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Pachyonychia Congenita Gene_reviews

International Pachyonychia Congenita Research Registry (IPCRR) Data Summary (as of 10 May 2017) View in own window Gene in Which Pathogenic Variants Were Confirmed KRT6A KRT6B KRT6C KRT16 KRT17 TOTAL Number evaluated for finding 1 304 71 22 247 130 774 Toenails thickened 10 toenails 286 (94%) 26 (37%) 0 (00%) 99 (40%) 100 (77%) 511 (66%) 7-9 toenails 9 (03%) 14 (20%) 0 (00%) 52 (21%) 11 (08%) 86 (11%) 4-6 toenails 2 (01%) 21 (30%) 3 (14%) 63 (26%) 7 (05%) 96 (12%) 1-3 toenails 4 (01%) 9 (13%) 10 (45%) 44 (18%) 8 (06%) 75 (10%) Total w/toenails thickened 301 (99%) 70 (99%) 13 (59%) 238 (96%) 126 (97%) 748 (97%) Age at onset Birth - <1 yr 264 (88%) 10 (14%) 1 (08%) 45 (19%) 92 (73%) 412 (54%) 1-4 yrs 33 (11%) 19 (27%) 6 (46%) 78 (33%) 24 (19%) 160 (21%) 5-14 yrs 4 (01%) 34 (49%) 4 (31%) 74 (31%) 10 (08%) 126 (17%) ≥15 yrs 0 (00%) 7 (10%) 2 (15%) 43 (18%) 1 (01%) 53 (07%) Fingernails thickened 10 fingernails 271 (89%) 4 (06%) 0 (00%) 73 (30%) 62 (48%) 410 (53%) 7-9 fingernails 10 (03%) 4 (06%) 0 (00%) 11 (04%) 13 (10%) 38 (05%) 4-6 fingernails 14 (05%) 17 (24%) 0 (00%) 30 (12%) 28 (22%) 89 (11%) 1-3 fingernails 6 (02%) 7 (10%) 0 (00%) 28 (11%) 9 (07%) 50 (06%) Total w/fingernails thickened 301 (99%) 32 (45%) 0 (00%) 142 (57%) 112 (86%) 587 (76%) Age at onset Birth - <1 yr 267 (89%) 4 (13%) 0 (00%) 33 (23%) 85 (76%) 389 (66%) 1-4 yrs 30 (10%) 8 (25%) 0 (00%) 42 (30%) 19 (17%) 99 (17%) 5-14 yrs 3 (01%) 11 (34%) 0 (00%) 34 (24%) 6 (05%) 54 (09%) ≥15 yrs 1 (00%) 10 (31%) 0 (00%) 34 (24%) 3 (03%) 48 (08%) Plantar keratoderma Always (never completely goes away) 254 (84%) 67 (94%) 19 (86%) 240 (97%) 86 (66%) 666 (86%) Sometimes (feet clear up completely at times) 7 (02%) 1 (01%) 0 (00%) 1 (00%) 14 (11%) 23 (03%) Seldom (feet usually clear of symptoms) 5 (02%) 0 (00%) 0 (00%) 0 (00%) 4 (03%) 9 (01%) Total w/plantar keratoderma 266 (88%) 68 (96%) 19 (86%) 241 (98%) 104 (80%) 698 (90%) Age at onset Birth - <1 yr 39 (15%) 2 (03%) 1 (05%) 23 (10%) 12 (12%) 77 (11%) 1-4 yrs 152 (57%) 23 (34%) 9 (47%) 130 (54%) 35 (34%) 349 (50%) 5-14 yrs 70 (26%) 42 (62%) 9 (47%) 82 (34%) 43 (41%) 246 (35%) ≥15 yrs 5 (02%) 1 (01%) 0 (00%) 8 (03%) 15 (14%) 29 (04%) Plantar pain w/plantar keratoderma 2 Often require medication for pain 65 (24%) 12 (18%) 5 (26%) 74 (31%) 19 (18%) 175 (25%) Very painful, but do not use medication 114 (43%) 32 (47%) 11 (58%) 111 (46%) 34 (33%) 302 (43%) Somewhat painful 77 (29%) 24 (35%) 3 (16%) 50 (21%) 36 (35%) 190 (27%) Total w/plantar keratoderma/pain 256 (96%) 68 (100%) 19 (100%) 235 (98%) 89 (86%) 667 (96%) Palmar keratoderma Always (never completely goes away) 86 (28%) 11 (15%) 2 (09%) 148 (60%) 21 (16%) 268 (35%) Sometimes (hands clear up completely at times) 32 (11%) 7 (10%) 1 (05%) 15 (06%) 22 (17%) 77 (10%) Seldom (hands usually clear of symptoms) 49 (16%) 13 (18%) 3 (14%) 22 (09%) 27 (21%) 114 (15%) Total w/palmar keratoderma 167 (55%) 31 (44%) 6 (27%) 185 (75%) 70 (54%) 459 (59%) Additional findings Oral leukokeratosis 269 (88%) 18 (25%) 4 (18%) 88 (36%) 34 (26%) 413 (53%) Cysts 188 (62%) 49 (69%) 4 (18%) 64 (26%) 121 (93%) 426 (55%) Follicular hyperkeratosis 162 (53%) 30 (42%) 0 (00%) 30 (12%) 86 (66%) 308 (40%) Natal or prenatal teeth 12 (04%) 0 (00%) 0 (00%) 0 (00%) 99 (76%) 111 (14%) 1.

KRT17, KRT16, KRT6A, KRT6B, KRT10, KRT6C, KRT80, SLURP1, PNOC, NFE2L2, AQP5, FLG, KRT1, KLKB1, GJB2, GABPA, MTOR, KRT9
- Pachyonychia Congenita 4 Omim
  
  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 Orphanet
  
  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 Gard
  
  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.
- Pachyonychia Congenita, Autosomal Recessive Omim
  
  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
- Pachyonychia Congenita 3 Omim
  
  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.
- Pachyonychia Congenita 2 Omim
  
  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.
- Pachyonychia Congenita 1 Omim
  
  A number sign (#) is used with this entry because pachyonychia congenita-1 (PC1) is caused by heterozygous mutation in the keratin-16 gene (KRT16; 148067) 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). Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita. PC type 1, the Jadassohn-Lewandowsky type, shows oral leukokeratosis.
African Trypanosomiasis Wikipedia

The World Health Organization plans to eradicate sleeping sickness by the year 2030. [37] [38] Trypanosoma brucei gambiense [39] 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 Angola 1498 2094 2406 1796 1274 2441 6726 8275 6610 5351 4546 4577 3621 3115 2280 1727 1105 648 517 247 211 154 70 69 36 35 19 18 79 30 Benin 0 0 2 1 0 0 0 0 0 20 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Burkina Faso 27 27 20 17 18 13 12 1 15 15 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 Cameroon 86 69 21 3 20 21 17 10 54 32 27 14 32 33 17 3 15 7 13 24 16 15 7 6 7 6 6 5 7 17 Central African Republic 308 197 362 262 368 676 492 730 1068 869 988 718 572 539 738 666 460 654 1194 1054 395 132 381 59 194 147 124 76 57 86 Chad 20 221 149 65 214 315 178 122 134 187 153 138 715 222 483 190 276 97 196 510 232 276 197 195 95 67 53 28 12 16 Congo 580 703 727 829 418 475 474 142 201 91 111 894 1005 717 873 398 300 189 182 87 87 61 39 20 21 36 18 15 24 17 Côte d'Ivoire 365 349 456 260 206 326 240 185 121 104 188 92 97 68 74 42 29 13 14 8 8 10 9 7 6 3 0 3 2 1 Democratic Republic of the Congo 7515 5825 7757 11384 19021 18182 19342 25094 26318 18684 16951 17300 13816 11459 10339 10249 8013 8155 7318 7178 5624 5590 5968 5647 3205 2351 1769 1110 660 604 Equatorial Guinea 63 36 45 30 85 37 46 67 62 28 16 17 32 23 22 17 13 15 11 7 8 1 2 3 0 0 3 4 4 3 Gabon 80 45 33 80 61 20 32 11 6 38 45 30 26 26 49 53 31 30 24 14 22 17 9 17 10 9 10 9 16 8 Ghana 3 6 16 0 0 0 1 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 Guinea 52 29 24 27 26 33 38 88 99 68 52 72 132 130 95 94 48 69 90 79 68 57 70 78 33 29 107 140 74 69 Mali 0 0 0 27 17 11 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Nigeria 24 0 0 0 0 0 0 0 0 27 14 14 26 31 10 21 3 0 0 0 2 3 2 0 0 0 1 0 0 0 South Sudan 67 58 28 62 69 56 157 737 1726 1312 1801 1919 3121 3061 1742 1853 789 469 623 373 199 272 317 117 63 45 17 12 17 11 Togo 2 0 0 0 0 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Uganda 2066 1328 2042 1764 1469 1062 981 1123 971 1036 948 310 604 517 378 311 290 120 198 99 101 44 20 9 9 4 4 0 1 2 Total 12756 10987 14088 16607 23266 23671 28736 36585 37385 27862 25841 26095 23799 19941 17100 15624 11372 10466 10380 9680 6973 6632 7091 6228 3679 2733 2131 1420 953 864 Trypanosoma brucei rhodesiense [40] 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 Kenya 91 8 4 2 1 0 2 5 14 22 15 10 11 0 0 0 1 0 0 1 0 0 2 0 0 0 0 0 0 0 Malawi 228 195 143 53 31 15 8 7 10 11 35 38 43 70 48 41 58 50 49 39 29 23 18 35 32 30 37 7 15 91 Mozambique 3 7 24 10 16 No data No data No data No data No data No data No data 1 No data 1 No data No data No data No data No data No data No data No data No data No data No data No data No data No data No data Uganda 1417 832 606 503 342 497 178 217 283 283 300 426 329 338 335 473 261 119 138 129 112 84 71 43 70 28 10 13 4 5 United Republic of Tanzania 187 177 366 262 319 422 400 354 299 288 350 277 228 113 159 186 127 126 59 14 5 1 4 1 1 2 3 3 0 3 Zambia 7 No data 4 1 1 1 3 No data No data 15 9 4 5 15 9 7 6 10 13 4 8 3 6 6 12 8 2 3 5 15 Zimbabwe No data No data No data No data 1 No data No data 9 No data No data No data No data No data No data No data 3 No data No data 0 3 2 4 9 1 3 3 1 1 0 2 Total 1933 1219 1147 831 710 935 591 583 606 619 709 755 617 536 552 707 453 305 259 187 154 111 101 85 115 68 52 27 24 116 History [ edit ] In 1903, David Bruce recognized the tsetse fly as the arthropod vector. ... The results showed efficacy and safety in both stages of the disease, both in adults and children ≥ 6 years old and weighing ≥ 20 kg. [56] The European Medicines Agency approved it for first and second stage disease outside of Europe in November 2018. [57] The treatment was approved in the DRC in December 2018. [58] Funding [ edit ] For current funding statistics, human African trypanosomiasis is grouped with kinetoplastid infections. ... Lancet . 380 (9859): 2095–128. doi : 10.1016/S0140-6736(12)61728-0 . hdl : 10536/DRO/DU:30050819 . PMID 23245604 . ... Parasites & Vectors . 8 : 236. doi : 10.1186/s13071-015-0851-0 . PMC 4436790 . PMID 25928366 . ^ a b Brun R, Blum J, Chappuis F, Burri C (January 2010). ... Cambridge University Press. p. 748. ISBN 978-0-521-22803-9 . Archived from the original on 18 March 2015. ^ Steverding D (March 2010).

NOS2, APOL1, TMPRSS11D, APBB3, SRA1, MSR1, IL10, LSAMP, LAMP3, HPR, NXT1, SERPINA1, IL6, ODC1, RMDN1, SMUG1, VSX2, MRPL28, STT3B, SUB1, MCF2L, SEC14L2, DNAJB1P1, TIMM10, CMTR2, RMDN3, SYBU, PAQR7, RMDN2, TUT1, TIMM9, NXF1, CDKN2B, GMPS, SLC9A6, DNAJB1, SARDH, DNAH8, FLNB, GAPDH, UTS2R, HLA-G, HP, PRMT1, IL1A, PEX16, IL1RN, CXCL10, STT3A, SRL, TNF, USO1, DDOST, NR1I2, H3P9
- African Trypanosomiasis Orphanet
  
  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.
Glycogen Storage Disease Type 0 Medlineplus

Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired. The signs and symptoms of muscle GSD 0 typically begin in early childhood. ... Because some people with muscle GSD 0 die from sudden cardiac arrest early in life before a diagnosis is made and many with liver GSD 0 have mild signs and symptoms, it is thought that GSD 0 may be underdiagnosed. Causes Mutations in the GYS1 gene cause muscle GSD 0, and mutations in the GYS2 gene cause liver GSD 0.

GYS2
- Glycogen Storage Disease 0, Liver Omim
  
  A number sign (#) is used with this entry because of evidence that liver glycogen storage disease-0 (GSD0A) is caused by homozygous or compound heterozygous mutation in the GYS2 gene (138571), which encodes glycogen synthase-2, on chromosome 12p12. ... Mapping Orho et al. (1998) established linkage of glycogen storage disease 0 to intragenic and flanking polymorphic markers of the GYS2 gene on chromosome 12p12.2. Molecular Genetics In affected members of 5 families with liver glycogen storage disease 0, Orho et al. (1998) identified homozygous or compound heterozygous mutations in the GYS2 gene (138571.0001-138571.0008) Inheritance - Autosomal recessive Neuro - Seizures Lab - Glycogen synthetase deficiency Metabolic - Neonatal hypoglycemia - Fasting hypoglycemia - Fasting hyperketonemia - Hyperglycemia and hyperlactatemia with feeding ▲ Close
- Glycogen Storage Disease Due To Hepatic Glycogen Synthase Deficiency Orphanet
  
  A genetically inherited anomaly of glycogen metabolism and a form of glycogen storage disease (GSD) characterized by fasting hypoglycemia. This is not a glycogenosis, strictly speaking, as the enzyme deficiency decreases glycogen reserves. Epidemiology It is an extremely rare disease; about 20 cases have been reported in the literature so far. Clinical description It commonly appears in infancy or in early childhood. Patients present with morning fatigue and fasting hypoglycemia (without hepatomegaly) associated with hyperketonemia but without hyperalaninemia or hyperlactacidemia.
- Glycogen Storage Disease Type 0, Liver Gard
  
  Glycogen storage disease type 0, liver (liver GSD 0), a form of glycogen storage disease (GSD), is a rare abnormality of glycogen metabolism (how the body uses and stores glycogen, the storage form of glucose). Unlike other types of GSD, liver GSD 0 does not involve excessive or abnormal glycogen storage, and causes moderately decreased glycogen stores in the liver. ... This condition differs from another form of GSD 0 which chiefly affects the muscles and heart ( Glycogen storage disease type 0, muscle ) and is thought to be caused by mutations in the GYS1 gene.
Primary Cutaneous Adenoid Cystic Carcinoma Wikipedia

Andrews' Diseases of the Skin: Clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... "Primary cutaneous adenoid cystic carcinoma". J. Am. Acad. Dermatol . 58 (4): 636–41. doi : 10.1016/j.jaad.2007.12.005 .

MYBL1
Cervical Polyp Wikipedia

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) .

BMI1, CDKN2A, COMMD3-BMI1
Glycogen Storage Disease Type 0 Wikipedia

Glycogen storage disease type 0 Glycogen storage disease type 0 has defect in glycogen synthase Specialty Medical genetics Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). ... Serum electrolytes calculate the anion gap to determine presence of metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an anion gap in the reference range and no acidosis. ... In patients with glycogen-storage disease type 0, hyperlipidemia is absent or mild and proportional to the degree of fasting. ... In patients with glycogen-storage disease type 0, urine ketones findings are positive, and urine-reducing substance findings are negative. ... The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [2] Mortality/Morbidity [ edit ] The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency.

GYS2, CPLANE1
Severe Acute Respiratory Syndrome Wikipedia

While diarrhea is common in people with SARS, the fecal–oral route does not appear to be a common mode of transmission. [9] The basic reproduction number of SARS-CoV, R 0 , ranges from 2 to 4 depending on different analyses. ... As a result of quarantine procedures, some of the post-SARS patients have been documented as suffering from post-traumatic stress disorder (PTSD) and major depressive disorder . [31] [32] Epidemiology [ edit ] Main article: 2002–2004 SARS outbreak SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%. [4] The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient. [9] Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%). [33] As with MERS and COVID-19 , SARS resulted in significantly more deaths of males than females. 2003 Probable cases of SARS – worldwide Probable cases of SARS by country or region, 1 November 2002 – 31 July 2003 [34] Country or region Cases Deaths Fatality (%) China [a] 5,327 349 6.6 Hong Kong 1,755 299 17.0 Taiwan [b] 346 73 [35] [36] 21.1 Canada 251 43 17.1 Singapore 238 33 13.9 Vietnam 63 5 7.9 United States 27 0 0 Philippines 14 2 14.3 Thailand 9 2 22.2 Germany 9 0 0 Mongolia 9 0 0 France 7 1 14.3 Australia 6 0 0 Malaysia 5 2 40.0 Sweden 5 0 0 United Kingdom 4 0 0 Italy 4 0 0 Brazil 3 0 0 India 3 0 0 South Korea 3 0 0 Indonesia 2 0 0 South Africa 1 1 100.0 Colombia 1 0 0 Kuwait 1 0 0 Ireland 1 0 0 Macao 1 0 0 New Zealand 1 0 0 Romania 1 0 0 Russia 1 0 0 Spain 1 0 0 Switzerland 1 0 0 Total excluding China [a] 2,769 454 16.4 Total (29 territories) 8,096 774 9.6 ^ a b Figures for China exclude Hong Kong and Macau, which are reported separately by the WHO . ^ After 11 July 2003, 325 Taiwanese cases were 'discarded'. ... He also persuaded the Vietnamese Health Ministry to begin isolating patients and screening travelers, thus slowing the early pace of the epidemic. [55] He subsequently contracted the disease himself, and died in March 2003. [56] [57] The CDC and Canada's National Microbiology Laboratory identified the SARS genome in April 2003. [58] [59] Scientists at Erasmus University in Rotterdam , the Netherlands demonstrated that the SARS coronavirus fulfilled Koch's postulates thereby suggesting it as the causative agent.

ACE, CXCL6, CXCL1, ACE2, SARS1, VTN, CDSN, SARS2, MBL2, SH2D3A, CXCL10, HLA-A, TMPRSS2, IFNG, CLEC4M, IL6, MX1, IFNB1, HLA-DRB1, MBL3P, CCL2, TNF, OAS1, MYOM2, CCL5, HLA-B, NLRP3, IL10, BST2, IL2, IFNA13, IFNA1, RBM45, ERVK-6, SPECC1, GPT, CD209, EGFR, ERVK-32, MERTK, EBI3, POLDIP2, LINC01672, THPO, COPD, RNF19A, TPO, TRAF3, UBE2I, CBLL2, TRIM25, AIMP2, BCAR3, IL18R1, MUL1, IFIH1, ADAM17, GRAP2, NPIPB3, TMPRSS11D, RIPK3, BAG3, SDS, ISG15, FGL2, MASP2, CKLF, AHSA1, PRRT2, SOCS3, ABCA4, SULT1E1, CR1, FN1, FCER2, ESR1, CTSL, CTRL, MAPK14, CRK, ATF2, CREB1, MAP3K8, RTN2, CD14, CASP3, CASP1, CALR, BCL2L1, B2M, ANPEP, AHSG, AGT, GAPDH, GNL1, GOT1, GPER1, BRD2, RNASEL, RNASE2, RB1, PLAAT4, MAPK1, ACRV1, PRKCA, PPIA, PI4KB, PRKN, NM, NFIC, MIP, IRF3, IL12RB1, CXCL8, IFN1@, ICAM3, PRKCB
- Severe Acute Respiratory Syndrome (Sars) Mayo_clinic
  
  Overview Severe acute respiratory syndrome (SARS) is a contagious and sometimes fatal respiratory illness. severe acute respiratory syndrome (SARS) first appeared in China in November 2002. Within a few months, SARS spread worldwide, carried by unsuspecting travelers. SARS showed how quickly infection can spread in a highly mobile and interconnected world. On the other hand, a collaborative international effort allowed health experts to quickly contain the spread of the disease. There has been no known transmission of SARS anywhere in the world since 2004.
- Severe Acute Respiratory Syndrome Orphanet
  
  A rare pulmonary disease induced by SARS-CoV coronavirus infection, with a reported incubation period varying from 2 to 7 days. Patients present flu-like symptoms, including fever, malaise, myalgia, headache, diarrhoea, and rigors. Dry, nonproductive, cough and dyspnea are frequently reported. Severe cases evolve rapidly, progressing to respiratory distress and failure, requiring intensive care. Mortality rate is 10%. The disease appeared in 2002 in southern China, subsequently spreading in 2003 to 26 countries. Reported human-to-human transmission occurred in Toronto (Canada), Hong Kong Special Administrative Region of China, Chinese Taipei, Singapore, and Hanoi (Viet Nam).
Scrupulosity Wikipedia

J Anxiety Disord . 2008;22(6):1042–58. doi : 10.1016/j.janxdis.2007.11.004 . ... Religion and Psychiatry: Beyond Boundaries . Wiley; 2010. ISBN 978-0-470-69471-8 . p. 211–33. ^ Ciarrocchi JW. ... Mahwah, NJ: Paulist Press; 1995. ISBN 0-8091-3553-1 . Scruples: common and uncommon. p. 32–47. ^ a b Taylor CZ. ... Mahwah, NJ: Paulist Press; 1999. ISBN 0-8091-3771-2 . p. 209–18. ^ Monahan J. ... Crossroad Publishing; 1997. ISBN 0-8245-1605-2 . Shapiro, Leslie (2015).
Paraphilic Infantilism Wikipedia

John Wiley and Sons. p. 719 . ISBN 978-0-470-57712-7 . ^ Becker, Judith V.; Stinson, Jill D. (2008). ... John Wiley & Sons . pp. 522 . ISBN 978-0-470-25721-0 . ^ Money 1986 , p. 290 . ^ Money 1986 , p. 34 . ^ Money, J. (1984). ... Prometheus Books . p. 147. ISBN 978-0-87975-277-4 . ^ Wilson, Glen Daniel (1987). ... Taylor and Francis. pp. 107–11 . ISBN 978-0-7099-3698-5 . ^ Kaufman, F (1997). ... Washington Square Press. ISBN 978-0-87140-840-2 . Further reading [ edit ] Love, B (1992).
Breast Fetishism Wikipedia

Greenwood Publishing Group. ISBN 978-0-313-31520-6 , p. 402. ^ Miller, Laura. (2006). ... University of California Press. ISBN 978-0-520-24509-9 ^ Latteier 1998 ^ Buss, David (2019). ... El Rio, TX: Hauck Pub Co. ISBN 978-0-9621797-2-3 . ^ McDonough, Jimmy (2005). ... University of California Press. ISBN 978-0-520-24509-9 ^ Latteier 1998 Further reading [ edit ] Block, Susan (2004). ... The Breast Fetish (pg. 29). Palgrave Macmillan. ISBN 0-312-22129-0 . Glazier, Stephen D. ; Flowerday, Charles (2003).
Dependent Personality Disorder Wikipedia

Springer, Boston, MA. pp. 230–237. doi : 10.1007/978-0-387-28370-8_22 . ISBN 978-0-387-28369-2 . ^ a b Coolidge, F.L.; Thede, L.; Jang, K.L. (2 December 2013). ... Springer, Boston, MA. pp. 230–237. doi : 10.1007/978-0-387-28370-8_22 . ISBN 978-0-387-28369-2 . ^ Nolen-Hoeksema, Susan (2014). ... New York: Guilford Press. ISBN 978-0-89862-434-2 . Millon, Theodore; Davis, Roger Dale (1996). ... Personality Disorders in Modern Life . Wiley. ISBN 978-0-471-66850-3 . Millon, Theodore (2006). ... Diagnosis and Treatment of the Personality Disorders . Ishiyaku EuroAmerica. ISBN 978-0-912791-89-0 . Ellison, J. M.; Adler, D.

DRD4
Estrogen-Dependent Condition Wikipedia

Jaypee Brothers Publishers. 2007. pp. 347–. ISBN 978-81-8061-996-0 . ^ Leonard J. Deftos (1 January 1998). ... 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). ... Elsevier Health Sciences. pp. 1281–. ISBN 978-0-323-08678-3 . ^ Guy I. Benrubi (28 March 2012).
Androgen-Dependent Condition Wikipedia

Neonatal Skin: Structure and Function . CRC Press. pp. 67–. ISBN 978-0-8247-0887-0 . ^ Mariagrazia Stracquadanio; Lilliana Ciotta (20 April 2015). ... A Woman Doctor's Guide to Skin Care: Essential Facts and Information on Keeping Skin Healthy . Hyperion. ISBN 978-0-7868-8100-0 . ^ Sarah Bekaert (2007). ... CUP Archive. pp. 321–. ISBN 978-0-521-22673-8 . ^ Raphael Rubin; David S. ... Lippincott Williams & Wilkins. pp. 816–. ISBN 978-0-7817-9516-6 . ^ Andrea Dunaif; R. ... Academic Press. 3 October 1994. pp. 1994–. ISBN 978-0-08-058373-0 . Further reading [ edit ] Shukla, G.
Laryngotracheoesophageal Cleft Type 0 Orphanet

Laryngo-tracheo-esophageal cleft (LC) type 0 is a congenital respiratory tract anomaly characterized by a submucosal laryngo-tracheo-esophageal cleft with minor symptoms or an asymptomatic course. ... Clinical description Subjects with type 0 LC may have no obvious symptoms or mild symptoms such as occasional aspirations.
Doege–potter Syndrome Wikipedia

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
Hydroa Vacciniforme Wikipedia

Feb, 42(2 Pt 1) (2): 208–13. doi : 10.1016/s0190-9622(00)90127-0 . PMID 10642674 . ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Rezk SA, Zhao X, Weiss LM (September 2018).

CD4, CCR4, GATA2, PLK2
- Hydroa Vacciniforme Orphanet
  
  A rare photodermatosis characterized by the development of pruritic or painful vesicles in a photodistributed pattern in response to sunlight exposure. The lesions heal with permanent varioliform scarring. Ocular involvement, deformities of ears and nose, or contractures of the fingers may occasionally be observed. Systemic signs and symptoms are absent. The condition typically occurs in childhood and regresses spontaneously in adolescence or young adulthood.
Nevus Comedonicus Wikipedia

Louis: Mosby. p. 1673. ISBN 1-4160-2999-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . This Epidermal nevi, neoplasms, cysts article is a stub .

NEK9, IL6, AKT1, SRD5A2, MIR511, PCSK9, ASXL1, ABCA12, MCF2L, JMJD6, PRSS21, VEGFA, TOP2A, TOP1, TNFAIP6, TNF, SKP2, BAX, CCL4, PTH, POMC, PECAM1, OPRL1, LRP2, KRT15, KRT10, IL7R, CYP21A2, CASP3, BCL2, MIR146B
- Nevus Comedonicus Omim
  
  A number sign (#) is used with this entry because of evidence that nevus comedonicus (NC) is caused by somatic mutation in the NEK9 gene (609798) on chromosome 14q24. Description Nevus comedonicus (NC) is a rare type of epidermal nevus with predilection for the face and neck area. The condition develops within the first decade of life in most patients. NC is characterized by dilated, plugged follicular ostia containing lamellar keratinaceous material and grouped in a honeycomb pattern; the distribution of lesions may be unilateral, bilateral, linear, interrupted, segmental, or along the lines of Blaschko. NC may be nonpyogenic with an acne-like appearance or associated with the formation of cysts, papules, pustules, and abscesses.
- Nevus Comedonicus Syndrome Orphanet
  
  A rare, syndromic nevus characterized by the association of typically unilateral, closely arranged, linear, slightly elevated, multiple, nevus comedonicus lesions located usually on the face, neck, trunk or limbs (with or without a central, dark, firm, hyperkeratotic plug and secondary acneiform lesions) with extracutaneous ocular, skeletal, and/or central nervous system abnormalities, such as ipsilateral cataract, corneal erosion, poly-/syndactyly, absent fifth finger, scoliosis, vertebral defects, corpus callosum agenesis, seizures, interhemispheric cyst, intellectual deficiency, and/or developmental delay.
- Nevus Comedonicus Syndrome Wikipedia
  
  Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . External links [ edit ] Classification D ICD - 10 : Q82.5 OMIM : 617025 External resources Orphanet : 64754 This Epidermal nevi, neoplasms, cysts article is a stub .
Acephalgic Migraine Wikipedia

Lippincott Williams & Wilkins. p. 1152. ISBN 0-7817-7513-2 . ^ Pryse-Phillips, William (2003). ... Oxford University Press US. p. 587. ISBN 0-19-515938-1 . ^ Bradley, Walter George (2004). ... Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... Lippincott Williams & Wilkins. p. 1289. ISBN 0-7817-4811-9 . ^ a b Loder, Elizabeth; Dawn A. ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007).
Persistent Left Superior Vena Cava Wikipedia

.), "92 - Anomalies of Systemic Venous Return" , Obstetric Imaging: Fetal Diagnosis and Care (Second Edition) , Elsevier, pp. 411–414.e1, doi : 10.1016/b978-0-323-44548-1.00092-9 , ISBN 978-0-323-44548-1 , retrieved 2020-11-16 ^ a b c Fligner, Corinne L.; Clark, John I.; Clark, Judy M.; Larson, Lyle W.; Poole, Jeanne E. (2018-01-01), Poole, Jeanne E.; Larson, Lyle W. (eds.), "2 - Surgical Anatomy for the Implanting Physician" , Surgical Implantation of Cardiac Rhythm Devices , Elsevier, pp. 13–58, doi : 10.1016/b978-0-323-40126-5.00002-1 , ISBN 978-0-323-40126-5 , retrieved 2020-11-16 ^ Berg C, Knüppel M, Geipel A, et al.

RBM10, HTC2
Neurosis Wikipedia

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. ... New York: Anchor Books / Doubleday . ISBN 0-385-05221-9 . Ladell, R. M., and T. ... Albany: State University of New York Press. ISBN 0-7914-5754-0 Winokur, Jon . 2005. Encyclopedia Neurotica. ISBN 0-312-32501-0 . External links [ edit ] Classification D ICD - 10 : F40 - F40.8 Library resources about Neurosis Resources in your library Resources in other libraries Janov, Arthur (1991).

GPC6, NKAIN2, MDGA2, ABO, COMT, CRP, NHS