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  • Fowler's Syndrome Wikipedia
    The usual findings are complex repetitive discharges without and with deceleration (decelerating bursts), suggesting an impairment in sphincter muscle relaxation. [7] [4] Treatment [ edit ] Sacral neuro modulation is the commonly practiced treatment for restoration of normal micturition. This technique involves modulation of micturition reflex by stimulating S3 nerve root. [8] [9] History [ edit ] This disease was described first by Fowler et al in 1985. [10] References [ edit ] ^ Wein, Alan J. (2012), "Pathophysiology and Classification of Lower Urinary Tract Dysfunction", Campbell-Walsh Urology , Elsevier, pp. 1834–1846.e1, doi : 10.1016/b978-1-4160-6911-9.00061-x , ISBN 978-1-4160-6911-9 ^ a b Panicker, Jalesh N; Pakzad, Mahreen; Fowler, Clare J (April 2018). ... Videosurgery and Other Miniinvasive Techniques . 14 (4): 476–485. doi : 10.5114/wiitm.2019.85352 . ... "Abnormal Electromyographic Activity of the Urethral Sphincter, Voiding Dysfunction, and Polycystic Ovaries: A New Syndrome?" . BMJ . 297 (6661): 1436–1438. doi : 10.1136/bmj.297.6661.1436 .
    FLVCR2, TTLL5
    • Proliferative Vasculopathy And Hydranencephaly-Hydrocephaly Syndrome Omim
      A number sign (#) is used with this entry because of evidence that proliferative vasculopathy and hydranencephaly-hydrocephaly syndrome (PVHH), also known as encephaloclastic proliferative vasculopathy, is caused by homozygous or compound heterozygous mutation in the FLVCR2 gene (610865) on chromosome 14q24. Description The proliferative vasculopathy and hydranencephaly-hydrocephaly syndrome is a rare, autosomal recessive, usually prenatally lethal disorder characterized by hydranencephaly, a distinctive glomerular vasculopathy in the central nervous system and retina, and diffuse ischemic lesions of the brain stem, basal ganglia, and spinal cord with calcifications. It is usually diagnosed by ultrasound between 26 and 33 weeks' gestation (summary by Meyer et al., 2010). Rarely, affected individuals may survive, but are severely impaired with almost no neurologic development (Kvarnung et al., 2016). Clinical Features In identical male twins, Moeschler and Marin-Padilla (1989) described a disorder that had been reported in 5 sibs by Fowler et al. (1972) and in 2 sibs by Harper and Hockey (1983).
    • Fowler Vasculopaty Orphanet
      A rare, genetic neurological disorder characterized by hydranencephaly, distinctive glomeruloid vasculopathy in the central nervous system and retina, polyhydramnios and fetal akinesia with arthrogryposis. The disorder is usually prenatally lethal. In rare reported cases that survived beyond infancy, severe intellectual and neurologic disability with seizures, microcephaly and absence of functional movements were reported.
  • Silent Stroke Wikipedia
    Sickle cell anemia [ edit ] Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity , as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality. [50] [51] See also [ edit ] Stroke Hypertension Cerebral hypoxia DASH diet (Dietary Approaches to Stop Hypertension) References [ edit ] ^ Miwa, K; Hoshi, T; Hougaku, H; Tanaka, Makiko; Furukado, Shigetaka; Abe, Yuko; Okazaki, Shuhei; Sakaguchi, Manabu; et al. (2010). ... Clinical and Experimental Hypertension (New York, N.Y. : 1993) . 24 (7–8): 669–76. doi : 10.1081/CEH-120015343 . ... "Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality" . ... "The use of transcranial ultrasonography to predict stroke in sickle cell disease". The New England Journal of Medicine . 326 (9): 605–10. doi : 10.1056/NEJM199202273260905 .
  • Hemochromatosis Mayo_clinic
    These blood tests for iron are best performed after you have been fasting. Elevations in one or all of these tests can be found in other disorders. ... These tests can help identify liver damage. MRI . An MRI is a fast and noninvasive way to measure the degree of iron overload in your liver. ... Are there any brochures or other printed material that I can take with me? What websites do you recommend? Don't hesitate to ask other questions during your appointment.
    HFE, HAMP, TFR2, HJV, SLC40A1, SLC11A2, TNF, BMP6, CP, HP, BMP2, AKR1D1, B2M, HMOX1, ALAD, HLA-A, TFRC, HLA-H, CYBRD1, FTL, HLA-B, TMPRSS6, APOE, TF, UBE2D1, TIMP1, GNPAT, TLR4, ACO1, MMP2, HEPH, FTH1, EPO, SUCNR1, COX8A, F5, PPP1R11, SOD2, SOD1, SHBG, ADIPOQ, TP53, UROD, ZKSCAN8, PCSK7, S100A9, GDF15, PIEZO1, TRIM31, NUP42, TNMD, SLC46A1, BTBD9, MCIDAS, LINC01194, CCL2, MDM2, UBL3, SERPINA1, GABPA, GAST, FXN, FOXC2, ELANE, CYLD, CTNNB1, CFTR, CELP, CD68, CALR, ARNTL, ALDH2, ALB, ALAS2, GAPDH, GNRH1, GPT, SMAD1, PGF, NMBR, NFE2L2, MPO, MMP3, SMAD7, IREB2, GSTP1, IL10, IL6, IGHG3, IGFALS, IFNG, HLA-F, MFT2
    • Rare Hereditary Hemochromatosis Orphanet
      Rare hereditary hemochromatosis comprises the rare forms of hereditary hemochromatosis (HH), a group of diseases characterized by excessive tissue iron deposition. These rare forms are hemochromatosis type 2 (juvenile), type 3 (TFR2-related), and type 4 (ferroportin disease) (see these terms). Hemochromatosis type 1 (also called classic hemochromatosis; see this term) is not a rare disease. Epidemiology The rare forms of HH have a broad geographical distribution with few cases described. Clinical description Hemochromatosis causes chronic fatigue and bronzed skin pigmentation, with severe tissue damage in the liver, pancreas, joints, bone, endocrine glands, or heart, which results in various complications usually in adulthood including liver fibrosis (cirrhosis with the risk of hepatocellular carcinoma), diabetes mellitus, arthropathy, osteoporosis, hypogonadotropic hypogonadism, and cardiac failure.
    • Hereditary Haemochromatosis Wikipedia
      Diabetes is, in turn, the leading cause of new blindness in adults and may be involved in kidney failure and cardiovascular disease . ... Retrieved 2011-06-03 . ^ "The interaction of iron and erythropoietin" . ^ a b Iron Overload and Hemochromatosis Centers for Disease Control and Prevention ^ "News | Penn State University" . news.psu.edu . ... Department of Health and Human Services ^ a b c Pietrangelo A (June 2004). "Hereditary hemochromatosis—a new look at an old disease". N. Engl. ... "Hemochromatosis and iron-overload screening in a racially diverse population" . The New England Journal of Medicine . 352 (17): 1769–78. doi : 10.1056/nejmoa041534 . ... "Survival and Causes of Death in Cirrhotic and in Noncirrhotic Patients with Primary Hemochromatosis". New England Journal of Medicine . 313 (20): 1256–1262. doi : 10.1056/NEJM198511143132004 .
  • Vulvodynia Mayo_clinic
    Although there's little evidence that alternative techniques work, some women get some relief from yoga, meditation, massage and other stress reducers. ... Do you have brochures or other printed material I can have? What websites do you recommend? Don't hesitate to ask other questions.
    NGF, AGT, COMT, CYP19A1, KNG1, CPP
  • Ectropion Mayo_clinic
    Understanding how other conditions cause ectropion is important in choosing the correct treatment or surgical technique. Treatment If your ectropion is mild, your doctor might recommend artificial tears and ointments to ease the symptoms. ... Do you have any brochures or other printed material that I can take with me? What websites do you recommend? What to expect from your doctor Your doctor is likely to ask you a number of questions, such as: When did you begin experiencing symptoms?
    TGM1, ABCA12, ABCA1, PLEC, SULT2B1, TNFRSF1B, UROS, XPA, XPC, RNF113A, POLR3A, ABHD5, MBTPS2, FERMT1, ALOXE3, TWIST2, SDR9C7, CYP4F22, MPLKIP, CERS3, PNPLA1, NIPAL4, GTF2H5, ALOX12B, POLH, ERCC6, MMP1, APC, CD28, COL7A1, CTLA4, DDB2, DHODH, ERCC2, ERCC3, ERCC4, ERCC5, LIPN, FOXC2, FLI1, GATA1, GBA, GTF2E2, ITGA6, ITGB4, LRP4, VEGFA, CYP1B1, TIMP2, NF1
    • Ectropion Wikipedia
      Not to be confused with Cervical ectropion . Ectropion Cycatricial ectropion of lower lids - eyes open Specialty Ophthalmology Cycatricial ectropion - closed eyes Ectropion is a medical condition in which the lower eyelid turns outwards. It is one of the notable aspects of newborns exhibiting congenital Harlequin-type ichthyosis , but ectropion can occur due to any weakening of tissue of the lower eyelid. The condition can be repaired surgically . Ectropion is also found in dogs as a genetic disorder in certain breeds. [ citation needed ] Contents 1 Causes 2 Diagnosis 3 Ectropion in dogs 4 See also 5 References 6 External links Causes [ edit ] Congenital Aging Scarring Mechanical Allergic Facial nerve palsy Anti-cancer treatments such as erlotinib, cetuximab, and panitumumab, which block the function of EGFR (the epidermal growth factor receptor). Diagnosis [ edit ] Ectropion can usually be diagnosed with a routine eye exam and physical. The eyelid's muscle tone and tightness can be assessed by pulling gently on the eyelid. [1] Ectropion in dogs [ edit ] Ectropion in dogs usually involves the lower eyelid.
  • Trichorrhexis Nodosa Wikipedia
    Hair conditioners should be used. [ citation needed ] Prognosis [ edit ] This condition is self-limiting. Improvements in grooming techniques and in environmental conditions will correct the abnormality. ... References [ edit ] MedlinePlus Encyclopedia : Trichorrhexis nodosa External links [ edit ] Classification D ICD - 10 : L67.0 ICD - 9-CM : 704.2 DiseasesDB : 29680 External resources MedlinePlus : 001449 v t e Disorders of skin appendages Nail thickness: Onychogryphosis Onychauxis color: Beau's lines Yellow nail syndrome Leukonychia Azure lunula shape: Koilonychia Nail clubbing behavior: Onychotillomania Onychophagia other: Ingrown nail Anonychia ungrouped: Paronychia Acute Chronic Chevron nail Congenital onychodysplasia of the index fingers Green nails Half and half nails Hangnail Hapalonychia Hook nail Ingrown nail Lichen planus of the nails Longitudinal erythronychia Malalignment of the nail plate Median nail dystrophy Mees' lines Melanonychia Muehrcke's lines Nail–patella syndrome Onychoatrophy Onycholysis Onychomadesis Onychomatricoma Onychomycosis Onychophosis Onychoptosis defluvium Onychorrhexis Onychoschizia Platonychia Pincer nails Plummer's nail Psoriatic nails Pterygium inversum unguis Pterygium unguis Purpura of the nail bed Racquet nail Red lunulae Shell nail syndrome Splinter hemorrhage Spotted lunulae Staining of the nail plate Stippled nails Subungual hematoma Terry's nails Twenty-nail dystrophy Hair Hair loss / Baldness noncicatricial alopecia : Alopecia areata totalis universalis Ophiasis Androgenic alopecia (male-pattern baldness) Hypotrichosis Telogen effluvium Traction alopecia Lichen planopilaris Trichorrhexis nodosa Alopecia neoplastica Anagen effluvium Alopecia mucinosa cicatricial alopecia : Pseudopelade of Brocq Central centrifugal cicatricial alopecia Pressure alopecia Traumatic alopecia Tumor alopecia Hot comb alopecia Perifolliculitis capitis abscedens et suffodiens Graham-Little syndrome Folliculitis decalvans ungrouped: Triangular alopecia Frontal fibrosing alopecia Marie Unna hereditary hypotrichosis Hypertrichosis Hirsutism Acquired localised generalised patterned Congenital generalised localised X-linked Prepubertal Acneiform eruption Acne Acne vulgaris Acne conglobata Acne miliaris necrotica Tropical acne Infantile acne / Neonatal acne Excoriated acne Acne fulminans Acne medicamentosa (e.g., steroid acne ) Halogen acne Iododerma Bromoderma Chloracne Oil acne Tar acne Acne cosmetica Occupational acne Acne aestivalis Acne keloidalis nuchae Acne mechanica Acne with facial edema Pomade acne Acne necrotica Blackhead Lupus miliaris disseminatus faciei Rosacea Perioral dermatitis Granulomatous perioral dermatitis Phymatous rosacea Rhinophyma Blepharophyma Gnathophyma Metophyma Otophyma Papulopustular rosacea Lupoid rosacea Erythrotelangiectatic rosacea Glandular rosacea Gram-negative rosacea Steroid rosacea Ocular rosacea Persistent edema of rosacea Rosacea conglobata variants Periorificial dermatitis Pyoderma faciale Ungrouped Granulomatous facial dermatitis Idiopathic facial aseptic granuloma Periorbital dermatitis SAPHO syndrome Follicular cysts " Sebaceous cyst " Epidermoid cyst Trichilemmal cyst Steatocystoma simplex multiplex Milia Inflammation Folliculitis Folliculitis nares perforans Tufted folliculitis Pseudofolliculitis barbae Hidradenitis Hidradenitis suppurativa Recurrent palmoplantar hidradenitis Neutrophilic eccrine hidradenitis Ungrouped Acrokeratosis paraneoplastica of Bazex Acroosteolysis Bubble hair deformity Disseminate and recurrent infundibulofolliculitis Erosive pustular dermatitis of the scalp Erythromelanosis follicularis faciei et colli Hair casts Hair follicle nevus Intermittent hair–follicle dystrophy Keratosis pilaris atropicans Kinking hair Koenen's tumor Lichen planopilaris Lichen spinulosus Loose anagen syndrome Menkes kinky hair syndrome Monilethrix Parakeratosis pustulosa Pili ( Pili annulati Pili bifurcati Pili multigemini Pili pseudoannulati Pili torti ) Pityriasis amiantacea Plica neuropathica Poliosis Rubinstein–Taybi syndrome Setleis syndrome Traumatic anserine folliculosis Trichomegaly Trichomycosis axillaris Trichorrhexis ( Trichorrhexis invaginata Trichorrhexis nodosa ) Trichostasis spinulosa Uncombable hair syndrome Wooly hair nevus Sweat glands Eccrine Miliaria Colloid milium Miliaria crystalline Miliaria profunda Miliaria pustulosa Miliaria rubra Occlusion miliaria Postmiliarial hypohidrosis Granulosis rubra nasi Ross’ syndrome Anhidrosis Hyperhidrosis Generalized Gustatory Palmoplantar Apocrine Body odor Chromhidrosis Fox–Fordyce disease Sebaceous Sebaceous hyperplasia
    TTC37, HEPHL1, ASL, ERCC2, SKIV2L, SPINK5, MPLKIP, KRT25
  • Eruptive Vellus Hair Cyst Wikipedia
    The cysts appear similar clinically to steatocystoma multiplex , as well as acneiform eruptions and milia . Therapeutic techniques that are safe and effective are rare, with incision and drainage being the primary form of treatment when sporadic regression does not occur. [3] It was first described in 1977. [4] Contents 1 Signs/symptoms 2 Cause 3 Diagnosis 3.1 Associations 4 Treatment 5 See also 6 References 7 Further reading Signs/symptoms [ edit ] This section is empty. ... PMID 21958358 . v t e Disorders of skin appendages Nail thickness: Onychogryphosis Onychauxis color: Beau's lines Yellow nail syndrome Leukonychia Azure lunula shape: Koilonychia Nail clubbing behavior: Onychotillomania Onychophagia other: Ingrown nail Anonychia ungrouped: Paronychia Acute Chronic Chevron nail Congenital onychodysplasia of the index fingers Green nails Half and half nails Hangnail Hapalonychia Hook nail Ingrown nail Lichen planus of the nails Longitudinal erythronychia Malalignment of the nail plate Median nail dystrophy Mees' lines Melanonychia Muehrcke's lines Nail–patella syndrome Onychoatrophy Onycholysis Onychomadesis Onychomatricoma Onychomycosis Onychophosis Onychoptosis defluvium Onychorrhexis Onychoschizia Platonychia Pincer nails Plummer's nail Psoriatic nails Pterygium inversum unguis Pterygium unguis Purpura of the nail bed Racquet nail Red lunulae Shell nail syndrome Splinter hemorrhage Spotted lunulae Staining of the nail plate Stippled nails Subungual hematoma Terry's nails Twenty-nail dystrophy Hair Hair loss / Baldness noncicatricial alopecia : Alopecia areata totalis universalis Ophiasis Androgenic alopecia (male-pattern baldness) Hypotrichosis Telogen effluvium Traction alopecia Lichen planopilaris Trichorrhexis nodosa Alopecia neoplastica Anagen effluvium Alopecia mucinosa cicatricial alopecia : Pseudopelade of Brocq Central centrifugal cicatricial alopecia Pressure alopecia Traumatic alopecia Tumor alopecia Hot comb alopecia Perifolliculitis capitis abscedens et suffodiens Graham-Little syndrome Folliculitis decalvans ungrouped: Triangular alopecia Frontal fibrosing alopecia Marie Unna hereditary hypotrichosis Hypertrichosis Hirsutism Acquired localised generalised patterned Congenital generalised localised X-linked Prepubertal Acneiform eruption Acne Acne vulgaris Acne conglobata Acne miliaris necrotica Tropical acne Infantile acne / Neonatal acne Excoriated acne Acne fulminans Acne medicamentosa (e.g., steroid acne ) Halogen acne Iododerma Bromoderma Chloracne Oil acne Tar acne Acne cosmetica Occupational acne Acne aestivalis Acne keloidalis nuchae Acne mechanica Acne with facial edema Pomade acne Acne necrotica Blackhead Lupus miliaris disseminatus faciei Rosacea Perioral dermatitis Granulomatous perioral dermatitis Phymatous rosacea Rhinophyma Blepharophyma Gnathophyma Metophyma Otophyma Papulopustular rosacea Lupoid rosacea Erythrotelangiectatic rosacea Glandular rosacea Gram-negative rosacea Steroid rosacea Ocular rosacea Persistent edema of rosacea Rosacea conglobata variants Periorificial dermatitis Pyoderma faciale Ungrouped Granulomatous facial dermatitis Idiopathic facial aseptic granuloma Periorbital dermatitis SAPHO syndrome Follicular cysts " Sebaceous cyst " Epidermoid cyst Trichilemmal cyst Steatocystoma simplex multiplex Milia Inflammation Folliculitis Folliculitis nares perforans Tufted folliculitis Pseudofolliculitis barbae Hidradenitis Hidradenitis suppurativa Recurrent palmoplantar hidradenitis Neutrophilic eccrine hidradenitis Ungrouped Acrokeratosis paraneoplastica of Bazex Acroosteolysis Bubble hair deformity Disseminate and recurrent infundibulofolliculitis Erosive pustular dermatitis of the scalp Erythromelanosis follicularis faciei et colli Hair casts Hair follicle nevus Intermittent hair–follicle dystrophy Keratosis pilaris atropicans Kinking hair Koenen's tumor Lichen planopilaris Lichen spinulosus Loose anagen syndrome Menkes kinky hair syndrome Monilethrix Parakeratosis pustulosa Pili ( Pili annulati Pili bifurcati Pili multigemini Pili pseudoannulati Pili torti ) Pityriasis amiantacea Plica neuropathica Poliosis Rubinstein–Taybi syndrome Setleis syndrome Traumatic anserine folliculosis Trichomegaly Trichomycosis axillaris Trichorrhexis ( Trichorrhexis invaginata Trichorrhexis nodosa ) Trichostasis spinulosa Uncombable hair syndrome Wooly hair nevus Sweat glands Eccrine Miliaria Colloid milium Miliaria crystalline Miliaria profunda Miliaria pustulosa Miliaria rubra Occlusion miliaria Postmiliarial hypohidrosis Granulosis rubra nasi Ross’ syndrome Anhidrosis Hyperhidrosis Generalized Gustatory Palmoplantar Apocrine Body odor Chromhidrosis Fox–Fordyce disease Sebaceous Sebaceous hyperplasia
  • Maladaptive Daydreaming Wikipedia
    Find sources: "Maladaptive daydreaming" – news · newspapers · books · scholar · JSTOR ( December 2020 ) ( Learn how and when to remove this template message ) ( Learn how and when to remove this template message ) Maladaptive daydreaming , also called excessive daydreaming, is a proposed diagnosis of a disordered form of dissociative absorption associated with excessive fantasy that is not recognized by any major medical or psychological criteria. ... "Maladaptive daydreaming as a new form of behavioral addiction" . Journal of Behavioral Addictions. doi : 10.1556/2006.7.2018.95 . ... Retrieved 2020-07-17 . ^ Singer, J. L. (1966) Daydreaming . New York, NY: Random House ^ Somer, E.; Somer, L.; Jopp, S.D. (9 June 2016). ... (August 2018). "Maladaptive daydreaming as a new form of behavioral addiction" . Journal of Behavioral Addictions . 7 (3): 838–843. doi : 10.1556/2006.7.2018.95 . ... PMID 29867613 . ^ Bershtling, O., & Somer, E. (27 August 2018). "The Micro-Politics of a New Mental Condition: Legitimization in Maladaptive Daydreamers' Discourse" .
  • Parkinson's Disease Mayo_clinic
    Clinical trials Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition. ... An occupational therapist can show you techniques that make daily life easier. If you are having trouble talking, a speech therapist may be able to help. ... You may modify most poses to fit your physical abilities. Alexander technique. This technique — which focuses on muscle posture, balance and thinking about how you use muscles — may reduce muscle tension and pain. ... Having a dog or cat may increase your flexibility and movement and improve your emotional health. Relaxation techniques. These practices help lower your blood pressure, reduce your heart rate and improve muscle tone. ... Are there any brochures or other printed material that I can take home with me? What websites do you recommend? In addition to the questions that you've prepared to ask your care team, don't hesitate to ask questions that occur to you during your appointment.
    SNCA, PINK1, DRD2, TH, DDC, MAOB, ATP13A2, PRKN, SLC18A2, PARK7, DRD1, IGF1R, LRRK2, BST1, MAPT, GBA, GAK, HLA-DRA, CYP2D6, CP, PPARGC1A, TNF, SOD2, SOD1, BDNF, ABCB1, VPS35, IL6, NOS1, PARK16, MTHFR, GDNF, GFAP, TMEM230, MAOA, DNM1L, GSTM1, HFE, HMOX1, HSPA9, SLC6A3, DDIT4, GSTP1, CYP2E1, MAP3K5, NGF, AIF1, NQO1, IGF2, GSTA4, TRPM2, IGF2R, INS, HLA-DRB5, GPX1, TCL1B, MIR181C, MTA1, ENO2, BAG5, MAG, FCER2, HGF, HSPA1A, FBP1, INSR, HSPA8, NCAPG2, HBG1, RPL23A, GSK3B, HSPA4, NR4A2, RPS8, COL19A1, TALDO1, SLC30A10, DRAXIN, PITX3, CNTNAP2, NECTIN2, IL1B, ADARB2, CEACAM6, TFAM, MAP2, EDN1, FGB, KCNJ4, RPL6, RPL14, SLC2A14, OPTN, SPR, TWNK, ATG7, GRK5, HTR1A, PENK, GDF5, PPP1R9B, ADH7, DLG4, ABL1, HSF1, LEP, PTN, HSPD1, ND3, GRK6, DLG1, DBN1, ADCY5, HCN3, CCN2, FEZ1, APOE, FASLG, COX10, GJC2, RRN3, RIT2, GCH1, ARPC3, GRK3, GRK2, STK39, LAMP3, SLC41A1, CCDC62, MCCC1, GPNMB, DGKQ, TMEM175, VPS13C, STH, HLA-DRB1, SIPA1L2, CTSB, SREBF1, HIP1R, NUCKS1, MAPT-AS1, RAI1, BCKDK, BIN3, RREB1, TCEANC2, TPM1, PAM, DLG2, ITPKB, MMRN1, KANSL1, FAM47E, ITGA8, LHFPL2, SH3GL2, LMNA, FAM47E-STBD1, NSF, INPP5F, TMC3-AS1, CCDC82, DRD3, SLC50A1, DSCAS, MUL1, RABEP2, NOS2, MANF, ADORA2A, WBP1L, AIMP2, PLPPR1, PTEN, GBF1, EEF1A2, DNAJC1, BAP1, NEFL, SQSTM1, PIP4P2, EIF4G1, PLA2G6, GPR65, MX2, ESR1, PDSS2, NFE2L2, TBC1D5, LINC02224, SMUG1, HTT, SIRT1, TARDBP, SF3B1, GSTT1, LAMC2, GRM5, LRRK2-DT, FRY, FBXO7, GRIN2B, RNF19A, GRN, LINC02451, ACHE, SYNM, RAB29, AHSA1, IL1A, IL10, IGFALS, IGF1, CIT, ITIH1, SIRT2, MCF2L, RET, LOC107987479, TBC1D9, MPHOSPH6, SYT11, TNK2, GPR37, GIGYF2, POLDIP2, MAP4K4, SNCAIP, IP6K2, FYN, MTOR, ATXN3, SYT17, FMR1, FGF20, DCUN1D1, GRAP2, TREM2, MPZ, TET2, CNNM2, GABPA, CHCHD2, GAPDH, ZNF646, GBAP1, GCG, LINC02210-CRHR1, LINC02471, CTNNA3, REM1, HTRA2, HPGDS, GLP1R, CTIF, LY6E, PLEKHM1, LRP2, KCNIP4, ATXN2, ZP3, PARK3, TPTE2P6, PM20D1, LINC02210, MAPK1, TP53, TPO, LINC01121, SLCO6A1, DPY19L2P3, CA8, CDNF, TYW1B, APP, POLG, CNTN1, COL5A2, COL13A1, KLHDC1, COMT, BORCS7, AGAP1, CRHR1, CRK, PIK3CD, CRP, RAB39B, GSTK1, TLR4, CHM, CASP3, PIK3CG, PRSS53, PIK3CB, PIK3CA, TMC3, ALDH1A1, C9orf72, NAT2, ASXL1, PARK10, SPTSSB, SPPL2C, CDH8, CDK5, PRNP, MCIDAS, MDGA2, TMEM229B, PTGS2, CBLL2, THY1, CNKSR3, CASC16, TMPRSS9, SNCA-AS1, NLRP3, RPA2P1, MAPK14, NDUFAF2, UCHL1, SMPD1, YWHAE, BCHE, ALDH2, BCL2, SCN2A, CCL2, AKT1, LINGO1, WNT3, VDR, SLC45A3, CYP17A1, MAPT-IT1, UNC13C, SNCG, CCNT2-AS1, ADAMTSL1, CTSD, TPTE2, BORCS7-ASMT, ZNF165, PREP, SLC2A13, PON1, SNCB, BRINP1, CSF2, ACE, PAFAH1B1, ZSCAN16-AS1, NRTN, CAB39L, DBH, VEGFA, HCRT, GAD1, FUS, SLC11A2, CXCL8, SLC6A4, PARP1, CRMP1, DENR, PPARG, ULK1, DNAJC13, P2RX7, REG1A, IFNG, UTRN, MIR133B, DAPK2, LAMP2, APLN, CTNNB1, TYR, HIF1A, ESR2, PAEP, HNMT, CYP1A2, MC1R, EHMT1, LRRK1, ACMSD, CALB1, USP24, NUP62, CASP9, GRIN2A, TSPO, S100B, CAT, LMX1A, TAC1, GTF2H1, UBE2K, SIRT3, TLR2, LINC01672, DYRK1A, CNR2, ADRB2, CNR1, PDE10A, SYNJ1, HSP90AA1, KHDRBS1, SLC1A2, TPPP, ANG, DNAJB1, ZGLP1, CHRNA4, RMDN3, SCARB2, GIP, LILRB1, DCTN4, PSPN, ROS1, TGFB1, ACTB, SERPINA3, DECR1, IL17A, GRM4, PSPH, CRYZ, STX1B, HTR2A, SLC6A2, BPIFA2, STXBP3, MSMB, MPO, AGER, MAPK8, MEF2D, LMX1B, RIDA, HMGB1, CAV1, CXCR4, CYBB, TOMM40, POTEKP, CCR2, REST, MIR433, AQP4, AGFG1, POTEM, SIGMAR1, ACOT7, ACTG1, MIR34B, ZFPM1, RPS27A, RMDN2, CLOCK, FHL5, NMS, COX2, GSTO2, SUCLA2, SYBU, UBC, BECN1, CST3, CYP1A1, NTS, NNMT, NTF3, DRD4, TFEB, PPP1R2C, RMDN1, MMP9, NQO2, MIR221, TBP, ACTG2, ACTBL2, STAT3, CHMP2B, MFN2, CHCHD10, GSTM2, DNAJC6, GLA, CCK, PLK2, NEDD4, NPC1, VCP, PICALM, NGFR, SYP, SEPTIN4, TRPV1, PTPA, NPY, XBP1, LCN2, TFRC, MAPK3, SKP1, AKR1A1, PRDX2, GDF15, GSTO1, MMP3, LAG3, KLK6, OGA, PSEN1, DNAJB6, PHOX2B, CDK5R1, CXCL12, TCF3, CX3CL1, A2M, REN, CREB1, SNHG1, MIR34A, MIR205, DNM3, MALAT1, NEAT1, GLRX, RLS1, DNAJB1P1, LINGO2, ZNF746, CUX1, SV2C, CYP2D7, DMRT1, NIF3L1, ELAVL4, FKBP1A, ELK3, EPHB1, SLC2A9, FGF2, PTK2B, FABP3, ATF4, RHOT1, MIR4697, HP, HSPA5, ADCYAP1, ICAM1, APOA1, IAPP, CX3CR1, MAP1LC3B, WNT1, AGT, CYP2B6, VIPR2, OGDH, OGG1, VDAC1, APRT, NRGN, P2RX3, VCAM1, AGTR1, UCP2, CTSL, PEBP1, UBB, PINK1-AS, PROKR2, TMEM163, RAB10, NRF1, ADH1B, MOK, RAC1, NR1I2, PARL, F2, ACP3, RAB1A, EPHB2, MARK2, NDUFV2, TRPC1, NEDD9, PVALB, RTN4R, RIC3, HSD3B7, DNMT1, ADH1C, DNAJC5, YWHAZ, TSC2, CLU, PCNA, PACRG, PSMC4, PON2, PPARA, PPARD, MIR29C, PRKAA1, HOTAIR, PRKAA2, PRKAB1, AVP, SMN2, SMN1, PRKAR2A, PRKD1, SGCA, MIR135B, ASAH1, ARNTL, WASH6P, FAS, SKIL, APEX1, MIR200A, SEPTIN5, ATXN8OS, SIAH1, PDE4A, CHRM3, PDYN, TIMP2, ALB, CFP, CDKN2D, CDKN2A, CD38, MIR19B1, WASHC1, USP40, APAF1, PIN1, CASP1, CALCA, SST, PNOC, MIR195, TFR2, IL4, DCTN1, DCDC2, FKBP1AP2, FOXA2, TRAP1, ATG12, GAP43, GRIA2, FKBP1AP3, FKBP1AP4, PRRX2, HMOX2, FTL, MSC, MEFV, FKBP4, ISYNA1, GPX4, NCS1, PPIG, FOXO1, LSAMP, TLR9, LGALS4, MACF1, LAMP1, LRPPRC, ATG5, GRIN2D, MFAP1, BAG3, LDLR, LRP10, GRM2, IREB2, KEAP1, COQ2, FAF1, SBNO2, VPS41, SGSM3, NOX1, SEMA5A, IL1RN, PSIP1, FKBP1AP1, TOMM20, CYP4F3, SLC40A1, PTPN22, GLUD2, SBNO1, IL18, MIR27A, MIR185, MIR137, SNAP25, MIR132, MIR126, TAL1, MIR29A, SP1, SRY, PPIF, MIR204, SPG7, SPP1, FBXO8, MIR21, HDAC6, MIR212, MIR223, USP15, MIR22, RNF11, SOAT1, SNRPF, SNRNP70, SOD3, BDNF-AS, BACE1, FST, ARL6IP5, NLRP1, P2RX5-TAX1BP3, SCD, TXNIP, MGLL, CHP1, MIR4519, HRH3, NES, OPN1MW3, RIPK3, RAB32, TMED10, RNASE4, RNASE1, MTCO2P12, PRSS21, TRIM27, RFC1, LINC02605, H3P13, RENBP, CCL5, P2RX2, ATP6AP2, ABCA7, SMARCA1, CD2AP, SLC22A1, SLC18A3, SRRM2, MIR326, SLC16A1, SLC8A1, MIR494, MIR505, ARC, UCA1, RNF41, MPRIP, HMGXB3, ST3GAL2, MIR563, SI, SHMT2, TRIM32, SHMT1, OPN1MW2, SGTA, SIGLEC7, SPHK1, ERCC6L2, TET1, P2RX6, AXIN2, NEUROG2, NOD2, FBRS, HS1BP3, DDRGK1, SLC52A2, PANK2, MAP3K13, NELFE, H3C1, RAB7A, XPR1, COASY, ZNF184, NDFIP1, EGLN1, MFHAS1, GPR55, KLF4, RNF146, HIVEP3, H3C4, XIST, TMED9, TRPM7, CISD1, RIPK1, DNAJC12, B3GALT4, H3C7, PDE8B, KHSRP, SLC17A6, MGAM, STBD1, H3C3, NOL3, SEMA6A, H3C2, H3C10, H3C12, TMEM106B, H3C8, H3C11, H3C6, TRIB3, C19orf12, SESN2, TCOF1, TIMP3, TRAF2, MZB1, SESN3, GAL, TNFRSF1B, PWAR1, TRAT1, PLB1, TLN1, HDAC4, ATG13, CD200R1, TAS2R13, BMS1, RMC1, EIF2B3, MCAT, MTIF3, ANKK1, PGP, RAB7B, HCAR2, TRH, TTR, PPP1R1B, IL23A, SYVN1, GPR88, HOMER1, SHC3, VIM, ATAD1, MIDN, SELENOT, ROCK2, SLC25A27, DNER, TPH2, USP1, SCLY, UCHL3, FTMT, OPN4, UBE2L3, TXNRD3, VPS26A, CARD16, TXN, TGM2, TGFB2, IDUA, CHRNA5, HK2, LGALS1, BAG1, PLA2G1B, F9, HLA-C, LBP, E2F1, BAX, CLK1, NCL, HCN2, F2R, NR4A1, FOXA1, NDUFA1, NDUFA2, NDUFS3, PLD2, HK1, HOXD13, TOR1A, COL17A1, COL11A2, PPID, FCGR3A, POU2F1, POMC, POLB, ARSA, ASCL1, LGALS3, HCLS1, PLXNA2, LIFR, FAAH, ATM, ATOX1, NRG1, ATP1A3, BNIP3L, NDUFS4, PDIA3, CBS, P2RY2, IL7, KCNJ6, P2RY1, P2RX5, P2RX4, P2RX1, OPRL1, CCKAR, KDR, GPR143, NUCB2, IL13RA1, ISG20, ITGAM, NTRK2, NT5E, CD19, IL2RB, IL2RA, EGF, PCP4, HRES1, NEFM, CHAT, CTSC, ERG, CEBPB, PDC, NFKB1, EGR1, CAST, HTC2, CACNA1A, NHS, HTR1B, KRT7, IDE, CAPN1, NOS3, COX8A, ELAVL2, FRAXE, CBLIF, RBM3, PSMB8, DDIT3, CD200, DAPK1, CSF3, PSEN2, APOD, PSAP, CYTB, GPX7, APOB, DNMT3B, MFGE8, ADCYAP1R1, FXN, GLB1, PTBP1, GLUL, GRP, FTH1, PTPRC, ALOX5, AKR1B1, MSRA, ADH4, MEF2C, GAD2, AHR, GALC, MS, DPEP1, FOSL2, ND1, ATF2, CYP3A4, DRD5, MIF, ACACA, MTRR, NR3C1, MTR, DPYSL2, MAPK10, DPP4, KLK3, ND5, MRC1, FOXO3, OPN1MW, GC, CD55, ND2, CRY1, SLC39A8, FSD1L, SNX6, CYP27B1, KREMEN1, TNMD, DLGAP3, EHHADH, ANO3, GBA2, CYP3A5, TINAGL1, MAK16, DTNBP1, EIF2B1, NEUROD6, LSM2, ATP13A4, MINDY4, DAPK3, TLCD3B, FKBP10, EIF4E, PROK2, EIF4EBP1, HAPLN2, HAMP, LGR6, ACE2, EIF4A2, LIN28A, APH1B, PAGR1, DOCK3, SLC8B1, ASPSCR1, ELOVL7, FA2H, DHRS11, BRCC3, FSD1, CWC22, DHDDS, XYLT2, DVL1, DUSP8, TNFAIP8L2, MCPH1, PEAK1, NEIL1, RTL10, ATN1, DUSP2, DUSP26, DMPK, DLD, TIMM8A, SLC25A28, TFB2M, MS4A6A, EGFR, MEGF8, HIF3A, RAB1B, CSMD1, DAXX, DBI, DCC, DCN, TAS1R2, ZNF436, PDIA2, EEF2, RAPH1, TNKS2, EEF1A1, FYCO1, REL, USP37, FBXO42, FPR2, WWOX, INPP5K, IL17D, PANK1, FN1, PPIL3, IMMTP1, AFF2, FLNB, H2BS1, FKBP5, TREM1, WNT4, FKBP3, ATG16L1, FKBP2, UGT1A9, FKBP1B, FGG, MARCHF5, FGF13, FGF9, FGF8, NDE1, FGF1, GPC4, FDXR, ANKHD1, FCGR3B, VPS29, TRAPPC2L, NUB1, FKBP7, GDF1, DPP7, PSAT1, UBQLN2, UBQLN1, SLC39A2, OBP2A, VSX1, NOX4, ASAP1, GATA2, SOST, TMED7, ST8SIA3, NMD3, POLR1D, GALNS, TFB1M, B4GALNT1, TRIM17, GABBR1, TRAPPC4, G6PD, GAST, HSD17B7, FRAXA, SIRT7, RAB6B, PPIL1, HEATR3, OXR1, SH3RF1, PELI1, EPRS1, NPDC1, TCIM, PNO1, EPO, PAK6, ARNTL2, ZGPAT, RGMA, EPHX2, CASS4, TIGAR, EPHX1, PGLYRP4, ENDOG, THAP1, ANKRD50, VN1R1, MCOLN1, CYP20A1, NDRG2, PPM1H, ZNF512B, NLN, XPO5, GPR158, NUFIP2, NCEH1, ELF4, ELAVL1, ERBB2, ERBB3, CTNNBL1, ZNF253, MTPAP, FCGR2B, MAP1S, FASN, RCBTB1, ADI1, QRSL1, F12, FBXW7, CHDH, YOD1, TRPV6, GPRC5D, SAGE1, SMPD3, F2RL1, SOX6, AMBRA1, EZH2, MECOM, ARFGAP1, MBD5, VPS11, ESRRG, PSENEN, GPRC5C, ERN1, MYO5C, MYDGF, MAP1LC3A, CRY2, EBPL, GET3, MIR342, MIR335, MIR331, ASIP, MIR324, MIR148B, GPR166P, SPAG11A, VN1R17P, ATP5F1B, ATP7A, ATR, MIR96, MIR34C, PLF, MIR425, FBXO48, MIR410, ARRB1, MIR520D, ARR3, MIR486-1, ARG1, POU5F1P3, ARF3, AR, POU5F1P4, CCDC154, NORAD, LINC00273, AQP9, ADGRB1, MIR320A, MIR30E, MIR19A, MIR107, CA12, CA2, MIR134, C4B, MIR142, MIR144, MIR15B, MIR181A2, C4A, MIR183, C1R, MIR190A, KLF9, BRAF, MIR30C2, DST, BMX, BMP2, BMI1, MIR214, MIR217, BGLAP, CFB, MIR222, BCR, MIR27B, BCL2L1, MIR30A, MIR30C1, CXADRP1, AQP1, MIRLET7D, PGR-AS1, LOC102724334, MIR8061, LOC101928100, ADORA1, UCHL1-AS1, TLE5, APLNR, OCM, ERVW-4, MIR4639, ALAD, MICOS10-NBL1, AMFR, BIN1, CBSL, HAGLROS, TP53COR1, APOA1-AS, SNHG14, ADAM10, ADA, ACO2, SIRT1-AS, BUB1B-PAK6, ACO1, ASIC2, LOC110366354, LOC110806262, AOC1, ABCA1, H3P17, MIR3143, ANGPT1, TMED7-TICAM2, PLIN4, MIR545, MIR542, PARK12, MIR561, MIR579, MIR590, MIR599, MIR613, MIR625, MIR626, MIR634, ATXN8, POTEF, APOC3, MIR671, C4B_2, XIAP, VTRNA2-1, MIR543, APC, MUPP, APBB1, ANXA5, ANK2, ANK1, CD24, MIR1224, MFT2, ANGPT2, TIMM23, MIR100, CALB2, SPZ1, KLF6, CCR7, ABCC2, CNGA1, CNTF, GPR139, MTFMT, CPOX, CHI3L1, CRAT, EXOSC6, MRGPRX4, MRGPRX3, RAB3IP, NUS1, GNPDA2, CCR5, GPR151, CCR3, PXDNL, CMA1, SIRPA, STK35, CACUL1, CLN3, CHRNB4, ZFP90, CHRNB3, ZNF569, GLIS1, PDIK1L, FBXO41, PGLYRP3, PGLYRP2, EEF2K, PLXNA4, CYP2C9, USP30, PTPN5, ORAI1, CYP2C19, CYP1B1, PPIL4, DNAJC14, CYLD, CHRFAM7A, CYC1, MCU, IL33, TRIM41, DEPDC7, CRYAB, CXADR, MTDH, CTSZ, CTSK, PRDM6, CTRL, CADPS2, CTNS, CSNK1D, TGS1, NACC1, TRIM9, CSF1R, CSF1, CHIT1, CEL, HSP90AB2P, TMED10P1, CASR, GOLGA6A, CPP, RSPO2, CAV2, RUNX1, PPIL6, SHOC1, FBXW12, ZNF763, LYPD5, CCKBR, CCND3, OR10A4, NANOS3, HSD17B13, PFN3, CASP8, CASP7, SEPTIN14, AMIGO2, HCN1, TICAM2, CASP6, NDUFS7, CALR, CALD1, CALCR, TMEM189, TMEM189-UBE2V1, UOX, CD14, SELENOH, MRGPRX1, ARID2, CDKN1B, CDKN1A, FSIP1, CDK6, CDC42, TMPRSS6, OXER1, CDK1, DDX53, CDA, CD69, RHOV, CD59, CD47, MLKL, GPX6, CDCP2, PRSS55, CD44, CD36, TPCN2, ZUP1, GPRC6A, CD34, IL27, LCLAT1, EBF3, PHYHD1, CD28, GK5, HOOK2, GPR3, USP25, UMOD, VHL, VGF, OPA1, OPRM1, UQCRH, UQCRFS1, UCP1, NPPC, UCN, P2RY6, P4HB, UBTF, UBE3A, UBE2V1, OMP, VIP, VIPR1, VSNL1, WAS, WFS1, NUCB1, WNT5A, NTRK1, NTF4, XK, XRCC1, XRCC3, YWHAG, YWHAH, NPTX2, CNBP, PRDX1, PAH, SERPINE1, TRAF6, PECAM1, TKT, PDR, PDPK1, PDHA1, TM7SF2, PDE1B, PDE7A, PDCD2, PDB1, TPT1, CRISP2, NR2C1, HSP90B1, PCNT, TYROBP, PCMT1, TRPC6, SERPINA5, PAX4, PHLDA2, TST, PAWR, TUBA4A, TUFM, TNFRSF4, REG3A, TXNRD1, TYMS, PAK1, ZSCAN21, NPPB, EIF2S2, MYOC, PEA15, MYL4, EIF3A, HSD17B6, TP63, PSMG1, USO1, NPPA, PRKRA, CASK, NAGLU, PDXK, NBL1, LGR5, MYD88, SNX3, MYCN, MYC, TNFRSF14, FADD, SNAP23, RGS9, MTX1, FGF18, CCN6, TRNL1, ASAP2, MTTP, MTNR1B, FUBP1, EIF2B4, CHST1, DGKD, NUBP1, SLC14A2, MAP3K12, PRDM2, LRP8, TUBA1A, NPM1, NPAS2, NOTCH4, ST8SIA4, NOTCH2, LAP, NKTR, CSRP3, FGF23, SLC7A5, MLRL, CUL1, SYN3, GTPBP6, NFKBIA, AXIN1, NFKB2, FZD4, NFE2L1, NFE2, NEK1, NEFH, NEDD8, NDN, NR0B2, NCK2, SERPINF1, TIMP1, TIAL1, PSMC1, PSMA2, SGK1, SELENOP, SELE, SEL1L, PSMB9, PSMD11, PER1, CCL3, SCN9A, SCN8A, TAS2R38, SCN1A, PTGER2, PSG5, SHH, HTRA1, KLK7, PRSS2, LGMN, PROS1, SLC1A1, PROP1, SLC1A6, SLC2A1, SLC2A4, PROC, PRL, MAP2K7, SLC6A8, SLC6A11, PTGER4, PTH, SATB1, ROCK1, RB1, RAP2B, RAP1B, RAN, RGS2, RGS4, RGS10, RHEB, RAD51B, RING1, RAD51, RAB6A, RNH1, RNY1, RAB3B, SAT1, QDPR, PTX3, RPL32, RPS6, RPS6KB1, PTPRA, RRAS, PTPN6, RTN1, RXRA, S100A9, S100A10, QSOX1, SALL1, SLC6A13, SLC7A1, MAP2K6, DYNLT3, CDKL5, STXBP1, SERPINF2, ABCC8, PLEK, PLG, ADAM17, TACR1, TAF1, PLD1, TAP1, CNTN2, PLAG1, PKD1, PITX2, STAT4, TEF, TMBIM6, TF, PIK3C2B, TFDP2, PIGC, SERPINA1, PHF1, SLC25A3, PHB, PGK1, THAS, THBS1, THOP1, STIM1, PLK1, SLC8A3, PPP3R1, SLC11A1, MAP2K2, PRKCG, SLC19A1, SLC20A2, PRKCD, SLC22A5, PRKAR1B, PRKAR1A, PRKACB, PRKACA, SMPD2, SMS, PPY, PPP4C, STAT1, PPP2R2B, PPP1R1A, PPBP, MED1, POU5F1, SORL1, SOX2, SPN, PODXL, PNMT, SPTBN1, PRRX1, FXYD1, ST13, EIF2B2, ENDOU, GFPT1, SARM1, HLA-A, HLA-B, ACSBG1, HLA-DQB1, KDM6B, CUL9, SMG1, GSR, TNIK, FAIM2, HLF, HNF4A, HNRNPA1, SEPHS1, SATB2, NEDD4L, HEXA, ZNF629, NCSTN, HDAC2, DICER1, SIRT5, HDAC1, HCRTR1, TPSD1, HAS2, ATP1B4, HSD17B10, ABCA5, TRAM1, GTF2H4, TLX2, RPH3A, HPD, RER1, MRPS30, JTB, PNPLA6, SUGT1, PAPOLA, RALBP1, PRDX3, IKBKB, IGHG3, COPS5, IMMT, RAB35, IFNAR1, STMN2, HTR6, DLGAP4, SLC2A6, PTGDR2, HSPB2, HSPB1, COPE, ECD, FKBP9, HSPA1L, PDAP1, TUSC2, GABARAP, HSPA1B, GABARAPL2, RRAS2, ZFYVE26, SEC14L2, MBD2, PDE7B, GLI1, RBMS3, SIT1, GLI2, GPR78, AGO2, CACYBP, LPAR3, CACNG5, B3GAT1, GLS, GLUD1, GNAL, ACAD8, TOX3, GJB2, GJB1, MAT2B, TOR2A, GHSR, GIT1, ACAD9, FLVCR1, MCTS1, DBNL, HIPK2, GHR, SETD2, SCG3, PYCARD, TBK1, ATP2C1, GNAQ, SEC22A, ARIH1, GSPT1, PDSS1, OPN3, MKRN2, GRM8, GRM3, LDOC1, PPP1R15A, SLC7A11, PPIL2, MAFF, GRIN2C, ATXN10, NOCT, TPSG1, CHORDC1, PRDX5, BACE2, PART1, GRIN1, GRIK3, GORASP2, FFAR1, GPER1, MCHR1, GPR17, UTS2R, FBXO2, FBXO9, GPR6, IL9, PPP1R13L, IL13, MICD, MAP3K3, RAB8A, PTGES, MGMT, TMEM59, NPEPPS, TBX4, PPP1R17, MAPK8IP1, MIP, MAP3K11, SH3BP5, KMT2A, AFF1, DNAJB9, ISG15, MCL1, HERPUD1, MBP, SART3, HDAC9, SETD1A, CLSTN3, PHACTR2, MATN3, MAS1, MARK1, PIEZO1, MAP6, MAP1B, CD180, AFDN, NR3C2, MME, MSX1, MTHFD1, NUDT1, USP13, MT3, HSPB3, PGLYRP1, MT2A, SOCS3, MT1E, ERDA1, MT1B, MT1A, PIAS2, USP10, AIFM1, COX5A, OSMR, SLC16A7, SLC33A1, VAPB, MOG, MMP8, GPR37L1, MMP7, MMP2, TAOK2, MMP1, LONP1, KL, ADIPOQ, LTF, LTA, LRPAP1, NXF1, SPRY1, STUB1, DNAJA2, KLC1, DLEU1, KNG1, CCL26, KLK2, NPM3, NDRG1, SPAG11B, UBAC1, KIF2A, KCNMA1, CIB1, CALCOCO2, PROCR, KCNA5, ARFGEF1, NPC2, SCGN, JUP, TRIM3, ITPR3, YKT6, ITPR1, ITGB2, PTGES3, GJB6, CPLX1, KRT10, STX6, HEPH, LPA, PSMD6, SV2B, SRGAP3, RBM19, NCAPD2, SEC16A, LRP6, LRP1, USP3, MVP, NR1I3, SRA1, LPO, BCL2L11, ABCB6, EIF1, LIG4, PTPRU, PQBP1, LIF, TRIM10, LCN1, G3BP1, RPSA, WASF2, LAMB2, LAD1, L1CAM, KRT31, TRIM13, H3P42
    • Parkinson's Disease Wikipedia
      A feature of tremor is pill-rolling , the tendency of the index finger and thumb to touch and perform together a circular movement. [31] [32] The term derives from the similarity between the movement of people with PD and the early pharmaceutical technique of manually making pills. [32] Bradykinesia (slowness of movement) is found in every case of PD, and is due to disturbances in motor planning of movement initiation, and associated with difficulties along the whole course of the movement process, from planning to initiation to execution of a movement. ... Symptoms of apathy include reduced initiative/interests in new activities or the world around them, emotional indifference, and loss of affection or concern for others. [10] Apathy is associated with deficits in cognitive functions including executive and verbal memory. [50] Other Sleep disorders are a feature of the disease and can be worsened by medications. [31] Symptoms can manifest as daytime drowsiness (including sudden sleep attacks resembling narcolepsy ), disturbances in REM sleep, or insomnia . [31] REM behavior disorder (RBD), in which people act out dreams, sometimes injuring themselves or their bed partner, may begin many years before the development of motor or cognitive features of PD or DLB . [52] Alterations in the autonomic nervous system can lead to orthostatic hypotension (low blood pressure upon standing), oily skin and excessive sweating, urinary incontinence , and altered sexual function. [31] Constipation and impaired stomach emptying (gastric dysmotility) can be severe enough to cause discomfort and even endanger health. [17] Changes in perception may include an impaired sense of smell, disturbed vision, pain, and paresthesia (tingling and numbness). [31] All of these symptoms can occur years before diagnosis of the disease. [31] Causes Main article: Causes of Parkinson's disease Many risk factors have been proposed, sometimes in relation to theories concerning possible mechanisms of the disease; however, none have been conclusively proven. [53] The most frequently replicated relationships are an increased risk in those exposed to pesticides, and a reduced risk in smokers. [53] [54] There is a possible link between PD and H. pylori infection that can prevent the absorption of some drugs including levodopa. [55] [56] Environmental factors and exposures Exposure to pesticides and a history of head injury have each been linked with Parkinson disease (PD), but the risks are modest. ... Treating motor symptoms with surgery was once a common practice, but since the discovery of levodopa, the number of operations has declined. [126] Studies in the past few decades have led to great improvements in surgical techniques, so that surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. [126] Surgery for PD can be divided in two main groups: lesional and deep brain stimulation (DBS). ... Generally DBS is associated with 30–60% improvement in motor score evaluations. [ citation needed ] Rehabilitation Further information: Rehabilitation in Parkinson's disease Exercise programs are recommended in people with Parkinson's disease. [18] There is some evidence that speech or mobility problems can improve with rehabilitation, although studies are scarce and of low quality. [129] [130] Regular physical exercise with or without physical therapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. [130] When an exercise program is performed under the supervision of a physiotherapist, there are more improvements in motor symptoms, mental and emotional functions, daily living activities, and quality of life compared to a self-supervised exercise program at home. [131] In terms of improving flexibility and range of motion for people experiencing rigidity , generalized relaxation techniques such as gentle rocking have been found to decrease excessive muscle tension. Other effective techniques to promote relaxation include slow rotational movements of the extremities and trunk, rhythmic initiation, diaphragmatic breathing , and meditation techniques. [132] As for gait and addressing the challenges associated with the disease such as hypokinesia (slowness of movement), shuffling and decreased arm swing; physiotherapists have a variety of strategies to improve functional mobility and safety.
  • Fear Of Missing Out Wikipedia
    Grohol, founder and Editor-in-Chief of Psych Central , FOMO may lead to a constant search for new connections with others, abandoning current connections to do so. ... Maybe it's your Facebook wall" . The New York Times . ^ Shea, Michael (27 July 2015). ... "Internet Gratifications and Internet Addiction: On the Uses and Abuses of New Media". CyberPsychology & Behavior . 7 (4): 384–394. doi : 10.1089/cpb.2004.7.384 . PMID 15331025 . ^ Herman, Dan (2000-05-01). "Introducing short-term brands: A new branding tool for a new consumer reality". ... "The Inventor of FOMO is Warning Leaders About a New, More Dangerous Threat" . Inc.com .
  • Lissencephaly Type Iii And Bone Dysplasia Omim
    The fetus had a normal XY karyotype. Like the index case, he had craniofacial edema and arthrogryposis, as well as epiphyseal stippling of cervical vertebrae, feet, and sacrum. ... Attia-Sobol et al. (2001) suggested that the disorder in this family is a new type III lissencephaly syndrome because of epiphyseal calcifications and metacarpal phalangeal bone dysplasia.
    • Lissencephaly Type 3-Metacarpal Bone Dysplasia Syndrome Orphanet
      This syndrome is characterised by severe microcephaly, agyria, agenesis of the corpus callosum, cerebellar hypoplasia, facial dysmorphology and epiphyseal stippling of the metacarpal bones. It has been described in two brothers. The syndrome is transmitted as an autosomal recessive trait and may be an allelic variant of Neu-Laxova syndrome and Lissencephaly type III with cystic dilations of the cerebellum and foetal akinesia sequence (see these terms).
  • Wasting Wikipedia
    WFH as % of median reference value is calculated this way: W F H = weight of a given child median weight for a given child of that height × 100 {\displaystyle \mathrm {WFH} ={\frac {\mbox{weight of a given child}}{\mbox{median weight for a given child of that height}}}\times 100} Cutoff points may vary, but <80% (close to −2 Z-score ) is often used. Adults: Body Mass Index (BMI) is the quotient between weight and height squared (kg/m 2 ). ... UNICEFWHO- World Bank Joint Child Malnutrition Estimates. (UNICEF, New York; WHO, Geneva; The World Bank, Washington, DC; 2012) ^ Michael Powers, "Performance-Enhancing Drugs" in Joel Houglum, in Gary L.
    DMD, FGF23, BEST1, TNF, AHR, CCL2, TSC22D4, SARS2, FOXP3, GDF11, ZNF185, TTR, SHOX2, SARS1, CA12, REN, PLG, SERPINA1, PDCD1, IL6, HLA-G, GH1, MSTN, CYP21A2, CDC42, MIR142
  • Cold Urticaria Mayo_clinic
    Do you have any brochures or other printed material I can take with me? What websites do you recommend? What to expect from your doctor Your doctor is likely to ask you questions such as: When did you begin experiencing symptoms? ... Do others in your family have similar symptoms? Have you taken any new medications recently? Have you tried any new foods? Have you traveled to a new place? Does anything seem to improve your symptoms?
    SERPINA3, PLCG2, TRPM8, NLRP12
    • Cold Urticaria Wikipedia
      The hives may be the shape of the ice, or it may radiate from the contact area of the ice. [20] However, while these techniques assist in diagnosis, they do not provide information about temperature and stimulation time thresholds at which patients will start to develop symptoms, [20] which is essential because it can establish disease severity and monitor the effectiveness of treatment. [20] Treatment [ edit ] The first-line therapy in ColdU, as recommended by EAACI/GA2 LEN/EDF/WAO guidelines , is symptomatic relief with second-generation H1- antihistamines. if standard doses are ineffective increasing up to 4-fold is recommended to control symptoms. [21] The second-generation H1-antihistamine, rupatadine , was found to significantly reduce the development of chronic cold urticaria symptom without an increase in adverse effects using 20 and 40 mg. [20] Allergy medications containing antihistamines such as diphenhydramine ( Benadryl ), cetirizine (Zyrtec), Loratadine (Claritin), cyproheptadine (Periactin), and fexofenadine (Allegra) may be taken orally to prevent and relieve some of the hives (depending on the severity of the allergy). [22] For those who have severe anaphylactic reactions, a prescribed medicine such as doxepin, which is taken daily, should help to prevent and/or lessen the likelihood of a reaction and thus, anaphylaxis. ... ISBN 0-7216-2921-0 . ^ Hoffman HM, Mueller JL, Broide DH, Wanderer AA, Kolodner RD (November 2001). "Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome" . ... "Cold Urticaria: Release into the Circulation of Histamine and Eosinophil Chemotactic Factor of Anaphylaxis during Cold Challenge". New England Journal of Medicine . 294 (13): 687–90. doi : 10.1056/nejm197603252941302 . PMID 55969 . ^ News published on the National Institute of Allergy and Infectious Diseases (NIAID) website (Jan. 11, 2012) ^ a b c d Abajian M.; Curto-Barredo L.; Krause K.; Santamaria E.; Izquierdo I.; Church M.; Maurer M.; Giménez-Arnau A. (2016).
    • Cold Urticaria Gard
      Cold urticaria is an allergic condition that affects the skin. Symptoms usually start in early adulthood. The most common symptom is a red, itchy rash that appears on the skin when it is exposed to the cold (e.g. cold weather or cold water). This reaction usually occurs within 5-10 minutes after exposure and can last for 1-2 hours. The exact cause of cold urticaria is unknown. In some cases, it may be associated with an infection , insect bite, or blood cancer. It is diagnosed based on the symptoms and confirmed through tests that look for a specific reaction to cold.
  • Bleeding Canker Of Horse Chestnut Wikipedia
    Infections by the gram-negative fluorescent bacterium Pseudomonas syringae pathovar aesculi are a new phenomenon, and have caused most of the bleeding cankers on horse chestnut that are now frequently seen in Britain. [1] Contents 1 Disease cycle 2 Causes 2.1 Pseudomonas syringae pathovar aesculi 3 Management 4 Importance 5 References 6 External links Disease cycle [ edit ] Pseudomonas syringae pv. ... Causes [ edit ] Pseudomonas syringae pathovar aesculi [ edit ] In the past few years, the bacterial pathogen Pseudomonas syringae pv. aesculi has emerged as a new and virulent agent for this disease in Western Europe. ... "Isolation and identification of Pseudomonas syringae pv. aesculi causing bleeding canker of horse chestnut in the UK" . New Disease Reports . British Society for Plant Pathology (BSPP) . ... External links [ edit ] UK Forest Research Kew Royal Botanical Gardens- (Aesculus indica) Indian horse chestnut Forestry Commission Website Working group Aesculaap
  • Idiopathic Postprandial Syndrome Wikipedia
    The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars . ... Non-disease [ edit ] In October 1974, The New England Journal of Medicine carried an article "Non-hypoglycemia as an epidemic condition" which described the condition as a "non-disease". [4] The authors claim Over the past few years people have appeared in droves with the self-diagnosis of "hypoglycemia" – a term that has become the layman's final common pathway for a variety of conditions, only a few of which are related to endocrinologic abnormalities. ... Young (1974) "Non-hypoglycemia as an epidemic condition", The New England Journal of Medicine 291:907,8 ^ George F. ... Stuart Soeldner (1974) "A non-editorial on non-hypoglycemia", The New England Journal of Medicine 291: 905,6 ^ "postprandiale Hypoglykämie" .
  • Collapsed Vein Wikipedia
    Unsourced material may be challenged and removed. Find sources: "Collapsed vein" – news · newspapers · books · scholar · JSTOR ( July 2007 ) ( Learn how and when to remove this template message ) Collapsed veins are a common injury that results from repeated use of intravenous injections . ... Contents 1 Causes 2 Mechanism 3 Prognosis 4 See also 5 References Causes [ edit ] Permanent vein collapse occurs as a consequence of: Repeated injections, especially with blunt needles. Poor injection technique. Injection of substances which irritate the veins; in particular, injection of liquid methadone intended for oral use.
  • Angina Mayo_clinic
    It may feel like a heavy weight lying on the chest. Angina may be a new pain that needs to be checked by a health care provider, or recurring pain that goes away with treatment. ... Any new or worsening angina symptoms need to be evaluated immediately by a health care provider who can determine whether you have stable or unstable angina. ... An ECG can show if the heart is beating too fast, too slow or not at all. Your health care provider also can look for patterns in the heart rhythm to see if blood flow through the heart has been slowed or interrupted. ... Clinical trials Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition. ... Are there any brochures or other printed materials that I can take home with me? What websites do you recommend visiting? Don't hesitate to ask any other questions that you may have during your appointment.
    AVP, PLAU, APOE, LDLR, GLA, CRELD1, ABCG8, ABCG5, GATA4, GATA6, XYLT2, XYLT1, NR2F2, LMNA, LCAT, JAK2, HLA-DPA1, HLA-DPB1, LDLRAP1, IDUA, LIPC, CYP27A1, TET2, PRTN3, ZMPSTE24, CTLA4, SCN5A, PTEN, MPL, ENPP1, PIGA, PCSK9, PTPN22, ABCC6, VEGFA, PMM2, APOB, ACE, CRP, CAD, CCS, IL6, SERPINE1, ITGB2, TNNI3, DLD, CXCL16, OXCT1, LAD1, SERPINA5, PLA2G1B, APOA1, TNF, NOS3, PLB1, KLF14, PLA2G7, PLA2G6, YWHAZ, IL37, NEAT1, VIP, MIR208A, MIR34A, MIR499A, TNFRSF1B, ZGLP1, CYP4F2, PROM1, TNFSF10, CPSF4, HDL3, MOCOS, QRSL1, POC1A, TBC1D9, JTB, ZC4H2, CMAS, SELL, EHMT1, PPP1R2C, FERMT3, ADIPOQ, WASF1, NLRP3, NR1I2, FGF21, ADAM10, CCL2, EDN1, ICAM1, HSPA5, GNB3, GLP1R, GLB1, GDF10, GCG, FGF4, F5, F3, CYP19A1, RENBP, CPB2, CLCN1, CETP, CD34, CD14, VPS51, KLK3, APOC3, ALB, AGTR1, IFNG, IGF2R, IL1A, IL1B, PYGM, PRKCD, PLXNA2, PLA2G2A, ABCB1, PAPPA, CNTN3, ADRB1, OPA1, NOS2, NOS1, MPI, MMP3, SMCP, LPA, KDR, ITGA2B, IL10, CXCL8, IL7, IL1RN, LINC02605
    • Angina Wikipedia
      Unstable angina [ edit ] Unstable angina (UA) (also " crescendo angina "; this is a form of acute coronary syndrome ) is defined as angina pectoris that changes or worsens. [6] It has at least one of these three features: it occurs at rest (or with minimal exertion), usually lasting more than 10 minutes it is severe and of new onset (i.e., within the prior 4–6 weeks) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before). ... The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant. [41] Microvascular angina in women [ edit ] Women with myocardial ischemia often have either no or atypical symptoms, such as palpitations, anxiety, weakness, and fatigue. ... The diagnosis of MVA may require catheterization during which there is assessment of the microcirculatory response to adenoside or acetylcholine and measurement of coronary and fractional flow reserve. New techniques include positron emission tomography (PET) scanning, cardiac magnetic resonance imaging (MRI), and transthoracic Doppler echocardiography. ... The combination of nonnitrate vasodilators, such as calcium channel blockers and angiotensin converting enzyme (ACE) inhibitors along with HMG-CoA reductase inhibitors (statins), also has been shown to be effective in many women, and new drugs, such as Ranolazine and Ivabradine, have shown promise in the treatment of MVA. ... Pharmacotherapy Handbook (7th ed.). New York: McGraw-Hill. p. 140 . ISBN 978-0-07-148501-2 . ^ "Health Benefits of Cessation" .
  • Antimicrobial Resistance Wikipedia
    Clinical resistance is shown through the failure of many therapeutic techniques where the bacteria that are normally susceptible to a treatment become resistant after surviving the outcome of the treatment. ... Given that lifespans and production of new generations can be on a timescale of mere hours, a new (de novo) mutation in a parent cell can quickly become an inherited mutation of widespread prevalence, resulting in the microevolution of a fully resistant colony. ... In recent years, the emergence and spread of β-lactamases called carbapenemases has become a major health crisis. [100] One such carbapenemase is New Delhi metallo-beta-lactamase 1 (NDM-1), [101] an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics . ... Drug resistance has "become a major concern". [116] History [ edit ] The 1950s to 1970s represented the golden age of antibiotic discovery, where countless new classes of antibiotics were discovered to treat previously incurable diseases such as tuberculosis and syphilis. [117] However, since that time the discovery of new classes of antibiotics has been almost nonexistent, and represents a situation that is especially problematic considering the resiliency of bacteria [118] shown over time and the continued misuse and overuse of antibiotics in treatment. [119] The phenomenon of antimicrobial resistance caused by overuse of antibiotics was predicted as early as 1945 by Alexander Fleming who said "The time may come when penicillin can be bought by anyone in the shops. ... Furthermore, if the use of vaccines increases, there is evidence that antibiotic resistant strains of pathogens will decrease; the need for antibiotics will naturally decrease as vaccines prevent infection before it occurs. [132] However, new strains that escape immunity induced by vaccines may evolve ; for example, an updated influenza vaccine is needed each year.
  • Apert Syndrome Wikipedia
    However, the typical hand deformities in patients with Apert syndrome distinguish it from the other syndromes. [8] The hands in patients with Apert syndrome always show four common features: [9] a short thumb with radial deviation complex syndactyly of the index, long and ring finger symbrachyphalangism simple syndactyly of the fourth webspace The deformity of the space between the index finger and the thumb may be variable. ... The thumb shows radial deviation and clinodactyly but is separated from the index finger. The index, long and ring finger are fused together in the distal interphalangeal joints and form a flat palm. ... This is a more serious anomaly since the thumb is fused to the index finger by simple complete or incomplete syndactyly. Only the distal phalanx of the thumb is not joined in the osseous union with the index finger and has a separate nail. ... In both type I and type II, the recurrent syndactyly of the second web space will occur because of a pseudoepiphysis at the base of the index metacarpal. This should be corrected by later revisions.
    FGFR2, TWIST1, FGF8
    • Acrocephalosyndactyly Orphanet
      A rare group of inherited congenital malformation disorders characterized by craniosynostosis and fusion or webbing of the fingers or toes, often with other associated manifestations. Epidemiology The exact prevalence and birth incidence of ACS syndromes are not known. Overall incidence of all forms of craniosynostosis is reported to be 1/2,000 to 1/2,500 live births, but only small minorities of these cases are syndromic and the ACS syndromes are only one of many that have craniosynostosis as a finding. Clinical description Acrocephalosyndactyly includes a number of syndromes with similar and sometimes overlapping clinical manifestations. All include single-suture or multisutural craniosynostosis with distinctive facial features, variable intellectual and developmental deficits, and variable forms of hand or foot abnormalities.
    • Apert Syndrome Omim
      A number sign (#) is used with this entry because Apert syndrome is caused by heterozygous mutation in the FGFR2 gene (176943) on chromosome 10q26. Crouzon syndrome (123500) and Pfeiffer syndrome (101600) are allelic disorders with overlapping features. Description Apert syndrome is a congenital disorder characterized primarily by craniosynostosis, midface hypoplasia, and syndactyly of the hands and feet with a tendency to fusion of bony structures. Most cases are sporadic, but autosomal dominant inheritance has been reported (Mantilla-Capacho et al., 2005). Cohen (1973) provided a review of all the 'craniosynostosis syndromes.'
    • Acrocephalosyndactylia Wikipedia
      "Acrocephalopolysyndactyly type IV: a new genetic syndrome in 3 sibs". Clin.
    • Apert Syndrome Gard
      It is inherited in an autosomal dominant manner, but many cases result from a new mutation in a person with no family history of the disorder (a de novo mutation).
  • Age Spots (Liver Spots) Mayo_clinic
    Risk factors You might be more likely to develop age spots if you: Have light skin Have a history of frequent or intense sun exposure or sunburn Prevention To help avoid age spots and new spots after treatment, follow these tips for limiting your sun exposure: Avoid the sun between 10 a.m. and 2 p.m. ... Dermabrasion sands down the surface layer of skin with a rapidly rotating brush. New skin grows in its place. You may need to undergo the procedure more than once. ... If you have rosacea or tiny red veins on your face, this technique could make the condition worse. ... This method involves applying a chemical solution to the skin to remove the top layers. New, smoother skin forms to take its place. ... Also, make sure your dermatologist is specially trained and experienced in the technique you're considering. Self care Many nonprescription fade creams and lotions for lightening age spots are available for sale.
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