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  • Neurodegeneration With Brain Iron Accumulation Wikipedia
    Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). ... Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). ... Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). ... Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). ... Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.).
    WDR45, PANK2, C19orf12, PLA2G6, PLB1, FA2H, YWHAZ, PLA2G1B, ATP13A2, FTL, COASY, SOD1, DCAF17, PANK1, FBXO7, CRAT, CP, C9orf72, GLB1, F5, RAB39B, SLC52A3, REPS1, FXN, DDHD1, GCH1, GFER, GJA1, SPARC, TFRC, IGFALS, PRKN, PLA2G4A, PRPS1, SPAG9, PRKRA, SGSH, SLC6A3, HSP90B2P, PINK1
    • Neurodegeneration With Brain Iron Accumulation Gard
      Neurodegeneration with brain iron accumulation (NBIA) is a group of inherited neurologic disorders in which iron accumulates in the basal ganglia. Symptoms include progressive dystonia (a movement disorder resulting in muscular spasms, twisting, and repetitive movements) spasticity, parkinsonism (slurred or slow speech, stiffness of the muscles, slow movement, and visible tremors), inability to coordinate movements (ataxia), neuropsychiatric abnormalities (confusion, disorientation, seizures, stupor, dementia), and eye problems, such as optic atrophy or retinal degeneration. The age of onset ranges from infancy to late adulthood, and the rate of progression varies. Some subtypes have cognitive decline. Cerebellar atrophy is common in many cases. There are ten recognized types of NBIA, classified according to the altered gene that causes the disease.
    • Neurodegeneration With Brain Iron Accumulation Orphanet
      Neurodegeneration with brain iron accumulation (NBIA, formerly Hallervorden-Spatz syndrome) encompasses a group of rare neurodegenerative disorders characterized by progressive extrapyramidal dysfunction (dystonia, rigidity, choreoathetosis), iron accumulation in the brain and the presence of axonal spheroids, usually limited to the central nervous system. Epidemiology An estimated prevalence of 1-3/1,000,000 has been suggested based on observed cases in a population. The most common form of NBIA is pantothenate kinase-associated neurodegeneration (PKAN; see this term), which accounts for approximately 50% of cases. Clinical description NBIA can present as early onset with rapid progression: classic pantothenate kinase-associated neurodegeneration (PKAN), infantile neuroaxonal dystrophy (INAD) and atypical neuroaxonal dystrophy (atypical NAD) (see these terms); or later onset with slower progression: atypical PKAN, neuroferritinopathy and aceruloplasminemia (see these terms). Idiopathic NBIA can have either type of onset and progression. Etiology Classic and atypical PKAN are caused by mutations in the PANK2 gene (20p13-p12.3), infantile and atypical neuroaxonal dystrophy are caused by mutation in the PLA2G6 gene (22q13.1), aceruloplasminemia is caused by mutation of the ceruloplasmin (CP) gene (3q23-q24) and neuroferritinopathy is caused by mutations in the ferritin light chain (FTL1) gene (19q13.3-q13.4).
  • Obesity In Pets Wikipedia
    Canine and Feline Nutrition: A Resource for Companion Animal Professionals (Third ed.). ... Blackwell's Five-Minute Veterinary Consult: Canine and Feline (Sixth ed.). ... PMID 19545467. ^ Rand, J, ed. (2007). "Obesity". Problem-based feline medicine (Repr. ed.). ... ISBN  9781437703023 . ^ Lappin, MR, ed. (2001). "Obesity and polyphagia". ... Black's Student Veterinary Dictionary (22nd ed.). Bloomsbury Publishing. p. 621.
  • Gastric Atresia Wikipedia
    Sleisenger and Fordtran's Gastrointestinal and Liver Disease (10 ed.). Elsevier. pp. 801–803. ^ a b c Avery's Diseases of the Newborn (10 ed.). Elsevier. 2018. pp. 1039–1053. ^ Fetal and Neonatal Physiology (5 ed.).
  • Head Pressing Wikipedia
    Canine Medicine and Disease Prevention (5th ed.). Animal Health Publications. ... (eds.). Veterinary Microbiology (3rd ed.). John Wiley & Sons. p. 573.
  • Mycotic Aneurysm Wikipedia
    In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia: Churchill Livingstone; 2000:888-892. ^ Jarrett F, Darling RC, Mundth ED, Austen WG.
  • Neurothekeoma Wikipedia
    Reed (1969), Tumors of the Peripheral Nervous System, in Armed Forces Institute of Pathology, ed: Atlas of Tumor Pathology, 2nd series, fascicle 3, Washington, D.C.: Armed Forces Institute of Pathology ^ a b c Pulitzer DR, Reed RJ (October 1985). ... (eds.), Lever's Histopathology of the Skin (Ninth ed.), Philadelphia: Lippincott Raven, ISBN  978-0781773638 This Dermal and subcutaneous growths article is a stub.
    ABCB1, TBC1D9
  • Zymotic Disease Wikipedia
    Hospitalism and Zymotic Disease (2nd ed.). London: Longmans, Green, and Co. ^ a b c Chisholm, Hugh, ed. (1911). ... Encyclopædia Britannica (11th ed.). Cambridge University Press. ^ Hess, David J. (1997).
  • Sexual Sadism Disorder Wikipedia
    Millon (Eds.), Oxford textbook of psychopathology (3rd ed.) (pp. 589–614). ... Diagnostic and Statistical Manual of Mental Disorders (3rd ed., revised). ... Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington, DC: Author. ^ American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.). ... Diagnostic and Statistical Manual of Mental Disorders (3rd ed.). Washington, DC: Author. ^ American Psychiatric Association. (1968).
  • Eosinophilic Cystitis Wikipedia
    Eosinophilic cystitis Specialty Urology Eosinophilic cystitis is a rare condition where eosinophiles are present in the bladder wall.[1] Signs and symptoms are similar to a bladder infection.[1] Its cause is not entirely clear; however, may be linked to food allergies, infections, and medications among others.[2] Management[edit] Treatment involves avoiding the trigger if that can be determined.[1] Prognosis[edit] Long term outcomes in children are generally good.[1] References[edit] ^ a b c d Kramer, ed. by A. ... Clinical pediatric urology (4. ed.). London: Dunitz. p. 338. ISBN  9781901865639 .CS1 maint: extra text: authors list (link) ^ Popescu, OE; Landas, SK; Haas, GP (Feb 2009).
    BRAF
    • Eosinophilic Cystitis Gard
      Eosinophilic cystitis (EC) is a rare inflammatory bladder condition caused by the build up of eosinophils in the bladder. The exact cause of this condition is not known. However, EC has been found in those with allergies and asthma, and in those with a history of bladder trauma or infection, open bladder surgery, or surgery for a bladder tumor. EC has also been found in those who take certain medications.
  • Ocular Melanosis Wikipedia
    (ed.) (1999). Veterinary Ophthalmology (3rd ed.). Lippincott, Williams & Wilkins.
    PLCB4, BAP1
  • Median Nail Dystrophy Wikipedia
    Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ... Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders.
  • Bubble Hair Deformity Wikipedia
    Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ... Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders.
  • Eclampsia Wikipedia
    Emergency medicine (8th ed.). New York: McGraw-Hill. ISBN  9780071840613 . ... Wayne (Eighth ed.). Philadelphia, PA: Saunders, Elsevier. pp. 626–637. ... (Tenth ed.). [New York]: McGraw-Hill Education. ISBN  9781259589287 . ... Larry,, Loscalzo, Joseph (19th ed.). New York: McGraw-Hill Education. ... (Sixtieth ed.). New York. 10 September 2020. ISBN  978-1-260-46986-8 .
    IL6, NOS3, STOX1, CORIN, LMNA, CD46, CFH, HELLPAR, VEGFA, AGT, PPARG, TNF, CFI, PGF, HLA-G, LEP, MTHFR, ADIPOQ, ACE, F5, HIF1A, IL1B, FOXP3, FLT1, TAC3, REN, SERPINE1, IL10, FAS, AGTR1, COMT, APOE, PTGS2, FASLG, MIR210, TGFB1, ACVR2A, MBL2, MMP9, EPHX1, PAPPA, SLC2A1, PTGS1, ERVW-1, COX1, IL1RN, IL4, ILK, KIR2DL4, TNFRSF11B, LPA, COX2, PAPPA2, MTCO2P12, HSPA4, AVP, FABP4, ENG, AQP4, F2, MIR155, EGF, CRP, EDN1, CALR, IL27, ADM, H19, MIF-AS1, SUMO4, MIR204, TLR4, TLR2, TP53, HTRA4, TXN, UCN, MIR203A, THBD, IL23R, MIR126, CFAP97, TERC, STAT1, CCL2, GHET1, CXCL12, PRNCR1, SNCA, RPL17-C18orf32, SORD, SRY, STAT5A, WAS, CD24, MIR885, SYT1, MIR454, POTEF, UCA1, TAP1, TAP2, LINC00261, CUL3, NPHS2, INTS6, IGF2BP2, ADIPOR2, RPL17, PLAC1, WNK1, RASSF1, SEC14L2, PART1, IL37, ADAM12, CTNNA3, GORASP1, HIF3A, C19orf33, IL23A, IL17D, MYDGF, RETN, NXF1, FST, FSTL3, WASF2, ACKR3, GCM1, BHLHE40, TNFSF11, USO1, IL18R1, CLIC3, DGKI, KISS1R, EBAG9, PROK1, ROCK2, INO80B, SPATA2, EBI3, NECTIN4, ATP6AP2, S100B, ABCA1, BRD2, FSHR, ELF5, ESR1, F2R, F10, FBN2, FGFR4, FLNB, FOS, FOSB, GEM, DUSP9, GIP, GLRX, GPT, GSTM1, GZMA, HLA-A, HLA-B, HLA-C, HLA-DPB1, EDN2, HBEGF, RHD, AQP9, ACTB, ADH5, ADORA2B, AFM, ALB, ANGPT1, ANXA2, ANXA5, XIAP, AVPR1A, DECR1, CD14, CD59, CSF1R, CCN2, CYBA, CYP2C9, CYP2D6, CYP11B2, DAP, HLA-DQA1, HLA-E, HSD11B2, NOTCH1, KLRB1, KLRC2, LHCGR, LPL, NR3C2, MMP2, ABO, RNR2, NFATC2, NOTCH2, ICA1, PAX3, PDCD1, PRKCB, PRKCD, PROS1, PSG5, PTPN2, RBP4, RELA, KIR3DL1, KIR2DL1, KDR, JUND, IFNG, IFNGR1, IGF2, IGFBP1, IGFBP5, CCN1, IL2, IL2RA, CXCL8, IL15, IL18, IDO1, INHBA, INS, INSR, EIF3E, ISG20, JUN, JUNB, MTF1
  • Synchysis Scintillans Wikipedia
    (ed.) (1999). Veterinary Ophthalmology (3rd ed.). Lippincott, Williams & Wilkins.
    CAT, ELANE
  • Erosive Pustular Dermatitis Of The Scalp Wikipedia
    Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ... Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders.
    • Erosive Pustular Dermatosis Of The Scalp Orphanet
      Erosive pustular dermatosis of the scalp is a rare chronic inflammation of the scalp usually occurring in elderly women (>70 years old) and characterized by the development of painful pustules, shallow erosions, and crusting on atrophic skin that eventually result in cicatricial alopecia.
  • Corneodermatoosseous Syndrome Wikipedia
    (eds.). Fitzpatrick's Dermatology in General Medicine (6th ed.). McGraw-Hill. p. 513.
  • Kinking Hair Wikipedia
    Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ... Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders.
  • Cavitation (Bone) Wikipedia
    Cranial Manipulation: Theory and Practice: Osseous and Soft Tissue Approaches (2 ed.). ... Retrieved 2019-12-22. ^ Sinatra, Stephen T.; Houston, Mark C., eds. (2015).
  • Tethered Spinal Cord Syndrome Wikipedia
    In Yamada, Shokei (ed.). Tethered Cord Syndrome in Children and Adults (Rev. ed.). ... In Yamada, Shokei (ed.). Tethered Cord Syndrome in Children and Adults (Rev. ed.). ... In Yamada, Shokei (ed.). Tethered Cord Syndrome in Children and Adults (Rev. ed.). ... In Yamada, Shokei (ed.). Tethered Cord Syndrome in Children and Adults (Rev. ed.). ... In Yamada, Shokei (ed.). Tethered Cord Syndrome in Children and Adults (Rev. ed.).
    MTHFR, PAX3, PDGFRA, VANGL2, PCMT1, CFL1, PON1, CHKA, CCL2, TXN2, PCYT1A, FGFR2, RNF2, SUZ12, MTRR, MTR, MTHFD1, BRCA1, SLC25A1, PTCH1, DLL4, FLI1, FANCL, RFWD3, FANCI, TRIM36, FANCC, SUFU, PSAT1, UBE2T, PHGDH, FANCF, HAAO, MEOX1, PTCH2, MAD2L2, LMX1B, RBM8A, BMS1, KIF22, FANCG, GDF3, FANCB, CREBBP, BRIP1, BRCA2, RAD51C, SLX4, RAD51, PALB2, FANCE, RMRP, PORCN, XRCC2, GDF6, SLC25A19, FANCM, ERCC4, FANCA, FANCD2, ZIC2, DHFR, GRHL3, FUZ, BHMT, CELSR1, TYMS, PTK7, CBS, NOS3, LEPR, NAT1, PAX1, PRCP, SLC19A1, TIMP2, CYP26A1, GRHL2, CBSL, AFP, PGPEP1, FOLR1, FOLR2, SCRIB, COMT, BMP1, ZIC1, VSIR, PKD2L1, VANGL1, ANKEF1, CD200R1, PRICKLE2, UCP2, PCSK9, TP53, SLC5A11, SLC39A4, CCDC88A, ALDH1A2, ISYNA1, TGIF1, TRIM26, FZD3, FKBP8, BHMT2, GPR161, CUBN, DVL1P1, FOXN1, ALDH1L1, MTHFD2, TNIP1, NKX2-8, NNMT, TGFB1, SOX3, GCKR, FOSB, FOS, FOLH1, FLT4, GPC5, FGF3, FAP, ERCC2, EPHA4, DVL3, DVL1, DPP4, TRDMT1, SARDH, CSF2, CRABP2, ABCC2, CD38, CASP8, CASP3, BMP4, BDNF, ARSA, APOE, APOB, APEX1, APAF1, ABO, GLI2, GNAS, UTS2R, LAMC2, SLC2A1, SKI, RFC1, PRKCB, PRKCA, NAT2, NGF, MS, CD200, MMP2, LRP6, LMNB1, LEP, JUND, HK1, JUNB, JUN, JARID2, ITPK1, IL18, IL13, IL10, HOXD@, HOXC@, HOXB@, HOXA@, HMOX1, HLA-DRB4, RN7SL263P
    • Spina Bifida Wikipedia
      Pediatric life care planning and case management (2nd ed.). Boca Raton, FL: CRC Press. p. 392. ... Newborn surgery (3 ed.). London: Hodder Arnold. p. 811. ISBN  9781444149494 . ^ a b Ferri, Fred F. (2016).
    • Neural Tube Defects, Folate-Sensitive Omim
      A number sign (#) is used with this entry because folate-sensitive neural tube defects (NTDFS) have been associated with variation in a number of genes involved in folate and homocysteine metabolism, including 5,10-methylenetetrahydrofolate reductase (MTHFR; 607093), methionine synthase (MTR; 156570), methionine synthase reductase (MTRR; 602568), and methylenetetrahydrofolate dehydrogenase-1 (MTHFD1; 172460). See also 182940 for a discussion of neural tube defects that are not associated with folate metabolism. See also 601775 for a description of variation of folate levels in erythrocytes. Description Neural tube defects have a birth incidence of approximately 1 in 1,000 in American Caucasians and are the second most common type of birth defect after congenital heart defects. The most common NTDs are open spina bifida (myelomeningocele) and anencephaly (206500) (Detrait et al., 2005).
    • Rachischisis Wikipedia
      Neural tube defect in which the spinal cord is exposed Rachischisis Craniorachischisis in a mouse embryo at day 18.5 Specialty Medical genetics  Rachischisis (Greek: "rhachis - ῥάχις" - spine, and "schisis - σχίσις" - split) is a developmental birth defect involving the neural tube. This anomaly occurs in utero, when the posterior neuropore of the neural tube fails to close by the 27th intrauterine day. As a consequence the vertebrae overlying the open portion of the spinal cord do not fully form and remain unfused and open, leaving the spinal cord exposed. Patients with rachischisis have motor and sensory deficits, chronic infections, and disturbances in bladder function. This defect often occurs with anencephaly. Craniorachischisis is a variant of rachischisis that occurs when the entire spinal cord and brain are exposed - simultaneous complete rachischisis and anencephaly.
    • Spina Bifida Gard
      Spina bifida is a type of neural tube defect in which the neural tube (the structure in an embryo that becomes the brain and spinal cord) does not completely close during development in the womb. This may result in part of the spinal cord sticking out through an opening in the spine, leading to permanent nerve damage. Babies born with spina bifida often have a fluid-filled sac, covered by skin, on their back. This is called a meningocele. If the sac contains part of the spinal cord and its protective covering, it is known as a myelomeningocele. The signs and symptoms of spina bifida can range from mild to severe, depending on the location and extent of spinal cord involvement.
    • Isolated Spina Bifida Orphanet
      A group of rare neural tube defect disorders characterized by improper closure of the spinal column during embryonal development, not associated with other major congenital malformations nor ventriculomegaly. The extent of the closure defect may vary, ranging from spina bifida occulta, in which the site of the lesion is not exposed (e.g. an isolated posterior vertebral arch defect), to spina bifida aperta, in which the lesion may be conformed of proturding spinal cord and meninges (myelomeningocele) or meninges exposure only (meningocele), with or without a proturding sac at the site of the lesion, to the most severe defect which includes total exposure of the spinal cord along its full length (rachischisis). Depending on the type, size and site of the defect, severe morbidity, typically inlcuding motor, sensory and sphincter dysfunction, and mortality may be associated. Spina bifida occulta may be asymptomatic.
    • Neural Tube Defects, X-Linked Omim
      For a general phenotypic description and a discussion of genetic heterogeneity of neural tube defects, see 182940 and 601634. Inheritance Toriello et al. (1980) observed either anencephaly or spina bifida in 5 males in 5 different sibships spanning 4 generations genealogically connected through females. Baraitser and Burn (1984) and Toriello (1984) reported additional kindreds with pedigree patterns strongly supporting X-linked recessive inheritance. Baraitser and Burn (1984) reported a nonconsanguineous Pakistani Muslim family in which a woman had 3 brothers and 3 sons with neural tube defects, including posterior encephalocele and spina bifida cystica. Jensson et al. (1988) reported an Icelandic family in which 5 males had either anencephaly or spina bifida: 2 had spina bifida, 2 sibs had anencephaly, and 1 had both high and low spinal lesions.
    • Neural Tube Defects, Susceptibility To Omim
      A number sign (#) is used with this entry because of evidence that susceptibility to the development of neural tube defects (NTDs) is conferred by variation in the VANGL1 (610132), VANGL2 (600533), CELSR1 (604523), or FUZ (610622) genes. An association has been reported with variants in the T locus (601397) on chromosome 6q. Description Neural tube defects are the second most common type of birth defect after congenital heart defects. The 2 most common NTDs are open spina bifida, also known as spina bifida cystica (SBC) or myelomeningocele, and anencephaly (206500) (Detrait et al., 2005). Spina bifida occulta (SBO), a bony defect of the spine covered by normal skin, is a mild form of spina bifida that is often asymptomatic.
  • Erythroplakia Wikipedia
    Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0-07-138076-0. ^ a b c d Barnes L, ed. (2008). Surgical pathology of the head and neck Vol. 1 (3rd ed.). ... Oral and maxillofacial medicine: the basis of diagnosis and treatment (3rd ed.). ... ISBN  978-0-7020-4948-4 . ^ a b Katsambas AD, Lotti TM, eds. (2003). European handbook of dermatological treatments (2nd ed.). ... "Head and Neck Tumors" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008. ^ Hashibe M, Mathew B, Kuruvilla B, et al.
    TP53, EGFR, FHIT, OSTF1
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