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Lichen Spinulosus Wikipedia

Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . References [ edit ] Friedman S (1990). ... PMID 2179296 . External links [ edit ] Derm Net NZ Emedicine Thehinhso v t e Diseases of the skin and appendages by morphology Growths Epidermal Wart Callus Seborrheic keratosis Acrochordon Molluscum contagiosum Actinic keratosis Squamous-cell carcinoma Basal-cell carcinoma Merkel-cell carcinoma Nevus sebaceous Trichoepithelioma Pigmented Freckles Lentigo Melasma Nevus Melanoma Dermal and subcutaneous Epidermal inclusion cyst Hemangioma Dermatofibroma (benign fibrous histiocytoma) Keloid Lipoma Neurofibroma Xanthoma Kaposi's sarcoma Infantile digital fibromatosis Granular cell tumor Leiomyoma Lymphangioma circumscriptum Myxoid cyst Rashes With epidermal involvement Eczematous Contact dermatitis Atopic dermatitis Seborrheic dermatitis Stasis dermatitis Lichen simplex chronicus Darier's disease Glucagonoma syndrome Langerhans cell histiocytosis Lichen sclerosus Pemphigus foliaceus Wiskott–Aldrich syndrome Zinc deficiency Scaling Psoriasis Tinea ( Corporis Cruris Pedis Manuum Faciei ) Pityriasis rosea Secondary syphilis Mycosis fungoides Systemic lupus erythematosus Pityriasis rubra pilaris Parapsoriasis Ichthyosis Blistering Herpes simplex Herpes zoster Varicella Bullous impetigo Acute contact dermatitis Pemphigus vulgaris Bullous pemphigoid Dermatitis herpetiformis Porphyria cutanea tarda Epidermolysis bullosa simplex Papular Scabies Insect bite reactions Lichen planus Miliaria Keratosis pilaris Lichen spinulosus Transient acantholytic dermatosis Lichen nitidus Pityriasis lichenoides et varioliformis acuta Pustular Acne vulgaris Acne rosacea Folliculitis Impetigo Candidiasis Gonococcemia Dermatophyte Coccidioidomycosis Subcorneal pustular dermatosis Hypopigmented Tinea versicolor Vitiligo Pityriasis alba Postinflammatory hyperpigmentation Tuberous sclerosis Idiopathic guttate hypomelanosis Leprosy Hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized Drug eruptions Viral exanthems Toxic erythema Systemic lupus erythematosus Localized Cellulitis Abscess Boil Erythema nodosum Carcinoid syndrome Fixed drug eruption Specialized Urticaria Erythema ( Multiforme Migrans Gyratum repens Annulare centrifugum Ab igne ) Nonblanchable Purpura Macular Thrombocytopenic purpura Actinic/solar purpura Papular Disseminated intravascular coagulation Vasculitis Indurated Scleroderma / morphea Granuloma annulare Lichen sclerosis et atrophicus Necrobiosis lipoidica Miscellaneous disorders Ulcers Hair Telogen effluvium Androgenic alopecia Alopecia areata Systemic lupus erythematosus Tinea capitis Loose anagen syndrome Lichen planopilaris Folliculitis decalvans Acne keloidalis nuchae Nail Onychomycosis Psoriasis Paronychia Ingrown nail Mucous membrane Aphthous stomatitis Oral candidiasis Lichen planus Leukoplakia Pemphigus vulgaris Mucous membrane pemphigoid Cicatricial pemphigoid Herpesvirus Coxsackievirus Syphilis Systemic histoplasmosis Squamous-cell carcinoma This condition of the skin appendages article is a stub .

Histiocytosis Wikipedia

Information concerning histiocytosis and clinicians located in European countries may be found in many languages at the web portal of Euro Histio Net (EHN). This is a project funded by the European Union, coordinated by Jean Donadieu, APHP , Paris, France. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Goldberg, J; Nezelof, C (1986), "Lymphohistiocytosis: a multi-factorial syndrome of macrophagic activation clinico-pathological study of 38 cases", Hematol Oncol , 4 (4): 275–289, PMID 3557322 . ^ Egan, Caoimhe; Jaffe, Elaine S. (2018). ... Springer Science & Business Media. p. 383. ISBN 978-0-387-73743-0 . External links [ edit ] Classification D ICD - 10 : C96.1 , D76.0 ICD - 9-CM : 202.3 , 277.89 MeSH : D015614 SNOMED CT : 60657004 External resources MedlinePlus : 000068 eMedicine : ped/1997 v t e Histiocytosis WHO-I/ Langerhans cell histiocytosis / X-type histiocytosis Letterer–Siwe disease Hand–Schüller–Christian disease Eosinophilic granuloma Congenital self-healing reticulohistiocytosis WHO-II/ non-Langerhans cell histiocytosis / Non-X histiocytosis Juvenile xanthogranuloma Hemophagocytic lymphohistiocytosis Erdheim-Chester disease Niemann–Pick disease Sea-blue histiocyte Benign cephalic histiocytosis Generalized eruptive histiocytoma Xanthoma disseminatum Progressive nodular histiocytosis Papular xanthoma Hereditary progressive mucinous histiocytosis Reticulohistiocytosis ( Multicentric reticulohistiocytosis , Reticulohistiocytoma ) Indeterminate cell histiocytosis WHO-III/ malignant histiocytosis Histiocytic sarcoma Langerhans cell sarcoma Interdigitating dendritic cell sarcoma Follicular dendritic cell sarcoma Ungrouped Rosai–Dorfman disease

SLC29A3, IFNGR1, BRAF, ALK, MAP2K7, PTPRC, EPHB2, MAPK1, MAP2K1, MAP2K2, S100A1, ARAF, TLR7, CD274, ZHX2, PPT2, CD163, TP53, TIMP1, S100B, CD68, RET, RAF1, CSF1R, PTGS1, XIAP, POU6F1, KIF5B, IL6, CD1A, HPRT1, SEMA6A

Glaucoma 1, Open Angle, M Omim

Affected individuals were typically diagnosed before 35 years of age and had grade III-IV gonioscopy of the anterior chamber, intraocular pressures greater than or equal to 22 mm Hg, and chacteristic optic disc and visual field changes. ... They obtained a maximum lod score of 4.82 (theta = 0) at marker D5S2011 when unaffected family members under the age of 35 were considered to have 'unknown' status.

CYP1B1, MYOC, PAX6, FOXC1, PITX2, ADAR, CHST3, CYP1B1-AS1, CANT1, RNASEH2C, RNASEH2B, IFIH1, B3GAT3, SAMHD1, TREX1, RNASEH2A, SRY, PYCR1, LTBP2, FLNA, FOXE3, PXDN, VAV3, ARSD, PLXNA2, NUFIP2, LGALS7, GJA1, FUT8, LGALS7B

Glaucoma 1, Open Angle, J Omim

For a general phenotypic description and a discussion of genetic heterogeneity of primary open angle glaucoma (POAG), see 137760. Wiggs et al. (2004) identified 25 pedigrees with typical juvenile-onset primary open angle glaucoma (JOAG), demonstrating autosomal dominant inheritance. They sequenced the myocilin gene (MYOC; 601652) in probands from each family and found mutations in 8%. To identify novel genes responsible for JOAG, they used families that did not have myocilin mutations for a genomewide screen. Multipoint linkage analysis of chromosome 9 markers achieved a peak hlod score of 4.0 between markers D9S1803 and D9S196 on chromosome 9q22.
Glaucoma 1, Open Angle, N Omim

For a general phenotypic description and a discussion of genetic heterogeneity of primary open angle glaucoma (POAG), see 137760. Clinical Features Wang et al. (2006) reported a 3-generation Chinese family in which 8 members had confirmed autosomal dominant juvenile-onset primary open angle glaucoma (JOAG; see 137750). Age at diagnosis ranged from 12 to 32 years. All of those affected showed notable increase in intraocular pressure and severe visual loss. All had a wide anterior chamber. Although most of them had typical glaucoma changes in optic disc and visual field, they all showed a normal iris, no anterior segment anomalies, and corneal thickness and anterior chamber depth within normal ranges. Mapping In 8 affected members of a Chinese family segregating autosomal dominant JOAG, Wang et al. (2006) excluded mutations in the MYOC (601652), OPTN (602432), and WDR36 (609669) genes.
Glaucoma 1, Open Angle, K Omim

For a general phenotypic description and a discussion of genetic heterogeneity of open angle glaucoma (POAG), see 137760. Mapping Wiggs et al. (2004) identified 25 pedigrees with typical juvenile-onset OAG (JOAG), demonstrating autosomal dominant inheritance. They sequenced the myocilin gene (MYOC; 601652) in probands from each family and found mutations in 8%. To identify novel genes responsible for JOAG, they used families that did not have myocilin mutations for a genomewide screen. Multipoint linkage analysis of chromosome 20 markers achieved a peak hlod score of 4 between markers D20S189 and D20S104 on chromosome 20p12.
Glaucoma 1, Open Angle, A Omim

The intraocular pressures of affected individuals were commonly more than 50 mm Hg when they were first examined. Gonioscopy showed open angles, with no abnormal pigmentation, iris processes, or embryonic tissue. ... In the 23 affected patients, the average age of diagnosis was 18.5 years (range, 5 to 30 years), and the average initial intraocular pressure was 38.5 mm Hg (range, 30 to 53 mm Hg). Myopia was present in 87% of affected individuals, and 83% required surgical treatment for glaucoma. ... Clinical features associated with these 6 mutations included an age at diagnosis ranging from 8 to 77 years and maximal recorded intraocular pressures ranging from 12 to 77 mm Hg. The spectrum of disease, as indicated by this survey, can range from juvenile glaucoma to typical late-onset primary open angle glaucoma.
Juvenile Glaucoma Orphanet

A primary early-onset glaucoma that is characterized by early onset, severe elevation of intra ocular pressure of rapid progression, leading to optic nerve excavation and, when untreated, substantial visual impairment. Epidemiology The disorder is estimated to occur in 0,32/100 000 individuals before the age of 20 years. Clinical description Juvenile glaucoma (JG) typically presents between the ages of 5 to 18 years, but it can appear later. Patients are initially asymptomatic and are often discovered incidentally on a routine examination. JG is generally bilateral; there can be a marked asymmetry between the two eyes.

Retiform Parapsoriasis Wikipedia

Retiform parapsoriasis Specialty Dermatology Retiform parapsoriasis is a cutaneous condition, considered to be a type of large-plaque parapsoriasis . [1] It is characterized by widespread, ill-defined plaques on the skin, that have a net-like or zebra-striped pattern. [2] Skin atrophy , a wasting away of the cutaneous tissue , usually occurs within the area of these plaques. [1] See also [ edit ] Parapsoriasis Poikiloderma vasculare atrophicans List of cutaneous conditions References [ edit ] ^ a b Lambert WC, Everett MA (Oct 1981). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . External links [ edit ] Classification D ICD - 10 : L41.5 ICD - 9-CM : 696.2 v t e Papulosquamous disorders Psoriasis Pustular Generalized pustular psoriasis ( Impetigo herpetiformis ) Acropustulosis / Pustulosis palmaris et plantaris ( Pustular bacterid ) Annular pustular psoriasis Localized pustular psoriasis Other Guttate psoriasis Psoriatic arthritis Psoriatic erythroderma Drug-induced psoriasis Inverse psoriasis Napkin psoriasis Seborrheic-like psoriasis Parapsoriasis Pityriasis lichenoides ( Pityriasis lichenoides et varioliformis acuta , Pityriasis lichenoides chronica ) Lymphomatoid papulosis Small plaque parapsoriasis ( Digitate dermatosis , Xanthoerythrodermia perstans ) Large plaque parapsoriasis ( Retiform parapsoriasis ) Other pityriasis Pityriasis rosea Pityriasis rubra pilaris Pityriasis rotunda Pityriasis amiantacea Other lichenoid Lichen planus configuration Annular Linear morphology Hypertrophic Atrophic Bullous Ulcerative Actinic Pigmented site Mucosal Nails Peno-ginival Vulvovaginal overlap synromes with lichen sclerosus with lupus erythematosis other: Hepatitis-associated lichen planus Lichen planus pemphigoides Other Lichen nitidus Lichen striatus Lichen ruber moniliformis Gianotti–Crosti syndrome Erythema dyschromicum perstans Idiopathic eruptive macular pigmentation Keratosis lichenoides chronica Kraurosis vulvae Lichen sclerosus Lichenoid dermatitis Lichenoid reaction of graft-versus-host disease This dermatology article is a stub .

Poikiloderma Vasculare Atrophicans Wikipedia

Poikiloderma vasculare atrophicans Other names Parapsoriasis variegata [1] or Parapsoriasis lichenoides [2] Typical skin changes and discoloration described as poikiloderma vasculare atrophicans Specialty Dermatology Poikiloderma vasculare atrophicans ( PVA ), is a cutaneous condition ( skin disease ) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation , respectively), telangiectasia and skin atrophy . [3] [4] [5] Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis . [6] The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. [7] PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". [3] On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin). [3] [6] Mycosis fungoides, a type of skin lymphoma , may be a cause of PVA. The condition may also be caused by, associated with or accompany any of the following conditions or disorders: other skin lymphomas, dermatomyositis , lupus erythematosus , Rothmund–Thomson syndrome , Kindler syndrome , dyskeratosis congenita , and chronic radiodermatitis . [4] Rare causes include arsenic ingestion, and the condition can also be idiopathic . [1] [3] [5] PVA may be considered a rare variant of cutaneous T-cell lymphoma , a non-Hodgkin's form of lymphoma affecting the skin. [7] It may also be included among a number of similar conditions that are considered as precursors to mycosis fungoides . PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis ; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis . [5] Contents 1 Presentation 2 Cause 3 Diagnosis 3.1 Classification 4 Management 5 See also 6 References 7 External links Presentation [ edit ] The layers of the epidermis (left). Melanocytes (rlght), located in the bottom epidermal layer, produce melanin. PVA can be characterized by speckled, combined hyper- and hypopigmentation in the plaques or patches of affected skin. [5] Hyperpigmentation is excess coloration, or darkening of the skin, [8] while hypopigmentation is a diminished or pallid coloring to the skin.

Hypomagnesemia, Hypertension, And Hypercholesterolemia, Mitochondrial Omim

Including the index case, 38 members had hypertension (blood pressure greater than 140/90 mm Hg or on treatment for hypertension), 33 had hypercholesterolemia (with total cholesterol greater than 200 mg/dl or on treatment for hypercholesterolemia), and 32 had clinically significant hypomagnesemia (range 0.8 to 1.7 mg/dl, normal 1.8 to 2.5 mg/dl). ... Affected fathers never transmitted the trait to their offspring (0 of 17 offspring), whereas affected mothers transmitted the trait to a high fraction of their offspring (16 of 21). ... Among adults age 18 to 60, maternal lineage increased systolic blood pressure by an average of 13 mm Hg and diastolic blood pressure by 5 mm Hg.

TRNI

Affluenza Wikipedia

Affluenza: How to Be Successful and Stay Sane . Vermilion . ISBN 978-0-09-190011-3 . ^ James, Oliver (2008). The Selfish Capitalist . Vermilion . ISBN 978-0-09-192381-5 . ^ James, Oliver (2007). ... London: Vermilion. p. 344 . ISBN 978-0-09-190010-6 . 1. The mean prevalence of emotional distress for the six English-speaking nations combined was 21.6%. ... (Archive is the same work, but on a different website) Further reading [ edit ] The Circle of Simplicity , Cecile Andrews, ISBN 0-06-092872-7 The Golden Ghetto: The Psychology of Affluence , Jessie H. O'Neill, ISBN 978-0-9678554-0-0 Voluntary Simplicity , Duane Elgin, ISBN 0-688-12119-5 Voluntary Simplicity , Daniel Doherty & Amitai Etzioni, ISBN 0-7425-2066-8 How Much Is Too Much?

Giant Condyloma Acuminatum Wikipedia

Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ "Condyloma Acuminata" . ... Accessed April 15, 2020. ^ a b Kim HG, Kesey JE, Griswold JA. Giant anorectal condyloma acuminatum of Buschke-Löwenstein presents difficult management decisions.

Kindler Syndrome Wikipedia

Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Bardhan, Ajoy; Bruckner-Tuderman, Leena; Chapple, Iain L. ... Nature Reviews Disease Primers . 6 (1): 78. doi : 10.1038/s41572-020-0210-0 . ISSN 2056-676X . PMID 32973163 . ... Retrieved November 18, 2018 . ^ Siegel DH, Ashton GH, Penagos HG, Lee JV, Feiler HS, Wilhelmsen KC, et al.

FERMT1, ACTB, FBLIM1, FERMT2, UVRAG, COMMD3-BMI1, FERMT3, CKAP4, TP63, XPC, RPE65, BMI1, PXN, MAPK8, PLEK, KRT5, COL7A1, CDKN2A, CDK2, CDK1, H3P10

Kindler Syndrome Gene_reviews

Summary Clinical characteristics. Kindler syndrome (KS), a rare subtype of inherited epidermolysis bullosa, is characterized by skin fragility and acral blister formation beginning at birth, diffuse cutaneous atrophy, photosensitivity (which is most prominent during childhood and usually decreases after adolescence), poikiloderma, diffuse palmoplantar hyperkeratosis, and pseudosyndactyly. Mucosal manifestations are also common and include hemorrhagic mucositis and gingivitis, periodontal disease, premature loss of teeth, and labial leukokeratosis. Other mucosal findings can include ectropion, esophageal strictures/stenosis, anal stenosis, colitis, urethral stenosis/strictures, and severe phimosis. Severe long-term complications of KS include periodontitis, mucosal strictures, and aggressive squamous cell carcinomas. Manifestations can range from mild to severe. Diagnosis/testing. The diagnosis of Kindler syndrome is established in a proband with characteristic clinical findings and identification of either biallelic FERMT1 pathogenic variants on molecular genetic testing or suggestive histologic findings and/or immunolabeling on skin biopsy.
Kindler Syndrome Omim

A number sign (#) is used with this entry because of evidence that Kindler syndrome (KNDLRS) is caused by homozygous mutation in the FERMT1 (KIND1; 607900) gene on chromosome 20p12. Description Kindler syndrome is an autosomal recessive dermatosis characterized by congenital blistering, skin atrophy, photosensitivity, skin fragility, and scaling (summary by Jobard et al., 2003). Clinical Features Kindler (1954) described an English girl with unusual congenital blistering of her hands and feet. Later in childhood, the patient developed reticulate erythema and diffuse cutaneous atrophy, beginning in sun-exposed areas. Her gums bled easily, and the skin of the dorsal hands and feet had a thin, wrinkled appearance.
Kindler Syndrome Medlineplus

Kindler syndrome is a rare type of epidermolysis bullosa, which is a group of genetic conditions that cause the skin to be very fragile and to blister easily. From early infancy, people with Kindler syndrome have skin blistering, particularly on the backs of the hands and the tops of the feet. The blisters occur less frequently over time, although repeated blistering on the hands can cause scarring that fuses the skin between the fingers and between the toes. Affected individuals also develop thin, papery skin starting on the hands and feet and later affecting other parts of the body. Other skin abnormalities that occur with Kindler syndrome include patchy changes in skin coloring and small clusters of blood vessels just under the skin (telangiectases), a combination known as poikiloderma.
Kindler Syndrome Gard

Kindler syndrome is a rare type of epidermolysis bullosa , a group of inherited conditions that cause fragile and blistering skin. Kindler syndrome causes skin to blister beginning in early infancy. Other symptoms may include increased sensitivity to light (photosensitivity); patchy discoloration of the the skin and small clusters of blood vessels (poikiloderma); thickening and hardening of the skin on the palms of the hands and soles of the feet (hyperkeratosis); and an increased risk for squamous cell carcinoma. The condition can also affect the moist lining of the mouth, eyes, esophagus, intestines, genitals, and urinary system. Kindler syndrome is caused by mutations in the FERMT1 gene (also called the KIND1 gene) and is inherited in an autosomal recessive manner. Treatment consists of avoiding skin injury, limiting sun exposure, and carefully tending to blisters (often with antibiotics).
Kindler Syndrome Orphanet

Kindler syndrome (KS) is the fourth major type of epidermolysis bullosa (EB), besides simplex, junctional and dystrophic forms, and is characterized by skin fragility and blistering at birth followed by development of photosensitivity and progressive poikilodermatous skin changes. Epidemiology Prevalence is unknown. More than 250 cases have been reported to date. Clinical description The disease usually manifests at birth with trauma-induced skin blistering that is more prominent on extremities and tends to regress with age, becoming rare in adulthood. Healing of blisters occurs with minimal scarring. With age, additional skin findings are observed: (i) in most patients, photosensitivity with erythema and photo-induced blisters is obvious since early childhood and often diminishes after adolescence, (ii) progressive skin poikiloderma (atrophy, telangiectases, and reticular pigmentation) manifests from childhood and is predominantly localized to the face and neck, and (iii) skin atrophy is localized to hands and feet in the first years of life but becomes generalized by adolescence. Blisters also affect the mucosae. In the oral cavity, chronic gingivitis and periodontitis are frequent and prominent features in adulthood.

Glaucoma 1, Open Angle, P Omim

POAG that occurs with an IOP below an arbitrary threshold of 21 mm Hg is often termed 'normal tension glaucoma' (summary by Fingert et al., 2011). ... Five of the 6 affected family members with extensive ophthalmologic records had a maximum IOP of 21 mm Hg or less and met criteria for a diagnosis of normal tension glaucoma, whereas 1 patient had a maximum IOP of 22 mm Hg. Mapping In affected individuals from a 4-generation African American pedigree with NTG who were negative for mutation in the known glaucoma genes MYOC (601652) and OPTN (602432) and did not show linkage to either of those loci, Fingert et al. (2011) performed genomewide linkage analysis and obtained a maximum genomewide lod score of 2.7 at theta = 0 on chromosome 12q14. All 10 affected family members shared at least 1 allele of 1,869 contiguous SNPs on 12q14, defining a 9.47-Mb locus between rs12227270 and rs7488555. ... One was a sporadic NTG patient with a maximum IOP of 20 mm Hg and a 300-kb duplication. The other patient, who had a 650-kb duplication, came from an NTG family previously described by Bennett et al. (1989); DNA was available from 3 additional affected members, who all carried the duplication, whereas it was not found in 3 unaffected family members. ... Using quantitative PCR, Kawase et al. (2012) analyzed 252 unrelated Japanese NTG patients who had open angle glaucoma and maximum untreated IOPs of 21 mm Hg or less, 202 Japanese controls, 29 NTG patients from North Carolina, and 28 NTG patients from New York.

Amoebic Gill Disease Wikipedia

The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile. [2] It was first diagnosed in the summer of 1984/1985 in populations of Atlantic salmon off the east coast of Tasmania and was found to be caused by N. perurans n.sp. [3] Contents 1 Clinical signs and diagnosis 2 Treatment and control 3 Notes 4 References Clinical signs and diagnosis [ edit ] Symptoms typically begin to appear two months after the fish are transferred from freshwater hatcheries to open net sea cages. [4] Symptoms include mucus build-up on the gills of infected fish and hyper-plastic lesions, causing white spots and eventual deterioration of the gill tissue. ... searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] ^ "Neoparamoeba perurans n. sp., an agent of amoebic gill disease of Atlantic salmon (Salmo salar)". ... searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] ^ https://www.int-res.com/articles/dao/25/d025p023.pdf ^ http://eafp.org/display/Search?searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] References [ edit ] Amoebic Gill Disease Wikivet .

Afterdepolarization Wikipedia

They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. [3] [4] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia . ... Neuroscience. ^ Katzung, B: Basic and Clinical Pharmacology (10th ed.), chapter 14: "Agents Used in Cardiac Arrhythmias", The McGraw-Hill Companies, 2007, ISBN 978-0-07-145153-6 ^ Lilly, L: "Pathophysiology of Heart Disease", chapter 11: "Mechanisms of Cardiac Arrhthmias", Lippencott, Williams and Wilkens, 2007 This article about a medical condition affecting the circulatory system is a stub .

Morbid Obesity And Spermatogenic Failure Omim

Obese family members all fulfilled criteria consistent with metabolic syndrome, including hypertension with systolic blood pressure greater than 140 mm Hg, fatty liver disease by ultrasound, and insulin resistance. ... Mapping By positional cloning in a large multigenerational Arab family with morbid obesity and spermatogenic failure, Shalata et al. (2013) localized the disease gene to a 5.5-Mb region between markers D3S2418 and D3S3550 on the telomeric end of chromosome 3q29 (lod score of 9.7 at theta = 0). Heterozygosity and haplotype analysis narrowed the critical region to a 1.6-Mb interval between D3S2306 and D3S3550.

CEP19, PIGX

Peripheral Artery Disease Wikipedia

This classification system consists of four grades and seven categories (categories 0–6): [43] [51] Grade 0, Category 0: asymptomatic Grade I, Category 1: mild claudication Grade I, Category 2: moderate claudication Grade I, Category 3: severe claudication Grade II, Category 4: rest pain Grade III, Category 5: minor tissue loss; ischemic ulceration not exceeding ulcer of the digits of the foot Grade IV, Category 6: major tissue loss; severe ischemic ulcers or frank gangrene Moderate to severe PAD classified by Fontaine's stages III to IV or Rutherford's categories 4 to 5, presents limb threat (risk of limb loss) in the form of critical limb ischemia . [52] Recently, the Society for Vascular Surgery came out with a classification system based on "wound, ischemia and foot Infection" (WIfI). [53] This classification system, published in 2013 was created to account for the demographic changes that have occurred over the past forty years including increased incidence of high blood sugar and evolving techniques and ability for revascularization . This system was created on the basis of ischemia and angiographic disease patterns not being the sole determinants of amputation risk. [54] The WIfI classification system is broken up into two parts: wounds and ischemia. Wounds are graded 0 through 3 on the presence of ulceration and/or gangrene and ischemia. [53] Grade 0: no ulcer, no gangrene Grade 1: small, shallow ulcer; no gangrene Grade 2: deep ulcer with exposed tendon or bone, gangrene limited to toes Grade 3: extensive, full-thickness ulcer; gangrene extending to forefoot or midfoot Ischemia is graded 0 through 3 based on ABI, ankle systolic pressure, and toe pressure. [53] Grade 0: ABI 0.8 or higher, ankle Grade 1: arterial brachial index 0.6 to 0.79, ankle pressure 70 to 100 mm Hg, toe pressure 40 to 59 mm Hg Grade 2: ABI 0.4–0.59, ankle pressure 50 to 70 mm Hg, toe pressure 30 to 39 mm Hg The TASC (and TASC II) classification suggested PAD treatment is based on the severity of disease seen on angiogram . [43] Screening [ edit ] It is not clear if screening for disease in the general population is useful as it has not been properly studied. [19] This includes screening with the ankle-brachial index . [55] Testing for coronary artery disease or carotid artery disease is of unclear benefit. [18] While PAD is a risk factor for abdominal aortic aneurysms (AAA), there is no data on screening individuals with asymptomatic PAD for abdominal aortic aneurysms. [18] In people with symptomatic PAD screening by ultrasound for AAA is not unreasonable. [18] Treatment [ edit ] Depending on the severity of the disease, these steps can be taken, according to these guidelines: [56] Lifestyle [ edit ] Stopping smoking (cigarettes promote PAD and are a risk factor for cardiovascular disease) Regular exercise for those with claudication helps open up alternative small vessels (collateral flow) and the limitation in walking often improves. ... Lancet . 382 (9901): 1329–40. doi : 10.1016/s0140-6736(13)61249-0 . PMID 23915883 . S2CID 38652734 . ^ a b "How Is Peripheral Arterial Disease Diagnosed?"

BMP8A, BMP2, LPA, ABO, F5, LPL, TCF7L2, OSBPL10, TNIK, MACF1, COL4A1, CNNM1, PADI4, MTHFD1L, HDAC9, WWOX, CRP, TRAM2, ZYG11B, FEZ1, MMP3, NDUFB9, VEGFA, UTRN, UGDH, CNOT4, CNTN3, CELSR2, VIT, ATXN2, PPP2R2C, DHX40, PTPN11, LRRTM4, RILPL2, PKN2-AS1, UGDH-AS1, CDKN2B-AS1, PPIEL, PDYN-AS1, HGF, UBAC2, GOT1, NSMCE1, IL6, RBFOX1, SYTL3, PPP4R2, TLR10, PAQR8, TRIM5, CREB3L1, EFHC1, OPN4, ACE, PCSK9, ALB, APOB, MTHFR, TNF, P2RY12, THBS1, CCL2, ARSA, IL1B, F2, HIF1A, TNFRSF11B, NOS3, FABP4, HMGB1, MMP2, LGALS3, ADIPOQ, CST3, SELENBP1, ADA, AHSG, APOE, RETN, CCHCR1, HMOX1, SHBG, STAT3, TLR4, PON1, MIR93, SELENOP, COPD, CXCL8, JAK2, KNG1, PTCRA, LIPC, PCYT1A, SLC5A2, S100A9, GDF15, FURIN, PLA2G7, BEST1, PTX3, CERNA3, AVP, FGF2, EDN1, CHI3L1, GCH1, CDKN1A, F11, ANGPT2, AGTR1, AGER, F2R, F10, DPP4, B2M, SGSM3, EIF3K, SETD2, PADI1, IL22, SDF4, IL1A, BFAR, CETN1, FXYD5, UGT1A1, AGGF1, ADI1, CHDH, ZNF415, ACSS2, ANGPTL8, CEBPA, CHRNA3, FGF21, PPARGC1A, CSF2, CS, ZEB2, NR1H4, CASP8AP2, SH2B3, ABCB6, IL18BP, PSMD14, FBLN5, TCFL5, ADAMTS13, SOSTDC1, ADAMTS5, ADAMTS7, PADI2, NLRP1, COX8A, TRS-AGA2-3, ANGPTL2, MAP3K8, CHRNB4, PLA2G15, FAM20C, SCARB1, SLC52A2, RTN4, MIR125A, ARG2, ABCC6, AR, TET3, PRSS55, APOH, APOA1, ANGPT1, MIRLET7G, MIR106B, MIR140, CSMD1, MIR15B, MIR18A, MIR29A, AGT, ACOD1, ADRB2, HLP, ADD1, ACR, CBSL, ALDH7A1, PWAR1, LRG1, NUS1, CD36, TBPL1, CD34, CD14, CBS, PPP1R2C, SLC2A10, CASR, ANGPTL6, SPRTN, ANTXR1, ZGPAT, SPZ1, TRIM63, ACCS, CAD, BLM, BCL2, CCND1, CARD16, ATP7B, CSF3, IL1RL1, CSTB, CX3CR1, NFE2L2, FOXO1, FGG, NPY, NPPB, NPPC, NPR3, NT5E, NUCB2, FGF1, FGB, SERPINA5, FAP, ENPP1, PECAM1, F13A1, ABCB1, PLG, PODXL, F12, PON3, MAPK1, EIF2AK2, FLNA, MYB, MTTP, LEP, SERPIND1, HARS1, IL10, IL18, GPX4, KDR, GNB3, IPO5, LAMP2, LDLR, GIP, FLT1, GABPA, FSHMD1A, MCAM, MFAP4, FOS, FN1, MMP9, MMP13, MPO, MT1B, PTGS1, PTGS2, F8, CYBB, TNFRSF1A, TNFRSF1B, TP53, CRISP2, DAPK3, CYP2C19, VCAM1, CYP2B6, CYP1A2, WRN, CUBN, TLR2, BRAP, YBX3, PRKRA, TNFSF11, NR1I2, TRPA1, CYBA, HGS, IFNG, ADGRG1, DECR1, THBS4, RAP2A, SFTPD, RBBP6, REN, SORT1, F3, SAA1, EPHB2, CXCL12, SELP, ENG, SRSF5, MARK2, ATN1, SHH, EDNRA, SLC25A1, SRD5A1, SRD5A2, SULT1E1, TAC1, DUSP5, TEK, TERF2, NAT2

Chondrodystrophy Wikipedia

Other probabilities for the other possible allele combinations concerning this gene are: 0% chance of affected offspring if only one parent is a carrier, 0% chance of affected offspring if one parent is affected and the other does not carry the allele, and 50% chance of affected offspring if one parent is affected and the other is a carrier. ... Percentage risk of inheritance [ edit ] Both average parents A couple already has a child with chondrodystrophy; the risk of inheritance for the next child to have the disorder is 0.1% (less than 1 in 1,000) The risk that the normal-statured child will have at least one offspring with this disorder is 0.01% (less than 1 in 10,000) One parent with chondrodystrophy and one parent without One child with normal height; the probability of that child having offspring with chondrodystrophy is 0.01% (less than 1 in 10,000) One child with normal stature; the probability of the next having chondrodystrophy is 50% (1 in 2) One child with normal stature; the probability of the next not having chondrodystrophy is 50% (1 in 2) Both parents with chondrodystrophy The probability of offspring affected by chondrodystrophy is 100% (4 in 4) The probability of offspring to be of normal size is 0% (0 in 4) Diagnosis [ edit ] There are several ways to determine if a child has chondrodystrophy, including parent testing and x-rays. ... Modification suggestions [ edit ] Height adjustments for goals and volleyball nets. Modified rules to accommodate size and structure.

ATF2, TGFB2, TGFBR1, ACAN, COL1A2, COL2A1, FGF4, IGF1, CUL7

Allergies In Cats Wikipedia

"Dermatologic manifestations and nutritional management of adverse food reactions" . dvm360.com . Retrieved 2017-11-29 . ^ Scott, D. (2001). ... Muller & Kirk's Small Animal Dermatology . pp. 543–666. doi : 10.1016/B978-0-7216-7618-0.50012-2 . ISBN 978-0-7216-7618-0 . ^ Carlotti, Didier N. (2013).

Glass Delusion Wikipedia

The Anatomy of Melancholy . ^ Burton, Com.1 Sec.3 comment no. 52 ^ de Cervantes, Miguel (1613). ... Meditations on First Philosophy . ISBN 0-87484-893-8 . ^ Locke J (1690) An Essay Concerning Humane Understanding .

Closed-Eye Hallucination Wikipedia

[Place of publication not identified]: Lulu Com. p. 201. ISBN 978-1105482885 . OCLC 939782198 . ^ Ladd, Trumbull (1894). ... Essay on the origin of thought . Ohio University Press. ISBN 0-8214-0156-4 . ^ Lilly, John C. (1990). ... Marion Boyars Publishers Ltd. ISBN 0-7145-0961-2 ^ Lilly, John C. (1981). The Deep Self: Profound Relaxation and the Tank Isolation Technique . Warner Books. ISBN 0-446-33023-X ^ Stephen LaBerge (1990).

Coarctation Of The Aorta Wikipedia

Philadelphia: Lippincott Williams & Wilkins. ISBN 978-0-7817-1433-4 . [ page needed ] ^ Cotran, R.; V. ... Robbins Pathologic Basis of Disease (7th ed.). W.B. Saunders. ISBN 978-0-8089-2302-2 . [ page needed ] ^ a b Völkl, Thomas M. ... Pearls of Wisdom. McGraw-Hill. ISBN 978-0-07-146431-4 . [ page needed ] ^ Pregerson, Brady (October 1, 2006). Quick Essentials: Emergency Medicine (2nd ed.). ED Insight Books. ISBN 978-0-9761552-7-0 . [ page needed ] ^ Aortic Coarctation Imaging at eMedicine ^ Nielsen, J. ... The Journal of Thoracic and Cardiovascular Surgery . 108 (3): 525–31. doi : 10.1016/S0022-5223(94)70264-0 . PMID 8078345 . Jenkins, N.P. (1999).

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Coarctation Of The Aorta Mayo_clinic

Overview The aorta is the largest artery in the body. It moves oxygen-rich blood from the heart to the rest of the body. Aortic coarctation (ko-ahrk-TAY-shun) is a narrowing of the aorta. It forces the heart to pump harder to move blood through the aorta. Coarctation of the aorta is generally present at birth (congenital heart defect). Symptoms can range from mild to severe. The condition might not be detected until adulthood. Coarctation of the aorta often occurs along with other congenital heart defects.
Critical Congenital Heart Disease Medlineplus

Critical congenital heart disease (CCHD) is a term that refers to a group of serious heart defects that are present from birth. These abnormalities result from problems with the formation of one or more parts of the heart during the early stages of embryonic development. CCHD prevents the heart from pumping blood effectively or reduces the amount of oxygen in the blood. As a result, organs and tissues throughout the body do not receive enough oxygen, which can lead to organ damage and life-threatening complications. Individuals with CCHD usually require surgery soon after birth. Although babies with CCHD may appear healthy for the first few hours or days of life, signs and symptoms soon become apparent.
Coarctation Of Aorta Omim

Gough (1961) described the anomaly in father and son. He found 6 other reports of familial coarctation. In a systematic study of coarctation, Boon and Roberts (1976) discerned familial aggregation with multifactorial inheritance. Recurrence risks in sibs was about 0.5% for coarctation and 1.0% for any form of congenital heart defect. Beekman and Robinow (1985) described coarctation of the aorta in 4 generations. In 2 members of the family, mother and son, in the third and fourth generations, the coarctation was minimal; in the mother, for example, a gradient in the aorta was demonstrated mainly after peak exercise.

Dogger Bank Itch Wikipedia

In Dogger Bank itch, sensitivity is acquired after repeated handling of the sea chervils that become entangled in fishing nets. [ citation needed ] The specific toxin responsible for the rash was determined to be the sulfur -bearing salt (2-hydroxyethyl) dimethylsulfoxonium chloride. [3] This salt is also found in some sea sponges and has potent in vitro activity against leukemia cells. [4] Treatment [ edit ] A study of two cases in 2001 suggests that the rash responds to oral ciclosporin . ... The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Bonnevie, P. (1948).

Torsades De Pointes Wikipedia

This effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel and, in some cases, augmentation of the late sodium channel . [12] Risk factors [ edit ] Lead II ECG showing a TdP patient being shocked by an implantable cardioverter-defibrillator back to their baseline cardiac rhythm The following is a partial list of factors associated with an increased tendency towards developing torsades de pointes: [13] Medications Hypokalemia (low serum potassium) Hypomagnesemia (low serum magnesium) Hypocalcemia (low serum calcium) Bradycardia (slow heartbeat) Heart failure Left ventricular hypertrophy Hypothermia Subarachnoid hemorrhage Hypothyroidism Pathophysiology [ edit ] Action potential of cardiac muscles can be broken down into five phases: Phase 0: Sodium channels open, resulting in the entrance of Na + into the cells; this results in the depolarization of the cardiac muscles. ... Phase 3: Calcium channels close (inward Ca ++ stops), but potassium channels are still open (outward K + current); this persists until the cells gain back normal polarization (repolarization achieved). Please note that phase 0 leads to a net gain of Na + , while phases 1-3 lead to a net loss of K + . ... Sanoski, Cynthia A.,, Deglin, Judith Hopfer, 1950- (Fourteenth ed.). Philadelphia. ISBN 978-0-8036-4085-6 . OCLC 881473728 . ^ Lenz T. ... United Kingdom: Elsevier. p. 568. ISBN 978-0-7020-3084-0 . ^ a b Yap, Yee Guan; Camm, A John (2017-01-17).

KCNH2, SCN5A, CYP3A4, KCNQ1, KCNE1, ANK2, KCNE2, NAA10, KCNJ5, SCN4B, SCN10A, SNTA1, ALG10B, CAV3, CALM2, CALM1, AKAP9, TRDN, C18orf21, NOS1AP, IL6, KCNK3, KCNA5, ATP12A, ATP4A, CYP19A1, KCNA4, ACE, SLC24A3, SLCO3A1, RAPGEF4, SLCO1B1, ATP5F1A, CRP, CYP2D6, NR1I2, TNF, SRL, SARDH, TLX2, HTR4, RYR2, RNPEP, ABCB1, ORM1, MSD, LBR, IL1A, ADRB1, IL1B, ADRA2C