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  • Primary Biliary Cholangitis Wikipedia
    Anti-gp210 antibodies are found in 47 percent of PBC patients. [26] [27] Anti-centromere antibodies often correlate with developing portal hypertension. [28] Anti-np62 [29] and anti-sp100 are also found in association with PBC. ... "Primary Biliary Cirrhosis: Getting a Diagnosis" (online) . At Home Magazine . Retrieved 28 July 2015 . ^ Jacoby A, Rannard A, Buck D, et al.
    IL12A, SPIB, IL12RB1, ABCC2, NOS2, MMEL1, TNFSF15, STAT4, POU2AF1, NFKB1, CLEC16A, IRF5, TNPO3, TYK2, IL7R, DENND1B, TNFRSF1A, SLC4A2, ABCB4, ALB, CD80, CXCL10, NFE2L2, TGFB1, LOXL2, IL12B, CXCL9, LOX, CXCR5, HIF1A, NOS3, KEAP1, SLC51A, ICAM3, MAPK14, CYGB, CDH5, SLC51B, IGFBP1, RELA, CCL5, UBD, ENTPD2, ABCG2, CD3D, NSA2, KRT7, IL4, PPARGC1A, HAMP, ACE, VEGFA, JAK2, SLCO1C1, MMP13, HMOX1, ACE2, DAG1, HHIP, CPEB1, MAS1, MAP3K14, MMP2, MMP3, PDE5A, MMP9, RPS6KB1, AGT, COL1A1, REN, CCN2, AQP4, HLA-DPB1, IL12RB2, IKZF3, HLA-DRA, IL16, GSDMB, IL21R, PRKCB, SYNGR1, ORMDL3, ZPBP2, TNFSF8, PAX3, DGKQ, MAPK8IP1P1, PLCL2, KANSL1-AS1, MAPK8IP1P2, PLCB1, RPL3, TP63, IL10, NSF, RAD51B, KANSL1, CD58, PSMG4, CYP21A2, ATXN2, LINC01100, LINC02820, LINC02210-CRHR1, SKIV2L, RPS6KA4, SP100, MAPT, MANBA, TSBP1-AS1, IL12A-AS1, ELMO1, LTBR, EIF4EP2, SH2B3, DLEU1, STAT1, MAPT-IT1, NAB1, TSBP1, DELEC1, MAPT-AS1, CCDC88B, ARHGAP31, PRICKLE1, GLI3, PSMD3, TMEM39A, LINC02210, SPPL2C, WNT3, SDK1, COL17A1, SLC22A23, SLC17A8, CNTN5, PRDM16, CTLA4, CDK12, GRIK1, HLA-DRB1, MED1, EIF4E, RBM45, ARID3A, TIMMDC1, STH, FBXL20, EXOC3L4, DLAT, RMI2, DDX6, TNF, VDR, IFNG, NUP210, PML, TLR4, FOXP3, CDKN1A, FGF19, IL17A, GPT, OGDH, IL1B, CD40LG, CXCL8, SQSTM1, CYP7A1, ABCB11, CDKN2A, HLA-DOA, PPARA, HK1, BCL2, DLST, PDC, ABCB1, TNFSF11, PDHX, TRIM21, NR1I2, ICAM1, SLPI, ATHS, MIR506, GGT1, CD14, SLC12A9, NAT10, HGF, GGTLC5P, HLA-DQA1, GGTLC3, GGT2, CD40, GGTLC4P, PDLIM3, CD19, PTPN22, IL2, ATRNL1, IL5, ASRGL1, ATN1, TBC1D9, MIR21, CCL27, DBT, ALPP, TGFBR2, XPR1, SULT2A1, SYCE1L, C4B_2, LOC102723407, LOC102724197, LOC102724971, TLR2, IL21, GPBAR1, SLC22A1, SLCO1B1, KHDRBS1, BTG3, NUP62, ABCC3, SOCS1, B3GAT1, DCTN4, GGTLC1, CDR3, NELFCD, KRT20, KLHL1, NR1H4, KLHL12, TP53, SLC10A2, H3P10, ESR2, LGALS3BP, HLA-A, CDKN1B, C4A, CYP3A4, C4B, CX3CR1, GTF2H1, POU2F1, MS4A1, CTSZ, GABPA, NRAS, CCR5, CD86, CXCR3, IL7, CD79A, FBL, ESR1, SLC10A1, HLA-DRB3, APOE, HNF4A, IL2RA, HSPD1, PPP1R2C, GLB1, GATM, PDCD1LG2, LRRC32, PNPLA3, MARCKSL1, FOXO3, FOXO1, WLS, FH, AGBL2, VTCN1, TNFAIP8L2, SLC25A1, POGLUT1, NR3C1, SIAE, IGF1, IFI27, SOST, TMED7, HMGB1, IL23A, HLA-DQB1, HLA-DPA1, HLA-B, TLR9, PDP1, COG6, RBFOX1, DPP8, GZMB, ITLN1, PRPF40A, WDR11, GSTM2, PRAM1, GSTM1, JPH3, JAM3, NQO1, NBPF3, MIR223, MIR505, CD1D, CD1C, DDR1, SPATA31A3, BRCA1, BHMT, BCR, BCL3, ATM, AREG, ABCC6, DEFB4B, FASLG, TMED7-TICAM2, FAS, APEX1, AIRE, ANXA11, ANXA2, ACTB, LINC02605, H3P23, MIR425, MIR210, DNMT1, CD28, DPP9, DNASE1, DMBT1, SP140L, TBX21, DBA2, DEFB4A, FCRL3, CTHRC1, DEFB1, LRG1, CYP2D6, COL9A3, CNGB1, CCR7, CHUK, CHRM3, CFTR, CD74, LINC01193, TICAM2, MIR155, MIR197, CD207, CD274, SCHIP1, POLR2G, SERPINA1, WNT2B, PRRC2A, PDK4, FOSL1, KMT2D, CDK2AP1, PDGFB, NR0B2, PDCD1, OPRM1, RNASET2, TNFRSF11B, DDR2, NOTCH1, TNFSF10, TNFSF9, TNFRSF11A, IL18R1, NFYA, MYD88, WASF1, ABCC1, HAP1, MIF, PIK3CA, VCAM1, EBAG9, UGT2B4, SOAT1, CXCL12, CCL24, SPINT1, SPP1, SRY, CCL20, CCL11, STAT3, SCTR, STAT5A, STAT5B, SERPINB3, TFF3, S100A12, RDX, TGM2, PTGS2, TLR3, PSMD9, PSMA4, PRF1, PPARG, TPMT, TNFSF4, CD99, MBL2, ICOS, TNFSF13B, ITGB2, ITGAV, RIPK3, ITGAL, PDZD2, ITGA5, ITGA1, ISG20, IL18, IL13, ICOSLG, SLC44A1, CLDN14, IL6, SS18L1, IL1RN, IL1A, INTU, AGO2, IL37, IGHG3, HPGDS, SLCO1B3, TRBV10-1, ABO, ITIH4, DCTN6, KLF4, KRT18, SLIT2, NTN1, SMAD3, HDAC9, KMT2B, SMAD2, CD180, LTA, LRP1, NR1I3, LPA, DGCR2, LORICRIN, EBI3, KLRG1, CALCOCO2, ABCC4, CCL26, LGALS3, CIB1, ZNRD2, LEP, GNLY, LAMP1, L1CAM, ABCA1
    • Biliary Cirrhosis, Primary, 5 OMIM
      Description Primary biliary cirrhosis (PBC) is a chronic, progressive cholestatic liver disease that usually affects middle-aged women and eventually leads to liver failure (summary by Kaplan, 1996). For a discussion of genetic heterogeneity of primary biliary cirrhosis (PBC), see PBC1 (109720). Mapping To replicate the findings of Hirschfield et al. (2009) and to evaluate the relevance of identified loci to PBC susceptibility, Hirschfield et al. (2010) tested an additional independent cohort of 857 individuals with PBC and 3,198 controls, all of European descent, for PBC associations with 36 SNPs across 24 loci. The combination of these replication results and the prior genomewide association data yielded a genetic dataset derived from 1,351 PBC cases and 4,700 controls. Hirschfield et al. (2010) identified association with PBC at a region on chromosome 17q12-q21 represented by SNP rs11557467 in the ZPBP2 gene (608499) (combined p = 3.5 x 10(-13), OR = 0.72).
    • Biliary Cirrhosis, Primary, 2 OMIM
      Description Primary biliary cirrhosis (PBC) is a chronic, progressive cholestatic liver disease that usually affects middle-aged women and eventually leads to liver failure (summary by Kaplan, 1996). For a discussion of genetic heterogeneity of primary biliary cirrhosis (PBC), see PBC1 (109720). Mapping In a 2-stage genomewide association study involving a total of 536 patients with primary biliary cirrhosis and 1,536 controls, Hirschfield et al. (2009) found significant association between PBC and 13 loci across the HLA class II region on chromosome 6p21.3, with HLA-DQB1 (604305) having the strongest association (combined p for rs2856683 = 1.78 x 10(-19); odds ratio, 1.75).
    • Biliary Cirrhosis, Primary, 3 OMIM
      Description Primary biliary cirrhosis (PBC) is a chronic, progressive cholestatic liver disease that usually affects middle-aged women and eventually leads to liver failure (summary by Kaplan, 1996). For a discussion of genetic heterogeneity of primary biliary cirrhosis (PBC), see PBC1 (109720). Mapping In a 2-stage genomewide association study involving a total of 536 patients with primary biliary cirrhosis and 1,536 controls, Hirschfield et al. (2009) found significant association between PBC and rs3790567 at the IL12RB2 locus (601642) on chromosome 1p31.2 (combined p = 2.76 x 10(-11); odds ratio, 1.51).
    • Biliary Cirrhosis, Primary, 1 OMIM
      Description Primary biliary cirrhosis (PBC) is a chronic, progressive cholestatic liver disease that usually affects middle-aged women and eventually leads to liver failure (summary by Kaplan, 1996). Genetic Heterogeneity of Primary Biliary Cirrhosis Primary biliary cirrhosis-1 (PBC1) is significantly associated with SNPs at the IL12A locus (161560) on chromosome 3p12-q13.2. Significant association of PBC has also been shown with SNPs at the HLA-DQB1 locus (604305) on chromosome 6p21.3 (PBC2; 613007), at the IL12RB2 locus (601642) on chromosome 1p31.2 (PBC3; 613008), at the IRF5 (607218)-TNPO3 (610032) locus on chromosome 7q32 (PBC4; 614220), and at the ZPBP2 locus (608499) on chromosome 17q12-q21 (PBC5; 614221). See also Reynolds syndrome (613471), in which primary biliary cirrhosis is a feature. Clinical Features Jaup and Zettergen (1980) studied familial incidence of primary biliary cirrhosis.
    • Primary Biliary Cholangitis Orphanet
      A rare autoimmune cholestatic liver disease characterized by autoimmune mediated damage of small intrahepatic bile ducts leading to cholestasis, fibrosis, and potential cirrhosis. Epidemiology Primary biliary cholangitis (PBC) incidence rates range from 0.33 to 5.8 per 100,000 inhabitants/year and prevalence rates range from 1.91 to 40.2 per 100,000 inhabitants Women are predominantly affected with a sex ratio of 9:1. Clinical description Onset is generally in the 4th to 6th decades of life. Many patients are asymptomatic at diagnosis and are identified incidentally. The initial presenting manifestations include fatigue (80%) and pruritus (20-70%), both of which fluctuate throughout the disease course.
    • Primary Biliary Cholangitis Mayo Clinic
      Overview Primary biliary cholangitis, previously called primary biliary cirrhosis, is a chronic disease in which the bile ducts in your liver are slowly destroyed. Bile is a fluid made in your liver. It aids with digestion and helps you absorb certain vitamins. It also helps your body get rid of cholesterol, toxins and worn-out red blood cells. Chronic inflammation in the liver can lead to bile duct damage, irreversible scarring of liver tissue (cirrhosis) and eventually, liver failure. Although it affects both sexes, primary biliary cholangitis mostly affects women.
    • Primary Biliary Cholangitis GARD
      Primary biliary cholangitis (PBC) is a chronic, progressive liver disease in which the bile ducts become inflamed and damaged. This leads to the buildup of bile and causes liver problems such as scarring, cirrhosis (scarring and poor liver function), and eventual liver failure . PBC is more common in women. Many people do not have symptoms when they are first diagnosed and may not develop symptoms for several years. Early symptoms may include fatigue (the most common symptom), itchy skin ( pruritus ), and abdominal pain. As the disease progresses, people with PBC may develop weakness, nausea, diarrhea, swelling in the legs and feet (edema), bone and joint pain, jaundice, dark urine, and xanthomas .
    • Biliary Cirrhosis, Primary, 4 OMIM
      Description Primary biliary cirrhosis (PBC) is a chronic, progressive cholestatic liver disease that usually affects middle-aged women and eventually leads to liver failure (summary by Kaplan, 1996). For a discussion of genetic heterogeneity of primary biliary cirrhosis (PBC), see PBC1 (109720). Mapping To replicate the findings of Hirschfield et al. (2009) and to evaluate the relevance of identified loci to PBC susceptibility, Hirschfield et al. (2010) tested an additional independent cohort of 857 individuals with PBC and 3,198 controls, all of European descent, for PBC associations with 36 SNPs across 24 loci. The combination of these replication results and the prior genomewide association data yielded a genetic dataset derived from 1,351 PBC cases and 4,700 controls. The locus on chromosome 7q32 near the IRF5 (607218)-TNPO3 (610032) genes was confirmed by this analysis (SNP rs10488631, replication dataset p = 1.13 x 10(-8), OR = 1.58; combined dataset p = 8.66 x 10(-13), OR = 1.57).
  • Dutch Elm Disease Wikipedia
    A policy of sanitary felling has kept losses in the city to an average of 1000 a year. [28] Elm was the most common tree in Paris from the 17th century; before the 1970s there were some 30,000 ormes parisiens . ... Contact (in French). Laval University. 28 (1). ^ CFIA annual pest survey report. 1999 Summary of Plant Quarantine Pest and Disease Situations in Canada (report available upon demand at the Canadian Food Inspection Agency: http://publications.gc.ca/site/eng/9.831610/publication.html ) ^ "Dutch Elm Disease" . ... Archived from the original (PDF) on 28 June 2007. ^ Screening European Elms for resistance to 'Ophiostoma novo-ulmi' ( Forest Science 2005) [2] ^ ‘Spanish Clones’ (Oct. 2013) resistantelms.co.uk ^ Δoκιμή ανθεκτικότητας ελληνικών γενoτύπων πεδινής φτελιάς (Ulmus minor) κατά της Oλλανδικής ασθένειας , Σ. ... Retrieved 16 November 2013 . ^ Coleman 2009 ^ 'First Genetically Modified Dutch Elm Trees Grown', unisci.com ^ resistantelms.co.uk, FAQ 'Disease Control' ^ Coleman 2009 , p. 17 ^ "The mid-Holocene Ulmus decline: a new way to evaluate the pathogen hypothesis" . Archived from the original on 28 September 2011 . Retrieved 4 November 2011 . ^ Oliver Rackham, The History of the Countryside (London 1986), pp. 242–243, 232 ^ Meulemans, M.; Parmentier, C. (1983).
  • Medial Knee Injuries Wikipedia
    This soft-tissue attachment can be reproduced with a suture anchor [28] placed 12.2 mm distal to the medial joint line (average location), directly medial to the anterior arm of the semimembranosus tibial attachment. [27] Once this aspect of the sMCL is secured to the suture anchor, the knee is put through range of motion testing by the physician to determine the "safe zone" of knee motion which is used during the first post-operative day rehabilitation (below). [27] Rehabilitation [ edit ] Nonoperative Rehabilitation As mentioned in the Nonoperative Treatment section, the principles of rehabilitation are to control swelling , protect the knee (bracing), reactivate the quadriceps muscle, and restore range of motion . ... The Physician and Sportsmedicine . 41 (3): 19–28. doi : 10.3810/psm.2013.09.2023 . ... PMID 20563561 . ^ Crawford, Duncan (28 January 2010). "Northern Ireland kneecapping victim 'shot four times ' " .
  • Chytridiomycosis Wikipedia
    Excessive shedding of skin is seen in most frog species affected by B. dendrobatidis . [6] These pieces of shed skin are described as opaque, gray-white, and tan. [6] Some of these patches of skin are also found adhered to the skin of the amphibians. [6] These signs of infection are often seen 12–15 days following exposure. [20] The most typical symptom of chytridiomycosis is thickening of skin, which promptly leads to the death of the infected individuals because those individuals cannot take in the proper nutrients, release toxins, or, in some cases, breathe. [6] Other common signs are reddening of the skin, convulsions, and a loss of righting reflex . [20] In tadpoles, B. dendrobatidis affects the mouthparts, where keratin is present, leading to abnormal feeding behaviors or discoloration of the mouth. [6] Research and impact [ edit ] The amphibian chytrid fungus appears to grow best between 17 and 25 °C, [21] and exposure of infected frogs to high temperatures can cure the frogs. [26] In nature, the more time individual frogs were found at temperatures above 25 °C, the less likely they were to be infected by the amphibian chytrid. [27] This may explain why chytridiomycosis-induced amphibian declines have occurred primarily at higher elevations and during cooler months. [28] Naturally produced cutaneous peptides can inhibit the growth of B. dendrobatidis when the infected amphibians are around temperatures near 10 °C (50 °F), allowing species like the northern leopard frog ( Rana pipiens ) to clear the infection in about 15% of cases. [29] Although many declines have been credited to the fungus B. dendrobatidis - although likely prematurely so in many cases [4] - some species resist the infection and some populations can survive with a low level of persistence of the disease. [30] In addition, some species that seem to resist the infection may actually harbor a nonpathogenic form of B. dendrobatidis . ... S2CID 4421285 . ^ "Amphibian 'apocalypse' caused by most destructive pathogen ever" . Animals . 2019-03-28 . Retrieved 2019-04-06 . ^ Briggs, Helen (29 March 2019). ... Retrieved 29 March 2019 . ^ Scheele, Ben C.; Pasmans, Frank; Skerratt, Lee F.; et al. (28 March 2019). "Amphibian fungal panzootic causes catastrophic and ongoing loss of biodiversity" (PDF) .
  • Alcohol And Pregnancy Wikipedia
    Support groups and talk therapy not only help the children suffering from FAS, but also help the parents and siblings of these children. [28] Treatment [ edit ] A woman may elect to discontinue alcohol once she knows that she is pregnant.
  • Rheumatic Fever Wikipedia
    Duckett Jones, MD. [25] They have been periodically revised by the American Heart Association in collaboration with other groups. [26] According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre [27] or Anti-DNase B . [28] [8] A recurrent episode is also diagnosed when three minor criteria are present. [29] Exceptions are chorea and indolent carditis , each of which by itself can indicate rheumatic fever. [30] [31] [32] An April 2013 review article in the Indian Journal of Medical Research stated that echocardiographic and Doppler (E & D) studies, despite some reservations about their utility, have identified a massive burden of rheumatic heart disease, which suggests the inadequacy of the 1992 Jones' criteria.
    MYOM2, CDKN2A, TP53, TNF, HLA-DRB1, MDM2, BMI1, PAGR1, RBM45, GALNS, GAST, COMMD3-BMI1, NPM1, MBL2, TLR2, IL6, CDK4, PTEN, TGFB1, CTLA4, IL10, ATM, IL17A, HLA-A, RUNX1T1, TBX3, FCN2, MASP2, EGFR, CBX7, HNF1A, TBX2, TRIM21, TCF7, RHD, RARB, TRBV20OR9-2, PTH, CDK5RAP3, VIM, POTEF, TWIST1, VEGFA, CCDC6, RAB11A, PRC1, DMTF1, LINC01194, HAVCR2, HUWE1, POSTN, RASSF1, HARS2, SLC25A19, MBD2, ABL1, PIK3C3, E2F1, HARS1, GC, FOXM1, FGF1, FCN1, FCGR3B, FCGR2A, DMP1, NOTCH1, CRH, CLU, CDKN2B, RUNX1, BCR, PARP1, ACTB, HLA-DQA1, HLA-DQA2, HLA-DQB1, AGFG1, MYC, MUC1, MTTP, MNT, MEFV, ABO, CXCL10, IL2RG, IL1RN, IL1B, IGHG3, IGFBP2, IFNG, IDH1, ICAM1, H3P10
    • Rheumatic Fever-Related Antigen OMIM
      Genetic predisposition to rheumatic fever has intrigued investigators since Cheadle (1889) first noted the familial aggregation of rheumatic fever. Wilson et al. (1943) suggested that susceptibility might be an autosomal recessive trait. Taranta et al. (1959) suggested reduced penetrance because of a low concordance in monozygotic twins. Patarroyo et al. (1979) found that a serum from a multiparous woman identified a novel B-cell alloantigen marker, 883, in persons previously identified as having had rheumatic fever with or without subsequent rheumatic heart disease. They found that 71% of patients typed in New York and 74% of patients typed in Bogota expressed this antigen on their B cells as compared with only 17% in the 2 disease-free control groups tested.
    • Rheumatic Fever Orphanet
      Rheumatic fever (RF) is a multisystem inflammatory disease occurring as a post-infectious, nonsuppurative sequela of untreated streptococcus pyogenes (Group A streptococcus [GAS]) pharyngitis, and mainly occurs in individuals aged 5 to 15 years. The most common presenting signs are fever, migratory polyarthritis and carditis. Epidemiology The incidence of RF in industrialized countries, due to sporadic outbreaks, is typically less than 1/20, 000 individuals. In the developing world, the annual incidence is at least 100 times higher with some reports of > 1/200 individuals in select subpopulations, such as Australian Aboriginals. RF remains a major cause of acquired cardiac morbidity and mortality among people under 50 years of age.
    • Rheumatic Fever GARD
      Rheumatic fever is an inflammatory condition that may develop after infection with group A Streptococcus bacteria, such as strep throat or scarlet fever . It is primarily diagnosed in children between the ages of 6 and 16 and can affect the heart, joints, nervous system and/or skin. Early signs and symptoms include sore throat; swollen red tonsils; fever; headache; and/or muscle and joint aches. Some affected people develop rheumatic heart disease, which can lead to serious inflammation and scarring of the heart valves. It is not clear why some people who are infected with group A Streptococcus bacteria go on to develop rheumatic fever, while others do not; however, it appears that some families may have a genetic susceptibility to develop the condition.
    • Rheumatic Fever Mayo Clinic
      Overview Rheumatic fever is an inflammatory disease that can develop when strep throat or scarlet fever isn't properly treated. Strep throat and scarlet fever are caused by an infection with streptococcus (strep-toe-KOK-us) bacteria. Rheumatic fever most often affects children ages 5 to 15. But it can develop in younger children and adults. Although strep throat is common, rheumatic fever is rare in the United States and other developed countries. Rheumatic fever can cause permanent damage to the heart, including damaged heart valves and heart failure.
  • Abusive Head Trauma Wikipedia
    Furthermore, shaking cervical spine injury can occur at much lower levels of head velocity and acceleration than those reported for SBS." [19] Other authors were critical of the mathematical analysis by Bandak, citing concerns about the calculations the author used concluding "In light of the numerical errors in Bandak’s neck force estimations, we question the resolute tenor of Bandak’s conclusions that neck injuries would occur in all shaking events." [20] Other authors critical of the model proposed by Bandak concluding "the mechanical analogue proposed in the paper may not be entirely appropriate when used to model the motion of the head and neck of infants when a baby is shaken." [21] Bandak responded to the criticism in a letter to the editor published in Forensic Science International in February 2006. [22] Diagnosis [ edit ] Diagnosis can be difficult as symptoms may be nonspecific. [1] A CT scan of the head is typically recommended if a concern is present. [1] While retinal bleeding is common, it can also occur in other conditions. [1] It is unclear how useful subdural haematoma, retinal hemorrhages, and encephalopathy are alone at making the diagnosis. [23] A skull fracture from abusive head trauma in an infant 3D CT reconstruction showing a skull fracture in an infant 3D CT reconstruction showing a skull fracture in an infant Triad [ edit ] While the findings of AHT are complex and many, [24] they are often incorrectly referred to as a "triad" for legal proceedings; distilled down to retinal hemorrhages , subdural hematomas , and encephalopathy. [25] AHT may be misdiagnosed, underdiagnosed, and overdiagnosed, [26] and caregivers may lie or be unaware of the mechanism of injury. [11] Commonly, there are no externally visible signs of the condition. [11] Examination by an experienced ophthalmologist is often critical in diagnosing shaken baby syndrome, as particular forms of ocular bleeding are quite characteristic. [27] Magnetic resonance imaging may also depict retinal hemorrhaging; [28] this may occasionally be useful if an ophthalmologist examination is delayed or unavailable. [ citation needed ] Conditions that are often excluded by clinicians include hydrocephalus , sudden infant death syndrome (SIDS), seizure disorders , and infectious or congenital diseases like meningitis and metabolic disorders . [29] [30] CT scanning and magnetic resonance imaging are used to diagnose the condition. [11] Conditions that may accompany AHT include bone fractures , injury to the cervical spine (in the neck), retinal bleeding, cerebral bleed or atrophy , hydrocephalus , and papilledema (swelling of the optic disc ). [12] The terms non-accidental head injury or inflicted traumatic brain injury have been suggested instead of Abusive head trauma or "SBS". [31] Classification [ edit ] The term abusive head trauma is preferred as it better represents the broader potential causes. [13] The US Centers for Disease Control and Prevention identifies SBS as "an injury to the skull or intracranial contents of an infant or young child (< 5 years of age) due to inflicted blunt impact and/or violent shaking". [32] In 2009, the American Academy of Pediatrics recommended the use of the term abusive head trauma to replace SBS, in part to differentiate injuries arising solely from shaking and injuries arising from shaking as well as trauma to the head. [33] SBS was previously believed to present with constellation of findings (often referred to as a " triad "): subdural hematoma ; retinal bleeding ; and brain swelling or encephalopathy – which has controversially been used to infer child abuse caused by violent shaking or traumatic shaking. [13] The diagnostic accuracy of the triad, linked to episodes of traumatic shaking is controversial with a 2016 systematic review finding limited scientific evidence associating the triad to episodes of traumatic shaking, and insufficient evidence for using the triad to identify such episodes. [13] The connection is controversial in part following cases where parents of children exhibiting the triad have, in addition to losing custody, been jailed or sentenced to death. [34] The Crown Prosecution Service for England and Wales recommended in 2011 that the term shaken baby syndrome be avoided and the term non accidental head injury ( NAHI ) be used instead. [35] Differential diagnosis [ edit ] Vitamin C deficiency [ edit ] Some authors have suggested that certain cases of suspected shaken baby syndrome may result from vitamin C deficiency. [36] [37] [38] This contested hypothesis is based upon a speculated marginal, near scorbutic condition or lack of essential nutrient(s) repletion and a potential elevated histamine level.
    • Shaken Baby Syndrome Mayo Clinic
      Overview Shaken baby syndrome is a serious brain injury resulting from forcefully shaking an infant or toddler. It's also known as abusive head trauma, shaken impact syndrome, inflicted head injury or whiplash shaken infant syndrome. Shaken baby syndrome destroys a child's brain cells and prevents his or her brain from getting enough oxygen. This form of child abuse can cause permanent brain damage or death. Shaken baby syndrome is preventable. Help is available for parents who are at risk of harming a child. Parents also can educate other caregivers about the dangers of shaken baby syndrome.
  • Hiv-Associated Neurocognitive Disorder Wikipedia
    Neuroimaging studies of HIV patients indicate that significant volume reductions are apparent in the frontal white matter, whereas subcortically, hypertrophy is apparent in the basal ganglia, especially the putamen . [16] Moreover, the results of some studies suggest loss of brain volume in cortical and subcortical regions even in asymptomatic HIV patients and patients who were on stable treatment. [24] A recent longitudinal study of a small representative cohort of HIV-positive patients on stable medication regiments suggests that this cortical atrophy is progressive, and is in part related to nadir CD4. [25] Cerebral brain volume is associated with factors related to duration of the disease and CD4 nadir; patients with a longer history of chronic HIV and higher CD4 nadir loss present with greater cerebral atrophy. [24] CD4 lymphocyte counts have also been related to greater rates of brain tissue loss. [26] Current factors, such as plasma HIV RNA, have been found to be associated with brain volumes as well, especially with regards to basal ganglia volume [24] and total white matter. [27] Loss of cortical grey matter oligodendrocytes might also contribute to the symptomatology. [28] Changes in the brain may be ongoing but asymptomatic, that is with minimal interference in functioning, making it difficult to diagnose HIV-associated neurocognitive disorders in the early stages. [29] Diagnostic criteria [ edit ] Marked acquired impairment of at least two ability domains of cognitive function (e.g. memory, attention): typically, the impairment is in multiple domains, especially in learning, information processing and concentration/attention.
    ADRB2, OPRM1, IL1B, NALCN, SLC8A1, SLC8A1-AS1, TNF, ITIH4, APOE, CXCR4, CCR5, EDN1, CXCL10, MMP9, CCL3, CCL4, TAT, TGFB1, GLS, TP53, S100B, CCL4L2, ABCB6, RRP8, CCL4L1, CCR2, CCL2, PTGDS, PTPRC, KCNK1, GPI, HCK, HLA-C, IGF1, FGF2, IL6, MAP2, PTGS2, MMP2, MMP7, NEFL, ENPEP, PCNA, GLUL, NGF
  • Tetralogy Of Fallot Wikipedia
    It is associated with chromosome 22 deletions and DiGeorge syndrome . [22] : 62 Specific genetic associations include: JAG1 , [23] NKX2-5 , [24] ZFPM2 , [25] VEGF , [26] NOTCH1 , TBX1 , and FLT4 . [27] Embryology studies show that it is a result of anterior malalignment of the aorticopulmonary septum , resulting in the clinical combination of a VSD, pulmonary stenosis, and an overriding aorta. [18] : 200 Right ventricular hypertrophy develops progressively from resistance to blood flow through the right ventricular outflow tract. [9] Pathophysiology [ edit ] Play media Video explanation The main anatomic defect in TOF is the anterior deviation of the pulmonary outflow septum. [9] This defect results in narrowing of the right ventricular outflow tract (RVOT), override of the aorta, and a ventricular septal defect (VSD). [28] Four malformations [ edit ] " Tetralogy " denotes four parts, here implying the syndrome's four anatomic defects. [2] This is not to be confused with the similarly named teratology , a field of medicine concerned with abnormal development and congenital malformations (including tetralogy of Fallot). ... Archived from the original on 2008-10-16 . Retrieved 2009-02-28 . ^ " ' Little Darth Vader' reveals face behind the Force" . 7 February 2011. ^ "Aide to All the Times Jimmy Kimmel Has Gotten Political" .
    ZFPM2, NKX2-5, JAG1, GATA4, TBX1, GATA6, GDF1, GJA5, CITED2, FLT4, GATA5, NKX2-6, FOXC2, FOXH1, HAND2, FGF8, FOXC1, HEY2, MKS1, BMP10, NTF3, INVS, DNAH5, PHC1, DOCK1, NRP1, HIRA, UFD1, NOTCH1, COMT, PTPN11, FN1, TAB2, MKKS, RFC2, RET, NOTCH2, NODAL, UBE2T, INTU, ROR2, CCDC22, SPECC1L, RAD51C, RAD51, DLL1, PTCH1, PIGN, NIPBL, RPH3A, TBL2, PAH, HIBCH, ATXN2, CERS1, RPL5, TDGF1, GTF2IRD1, PIGL, NR2F2, TGIF1, TPM1, UBE2A, SLC35A2, BAZ1B, CLIP2, WT1, XRCC2, ZIC2, CXCR4, ALX1, SEC24C, TTC37, SEMA3E, SIX3, RREB1, MAD2L2, SF3B4, SALL1, CDON, SHH, SKI, TMEM94, SKIV2L, PQBP1, SH2B3, RBM8A, WASHC5, FIG4, NID1, LINC02676, DACT1, STRA6, DDX59, NAA25, EHMT1, PALB2, CRELD1, NXN, ELN, SLX4, EPHB4, ERCC4, PRDM16, FANCM, FANCA, COX3, BRIP1, DISP1, FANCE, BRAF, ZFPM2-AS1, RNU4ATAC, ALX3, ARVCF, RERE, BRCA1, BRCA2, COL2A1, EOGT, MYRF, HECTD4, JMJD1C, CHD4, CHRM3, FANCD2, FANCC, FANCB, SALL4, COX2, COX1, SUFU, RAB23, DLL4, KCNAB2, FANCL, RFWD3, FANCI, CHD7, LIMK1, VAC14, FANCF, HDAC8, RBPJ, RBM10, FOXF1, FANCG, GTF2I, ARID1B, DOCK6, GP1BB, GLI2, ARHGAP31, FGFR1, GPC5, GAS1, GABRD, VEGFA, TBX20, CHDH, HAND1, GJA1, KDR, TGFB1, VANGL2, MIR421, MIR1233-1, SULT1E1, MTHFR, APOE, HIF1A, REN, PVR, PITX2, MMP9, NPPB, MEIS2, FBN2, MAVS, GPR42, HAS2, MMP3, HOXA1, ACKR3, DGCR8, MMP2, HTC2, JARID2, FBN1, LPA, LRPAP1, LSAMP, MAP4, MBNL1, FEZF2, SLC50A1, IQGAP1, F5, TSPYL2, ADRA2B, AGT, ALDH2, MIR625, MIR424, BRS3, CAD, CD48, CRKL, CRP, CYBA, ACE, DMD, FSD1L, DNAH8, DNMT1, DNMT3B, DNTT, CORO7, FSD1, DVL2, EDNRA, EGF, F2, MYL4, CHMP5, TCF21, SLN, SNAI2, SCO2, REC8, SMN1, SMN2, SSTR4, ADRA1A, TADA2A, TBX5, RGS6, WNT11, TFAP2B, CHD1L, TFAP2C, TTN, VIM, LPAR2, BEST1, MBD2, AVSD1, ALDH1A2, MBNL2, ACSM3, RYR2, RXRA, NTRK3, OPRD1, PBX1, PBX3, PDGFA, LAMP3, PECAM1, AATF, PFKL, SUN2, PLN, PTH, DICER1, RASA1, MMRN1, ROBO1, BVES, WWP2, PPARGC1A, ROCK1, CXCR6, ACTC1
    • Tetralogy Of Fallot Orphanet
      Tetralogy of Fallot is a congenital cardiac malformation that consists of an interventricular communication, also known as a ventricular septal defect, obstruction of the right ventricular outflow tract, override of the ventricular septum by the aortic root, and right ventricular hypertrophy. Epidemiology This combination of lesions occurs in 1 of every 35,0000-30,000 live births, and accounts for 7-10% of all congenital cardiac malformations. Clinical description Patients nowadays usually present as neonates, with cyanosis of varying intensity based on the degree of obstruction to flow of blood to the lungs. Etiology The aetiology is multifactorial, but reported associations include untreated maternal diabetes, phenylketonuria, and intake of retinoic acid. Associated chromosomal anomalies can include trisomies 21, 18, and 13, but recent experience points to the much more frequent association of microdeletions of chromosome 22.
    • Tetralogy Of Fallot GARD
      Tetralogy of Fallot is a complex congenital heart defect characterized by a large ventricular septal defect (hole between the right and left ventricles), pulmonary stenosis (narrowing of the valve and artery that connect the heart with the lungs), an overriding aorta (the aorta - the artery that carries oxygen-rich blood to the body - is shifted over the right ventricle and ventricular septal defect, instead of coming out only from the left ventricle), and right ventricular hypertrophy (the muscle of the right ventricle is thicker than usual). Tetralogy of Fallot causes low oxygen levels in the blood, which can lead to cyanosis (a bluish-purple color to the skin). The cause of this condition is unknown. Treatment involves surgery to repair the heart defects. Sometimes more than one surgery is needed.
    • Tetralogy Of Fallot Mayo Clinic
      Overview Tetralogy of Fallot (teh-TRAL-uh-jee of fuh-LOW) is a rare condition caused by a combination of four heart defects that are present at birth (congenital). These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin because their blood doesn't carry enough oxygen. Tetralogy of Fallot is often diagnosed while the baby is an infant or soon after. Sometimes, depending on the severity of the defects and symptoms, tetralogy of Fallot is not detected until adulthood.
    • Tetralogy Of Fallot OMIM
      A number sign (#) is used with this entry because tetralogy of Fallot (TOF) can be caused by heterozygous mutation in the JAG1 gene (601920) on chromosome 20p12, the NKX2-5 gene (600584) on chromosome 5q35, the GATA4 gene (600576) on chromosome 8p23. Tetralogy of Fallot is also a well-recognized feature of many syndromes, including the 22q11 microdeletion syndrome (188400) and trisomy 21 (190685), and has been found to be caused by mutations in several genes, including ZFPM2 (603693), TBX1 (602054), and GATA6 (601656). Inheritance Pitt (1962) described a family in which 11 persons had either TOF or one of its components. The diagnosis was confirmed at operation or autopsy in 5 of the 11. The large study of Boon et al. (1972) led to the conclusions that heritability is about 54% and that in sibs the recurrence risk is about 1% for Fallot tetralogy and about 2% for any cardiac defect. The family that Der Kaloustian et al. (1985) reported may be a special type of Fallot tetralogy, inherited, the authors suggested, as an autosomal recessive.
  • Pain Management In Children Wikipedia
    Breastmilk or 'sugar' water has a similar effect, though studies in preterm infants have yet to be done. [26] Skin-to-skin care ( kangaroo care ) is thought be effective for pain control during painful procedures. [27] For children and adolescents who experience chronic pain- behavioral treatment, relaxation training, cognitive behavioral therapy (CBT) and acupuncture have been proven to be effective for some patients. [28] For recurrent abdominal pain a 2017 Cochrane review found some evidence that CBT and hypnotherapy were effective in reducing pain for the short term. [29] Medication [ edit ] Further information: Analgesic adjuvant Acute pain, chronic pain, neuropathic pain and recurrent pain in children is most often managed with medication.
  • Nephritic Syndrome Wikipedia
    Jugular venous distention (JVD) may also be appreciated when visualizing the veins of the neck on physical exam. [9] Elevated blood pressure - Measured at least two separate times with at least two minutes between measurements using a sphygmomanometer or equivalent method. [28] Abnormal heart sounds - If the underlying cause is cardiac in nature (such as infective endocarditis ), then you may appreciate abnormal heart sounds during auscultation of the heart. [29] Laboratory testing [ edit ] If the physician is suspicious of a possible nephritic syndrome, then he/she may order some common lab tests including: Serum electrolytes - The kidney is one of the main regulators of electrolytes in the human body and measuring the different electrolyte levels using either a basic metabolic panel (BMP) or comprehensive metabolic panel (CMP) can be a useful indicator of the underlying pathology. [30] Serum creatinine - Also measured using a BMP or CMP , creatinine is one of the most important indicators of current kidney function and is used to calculate the glomerular filtration rate (GFR).
    NPHS2, C3, CCN2, ESR1, HMGB1, SSRP1, CXCL16, IGAN1
  • Viral Hemorrhagic Septicemia Wikipedia
    Clair . [27] The isolate was named MI03GL and was sequenced for its entire genome. [28] The North American genotype of the virus, in addition to moderate mortality to salmonid species, including various varieties of trout, is also proving virulent among a wide variety of warm-water species previously considered resistant to VHS.
    CAV1, HIF1A, JAG2, THBS1, CDR3, MYOM2, MIR10A
  • Multiple Myeloma Wikipedia
    HIV/AIDS , organ transplantation , or a chronic inflammatory condition such as rheumatoid arthritis . [28] EBV-positive multiple myeloma is classified by the World Health Organization (2016) as one form of the Epstein-Barr virus-associated lymphoproliferative diseases and termed Epstein-Barr virus-associated plasma cell myeloma . ... Epidemiology [ edit ] Deaths from lymphomas and multiple myeloma per million persons in 2012 0-13 14-18 19-22 23-28 29-34 35-42 43-57 58-88 89-121 122-184 Age-standardized death from lymphomas and multiple myeloma per 100,000 inhabitants in 2004. [94] no data less than 1.8 1.8–3.6 3.6–5.4 5.4–7.2 7.2–9 9–10.8 10.8–12.6 12.6–14.4 14.4–16.2 16.2–18 18–19.8 more than 19.8 Globally, multiple myeloma affected 488,000 people and resulted in 101,100 deaths in 2015. [8] [9] This is up from 49,000 in 1990. [95] United States [ edit ] In the United States in 2016, an estimated 30,330 new cases and 12,650 deaths were reported. [7] These numbers are based on assumptions made using data from 2011, which estimated the number of people affected as 83,367 people, the number of new cases as 6.1 per 100,000 people per year, and the mortality as 3.4 per 100,000 people per year. ... National Cancer Institute . 1980-01-01 . Retrieved 28 November 2017 . ^ Ferri, Fred F. (2013). ... OCLC 888026338 . ^ Landgren O, Kyle RA, Pfeiffer RM, Katzmann JA, Caporaso NE, Hayes RB, Dispenzieri A, Kumar S, Clark RJ, Baris D, Hoover R, Rajkumar SV (28 May 2009). "Monoclonal gammopathy of undetermined significance (MGUS) consistently precedes multiple myeloma: a prospective study" .
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ABL1, COX8A, BMP6, TFRC, LY9, CR2, TLR4, CXCR5, TRIAP1, MICA, JUN, TRPV2, TXN, UBE2I, CD82, TYMS, ITGA5, PARP14, PTPRA, PCDH10, PRKN, HAMP, PDK1, IL21, RAF1, CD276, CDK9, SPANXA2, RAC1, PVR, CD79A, KLF6, CDK2, PTGS1, POU2AF1, POU2F2, EPHA3, PTCH1, SRGN, RTL10, PSMD2, CDK1, MUL1, RPS6KA3, PAEP, S100A9, CEBPA, RAB8A, COL1A1, AURKA, TUG1, ABCC2, CCR7, MEG3, CD24, CCR5, COX1, MTR, TRIM63, SLC2A4, SLAMF1, SKP2, PMEL, NGF, ASCC2, SPHK2, CD27, CHEK1, OAS3, ODC1, ITGB7, RELN, AREG, HLA-G, FOS, SIRT1, HMOX1, CCN1, FLT1, IGHV3-52, FOXM1, TCL1A, IL1A, ATM, HLA-DRB1, CYP2C8, CFDP1, MIR192, HDAC4, TPX2, NAMPT, HNF4A, CXCR3, AGO2, USP14, HP, CRTC1, PKD2L1, TNFRSF10A, DAZAP2, ALDH1A1, MIR125A, FOXP1, GJA1, SND1, XIAP, HLA-E, CIB1, XRCC4, RASSF1, E2F1, ADM, GEMIN4, GDF15, PRDX5, XRCC5, BCL9, CTAG2, CXCL10, CBLL2, BDNF, MIR497, BGLAP, EPAS1, ZDHHC9, ANGPT1, ESR1, EIF4G2, SPANXA1, HK2, USP7, USP5, EZH1, ADAR, F9, DPP4, RRM1, MELK, MIB1, TCL1B, ALPP, ALPI, CCL20, CX3CL1, APC, ADAMTS9, CCL5, RUNX2-AS1, 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MCIDAS, PABPC1P1, BLOC1S2, PPP1R16B, MIR338, ZNF763, SPDYA, IGHV5-78, LINC01193, STEAP1, GPSM1, AATF, FOXD3, HOXC-AS3, PTENP1-AS, NUPR1, PABPC1, ABCB5, MYCBP, MIR335, RICTOR, LAMA5-AS1, BBC3, MIR331, NANOS3, CLEC4D, MIR425, TINF2, LINC00515, DIMT1, FBXO9, PDCD4, PHF19, GSTK1, APEX2, MMP28, IBTK, MRAS, MIR197, MLXIP, MIR193A, CLSTN1, LINC02605, CARD8, RNA28S5, MIR182, RNA28SN4, MMRN1, ATF6, RPIA, MIR30E, PRAL, MIR320A, MIR150, MTCO2P12, TNIK, SMG1, MTF2, MIR30D, CIC, VSIG4, MIR301A, RPP14, CIT, CDC37, GLMN, MIR28, MIR27A, MIR26B, MIR23B, MIR30A, SLC2A6, MIR30C1, PTENP1, PADI2, H3P8, MIR30C2, CHP1, H3P13, MIR215, KDM6B, MIR34B, MAST4, MAPK8IP2, PSD4, LPAR3, CSAG3, PADI4, CSAG2, MIR93, LIN28B, DAPK2, NUP62, ANXA2R, SGK3, HES5, PSMA3-AS1, MAFF, MIR9-3, CA13, RCHY1, POT1, SOSTDC1, SEZ6L, MIR9-2, RN7SL263P, IGHV4-34, ACSBG1, MIR130A, RHOBTB2, MIR127, DNMBP, USP24, MIR126, ZNF629, PPP1R13B, MIR124-1, MIR10A, CERNA3, SIRT3, MIRLET7B, RYBP, MIR9-1, SF3B1, PERCC1, IRAIN, CABIN1, TRAT1, ZUP1, FERMT3, PAG1, USE1, PBK, GPRC5C, PROK1, SLC2A9, RPAIN, TCHP, MAGED4, RNASEH2C, TCIM, PMEPA1, VTRNA2-1, CHPT1, SLC12A9, KREMEN1, EIF2A, CIAPIN1, RASSF4, CRISPLD2, PDXP, DOT1L, NUP133, NLRP2, ORAI1, MIR1246, PRINS, SNORD14B, LGR4, RBPMS, ZNF331, CAMK2N1, ATAD1, HES6, HAVCR2, MIR631, RIOX2, SOX6, SUPT20H, MIR33B, SPZ1, SNORD35B, DEPDC1, MIR532, MIR610, PCBP4, PLSCR4, DLL1, GOPC, ZKSCAN3, ASRGL1, UBE2O, ZC3H12A, DHDDS, TXNDC15, LIN28A, DHX40, TINAGL1, IFIH1, FAM72D, MMP25, GORASP1, PDIA2, OIP5-AS1, RAPH1, NEIL1, WNK1, SLC2A11, TRPM8, MAPKAP1, CEP70, ULBP2, PDCD1LG2, WDR19, RALGAPB, TP73-AS1, RNA28SN5, MIR765, RPTOR, SESN2, SEMA6A, RASSF5, KIF18A, POTEF, HPSE2, TLR10, CTDSP1, RHOU, MAGED4B, SLC38A1, SCPEP1, ZNF436, BACH2, COL18A1, SNORD14C, MSTO1, SNORD14D, SNORD14E, MIR193B, TENT5D, DERL1, SLC30A8, BHLHA15, CLEC12A, FEZF1-AS1, SLC2A12, MIR520G, DTX3L, GOLT1B, IL23R, ANGPTL4, ZNF569, SLC45A2, IL34, LINC00328, ARMH4, DCTN4, MIR509-1, SLC25A37, RHOV, MIR4741, PDIA3P1, MPEG1, LAMTOR2, MCTS1, ALKBH3, UBE2T, MARCHF8, MYLIP, MIR410, DEL13Q14, RMC1, PSC, MIR4505, PRSS55, PADI1, MIR485, PIKFYVE, SLC2A8, MIR490, ERO1A, MIR4449, SOX8, RPL17-C18orf32, A2ML1, MS4A4A, EGLN1, MIR155HG, NLRP3, SLC35A4, TP53RK, SHC3, TERF2IP, CYTOR, DDX4, DDIT4, FOXP2, ZNF501, FBLIM1, PPP1R12C, TET2, DPP8, DCAF15, CASZ1, NSD3, SLC25A21, ITPRIP, ADA2, MIR4254, FZR1, LINC01672, CACUL1, MIB2, NRSN1, SCARA3, PASD1, SLCO6A1, EVL, CPT1C, LINC01234, ETV7, LINC00461, SIRT6, SEZ6, SNHG18, NBAS, SF3B6, RASD1, CRNDE, ZNF44, IGLL5, RITA1, NAT1, GLIPR1, IGF2, IGHM, IGHG1, IGHDOR15@, IGFBP7, IGFBP4, IGF2R, IFNB1, IL2RB, IDUA, ID1, HSPA8, HSPA1B, HSPA1A, HES1, JCHAIN, IL2RG, ITGAV, ILF2, IRF1, IRAK1, INPPL1, INPP5D, IDO1, ILK, IL18, IL5, IL13, IL12RB2, IL11RA, IL10RB, IL10RA, IL7, HOXC10, HOXB7, HOXA11, GFER, GPR42, CCR10, SFN, GOT2, GLO1, GLB1, GDF1, HOXA1, GCG, GBP1, GARS1, GAB1, XRCC6, IFI6, GRB2, GRM3, GTF2H1, GZMB, H2AX, HAS2, HCK, HDAC2, HFE, HGFAC, HIC1, HLA-DOB, HLA-DQB1, HLA-DRB5, HMBS, NR4A1, HOXA@, ITGAL, ITGAX, MMP24, COX2, NEDD4, NDP, NBN, NAGLU, MUC4, NUDT1, MSX1, NOS2, MRC1, MPZ, MPST, MPG, MMP15, MMP8, NOS1, NOS3, ITGB2, PAFAH1B1, PDC, PCYT1A, PCM1, PBX3, PAM, SERPINE1, FURIN, NOTCH3, PEBP1, ORC4, ROR1, NTF3, NPPB, NPC1, MMP1, MAP3K10, MLH1, STMN1, CD180, LTBP3, LIF, LGALS8, LEPR, LCN2, LAMP1, MITF, LAMA5, KRT81, KPNA2, KLRB1, KIR3DS1, ITGB3, EPCAM, MARCKS, SMAD1, SMAD2, SMAD3, SMAD5, MAGEA1, MAOA, MAX, MBD1, CD46, MEIS2, MAP3K5, MFAP1, MGST1, CIITA, MIF, FUT1, FOLR2, FOLR1, CASP2, CD247, CD1D, CCNB1, CCK, RUNX3, CAV1, CANX, TNFRSF8, CALCR, DDR1, BUB1B, BTF3P11, KLF9, BRS3, CD22, TNFSF8, FLII, CHUK, CNR2, CCR4, CMA1, TPP1, CLCN5, CISH, CHI3L1, CD48, CDKN2D, CDK7, CDC42, CDC25C, CDC20, CD68, BRCA2, BMPR1A, CEACAM1, AHCY, AMY1B, AMY1A, AMBP, ALOX5, ALK, CRYBG1, AGER, BCL3, ADRA2B, ADRA1A, ADK, ACVRL1, ACVR2A, ACP5, AMY1C, ANG, ANGPT2, ANXA1, APOA1, APOB, APRT, ARF1, ARG1, RHOH, ARNT, ARNTL, ATF3, ATP7A, AXL, BCHE, BCL2A1, COL4A1, SLC31A2, MAP3K8, EPOR, ETFA, ERG, ERCC3, ERCC2, ERBB3, ERBB2, ENO1, EDN1, ENDOG, EMX2, ELF4, ELAVL2, EIF4EBP1, EEF1A2, ETS1, F2, F3, F10, FASN, FCAR, FCER2, FCGR2B, FCGRT, FDPS, FGA, FGF1, FGF13, FGFR4, FH, FHIT, FLI1, EDNRB, LPAR1, CPOX, CYP1B1, DCN, DAPK1, CYP3A4, CYP2D6, CYP2C9, CYP2B6, CYLD, S1PR1, CTSK, CCN2, CSNK1A1, HAPLN1, CREBBP, CREB1, ACE, DDB1, DDX5, TIMM8A, DHCR24, DHFR, DIO3, DKC1, DLD, DMD, DNASE1, DNMT3A, SLC26A3, TSC22D3, DUSP5, DUSP8, TYMP, ENPP1, ENPP2, PDZK1, TNKS, TNFRSF10C, TNFRSF18, TNFRSF6B, ADAM23, TNFSF9, RIPK1, DYNLL1, PROM1, NCOA1, USO1, KMO, IKBKG, ITGA8, ENC1, SOCS2, DLEU2, UCN, CDY1, LPAR2, PDCD5, CBFA2T2, SLC16A3, SLC16A4, FCGR2C, PRC1, NR1I2, SEMA5A, MAP3K14, BTRC, MBD2, SPHK1, ARHGEF7, OFD1, SMARCA5, CUL4A, VWF, ZAP70, YWHAE, YY1, WT1, WNT5A, WEE1, VRK1, DYRK2, TRPV1, BEST1, VIM, VDAC1, USP1, NR1H2, ZNF70, TRIM25, ZMYM2, LAPTM5, EVI5, DEK, BAG6, RNF217-AS1, TFPI2, FGF23, CLLS2, NCOA3, USP9Y, ARID1A, TRRAP, BCAR3, RECK, SLC16A7, MTA2, PTTG1, CDK2AP2, CRTAP, TACC3, PRMT5, ST3GAL6, RACK1, STUB1, TRIB1, AKT3, PSMD14, PSME3, PDZK1IP1, ARPC5, EDIL3, ABCC5, SEMA4D, PRDX4, ARPC1A, CXCL13, GNLY, COLEC10, KHDRBS1, CXCR6, NRG3, OGA, NES, KDM5B, ZMYND11, CCL27, LILRB1, SLC26A1, MALT1, BCL2L10, SCO2, PDLIM7, NCR2, CHD1L, VPS4B, TBPL1, NAPSA, HOMER1, NCR1, COX5A, USP15, KL, LONP1, KLF4, ASIC3, CD83, ITGB1BP1, MINPP1, SOX13, APOBEC3B, RBM39, CYTIP, CARTPT, NCOR2, TTI1, HERPUD1, DCAF1, RAPGEF5, MTSS1, SPATA2, GAB2, TELO2, UBAP2L, DLEC1, UGCG, UCHL1, PFKFB3, RBBP8, RNASE2, RGS1, RENBP, REG1A, RECQL, OPN1LW, RBBP5, RNF6, RARA, RANBP2, RAG2, MOK, RAD23B, PTN, RNASE3, RNH1, UBE2G1, ATXN1, SELL, SELE, CXCL11, CCL8, CCL7, SCN7A, RYR1, SNORD15A, RRM2, RPS27A, RPS27, RPL17, RPL5, RPA1, PTBP1, PSME2, PSMD10, PLAUR, PPP3CA, PON1, POLD1, PMP22, PML, PLXNB1, PLAT, PSMD4, PKM, PIK3R2, PIK3R1, PIGA, ABCB4, PFN1, PRB1, PRKAA1, PRKAA2, MAPK7, MAPK9, MAP2K1, PSAP, PSMA3, PSMA6, PSMB1, PSMB4, PSMB5, PSMB8, PSMB9, PSMB10, PSMC1, PSMC6, SELP, SEMG1, SELENOW, TERF1, KLF10, THBS2, THBD, TGFA, TFPI, NAT2, TERC, ADAM17, TEAD1, TDG, TCF19, GCFC2, SERPINA7, TAPBP, TIMP3, TJP1, TLR3, TSPAN7, TMSB4X, TNFAIP3, TNFRSF1B, TOP1, TPO, CRISP2, TRAF2, TRPC1, TSC2, TSHR, TTK, TYRO3, UBA1, TAP2, SYT1, SFRP1, SKIV2L, SNCA, SIGLEC1, SMO, SMARCB1, SLC3A2, SKP1, SKI, SYCP1, SIM2, SH3GL3, SH3GL1, SGK1, SRSF2, SFRP5, FSCN1, SOD1, SORL1, SOX1, SOX2, SOX4, SOX11, SRI, ITPRID2, SSTR4, SSX1, SSX4, STAT5A, STAT5B, STK11, STX4, SULT1A1, TERF2
    • Myeloma, Multiple OMIM
      A number sign (#) is used with this entry because several chromosome aberrations, including recurrent translocations and deletions, have been found to be related to the development or progression of multiple myeloma; see CYTOGENETICS section. Description Multiple myeloma is a neoplastic plasma cell disorder characterized by clonal proliferation of malignant plasma cells in the bone marrow microenvironment, monoclonal protein in the blood or urine, and associated organ dysfunction (Palumbo and Anderson, 2011). Clinical Features Leoncini and Korngold (1964) described multiple myeloma in 2 sisters and reviewed the literature on familial cases. Manson (1961) reported affected sisters, one of whom also had pernicious anemia. Myeloma has also been observed in father and son (Nadeau et al., 1956).
    • Multiple Myeloma Mayo Clinic
      Overview Multiple myeloma is a cancer that forms in a type of white blood cell called a plasma cell. Healthy plasma cells help you fight infections by making antibodies that recognize and attack germs. In multiple myeloma, cancerous plasma cells accumulate in the bone marrow and crowd out healthy blood cells. Rather than produce helpful antibodies, the cancer cells produce abnormal proteins that can cause complications. Treatment for multiple myeloma isn't always necessary right away. If the multiple myeloma is slow growing and isn't causing signs and symptoms, your doctor may recommend close monitoring instead of immediate treatment.
    • Multiple Myeloma Orphanet
      Multiple myeloma (MM) is a malignant tumor of plasma cell characterized by overproduction of abnormal plasma cells in the bone marrow and skeletal destruction. The clinical features are bone pain, renal impairment, immunodeficiency, anemia and presence of abnormal immunoglobulins (Ig).
    • Multiple Myeloma GARD
      Multiple myeloma is a form of cancer that occurs due to abnormal and uncontrolled growth of plasma cells in the bone marrow. Some people with multiple myeloma, especially those with early stages of the condition, have no concerning signs or symptoms. When present, the most common symptom is anemia, which can be associated with fatigue and shortness of breath. Other features of the condition may include multiple infections; abnormal bleeding; bone pain; weak and/or easily broken bones; and numbness and/or weakness of the arms and legs. The exact underlying cause of multiple myeloma is currently unknown. Factors that are associated with an increased risk of developing multiple myeloma include increasing age, male sex, African American race, radiation exposure, a family history of the condition, obesity, and/or a personal history of monoclonal gammopathy of undetermined significance (MGUS ).
  • Brachial Plexus Injury Wikipedia
    Recovery takes place without wallerian degeneration . [26] [27] Axonotmesis : Involves axonal degeneration, with loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and perineurium , are preserved). [26] [28] Neurotmesis : The most severe form of nerve injury, in which the nerve is completely disrupted by contusion, traction or laceration.
    SEMA3F, SEMA3A
  • First Red Scare Wikipedia
    The Senators heard various views of women in Russia, including claims that women were made the property of the state. [27] The press reveled in the investigation and the final report, referring to the Russians as "assassins and madmen," "human scum," "crime mad," and "beasts." [28] The occasional testimony by some who viewed the Bolshevik Revolution favorably lacked the punch of its critics.
  • Hiv/aids In New York City Wikipedia
    Joseph credited activists such as Yolanda Serrano , the head of the Association for Drug Abuse Prevention and Treatment (ADAPT) for calling attention to how the problem of addiction was far less dire than the overwhelming number of deaths from the rapidly spreading AIDS epidemic. [21] : 6 However, at the start of Mayor David Dinkins administration in 1990, the only legal needle exchange program was shut down. [25] Following new studies that demonstrated reduction in HIV infection rates, new programs restarted in New York City in 1992. [28] Comparison with San Francisco [ edit ] No two cities were more prominent in the battle against AIDS in the 1980s than New York and San Francisco. ... Rockwell; D.C.D. Jarlais; R. Elovich (28 December 2006). "Harm reduction theory: Users culture, micro-social indigenous harm reduction, and the self-organization and outside-organizing of users' groups" . ... Koch Collection, Koch Oral History Collection. Koch, Edward I. (28 July 2011). "LaGuardia and Wagner Archives Oral History: Mayor Ed Koch discusses the needle exchange program" (Video) .
  • Scurvy Wikipedia
    In the 1497 expedition of Vasco da Gama , the curative effects of citrus fruit were already known [25] [26] and confirmed by Pedro Álvares Cabral and his crew in 1507. [27] The Portuguese planted fruit trees and vegetables in Saint Helena , a stopping point for homebound voyages from Asia, and left their sick, who had scurvy and other ailments, to be taken home by the next ship if they recovered. [28] In 1500, one of the pilots of Cabral 's fleet bound for India noted that in Malindi , its king offered the expedition fresh supplies such as lambs, chickens, and ducks, along with lemons and oranges, due to which "some of our ill were cured of scurvy". [29] [30] Unfortunately, these travel accounts did not stop further maritime tragedies caused by scurvy, first because of the lack of communication between travelers and those responsible for their health, and because fruits and vegetables could not be kept for long on ships. [31] In 1536, the French explorer Jacques Cartier , exploring the St. ... Westmead Institute for Medical Research . 28 November 2016. Archived from the original on 23 August 2017 .
  • Chronic Cerebrospinal Venous Insufficiency Controversy Wikipedia
    Problems with the innominate vein and superior vena cava have also been reported to contribute to CCSVI. [26] A vascular component in MS had been cited previously. [27] [28] Several characteristics of venous diseases make it difficult to include MS in this group. [14] In its current form, CCSVI cannot explain some of the epidemiological findings in MS. ... Consensus document of the International Union of Phlebology (IUP)-2009". International Angiology . 28 (6): 434–51. PMID 20087280 . ^ "CCSVI – current studies" . mssociety.org.uk .
  • Doping In Sport Wikipedia
    The chairman of the Dutch cycling federation, Piet van Dijk, said of Rome that "dope – whole cartloads – [were] used in such royal quantities." [28] The 1950s British cycling professional Jock Andrews would joke: "You need never go off-course chasing the peloton in a big race – just follow the trail of empty syringes and dope wrappers." [29] The Dutch cycling team manager Kees Pellenaars told of a rider in his care: I took him along to a training camp in Spain.
  • Lung Cancer Wikipedia
    As more damage accumulates, the risk for cancer increases. [24] Smoking [ edit ] Tobacco smoking is by far the main contributor to lung cancer. [4] Cigarette smoke contains at least 73 known carcinogens , [25] including benzo[ a ]pyrene , [26] NNK , 1,3-butadiene , and a radioactive isotope of polonium – polonium-210 . [25] Across the developed world, 90% of lung cancer deaths in men and 70% of those in women during the year 2000 were attributed to smoking. [27] Smoking accounts for about 85% of lung cancer cases. [7] A 2014 review found that vaping may be a risk factor for lung cancer but less than that of cigarettes. [28] Passive smoking – the inhalation of smoke from another's smoking – is a cause of lung cancer in nonsmokers.
    FGF9, FOXM1, HP, KRAS, PTGS2, ROBO1, XPC
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