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Philadelphia Chromosome
Wikipedia
For second remission (CR2), if achieved, both chemotherapy and transplant options are possible, and many physicians prefer transplant. [ citation needed ] History [ edit ] The Philadelphia chromosome was first discovered and described in 1959 by David Hungerford from Fox Chase Cancer Center (then the Institute for Cancer Research) and Peter Nowell from the University of Pennsylvania School of Medicine , and was named after the city in which both facilities are located. [1] [27] [28] Hungerford was writing his doctoral thesis on chromosomes in a genetics lab at Fox Chase Cancer Center, and detected a tiny flaw in chromosomes from the blood cells of patients with a type of leukemia.
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Sarcoma
Wikipedia
Around 50% of bone sarcomas and 20% of soft-tissue sarcomas are diagnosed in people under the age of 35. [28] Some sarcomas, such as leiomyosarcoma , chondrosarcoma , and gastrointestinal stromal tumor (GIST), are more common in adults than in children. [2] Most high-grade bone sarcomas, including Ewing's sarcoma and osteosarcoma , are much more common in children and young adults. [2] In fossils [ edit ] In 2016, scientists reported the discovery of an osteosarcoma tumor in a 1.6-1.8 million-year-old fossil from the skeleton of now-extinct hominin species, making it the earliest-known case of human cancer. [29] Research [ edit ] Treatment of sarcoma, especially when the sarcoma has spread, or "metastasized", often requires chemotherapy but existing chemotherapeutic medicines are associated with significant toxicities and are not highly effective in killing cancer cells. [3] Therefore, research to identify new medications to treat sarcoma is being conducted as of 2019 [update] . [3] One possibility is the use of cancer immunotherapy (e.g., immune checkpoint inhibitors like anti-PD1, anti-PDL1, and anti-CTLA4 agents) to treat sarcomas. [30] This is not yet an established treatment tool. [30] Other strategies, such as small-molecule targeted therapy , biologic agents (e.g., small interfering RNA molecules), and nanoparticle-directed therapy, also are being investigated. [3] Research to understand the specific genetic and molecular factors that cause sarcoma to develop is underway. [3] This could allow for the design of new targeted therapies and allow physicians to more accurately predict a patient's prognosis. [3] Presence of the H3-B3 immunoregulatory checkpoint receptor in the tumor cells provides the opportunity for clinical trial testing of new drugs and targeted agents and immunotherapies in development.
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Hyperthyroidism
Wikipedia
This includes those that cannot tolerate medicines for one reason or another, people that are allergic to iodine, or people that refuse radioiodine. [27] If people have toxic nodules treatments typically include either removal or injection of the nodule with alcohol. [28] Radioiodine [ edit ] In iodine-131 ( radioiodine ) radioisotope therapy , which was first pioneered by Dr. ... Archived from the original on 19 January 2008 . Retrieved 28 January 2007 . ^ "Hyperthyroidism Overview" . Archived from the original on 28 April 2010 . Retrieved 27 April 2010 . ^ a b Andersson, Maria; Zimmermann, Michael B. (2010). Influence of Iodine Deficiency and Excess on Thyroid Function Tests . Endocrine Updates. 28 . pp. 45–69. doi : 10.1007/978-1-4419-1485-9_3 . ... Veterinary Information Network . Retrieved 28 January 2007 . Brent, Gregory A. (Ed.), Thyroid Function Testing , New York : Springer, Series: Endocrine Updates, Vol. 28, 1st Edition., 2010.CAT, GPX1, SOD1, GSR, TSHR, PON1, CARTPT, SOD2, AQP1, NR1D1, SERPINA7, PPARGC1A, UCP3, CP, PCSK1, CTSL, MTHFR, VIM, UGT1A1, CAB39, MCM7, HMOX1, IGF1R, ADIPOQ, BDH1, IL10, ANXA1, ANXA5, SLC34A1, ANXA2, APOC3, STK11, SLC9A1, APOA1, APOA2, THRB, AKT1, KCNJ18, GNAS, FOXP3, HLA-DRB1, ND6, TRNL1, TRNF, TRNH, RRM2B, TRNQ, TRNS1, ND5, RREB1, ND4, ND1, SLC25A4, MICOS10, COX3, COX2, COX1, POLG2, POLR3A, PDE10A, PDE8B, SEC24C, PTCSC2, GP1BB, TRNS2, MSTO1, TPO, JMJD1C, ARVCF, FAM227B, CACNA1S, TMEM71, TBX1, POLG, COMT, PIK3CA, LINC00511, PTEN, PRDM11, HIRA, TRNW, UFD1, BTNL2, TWNK, SLC16A2, HT, TG, SHBG, IGF1, REN, GH1, DIO2, VDR, VWF, SLC5A5, PAX8, MOK, LEP, PTH, PRL, TH, IL13, CLOCK, SST, RNH1, UCP2, NOS3, IL6, BCL2, CS, CST3, IL4, CTLA4, DIO1, EDN1, SHC3, SOST, F3, FN1, CD40, COX8A, PTPN22, BGLAP, GDF1, AHSG, AGT, PPP1R13L, AGTR1, AZGP1, MAGI3, WNK1, EHMT1, PGR-AS1, TM7SF2, GPR174, ZGLP1, THRA, CGB5, TGFB1, POTEF, MIR206, BCAR4, SYT1, LINC01193, CGB8, TXNRD3, COPD, PPARGC1B, NRG4, TNF, BACH2, GORASP1, DKK1, RAPGEF5, GDF15, ATG5, NAMPT, RNASET2, ATP6AP2, CPQ, LOH19CR1, FGF23, TXNRD2, STAT5B, TRPV1, SMG1, TRH, LMOD1, FGF21, MAT2B, SETD2, CD274, ICOS, CMAS, COQ9, RNF213, UCP1, TTN, TSHB, STAT6, ACP3, STAT5A, CGB3, CTH, CYP7A1, ACE, DIO3, DMD, DMP1, DNMT1, EGFR, EGR1, ELANE, EPHA3, F2, FCGRT, FLNB, XRCC6, GABPA, GCG, GIP, GJA1, GLP1R, GPX4, CPB2, CGA, STAT4, CETP, ADA, ADCY1, ADRB2, AGTR2, ALB, ANGPT1, APOB, APOD, APP, ARNTL, ATP2A2, BAAT, HCN2, BRCA1, C6, CA1, CALCA, SERPINA6, CBS, CD34, CD40LG, GSK3B, HIF1A, HLA-A, HLA-C, ACTB, NPY, NT5E, SERPINE1, PC, PDCD1, PDE3B, ENPP2, SLC26A4, ABCB1, PITX2, PPARA, PPARG, PRKAA1, PRKAA2, PRKAB1, RELA, RPS19, SLC2A1, SLC2A3, SLC2A4, NFE2L2, MYD88, MPST, IL2RA, HLA-DPB1, HLA-DQA1, HOXD13, HSPA4, HTC2, IFNG, IGFBP1, IGFBP3, IL2, CXCL8, MEN1, IL12B, ISG20, KNG1, KRT19, LDLR, LHB, LIPE, LPA, MBL2, CBSL
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Asperger Syndrome
Wikipedia
Pronunciation / ˈ æ s p ɜːr ɡ ər z / , [4] /- dʒ ər z / [5] Specialty Clinical psychology , psychiatry , pediatrics , occupational medicine Symptoms Problems with social interaction, non-verbal communication, restricted interests, and repetitive behavior [6] Complications Social isolation, employment problems, family stress, bullying , self-harm [7] Usual onset Before two years old [6] Duration Long term [6] Causes Unknown [6] Diagnostic method Based on the symptoms [8] Medication For associated conditions [9] Frequency 37.2 million (2015) [10] Asperger syndrome ( AS ), also known as Asperger's , is a neurodevelopmental disorder characterized by significant difficulties in social interaction and nonverbal communication , along with restricted and repetitive patterns of behavior and interests. [6] It is an autism spectrum disorder (ASD), [11] but differs from other ASDs by relatively unimpaired language and intelligence . [12] Although not required for diagnosis, physical clumsiness and unusual use of language are common. [13] [14] Signs usually begin before two years of age and typically last for a person's entire life. [6] The exact cause of Asperger's is unknown. [6] While it is largely inherited , the underlying genetics have not been determined conclusively. [13] [15] Environmental factors are also believed to play a role. [6] Brain imaging has not identified a common underlying condition . [13] In 2013, the diagnosis of Asperger's was removed from the Diagnostic and Statistical Manual of Mental Disorders ( DSM-5 ), with the symptoms now included within the autism spectrum disorder along with autism and pervasive developmental disorder not otherwise specified (PDD-NOS). [6] [16] It remains within the International Classification of Diseases ( ICD-11 ) as of 2019 [update] as a subtype of autism spectrum disorder. [17] [18] There is no single treatment, and the effectiveness of particular interventions is supported by only limited data. [13] Treatment is aimed at lowering obsessive or repetitive routines and improving communication skills and physical clumsiness. [9] Interventions may include social skills training, cognitive behavioral therapy , physical therapy , speech therapy , parent training, and medications for associated problems, such as mood or anxiety. [9] Most children improve as they grow up, but social and communication difficulties usually persist. [19] Some researchers and people on the autism spectrum have advocated a shift in attitudes toward the view that autism spectrum disorder is a difference rather than a disease that must be treated or cured. [20] [21] In 2015, Asperger's was estimated to affect 37.2 million people globally (about 0.5% of people). [10] Autism spectrum disorder is diagnosed in males more often than females, and females are typically diagnosed at a later age. [22] [23] The syndrome is named after the Austrian pediatrician Hans Asperger , who, in 1944, described children in his care who struggled to form friendships, did not understand others' gestures or feelings , engaged in one-sided conversations about their favorite interests, and were clumsy. [24] The modern conception of Asperger syndrome came into existence in 1981 and went through a period of popularization. [25] [26] [27] It became a standardized diagnosis in the early 1990s. [28] Many questions and controversies about the condition remain. [19] There is doubt about whether it is distinct from high-functioning autism (HFA). [29] Partly because of this, the percentage of people affected is not firmly established. [13] Contents 1 Classification 2 Characteristics 2.1 Social interaction 2.1.1 Violent or criminal behavior 2.2 Restricted and repetitive interests and behavior 2.3 Speech and language 2.4 Motor and sensory perception 3 Causes 4 Mechanism 4.1 Connectivity theory 4.2 Mirror neuron system (MNS) theory 5 Diagnosis 5.1 Differential diagnosis 6 Screening 7 Management 7.1 Therapies 7.2 Medications 8 Prognosis 9 Epidemiology 10 History 11 Society and culture 12 Further reading 13 References Classification The extent of the overlap between AS and high-functioning autism ( HFA – autism unaccompanied by intellectual disability ) is unclear. [29] [30] [31] The ASD classification is to some extent an artifact of how autism was discovered, [32] and may not reflect the true nature of the spectrum; [33] methodological problems have beset Asperger syndrome as a valid diagnosis from the outset. [34] [35] In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published in May 2013, [36] AS, as a separate diagnosis, was eliminated and folded into autism spectrum disorder. [37] Like the diagnosis of Asperger syndrome, [38] the change was controversial [38] [39] and AS was not removed from the WHO's ICD-10 or ICD-11 . [17] [40] The World Health Organization (WHO) defined Asperger syndrome (AS) as one of the autism spectrum disorders (ASD) or pervasive developmental disorders (PDD), which are a spectrum of psychological conditions that are characterized by abnormalities of social interaction and communication that pervade the individual's functioning, and by restricted and repetitive interests and behavior. ... Revista Brasileira de Psiquiatria (in Spanish). 28 (Suppl 1): S3–11. doi : 10.1590/S1516-44462006000500002 .DISC1, SLC6A4, VIP, ARSD, NLN, DISC2, NRXN1, TSNAX, OXTR, BDNF, NOS2, NOS1, MTHFR, MECP2, GABRB3, CTSL, SHANK3
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Confabulation
Wikipedia
Although confabulation is usually coherent in its presentation, confabulations of schizophrenic patients are often delusional [27] Researchers have noted that these patients tend to make up delusions on the spot which are often fantastic and become increasingly elaborate with questioning. [28] Unlike patients with Korsakoff's and Alzheimer's, patients with schizophrenia are more likely to confabulate when prompted with questions regarding their semantic memories, as opposed to episodic memory prompting. [29] In addition, confabulation does not appear to be related to any memory deficit in schizophrenic patients. ... Quarterly Journal of Experimental Psychology . 49A (1): 5–28. doi : 10.1080/713755608 . S2CID 54633639 . ^ Dalla Barba G (1993).
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Non-Hodgkin Lymphoma
Wikipedia
As a consequence, rates of non-Hodgkin lymphoma (NHL) in people infected with HIV has significantly declined in recent years. [13] Treatment [ edit ] The traditional treatment of NHL includes chemotherapy , radiotherapy , and stem-cell transplants . [26] [27] There have also been developments in immunotherapy used in the treatment of NHL. [28] Chemotherapy [ edit ] The most common chemotherapy used for B-cell non-Hodgkin lymphoma is R-CHOP , which is a regimen of four drugs (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus rituximab. [29] Treatment complications [ edit ] If participants receive stem-cell transplants, they can develop a graft-versus-host disease .RAD54L, RAD54B, BCL2, BCL6, FAS, CASP10, CSF3, MTHFR, HLA-DRB1, NPM1, TYMS, NBN, SHMT1, CBS, CD79B, BRAF, CYP2E1, PAX5, TFRC, IFNA2, BCL10, CSF2, CD79A, CHEK2, FPGS, PRF1, BHMT, SPEN, TBL1XR1, EPHX1, IKBKB, CREBBP, S1PR2, MTSS1, ATM, TET2, KIT, ASXL1, NTHL1, LTA, MS4A1, IL10, SRSF2, CD19, TNFRSF8, ABCB1, CCND1, IGH, IL2, KRT20, RTEL1, ALK, SMUG1, EZH2, CDKN2A, PDLIM7, MYC, VEGFA, TP53, TNF, NAT2, IL6, LEP, IL4, GSTP1, NLRP2, CD37, IL2RA, IRF4, CXADR, NAT1, PIK3CD, TRBV20OR9-2, SPG7, ARR3, CXCL12, NR1I3, PRKAR1A, TRIM13, CDR3, CASR, CD274, CXADRP1, FGF2, FCGR3A, ERCC2, GSTT1, RBM45, GSTM1, MTR, STAT3, CD70, LEPR, CD40LG, CD34, CXCL8, TNFSF10, NCAM1, NOS2, AICDA, MDM2, PIK3CA, TBC1D9, FCGR2A, MTRR, PIK3CB, TNFSF13B, TLR2, DLC1, PIK3CG, MAPK1, XRCC1, VDR, H3P10, AKT1, CD22, BCR, CASP8, CD44, CD40, CDKN2B, IL12A, CASP3, CD47, IFI27, ALDH1L1, HPGDS, CASP9, IL13, CXCR4, FOXP3, GPX1, CALM3, DCTN6, TLR9, ZNRD2, CALM2, FOXO1, PLK1, BCL2L11, CLLS2, IL1RN, DLEC1, HDAC9, PON1, CALM1, IGL, CDK2, TMED7, PSMD9, CD28, TP73, H3P23, HLA-DQB1, CTLA4, TMED7-TICAM2, SELL, CD38, MIR21, MRE11, RNASE3, CCR5, LINC01194, MSH2, TICAM2, KRIT1, AHR, NPAS2, NFKB1, CAMKMT, H2AX, SERPING1, RAF1, TNFRSF13C, MYD88, CCL21, BTK, RIT1, PTPN6, PTEN, TSPO, BRCA1, BRD2, PDCD1, PLXNA2, CCND3, MCL1, MGMT, MKI67, MMP2, MMP9, MOS, MPO, ABCC1, MTX1, PIM1, MUC1, MYOD1, NME1, NPR2, CAT, PCNA, SOD2, CASP1, SLC16A1, WRN, CXCR5, AURKA, POLDIP2, MCAT, MCTS1, NXT1, POLE3, MIB1, BACH2, MARCKSL1, WLS, ARHGAP24, TXLNA, IFNL3, CLEC4D, SLC35B2, ASPG, MIR150, MIR155, MIR203A, MIR34A, FAM72B, CCR2, FAM72A, MEF2B, KLRC4-KLRK1, ERVK-32, H3P9, H3P11, RNF19A, TNFAIP8, TOGARAM1, TP63, SYK, TGFB1, TIMP1, TIMP2, TLR1, BCL3, TRAF1, TRAF3, BAX, GPANK1, AIMP2, NR0B2, DYNLL1, ANXA5, TNFRSF10B, SOCS3, GRAP2, KLK3, HDAC6, RAD50, CIB1, MRPL28, AHSA1, SUB1, XIAP, KLRK1, LTB, CRK, FH, CCR7, ERBB2, CYBA, KDR, HLA-G, FN1, ISG20, CYP2B6, CYP2C9, CDKN1B, IL18, HLA-B, HLA-A, CDC25A, CEBPA, FGFR4, EPO, CYP1A1, DDIT3, MAPK14, GBA, CMA1, IRF8, LGALS1, LYVE1, TPX2, GOLGA7, LEF1, CCR9, ACSBG1, HSPH1, ANXA1, FCGR1A, CES1, PLEKHO1, WT1-AS, FCGR2B, FCN2, SF3B1, CCL27, RASSF1, UBE2C, EBNA1BP2, FCGR3B, C1RL, ALPP, ANPEP, ERCC5, GPR132, PSAT1, ERVW-1, DLL1, IGHV1-12, SMARCAL1, IGHV3-69-1, IGHV3OR16-7, CHEK1, PDLIM3, ICOS, EPHX2, ESR1, MASP2, ATRNL1, ETS1, PART1, DERL2, CFL1, ANG, CADM1, LMNA, BIRC5, FRA16B, FASLG, BCLAF1, CDKN2C, RGS6, TCL1B, NCOR2, CYTIP, CLOCK, BAG5, EEF1E1, NPEPPS, ADIPOQ, CD52, KLF4, AR, ARG1, ARHGEF2, FCGR2C, ARTN, MTOR, LIMD1, MBD2, RHOA, PER3, BMS1, SLC23A2, SLC23A1, FLT4, KHDRBS1, SLCO1B1, FGFR1, GDE1, FOXM1, CRTAP, APOH, TUBA1B, TLR6, AKR1A1, TNIP1, LANCL1, DLEU1, SPRY2, RABEPK, APRT, ZNF197, FLT1, EDIL3, SMC4, FLT3, FLT3LG, TANK, ATRAID, TMEM260, ALDH1A1, EPHB2, MIR28, MIR26B, CYP1B1, MIR200B, MIR152, CYP17A1, MIR143, MIR124-1, MIRLET7B, CYP24A1, LOC390714, KMT5A, CYP27B1, GSTK1, CD55, DAPK1, ARMH1, DCC, H19, ACE, CTAG1A, TIGIT, AKR1C1, ACACA, RMDN2, MIR17HG, XRCC6P5, MIR148B, ERVK-20, H3P5, H3P28, CR2, COMT, CSF3R, LOC105379528, UPK3B, LOC102724971, LOC102723407, ERVK-18, H3P12, CTAG1B, KIR2DL5B, CTNNB1, CUX1, CX3CR1, MIR618, OCM, LGALS7B, ACAA1, SCFV, MIR502, MIR202, H4C15, SLCO6A1, PARP1, TPPP2, DHX33, E2F1, IL21, CXCL16, C6orf47, POLD4, CFAP97, EEF2, SCYL1, EIF4A2, KIR2DL5A, GOPC, POLE4, ERVK-6, PCDHGB7, CFC1, CCAR1, AIF1, NAT10, LAMTOR1, GGH, EIF4E, FBLIM1, ALB, EIF4G1, IGAN1, PLEKHG2, H4-16, CARD11, MIR155HG, TIRAP, NLRP3, CDCA5, PRRT2, MUC16, MTDH, TSLP, DIXDC1, PWWP3A, HAVCR2, MIXL1, RAPH1, DDT, TLR10, DEFB126, RNF34, ASRGL1, DECR1, DNMT1, AGRP, VTCN1, BIRC7, DPP4, CDK5R1, RHOH, NRP1, P2RX7, PRKCB, PRKCA, FMNL1, CDH13, IL1B, PMS1, PML, CDC6, PLAG1, IL2RG, CDK11B, IL5, CD59, IL7R, IL9, PDGFRB, PDGFRA, PDE6H, IL10RA, IL12B, SERPINA5, PC, IL12RB1, PAFAH1B1, PAEP, IFNGR2, MAPK3, MAPK8, PTPRC, ICAM1, RMD1, ID4, RING1, RFC1, RCD1, RB1, IDH1, RAC2, NECTIN2, PTPRJ, PTPN13, MAP2K1, PTPN11, IDH2, PTGS2, CDK4, IFNG, PSMD7, PSMB9, PSMB6, RELN, PROS1, PRL, PEBP1, ORC4, RORB, OGG1, MSMB, MSH5, KIR2DS1, KIR3DS1, KRAS, KRT81, MNAT1, LAIR1, MMP3, RPSA, MMP1, MME, KMT2A, LBR, CD33, MFAP1, MDM4, TNFSF8, MDK, MBP, EPCAM, SH2D1A, LTK, LGALS3, LGALS7, MTAP, MTHFD1, CD14, NFKBIL1, NTRK1, IL15, IL16, CAV3, TNFRSF9, NOTCH4, NPY, NOS3, SERPINA6, NOS1, NGF, IDO1, CD5, NEDD9, NCF4, CCK, INSL3, INSR, MYCN, MYCL, CCND2, ISL1, ITGB3, JAK2, RORA, RPS6, CES2, GZMB, ADAM12, MAFK, GPT, GSTM3, PRRC2A, IL1R2, ZMYM2, ZBTB16, ZAP70, YWHAE, YY1, XRCC4, B2M, XPO1, CDKN1A, VIPR1, VIP, MSH6, BCHE, VCAM1, UCP1, UBE2I, TYRO3, BCL2L1, TRAF6, KMT2D, GPR34, TCL1A, H4C14, TNFRSF10A, G6PD, TNFRSF14, LSP1, TNFSF13, NCOA1, AKR1C3, GCHFR, DYRK2, ATHS, GNA15, H4C13, ATIC, H4C5, H4C2, H4C8, H4C3, H4C11, H4C12, H4C6, H4C4, H4C1, H4C9, NCOA3, GUCY2D, TPM3, RRM1, HBB, SRC, SPP1, SPN, HOXC5, HOXC6, SOAT1, SLPI, SLC19A1, HRAS, STIL, PMEL, SHMT2, HSPA1L, BRCA2, SEMG1, HSPA4, SELE, HSPD1, TNC, CCL5, CCL1, SAI1, S100A4, RYR3, RXRB, SST, BLM, STAT6, THY1, HGF, TNFRSF1B, TNFRSF1A, TNFAIP3, BCL7A, TSPAN7, TNFRSF17, HIC1, TJP1, HIF1A, TIA1, TGFBR3, HMGB1, TGFBR2, TGFBR1, CDK6, TFDP1, TERT, TERC, CRY2, TCN1, TCF3, TAT, TAP2, BDNF
- Citrullinemia Type I Gene_reviews
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Postpartum Psychosis
Wikipedia
But there is evidence of four other triggers – late postpartum, [27] prepartum, [28] post-abortion [29] and weaning. [30] Marcé, widely considered an authority on puerperal psychoses, [31] claimed that they could be divided into early and late forms; the late form begins about six weeks after childbirth, associated with the return of the menses. [32] His view is supported by the large number of cases in the literature with onset 4-13 weeks after the birth, mothers with serial 4-13 week onsets and some survey evidence. [33] The evidence for a trigger acting in pregnancy is also based on the large number of reported cases, and particularly on the frequency of mothers suffering two or more prepartum episodes.ESR1, STS, CXCL8, MIR212, MIR146A, TNF, THRA, SLC6A4, CCN3, ITGAX, IL6, CSTB, IGFBP2, HTR2C, NR3C1, EIF4EBP1, DLX4, CCN2, THRA1/BTR
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Nemaline Myopathy
Wikipedia
Another group of Australian researchers has since published an article recognizing Reye for his work. [28] "Nemaline myopathy" was first named in a published paper in 1963 by North American researchers P.E.TNNT1, NEB, TPM3, TPM2, ACTA1, KLHL41, KLHL9, NEFL, SRPK3, POMGNT1, FKTN, CHKB, B4GAT1, ITGA7, LMNA, POMT1, FKRP, LARGE1, CFL2, RIF1, ACTB, TPM1, KLHL40, LMOD3, RYR1, KBTBD13, MSTN, ACTC1, HTC2, CUL3, DES, C16orf82, ACTA2, MYO18B, MYPN, MCOLN1, ACTN1, UCP3, EMD, EIF3K, HK1, GJB6, MYH7, NRAP, MYOT, TNNT3, ACHE
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Macular Degeneration
Wikipedia
Absence of the complement factor H-related genes R3 and R1 protects against AMD. [26] [27] Two independent studies in 2007 showed a certain common mutation Arg80Gly in the C3 gene, which is a central protein of the complement system , is strongly associated with the occurrence of AMD. [28] [29] The authors of both papers consider their study to underscore the influence of the complement pathway in the pathogenesis of this disease. ... "Diagnostic accuracy of the Amsler grid and the preferential hyperacuity perimetry in the screening of patients with age-related macular degeneration: systematic review and meta-analysis" . Eye . 28 (7): 788–96. doi : 10.1038/eye.2014.104 .FSCN2, ABCA4, CRYAB, CD36, SERPINF1, PRPH2, BBS10, DYRK1A, TUBB6, CNGA3, AFG3L2, ELOVL4, BEST1, C1QTNF5, CFH, RS1, TST, RPGR, VEGFA, ATXN7, CRP, EFEMP1, RPE, PRPF31, CP, CDHR1, MFRP, COL18A1, LRRTM4, CX3CR1, CNGB3, VSX1, E2F2, HTRA1, F3, PROM1, GPX3, TTPA, IMPDH1, TLR2, TIMP3, MMP2, PLXNA2, ARMS2
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Graves' Disease
Wikipedia
Smoking was shown to have an impact independent to a positive TSHR-Ab. [28] Radioiodine [ edit ] Scan of affected thyroid before ( top ) and after ( bottom ) radioiodine therapy Radioiodine (radioactive iodine-131) was developed in the early 1940s at the Mallinckrodt General Clinical Research Center . ... Louis, Missouri: Missouri History Museum. ^ Altman LK (1991-05-28). "The Doctor's World — A White House Puzzle: Immunity Ailments-Science Section" . ... "Rare Disease Could Whack Sammy Bull" . New York Post . Retrieved January 28, 2020 . ^ "Hamilton talks about his disease on his podcast" .
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Depersonalization-Derealization Disorder
Wikipedia
It has been thought that depersonalization can be caused by a biological response to dangerous or life-threatening situations which causes heightened senses and emotional numbing. [11] Psychosocial [ edit ] There is growing evidence linking physical and sexual abuse in childhood with the development of dissociative disorders. [23] Childhood interpersonal trauma – emotional abuse in particular – is a significant predictor of a diagnosis of DPDR. [25] Compared to other types of childhood trauma, emotional abuse has been found to be the most significant predictor both of a diagnosis of depersonalization disorder and of depersonalization scores, but not of general dissociation scores. [26] Some studies suggest that greater emotional abuse and lower physical abuse predict depersonalization in adult women with PTSD. [27] Patients with high interpersonal abuse histories (HIA) show significantly higher scores on the Cambridge Depersonalization Scale, when compared to a control group. [28] [7] Earlier age of abuse, increased duration and parental abuse tend to correlate with severity of dissociative symptoms. [23] [29] Besides traumatic experiences, other common precipitators of the disorder include severe stress , major depressive disorder , panic attacks , and psychoactive substances. [30] People who live in highly individualistic cultures may be more vulnerable to depersonalization, due to threat hypersensitivity and an external locus of control . [31] Neurobiology [ edit ] Animated image showing prefrontal cortex which is thought to play a role in DPDR There is converging evidence that the prefrontal cortex may inhibit neural circuits that normally form the basis of emotional experience. [32] In an fMRI study of DPD patients, emotionally aversive scenes activated the right ventral prefrontal cortex . ... S2CID 220602831 . ^ Aponte-Soto, Michell; Martinez-Taboas, Alfonso; Vélez-Pastrana, María C.; González, Rafael A. (28 June 2019). "The Relationship between Interpersonal Abuse and Depersonalization Experiences" .
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Malocclusion
Wikipedia
A deep bite (also known as a Type II Malocclusion) is a condition in which the upper teeth overlap the lower teeth, which can result in hard and soft tissue trauma, in addition to an effect on appearance. [25] It has been found to occur in 15-20% of the US population. [26] An open bite is a condition characterised by a complete lack of overlap and occlusion between the upper and lower incisors. [27] In children, open bite can be caused by prolonged thumb sucking. [28] Patients often present with impaired speech and mastication. [29] Overbites [ edit ] This is a vertical measurement of the degree of overlap between the maxillary incisors and the mandibular incisors. ... "An Introduction to Orthodontics, 2nd edn". Journal of Orthodontics . 28 (4): 320. doi : 10.1093/ortho/28.4.320 . ^ a b Houston, W. ... Progress in Orthodontics . 19 (1): 28. doi : 10.1186/s40510-018-0218-0 .
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Mental Disorder
Wikipedia
Some neurologists argue that classification will only be reliable and valid when based on neurobiological features rather than clinical interview, while others suggest that the differing ideological and practical perspectives need to be better integrated. [26] [27] The DSM and ICD approach remains under attack both because of the implied causality model [28] and because some researchers believe it better to aim at underlying brain differences which can precede symptoms by many years. [29] Dimensional models The high degree of comorbidity between disorders in categorical models such as the DSM and ICD have led some to propose dimensional models.
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Wolf-Hirschhorn Syndrome
Omim
The crude infant mortality rate was 23 of 132 (17%), and in the first 2 years of life the mortality rate was 28 of 132 (21%). Cases with large de novo deletions (proximal to and including p15.2) were more likely to have died than those with smaller deletions (odds ratio = 5.7; 95% confidence interval 1.7 to 19.9).NSD2, LETM1, FGFRL1, NELFA, MSX1, WHCR, CPLX1, WTRS, CTBP1, HTC2, IL1RL1, FGFR3, SET, CDKN2A, C4orf48, TACC3, LAP3, LAMTOR2, H3P8, RPP14, SUB1, SF3B6, ALB, CDK2AP2, SLBP, ZNF141, WFS1, S100A9, OXA1L, RBPJ, GH1, EZH2, DRD5, H3P10
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Borderline Personality Disorder
Wikipedia
This phenomenon is sometimes called splitting . [25] Combined with mood disturbances, idealization and devaluation can undermine relationships with family, friends, and co-workers. [26] While strongly desiring intimacy, people with BPD tend toward insecure, avoidant or ambivalent, or fearfully preoccupied attachment patterns in relationships, [27] and often view the world as dangerous and malevolent. [23] Like other personality disorders, BPD is linked to increased levels of chronic stress and conflict in romantic relationships, decreased satisfaction of romantic partners, abuse , and unwanted pregnancy . [28] Behavior [ edit ] Impulsive behavior is common, including substance or alcohol abuse , eating in excess , unprotected sex or indiscriminate sex with multiple partners , reckless spending , and reckless driving . [29] Impulsive behavior may also include leaving jobs or relationships, running away, and self-injury. [30] People with BPD might do this because it gives them the feeling of immediate relief from their emotional pain , [30] but in the long term they feel increased shame and guilt over the inevitable consequences of continuing this behavior. [30] A cycle often begins in which people with BPD feel emotional pain, engage in impulsive behavior to relieve that pain, feel shame and guilt over their actions, feel emotional pain from the shame and guilt, and then experience stronger urges to engage in impulsive behavior to relieve the new pain. [30] As time goes on, impulsive behavior may become an automatic response to emotional pain. [30] Self-harm and suicide [ edit ] Scarring as a result of self-harm, which is a common sign in borderline personality disorder. [4] Self-harming or suicidal behavior is one of the core diagnostic criteria in the DSM-5 . [5] Self-harm occurs in 50 to 80% of people with BPD. ... However, these links may apply to personality disorders in general. [28] Adolescence [ edit ] Onset of symptoms typically occurs during adolescence or young adulthood, although symptoms suggestive of this disorder can sometimes be observed in children. [93] Symptoms among adolescents that predict the development of BPD in adulthood may include problems with body-image, extreme sensitivity to rejection, behavioral problems, non-suicidal self-injury, attempts to find exclusive relationships, and severe shame. [13] Many adolescents experience these symptoms without going on to develop BPD, but those who experience them are 9 times as likely as their peers to develop BPD.DPPA3, SLC6A4, BDNF, NR3C1, COMT, TPH1, HTR2A, ANK3, MAOA, CACNA1C, TPH2, SLC6A3, P2RX7, GAD1, FKBP5, DISC1, CLOCK, ZNF804A, MTHFR, MCF2, MAOB, MCPH1, HTR2C, HTR1B, P2RX1, HTR1A, NRG1, GSTT1, GSTM1, DGKH, P2RX5-TAX1BP3, NFKB1, P2RX3, P2RX2, P2RX4, P2RX5, P2RY1, P2RY2, ASCC1, SGSM3, GABRB2, BRD1, VEGFA, ARHGEF7, P2RX6, MTA2, BAG3, APBA3, TH, H3P40, DNMT1, DBT, CHRNA7, ERBB4, DPYSL2, GRK3, DRD2, DRD4, CD40, PDLIM5, CXCR6, WASF3, PDE10A, RAB40B, SHANK2, SIRT1, BPI, SYNE1, CACNG2, BCL2, TENM4, INTU, AVP, HPGDS, CAP2, G6PD, TRIM13, CASR, VASP, CHRM2, XBP1, SLC14A2, TAM, MAD1L1, SYNJ1, WASF1, LPAR2, IL18BP, VAPA, CAMK2A, NRXN3, CALB2, CACNA1E, BRS3, ZBED4, MCAT, NR1I3, ZDHHC8, ARR3, PRIMA1, SERINC5, ADRA2B, CEP85L, NPSR1, MIR124-3, MIR30A, MDD1, BDNF-AS, CXADRP1, WASH6P, ZGLP1, TAF9BP2, DIP, WASHC1, LINC01672, ADRA1A, STIN2-VNTR, KANK4, AKT1, REM1, CACNA2D4, TSPAN8, SHANK1, APOE, MZB1, NRN1, CDCA8, MSTO1, CHDH, ACKR3, NIF3L1, NPAS3, ETNPPL, MPPE1, APBA2, EHMT1, LMAN2L, ANGPT1, CHRNA2, TAC1, THAS, NR3C2, ENPEP, ENG, HTR1D, EGFR, EDNRA, HTR3A, ID2, IGFBP2, IL18, IMPA2, KCNQ2, KCNQ3, LDHA, LEP, FADS1, LPP, MAS1, HIF1A, HDAC2, HDAC1, GPC1, FGFR2, GAD2, GCG, GCH1, GFAP, GLP1R, GNAS, UTS2R, GSTZ1, MCHR1, GPR42, GRN, GRIK2, FGF9, F2R, EYA1, MAP3K10, MPST, TERC, DDC, SCN4B, SCN8A, SCN9A, CCL24, SLC1A2, SLC6A2, CRH, CMKLR1, SLC16A1, SLC18A1, SLC18A2, SMARCA4, SPG7, SST, SSTR4, VAMP7, FLNA, RARA, PVALB, RELN, OXTR, NGF, NHS, NINJ2, NOS3, NOTCH3, NR4A2, OTSC1, ACE, MAPK1, CXADR, CRP, ADCYAP1, CRHR2, CRHR1, PLCG1, PRKAR1A, ADCY2
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Respiratory Arrest
Wikipedia
Noninvasive positive pressure ventilation can be used in an outpatient setting for patients with obstructive sleep apnea. [28] See also [ edit ] Crash cart Respiratory failure References [ edit ] ^ Heilman, MD, James (2014-07-17), "Bagging" , Wikimedia Commons , retrieved 2019-11-25 ^ a b c "Overview of Respiratory Arrest - Critical Care Medicine" .
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Pulmonary Contusion
Wikipedia
In the inertial effect , the lighter alveolar tissue is sheared from the heavier hilar structures, an effect similar to diffuse axonal injury in head injury. [5] It results from the fact that different tissues have different densities, and therefore different rates of acceleration or deceleration. [10] In the spalling effect , lung tissue bursts or is sheared where a shock wave meets the lung tissue, at interfaces between gas and liquid. [20] The alveolar walls form such a gas-liquid interface with the air in the alveoli. [5] [27] The spalling effect occurs in areas with large differences in density; particles of the denser tissue are spalled (thrown) into the less dense particles. [28] The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas: the bubbles first implode, then rebound and expand beyond their original volume. [29] The air bubbles cause many tiny explosions, resulting in tissue damage; [29] the overexpansion of gas bubbles stretches and tears alveoli. [30] [31] This effect is thought to occur microscopically when the pressure in the airways increases sharply. [26] Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury , a contrecoup contusion may occur at the site opposite the impact as well. [24] A blow to the front of the chest may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. ... "Thoracic trauma: The deadly dozen". Critical Care Nursing Quarterly . 28 (1): 22–40. doi : 10.1097/00002727-200501000-00004 .
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Lymphocytic Choriomeningitis
Wikipedia
The island of Vir in Croatia is one of the biggest described endemic places of origin of LCMV in the world, with IFA testing having found LCMV antibodies in 36% of the population. [27] [28] Individuals with the highest risk of infection are laboratory personnel who handle rodents or infected cells. [7] Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter [7] when mice tend to move indoors. ... Charles River Laboratories International, Inc, 2009. Web. 28 Oct 2009. "Prevent LCMV from wild rodents."IFNG, IFNA1, IFNA13, TNF, ERVW-1, ERVK-6, ERVK-20, GZMB, AGFG1, TLR4, LAMTOR2, IL10, RPP14, SUB1, IL6, IRF9, CDK2AP2, TOX, DCAF1, S100A9, RIPK1, TRAF1, PDCD1, H3P8, RPAIN, SF3B6, TMBIM4, CDKN2A, HAVCR2, IL23A, IFNLR1, YME1L1, UBD, SPRY1, NR1H4, IL33, CLEC12A, IL27RA, IL21, ADAM7, IL27, STX11, NR0B2, WAS, KDM6A, TYROBP, VHLL, FGL2, GOPC, PRDX3, NELFCD, FOXP3, IL22, SH3KBP1, IL17D, ICOS, TREM1, LINC02605, KRT20, CD274, MIR31, CPVL, PTPN22, SOSTDC1, FBLIM1, CD2AP, CABIN1, KDM1A, USP18, DUSP10, MUPP, ADAR, TLR2, IL2, HLA-A, HIF1A, GYPC, GRN, CXCR3, NR5A2, MTOR, FOXO3, FCGR2B, FCER1G, FAT1, EZH2, EGR2, CTNNB1, CTLA4, CSF2, CHAT, CDC42, CD47, CD44, TNFRSF8, CD27, MS4A1, CA9, CEACAM1, ATP5F1B, FAS, IFN1@, IL7, THBS1, IL7R, TCF7, HNF1A, STAT4, ADM, STAT1, SOX2, SLAMF1, SELL, CCL2, RAG1, RAB5C, PTPN2, PSMB10, PSMB8, PRF1, PML, PHB, NPC1, MYD88, MBP, SH2D1A, KRT1, IRF7, CXCL10, IMPDH2, TNFRSF9, CXCL8, STAT2
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Dementia
Wikipedia
Subtypes may be based on various symptoms as may be due to a neurodegenerative disorder such as Alzheimer's disease ; frontotemporal lobar degeneration for frontotemporal dementia ; or Lewy body disease for dementia with Lewy bodies . [4] [13] More than one type of dementia, known as mixed dementia , may exist together. [4] Diagnosis is usually based on history of the illness and cognitive testing with imaging , and blood tests to rule out other possible causes, [5] and to determine the particular subtype. [14] The mini mental state examination is one commonly used cognitive test . [3] The greatest risk factor for developing dementia is aging, however dementia is not a normal part of aging. [4] Several risk factors for dementia are described with some such as smoking, and obesity being preventable by lifestyle changes. [7] Screening the general population for the disorder is not recommended. [15] There is no known cure for dementia. [2] Acetylcholinesterase inhibitors such as donepezil are often used and may be beneficial in mild to moderate disorder. [8] [16] [17] Overall benefit, however, may be minor. [8] [9] There are many measures that can improve the quality of life of people with dementia and their caregivers . [2] Cognitive and behavioral interventions may be appropriate. [2] Educating and providing emotional support to the caregiver is important. [2] Exercise programs may be beneficial with respect to activities of daily living and potentially improve outcomes. [18] Treatment of behavioral problems with antipsychotics is common but not usually recommended, due to the limited benefit and the side effects, including an increased risk of death. [19] [20] It was estimated in 2020 that dementia affected about 50 million people worldwide. [4] This is an increase on the 2015 estimate of 46 million. [21] About 10% of people develop the disorder at some point in their lives, [22] commonly as a result of aging . [23] About 3% of people between the ages of 65–74 have dementia, 19% between 75 and 84, and nearly half of those over 85 years of age. [24] In 2015 dementia resulted in about 1.9 million deaths, up from 0.8 million in 1990. [10] In 2020 it was reported that dementia was listed as one of the top ten causes of death worldwide. [25] As more people are living longer, dementia is becoming more common. [23] For people of a specific age, however, it may be becoming less frequent, at least in the developed world, due to a decrease in risk factors. [23] It is one of the most common causes of disability among the old. [3] Worldwide the cost of dementia in 2015 was put at US$818 billion . [4] People with dementia are often physically or chemically restrained to a greater degree than necessary, raising issues of human rights . [2] Social stigma against those affected is common. [3] Contents 1 Signs and symptoms 2 Stages 2.1 Mild cognitive impairment 2.2 Early stages 2.3 Middle stages 2.4 Late stages 3 Subtypes 3.1 Alzheimer's disease 3.2 Vascular dementia 3.3 Dementia with Lewy bodies 3.4 Frontotemporal dementia 3.5 Progressive supranuclear palsy 3.6 Corticobasal degeneration 3.7 Dementia due to prion disease 3.8 Alcohol-related dementia 4 Other conditions 4.1 Slowly progressive 4.2 Mixed dementia 5 Diagnosis 5.1 Cognitive testing 5.2 Laboratory tests 5.3 Imaging 6 Prevention 6.1 Risk factors 6.2 Dental health 6.2.1 Oral bacteria 6.2.2 Oral viruses 6.3 Other interventions 7 Management 7.1 Psychological and psychosocial therapies 7.2 Medications 7.3 Pain 7.4 Eating difficulties 7.5 Diet 7.6 Exercise 7.7 Alternative medicine 7.8 Palliative care 8 Epidemiology 9 History 9.1 Terminology 10 Society and culture 11 Notes 12 References 13 External links Signs and symptoms [ edit ] A drawing of a woman diagnosed with dementia A drawing of an old man diagnosed with senile dementia The signs and symptoms of dementia, are behavioral and psychological and termed as the behavioral and psychological symptoms of dementia . [26] Behavioral symptoms can include agitation, restlessness, inappropriate behavior, sexual disinhibition, and aggression which can be verbal or physical. [26] Psychological symptoms can include depression, psychotic hallucinations and delusions, apathy, and anxiety. [26] [27] The rate of their progression varies across the dementia subtypes. [28] [29] [30] The most commonly affected areas include memory , visuospatial function affecting perception and orientation, language , attention and problem solving .TREM2, APP, MAPT, PRNP, NOTCH3, GRN, PSEN2, CST3, DNMT1, CP, HTRA1, FUS, TYROBP, SLC6A3, CSF1R, COL4A1, SLC9A8, C9orf72, ITM2B, APOE, LRRK2, SNCA, PSEN1, VCP, CHMP2B, ATP13A2, SNCB, FMR1, SPAST, GBA, PINK1, SERPINI1, TTR, NOS3, TBP, TMEM106B, ARSA, ATXN2, JPH3, OPA1, SNCAIP, WDR45, ABCD1, NPC2, C19orf12, TRPM7, COX2, SPG21, NPC1, IRF6, NAGLU, AARS2, CLN6, DCTN1, CISD2, MECP2, PPP2R2B, HTT, CERS1, EIF4G1, SDHB, ATN1, ATP7B, EPM2A, HFE, CTSF, MPO, ATXN3, DNAJC5, SMOX, RNF216, GBE1, FTL, ATP6, AMN, VPS13C, APTX, LAMC2, PANK2, GLUD2, IGFALS, VPS35, GM2A, ROGDI, TWNK, HEXA, PRDM8, IL6, HLA-DQB1, IRF2BPL, IL1B, GBA2, TRNC, ADA2, COX1, SDHD, BACE1, PSAP, SMUG1, ATP6V0A2, NECTIN2, ALDH18A1, TARDBP, DNAJC13, ATXN8OS, SDHA, SLC2A3, ATXN10, TREX1, SOD1, PNPLA6, TUBB4A, TNF, DNM1L, MATR3, WFS1, CUBN, XPR1, FBXO7, POLG, COX3, TRNS2, CYTB, ND1, ND5, ND6, TRNE, TRNF, TRNK, TRNL1, TRNQ, TRNS1, TRNV, MMACHC, TRNW, NDP, NEFL, MBTPS2, NR4A2, RRM2B, PRDX1, PDGFB, PLAU, GIGYF2, OSBPL1A, A2M, TYMP, ASAH1, PRICKLE1, ACE, KCTD7, ACHE, MCIDAS, TIMM8A, CRP, BDNF, CYP27A1, DGUOK, SCARB2, CSF2, CSTB, SLC13A5, ATP6V1A, CDR1, ATP6V1E1, ADH1C, ERCC8, SDHAF1, CLN3, ESR1, BCHE, NHLRC1, CHI3L1, COMT, CLU, IGF1, IL1A, SERPINA3, MTHFR, PAEP, RUNX1T1, PON1, ITIH4, NHS, LEP, AKR1C4, UBQLN2, CCL2, ALB, DYRK1A, SLC6A4, CIT, DPP4, IDE, ABCB6, COPD, NRGN, GFAP, ADIPOQ, SORL1, SIRT1, AGER, CHRNA4, ST3GAL4, CHRNA7, SQSTM1, BCL2, APOC1, AGPS, TSHZ1, TGFB1, SCD, MCF2L, LRP2, ADAMTS2, CHAT, PRKN, CYP19A1, NDUFAB1, CETP, ALDH2, TOMM40, CYP2D6, BPIFA4P, FASTK, NGF, MME, MOK, IAPP, IGF1R, DHDDS, SERPINA1, HTR6, STH, ICAM1, S100B, VCAM1, APOA1, WWC1, IL10, SUCLA2, IL1RN, PLA2G7, CPAT1, MIR132, ATM, CCL4, PPARG, CXCL12, PART1, ERVW-1, ATP2B3, EBP, RELN, OPN1SW, REN, SEC14L2, MIR659, TGDS, TXNIP, RAB3A, NF1, APOB, MIR155, AKT1, PDC, SLC18A3, SERPINE1, PAFAH1B1, PDYN, SNAP25, SNCG, CHCHD10, SLC1A3, ABCB1, SLC1A2, NOS2, SHBG, SGCA, SFTPC, PIN1, PARK7, STAR, EDAR, REM1, TBK1, MMP9, SLC30A6, CHRFAM7A, TPI1, GAP43, USO1, GCG, IL18, TRPM2, PLA2G6, SPG11, GLS, SLC17A7, DBN1, ASXL1, PICALM, AKAP6, ACTB, AGTR1, GDF15, HTR2A, ERVK-6, HSD11B1, DRD3, YWHAE, DLG4, ERVK-32, SIGMAR1, INSRR, TIMP1, MTOR, FLNB, MMP2, ESR2, MFGE8, THBS1, TET2, NXF1, TAS2R62P, MAOA, SF3B1, KL, SPTLC1, EPO, ERVK-20, ABCA1, LPA, ABCA7, JAG1, MMP3, CCL4L2, LGI1, AD10, H6PD, H3P28, TRIM2, ASTN2, FAM72A, ATG5, UBR4, TAOK2, FHL5, NCSTN, GRAP2, LIPG, PHLPP1, CYTIP, FPGT-TNNI3K, NBEAL2, RABEPK, MCI2, AD16, MIR2113, LANCL1, ADAMTS13, CNMD, SDS, EBNA1BP2, SPON1, CFDP1, OLFM1, PPARGC1A, NES, FAS-AS1, CRTAP, RIDA, WDHD1, SIRT2, WIF1, ABCG1, FASTKD2, ACOT7, MTCO2P12, RAPGEF5, AD17, PGR-AS1, RBM8A, ZGLP1, CCS, AD11, GNE, WASF2, ERVK-18, MPZL2, LRRC37A, SLCO6A1, FAM72B, ACE2, ANKK1, PCSK9, KIDINS220, PLEKHG5, AICDA, MCOLN1, TIGAR, SLC17A6, PDXP, ACKR3, CHPT1, MRGPRX1, FMN2, RETN, ASAH2, USE1, MBD5, ATF7IP, ADI1, SLC52A1, MARCHF1, HCCAT5, INTS11, DYM, ARHGEF2, ARMH1, NANOS3, ACTBL2, PWAR4, HAMP, LGR6, CABIN1, CLSTN2, MRGPRX3, ESCO1, CSMD2, NLRP3, TMEM54, ATPAF2, GPR151, SHANK3, BPIFA2, CACUL1, COL25A1, TOM1L2, PPP1R2C, NAA50, OXER1, RIN3, EHMT1, DHX40, PTCRA, FTO, UBE2Z, WNK1, GPRC6A, CSMD1, CIAO3, HHIP, ROBO3, FNDC5, ABCG4, GSTK1, SERPINA13P, DNAJC10, CCL4L1, CYFIP2, SLC17A5, SEZ6L2, HSPB8, FBXW8, PTPN22, VN1R17P, LRP10, GPR166P, PLF, SH2B1, MIR384, BACE2, BDNF-AS, PRDX5, TPSG1, MIR193B, GCA, BRI3, QPCT, NPS, POTEM, LOC643387, CD2AP, KLHDC2, DDX58, PADI4, LPAR3, LINC00273, GLS2, POTEKP, SIT1, MIR21, MIRLET7B, MIR106B, MIR107, MIR125A, POLE3, INPP5K, WWOX, UBR5, PLA1A, MIR181C, MIR195, MIR206, CHCHD2, SAR1B, HPGDS, TNNI3K, GEMIN4, MIR210, IL22, DELEC1, NOX4, MIR212, MIR223, KCNIP3, CD274, MIR29A, MRGPRX4, PYCARD, SLC33A1, CCL21, HGS, HHEX, GHR, CBLIF, GCLC, GLP1R, GLRA2, GPR39, GRK5, GPX1, GPX4, GRIN2B, NR3C1, GSK3B, GYPC, HARS1, HDAC2, GH1, GDNF, GDF1, PTK2B, EIF4G2, ELF3, EPHX2, F2RL1, F11, FANCD2, FANCB, GAPDH, FDXR, FOXO3, FLT1, FN1, FOLH1, G6PD, HGF, HLA-C, LRPAP1, HMGB1, IL12B, IL13, IL15, IL17A, CXCL10, INPP5D, INSR, IRS1, ITGB2, KNG1, LAD1, RPSA, LIMK1, LMNA, LPL, IL12A, IL9, CXCL8, IDH2, HMOX1, HP, HSF1, HSPG2, HTR1A, IDH1, IFNG, IL7, IGF2, IGFBP2, IGFBP3, IKBKB, IL4, IL6R, EGFR, EEF1A2, EDN1, ECE1, BAX, BCL2A1, DST, BRCA1, BRCA2, TSPO, SERPING1, CA11, CASP1, CASP2, CASP6, CAV1, CBS, CCT, CD4, BACH1, ATR, ATP7A, AGT, ACTG1, ACTG2, ACY1, ADA, ADAM10, ADSL, AGTR2, APOC3, AHR, AKR1B1, ALK, BIN1, ANGPT1, ANXA1, CD14, CD38, CDKN1A, DIH1, CSF3, CSPG4, CTSB, CTSD, CUX1, DAG1, DLD, CREB1, SARDH, DPP6, DRD2, DSC3, DSPP, E2F1, CRYGD, CPE, CDR2, CHD2, CEACAM5, CEBPB, CECR, CGA, CEACAM3, CEACAM7, CHIT1, COL4A2, CHM, CHRM1, CHRNB2, TPP1, CCR5, CNR1, LRP5, LY6E, F2RL3, TLR2, SST, ST13, STAT1, STC1, STXBP3, SULT1A1, SYP, TAC1, TBCA, TCEA1, TFAM, TFPI, TGFB2, THOP1, TIMP2, SREBF1, SPP1, SORD, SELP, CCL3, CCL11, NAT2, CX3CL1, SEL1L, SELE, SET, SOD2, SFPQ, SRSF5, SLC5A2, SMARCA1, SMPD1, SNTA1, TIMP4, TLR4, MAP2, CLDN5, TFEB, NTT, NUP214, FGF23, CNSN, COLQ, FZD4, SRPX, BHLHE40, STK16, TP63, FADD, NR1I2, SYNJ1, WASF1, DEK, CXCR4, LRP8, TYRP1, TNNI3, TP53, TPO, HSP90B2P, TSC2, TYMS, UBB, VWF, UBE2H, UCHL1, UGCG, NR1H2, UROD, VLDLR, ATXN1, RPL29, BRD2, REG1A, NTRK2, NTS, OXT, P2RY11, P4HB, PEBP1, REG3A, PAWR, SERPINA5, PDE9A, SLC26A4, PENK, PER1, PFN1, PGF, NPTX2, NOTCH4, NOS1, MTR, SMCP, MDM2, MDM4, MEF2C, MSD, MSMB, MYLK, NINJ2, NDUFS3, NFIA, NFATC3, NFIB, NFIC, NFIX, PIK3CA, PIK3CB, PIK3CD, PTGS2, KLK10, PSG2, PSMD2, PSMD7, PSPH, PTH, PTHLH, PSPN, PTK2, PZP, RAP1GDS1, PLAAT4, RBP4, RCN1, KLK7, MAPK3, PIK3CG, PNN, PITX2, PITX3, PKNOX1, PLAUR, PLD1, PLP1, POLE, MAPK1, PON2, PPARA, PPP3CA, PREP, PRKAR1B, PRKCB, H3P11
