able to walk without the support of their shoes, and thus would have been severely limited in their mobility. [27] Women with bound feet who wore handmade shoes would also show that she was good at her craft. [28] However, many women with bound feet were still able to walk and work in the fields, albeit with greater limitations than their non-bound counterparts. ... Reform-minded Chinese intellectuals began to consider footbinding to be an aspect of their culture that needed to be eliminated. [38] In 1883, Kang Youwei founded the Anti-Footbinding Society near Canton to combat the practice, and anti-footbinding societies sprang up across the country, with membership for the movement claimed to reach 300,000. [39] The anti-footbinding movement, however, stressed pragmatic and patriotic reasons rather than feminist ones, arguing that abolition of footbinding would lead to better health and more efficient labour. [33] Reformers such as Liang Qichao , influenced by Social Darwinism , also argued that it weakened the nation, since enfeebled women supposedly produced weak sons. [40] At the turn of the 20th century, early feminists , such as Qiu Jin , called for the end of foot binding. [41] [42] Many members of anti-footbinding groups pledged to not bind their daughters' feet nor to allow their sons to marry women with bound feet. [35] [43] In 1902, the Cixi issued an anti-foot binding edict, but it was soon rescinded. [44] In 1912, the new Republic of China government banned foot binding, though the ban was not actively implemented, [45] and leading intellectuals of the May Fourth Movement saw foot binding as a major symbol of China's backwardness. [46] Local warlords such as Yan Xishan in Shanxi engaged in their own sustained campaign against foot binding with feet inspectors and fines for those who continued with the practice, [45] while regional governments of the later Nanjing regime also enforced the ban. [32] The campaign against foot binding was very successful in some regions; in one province, a 1929 survey showed that whereas only 2.3% of girls born before 1910 had unbound feet, 95% of those born after were not bound. [47] In a region south of Beijing , Dingxian , where over 99% of women were once bound, no new cases were found among those born after 1919. [48] [49] In Taiwan, the practice was also discouraged by the ruling Japanese from the beginning of Japanese rule , and from 1911 to 1915 it was gradually made illegal. [50] The practice lingered on in some regions in China; in 1928, a census in rural Shanxi found that 18% of women had bound feet, [29] while in some remote rural areas such as Yunnan Province it continued to be practiced until the 1950s. [51] [52] In most parts of China, however, the practice had virtually disappeared by 1949. [47] The practice was also stigmatized in Communist China, and the last vestiges of foot binding were stamped out, with the last new case of foot binding reported in 1957. [53] [54] By the 21st century, only a few elderly women in China still had bound feet. [55] [56] In 1999, the last shoe factory making lotus shoes, the Zhiqiang Shoe Factory in Harbin , closed. [57] Practice [ edit ] Variations and prevalence [ edit ] A comparison between a woman with normal feet (left) and a woman with bound feet in 1902 Foot binding was practiced in various forms and its prevalence varied in different regions. [58] A less severe form in Sichuan, called "cucumber foot" ( huanggua jiao ) due to its slender shape, folded the four toes under but did not distort the heel and taper the ankle. [29] [59] Some working women in Jiangsu made a pretense of binding while keeping their feet natural. [32] Not all women were always bound—some women once bound remained bound all through their lives, but some were only briefly bound, and some were bound only until their marriage. [60] Footbinding was most common among women whose work involved domestic crafts and those in urban areas; [32] it was also more common in northern China where it was widely practiced by women of all social classes, but less so in parts of southern China such as Guangdong and Guangxi where it was largely a practice of women in the provincial capitals or among the gentry. [61] [62] Foot binding limited the mobility of girls, so they became engaged in manual labor since childhood. [28] It is thought that the necessity for women labour in the fields due to a longer crop-growing season in the South and the impracticability of bound feet working in wet rice fields limited the spread of the practice in the countryside of the South. [63] The Manchu "flower bowl" shoes designed to imitate bound feet, mid 1880s. ... Mechanization resulted in women who worked at home facing a crisis. [28] Coupled with changes in politics and people's consciousness, the practice of foot binding disappeared in China forever after two generations. [58] [108] It has been argued that while the practice started out as a fashion, it persisted because it became an expression of Han identity after the Mongols invaded China in 1279, and later the Manchus' conquest in 1644, as it was then practiced only by Han women. [96] During the Qing dynasty, attempts were made by the Manchus to ban the practice but failed, and it has been argued the attempts at banning may have in fact led to a spread of the practice among Han Chinese in the 17th and 18th centuries. [110] In literature, film and television [ edit ] The bound foot has played a prominent part in many media works, both Chinese and non-Chinese, modern and traditional. [111] These depictions are sometimes based on observation or research and sometimes on rumors or supposition. ... "China's "Golden Lotus Feet" - Foot-binding Practice" . Archived from the original on 28 September 2013 . Retrieved 29 January 2012 . ^ Bossen, Laurel (2004). ... LONDON: Hodder and Stoughton. p. 111 . Retrieved June 28, 2010 . mohammedan. (Original from Harvard University) ^ a b c Jackson, Beverley (1997).
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Conjoined Twins
Wikipedia
The most common types of conjoined twins are: Thoraco-omphalopagus (28% of cases): [4] Two bodies fused from the upper chest to the lower chest. ... However, if the operation had not taken place, it was certain that both twins would die. [26] [27] Grace survived to enjoy a normal childhood. [28] In 2003, two 29-year-old women from Iran, Ladan and Laleh Bijani , who were joined at the head but had separate brains (craniopagus) were surgically separated in Singapore, despite surgeons' warnings that the operation could be fatal to one or both. ... The Journal of Law, Medicine & Ethics . 28 (3): 312–313. doi : 10.1111/j.1748-720x.2000.tb00678.x .
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Abortion In Mexico
Wikipedia
Abortion is the third cause of maternal mortality, and there are currently 20 women in prison for illegal abortions. [28] In October 2019, Las Comisiones Unidas de Procuración y Administración de Justicia y de Igualdad de Género (The United Commissions for the Procuration and Administration of Justice and Gender Equality) in Puebla vote against decriminalization of abortion and legalization of same-sex marriage . ... Retrieved 16 March 2014 . ^ Miller Llana, Sara (2008-08-28). "Mexico's Supreme Court upholds abortion law" . ... Retrieved January 10, 2006. ^ " Mexicans Support Birth Control, Not Abortion Archived March 31, 2007, at the Wayback Machine ." (March 28, 2007). Angus Reid Global Monitor.
