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Hereditary Mucoepithelial Dysplasia
Wikipedia
Hereditary mucoepithelial dysplasia Other names Urban-Schosser-Spohn syndrome, HMD Structure and location of desmosomes Gap junctions, connecting the interior of two cells Malformation of desmosomes and gap junctions are caused in this condition Specialty Dermatology Hereditary mucoepithelial dysplasia ( HMD ), or simply mucoepithelial dysplasia , [1] [2] is a rare autosomal dominant multiepithelial disorder causing systemic maldevelopment of the epithelia and mucous membranes that line the surface of tissues and structures throughout the body, particularly affecting systems affiliated with mucosa, which includes the respiratory , digestive , urinary , reproductive and immune systems . [2] [3] [4] [5] [6] The disorder is attributed to improper formation of desmosomes and gap junctions , which prevents proper cornification of the epithelial layer of the skin. [5] [7] Contents 1 Pathophysiology 2 Diagnosis 3 Treatment 4 References 5 External links Pathophysiology [ edit ] Desmosomes are extracellular protein structures responsible for cellular adhesion , whereby cells of the same type are held closely together. [8] Gap junctions are specialized channels located within the cell membrane of many animal cell types, which serve as gateways that connect the cytoplasmic interior of two adjacent cells, allowing the passage of small molecules such as ions , nucleotides , second messengers and others. [9] [10] The movement and exchange of small molecules between cells is an important part of intracellular communication processes like cell signaling . [11] Diagnosis [ edit ] This section is empty.
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Actinic Prurigo
Wikipedia
Some medical experts use the term actinic prurigo to denote a rare photodermatosis that develops in childhood and is chronic and persistent; this rare photodermatosis, associated with the human leukocyte antigen HLA-DR4, is often called "Familial polymorphous light eruption of American Indians" or "Hereditary polymorphous light eruption of American Indians" but some experts consider it to be a variant of the syndrome known as polymorphous light eruption (PMLE). [1] Some experts use the term actinic prurigo for Hutchinson's summer prurigo [2] (aka hydroa aestivale ) and several other photodermatoses that might, or might not, be distinct clinical entities. [3] [4] [5] Contents 1 Symptoms 2 Causes 3 Diagnosis 4 Treatment 5 History 6 See also 7 References 8 External links Symptoms [ edit ] AP is characterized by itchy, inflamed papules, nodules, and plaques on the skin.
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Solid Pseudopapillary Tumour
Wikipedia
PMID 1283055 . v t e Digestive system neoplasia GI tract Upper Esophagus Squamous cell carcinoma Adenocarcinoma Stomach Gastric carcinoma Signet ring cell carcinoma Gastric lymphoma MALT lymphoma Linitis plastica Lower Small intestine Duodenal cancer Adenocarcinoma Appendix Carcinoid Pseudomyxoma peritonei Colon/rectum Colorectal polyp : adenoma , hyperplastic , juvenile , sessile serrated adenoma , traditional serrated adenoma , Peutz–Jeghers Cronkhite–Canada Polyposis syndromes: Juvenile MUTYH-associated Familial adenomatous / Gardner's Polymerase proofreading-associated Serrated polyposis Neoplasm: Adenocarcinoma Familial adenomatous polyposis Hereditary nonpolyposis colorectal cancer Anus Squamous cell carcinoma Upper and/or lower Gastrointestinal stromal tumor Krukenberg tumor (metastatic) Accessory Liver malignant : Hepatocellular carcinoma Fibrolamellar Hepatoblastoma benign : Hepatocellular adenoma Cavernous hemangioma hyperplasia : Focal nodular hyperplasia Nodular regenerative hyperplasia Biliary tract bile duct : Cholangiocarcinoma Klatskin tumor gallbladder : Gallbladder cancer Pancreas exocrine pancreas : Adenocarcinoma Pancreatic ductal carcinoma cystic neoplasms : Serous microcystic adenoma Intraductal papillary mucinous neoplasm Mucinous cystic neoplasm Solid pseudopapillary neoplasm Pancreatoblastoma Peritoneum Primary peritoneal carcinoma Peritoneal mesothelioma Desmoplastic small round cell tumor
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Immunodeficiency 56
Omim
At age 5 years, she was admitted with severe interstitial pneumonia that rapidly progressed to acute respiratory distress syndrome requiring prolonged ventilation.
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Hyperphenylalaninemia
Wikipedia
Treatment for life is recommended to reduce the risk of long term neuropsychiatric problems and reduce the risk of maternal PKU syndrome. [ citation needed ] Outcome [ edit ] With treatment the outcome is excellent.
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Charcot-Marie-Tooth Disease, Demyelinating, Type 1f
Omim
Jordanova et al. (2003) noted that some of the patients were diagnosed with Dejerine-Sottas syndrome (DSS; 145900) because of early onset and increased severity.
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Type 2 Diabetes
Wikipedia
Consumption of sugar-sweetened drinks in excess is associated with an increased risk. [35] [36] The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk. [28] Eating a lot of white rice appears to play a role in increasing risk. [37] A lack of exercise is believed to cause 7% of cases. [38] Persistent organic pollutants may also play a role. [39] Genetics Main article: Genetic causes of type 2 diabetes Most cases of diabetes involve many genes , with each being a small contributor to an increased probability of becoming a type 2 diabetic. [10] The proportion of diabetes that is inherited is estimated at 72%. [40] More than 36 genes and 80 single nucleotide polymorphisms (SNPs) had been found that contribute to the risk of type 2 diabetes. [41] [42] All of these genes together still only account for 10% of the total heritable component of the disease. [41] The TCF7L2 allele , for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants. [13] Most of the genes linked to diabetes are involved in pancreatic beta cell functions. [13] There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or "other specific types of diabetes" ). [10] [13] These include maturity onset diabetes of the young (MODY), Donohue syndrome , and Rabson–Mendenhall syndrome , among others. [10] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people. [43] Medical conditions There are a number of medications and other health problems that can predispose to diabetes. [44] Some of the medications include: glucocorticoids , thiazides , beta blockers , atypical antipsychotics , [45] and statins . [46] Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes. [23] Other health problems that are associated include: acromegaly , Cushing's syndrome , hyperthyroidism , pheochromocytoma , and certain cancers such as glucagonomas . [44] Individuals with cancer may be at a higher risk of mortality if they also have diabetes. [47] Testosterone deficiency is also associated with type 2 diabetes. [48] [49] Eating disorders may also interact with type 2 diabetes, with bulimia nervosa increasing the risk and anorexia nervosa decreasing it. [50] Pathophysiology Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance . [13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver , and fat tissue. [51] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. [10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion. [13] Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells , resistance to and lack of incretin , high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system . [10] However, not all people with insulin resistance develop diabetes since an impairment of insulin secretion by pancreatic beta cells is also required. [13] In the early stages of insulin resistance, the mass of beta cells expands, increasing the output of insulin to compensate for the insulin insensitivity. [52] But when type 2 diabetes has become manifest, a type 2 diabetic will have lost about half of their beta cells. [52] Fatty acids in the beta cells activate FOXO1 , resulting in apopotosis of the beta cells. [52] Diagnosis WHO diabetes diagnostic criteria [53] [54] edit Condition 2-hour glucose Fasting glucose HbA 1c Unit mmol/L mg/dL mmol/L mg/dL mmol/mol DCCT % Normal < 7.8 < 140 < 6.1 < 110 < 42 < 6.0 Impaired fasting glycaemia < 7.8 < 140 6.1–7.0 110–125 42–46 6.0–6.4 Impaired glucose tolerance ≥ 7.8 ≥ 140 < 7.0 < 126 42–46 6.0–6.4 Diabetes mellitus ≥ 11.1 ≥ 200 ≥ 7.0 ≥ 126 ≥ 48 ≥ 6.5 The World Health Organization definition of diabetes (both type 1 and type 2) is for a single raised glucose reading with symptoms, otherwise raised values on two occasions, of either: [55] fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) or with a glucose tolerance test , two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl) A random blood sugar of greater than 11.1 mmol/l (200 mg/dl) in association with typical symptoms [23] or a glycated hemoglobin (HbA 1c ) of ≥ 48 mmol/mol (≥ 6.5 DCCT %) is another method of diagnosing diabetes. [10] In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥ 48 mmol/mol (≥ 6.5 DCCT %) should be used to diagnose diabetes. [56] This recommendation was adopted by the American Diabetes Association in 2010. [57] Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl). [56] ADA diabetes diagnostic criteria in 2015 [58] edit Diabetes mellitus Prediabetes HbA 1c ≥6.5% 5.7-6.4% Fasting glucose ≥126 mg/dL 100-125 mg/dL 2h glucose ≥200 mg/dL 140-199 mg/dL Random glucose with classic symptoms ≥200 mg/dL Not available Threshold for diagnosis of diabetes is based on the relationship between results of glucose tolerance tests, fasting glucose or HbA 1c and complications such as retinal problems . [10] A fasting or random blood sugar is preferred over the glucose tolerance test, as they are more convenient for people. [10] HbA 1c has the advantages that fasting is not required and results are more stable but has the disadvantage that the test is more costly than measurement of blood glucose. [59] It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease. [10] Type 2 diabetes is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. [60] This is in contrast to type 1 diabetes in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas and gestational diabetes that is a new onset of high blood sugars associated with pregnancy. [13] Type 1 and type 2 diabetes can typically be distinguished based on the presenting circumstances. [56] If the diagnosis is in doubt antibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes, [61] with C-peptide levels normal or high in type 2 diabetes, but low in type 1 diabetes. [62] Screening No major organization recommends universal screening for diabetes as there is no evidence that such a program improve outcomes. [63] [64] Screening is recommended by the United States Preventive Services Task Force (USPSTF) in adults without symptoms whose blood pressure is greater than 135/80 mmHg. [65] For those whose blood pressure is less, the evidence is insufficient to recommend for or against screening. [65] There is no evidence that it changes the risk of death in this group of people. [64] They also recommend screening among those who are overweight and between the ages of 40 and 70. [66] The World Health Organization recommends testing those groups at high risk [63] and in 2014 the USPSTF is considering a similar recommendation. [67] High-risk groups in the United States include: those over 45 years old; those with a first degree relative with diabetes; some ethnic groups, including Hispanics, African-Americans, and Native-Americans; a history of gestational diabetes ; polycystic ovary syndrome ; excess weight; and conditions associated with metabolic syndrome . [23] The American Diabetes Association recommends screening those who have a BMI over 25 (in people of Asian descent screening is recommended for a BMI over 23). [68] Prevention Main article: Prevention of type 2 diabetes Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise. [69] [70] Intensive lifestyle measures may reduce the risk by over half. [25] [71] The benefit of exercise occurs regardless of the person's initial weight or subsequent weight loss. [72] High levels of physical activity reduce the risk of diabetes by about 28%. [73] Evidence for the benefit of dietary changes alone, however, is limited, [74] with some evidence for a diet high in green leafy vegetables [75] and some for limiting the intake of sugary drinks. [76] There is an association between higher intake of sugar-sweetened fruit juice and diabetes, but no evidence of an association with 100% fruit juice. [77] A 2019 review found evidence of benefit from dietary fiber . [78] In those with impaired glucose tolerance , diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes. [25] [79] Lifestyle interventions are more effective than metformin. [25] A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal. [80] While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk. [81] Management Further information: Diabetes management Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range. [25] Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes may be used in combination with education, [82] although the benefit of self-monitoring in those not using multi-dose insulin is questionable. [25] In those who do not want to measure blood levels, measuring urine levels may be done. [82] Managing other cardiovascular risk factors, such as hypertension , high cholesterol , and microalbuminuria , improves a person's life expectancy. [25] Decreasing the systolic blood pressure to less than 140 mmHg is associated with a lower risk of death and better outcomes. [83] Intensive blood pressure management (less than 130/80 mmHg) as opposed to standard blood pressure management (less than 140-160 mmHg systolic to 85–100 mmHg diastolic) results in a slight decrease in stroke risk but no effect on overall risk of death. [84] Intensive blood sugar lowering (HbA 1c <6%) as opposed to standard blood sugar lowering (HbA 1c of 7–7.9%) does not appear to change mortality. [85] [86] The goal of treatment is typically an HbA 1c of 7 to 8% or a fasting glucose of less than 7.2 mmol/L (130 mg/dl); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy. [68] [87] [88] Hypoglycemia is associated with adverse outcomes in older people with type 2 diabetes. [89] Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms with long-term benefits, many people – for example people with a life expectancy of less than nine years who will not benefit, are over-treated . [90] It is recommended that all people with type 2 diabetes get regular eye examinations . [13] There is weak evidence suggesting that treating gum disease by scaling and root planing may result in a small short-term improvement in blood sugar levels for people with diabetes. [91] There is no evidence to suggest that this improvement in blood sugar levels is maintained longer than four months. [91] There is also not enough evidence to determine if medications to treat gum disease are effective at lowering blood sugar levels. [91] Lifestyle A proper diet and exercise are the foundations of diabetic care, [23] with a greater amount of exercise yielding better results. [92] Exercise improves blood sugar control, decreases body fat content and decreases blood lipid levels, and these effects are evident even without weight loss. [93] Aerobic exercise leads to a decrease in HbA 1c and improved insulin sensitivity. [94] Resistance training is also useful and the combination of both types of exercise may be most effective. [94] A diabetic diet which includes calorie restriction to promote weight loss is generally recommended. [95] [58] Other recommendations include emphasizing intake of fruits, vegetables, reduced saturated fat and low-fat dairy products, and with a macronutrient intake tailored to the individual, to distribute calories and carbohydrates throughout the day. [58] [96] Several diets may be effective such as the Dietary Approaches to Stop Hypertension (DASH), Mediterranean diet , low-fat diet , or monitored carbohydrate diets such as a low carbohydrate diet . [58] [97] [98] Viscous fiber supplements may be useful in those with diabetes. [99] Vegetarian diets in general have been related to lower diabetes risk, but do not offer advantages compared with diets which allow moderate amounts of animal products. [100] There is not enough evidence to suggest that cinnamon improves blood sugar levels in people with type 2 diabetes. [101] Culturally appropriate education may help people with type 2 diabetes control their blood sugar levels, for up to 24 months. [102] If changes in lifestyle in those with mild diabetes has not resulted in improved blood sugars within six weeks, medications should then be considered. [23] There is not enough evidence to determine if lifestyle interventions affect mortality in those who already have DM2. [71] As of 2015 [update] , there is insufficient data to recommend nonnutritive sweeteners, but note they may help reduce caloric intake. [103] Medications Metformin 500mg tablets. ... "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis" . ... "The role of testosterone in the metabolic syndrome: a review". The Journal of Steroid Biochemistry and Molecular Biology . 114 (1–2): 40–3. doi : 10.1016/j.jsbmb.2008.12.022 .PPP1R3A, HNF4A, PAX4, AKT2, GCK, IRS1, KCNJ11, HNF1A, HNF1B, SLC2A4, NEUROD1, PDX1, SLC2A2, IRS2, WFS1, HMGA1, ABCC8, CDKAL1, INS, INSR, ENPP1, ADCY5, CAPN10, TCF7L2, PPARG, TGFB1, LIPC, BCL2, MAPK8IP1, HP, NOS3, PPARGC1A, HMOX1, LEPR, ICAM1, UCP2, LEP, SIRT1, ADIPOQ, EDNRA, EDN1, TNF, TNFRSF1A, NOS2, KL, CPT1A, SNAP25, ATP2A2, EDNRB, RETN, GCKR, SLC30A8, GLIS3, GCGR, FTO, GLP1R, PTPN1, JAZF1, KCNQ1, IGF2BP2, MTNR1B, THADA, HMG20A, NOTCH2, PROX1, KCNK16, GPD2, UBE2E2, AP3S2, MAEA, CMIP, PEPD, GRB14, CCND2, PLEKHA1, DGKD, ZFAND3, ITGA1, PSMD6, PAM, KSR2, NFATC2, CAT, SHBG, MIR375, SLC2A1, BRAF, SLC1A2, ST6GAL1, HHEX, JADE2, IL13RA1, MIR126, SOD2, VPS26A, GSTM1, MOK, GNB3, GCG, CNKSR2, AUTS2, IGF2, GP2, INPPL1, SREBF1, SOD1, FGF21, LPL, ZNF257, FBN1, USP48, PPARA, SCTR, EPC2, IAPP, FAM234A, KLF14, CYBA, RNF6, IDE, ETS1, GIPR, CASP3, TNFRSF1B, SFRP4, OGG1, ND1, ADAMTS9, GPX1, AR, NFKB1, MIR27A, EGFR, MIR192, PCSK2, COX2, PRKCB, MIR144, HBA1, TIMP1, C2CD4A, ATF3, SLC22A3, MIR221, TMEM18, C3, C2CD4B, MIR483, MIR222, MIR423, RELA, FAS, CISD2, CBS, HK1, ATP2A3, MIR130B, HLA-DRB5, MIR203A, MIR142, CCDC92, MIR140, MIR200A, MIR98, MIR204, PAX6, ECE1, MIR214, ITLN1, MIR10B, MIR30A, MIR377, MIR1260A, CDO1, RARRES2, CCR5, SMAD5, MAT1A, NUS1, MIR1249, MIR1296, MAPK8, MIR1226, MIR1306, MRAS, MIR1228, MIR744, MIR939, CD36, MIR885, MIR1307, MIR151A, GPT, RBP4, IGF1, ID1, MIR127, MIR215, HSD11B1, MIR205, HPX, MIR195, MTOR, MIR141, GIP, HIF1A, MIR181C, GH1, UCP3, SOCS3, MIR17HG, MIR125B1, MIR432, MIR92B, MIR628, MIR532, MIR487B, BCL2L11, CYP1A2, S100A6, IL6, MIR485, MIR409, MIRLET7D, CCL2, MIR339, MIR335, MIR1301, MIR33B, MIR1908, MIR3173, MIR4482, BCL2L1, MIR4516, MIR8061, MIR6741, PRKAA1, PCK1, PCSK1, NFE2L2, BHMT, MIR7704, PPARD, MIR1260B, NUCB2, NKX6-1, ADRA2A, SERPINF1, AKT1, ZC3HC1, AGER, SERPINE1, MIR6803, KCNU1, AVP, MIR2116, MAPK1, TMEM155, MMP9, CASP8, PTGS2, G6PC, NR3C1, GSK3B, IGF1R, CCN2, REG3A, PIK3R1, CALCA, MAPK3, MAFA, HMGCR, MMP3, NPPB, SERPINA12, CRTC2, PC, ABCG2, CD38, BECN1, BAX, MMP1, PRKCZ, PTGDS, PRKN, MADD, HTR2C, AGTR2, TRPC1, ARRB2, LNPEP, AOC3, TRPC6, DCX, DEFB1, SMAD4, MIF, DNMT1, SLC9A1, CARTPT, NOG, PLAT, PLN, MTNR1A, UGT1A1, NFE2L1, DNM1L, CYP2E1, PPP1R3C, FOXM1, UGT1A6, SRD5A1, NR1D1, NOS1, THBD, AGRP, GJA1, PRKCE, CYB5R4, MAPK9, TGFBR2, CCKAR, CDKN2B, MAPK14, ACOT2, CYTB, MKI67, CTF1, SCN1B, DAG1, F7, ANKRD23, COL3A1, OXCT1, FEM1B, SRC, CALM1, CYP11A1, HSD3B1, KLF11, MAP1LC3A, KCNMB1, ARX, NCOA6, HSD17B3, TSPAN8, PNPLA3, GPT2, CASP7, BAD, ABCC2, ASIP, CASP12, PHOX2A, EPAS1, ATP2A1, PPP2CA, AK1, GADD45GIP1, AANAT, ATP5F1B, SLC16A11, STAR, BEST1, MPST, MTR, ALDOB, PRKCI, CCHCR1, MC4R, LMNA, CRHR1, EIF3F, SDF2L1, HLA-DQB1, SLC12A3, ATF6, CDKN2B-AS1, CAMK1D, NEUROG3, CTNNB1, ALMS1, ARAP1, ATM, UMOD, CDC123, ANK1, GRK5, DUSP9, NOX4, ABO, CYP19A1, ARL15, ELN, SRR, TP53INP1, CASR, TM6SF2, PTPN22, KIF11, CUBN, MAP2K7, TMEM163, GPR55, SCGN, TFAP2B, AGMO, HMGA2, DNER, ALDH7A1, RBMS1, HECTD4, RFC2, LAMA1, AHR, PRPF31, SLC26A9, PROM1, CTBP1-DT, ARG1, UBE2Z, DGKB, POU5F1, AHI1, ZMIZ1, RP9, INS-IGF2, ZRANB3, COBLL1, FAF1, TCF19, PRC1, ACSL1, TH, ND5, PTPRD, RASGRP1, GLP2R, RBPJ, TUB, GATAD2A, BAZ1B, LINGO2, NRL, ALK, PBX4, SSR1, NDUFAF6, PRKAG2, CLIP2, WRN, POC5, DHDDS, OAS1, SNHG17, ABCA4, SGCD, SLC16A13, CAMTA1, CTRB1, ADGRL3, EHMT2, SPPL3, STUB1, CAMK2G, TRDN, MACF1, TSBP1, STX8, TTLL6, PTPRN2, CAMKK2, RREB1, TRPM1, BCL9, LIG4, ATXN1, CTBP1, SUGP1, ROM1, TPCN2, MPHOSPH9, MCM6, SH2B3, POMGNT1, MASP1, FBXW7, RBPJL, SGCG, LIMK1, PPP2R2C, PDE6B, CERKL, FAM161A, RBP3, HIVEP2, HLA-DRB9, HLA-DOB, PRIM2, GPR119, MAGEC3, ASCC2, HK2, PRPH2, PEX10, HLA-DRB1, HGSNAT, SSTR4, NPY, SUMO4, ARL6, MNX1, GUCA1B, LCN2, UNC5D, MOG, OSBPL7, PCSK9, TRNL1, NECTIN2, PRKAA2, RTN4RL1, TCF7, TTC8, MAK, PYY, CYB5D2, TTC39C, MAP6, DLEU7, MFAP1, CFAP77, RELN, MBNL1, RFLNA, EDARADD, RDH12, MCC, LINC02694, LINC01344, RPSAP52, PSMD9, PCARE, TNFRSF11B, NTRK2, PRKAB1, MMP2, PDE6G, NRG4, ST6GALNAC3, APOA5, LPA, CTTNBP2, NTRK3, LRMDA, PDE6A, ZSWIM3, LTA, HFE, PTH1R, PTH, PTGFRN, PCNT, REG1A, RHO, OSBPL1A, SLC5A2, ZNF513, SELE, CCDC149, C8orf37, CCNQ, PRRX1, PLCD1, IFNG, SLC5A1, IDH3B, IMPDH1, LINC01010, PLCB3, IL17A, IDH3A, IL18, SLC9B2, C17orf58, ND6, PPARGC1B, SELP, ZNF775, IL10, PLG, TRNQ, TRNS1, TRNS2, TRNK, SI, TRNH, TRNW, IL1RN, TRNF, IL4, IL1B, TRNE, IL1A, ST3GAL4, ST3GAL3, PPIL6, PDILT, CXCL8, ARL9, NEK2, ND4, REN, RP1, EYS, KCNQ3, PIK3CD, SPP1, HORMAD2, CHCHD6, RP2, PIK3CB, PIK3CA, NLRP3, MTHFR, SLCO4C1, SDHAF4, MSH3, RLBP1, KIF9-AS1, RGS13, RGS7, RGR, RFC1, NFKBIL1, RPGR, RPE65, MRPL12, CNDP1, CDHR1, COX3, REEP6, COX1, FFAR4, GPBAR1, SCD, ATXN7, ATXN2, SLC22A1, SAG, HNF1A-AS1, ZNF101, GOLGA6A, PON1, PIK3CG, TTLL8, CHMP4B, IL17REL, EHMT1, LINC01122, KCNQ1OT1, INTS8, RAB3GAP1, ENPP7P10, RALY, NLGN1, CPEB3, MGLL, MINDY1, SPATA7, CD59, CD81, UBAP2, ARHGAP15, CDK5, NUDT6, POLR3A, KIZ, CDKN2A, TRIOBP, SNRNP200, PALLD, ZHX3, LINC00844, ABCB9, ABCB10, CRB1, PRC1-AS1, BRS3, ARHGEF18, RPGRIP1L, ADAMTS9-AS2, LINC01426, CAD, UBE2E2-AS1, PROX1-AS1, CA4, OSER1-DT, SLC30A10, FBXL7, CEP68, ZZEF1, ANGPTL8, APOM, ARPIN-AP3S2, LMCD1-AS1, CNR1, ZBED3-AS1, ACKR3, MERTK, PDSS2, ATP8B2, DLEU1, LRFN2, RAMP2, CALCOCO2, CPA1, GPR158, TOPORS, STARD9, NAMPT, FRY, CRP, CRX, PITPNM2, CNGA1, CNGB1, GTF2I, NFAT5, PNPLA6, CETP, KLHL7, TEX14, ANKH, LINC00271, RAI1, HMGA2-AS1, CXCR6, PRPF8, SUMO2P17, CHUK, YKT6, ZGLP1, TXNIP, CLCNKB, C1GALT1, PRCD, ARL2BP, BLM, NR2E3, LOC102723407, AGT, AGTR1, LRP12, LINC02030, AHSG, PURG, LINC02484, ALB, LINC02841, PELO, AKR1B1, EXOC6, HPGDS, PALD1, FOXP1, CCND2-AS1, NSG1, LINC02576, SND1, LRP1B, FSCN3, ADRB3, ADIPOR1, ABCA1, ANKFY1, SNX7, PEX5L, GLRX5, HSD17B12, ASB3, ANGPTL4, ADA, ADRB2, ADARB1, SOST, IMPG2, GHRL, SCAPER, LINC01611, ADRA1A, ADRA2B, TBL2, ANPEP, RCBTB1, VPS33B, HNF4A-AS1, OSBPL3, SCAANT1, TXNL4B, PTPN23, MIR5094, ABI3BP, PINX1, SAMM50, FSCN2, BBS2, PRPF6, SRBD1, DIANPH, BDNF, DARS2, BGLAP, SBNO1, AMACR, LINC00824, ASCL2, LINC02010, APP, GIN1, APOA1, APOB, APOC3, HORMAD2-AS1, IFT172, APOE, CNTLN, APRT, POLDIP2, ETS1-AS1, PABPC4-AS1, LINC01339, TSBP1-AS1, C5orf67, ARL3, PKN2-AS1, GPSM1, TSPAN3, PCSK6, CST3, AGBL5, PABPC4, PEA15, EXT2, EYA2, OASL, FABP4, GDAP1L1, FABP2, OFD1, GCC1, ADIPOR2, NPRL3, IFT88, FGF23, FGF14, ZNF408, BEST3, MIR29A, ESR1, ALDH1A2, PRPF3, PIM3, NRXN1, NRXN3, PIEZO2, LRAT, LPAR2, XYLT1, PRPF4, APLN, KIF9, SEMA4A, SELENBP1, CLN8, MGAM, MTMR3, AKTIP, ZSCAN20, ZIC1, THSD4, TLR4, TULP1, TNKS2, ZNF34, GOT2, TP53, TNFAIP6, SLC2A10, FFAR1, UCP1, C16orf74, GPR42, TGFBR3, MLX, LINC02245, GSTP1, GSTT1, SPHKAP, MIR146A, FOXO1, GABPA, XRCC4, SCD5, CPED1, PCNX2, VWF, VSNL1, BICC1, GABRA4, USH2A, GABRG3, GAD1, GAD2, VEGFA, VDR, VCAM1, CLRN1, MED23, YTHDC2, DPP4, UBE3C, GTF2IRD1, DSPP, RHOBTB1, ACE, G6PC2, DECR1, MAGI2, DBP, SLC7A14, CLOCK, FCHSD2, ACE2, SINHCAF, USP3, CELSR1, RBM19, FGF19, MIR4435-2HG, RAPGEF5, GDF15, MTSS1, UVSSA, SFI1, CYP2C9, WSCD2, DEPDC5, TRIB3, DHX38, IFT140, SENP2, CYP21A2, KIAA1549, DOCK4, DARS1, MRPS35, BCHE, LIPE, AIMP2, RNF19A, LDLR, USF1, ARNTL, NOS1AP, AHSA1, GSTK1, PTEN, RBM45, RENBP, CTLA4, IGFBP1, CRK, GRAP2, DMD, GYS1, PON2, CCL5, POMC, IGFBP3, MME, STAT3, LGALS3, CYP2C19, SLCO6A1, LPIN1, F3, STAP2, APOA2, AQP7, FOXA2, SST, SLC17A5, MET, HMGB1, GPR151, NIDDM1, SELENOP, NIDDM2, GPRC6A, PCK2, GGT1, OR10A4, DIO2, HSPA5, GC, CYP3A4, LINC01672, MPO, GGTLC5P, SIRT6, TLR2, GLO1, ELMO1, BCL11A, MLXIPL, ARID4B, NRF1, P2RX7, MIR155, MSTN, CYP2B6, ACR, GGTLC3, MRGPRX1, ALDH2, PDR, GGT2, MRGPRX3, APOL1, HSPA1A, SIRT3, GPR166P, VN1R17P, OXER1, SLC2A11, FZD4, FNDC5, SNCA, MRGPRX4, MIR21, HSPA4, ABCG1, HSPA1B, LPAR3, CHI3L1, NR3C2, FGF2, CD14, ISL1, HAMP, LGR6, ARNT, ZBTB7C, CAV1, GGTLC4P, SGK1, PSEN1, NR1H4, CISD1, SELENOS, CD163, TMBIM4, VIP, CCN4, MFN2, ROCK1, IL22, GGTLC1, VIM, SLC22A2, SOD3, PLIN1, OGA, CNBP, PLA2G2A, SAT1, HAVCR1, FETUB, SFRP5, NAT2, EPO, IARS1, GLUL, LBP, MIR27B, STS, APOA4, ACACB, KNG1, MIR29B1, GAS6, IL15, CD44, HLA-DQA1, ATN1, FXN, CD68, ADM, MIR29B2, LOC102724197, MEFV, CRY2, HGF, FGF1, MTTP, DDIT3, ANGPTL3, BCL2A1, SIRT2, DKK1, INSRR, KCNJ4, IL33, FADS2, CASP1, IL6R, IL37, CCK, SORT1, TBC1D4, MT1A, HEBP1, PRL, MBL2, PARP1, GRK2, ARHGEF11, ROS1, TRPM5, PTX3, FADS1, PYCARD, IL2RA, KRT16, IL5, XPR1, IL2, BMP4, HIRA, LPAL2, FABP1, PADI4, CHDH, FANCD2, PTK2B, BRCA2, SOCS1, FN1, XBP1, SLC47A1, FOXC2, SLBP, PLA2G7, FGB, GHSR, DGAT1, LIPG, EPHB2, IGFBP2, MIR34A, ELANE, MT2A, HSPG2, SOAT1, DPPA3, SULT1E1, TPD52, SH2B1, HHIP, HDLBP, NR1I2, AZU1, MIR122, BTC, CPE, MAP4K4, PDHX, STAM2, NCAM1, ACP1, CMKLR1, NGF, NHS, PKD1, UTS2, MYH9, PGC, MTCO2P12, IFNL3, RAPGEF1, SORCS1, KIR3DL1, GPX3, KDR, P2RY12, TIMP3, SNAP23, FLVCR1, GRN, HDAC9, AMY2A, TNFSF14, COMT, RPL29, GPD1, PDE3B, RAPSN, DACT1, SPX, TRAF6, PVT1, CYP2D6, AKR1A1, KEAP1, MIR223, ALOX12, HDAC3, MARCHF1, ISG20, RNU1-1, ANGPT1, C1QTNF9, TNMD, GAS5, IL13, CXCL12, SPARC, ENO1, CCL16, GPR142, CXCL10, ENHO, STRA6, ST13, TFRC, NPC1, CACNA1E, STK11, STX1A, CCR2, PDK4, RUNX2, NRG1, ERBB2, S100A9, SQSTM1, C1QL3, BCAR1, CLPS, LRG1, TOMM40, GEM, ACACA, DDAH2, FKBP5, CISH, CDK4, LGR5, METRN, MUSK, CREB1, MIR17, FLAD1, TAS2R13, CD40LG, PSMA6, MIR143, SLC39A7, CLU, POU2F1, NR1H3, PTGES2, FOXP3, OLR1, PCNA, LRP5, GAPDH, SLC2A9, ABCB6, PRKCA, NR0B2, XRCC1, ENSA, CXCR4, F5, PLA2G10, NR4A1, PLA2G6, ABCG5, ACHE, FOXO3, FBRS, STAT5A, P2RX3, CACNA1D, FSD1, HPSE, NPPA, FGFR1, KLK3, ARSA, PRMT1, IGF2R, CHGA, KLF4, PPP1R3B, DHX40, ANXA1, PNPLA2, ELAVL2, ERP44, CIDEC, PRDM16, FBXO8, BMP7, VPS13C, STEAP4, NNMT, CCNL1, MCIDAS, HSPA2, APOD, KHDRBS1, APOH, DST, MIR30D, ADAM17, FCGR3B, FCGR3A, ISYNA1, POU2F3, OSM, MIR145, SMUG1, B2M, NR1H2, NTS, MIR152, TNFSF10, WNK1, UTS2R, TM7SF2, GGCT, WNT5B, TNFRSF12A, NUP62, DDAH1, COL18A1, CMA1, IMPACT, HEMGN, GFAP, TNFSF11, F2, SP6, F2R, OGN, FAAH, PDE5A, BTF3P11, IL18R1, PBX1, ERBB4, NBEAL2, SIRT4, TCF4, SIRT5, HCCS, ELOVL6, GTF2H1, TTR, CILP2, TEK, FSD1L, TERF1, TFAM, PHLPP1, BACE2, TRPV1, MIR182, G6PD, ESR2, VEGFC, TGFBI, GRB10, TGM2, BMP2, OPA1, PARL, LINC01194, SLC6A4, ENTPD1, PRKG1, CENPJ, DRD2, LOX, KCNJ1, DCTN4, MC3R, PPIG, TUBB4B, JAK2, JAK1, S100A8, CERS6, ITGAM, NOD1, SPRY2, RNR2, JPH3, ITGA2B, LAD1, TMEM154, LITAF, STK38, PTPN2, RPS6KB1, KLB, PLF, MBOAT4, UCN3, KCNMA1, ALOX5, KCNJ15, TIMM8A, SGSM3, BRD2, PLTP, CEACAM5, RRAD, PRTN3, KCNJ9, H6PD, RXRA, MUTYH, PSAT1, PROS1, IRAK1, ITGA2, ANGPTL2, PGR, AMD1P2, EBI3, LRP2, C1QTNF5, CREBRF, PPIA, ADCY3, PHOSPHO1, ABCB1, RAC1, LRP1, SFTPD, EGR1, CYP2J2, FOXD3, CAPN1, RN7SL263P, BMS1, COPA, RAD1, TFB1M, TMPRSS6, SERPINA1, C1QTNF1, AMD1, NTN1, C5AR2, CDK9, CD33, MMP8, CASQ1, METRNL, ALX4, CYP2C18, NPC1L1, TLR9, SCARB1, INTU, SELL, LARS2, CYBB, ARID1B, KLF7, MIR495, SLCO1B1, CX3CR1, DOK5, CYP2C8, CYP1A1, P2RY1, NCOA5, SLC27A4, MAGEE1, FST, GFPT2, DUSP12, LRPPRC, CDKN1B, CELA3A, RNLS, FAT1, FBN2, SLC52A2, FCGR2B, ATP6AP2, CDKN1C, PREX1, KMT2D, SEMA6A, KLHL42, CHRM3, MICA, CPT2, CDKN1A, CP, CRYZ, CDC42, COX4I1, NR1I3, FCN3, CTSD, FABP6, MIR486-1, COX8A, PDLIM5, PTPRU, CDK2, IVNS1ABP, ABCC5, POSTN, OGT, CSF2, HOTAIR, NISCH, AGXT2, BSG, P2RX2, DEFB103A, XYLT2, COL9A3, DYRK1A, MIR30C2, P2RX6, CIB1, EP300, RCAN1, FAM3A, MIR30C1, ABCG8, ATG7, MIR29C, SLC30A6, CAV3, EPHX2, ARID3A, CEBPB, GGA3, CEL, DNAJB3, MIR33A, MIR34C, MIR320A, CELA1, CAMP, CPB2, CALR, EGF, IL32, CAPN2, ADAM28, CES1, LILRB1, SLC25A20, CAPN3, SULF2, NOD2, HSPB3, EPOR, ARHGEF12, VASH1, ESRRA, TRIM72, SERPING1, ZNF410, COMP, MIR20B, PINK1, ICOSLG, CD5L, CHPT1, DAPK3, ABHD6, CYP17A1, CYP11B2, KLF5, MEG3, PDAP1, CYP3A5, SUCLA2, TXNRD2, CNDP2, ARHGAP22, TBC1D1, MEPE, KLRK1, SEMA3A, NPEPPS, AAA1, SPHK1, ATF7IP, PER2, DNASE1, FOXO6, SORBS1, TSC22D1, SARDH, NQO1, DHCR7, SOCS2, GDF11, P2RY2, NR4A3, SLAMF1, LDHA, LECT2, LGALS1, LIF, C1QTNF3, FAM3B, LMX1A, DUOX1, PVALB, ICOS, PTPRN, PTPN9, RMC1, CYP2R1, APLNR, AFP, AFM, KIF6, SMAD7, KCNIP1, ADORA1, MAPT, DUOX2, MBP, IL20, ADH1B, PLIN2, MDM2, MEF2A, NANS, FRMD3, TERF2IP, ALOX5AP, IL1R1, IL6ST, SLC39A1, IL12B, SDC2, SDC1, CXCL5, SRL, ALOX15, SPINK4, ITGAX, MSMO1, TSPAN31, S100B, COPD, SFXN1, GHS, RXRG, KCNJ6, DESI1, RRAS, PRRT2, DLL1, RORC, NPAS4, KISS1, KLK1, KRT18, PRSS55, PRKCD, LARP1BP2, HDAC7, PIK3C2G, TAAR1, NM, SLC25A3, PHB, ATP6V1H, PGF, PFKM, NOTCH1, NT5C3A, PEG3, NPHS1, BFAR, IL23A, ERFE, TRPM6, ACAT1, PDCD1, PWAR1, PCYT1A, OCA2, R3HDML, PCBD1, OPRM1, P2RX1, P2RX4, P2RX5, PAK1, ACLY, NFKBIA, PRKAR1A, POR, PRKAB2, MMP7, MMP12, MMP13, SRGN, PTPA, MMP14, MRC1, RNU6-392P, GPRC5B, GAL, MT1E, FITM2, MT1X, NF2, MTHFD1, METTL9, PLXNA2, SLC35G1, PLK1, GNPDA2, PLD1, PLCG1, PLAGL1, PLAG1, PLA2G1B, PKNOX1, PKLR, IKBKB, CHIT1, CRISPLD2, AZGP1, GSN, KLRC4-KLRK1, GSR, UGT2B15, TF, TERT, GATA6, SERPINA3, ANGPTL6, TERC, TXN2, VIPR1, UCHL1, TMEM132A, TAPBP, CFH, VLDLR, ERVK-18, C1QTNF12, HLA-DMA, ATP5PF, GAST, VTN, STX4, BID, GFER, STAT5B, TLR3, TRH, ACAD10, CRISP2, GLA, CEP55, CD2AP, CBLIF, P2RX5-TAX1BP3, MIR107, BCR, CIMT, GPR39, THBS1, TTN, GHR, FFAR2, TLE1, TKT, TXN, GCA, GPS2, KLF10, SESN2, GFPT1, ARID5B, GORASP2, MIR199A1, FGL1, SPINK1, AQP9, SOX4, SORD, SNRNP70, FKBP4, AOC2, ANXA6, SPZ1, HTN1, SLC30A1, APPL1, HTR2A, SLC16A1, TRPM7, ANGPT2, GPC5, SLC6A2, ST8SIA4, SLC2A5, ANKRD55, IGFALS, QRSL1, FHL1, MIR199A2, MIR20A, STAT4, LINC-ROR, PGR-AS1, SSTR5, WNT5A, MIR130A, ONECUT1, FLT1, SREBF2, NAT10, C4B_2, MYDGF, LOC107832851, DMAP1, LARP6, LY75-CD302, RASD1, RBM14-RBM4, LSR, NBAS, DEFB4B, MCS+9.7, HMGA1P8, LOC110806263, MMP26, RHOT1, CCL28, ALG1, METTL3, LIN7C, LINC00994, DIP, RPS10-NUDT3, GNG12-AS1, RAB14, WASHC1, CYRIB, VIM-AS1, NDUFA12, SLC50A1, NEIL3, LOC102723996, SIRT1-AS, THRIL, MIR1910, SLC38A2, ALL2, NLGN3, CASZ1, ENAH, ZFAND6, OPN1MW3, VPS35, EXOSC4, RNPC3, UGT1A10, UGT1A8, UGT1A7, ERRFI1, UGT1A5, UGT1A9, MIR3188, TEMPS, UGT1A4, BNC2, TRPM4, TET2, FBLIM1, SALRNA1, CBSL, LOC102723971, UGT1A3, TREM2, MIR3939, APPL2, MOCOS, ZC4H2, LGR4, DEFB103B, COMMD3-BMI1, MIR4756, USE1, ASAH2, ENOX1, BOP, CAMK2N1, SLC6A20, SLC52A1, CST12P, SAGE1, PLUT, WWOX, LRP1-AS, ADA2, MIR3666, IL17D, SHC3, CERNA3, HDL3, FXYD5, MIR4463, PERCC1, SOX6, UGGT2, ROBO4, DUSP26, SUCNR1, IGSF21, CISD3, TIMD4, TRIM47, KCTD1, MIF-AS1, TTC28-AS1, EXOC3L2, SLC9C1, UCN2, CYP4V2, WNT3A, GALP, SLC22A16, LY86-AS1, KRT90P, DSEL, HCCAT5, GORAB, BIRC8, AD7, RNU12, AQP11, H19, TXNRD3, SLC46A1, OPN4, PRDM6, CGB8, CGB5, MUC19, LINC00523, PGP, TRMT10A, ABCC11, BPIFA4P, HS6ST3, MMAB, PHF6, ZACN, SLC27A1, LINC-PINT, MALAT1, PPP1R1B, KAT8, CHKB-CPT1B, SLC41A2, HORMAD1, IMMP2L, LEKR1, SAMD12, MIXL1, GPR61, LINC01193, PWAR4, C7orf50, GLYR1, UBASH3B, ORAI1, PTPN5, GPIHBP1, MFSD9, HCAR2, ZNF469, ZBED3, ZGPAT, BRINP3, ZFP69, HSD17B13, ACTBL2, L3MBTL3, TIRAP, TAS2R12P, TAS1R3, NRK, CLDN19, SIK1, UPP2, PPM1K, SLC2A12, CBLL2, FAM3D, ACVR1C, DQX1, SGMS2, NLRP6, ARID2, PIFO, MLKL, TET3, PDIK1L, MTPN, LRGUK, ROMO1, OR2AG1, PIWIL4, SESN3, FGFBP3, GSC, MT1P3, HT, GPAT4, BEAN1, CD300LG, PTPRVP, SLC30A7, IL23R, FAM78B, CENPX, KLHDC7A, SGMS1, MED19, CADM2, ANGPTL5, DCD, THEM4, TADA1, AKNAD1, SLC41A1, OLIG1, SLC22A12, CASC2, ANKK1, OSBPL8, PTF1A, WDR72, NEGR1, HCG27, IL27, SPESP1, MARCHF8, FOLH1B, TPRG1L, LYPLAL1, UNC5B, TCHHL1, SKA1, MSI2, GGTA2P, JMJD1C, SLC39A12, TPPP2, SPIC, RFX6, SLC29A4, SETDB2, INHBE, MICC, MT1IP, CCAR2, MIR323B, MARK4, MIR146B, MIR202, SPTBN4, MIR496, MIR499A, MIER1, USP37, NPS, CHD8, POTEM, TSHZ3, ECSCR, HNP1, MIR424, MIR382, SLC25A19, EIF2AK4, IGAN1, NIF3L1, ELOVL5, BACH2, EXOC4, RNASEK, MIR378A, PLIN5, POTEKP, PGBP, UBL5, CXCL16, NEUROD4, POU5F1P3, CHCHD2P9, TNFSF12-TNFSF13, USP36, KMT5AP1, MUC5B, OPN1MW2, CPA6, HYMAI, CDK11A, SLC12A9, ARNTL2, CA10, SMARCAD1, OCTN3, CELF4, SPHK2, MIR708, C20orf181, MIR661, GOPC, PELI1, KIDINS220, POU5F1P4, CXADRP1, NCF1, CFAP97, WASH6P, XPO5, MIR590, MIR657, MIR593, PLEKHG5, MRS2, GJD2, ATP10A, SLC39A10, PROK2, MIR99A, TOMM5, MUL1, ASRGL1, MIR15A, MIR15B, MIR18A, MIR187, STN1, MIR200B, ADM2, PRR5L, BBS10, LIN28A, NLRX1, NEIL1, MIR206, TNFAIP8L2, MIR154, MOGAT2, MIR147A, MIR106B, MFRP, MED25, TLR10, NIPA2, MOB2, COLEC12, SETD7, ALPK1, TAS1R2, MIR125A, MIR128-1, TSEN2, MIR132, COASY, MIR210, IRX3, MIR95, MBOAT7, WDR13, MIR296, PDIA2, GORASP1, DCLRE1C, GMCL2, GMCL1, NFKBIZ, NSD1, MIR30E, FN3K, DMRTA1, MIR31, SLC17A9, UBE2O, FNDC4, GNPNAT1, RFX7, GRAMD2B, MIR217, LY6G6E, MIR219A1, KCTD15, MIR22, VKORC1, MIR23A, SLC30A5, MIR23B, BRD9, WNK4, MIR26B, FRTS1, ACD, SCLY, UTRN, LARS1, HACD3, IK, IGH, IGFBP5, IGFBP4, IFNA13, IFNA1, ICAM3, HTR4, HTR2B, HTC2, HSPD1, HSP90AA1, HSPB2, HSPB1, HSPA9, HSD11B2, HES1, HRC, HRAS, HOXA5, HNRNPK, HNRNPF, HNRNPA1, FOXA3, HMBS, IL3, IL4R, IL7, KCNJ10, L1CAM, KRT31, KRT19, KRT7, KPNA1, KIR3DL2, KIR2DS1, KEL, KCNN3, KCNN2, KCNK3, KCNJ3, CXCR1, KCND3, KCNC4, KCNB1, ITGB2, INSIG1, IMPA1, ILK, TNFRSF9, IL16, IL15RA, IL12A, HLF, HLA-DRA, HLA-DQB2, GDF1, GNAO1, GLRX, GLS, GCLC, GLB1, GK, GJA8, GJA4, GH2, GDNF, GDF2, OPN1MW, SFN, GCH1, GBP2, GATA4, GATA3, GAP43, GALNT2, GABRG2, GABPB1, FUT6, FUT2, NR5A1, GOLGB1, GPI, HLA-DQA2, HSD17B10, HLA-DPB1, HLA-DOA, HLA-DMB, HLA-A, CFHR2, HCRT, HBA2, HAS3, HARS1, HADH, HADHA, GZMB, GPM6A, GYG1, GTF3A, GSTA4, GSTA1, GRB2, FFAR3, GPR35, GPER1, GPR21, CXCR3, GPR1, LAMB3, LAMP1, LAMC2, CCN3, OAS3, NR4A2, NUCB1, NTRK1, YBX1, SLC11A2, NPY2R, NPR3, NPR2, NPR1, NPM1, NME1, P4HB, NGFR, NFYC, NFYB, NFYA, NFATC1, NEFL, NDUFS4, NAGLU, MYO5A, MYLK, MYL2, OMG, PAEP, MYF5, PDK2, PIN1, PIK3C3, PIK3C2A, SERPINE2, SERPINB6, PGM1, PFKFB3, PFKFB2, PFDN2, PER1, PECAM1, PDHB, PRDX1, PDGFRB, PDGFB, PDE4D, PDC, PDB1, PCOLCE, SERPINA5, PCDH8, PAWR, PAPPA, SERPINB2, MYH6, MYD88, LAMP2, SH2D1A, MAX, MAS1, MAOA, MAN2A1, MAN1A1, MAFD2, SMAD3, SMAD2, SMAD1, MXD1, LYZ, LY75, MC5R, LY9, LTF, LTBR, CYP4F3, LRP6, LPP, LOXL2, FADS3, LIPA, LCN1, STMN1, MB, SMCP, MUC1, MST1, MTRR, RNR1, ATP8, MT1L, MT1M, MT1JP, MT1H, MT1G, MT1F, MT1B, MSX2, MSH5, ADAM11, MSH2, MPI, ALDH6A1, KMT2A, MGST3, MGP, MGAT2, MFAP2, MAP3K5, MEF2C, ME1, FOS, FOLR2, FOLR1, CA5A, CCND3, CCKBR, CBR3, CBR1, RUNX3, RUNX1, CAV2, CAMK2A, CALCR, CACNB3, CACNA1C, CA2, CD4, VPS51, C5, CAPN5, C4B, C4A, TSPO, BRCA1, BPI, BNIP3, BMP6, BMI1, CD247, CD86, BLK, CGA, AP3S1, CKM, CKB, CIDEA, CHRNB4, CHRNA4, CHN2, CHM, CEACAM7, CEACAM3, CGB3, CFTR, CD34, CTSC, CENPA, CECR, CEBPA, CDX2, CDKN3, CDK6, CDH13, CDH2, CD48, ENTPD3, BLVRA, BGN, CLCN3, AIF1, AMY1C, AMY1B, AMY1A, BIN1, AMPD1, AMH, ALPP, ALPL, ALDH3B1, ALCAM, ALAS1, AIC, ANXA5, ADORA3, ADORA2B, ADH1C, ADD1, ADCYAP1, ACVR2B, ACTG2, ACTG1, ACTB, ACAA1, AAVS1, ANK2, APCS, CFB, ATIC, BCS1L, OPN1SW, HCN2, BCAT1, AVPR2, ATP5PO, ATP7A, ATP5MC1, ATP4A, ATP2B1, ATP12A, ATHS, BIRC2, SERPINC1, ARSL, ARR3, RND3, RHOA, AQP5, AQP2, FASLG, APOC4, APOC2, BIRC3, CLCN2, CLCN5, FOLH1, EFNB3, EPHA4, ENO2, MARK2, ELK3, ELAVL1, EIF4G1, EIF4EBP1, EIF4A2, EGR3, EGR2, CELSR2, EFNB2, EPHX1, LPAR1, TYMP, EBM, E2F1, DUSP6, DRD3, DPYS, DPYD, DPT, DNTT, DMP1, EPHB1, ERBB3, DLD, FASN, FMO3, FLNA, FLII, FHIT, FGFR4, FGF11, GPC4, FDXR, FCP1, FCGRT, FBP1, FAP, ERG, FABP5, FABP3, F2RL2, F2RL1, EXT1, EVC, ETV3, ETFA, ESRRG, ESRRB, FBL, DMBT1, SEPTIN1, CLK2, COL17A1, CS, CRMP1, CREM, CREBBP, CRABP2, CPT1B, COX10, COX7A1, COX5B, MAP3K8, CORT, COL9A2, CSHL1, COL9A1, COL8A1, COL6A3, COL4A5, COL4A2, COL2A1, COL1A1, CNTF, CNR2, CMM, CCR1, CSF3, CST2, DIAPH2, BRINP1, CFD, DES, DEFB4A, DEFA3, DEFA1, DDX3X, DDT, AKR1C2, DCN, DBI, DBH, CYP27B1, CTAA1, CYP27A1, CYP8B1, CYP7A1, CYP2A6, CYP1B1, CYB5A, CXADR, CUX1, CTSL, CTSH, CTRL, PKM, PLA2G4A, PLEK, RBM14, SPTLC1, AGPAT1, PROCR, HYOU1, CARM1, UNC13B, CAP1, TIMM44, FAM3C, IFI30, LYPLA1, SPON1, SLC19A2, SPON2, NSA2, PEMT, ATP8A1, DLC1, CITED2, KLF2, WARS2, TCIRG1, SIGMAR1, FSTL3, SLC35A1, OLFM4, OLIG2, CCL27, BTN2A1, ADAMTS13, ESM1, LIAS, METAP2, EHD1, MALT1, FGL2, NMU, CD300C, CYP46A1, PPP1R13L, NPC2, CPLX1, WASF3, STARD10, SLC17A3, CAPN9, EBP, CD226, CTCF, IGF2BP3, IGF2BP1, USP16, ZMPSTE24, FLOT1, TREH, AIM2, GDF3, CXCL14, STXBP5L, GAL3ST1, ADAMTS2, ATG5, AKAP6, CHST3, FHL5, HOMER1, EIF2AK3, ITM2B, KIF20B, NCR1, TJP2, PEX16, TMPRSS11D, TGFBRAP1, ADGRG1, PIWIL1, ITGB1BP1, MSC, LARGE1, HACD1, SOX13, WTAP, TRIM13, MAFB, NUTF2, MPHOSPH10, TSHZ1, RBM6, HIPK3, PREB, AKT3, SCO2, KCNE2, THRAP3, EXOG, RNF10, NCOR1, SGSM2, HEPH, IP6K1, TOX, HDAC4, SART3, ECE2, AQR, EIF5B, LPIN2, NCOR2, PTPRT, MAP4K5, SLC16A7, DHDH, MCTS1, RGCC, SLC27A6, REM1, TRBV7-8, IGHD1-14, SLCO1B3, PCLO, MCAT, EIF3K, PDLIM3, SESN1, KLF15, SIT1, SERP1, IL17B, DISC1, DKK4, SIGLEC7, ACAD8, GREM1, BSCL2, PCOLCE2, CNNM1, DBNL, TBK1, HSPB8, MBL3P, CSAD, WAC, BPIFA1, TLR7, DNAJC27, IGF2-AS, GP6, IPO11, HSPA14, IRAK4, SLC35B3, G0S2, MYLIP, SLC40A1, TBX21, ERO1A, SLC2A8, SLC39A3, RHOD, PADI1, GPR132, HOOK2, CD274, CTNNA3, NUPR1, MYCBP, CHEK2, FAIM2, PSD3, SYNE1, TTC28, COBL, ARC, SIK2, FBXO28, SYT11, TBC1D9, CAND2, KDM1A, NT5C2, DICER1, RAB18, SACM1L, SBNO2, CARD8, MLXIP, COG2, ACOT7, MGAT4A, SLCO2B1, PTGDR2, AKAP13, CRTC1, NCS1, KLHL3, PANX1, PITPNC1, KIFBP, ATRNL1, TENM4, TKFC, PART1, MGAT4C, ARIH1, KLK5, TAFA5, SLC39A6, LY96, ZFPM2, BACE1, ZMYND8, DAPK2, FAM215A, SEC14L2, PES1, BRD4, TRAM1, NPTXR, TRS-AGA2-3, MLYCD, SLC33A1, ZBED1, SERPINF2, XCL1, SLC2A3, SLC1A7, SLC1A5, SKP2, SKIL, SIX3, SHC1, SRSF5, SELPLG, SDHA, CX3CL1, CCL22, SLC6A8, CCL20, CCL11, CCL8, CCL7, CCL4, CCL3, SCO1, SCN8A, SCN7A, SCN2A, SAA2, SLC5A5, SLC8A1, S100A12, SRI, TADA2A, TACR3, TAC3, TAC1, SYT4, SYT1, STXBP3, STX5, STIM1, STC1, SSTR2, SRD5A2, SLC9A3, SPRR2A, SPG7, SOX5, SOX2, SORL1, SIGLEC1, SMPD1, SLPI, SLCO1A2, SLC18A2, SLC10A2, SAA1, S100A4, TAL1, DNAJC3, PTMAP4, PTMA, PTGER3, PTBP1, PTAFR, PSMD3, PSMD2, PSMB6, PSMA7, PSG2, TMPRSS15, EIF2AK2, PTPN6, MAPK7, PRKD1, PPP1R2, POU3F1, POU2F2, PODXL, SEPTIN5, PNLIP, PMM2, PML, PMAIP1, PTPN4, PTPN11, RYR2, REG1B, RTN1, CLIP1, RPS19, RPS6KA3, RPS6KA2, RPN2, RPE, RORB, RNH1, RIT2, REV3L, REL, PTPRB, RCN2, RARB, RANGAP1, RAG1, RAB27A, RAB5B, RAB4A, PYGB, PTPRS, PTPRF, PTPRC, TAF1, TCP1, HTR3B, API5, ADAM19, MBTPS1, TNFRSF25, PAGE1, VAMP4, VAMP8, HSD17B6, JRK, KHSRP, DENR, PIAS1, CST7, TNFRSF14, DGKZ, IRS4, DOC2B, DYRK3, LOH19CR1, BRAP, PICALM, ZNF239, SLC14A2, AAAS, FOSL1, TNFSF12, RAB11A, MAFK, NOL3, PCSK7, HGS, MTMR7, USP2, USP14, PAPSS2, RPL14, CCRL2, TAF1C, F2RL3, KALRN, TRPA1, RIPK2, EIF2B5, ZPR1, FUBP1, PER3, TMEM11, BANF1, GALR2, TNFRSF11A, DLK1, TNFRSF18, SIGLEC5, ECB2, HBFQTL2, PRDX2, TLL1, HSP90B1, NR2C2, TPO, TPM4, TPM1, TOP2A, TOP1, TNFAIP3, NR2E1, TLR5, TLR1, TLE3, TRPM2, TJP1, TIMP2, TIAM1, THBS4, THBS2, TGFB2, TGFA, TFPI, TFAP2A, TERF2, TEP1, TRAF3, TST, TFEB, NSD2, LAP, PRRC2A, MANF, SLMAP, ZNF236, ZFP36, SF1, YWHAG, YY1, XDH, XBP1P1, WARS1, TNFRSF4, VPREB1, VEGFB, VDAC1, UPK2, UGT1A, UGCG, SCGB1A1, UBE2B, TYROBP, TYK2, TXNRD1, LINC02605
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Shox Deficiency Disorders
Gene_reviews
Cytogenetic testing. If either a contiguous gene syndrome encompassing signs of a SHOX deficiency disorder (in addition to other distinctive features) or an X;Y chromosomal translocation is suspected, a G-banded karyotype should be carried out [Ballabio et al 1989, Shears et al 1998, Shears et al 2002]. ... Differential Diagnosis The differential diagnosis of isolated SHOX-deficient short stature includes the following: Turner syndrome in females (see Genetically Related Disorders) Children of both sexes with short stature of unknown cause (often called idiopathic short stature [ISS]). ... The differential diagnosis of LWD caused by SHOX deficiency includes the following: Turner syndrome (see Genetically Related Disorders) LWD caused by pathogenic variants at an unidentified alternate locus or in gene(s) outside the SHOX locus Trauma to, infection of, or tumors in the distal radial growth plate Management Evaluations Following Initial Diagnosis To establish the extent of disease and needs in an individual diagnosed with SHOX deficiency, the evaluations summarized in this section (if not performed as part of the evaluation that led to the diagnosis) are recommended [Rappold et al 2007, Binder 2011]: Growth parameters. ... Treatment with high-dose rhGH augments the growth of children with SHOX deficiency to the same extent as in Turner syndrome according to a two-year randomized controlled trial [Blum et al 2007].
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Prss1-Related Hereditary Pancreatitis
Gene_reviews
Recurrent acute pancreatitis (RAP) is defined as a syndrome of multiple distinct acute inflammatory responses originating within the pancreas in individuals with genetic, environmental, traumatic, morphologic, metabolic, biologic, and/or other risk factors who experienced two or more episodes of documented acute pancreatitis, separated by at least three months [Guda et al 2018]. Chronic pancreatitis (CP) is defined as a pathologic fibro-inflammatory syndrome of the pancreas in individuals with genetic, environmental, and/or other risk factors who develop persistent pathologic responses to parenchymal injury or stress [Whitcomb et al 2016]. The features of established and advanced chronic pancreatitis include pancreatic atrophy, fibrosis, pain syndromes, duct distortion and strictures, and calcifications; pancreatic exocrine dysfunction; and pancreatic endocrine dysfunction and dysplasia [Whitcomb et al 2016]. ... Pain is usually sharp and stabbing in initial attacks, becoming deep and burning as the syndrome progresses. The most psychologically distressing pain is constant chronic pain, regardless of intensity [Machicado et al 2017].
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Autosomal Dominant Trpv4 Disorders
Gene_reviews
Affected individuals typically have either neuromuscular or skeletal manifestations alone, and in only rare instances an overlap syndrome has been reported. The three autosomal dominant neuromuscular disorders (mildest to most severe) are: Charcot-Marie-Tooth disease type 2C Scapuloperoneal spinal muscular atrophy Congenital distal spinal muscular atrophy The autosomal dominant neuromuscular disorders are characterized by a congenital-onset, static, or later-onset progressive peripheral neuropathy with variable combinations of laryngeal dysfunction (i.e., vocal fold paresis), respiratory dysfunction, and joint contractures. ... Spondyloepiphyseal dysplasia, Maroteaux type is also referred to as pseudo-Morquio syndrome type 2. Prevalence The prevalence of the autosomal dominant TRPV4 neuromuscular and skeletal dysplasias has not been well studied. ... Genes of Interest in the Differential Diagnosis of Intermediate and Severe Autosomal Dominant TRPV4 Skeletal Dysplasias View in own window Phenotype Gene MOI Disorder Intermediate COL2A1 AD (AR) Spondyloepiphyseal dysplasia congenita (see Type II Collagen Disorders Overview) GALNS AR Morquio syndrome type A (MPS IVA) GLB1 AR Morquio syndrome type B (MPS IVB) TRAPPC2 XL X-linked spondyloepiphyseal dysplasia tarda Severe COL2A1 AD Kniest dysplasia (see Type II Collagen Disorders Overview): platyspondyly & coronal cleft, shortened tubular bones & metaphyseal flaring, broad & short thorax COL11A1 COL11A2 AR AD Fibrochondrogenesis 1 & 2 (OMIM PS228520): rhizomelic limb shortening, broad dumbbell-shaped metaphyses, pear-shaped vertebral bodies, short & distally cupped ribs COL11A2 AR AD Otospondylomegaepiphyseal dysplasia 1 (OMIM 184840, 215150) HSPG2 AR Dyssegmental dysplasia, Silverman-Handmaker type (OMIM 224410) AD = autosomal dominant; AR = autosomal recessive; MOI = mode of inheritance; MPS = mucopolysaccharidosis; XL = X-linked 1. Autosomal recessive otospondylomegaepiphyseal dysplasia may also be referred to as Weissenbacher Zweymuller syndrome. Brachyolmia types 1 and 2 (OMIM 271530 and 613678) can also be considered in the differential diagnosis of intermediate autosomal dominant TRPV4 skeletal dysplasias.
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Mind-Blindness
Wikipedia
The triad consists of deficits in social, communication and imagination of others' minds. [22] Ozonoff and colleagues were able to discriminate between individuals diagnosed with the Asperger's syndrome and other individuals affected with autism by their ability to solve ToM tasks. ... Such subcategories include Asperger syndrome, pervasive developmental disorder, and disintegrative disorder. [25] Unfortunately, “despite this change in diagnostic criteria, the number of diagnosed cases of autism spectrum disorder (ASD) is much higher than expected”. [26] As reported by Johnson and Myers (2017), “ASDs are not rare [...] ... (July 1992). "Theory of Mind in Asperger's syndrome". Journal of Child Psychology and Psychiatry . 33 (5): 877–893. doi : 10.1111/j.1469-7610.1992.tb01962.x . PMID 1378848 . ^ Ozonoff, S; Rogers, S. & Pennington, B. (November 1991). "Asperger's syndrome: Evidence for an empirical distinction from high-functioning autism".
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Combat Stress Reaction
Wikipedia
Contents 1 Signs and symptoms 1.1 Fatigue-related symptoms 1.2 Autonomic nervous system – Autonomic arousal 1.2.1 Battle casualty rates 2 Diagnosis 2.1 Between the wars 2.2 World War II 2.2.1 American 2.2.2 British 2.2.3 Canadian 2.2.4 Germans 2.2.5 Finns 2.3 Post-World War II developments 2.3.1 Peacekeeping stresses 3 Pathophysiology 3.1 SNS activation 3.2 General adaptation syndrome 4 Treatment 4.1 7 Rs 4.2 BICEPS 4.2.1 Brevity 4.2.2 Immediacy 4.2.3 Centrality/Contact 4.2.4 Expectancy 4.2.5 Proximity 4.2.6 Simplicity 4.3 Predeployment preparation 4.3.1 Screening 4.3.2 Cohesion 4.3.3 Training 5 Prognosis 6 Controversy 7 See also 8 References 9 Further reading 10 External links Signs and symptoms [ edit ] Combat stress reaction symptoms align with the symptoms also found in psychological trauma , which is closely related to post-traumatic stress disorder (PTSD). ... By 1939, some 120,000 British ex-servicemen had received final awards for primary psychiatric disability or were still drawing pensions – about 15% of all pensioned disabilities – and another 44,000 or so were getting pensions for 'soldier's heart' or Effort Syndrome . There is, though, much that statistics do not show, because in terms of psychiatric effects, pensioners were just the tip of a huge iceberg." [6] War correspondent Philip Gibbs wrote: Something was wrong. ... Although the flight-or-fight-response normally ends with the removal of the threat, the constant mortal danger in combat zones likewise constantly and acutely stresses soldiers. [15] General adaptation syndrome [ edit ] The process whereby the human body responds to extended stress is known as general adaptation syndrome (GAS). ... "Stress and the General Adaptation Syndrome" . British Medical Journal . 1 (4667): 1383–1392. doi : 10.1136/bmj.1.4667.1383 .
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Hyperglycemia
Wikipedia
Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure. [6] Also, life-threatening consequences of hyperglycemia is nonketotic hyperosmolar syndrome. [1] Perioperative hyperglycemia has been associated with immunosuppression, increased infections, osmotic diuresis, delayed wound healing, delayed gastric emptying, sympatho-adrenergic stimulation, and increased mortality. In addition, it reduces skin graft success, exacerbates brain, spinal cord, and renal damage by ischemia, worsens neurologic outcomes in traumatic head injuries, and is associated with postoperative cognitive dysfunction following CABG. [7] Causes [ edit ] Hyperglycemia may be caused by: diabetes, various (non-diabetic) endocrine disorders (insulin resistance and thyroid, adrenal, pancreatic, and pituitary disorders), sepsis and certain infections, intracranial diseases (e.g. encephalitis, brain tumors (especially if near the pituitary gland), brain haemorrhages, and meningitis) (frequently overlooked), convulsions, end-stage terminal disease, prolonged/major surgeries, [8] excessive eating , severe stress, and physical trauma. [ citation needed ] Endocrine [ edit ] Chronic, persistent hyperglycaemia is most often a result of diabetes . [ citation needed ] Several hormones act to increase blood glucose levels and may thus cause hyperglycaemia when present in excess, including: cortisol, catecholamines, growth hormone, glucagon, [9] and thyroid hormones . [10] Hyperglycaemia may thus be seen in: Cushing's syndrome , [11] pheochromocytoma , [12] acromegaly , [13] hyperglucagonemia , [14] and hyperthyroidism . [10] Diabetes mellitus [ edit ] Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus . ... "Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management" . ... External links [ edit ] Classification D ICD - 10 : R73.9 ICD - 9-CM : 790.29 MeSH : D006943 DiseasesDB : 6234 External resources MedlinePlus : 007228 Hyperglycemia in infants – from MedlinePlus v t e Disease of the pancreas and glucose metabolism Diabetes Types type 1 type 2 gestational MODY 1 2 3 4 5 6 Complications See Template:Diabetes Abnormal blood glucose levels Hyperglycaemia Oxyhyperglycemia Hypoglycaemia Whipple's triad Insulin disorders Insulin resistance Hyperinsulinism Rabson–Mendenhall syndrome Other pancreatic disorders Insulinoma Insulitis v t e Clinical biochemistry blood tests Electrolytes Sodium Potassium Chloride Calcium Renal function Creatinine Urea BUN-to-creatinine ratio Plasma osmolality Serum osmolal gap Acid-base Anion gap Arterial blood gas Base excess Bicarbonate CO 2 content Lactate Iron tests Ferritin Serum iron Transferrin saturation Total iron-binding capacity Transferrin Transferrin receptor Hormones ACTH stimulation test Thyroid function tests Thyroid-stimulating hormone Metabolism Blood glucose Hemoglobin A1c Lipid panel LDL HDL Triglycerides Total cholesterol Basic metabolic panel Comprehensive metabolic panel Cardiovascular Cardiac marker Troponin test CPK-MB test Lactate dehydrogenase Myoglobin Glycogen phosphorylase isoenzyme BB Liver function tests Proteins Human serum albumin Serum total protein ALP transaminases ALT AST AST/ALT ratio GGT Bilirubin Unconjugated Conjugated Pancreas Amylase Lipase Pancreatic lipase Small molecules Blood sugar level Hypoglycemia Hyperglycemia Nitrogenous Azotemia Hyperuricemia Hypouricemia Proteins LFT Elevated transaminases Elevated ALP Hypoproteinemia Hypoalbuminemia Other Elevated alpha-fetoproteinINS, PRKCB, INSR, GCK, IL6, HNF1A, NOS3, LEP, GCG, NFE2L2, CCL2, AGER, ADIPOQ, PDX1, PTGS2, LEPR, IRS2, SP1, GPX1, NQO1, CD40, SIM1, HSD11B1, FBN1, FCGR3B, GLP1R, HMGA1, PRKAR1A, CD163, AKR1B1, PRDX4, ICAM1, COL3A1, IL1B, ITGAM, MMP9, PPARGC1A, AVP, PRKCZ, HCRT, GRK2, ADIPOR1, LDHA, PCSK1, HSPD1, HTR2A, PRNP, CBL, CYP11A1, EPAS1, STAT3, HRH3, PKLR, PPARG, CNTF, DRD1, PLA2G4A, ADA, ADRB1, HNF4A, HCRTR2, GIPR, ABCC8, KCNJ11, PIK3R1, PAX4, MC4R, NEUROD1, GATA6, APPL1, PLAGL1, ACAT1, KLF11, SLC2A4, IL10, PTF1A, IRS1, HYMAI, LMNA, ZFP57, CRK, SI, ST3GAL4, ITPR3, AHSA1, TXNIP, RFX6, SLC2A1, SLC5A2, MAPK14, ATN1, IGF1, DPP4, GIP, FGF21, GCGR, GABPA, PIK3CD, PTPN22, PIK3CB, POLDIP2, PRKAA1, FOXO1, PRKAA2, PIK3CA, PHKG2, GPT, EHMT1, ARMC5, MAPK1, RNF19A, HIF1A, REN, ROS1, PIK3CG, IAPP, CLCNKB, SIRT1, BLK, MGAM, TNF, ALB, AIMP2, VEGFA, ZMPSTE24, TCF7L2, TLR4, LRPPRC, TGFB1, AKT1, CEL, EIF2AK3, TP53, INS-IGF2, GRAP2, ZGLP1, SLC5A1, CAT, DECR1, PRKCA, SERPINE1, GH1, HMGB1, FN1, NLRP3, PRKAB1, PPARA, NOX4, ACE, DNM1L, MTOR, SOD2, AGT, WNK1, EPHB2, BDNF, SETD2, EPO, SYT1, CRP, APOE, SLC2A2, PTEN, GLO1, RELA, GCKR, HMOX1, IL18, VCAM1, THBS1, CYBB, POMC, GORASP1, GPBAR1, MOK, DAPK2, NFKB1, TXN, KDR, MIR146A, MIR126, UTRN, DENR, GSK3B, CRMP1, UCP2, RCBTB1, IL17A, CTNNB1, AGTR1, PDHX, TRPC6, GOLGA6A, VDR, MMP2, PON1, G6PC, FGF2, BCL2, FOXO3, APRT, PRRT2, ANGPT2, BGLAP, SLC17A5, SGK1, IFNG, CASP3, CD59, SIRT3, NFAT5, EDN1, MTNR1B, ALDH2, LOC102723407, EGR1, MAPK8, PTPN1, VWF, CXCL12, MFAP1, CD36, GYS1, ENPP1, PDK4, P2RX7, PARP1, SOCS3, MBL2, ACE2, PNPLA3, MAPT, LPL, ADCY5, TRIB3, BECN1, APOB, NR3C1, ROBO4, APOA1, AMY2A, IL22, GAL, TNFRSF11B, SERPINF1, FTO, MLXIPL, HK2, NUCB2, HSPA4, CXCL8, AKT2, NGF, HGF, IGF1R, FAM3B, MTHFR, IL1RN, IL4, FFAR1, SOD1, MIR223, MALAT1, CDH5, FGF1, FASN, CREM, PTK2B, ROCK1, SHBG, TDGF1P3, BMP7, F3, MAPK3, TGM2, ESR1, DIANPH, MIR34A, FST, ASPG, RAC1, SLC30A8, SELP, STK11, TLR2, ATF3, APP, VDAC1, PLA2G1B, ARG1, PLG, APOC3, TTR, PPARD, CASP1, SELE, HPSE, SELENOP, NSA2, KLF2, MST1, STAM, NR3C2, CCL5, SCT, PECAM1, SLC30A10, LOH19CR1, UNC13B, TNFSF10, SNAP25, LGALS3, PDE5A, SMN2, SMN1, SPP1, SREBF1, APOM, SMAD3, SREBF2, SLC5A3, MBD2, SST, MDM2, TCF21, NOS1, MYD88, KL, TKT, LONP1, PAX6, PC, BRD7, RAPGEF5, CRISP2, PCK2, TRPV1, TRPC3, PCNA, TSC2, MCAT, ABCG2, SERPINA1, HIPK2, REG3A, PRKCD, KLRK1, YWHAZ, NEU1, MMRN1, SLC39A7, RPS19, CXCR4, KDM1A, TEK, TFAM, PTH, NOS2, WFS1, RENBP, NOTCH1, NPY, NAMPT, SMUG1, ABCA1, DLK1, KMT5AP1, ESR2, CRY1, CSF1, DBP, HSPA12A, NRK, PRSS55, DNMT1, DRD2, RCAN1, CRTC2, PLB1, EGFR, SLC30A7, ENO2, FABP4, HHIP, FOXM1, FOS, FOSB, GFAP, GFPT1, SPZ1, GJA1, GLS, SETD7, GYS2, HBG2, CORO7, HMGCR, HOXD13, CREB1, COMP, MIR140, CHRM3, ACHE, ACTB, ADORA2B, ADRB3, AGTR2, KLRC4-KLRK1, FOXO6, C20orf181, ALOX15, ANPEP, AQP7, AQP9, ATIC, ATM, MIR375, BCHE, BNIP3, BTC, TSPO, VPS51, MIR26B, CAV1, CAV3, MIR24-1, CD86, MIR155, CDK4, CEBPA, FOXN3, P2RY12, DUSP1, HSF1, FAM3A, IDE, IGF2, G6PC2, IGFBP2, CXCL10, JUN, NOD2, HSPG2, JUNB, HSPA5, JUND, HSP90AA1, IL1R1, IL1A, MIR29A, SLC38A4, RACK1, SYCP2, MIR106B, MICU1, MIR23A, AGGF1, PNPO, IL21, MIR106A, TRPM7, ABCC4, MIR27A, RETSAT, CD226, LPCAT3, MIR29C, RHOT1, MIRLET7C, MIR301A, RASGRP1, CTDSP2, FBXW7, PPIF, NLRC4, VN1R17P, PTPRU, MIRLET7B, STAP2, MIR206, IFI30, MIR129-2, TRPV4, MIR132, CCT2, CASZ1, SLC35A1, SCPEP1, CYP2W1, PID1, ATG7, MIR144, DEAF1, MIR145, SEMA3C, MIR107, MIR150, FAM3C, MIR152, NCOA2, GER, VAT1, MIR17, MIR182, PDPN, THRAP3, MAD2L2, MIR200B, IGF2BP2, CXCR6, MIR200C, HCN4, XRCC6P5, GFPT2, MIR4454, SLC16A4, SLC16A3, PGR-AS1, P2RX6, LPAR2, SLC12A9, POLD4, KLF4, P2RX5-TAX1BP3, CHPT1, XPR1, MTA2, DIP, S1PR2, USP14, SNAP23, LOC102723971, F2RL3, TRPA1, DALIR, PERCC1, CST12P, SGPL1, SPHK1, RN7SL263P, ACKR3, RPTOR, ARHGEF7, KAT2B, H3P5, PROM1, TRAP, RETN, GPR166P, DCAF1, MIR503, MIR451A, GDF15, PTBP2, PRDX6, MIR423, HDAC9, POLE4, CTDSP1, ZDHHC7, BMS1, MIR135B, DDIT4, RNF10, DELYQ11, MIR486-1, GAL3ST1, ATG5, NCF1, PICK1, GGTLC5P, MAP4K4, ANGPTL8, MIR33B, MIR592, GGTLC3, POTEF, GGT2, SLC22A8, CCR2, GGTLC4P, SIX2, SMIM1, MAFA, GALP, NEXN, HSPB8, IL33, WNT3A, SIGLEC7, INTU, SERP1, QRFPR, ORAI1, HPGDS, BHLHE22, CNDP1, COX4I2, DESI1, DNER, FOXP2, FBXO8, FBXO2, EGLN3, MRAP2, MARCHF3, FN3K, KIFBP, NPVF, SNAP47, SNED1, MRGPRX3, GDE1, MRGPRX4, FTSJ3, MSI2, RPAIN, SIRT6, NES, DUOX2, TRPM5, CERS2, GGCT, A1CF, DUSP26, OBP2A, BRD9, HMCN1, HSPA14, ELOVL1, NEUROG3, TAS2R13, ASCC1, TVP23B, ABCG8, EFHD2, NOX5, GP6, ADIPOR2, NT5C3A, ASRGL1, NRN1, KLF15, HKDC1, SCUBE1, DACT1, KCNH6, TSC22D4, MCTS1, FLVCR1, SGSM3, RBM45, GPR151, NGDN, KRT20, METAP2, CAPN10, PSIP1, PTGDR2, GPRC6A, INPP5F, SIRT2, CHMP2B, DKK1, ERRFI1, P2RX2, NT5C2, UNC13A, SLC25A19, CADM2, PCSK9, EHMT2, LGR6, MTMR11, MRGPRX1, RAB10, C1QL1, OR10A4, ZFP69, QRFP, PWAR4, GPR142, ZACN, ENHO, FBRS, SRSF10, ELOVL5, MCF2L2, SLC24A3, SIK1, PTRH1, TRIM69, SH2B1, SRXN1, SIRPA, PART1, EMCN, TXN2, FTSJ1, FGFBP3, NRG4, TICAM1, LY96, LUC7L3, PROK2, ATG4B, LPAR3, DDAH2, PES1, SLC35G1, ANGPTL2, OXER1, GLIS3, SIRT5, NEDD4L, DUOX1, CENPX, ZBTB7C, PHLPP1, TBC1D1, SEMA6A, RPS6KB1, RIPK2, GCLC, GATA4, GCH1, GDF2, MSTN, GDNF, GFER, GGT1, GHR, GHSR, GLDC, GALNT2, GLUL, CXCR3, GPER1, GPR42, GPX5, GSTT1, GUSB, HAS2, HBB, GAS6, GALR1, TNFRSF14, F2, EEF1A2, EGF, ELAVL1, ENO1, EP300, EPHX2, EPOR, ESRRG, EZH2, FAAH, GAD1, FABP1, FANCC, FGB, FGL1, FGR, FLT1, FMO3, NR5A1, GAST, HCLS1, HCRTR1, HLA-B, KRAS, IL13, FOXK2, INSRR, IRF3, ITGA2, JAK2, KCNH2, KCNQ1, KNG1, LDLR, HLA-DMA, LECT2, LGALS1, LIPE, LOX, LRP5, LTA, LTBR, SMAD2, MAP2, IL7R, IL2RB, IL2, IKBKB, HLA-DMB, HLA-DRB1, NR4A1, SLC29A2, HNRNPA1, TLX2, HPRT1, AGFG1, PRMT1, HES1, HSPA1A, HSPA1B, HTR2C, IARS1, IRF8, IGFBP1, IGFBP3, IGFBP7, CCN1, EDNRA, S1PR3, S1PR1, CCND1, AQP5, AR, ARF6, ARRB1, ARRB2, ARSA, ASAH1, ATP2A3, BAX, HCN2, CD33, BMP4, BRS3, KLF9, C5AR1, CACNA1D, CAPN1, CASP8, CASR, RUNX2, AQP3, KLK3, APOA4, XIAP, ACACA, ACVRL1, ADCYAP1, PLIN2, ADK, ADM, ADRA1A, ADRA2B, JAG1, AHR, AHSG, AIF1, ALAD, ALDOB, ALK, ALX3, AMPD1, ANGPT1, ANXA5, MS4A1, ENTPD1, ECE1, DEFB1, CTLA4, CUX1, CYBA, CYC1, CYP1B1, CYP2E1, DAB2, DCN, DDIT3, TIMM8A, CD40LG, DIO2, DLD, DLG1, DMD, DMRT1, DYNC1H1, DUSP6, DUSP9, E2F1, CCN2, VCAN, CSF2, CSF1R, CD44, CD68, LRBA, CDC25C, CDC42, CDK2, CDK5, CDKN1A, CEACAM5, CMA1, CMKLR1, CNR1, COPA, COX4I1, CPT1A, CPT2, CREBBP, CRH, CRYZ, MDM4, MEFV, MAP3K5, SULT1E1, SNCA, SOAT1, SORD, SPARC, SRC, SSTR4, ST13, STAR, STAT5A, SUV39H1, TFPI, SYCP1, TAC1, TAT, TBX1, TBXA2R, TCF3, ZEB1, PPP1R11, TF, SMO, SNAI2, SLPI, SLC20A1, S100B, ACSM3, SAT1, SCD, SCN10A, SCP2, CCL3, CCL18, CXCL5, CX3CL1, SDC2, SDC4, SIX3, SLC1A3, SLC2A3, SLC6A6, SLC9A1, SLC16A1, SLC19A1, TFE3, TFRC, SORT1, ULK1, VIP, BEST1, CLIP2, YY1, CNBP, AIR, MLRL, FZD4, PLA2G6, STK24, TG, DOC2B, DGKD, APOL1, DEGS1, KHSRP, AOC3, NCOA1, RIPK1, TNFSF14, VIM, VEGFC, VEGFB, VDAC2, TGFB3, THBS2, KLF10, TIMP1, TIMP2, TIMP3, TLR1, TM7SF2, TMPRSS2, TNFRSF1A, TNFRSF1B, TPT1, TRH, UBE2V1, UCHL1, UCP3, UGCG, NR1H2, VASP, S100A8, S100A1, RAB8A, P2RX4, NTS, NR4A2, OGG1, OPA1, OPRK1, OPRM1, OSM, P2RX1, P2RX3, P2RX5, ABCB1, P2RY1, P2RY2, PAK1, PAWR, PAX3, PCK1, PDCD1, PDK1, PDR, DDR2, NRTN, SLC11A2, CCN3, MEN1, MFGE8, MIP, MITF, KMT2A, MMP3, MMP7, MMP16, MPG, MPO, ABCC1, MT2A, RNR2, MYC, MYLK, NCK1, NFE2, NFIL3, NFKBIA, PFKM, SLC25A3, CLIP1, RBP3, PTGDS, PTGS1, PTPN2, PTPN4, PTPN9, PTPRN, PTX3, RARA, RASGRF1, RBP4, PIM1, REG1A, RFC1, RHEB, BRD2, RORC, RPL10, RPL29, RPL36A, ABCA4, PTCH1, PROX1, MAP2K7, MAP2K6, PIN1, PIN4, PKM, PLA2G2A, PLAT, PLAUR, PLTP, PLXNA1, PML, PON2, POU1F1, CTSA, PPIA, PPID, PPP2CA, PTPA, PRKCI, PRKD1, MAPK7, H3P40
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Dysmenorrhea
Wikipedia
Dysmenorrhea at Curlie Classification D ICD - 10 : N94.4 - N94.6 ICD - 9-CM : 625.3 MeSH : D004412 DiseasesDB : 10634 External resources MedlinePlus : 003150 eMedicine : article/253812 Patient UK : Dysmenorrhea v t e Female diseases of the pelvis and genitals Internal Adnexa Ovary Endometriosis of ovary Female infertility Anovulation Poor ovarian reserve Mittelschmerz Oophoritis Ovarian apoplexy Ovarian cyst Corpus luteum cyst Follicular cyst of ovary Theca lutein cyst Ovarian hyperstimulation syndrome Ovarian torsion Fallopian tube Female infertility Fallopian tube obstruction Hematosalpinx Hydrosalpinx Salpingitis Uterus Endometrium Asherman's syndrome Dysfunctional uterine bleeding Endometrial hyperplasia Endometrial polyp Endometriosis Endometritis Menstruation Flow Amenorrhoea Hypomenorrhea Oligomenorrhea Pain Dysmenorrhea PMS Timing Menometrorrhagia Menorrhagia Metrorrhagia Female infertility Recurrent miscarriage Myometrium Adenomyosis Parametrium Parametritis Cervix Cervical dysplasia Cervical incompetence Cervical polyp Cervicitis Female infertility Cervical stenosis Nabothian cyst General Hematometra / Pyometra Retroverted uterus Vagina Hematocolpos / Hydrocolpos Leukorrhea / Vaginal discharge Vaginitis Atrophic vaginitis Bacterial vaginosis Candidal vulvovaginitis Hydrocolpos Sexual dysfunction Dyspareunia Hypoactive sexual desire disorder Sexual arousal disorder Vaginismus Urogenital fistulas Ureterovaginal Vesicovaginal Obstetric fistula Rectovaginal fistula Prolapse Cystocele Enterocele Rectocele Sigmoidocele Urethrocele Vaginal bleeding Postcoital bleeding Other / general Pelvic congestion syndrome Pelvic inflammatory disease External Vulva Bartholin's cyst Kraurosis vulvae Vestibular papillomatosis Vulvitis Vulvodynia Clitoral hood or clitoris Persistent genital arousal disorder v t e Menstrual cycle Events and phases Menstruation Follicular phase Ovulation Luteal phase Life stages Menarche Menopause Tracking Signs Basal body temperature Cervical mucus Mittelschmerz Systems Fertility awareness Calendar-based methods Billings Ovulation Method Creighton Model Suppression Extended cycle combined hormonal contraceptive Lactational amenorrhea Disorders Amenorrhea Anovulation Dysmenorrhea Hypomenorrhea Irregular menstruation Menometrorrhagia Menorrhagia Metrorrhagia Oligomenorrhea Related events Folliculogenesis Menstrual synchrony Premenstrual syndrome / Premenstrual dysphoric disorder / Menstrual psychosis Sexual activity In culture and religion Chhaupadi Feminine hygiene Sanitary napkin Tampon Menstrual cup Menstrual Hygiene Day Menstrual taboo Menstruation hut NiddahAVP, OXT, LMNA, ANTXR1, INHBA, PPARG, AIP, FOS, BSCL2, CYP17A1, GPR101, CYB5A, AGPAT2, CAVIN1, CAV1, MUC16, PTGS2, BDNF, ANXA2, CYP1A1, CGB5, OTC, OXTR, MTCO2P12, SERPINE1, PCNA, PPIA, PTH, SLC4A1, CCL11, TNF, VEGFA, TRPV1, PERCC1, NGF, MYL12A, MYL12B, CGB8, HPGDS, NOS3, ALOX5, COX2, MOS, BGLAP, CD34, CGA, CGB3, CLCN3, CLTC, CREB1, CTNNB1, CYP2B6, CYP2D6, DNMT3B, ESR1, FCER2, MSTN, GSTM1, GSTT1, HIF1A, HTC2, CCN1, IL1A, IL1RN, IL6, IL7, CXCL8, IL15, MEFV, MMP14, LOC107987479
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Thought Disorder
Wikipedia
FTD is a common, and core symptom of a psychotic disorder and may be seen as a marker of its severity, and also as a predictor of prognosis. [9] [11] It reflects a cluster of cognitive, linguistic, and affective disturbances, that has generated research interest from the fields of cognitive neuroscience, neurolinguistics, and psychiatry. [9] Eugen Bleuler , who named schizophrenia , held that thought disorder was its defining characteristic. [12] However, disturbances of thinking and speech such as clanging or echolalia may be present in Tourette syndrome , [13] or other symptoms as found in delirium . [14] A clinical difference exists between these two groups. ... FTD is a common, and core symptom of a psychotic disorder and may be seen as a marker of its severity, and also as a predictor of prognosis. [9] [11] It reflects a cluster of cognitive, linguistic, and affective disturbances, that has generated research interest from the fields of cognitive neuroscience, neurolinguistics, and psychiatry. [9] FTD is a complex, multidimensional syndrome characterized by deficiencies in the logical organizing of thought needed to achieve goals. ... This can be a symptom of Tourette's Syndrome, e.g. "What would you like for dinner?" ... Verbigeration [58] – Meaningless and stereotyped repetition of words or phrases replacing understandable speech, as seen in schizophrenia. [58] [59] Use of term [ edit ] Some recent (2015, 2017) psychiatric/psychological glossaries defined thought disorder as disturbed thinking or cognition that affects communication , language , or thought content including poverty of ideas , neologisms , paralogia, word salad , and delusions [7] [3] —which are disturbance of both thought content and thought form—and suggested the more specific terms of content thought disorder and formal thought disorder , [2] with content thought disorder defined as a thought disturbance characterized by multiple fragmented delusions, [16] [3] and formal thought disorder defined as disturbance in the form or structure of thinking. [60] [61] For example, DSM-5 (2013) only used the word formal thought disorder, mostly as a synonym of disorganized thinking and disorganized speech. [62] This is in contrast with ICD-10 (1992) which only used the word "thought disorder", always accompanied with "delusion" and "hallucination" separately, [63] and a general medical dictionary (2002) that although generally defined thought disorders similarly to the psychiatric glossaries, [64] but also used the word in other entries as ICD-10 did. [65] The recent psychiatric text (2017) also mentioned when describing thought disorder as a "disorganization syndrome" within the context of schizophrenia: "Thought disorder" here refers to disorganization of the form of thought and not content. ... PMID 8348799 . ^ Phenomenology of Schizophrenia (2017) , THE SYMPTOMS OF SCHIZOPHRENIA, Negative Symptoms. "The two-syndrome concept as formulated by T. J.
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Cerebellar Hypoplasia (Non-Human)
Wikipedia
In cats, this condition is also called "Wobbly Cat Syndrome." An animal with CH may be called ataxic or be described as a "bobble-head." ... Retrieved 2019-03-02 . ^ {{Cite web|url= https://www.vet.cornell.edu/departments-centers-and-institutes/cornell-feline-health-center/health-information/feline-health-topics/vestibular-syndrome feline vestibular syndrome|title=Feline infectious peritonitis}} ^ Skelly, Barbara J.; Franklin, Robin J. ... External links [ edit ] Video of a cat with cerebellar hypoplasia: This is Charlie Video of a dog with cerebellar hypoplasia: Samson: Lessons From A Blind Dog Super Hero The Hydrocephalic Cat and Zeke - SHAHS Non Profit Rescue Society Feline Vestibular Syndrome Life with CH Cats Kitty Cat Chronicles: Cerebellar Hypoplasia The Handicapped Pets Foundation donates new or reconditioned wheelchairs to pets-in-need.
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Bruxism
Wikipedia
The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. [3] [5] [7] [15] Indeed, the symptoms of TMD overlap with those of bruxism. [16] Others suggest that there is no strong association between TMD and bruxism. [4] A systematic review investigating the possible relationship concluded that when self-reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when stricter diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. [17] In severe, chronic cases, bruxism can lead to myofascial pain and arthritis of the temporomandibular joints. [ medical citation needed ] Causes [ edit ] The left temporalis muscle The left medial pterygoid muscle, and the left lateral pterygoid muscle above it, shown on the medial surface of the mandbilar ramus, which has been partially removed along with a section of the zygomatic arch The left masseter muscle (red highlight), shown partially covered by superficial muscles The muscles of mastication (the temporalis, masseter, medial and lateral pterygoid muscles) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. ... Possible associations [ edit ] Several associations between bruxism and other conditions, usually neurological or psychiatric disorders, have rarely been reported, with varying degrees of evidence (often in the form of case reports ). [1] [23] Examples include: Acrodynia [9] Atypical facial pain [27] Autism [10] Cerebral palsy [4] [8] Disturbed sleep patterns and other sleep disorders , such as obstructive sleep apnea , [23] snoring , [23] moderate daytime sleepiness , [ medical citation needed ] and insomnia [12] Down syndrome [4] Dyskinesias [7] Epilepsy [23] Eustachian tube dysfunction [ medical citation needed ] Infarction in the basal ganglia [23] Intellectual disability , particularly in children [27] Leigh disease [23] Meningococcal septicaemia [23] Multiple system atrophy [23] Oromandibular dystonia [31] Parkinson's diseases , [20] (possibly due to long-term therapy with levodopa causing dopaminergic dysfunction) [10] Rett syndrome [7] Torus mandibularis [9] and buccal exostosis [32] Trauma , [23] e.g. brain injury or coma [10] Diagnosis [ edit ] Early diagnosis of bruxism is advantageous, but difficult. ... The presence of other sleep disorders (e.g., obstructive sleep apnea syndrome). Definition examples [ edit ] Bruxism is derived from the Greek word βρύκειν ( brykein ) "to bite, or to gnash, grind the teeth". [35] [36] [37] People who suffer from bruxism are called bruxists or bruxers and the verb itself is "to brux".
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Blastocystosis
Wikipedia
"The role of Blastocystis sp. and Dientamoeba fragilis in irritable bowel syndrome: a systematic review and meta-analysis". ... "Blastocystis subtypes in irritable bowel syndrome and inflammatory bowel disease in Ankara, Turkey" . ... "Oh my aching gut: irritable bowel syndrome, Blastocystis, and asymptomatic infection" . ... "Oh my aching gut: irritable bowel syndrome, Blastocystis, and asymptomatic infection" . ... "Oh my aching gut: irritable bowel syndrome, Blastocystis, and asymptomatic infection" .
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Schizoid Personality Disorder
Wikipedia
He criticizes that this may be due to the current diagnostic criteria: They describe SPD only by an absence of certain traits, which results in a "deficit syndrome" or "vacuum". Instead of delineating the presence of something, they mention solely what is lacking. ... However, in OCPD the capacity to develop intimate relationships is usually intact, but deep contacts may be avoided because of an unease with emotions and a devotion to work. [13] [19] Asperger syndrome There may be substantial difficulty in distinguishing Asperger syndrome (AS), sometimes called "schizoid disorder of childhood", from SPD. ... A 2011 study on suicidal inpatients at a Moscow hospital found that schizoids were the least common patients, while those with cluster B personality disorders were the most common. [59] Asperger syndrome [ edit ] Several studies have reported an overlap or comorbidity with the autism spectrum disorder Asperger syndrome . [60] [15] [16] Asperger syndrome had traditionally been called " schizoid disorder of childhood ", and Eugen Bleuler coined both the terms "autism" and "schizoid" to describe withdrawal to an internal fantasy, against which any influence from outside becomes an intolerable disturbance. [61] In a 2012 study of a sample of 54 young adults with Asperger syndrome, it was found that 26% of them also met criteria for SPD, the highest comorbidity out of any personality disorder in the sample (the other comorbidities were 19% for obsessive–compulsive personality disorder , 13% for avoidant personality disorder and one female with schizotypal personality disorder ). Additionally, twice as many men with Asperger syndrome met criteria for SPD than women. ... The study found that social interaction impairments, stereotyped behaviours and specific interests were more severe in the individuals with Asperger syndrome also fulfilling SPD criteria, against the notion that social interaction skills are unimpaired in SPD.
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Bipolar Ii Disorder
Wikipedia
Even though hypomania may increase functioning, episodes need to be treated because they may precipitate a depressive episode. [1] [2] Depressive episodes [ edit ] It is during depressive episodes that BP-II patients often seek help. Symptoms may be syndromal or subsyndromal . [1] Depressive BP-II symptoms may include five or more of the below symptoms (at least one of them must be either depressed mood or loss of interest/pleasure). ... Relapse can still occur, even with continued medication and therapy. [25] Prognosis [ edit ] There is evidence to suggest that bipolar II has a more chronic course of illness than bipolar I disorder . [26] This constant and pervasive course of the illness leads to an increased risk in suicide and more hypomanic and major depressive episodes with shorter periods between episodes than bipolar I patients experience. [26] The natural course of bipolar II disorder, when left untreated, leads to patients spending the majority of their lives unwell with much of their suffering stemming from depression . [20] Their recurrent depression results in personal suffering and disability. [20] This disability can present itself in the form of psychosocial impairment, which has been suggested to be worse in bipolar II patients than in bipolar I patients. [27] Another facet of this illness that is associated with a poorer prognosis is rapid cycling , which denotes the occurrence of four or more major Depressive, Hypomanic, and/or mixed episodes in a 12-month period. [26] Rapid cycling is quite common in those with Bipolar II, much more so in women than in men (70% vs. 40%), and without treatment leads to added sources of disability and an increased risk of suicide. [20] To improve a patient's prognosis, long-term therapy is most favorably recommended for controlling symptoms, maintaining remission and preventing relapses. [28] With treatment, patients have been shown to present a decreased risk of suicide (especially when treated with lithium ) and a reduction of frequency and severity of their episodes, which in turn moves them toward a stable life and reduces the time they spend ill. [29] To maintain their state of balance, therapy is often continued indefinitely, as around 50% of the patients who discontinue it relapse quickly and experience either full-blown episodes or sub-syndromal symptoms that bring significant functional impairments. [28] Functioning [ edit ] The deficits in functioning associated with Bipolar II disorder stem mostly from the recurrent depression that Bipolar II patients suffer from. Depressive symptoms are much more disabling than hypomanic symptoms and are potentially as, or more disabling than mania symptoms. [27] Functional impairment has been shown to be directly linked with increasing percentages of depressive symptoms, and because sub-syndromal symptoms are more common—and frequent—in Bipolar II disorder, they have been implicated heavily as a major cause of psychosocial disability. [20] There is evidence that shows the mild depressive symptoms, or even sub-syndromal symptoms, are responsible for the non-recovery of social functioning, which furthers the idea that residual depressive symptoms are detrimental for functional recovery in patients being treated for Bipolar II. [30] It has been suggested that symptom interference in relation to social and interpersonal relationships in Bipolar II Disorder is worse than symptom interference in other chronic medical illnesses such as cancer. [30] This social impairment can last for years, even after treatment that has resulted in a resolution of mood symptoms. [30] The factors related to this persistent social impairment are residual depressive symptoms, limited illness insight (a very common occurrence in patients with Bipolar II Disorder), and impaired executive functioning. [30] Impaired ability in regards to executive functions is directly tied to poor psychosocial functioning, a common side-effect in patients with Bipolar II. [31] The impact on a patient's psychosocial functioning stems from the depressive symptoms (more common in Bipolar II than Bipolar I). [27] An increase in these symptoms' severity seems to correlate with a significant increase in psychosocial disability. [31] Psychosocial disability can present itself in poor semantic memory , which in turn affects other cognitive domains like verbal memory and (as mentioned earlier) executive functioning leading to a direct and persisting impact on psychosocial functioning. [32] An abnormal semantic memory organization can manipulate thoughts and lead to the formation of delusions and possibly affect speech and communication problems, which can lead to interpersonal issues. [32] Bipolar II patients have also been shown to present worse cognitive functioning than those patients with Bipolar I, though they demonstrate about the same disability when it comes to occupational functioning, interpersonal relationships, and autonomy . [31] This disruption in cognitive functioning takes a toll on their ability to function in the workplace, which leads to high rates of work loss in Bipolar II patient populations. [27] After treatment and while in remission, Bipolar II patients tend to report a good psychosocial functioning but they still score less than patients without the disorder. [20] These lasting impacts further suggest that a prolonged exposure to an untreated Bipolar II disorder can lead to permanent adverse effects on functioning. [30] Recovery and recurrence [ edit ] Bipolar II Disorder has a chronic relapsing nature. [28] It has even been suggested that Bipolar II patients have a higher degree of relapse than Bipolar I patients. [26] Generally, within four years of an episode, around 60% of patients will relapse into another episode. [28] Some patients are even symptomatic half the time, either with full on episodes or symptoms that fall just below the threshold of an episode. [28] Because of the nature of the illness, long-term therapy is the best option and aims to not only control the symptoms but to maintain sustained remission and prevent relapses from occurring. [28] Even with treatment, patients do not always regain full functioning, especially in the social realm. [30] There is a very clear gap between symptomatic recovery and full functional recovery for both Bipolar I and Bipolar II patients. [31] As such, and because those with Bipolar II spend more time with depressive symptoms that do not quite qualify as a major depressive episode, the best chance for recovery is to have therapeutic interventions that focus on the residual depressive symptoms and to aim for improvement in psychosocial and cognitive functioning. [31] Even with treatment, a certain amount of responsibility is placed in the patient's hands; they have to be able to assume responsibility for their illness by accepting their diagnosis, taking the required medication, and seeking help when needed to do well in the future. [33] Treatment often lasts after remission is achieved, and the treatment that worked is continued during the continuation phase (lasting anywhere from 6–12 months) and maintenance can last 1–2 years or, in some cases, indefinitely. [34] One of the treatments of choice is Lithium , which has been shown to be very beneficial in reducing the frequency and severity of depressive episodes. [29] Lithium prevents mood relapse and works especially well in Bipolar II patients who experience rapid-cycling. [29] Almost all Bipolar II patients who take lithium have a decrease in the amount of time they spend ill and a decrease in mood episodes. [29] Along with medication, other forms of therapy have been shown to be beneficial for Bipolar II patients.