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A number sign (#) is used with this entry because pachyonychia congenita-4 (PC4) is caused by heterozygous mutation in the KRT6B gene (148042) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Pachyonychia congenita (PC) is a rare genodermatosis predominantly featuring painful palmoplantar keratoderma, thickened nails, cysts and whitish oral mucosa. Epidemiology The prevalence is not known but approximately 1000 patients have been registered to date worldwide. Clinical description PC presents clinically as a spectrum of conditions. PC onset is variable with most cases manifesting soon after birth, others becoming clinically apparent only in late childhood and rarely in adulthood. The first signs of the disease usually are thickened nails or neonatal teeth.
Pachyonychia congenita (PC) is a rare inherited condition that primarily affects the nails and skin. The fingernails and toenails may be thickened and abnormally shaped . Affected people can also develop painful calluses and blisters on the soles of their feet and less frequently on the palms of their hands ( palmoplantar keratoderma ). Additional features include white patches on the tongue and inside of the mouth (leukokeratosis); bumps around the elbows, knees, and waistline (follicular hyperkeratosis); and cysts of various types including steatocystoma. Features may vary among affected people depending on their specific mutation.
For a phenotypic description and a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Inheritance Chong-Hai and Rajagopalan (1977) suggested autosomal recessive inheritance of pachyonychia congenita in a 4-year-old Malaysian girl with first-cousin parents, although they recognized new dominant mutation as a possibility. See also Sivasundram et al. (1985). INHERITANCE - Autosomal recessive HEAD & NECK Mouth - No oral leukoplakia SKIN, NAILS, & HAIR Skin - Horny papules (face, leg, buttocks) - No palmoplantar hyperkeratosis - No hyperhidrosis Nails - Episodic inflammatory swelling of nail bed - Recurrent shedding of nails - Hard,thickened nails (pachyonychia) - Subungual hyperkeratosis MISCELLANEOUS - See also pachyonychia congenita, type 3 (PC1, 167200 ) ▲ Close
A number sign (#) is used with this entry because pachyonychia congenita-3 (PC3) is caused by heterozygous mutation in the keratin-6a gene (KRT6A; 148041) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because of evidence that pachyonychia congenita-2 (PC2) is caused by heterozygous mutation in the KRT17 gene (148069) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Smith et al. (2005) identified keratin mutations in 30 probands from the International Pachyonychia Congenita Research Registry, including 8 patients with mutations in the KRT16 gene (see, e.g., 148067.0001-148067.0003 and 148067.0012).
Types, treatment methods, and prognosis". Postgrad Med . 73 (2): 161–8. doi : 10.1080/00325481.1983.11697763 . PMID 6823454 . ^ "Deaths in the district of Inveresk and Musselburgh in the County of Edinburgh" . Statutory Deaths 689/00 0032 . ScotlandsPeople . Retrieved 11 April 2015 . External links [ edit ] Classification D ICD-O : 8011/0, 8011/3 Wikimedia Commons has media related to Epithelioma .
Contents 1 Signs and symptoms 2 Cause 3 Diagnosis 3.1 Structure 4 Treatment 5 Prognosis 6 Epidemiology 7 See also 8 References 9 External links Signs and symptoms [ edit ] Cervical polyps often show no symptoms. [2] Where there are symptoms, they include intermenstrual bleeding, abnormally heavy menstrual bleeding ( menorrhagia ), vaginal bleeding in post- menopausal women, bleeding after sex and thick white vaginal or yellowish discharge ( leukorrhoea ). [3] [4] [5] [6] Cause [ edit ] The cause of cervical polyps is uncertain, but they are often associated with inflammation of the cervix. [7] They may also occur as a result of raised levels of estrogen or clogged cervical blood vessels. [3] Diagnosis [ edit ] Cervical polyps can be seen during a pelvic examination as red or purple projections from the cervical canal . [3] Diagnosis can be confirmed by a cervical biopsy which will reveal the nature of the cells present. [3] Structure [ edit ] Cervical polyps are finger-like growths, generally less than 1 cm in diameter. [3] [4] They are generally bright red in colour, with a spongy texture. [2] They may be attached to the cervix by a stalk (pedunculated) and occasionally prolapse into the vagina where they can be mistaken for endometrial polyps or submucosal fibroids . [4] Treatment [ edit ] Cervical polyps can be removed using ring forceps . [8] They can also be removed by tying surgical string around the polyp and cutting it off. [3] The remaining base of the polyp can then be removed using a laser or by cauterisation . [3] If the polyp is infected, an antibiotic may be prescribed. [3] Prognosis [ edit ] 99% of cervical polyps will remain benign and 1% will at some point show neoplastic change. [9] Cervical polyps are unlikely to regrow. [3] Epidemiology [ edit ] Cervical polyps are most common in women who have had children and perimenopausal women. [2] They are rare in pre-menstrual girls and uncommon in post-menopausal women. [6] See also [ edit ] Endometrial polyp References [ edit ] ^ Boon, Mathilde E.; Albert J. ... Lippincott Williams & Wilkins. pp. 254–256. ISBN 0-7817-3905-5 . ^ a b c d e f g h i Smith, Melanie N. (2006-05-10). ... Cambridge University Press . p. 77. ISBN 1-900151-51-0 . ^ Papadakis, Maxine A.; Stephen J. ... McGraw-Hill Professional. p. 60. ISBN 0-07-145892-1 . ^ a b Bosze, Peter; David M. ... Informa Health Care. p. 66. ISBN 963-00-7356-0 . ^ "Cervical Polyps" (PDF) .
Actual rates of hypoglycemia associated with a fibrous tumor are quite rare (a 1981 study of 360 solitary fibrous tumors of the lungs found that only 4% caused hypoglycemia [8] ), and are linked to large tumors with high rates of mitosis . [9] Removal of the tumor will normally resolve the symptoms. [1] [9] Tumors causing DPS tend to be quite large; [10] in one case a 3 kg (6.6 lb), 23×21×12 cm (9.1×8.3×4.7 in) mass was removed, sufficiently large to cause a collapsed lung . [5] In X-rays , they appear as a single mass with visible, defined borders, appearing at the edges of the lungs or a fissure dividing the lobes of the lungs. [10] Similar hypoglycemic effects have been related to mesenchymal tumors. [6] References [ edit ] ^ a b Balduyck B, Lauwers P, Govaert K, Hendriks J, De Maeseneer M, Van Schil P (July 2006). ... Exp. Clin. Endocrinol. Diabetes . 108 (8): 515–18. doi : 10.1055/s-2000-11007 . ... Surg . 119 (1): 185–7. doi : 10.1016/S0022-5223(00)70242-X . PMID 10612786 . Archived from the original on 2013-01-12. ^ a b Shields, TW; LoCicero J; Ponn RB; Rusch VW (2005). ... Hagerstwon, MD: Lippincott Williams & Wilkins. pp. 893 . ISBN 0-7817-3889-X . ^ Ellorhaoui M, Graf B (February 1976). ... Hagerstwon, MD: Lippincott Williams & Wilkins. pp. 172–3 . ISBN 978-0-7817-6957-0 . v t e Paraneoplastic syndromes Endocrine Hypercalcaemia SIADH Zollinger–Ellison syndrome Cushing's syndrome Hematological Multicentric reticulohistiocytosis Nonbacterial thrombotic endocarditis Neurological Paraneoplastic cerebellar degeneration Encephalomyelitis Limbic encephalitis Opsoclonus Polymyositis Transverse myelitis Lambert–Eaton myasthenic syndrome Anti-NMDA receptor encephalitis Musculoskeletal Dermatomyositis Hypertrophic osteopathy Mucocutaneous reactive erythema Erythema gyratum repens Necrolytic migratory erythema papulosquamous Acanthosis nigricans Ichthyosis acquisita Acrokeratosis paraneoplastica of Bazex Extramammary Paget's disease Florid cutaneous papillomatosis Leser-Trélat sign Pityriasis rotunda Tripe palms Other Febrile neutrophilic dermatosis Pyoderma gangrenosum Paraneoplastic pemphigus v t e Tumours of endocrine glands Pancreas Pancreatic cancer Pancreatic neuroendocrine tumor α : Glucagonoma β : Insulinoma δ : Somatostatinoma G : Gastrinoma VIPoma Pituitary Pituitary adenoma : Prolactinoma ACTH-secreting pituitary adenoma GH-secreting pituitary adenoma Craniopharyngioma Pituicytoma Thyroid Thyroid cancer (malignant): epithelial-cell carcinoma Papillary Follicular / Hurthle cell Parafollicular cell Medullary Anaplastic Lymphoma Squamous-cell carcinoma Benign Thyroid adenoma Struma ovarii Adrenal tumor Cortex Adrenocortical adenoma Adrenocortical carcinoma Medulla Pheochromocytoma Neuroblastoma Paraganglioma Parathyroid Parathyroid neoplasm Adenoma Carcinoma Pineal gland Pinealoma Pinealoblastoma Pineocytoma MEN 1 2A 2B
Hagerstown, MD: Lippincott Williams & Wilkins. p. 1150. ISBN 0-7817-2655-7 . Retrieved 2008-06-16 . ^ a b c d e f Scalea TM (2005). ... Boca Raton: CRC. pp. 26–32. ISBN 978-0-8493-8138-6 . Retrieved 2008-07-06 . ^ a b Porth, Carol (2007). ... Hagerstown, MD: Lippincott Williams & Wilkins. p. 838. ISBN 978-0-7817-7087-3 . Retrieved 2008-07-03 . ^ Pitkänen A, McIntosh TK (2006). ... Neurotrauma: New Insights Into Pathology and Treatment . Elsevier. pp. 13–19. ISBN 978-0-444-53017-2 . Retrieved 2008-06-10 . ^ a b Granacher RP (2007). ... Neuroscience . 101 (2): 289–95. doi : 10.1016/S0306-4522(00)00380-8 . PMID 11074152 . S2CID 20457228 . ^ Sauaia A, Moore FA, Moore EE, et al.
The coagulopathy can progress to disseminated intravascular coagulation and even death. [2] Hemolytic anemia secondary to microangiopathic destruction (physical damage) of the RBCs can be expressed as mild, moderate, or severe. [8] Diagnosis [ edit ] The diagnostic workup [8] is directed by the presenting signs and symptoms, and can involve: blood counts, clotting studies, and other laboratory testing imaging tests ( ultrasound , CT scan , MRI , sometimes angiography , and rarely nuclear medicine scans) Biopsy of the tumor is contraindicated due to risk of bleeding. ... Anticoagulant and antiplatelet medications can be used after careful assessment of the risks and benefits. [8] Definitive treatment [ edit ] Generally, treatment of the underlying vascular tumor results in resolution of Kasabach–Merritt syndrome. ... Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. p. 597. ISBN 978-0-7216-2921-6 . ^ a b c d e Hall G (2001). ... J Pediatr Surg . 23 (2): 109–11. doi : 10.1016/S0022-3468(88)80135-0 . PMID 3278084 . ^ a b c d Kasabach-Merritt Syndrome at eMedicine ^ Larsen, EC; Zinkham, WH; Eggleston, JC; Zitelli, BJ (June 1987). ... J Am Acad Dermatol . 42 (2 Pt 1): 225–35. doi : 10.1016/S0190-9622(00)90130-0 . PMID 10642677 . External links [ edit ] Classification D ICD - 10 : D69.5 ( ILDS D69.507) ICD - 9-CM : 287.39 OMIM : 141000 MeSH : D059885 DiseasesDB : 30701 SNOMED CT : 86635005 External resources eMedicine : med/1221 ped/1234 Orphanet : 2330
Animal Model In a mouse model of Kasabach-Merritt syndrome, Verheul et al. (1999) stimulated platelet production using Peg-rHuMGDF and observed a 7- to 8-fold increase in platelet counts and a significantly increased survival, with 50% of treated animals alive at 1 month versus none of the untreated controls.
Hemangioma thrombocytopenia syndrome is characterized by profound thrombocytopenia in association with two rare vascular tumors: kaposiform hemangioendotheliomas and tufted angiomas . The profound thrombocytopenia can cause life threatening bleeding and progress to a disseminated coagulopathy in patients with these tumors. The condition typically occurs in early infancy or childhood, although prenatal cases (diagnosed with the aid of ultrasonography), newborn presentations, and rare adult cases have been reported.
Kasabach-Merritt syndrome (KMS), also known as hemangioma-thrombocytopenia syndrome, is a rare disorder characterized by profound thrombocytopenia, microangiopathic hemolytic anemia, and subsequent consumptive coagulopathy in association with vascular tumors, particularly kaposiform hemangioendothelioma or tufted angioma.
Lack of awareness of the patient's predisposition to adverse effects (e.g. anxious patients and the elderly) and failure to attribute the adverse effects to the drug serves to compound the phobia. [8] [9] Starting at low doses and slowly increasing the medication dosage can avoid medication phobia secondary to adverse effects from developing. [9] Fears of medication use is also prevalent in people who have experienced unpleasant withdrawal effects from psychotropic drugs . [10] Sometimes patients wrongly associate symptoms of an acute disease or illness with medications used to treat the disease or illness. ... Clin Dermatol . 19 (1): 69–71. doi : 10.1016/S0738-081X(00)00215-7 . PMID 11369491 . ^ "Drugs that call for extra caution. ... New York: Simon Schuster. p. 56. ISBN 978-0-684-87309-1 . ^ M.d. Kamath, Bob (30 May 2007). ... Kendall Hunt Publishing. p. 25. ISBN 978-0-7872-8701-6 . ^ Ashton CH (2002).
Journal of Oral Pathology & Medicine . 37 (8): 504–10. doi : 10.1111/j.1600-0714.2008.00650.x . ... Kanski's clinical ophthalmology : a systematic approach (9th ed.). Edinburgh: Elsevier. ISBN 978-0-7020-7713-5 . OCLC 1131846767 . ^ a b c Lowry, R. ... United States Department of Health and Human Services . November 8, 2016. ^ a b Phillips, Jeffrey C.; del Bono, Elizabeth A.; Haines, Jonathan L.; Pralea, Anca Madalina; Cohen, John S.; Greff, Linda J.; Wiggs, Janey L. (1996). ... United States Department of Health and Human Services . November 8, 2016. ^ synd/1284 at Who Named It? ... Medical Intelligence Unit. Springer. doi : 10.1007/0-387-28672-1 . ISBN 978-0-387-28672-3 .
Nonocular features included characteristic facies (maxillary hypoplasia, short philtrum, and protruding lower lip of mild prognathism), dental anomalies (microdontia, hypodontia, and cone-shaped teeth), failure of involution of the umbilicus (often treated surgically in the neonatal period because of confusion with umbilical hernia), surgery for inguinal hernia in 8 persons, and hypospadias present in 4 males.
Axenfeld-Rieger syndrome (ARS) is a generic term used to designate overlapping genetic disorders, in which the major physical condition is anterior segment dysgenesis of the eye. Patients with ARS may also present with multiple variable congenital anomalies. Epidemiology The syndrome has an estimated prevalence of 1/200,000. Clinical description The clinical manifestations of ARS are highly variable. Features can be divided into ocular and non-ocular findings. Ocular abnormalities mainly affect the iris: hypoplasia, corectopia or hole formation in the iris mimicking polycoria; cornea: prominent and anteriorly displaced Schwalbe's line (posterior embryotoxon); and the chamber angle: iris strands bridging the iridocorneal angle to the trabecular meshwork. Eye dysgenesis in ARS may cause increased ocular pressure (IOP) leading to glaucoma.
Axenfeld-Rieger syndrome is a group of disorders that mainly affects the development of the eye. Common eye symptoms include cornea defects and iris defects. People with this syndrome may have an off-center pupil (corectopia) or extra holes in the eyes that can look like multiple pupils (polycoria). About 50% of people with this syndrome develop glaucoma, a condition that increases pressure inside of the eye, and may cause vision loss or blindness. Click here to view a diagram of the eye. Even though Axenfeld-Rieger syndrome is primarily an eye disorder, this syndrome can affect other parts of the body. Most people with this syndrome have distinctive facial features and many have issues with their teeth, including unusually small teeth (microdontia) or fewer than normal teeth (oligodontia).
Description Axenfeld-Rieger syndrome is a disorder of morphogenesis that results in abnormal development of the anterior segment of the eye, which results in blindness from glaucoma in approximately 50% of affected individuals. Systemic abnormalities, including cardiac and dental anomalies, are associated. For a general phenotypic description and a discussion of genetic heterogeneity and nomenclature of Axenfeld-Rieger syndrome, see RIEG1 (180500). Mapping Deletion of 13q14 was described in 2 cases of Rieger syndrome (Akazawa et al., 1981; Stathacopoulos et al., 1987). Phillips et al. (1996) performed linkage analysis of a large 4-generation family and demonstrated that Rieger syndrome was not linked to 4q25 but to markers on 13q14.
Ophthalmol. 114 (1): 35–44. doi : 10.1016/S0002-9394(14)77410-0 . PMID 1621784 . ^ Lisch W, Büttner A, Oeffner F, Böddeker I, Engel H, Lisch C, Ziegler A, Grzeschik K (October 2000). "Lisch corneal dystrophy is genetically distinct from Meesmann corneal dystrophy and maps to xp22.3". Am. J. Ophthalmol. 130 (4): 461–8. doi : 10.1016/S0002-9394(00)00494-3 .
Clinical Features Lisch et al. (1992) described 5 family members and 3 unrelated patients (4 males, 4 females), aged 23 to 71 years, with bilateral or unilateral, gray, band-shaped, and feathery opacities that sometimes appeared in whorled patterns. Retroillumination showed that the opacities consisted of intraepithelial, densely crowded, clear microcysts. Light and electron microscopy disclosed diffuse vacuolization of the cytoplasm of epithelial cells in the affected area. Visual acuity was so reduced in 3 patients that abrasion of the corneal epithelium was performed. The corneal abnormalities recurred within months, with the same reduction in visual acuity as before.
Lisch epithelial corneal dystrophy (LECD) is a very rare form of superficial corneal dystrophy characterized by feather-shaped opacities and microcysts in the corneal epithelium arranged in a band-shaped and sometimes whorled pattern, occasionally with impaired vision. Epidemiology Exact prevalence of this form of corneal dystrophy is not known but very few cases have been reported to date. LECD has been documented in one German family and in rare sporadic cases in Germany and the USA. Clinical description Lesions generally develop in childhood. Epithelial opacities are slowly progressive and painless blurred vision sometimes occurs after 60 years of age. Etiology The exact cause is unknown but appears to be genetic. The gene related to Lisch epithelial corneal dystrophy has been mapped to the short arm of the X chromosome (Xp22.3).
Rarely it is also caused by a skin infection surrounding the anus (perianal streptococcal dermatitis). [7] [8] Diagnosis [ edit ] Guttate psoriasis can typically be diagnosed by clinical examination alone. [9] Management [ edit ] The treatments used for plaque psoriasis can also be used for guttate psoriasis. ... Fitzpatrick's Dermatology in General Medicine (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James W, Berger T, Elston D (2005). Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Pardasani AG, Feldman SR, Clark AR (February 2000). ... Journal of the American Academy of Dermatology . 42 (5 Pt 2): 885–7. doi : 10.1016/s0190-9622(00)90263-9 . PMID 10767696 . ^ Mehlis S (2019). ... Archives of Dermatology . 132 (6): 717–8. doi : 10.1001/archderm.1996.03890300147032 .
Guttate psoriasis is a skin condition in which small, red, and scaly teardrop-shaped spots appear on the arms, legs, and middle of the body. It is a relatively uncommon form of psoriasis . The condition often develops very suddenly, and is usually triggered by an infection (e.g., strep throat, bacteria infection, upper respiratory infections or other viral infections). Other triggers include injury to the skin, including cuts, burns, and insect bites, certain malarial and heart medications, stress, sunburn, and excessive alcohol consumption. Treatment depends on the severity of the symptoms, ranging from at-home over the counter remedies to medicines that suppress the body's immune system to sunlight and phototherapy.
Springer Science & Business Media. pp. 423–. ISBN 978-1-84882-513-0 . ^ Merril D. Smith (8 September 2014). ... Rowman & Littlefield Publishers. pp. 73–. ISBN 978-0-7591-2332-8 . ^ Vasan; R.S. (1 January 1998). ... Biochemistry and Function of Sterols . CRC Press. pp. 26–27. ISBN 978-0-8493-7674-0 . ^ Michael Crocetti; Michael A. ... Lippincott Williams & Wilkins. pp. 564–. ISBN 978-0-7817-3770-8 . ^ W. Steven Pray (2006). ... Longo (8 November 2010). Cancer Chemotherapy and Biotherapy: Principles and Practice .
347 Strange Sightings, Incredible Occurrences, and Puzzling Physical Phenomena . Detroit: Visible Ink Press. ISBN 0-8103-9436-7 . ^ a b "At Night in Mattoon" . ... Borderlands: The ultimate exploration of the unknown . Overlook. ISBN 0-87951-724-7 . ^ Janet, Pierre (1965). ... Detroit: Visible Ink Press. pp. 239 . ISBN 0-8103-9436-7 . ^ Do Go On. "146 - The Mad Gasser of Mattoon" . ... New York: Paraview. ISBN 1-931044-84-8 . Maruna, Scott (2003). The Mad Gasser of Mattoon: Dispelling the Hysteria . Jacksonville, Ill.: Swamp Gas Book Co. ISBN 978-0-9728605-0-5 . Van Huss, William B. (2017) The Mad Gasser of Botetourt County ISBN 978-1979589246 External links [ edit ] "The Mad Gasser of Mattoon: how the press created an imaginary chemical weapons attack" from Skeptical Inquirer , 7/1/2002 Site with newspaper headlines and a list of victims and locations of incidents
Contents 1 Signs and symptoms 2 Pathophysiology 3 Diagnosis 4 Treatment 5 Prognosis 6 History 7 See also 8 References 9 External links Signs and symptoms [ edit ] The disease presents with the widespread formation of fluid-filled blisters that are thin walled and easily ruptured, and the patient can be positive for Nikolsky's sign . ... The Lancet . 156 (4011): 89–95. doi : 10.1016/S0140-6736(00)65681-7 . ^ Weisse, Martin E (31 December 2000). ... The Lancet . 357 (9252): 299–301. doi : 10.1016/S0140-6736(00)03623-0 . PMID 11214144 . S2CID 35896288 . ^ Powell, KR (January 1979). ... The Journal of Pediatrics . 78 (6): 958–67. doi : 10.1016/S0022-3476(71)80425-0 . PMID 4252715 . ^ Morens, David M; Katz, Alan R; Melish, Marian E (31 May 2001). ... The Lancet . 357 (9273): 2059. doi : 10.1016/S0140-6736(00)05151-5 . PMID 11441870 . S2CID 35925579 .
A rare staphylococcal toxemia caused by epidermolytic toxins of Staphylococcus aureus and characterized by the appearance of widespread erythematous patches, on which large blisters develop. Upon rupture of these blisters, the skin appears reddish and scalded. The lesions typically begin in the face and rapidly expand to other parts of the body. The disease may be complicated by pneumonia and sepsis. It most commonly affects newborns and infants.
Human African Trypanosomiasis (HAT), also called sleeping sickness, is a vector-borne parasitic disease caused by a protozoa of the Trypanosoma genus transmitted by the bite of a tsetse fly (genus Glossina ), that is found under its chronic form (average duration of 3 years) in western and central Africa (in case of the T. brucei gambiense sub-species), and under its acute form (lasting from few weeks to 6 months) in eastern and southern Africa (in case of the T. brucei rhodesiense sub-species). HAT comprises an initial hemo-lymphatic stage characterized by fever, weakness, musculoskeletal pain, anemia, and lymphadenopathy, along with dermatologic, cardiac and endocrine complications or hepatosplenomegaly, followed by a meningo-encephalitic stage characterized by neurologic involvement (sleep disturbances, psychiatric disorders, seizures) that progresses, in the absence of treatment, towards a fatal meningoencephalitis.
Characteristics [ edit ] Botellón usually begins around 11:00 p.m. and ends around 3:00 a.m. when many people move to a bar or club. ... In response to these problems, some municipal authorities have appointed special cleaning plans and attempted to charge participants a fine to offset the costs. [8] Economic issues : The higher cost of drinks in clubs and bars makes it difficult for young people with little or no income to go out to a bar or club and drink. ... Since botellón is usually a nighttime activity, Spain passed a law that prohibits stores to sell alcohol to the public after 10:00 p.m, hoping to persuade people to attend clubs or bars where alcohol must remain on site. [ citation needed ] However, the measure is a controversial one because people can still buy alcohol before the selling limit hour and consume it in public. ... CS1 maint: archived copy as title ( link ) ^ a b Mateo-Yanguas, Cristina (November 8, 2009). "Spanish teens fight for their right…to par-tay" . globalpost.com . ... CS1 maint: archived copy as title ( link ) ^ "Media España se cita en la Red para celebrar un macrobotellón el 17 de marzo" . 2006-03-07. ^ http://www.20minutos.es/noticia/97295/0/macrobotellones/ciudades/espana/ | Literally translated from Spanish ^ "El Ayuntamiento "no consentirá" el macrobotellón que se prepara en Moncloa" . 2006-03-07.
Its activity may be inhibited by warfarin . [8] It seems likely that warfarin induced embryotoxicity may be due at least in part to this inhibition. ... Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ Malou, E.; Gekas, J.; Troucelier-Lucas, V.; Mornet, E.; Razafimanantsoa, L.; Cuvelier, B.; Mathieu, M.; Thépot, F. (2001-02-01). ... Cytogenetic study and role of molecular biology]". Archives de Pédiatrie . 8 (2): 176–180. doi : 10.1016/S0929-693X(00)00181-0 . ... "Clinical and molecular analysis of arylsulfatase E in patients with brachytelephalangic chondrodysplasia punctata". Am. J. Med. Genet. A . 146A (8): 997–1008. doi : 10.1002/ajmg.a.32159 .
There is evidence of an increased grey matter volume in the left caudal intraparietal sulcus (IPS). [8] There was also found to be an increased grey matter volume in the right fusiform gyrus . ... Trends in Cognitive Sciences . 5 (1): 36–41. doi : 10.1016/S1364-6613(00)01571-0 . PMID 11164734 . S2CID 15092606 . ^ a b Jäncke, Lutz; Beeli, Gian; Eulig, Cornelia; Hänggi, Jürgen (March 2009). ... "Non-random associations of graphemes to colours in synaesthetic and non-synaesthetic populations". Cognitive Neuropsychology . 22 (8): 1069–85. doi : 10.1080/02643290500200122 . ... Journal of Consciousness Studies . 8 (12): 3–34. ^ Witthoft, N.; Winawer, N. (2006). ... Ninth IEEE International Symposium on Wearable Computers . pp. 108–113. doi : 10.1109/ISWC.2005.11 . ISBN 0-7695-2419-2 . S2CID 8221450 . Archived from the original (PDF) on 2007-03-29.
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State University of New York Press. ISBN 0-7914-5754-0 . ^ Jacobson, Kirsten. 2006. ... The Loss of Sadness . Oxford. ISBN 978-0-19-531304-8 . ^ Wilson, Mitchell. 1993. ... The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder . Oxford University Press. ISBN 978-0-19-531304-8 . Jung, Carl G. [1921] 1971. ... Jung 6). Princeton University Press. ISBN 0-691-01813-8 . —— 1966. Two Essays on Analytical Psychology , ( The Collected Works of C. ... Albany: State University of New York Press. ISBN 0-7914-5754-0 Winokur, Jon . 2005. Encyclopedia Neurotica.
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