• FindZebra
  • About
  • Contact
  • Help
  • Login
Advanced
  • Nosebleed Wikipedia
    Pronunciation Epistaxis / ˌ ɛ p ɪ ˈ s t æ k s ɪ s / EP -ih- STAK -sis Specialty Otorhinolaryngology Symptoms Bleeding from the nose [1] Usual onset Less than 10 and over 50 years old [2] Risk factors Trauma, Excessive Nose-picking , Certain infections , blood thinners , high blood pressure , alcoholism , seasonal allergies , dry weather [3] Diagnostic method Direct observation [1] Differential diagnosis Bleeding from the lungs , esophageal varices [1] Prevention Petroleum jelly in the nose [4] Treatment Pressure over the lower half of the nose, nasal packing , endoscopy [5] Medication Tranexamic acid [6] Frequency 60% at some point in time [7] Deaths Rare [3] A nosebleed , also known as epistaxis , is bleeding from the nose . [1] Blood can also flow down into the stomach and cause nausea and vomiting . [8] In more severe cases blood may come out of both nostrils . [9] Rarely bleeding may be so significant low blood pressure occurs. [1] Rarely the blood can come up the nasolacrimal duct and out from the eye. [10] Risk factors include trauma including putting the finger in the nose, blood thinners , high blood pressure , alcoholism , seasonal allergies , dry weather, and inhaled corticosteroids . [3] There are two types: anterior, which is more common; and posterior, which is less common but more serious. [3] Anterior nosebleeds generally occur from Kiesselbach's plexus while posterior bleeds generally occur from the sphenopalatine artery . [3] The diagnosis is by direct observation. [1] Prevention may include the use of petroleum jelly in the nose. [4] Initially treatment is generally by applying pressure for at least five minutes over the lower half of the nose. [5] If this is not sufficient nasal packing may be used. [5] Tranexamic acid may also be helpful. [6] If bleeding episodes continue endoscopy is recommended. [5] About 60% of people have a nosebleed at some point in their life. [7] About 10% of nosebleeds are serious. [7] Nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999. [11] Nosebleeds most commonly affect those younger than 10 and older than 50. [2] Contents 1 Cause 2 Pathophysiology 3 Prevention 4 Treatment 4.1 Nasal packing 4.2 Tranexamic acid 4.3 Cauterization 4.4 Surgery 4.5 Other 5 Society and culture 5.1 Etymology 6 References 7 External links Cause [ edit ] Two children boxing , the one on the right having a nosebleed due to a punch to the face. ... PMID 24439881 . ^ a b c d Tunkel, David E.; Anne, Samantha; Payne, Spencer C.; Ishman, Stacey L.; Rosenfeld, Richard M.; Abramson, Peter J.; Alikhaani, Jacqueline D.; Benoit, Margo McKenna; Bercovitz, Rachel S.; Brown, Michael D.; Chernobilsky, Boris; Feldstein, David A.; Hackell, Jesse M.; Holbrook, Eric H.; Holdsworth, Sarah M.; Lin, Kenneth W.; Lind, Meredith Merz; Poetker, David M.; Riley, Charles A.; Schneider, John S.; Seidman, Michael D.; Vadlamudi, Venu; Valdez, Tulio A.; Nnacheta, Lorraine C.; Monjur, Taskin M. (7 January 2020). ... Retrieved January 31, 2010 . ^ J. F. Lubianca Neto; F. D. Fuchs; S. R. Facco; M. Gus; L. Fasolo; R. Mafessoni; A. ... E.; Williams, R. J.; Kuhn, I.; Carrie, S. (December 2017). "Intranasal packs and haemostatic agents for the management of adult epistaxis: systematic review". ... Classification D ICD - 10 : R04.0 ICD - 9-CM : 784.7 MeSH : D004844 DiseasesDB : 18327 External resources MedlinePlus : 003106 eMedicine : emerg/806 ent/701 Patient UK : Nosebleed v t e Symptoms and signs relating to the respiratory system Auscultation Stethoscope Respiratory sounds Stridor Wheeze Crackles Rhonchi Stertor Squawk Pleural friction rub Fremitus Bronchophony Terminal secretions Elicited findings Percussion Pectoriloquy Whispered pectoriloquy Egophony Breathing Rate Apnea Prematurity Dyspnea Hyperventilation Hypoventilation Hyperpnea Tachypnea Hypopnea Bradypnea Pattern Agonal respiration Biot's respiration Cheyne–Stokes respiration Kussmaul breathing Ataxic respiration Other Respiratory distress Respiratory arrest Orthopnea / Platypnea Trepopnea Aerophagia Asphyxia Breath holding Mouth breathing Snoring Other Chest pain In children Precordial catch syndrome Pleurisy Nail clubbing Cyanosis Cough Sputum Hemoptysis Epistaxis Silhouette sign Post-nasal drip Hiccup COPD Hoover's sign asthma Curschmann's spirals Charcot–Leyden crystals chronic bronchitis Reid index sarcoidosis Kveim test pulmonary embolism Hampton hump Westermark sign pulmonary edema Kerley lines Hamman's sign Golden S sign Authority control GND : 4171181-6 NDL : 00560692
    ACVRL1, DNAH11, ZBTB16, WIPF1, WAS, VWF, TERT, TERC, TBXAS1, TBXA2R, STIM1, STAT5B, STAT3, RARA, PRTN3, PRKAR1A, PRKACG, PRF1, PML, GFI1B, FCGR2C, CACNA1D, RASGRP2, IRF2BP2, SLFN14, MCFD2, HPS4, DTNBP1, FIP1L1, HPS6, TBL1XR1, NABP1, P2RY12, BCOR, TET2, GP6, SBDS, PTPN22, NBEAL2, HPS5, PLAU, NUMA1, NPM1, MYH9, FGB, FGA, F13B, F13A1, F11, F10, F7, F5, F2, ETV6, EPOR, ENG, CYP11B2, CYP11B1, CTLA4, LYST, RUNX1, FGG, FYB1, GATA1, IFNG, MYD88, MPL, SMAD4, KCNJ5, JAK2, ITGB3, ITGA2B, HPS1, GBA, HLA-DPB1, HLA-DPA1, GP9, GP1BB, GP1BA, GGCX, GDF2, BLOC1S3
  • Leber Congenital Amaurosis Wikipedia
    . ^ a b Cideciyan AV, Hauswirth WW, Aleman TS, Kaushal S, Schwartz SB, Boye SL, et al. (August 2009). ... P.; Ardinger, H. H.; Pagon, R. A.; Wallace, S. E.; Bean LJH; Stephens, K.; Amemiya, A. (1993). ... PMID 20301475 . ^ Perrault I, Rozet JM, Calvas P, Gerber S, Camuzat A, Dollfus H, et al. (December 1996). ... Retrieved 2007-09-21 . ^ Dharmaraj S, Li Y, Robitaille JM, Silva E, Zhu D, Mitchell TN, et al. ... S2CID 27501557 . ^ Perrault I, Hanein S, Zanlonghi X, Serre V, Nicouleau M, Defoort-Delhemmes S, et al.
    RPGRIP1, CRX, CRB1, NMNAT1, RPE65, AIPL1, CEP290, IQCB1, LCA5, SPATA7, TULP1, KCNJ13, LRAT, IMPDH1, RD3, GUCY2D, RDH12, USP45, GDF6, MERTK, IFT140, PCYT1A, MPP5, ABCA4, CLUAP1, USH2A, SLC38A8, CDHR1, GRM6, RP2, AHI1, PDE6A, CNGB3, GIGYF2, ZFYVE26, NR2E3, RGS9, CRB2, LCA10, OTX2, CLTA, PTPRC, MYO7A, CNGA3, CCT2, GUCA1A, PRPH2, IMPG1, CABP4, GUCY2F, SLC7A14, GUCA1B, LPCAT1, HSD17B6, ENO2, CNTLN, PSMD13, PRPH, GUCY2EP, BCL2, MIR204, EGF, SP4, RPGR, NUB1, ADH7, NRL, TUB, ND4, FST, SLC19A2, PRPF8, PNPLA6, CILK1, NINL, SERPINF1, RPGRIP1L, MEF2C, TAP2, MEF2A, ELOVL4, IMPG2, PDE6B
    • Leber Congenital Amaurosis 17 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-17 (LCA17) is caused by compound heterozygous mutation in the GDF6 gene (601147) on chromosome 8q22. For a general phenotypic description and a discussion of genetic heterogeneity of Leber congenital amaurosis (LCA), see LCA1 (204000). Clinical Features Asai-Coakwell et al. (2013) studied a female LCA patient with compound heterozygous mutations in the GDF6 gene who had vision limited to detection of hand motions, with an extinguished electroretinogram (ERG) typical of the LCA phenotype. She did not have other ocular or systemic phenotypes, but the authors noted that she had not undergone radiologic imaging to detect milder GDF6-induced skeletal disease. Evaluation of her clinically unaffected mother revealed a delayed rod b-wave implicit time on ERG; similarly, her apparently unaffected father showed reduced b-wave amplitude.
    • Leber Congenital Amaurosis 12 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-12 (LCA12) is caused by homozygous mutation in the RD3 gene (180040) on chromosome 1q32. For a general phenotypic description and a discussion of genetic heterogeneity of LCA, see LCA1 (204000). Clinical Features Friedman et al. (2006) identified a sister and brother with Leber congenital amaurosis from a consanguineous Indian family. Both probands had had poor vision since birth. Nystagmus and atrophic lesions in the macular area with pigment migration were found on examination. Preising et al. (2012) reported a large consanguineous Kurdish family with LCA, in which 6 of 7 affected individuals were available for study.
    • Leber Congenital Amaurosis 9 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-9 (LCA9) is caused by homozygous or compound heterozygous mutation in the NMNAT1 gene (608700) on chromosome 1p36. For a general discussion of the phenotypic and genetic heterogeneity in Leber congenital amaurosis, see LCA1 (204000). Description Early-onset neurodegeneration in the human retina can lead to Leber congenital amaurosis (LCA), the most severe human form of inherited photoreceptor-neuron degeneration resulting in congenital blindness, with an incidence of approximately 1 in 80,000 (summary by Koenekoop et al., 2012). NMNAT1 (608700) mutations consistently cause severe and rapidly progressive macular degeneration leading to severe central atrophy with an appearance of congenital macular coloboma in the neonatal period, as well as an unusual early-onset atrophy of the optic nerve (Perrault et al., 2012). Clinical Features Koenekoop et al. (2012) reexamined affected individuals from 8 families with Leber congenital amaurosis in whom they had identified mutations in the NMNAT1 gene (608700), which is ubiquitously expressed (see MOLECULAR GENETICS).
    • Leber Congenital Amaurosis 5 OMIM
      A number sign (#) is used with this entry because Leber congenital amaurosis-5 (LCA5) is caused by homozygous mutation in the gene encoding lebercilin (LCA5; 611408) on chromosome 6q14. For a general phenotypic description and a discussion of genetic heterogeneity of LCA, see LCA1 (204000). Clinical Features Dharmaraj et al. (2000) described a multigenerational kindred of Old Order River Brethren, a religious isolate descended from Swiss immigrants to America in the 1750s (Brechbill, 1972), segregating Leber congenital amaurosis. LCA in this kindred was not associated with multisystem abnormalities. Renal function remained normal. Neurologic and hepatic function were within normal limits.
    • Leber Congenital Amaurosis 1 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-1 (LCA1) is caused by homozygous mutation in the gene encoding retinal guanylate cyclase (GUCY2D; 600179) on chromosome 17p13. Heterozygous mutation in the GUCY2D gene causes an allelic disorder, cone-rod dystrophy-6 (CORD6; 601777), and homozygous mutation in the same gene has also been found to cause autosomal recessive CORD (see 610777). Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009).
    • Leber Congenital Amaurosis GARD
      Leber congenital amaurosis (LCA) is an eye disorder that primarily affects the retina . People with this condition typically have severe visual impairment beginning in infancy. Other features include photophobia , involuntary movements of the eyes (nystagmus), and extreme farsightedness. The pupils also do not react normally to light. Additionally, the cornea may be cone-shaped and abnormally thin ( keratoconus ). Franceschetti's oculo-digital sign is characteristic of Leber congenital amaurosis.
    • Leber Congenital Amaurosis 11 OMIM
      A number sign (#) is used with this entry because Leber congenital amaurosis-11 (LCA11) is caused by heterozygous mutation in the IMPDH1 gene (146690) on chromosome 7q32. Heterozygous mutation in the IMPDH1 gene can also cause retinitis pigmentosa-10 (RP10; 180105). Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009).
    • Leber Congenital Amaurosis 16 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-16 (LCA16) is caused by homozygous mutation in the KCNJ13 gene (603208) on chromosome 2q37. For a general phenotypic description and a discussion of genetic heterogeneity of Leber congenital amaurosis, see LCA1 (204000). Clinical Features Sergouniotis et al. (2011) studied a consanguineous Middle Eastern family in which 2 brothers had nystagmus at birth and were diagnosed with Leber congenital amaurosis shortly thereafter. Poor night vision and difficulty reading print from an early age was reported for both patients; gradual progression of visual problems affecting central and peripheral vision was also noted. Both patients had bilateral cataract surgery in their third decade. Funduscopy revealed significant pigment in the retinal pigment epithelium (RPE), in a configuration unlike that of typical retinitis pigmentosa (see 268000).
    • Leber Congenital Amaurosis 7 OMIM
      A number sign (#) is used with this entry because Leber congenital amaurosis-7 can be caused by heterozygous or homozygous mutation in the CRX gene (602225) on chromosome 19q13. Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009). For a general description and a discussion of genetic heterogeneity of LCA, see 204000.
    • Leber Congenital Amaurosis 15 OMIM
      A number sign (#) is used with this entry because Leber congenital amaurosis-15 and juvenile retinitis pigmentosa are caused by homozygous or compound heterozygous mutation in the TULP1 gene (602280) on chromosome 6p21.3. Description Autosomal recessive childhood-onset severe retinal dystrophy is a heterogeneous group of disorders affecting rod and cone photoreceptors simultaneously. The most severe cases are termed Leber congenital amaurosis, whereas the less aggressive forms are usually considered juvenile retinitis pigmentosa (summary by Gu et al., 1997). Mutation in TULP1 can also cause a form of autosomal recessive retinitis pigmentosa (RP14; 600132). For a general phenotypic description and a discussion of the genetic heterogeneity of Leber congenital amaurosis, see LCA1 (204000); for retinitis pigmentosa, see 268000.
    • Leber Congenital Amaurosis 8 OMIM
      A number sign (#) is used with this entry because Leber congenital amaurosis-8 (LCA8) is caused by homozygous or compound heterozygous mutation in the CRB1 gene (604210) on chromosome 1q31. Homozygous or compound heterozygous mutation in CRB1 can also cause retinitis pigmentosa-12 (RP12; 600105). Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009).
    • Leber Congenital Amaurosis 6 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-6 (LCA6) is caused by homozygous or compound heterozygous mutation in the RPGRIP1 gene (605446) on chromosome 14q11. Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009). For a general description and a discussion of genetic heterogeneity of LCA, see 204000.
    • Leber Congenital Amaurosis 2 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-2 (LCA2) is caused by homozygous or compound heterozygous mutation in the RPE65 gene (180069) on chromosome 1p31. Mutations in this gene also cause retinitis pigmentosa (RP20; 613794). Description Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009).
    • Leber Congenital Amaurosis Orphanet
      Leber congenital amaurosis (LCA) is a retinal dystrophy defined by blindness and responses to electrophysiological stimulation (Ganzfeld electroretinogram (ERG)) below threshold, associated with severe visual impairment within the first year of life. Epidemiology The prevalence of LCA is 1/50,000 - 1/33,000 live births and accounts for 5% of all retinal dystrophies and 20% of blindness in school age children. Clinical description LCA is characterized by severely reduced visual acuity (less or equal 20/400) or blindness within in the first year of life. Sluggish pupillary responses, roving eye movement, photophobia, high hyperopia, nystagmus, convergent strabismus, or keratoconus may occur depending on the genetic cause. The Franceschetti's oculo-digital sign, comprising eye poking, pressing, and rubbing is pathognomonic.
    • Leber Congenital Amaurosis 10 OMIM
      A number sign (#) is used with this entry because of evidence that Leber congenital amaurosis-10 (LCA10) is caused by homozygous or compound heterozygous mutations in the CEP290 gene (610142) on chromosome 12q21. Description Leber congenital amaurosis is a severe retinal dystrophy, causing blindness or severe visual impairment at birth or during the first months of life (summary by den Hollander et al., 2006). For a general phenotypic description and a discussion of genetic heterogeneity of Leber congenital amaurosis, see LCA1 (204000). Clinical Features Den Hollander et al. (2006) reported a consanguineous French Canadian family in which 4 sibs had Leber congenital amaurosis. The sibs were blind or severely visually impaired at birth. Two of the 4 experienced seizures but had no other neurologic symptoms.
    • Retinal Aplasia OMIM
      Sorsby and Williams (1960) observed a family with multiple cases of retinal aplasia in which inheritance was autosomal dominant. 'Retinal aplasia' is the British term for what is called 'congenital amaurosis' on the continent. Much genetic heterogeneity exists as evidenced by the demonstration of both autosomal dominant and autosomal recessive forms. This disorder, which might be called an autosomal dominant form of Leber amaurosis congenita, must be very rare. Heckenlively (1988) reported a 6-generation family with a severe progressive retinal degeneration beginning in infancy.
  • Tropical Disease Wikipedia
    TDR history The current TDR disease portfolio includes the following entries: [5] Historical TDR disease portfolio Disease When added Pathogen Primary vector Primary endemic areas Frequency Annual deaths Symptoms Complications Malaria 1975 Plasmodium falciparum and four other Plasmodium species of protazoa Anopheles mosquitoes throughout the tropics 228 million (2018) 405,000 (2018) fever , tiredness , vomiting , headache yellow skin , seizures , coma , death Schistosomiasis / ˌ ʃ ɪ s t ə s ə ˈ m aɪ ə s ɪ s / [6] [7] (snail fever, bilharzia, "schisto") 1975 Schistosoma flatworms (blood flukes) freshwater snails throughout the tropics 252 million (2015) 4,400–200,000 abdominal pain , diarrhea , bloody stool , blood in the urine . ... Liver damage , kidney failure , infertility , bladder cancer Lymphatic filariasis 1975 Wuchereria bancrofti , Brugia malayi , and Brugia timori filarial worms mosquitoes throughout the tropics 38.5 million (2015) few lymphoedema , elephantiasis , hydrocele Onchocerciasis / ˌ ɒ ŋ k oʊ s ɜːr ˈ k aɪ ə s ɪ s , - ˈ s aɪ -/ [8] [9] (river blindness) 1975 Onchocerca volvulus filarial worms [10] Simuliidae black flies sub-Saharan Africa 15.5 million (2015) 0 itching , papules edema , lymphadenopathy , visual impairment , blindness Chagas disease (American trypanosomiasis) 1975 Trypanosoma cruzi protozoa Triatominae kissing bugs South America 6.2 million (2017) 7,900 (2017) fever , swollen lymph nodes , headache heart failure , enlarged esophagus , enlarged colon African trypanosomiasis (sleeping sickness) 1975 Trypanosoma brucei gambiense and T. b. rhodesiense protozoa Glossina tsetse flies sub-Saharan Africa 11,000 (2015) 3,500 (2015) first stage: fever , headache , itchiness , joint pain second stage: insomnia , confusion , ataxia , hemiparesis , paralysis anemia , endocrine disfunction , cardiac disfunction , kidney dysfunction , coma , death Leishmaniasis 1975 Leishmania protozoa Phlebotominae sandflies throughout the tropics 4–12 million 24,200 (2015) skin ulcers fever , anemia , enlarged liver , enlarged spleen , death Leprosy † (Hansen's disease) 1975 Mycobacterium leprae and M. lepromatosis mycobacteria extensive contact (probably airborne disease ) throughout the tropics 209,000 (2018) few skin lesions , [11] numbness permanent damage to the skin, nerves, limbs, and eyes Dengue fever 1999 dengue virus Aedes aegypti and other Aedes mosquitoes tropical Asia 390 million (2020) 40,000 fever , headache , muscle and joint pain , rash , vomiting , diarrhea low levels of blood platelets , hypotension , hemorrhage , shock Tuberculosis † (TB, consumption) 1999 Mycobacterium tuberculosis mycobacteria airborne disease worldwide 10 million (active, 2018), 2 billion (latent, 2018) 1.5 million (2018) chronic cough , fever , cough with bloody mucus , weight loss death TB-HIV coinfection ‡ 1999 HIV + Mycobacterium tuberculosis sexual contact + airborne disease Africa 1.2 million (2015) 251,000 (2018) Sexually transmitted infections (notably syphilis , gonorrhoea , chlamydia , trichomoniasis , hepatitis B , HSV , HIV , and HPV ) 2000 bacteria, parasite, viruses sexual contact worldwide various various † Although leprosy and tuberculosis are not exclusively tropical diseases, their high incidence in the tropics justifies their inclusion. ‡ People living with HIV are 19 (15-22) times more likely to develop active TB disease than people without HIV.
  • Gastric Antral Vascular Ectasia Wikipedia
    . ^ a b c d e f g h i j k l m n o p q r s Tuveri, Massimiliano; Borsezio, Valentina; Gabbas, Antonio; Mura, Guendalina (2007). ... PMID 21160630 . ^ a b El-Gendy, Hala; Shohdy, Kyrillus S.; Maghraby, Gehad G.; Abadeer, Kerolos; Mahmoud, Moustafa (2017-02-01). ... PMID 10205216 . ^ Krstić, M; Alempijević, T; Andrejević, S; Zlatanović, M; Damjanov, N; Ivanović, B; Jovanović, I; Tarabar, D; Milosavljević, T (2010). ... PMC 7045742 . PMID 17054131 . ^ a b c Saab S, Nieto JM, Lewis SK, Runyon BA (2006). ... PMID 14585429 . ^ Wells, C; Harrison, M; Gurudu, S; Crowell, M; Byrne, T; Depetris, G; Sharma, V (2008).
    CTC1, P4HB, DHX16, DDX21, DDX46, DDX19A, MIR3677
    • Watermelon Stomach GARD
      Watermelon stomach is a condition in which the lining of the stomach bleeds, causing it to look like the characteristic stripes of a watermelon when viewed by endoscopy. Although it can develop in men and women of all ages, watermelon stomach is most commonly observed in older women (over age 70 years). Signs and symptoms of watermelon stomach include blood in the stool , hematemesis (vomiting blood) and anemia. The exact cause of watermelon stomach is unknown; however, it is often diagnosed in people with other chronic (long-term) conditions such as cirrhosis (scarring of the liver and poor liver function), autoimmune disease, systemic sclerosis , and CREST syndrome . Treatment consists of surgery and/or medications to stop or control the bleeding.
  • Disseminated Intravascular Coagulation Wikipedia
    . ^ a b Robbins, Stanley L.; Cotran, Ramzi S.; Kumar, Vinay; Collins, Tucker (1999). ... PMID 17108099 . ^ Grewal, PK; Uchiyama, S; Ditto, D; Varki, N; Le, DT; Nizet, V; Marth, JD (June 2008). ... Thrombosis and Haemostasis . 86 (5): 1327–30. doi : 10.1055/s-0037-1616068 . PMID 11816725 . S2CID 39696424 . ^ Gando, S (2012). ... Lancet . 350 (9091): 1590–1593. doi : 10.1016/s0140-6736(97)06356-3 . PMID 9393338 . ^ Gando, S (1999). "Disseminated intravascular coagulation and sustained systemic inflammatory response syndrome predict organ dysfunctions after trauma: application of clinical decision analysis" . ... PMC 1191617 . PMID 9923809 . ^ Sallah, S (2001). "Disseminated intravascular coagulation in solid tumors: clinical and pathologic study".
    F3, F2, THBD, PROC, SERPINC1, OXT, F7, SERPINE1, IL6, TFPI, PLAT, FGA, PROS1, SERPIND1, NUMA1, NPM1, CFI, BCOR, NLRC4, CFH, NABP1, CD46, STAT5B, PML, TBL1XR1, ZBTB16, STAT3, FIP1L1, PRKAR1A, HELLPAR, RARA, IRF2BP2, HMGB1, PC, TNF, F10, MBL2, MPO, COX8A, BTBD8, OTOR, SLC25A10, ALB, TLR4, ZFP36, NCAM1, PLG, ADAMTS13, F5, ANGPT2, CD34, COLEC11, EGF, IL10, SH3BP4, SLC17A5, FCRL6, RN7SL263P, TEK, CABIN1, PGR-AS1, C20orf181, MIR122, ASPG, VEGFA, VTN, TAT, VWF, IL4I1, PROCR, RNF34, CLDN10, ARTN, DNAI2, RHOF, MBL3P, AGRP, TAL1, STIL, HGF, GPT, F13A1, F2R, EPHB2, EGFR, MAPK14, CRP, CPB2, COL4A2, CEACAM8, CD14, VPS51, BRAF, APOH, ANXA5, ALK, HLA-DOA, HMOX1, IFNG, PRH2, PMEL, SELL, SDC1, PTAFR, MASP1, MAPK8, MAPK1, PRH1, IL1B, PLD1, NRAS, MUC1, MMP10, ATXN3, MB, IL7, LINC02605
  • Antiphospholipid Syndrome Wikipedia
    Lupus anticoagulant (LAC) antibodies bind to prothrombin , thus increasing its cleavage to thrombin , its active form. [ citation needed ] In APS there are also antibodies binding to protein S , which is a co-factor of protein C. Thus, anti-protein S antibodies decrease protein C efficiency. [8] Annexin A5 forms a shield around negatively charged phospholipid molecules, thus reducing their availability for coagulation. ... Res . 67 (4): 355–65. doi : 10.1016/0049-3848(92)90266-d . PMID 1329261 . ^ a b Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R, Derksen RH, DE Groot PG, Koike T, Meroni PL, Reber G, Shoenfeld Y, Tincani A, Vlachoyiannopoulos PG, Krilis SA (February 2006). ... Retrieved 2020-08-31 . ^ de Jong PG, Goddijn M, Middeldorp S (2013). "Antithrombotic therapy for pregnancy loss" . ... PMID 6414579 . ^ Erkan D, Derksen R, Levy R, Machin S, Ortel T, Pierangeli S, Roubey R, Lockshin M (2011).
    APOH, PPARG, FRMD4A, TSHR, F5, F3, SYCP2L, F2, PTPRO, GPI, ANXA5, TLR4, SH2B2, KLK3, ANXA2, TNF, AGER, CPB2, MTOR, MTHFR, F10, PLG, HT, TFPI, PLAT, SELPLG, ACR, SERPINE1, MOK, LRP8, VWF, HMGB1, VIM, SELP, RAB4A, CCL2, CXCL12, ATXN2, RO60, S100A10, TRIM21, ABCA1, SSB, THBD, TNFRSF1B, NR1I2, ADIPOQ, SH2B3, PROCR, ADAMTS13, TREX1, PTPN22, FOXP3, SLC52A1, IL21, ANXA8, ANXA8L1, PROS1, NOS3, PON1, PLSCR1, HLA-DPB1, GP1BA, GCY, FGA, FCGR2A, F2RL1, EMD, EDN1, DECR1, CRP, CD36, CD1D, CALR, B2M, SERPINC1, AQP4, AMH, HLA-DRB1, HRES1, IDS, MBL2, PF4, PC, SERPINB2, TNFRSF11B, MYD88, MSN, MPL, LPA, IFNG, LGALS9, LCT, CXCL10, CXCL8, IL1B, IGFBP1, IGF1, C20orf181
    • Antiphospholipid Syndrome Mayo Clinic
      Deep vein thrombosis (DVT). Signs and symptoms of DVT s include swelling, redness, or pain in a leg or arm.
  • Latent Autoimmune Diabetes In Adults Wikipedia
    S2CID 2179462 . ^ a b c d e f g h Carlsson S. (2019). Environmental (Lifestyle) Risk Factors for LADA. ... P., Tuomi, T., Åsvold, B. O., & Carlsson, S. (2019). Interaction Between Overweight and Genotypes of HLA, TCF7L2, and FTO in Relation to the Risk of Latent Autoimmune Diabetes in Adults and Type 2 Diabetes. ... -O.; Dorkhan, M.; Groop, L.; Martinell, M.; Tuomi, T.; Wolk, A.; Carlsson, S. (October 2014). "Fatty fish consumption and risk of latent autoimmune diabetes in adults" . ... PMID 8425674 . ^ Hagopian, W A; Karlsen, A E; Gottsäter, A; Landin-olsson, M; Grubin, C E; Sundkvist, G; Petersen, J S; Boel, E; Dyrberg, T; Lernmark, A (January 1993). ... Sources [ edit ] Eisenbarth, George S., ed. (2010). Immunoendocrinology: Scientific and Clinical Aspects .
    PTPN22, INS, ATXN2, INS-IGF2, BACH2, SH2B3, CTLA4, DPP4, GAD2, TCF7L2, GAD1, LINC01193, SOX13, MICA, HLA-DQB1, HLA-DOA, HLA-DRB1, GCG, CCR2, CSN2, SUMO4, DSPP, SUV39H2, FTO, FABP5, SOST, FOXP3, GPT, KDM4C, HNF4A, TSPAN7, HLA-DQA1, PDE4B, LAD1, CCR5, IL18, IL6, IFNG, CD38
  • Anaplastic Large-Cell Lymphoma Wikipedia
    . ^ Kempf W, Pfaltz K, Vermeer MH, Cozzio A, Ortiz-Romero PL, Bagot M, Olsen E, Kim YH, Dummer R, Pimpinelli N, Whittaker S, Hodak E, Cerroni L, Berti E, Horwitz S, Prince HM, Guitart J, Estrach T, Sanches JA, Duvic M, Ranki A, Dreno B, Ostheeren-Michaelis S, Knobler R, Wood G, Willemze R. ... Retrieved 26 November 2018 . ^ Miranda RN, Aladily TN, Prince HM, Kanagal-Shamanna R, de Jong D, Fayad LE, Amin MB, Haideri N, Bhagat G, Brooks GS, Shifrin DA, O'Malley DP, Cheah CY, Bacchi CE, Gualco G, Li S, Keech JA Jr, Hochberg EP, Carty MJ, Hanson SE, Mustafa E, Sanchez S, Manning JT Jr, Xu-Monette ZY, Miranda AR, Fox P, Bassett RL, Castillo JJ, Beltran BE, de Boer JP, Chakhachiro Z, Ye D, Clark D, Young KH, Medeiros LJ. ... S2CID 19099328 . ^ a b Miranda RN, Aladily TN, Prince HM, Kanagal-Shamanna R, de Jong D, Fayad LE, Amin MB, Haideri N, Bhagat G, Brooks GS, Shifrin DA, O'Malley DP, Cheah CY, Bacchi CE, Gualco G, Li S, Keech JA Jr, Hochberg EP, Carty MJ, Hanson SE, Mustafa E, Sanchez S, Manning JT Jr, Xu-Monette ZY, Miranda AR, Fox P, Bassett RL, Castillo JJ, Beltran BE, de Boer JP, Chakhachiro Z, Ye D, Clark D, Young KH, Medeiros LJ. ... Invest . 88 (1): 48–57. doi : 10.1038/labinvest.3700696 . PMID 17965727 . ^ Park SJ, Kim S, Lee DH, et al. (August 2008). "Primary systemic anaplastic large cell lymphoma in Korean adults: 11 years' experience at Asan Medical Center" .
    ALK, STAT3, HSP90AA1, TWIST1, ACVRL1, NPM1, TP53, SLPI, TNFRSF8, IRF4, MYC, JUNB, TNF, JUN, CD274, CDKN1B, BCL2, DUSP22, COIL, IL1R1, WDR48, CDKN2A, NOS1, JUND, RTEL1, FOS, FOSB, NOS2, PDLIM7, NCAM1, BCL3, CEBPB, IGH, ATIC, KIT, TPM3, MCL1, PDGFRB, LGALS1, BATF3, NFKB1, MSN, RPE65, FAS, CLU, MAPK3, EZH2, IFNG, NTRK1, ANPEP, JAK3, CKAP4, AKT1, UVRAG, CIB1, GZMB, IL10, TP63, IL6, NOTCH1, IL5, PWWP3A, MIR155, MUC1, INSR, ISG20, IL17A, EML4, PDGFRA, KRT20, SMUG1, TFG, HERPUD1, BCL10, NR0B2, WAS, MAGEH1, VEGFA, IL22, FOXP3, TIMP1, TIA1, TRBV20OR9-2, STAT1, PIK3CA, IL2RA, SOAT1, SNAP25, CLIP1, PTPRC, PTPN11, PTPN6, MAPK8, PART1, PRF1, PNLIP, PIK3CD, PIK3CB, SPN, PIK3CG, IL2, CDKN2B, CASP3, MS4A1, CCR3, CLTC, TNFSF8, BSG, COL15A1, ETFA, DPP4, CDK6, CDKN1A, CD96, CHP1, NAPSA, CXCL14, CAPG, BCL2L11, TRAP1, EBI3, BTK, CALM2, BATF, MRPL28, CARS1, GNLY, SUB1, PSIP1, GRAP2, CFLAR, DOK2, ZAP70, TRAF1, TRAF2, CD44, TYK2, CD40, CD28, WIPF1, YY1, CLTCL1, SOCS3, CCNT1, CASP8, SKAP1, RIPK1, IL18R1, NRP1, ZHX2, ARHGEF7, ZNF652, TRIM32, CDC42, MIR146A, PDCD1LG2, BIRC2, TP53INP1, BMS1P20, IL17F, TCHHL1, RPTN, RHOV, RGL4, HRNR, MIR150, PDLIM2, AHR, MIR29A, MIR17HG, MIR135B, MIR494, LINC01013, CERNA3, H3P9, H3P42, H3P10, CARS2, TSPYL2, SMG1, BAK1, TBC1D9, BRAF, CADM1, PRDM1, BCL6, BCL2L1, NXT1, CCND1, BLNK, BAX, ASCC1, RBAK, GDE1, BACH1, ARNT, CROT, RHOA, FASLG, PRDM8, SLC12A9, BIRC3, RNF213, CD68, TMOD1, TNFRSF1B, FOXO1, FRA7H, MYH9, FN1, NFATC1, FLT4, NFKB2, NGF, FLT3, FOXO3, FKBP4, MTAP, FGFR4, PAEP, PAX5, PCYT1A, PDCD1, PTK2B, ETS1, ABCB1, SERPINA1, MTOR, FUT1, ERBB4, HDAC1, ID2, IL9, ICAM1, HSPA1B, HSPA1A, HOXC6, HOXC5, ITK, HDAC2, GTF2H4, CD99, GRB2, CXCR3, LDLR, GLI1, TACSTD2, MCC, FUT4, CD46, MDK, SERPINB9, EPHB2, TNFRSF1A, CCL22, RPS6KB1, MAPK14, S100A1, S100A10, S100B, SCT, CCL5, CCL11, CCL17, SHH, RPL18A, ST6GAL1, MAP3K8, CCR8, SQLE, CD52, STAT5B, TGFB1, CDK9, IGF1, RPS6, CSF1R, ADARB1, PTBP1, PKM, EGFR, E2F2, MAPK1, DUSP5, MAP2K7, PRSS1, PRSS2, PRSS3, PTEN, RORC, PTN, CYP51A1, CTNNB1, CSF2, RAF1, RAG1, RAG2, RB1, RENBP, H3P40
    • Anaplastic Large Cell Lymphoma GARD
      Anaplastic large cell lymphoma (ALCL) is a rare type of Non-Hodgkins lymphoma. Lymphoma is a cancer of the lymph system, part of our immune system. Non-Hodgkins lymphoma involves abnormal growth of white blood cells, either T cells or B cells. Anaplastic large cell lymphoma is an aggressive cancer that usually involves the T-cells. Cancer cells in ALCL can be identified by their appearance under the microscope and by the presence of a tumor marker called CD30 or Ki-1. There are two types of ALCL, a type that affects mainly the skin (cutaneous ALCL) and a type that affects other body organs (systmic ALCL).
    • Anaplastic Large Cell Lymphoma Orphanet
      A rare and aggressive peripheral T-cell non-Hodgkin lymphoma, belonging to the group of CD30-positive lymphoproliferative disorders, which affects lymph nodes and extranodal sites. It is comprised of two sub-types, based on the expression of a protein called anaplastic lymphoma kinase (ALK): ALK positive and ALK negative ALCL. Epidemiology ALCL accounts for approximately 3% of adult non-Hodgkin lymphomas and 10% to 20% of childhood lymphomas. Its prevalence is unknown. The ALK positive subtype usually affects children and young adults. The ALK negative subtype is more commonly found in older patients over the age of 40.
  • Fecal–oral Route Wikipedia
    . ^ Kal, K and Chambers, R (2008) Handbook on Community-led Total Sanitation Archived 2015-04-10 at the Wayback Machine , Plan UK Accessed 2015-02-26 ^ Hale TL, Keusch GT (1996). Baron S, et al. (eds.). Shigella in: Baron's Medical Microbiology (4th ed.). ... (via NCBI Bookshelf) . ^ Giannella RA (1996). Baron S; et al. (eds.). Salmonella :Epidemiology in: Baron's Medical Microbiology (4th ed.). ... (via NCBI Bookshelf) . ^ Finkelstein RA (1996). Baron S; et al. (eds.). Cholera, Vibrio cholerae O1 and O139, and Other Pathogenic Vibrio s in: Baron's Medical Microbiology (4th ed.). ... Retrieved 2016-04-18 . ^ Zuckerman AJ (1996). Baron S; et al. (eds.). Hepatitis Viruses in: Baron's Medical Microbiology (4th ed.). ... Retrieved 2020-02-04 . ^ Meyer EA (1996). Baron S; et al. (eds.). Other Intestinal Protozoa and Trichomonas Vaginalis in: Baron's Medical Microbiology (4th ed.).
  • Innate Resistance To Hiv Wikipedia
    This is attributed to individuals being heterozygous for the mutation, which prevents the delta mutation from effectively prohibiting HIV from entering immune cells. [23] See also [ edit ] Viruses portal Discovery and development of CCR5 receptor antagonists Entry inhibitor HIV tropism Timothy Ray Brown Stephen Crohn References [ edit ] ^ Scutti S (2014-11-20). "Why Some People Are Naturally Immune To HIV" . ... HIVPlusMag . Retrieved 2015-01-20 . ^ Nolen S (2007-05-27). "Staying alive: the women who are immune to Aids" . the Guardian . ... PMID 15556703 . ^ Hütter G, Nowak D, Mossner M, Ganepola S, Müssig A, Allers K, Schneider T, Hofmann J, Kücherer C, Blau O, Blau IW, Hofmann WK, Thiel E (February 2009). ... Blood . 117 (10): 2791–99. doi : 10.1182/blood-2010-09-309591 . PMID 21148083 . ^ Zhen A, Kitchen S (December 2013). "Stem-cell-based gene therapy for HIV infection" . ... PMC 4084652 . PMID 24597865 . ^ Rodríguez-Mora S, De Wit F, García-Perez J, Bermejo M, López-Huertas MR, Mateos E, Martí P, Rocha S, Vigón L, Christ F, Debyser Z, Jesús Vílchez J, Coiras M, Alcamí J (August 2019).
  • Pityriasis Alba Wikipedia
    .; King, Richard A.; Oetting, William S.; Ortonne, Jean-Paul (2008). The Pigmentary System: Physiology and Pathophysiology . ... PMID 2978289 . ^ Rigopoulos D, Gregoriou S, Charissi C, Kontochristopoulos G, Kalogeromitros D, Georgala S (2006). ... Journal of the European Academy of Dermatology and Venereology : JEADV . 16 (5): 463–468. doi : 10.1046/j.1468-3083.2002.00494.x . PMID 12428838 . ^ Dogra S, Kumar B (2003). "Epidemiology of skin diseases in school children: a study from northern India". ... PMID 14651562 . ^ Faye O, N'Diaye HT, Keita S, Traoré AK, Hay RJ, Mahé A (2005). ... PMID 10354028 . ^ Inanir I, Sahin MT, Gündüz K, Dinç G, Türel A, Oztürkcan S (2002). "Prevalence of skin conditions in primary school children in Turkey: differences based on socioeconomic factors".
  • Nail Clubbing Wikipedia
    Cite journal requires |journal= ( help ) ^ a b c d e Burcovschii, S; Aboeed, A (January 2019). "Nail Clubbing". ... Archived from the original (PDF) on 2003-11-01. ^ Epstein O, Dick R, Sherlock S (1981). "Prospective study of periostitis and finger clubbing in primary biliary cirrhosis and other forms of chronic liver disease" . ... PMID 11466101 . ^ Shah K, Ferrara TM, Jan A, Umair M, Irfanullah, Khan S, Ahmad W, Spritz RA (August 2017). ... Dermatol . 177 (2): 546–548. doi : 10.1111/bjd.15094 . PMID 27681482 . ^ a b Uppal S, Diggle CP, Carr IM, et al. (June 2008). ... PMID 2891996 . ^ Schamroth L (February 1976). "Personal experience". S. Afr. Med. J . 50 (9): 297–300. PMID 1265563 .
    CBR1, HPGD
  • Cryptogenic Organizing Pneumonia Wikipedia
    References [ edit ] ^ " bronchiolitis obliterans with organizing pneumonia " at Dorland's Medical Dictionary ^ White, Eric J. Stern, Charles S. (1999). Chest radiology companion . ... Retrieved 23 November 2012 . ^ Levy, Barry S.; Wegman, David H.; Baron, Sherry L.; Sokas, Rosemary K., eds. (2011). ... Retrieved June 23, 2015 . ^ Mukhopadhyay, Sanjay; Mehrad, Mitra; Dammert, Pedro; Arrossi, Andrea V; Sarda, Rakesh; Brenner, David S; Maldonado, Fabien; Choi, Humberto; Ghobrial, Michael (2019). ... ISSN 0002-9173 . PMID 31621873 . ^ Nogi, S; Nakayama, H; Tajima, Y; Okubo, M; Mikami, R; Sugahara, S; Akata, S; Tokuuye, K (2014).
    UNC119, CD68, CRP, NR3C1, HDAC2, CXCL8, TNF, TNFRSF1A, TNFRSF1B, CD163, ING4, COP1, HT, TOMM5, WG, SFTPA1
    • Bronchiolitis Obliterans Organizing Pneumonia GARD
      Bronchiolitis obliterans organizing pneumonia (BOOP) is a lung disease that causes inflammation in the small air tubes (bronchioles) and air sacs (alveoli). BOOP typically develops in individuals between 40-60 years old; however the disorder may affect individuals of any age. The signs and symptoms of BOOP vary but often include shortness of breath, a dry cough, and fever. BOOP can be caused by viral infections, various drugs, and other medical conditions. If the cause is known, the condition is called secondary BOOP. In many cases, the underlying cause of BOOP is unknown.
    • Cryptogenic Organizing Pneumonia Orphanet
      Cryptogenic organizing pneumonia (COP) is a form of idiopathic interstitial pneumonia characterized pathologically by organizing pneumonia (OP) that presents with non-specific flu-like symptoms, as well as cough and dyspnea and where no etiological agent is found. Epidemiology COP represents 5-10% of interstitial lung diseases. The annual incidence in Iceland has been estimated at 1/90,900. Clinical description Mean age of onset is 50-60 years of age and patients present with non specific features of mild fever, non-productive cough, malaise, anorexia, weight loss and progressive but mild dyspnea. At auscultation, focal and sparse crackles are often found over the involved areas with clinical features of consolidation in some. There is no sign of finger clubbing. There is often a delay of 3 months or more between the onset of first symptoms and diagnosis.
    • Cryptogenic Organizing Pneumonia GARD
      Cryptogenic organizing pneumonia (COP) is a form of idiopathic interstitial pneumonia characterized by lung inflammation and scarring that obstructs the small airways and air sacs of the lungs (alveoli). Signs and symptoms may include flu-like symptoms such as cough, fever, malaise , fatigue and weight loss. COP often affects adults in midlife (40 to 60 years of age). The exact underlying cause of the condition is unknown (idiopathic). Treatment varies based on the severity of the condition but generally includes glucocorticoids .
  • Gastric Dilatation Volvulus Wikipedia
    . ^ a b Beck J, Staatz A, Pelsue D, Kudnig S, MacPhail C, Seim H, Monnet E (2006). ... Retrieved 2007-04-17 . ^ a b Parton A, Volk S, Weisse C (2006). "Gastric ulceration subsequent to partial invagination of the stomach in a dog with gastric dilatation-volvulus". ... Assoc . 216 (1): 40–5. doi : 10.2460/javma.2000.216.40 . PMID 10638316 . ^ Braun L, Lester S, Kuzma A, Hosie S (1996). "Gastric dilatation-volvulus in the dog with histological evidence of preexisting inflammatory bowel disease: a retrospective study of 23 cases". ... Retrieved 2007-04-17 . ^ a b Rawlings C, Mahaffey M, Bement S, Canalis C (2002). "Prospective evaluation of laparoscopic-assisted gastropexy in dogs susceptible to gastric dilatation". ... Retrieved 15 October 2017 . ^ a b Mackenzie G, Barnhart M, Kennedy S, DeHoff W, Schertel E (March–April 2010).
  • Cadasil Wikipedia
    The disease progresses to subcortical dementia associated with pseudobulbar palsy and urinary incontinence . [ citation needed ] Ischemic strokes are the most frequent presentation of CADASIL, with approximately 85% of symptomatic individuals developing transient ischemic attacks or stroke(s). The mean age of onset of ischemic episodes is approximately 46 years (range 30–70). ... As with other individuals, people with CADASIL should be encouraged to quit smoking. [20] In one small study, around 1/3 of patients with CADASIL were found to have cerebral microhemorrhages (tiny areas of old blood) on MRI . [15] L-arginine, a naturally occurring amino acid, has been proposed as a potential therapy for CADASIL, [21] but as of 2017 there are no clinical studies supporting its use. [18] Donepezil , normally used for Alzheimer's Disease, was not shown not to improve executive functioning in CADASIL patients. [22] In popular culture [ edit ] John Ruskin has been suggested to have suffered from CADASIL. [23] Ruskin reported in his diaries having visual disturbances consistent with the disease, and it has also been suggested that it might have been a factor in causing him to describe James Whistler 's Nocturne in Black and Gold – The Falling Rocket as "ask[ing] two hundred guineas for throwing a pot of paint in the public's face". ... PMID 25824603 . ^ Joutel A, Andreux F, Gaulis S, et al. (March 2000). "The ectodomain of the Notch3 receptor accumulates within the cerebrovasculature of CADASIL patients" . ... PMID 7676806 . ^ Vlachakis D, Champeris Tsaniras S, Ioannidou K, Papageorgiou L, Baumann M, Kossida S (October 2014). ... PMID 20464302 . ^ a b Lesnik Oberstein, S. A.; van den Boom, R.; van Buchem, M.
    NOTCH3, HTRA1, EGF, COL4A1, COL18A1, NOTCH1, JAG1, APOE, APP, LPA, TREX1, GFAP, PLXNA2, CTSA, PROC, ACTB, SOD1, TGFB1, NOTCH2, LAP, MRS2, RNF213, NOX5, THBD, KDR, NEFL, ACTG2, RBPJ, FN1, FBN1, ELN, DVL1, DCN, CSF3, CSF1R, CLU, CACNA1A, BGN, APCS, LINC01191
    • Cadasil GeneReviews
      CADASIL ( c erebral a utosomal d ominant a rteriopathy with s ubcortical i nfarcts and l eukoencephalopathy) is characterized by mid-adult onset of recurrent ischemic stroke, cognitive decline progressing to dementia, a history of migraine with aura, mood disturbance, apathy, and diffuse white matter lesions and subcortical infarcts on neuroimaging. ... Diagnosis There are no generally accepted diagnostic criteria for CADASIL ( c erebral a utosomal d ominant a rteriopathy with s ubcortical i nfarcts and l eukoencephalopathy). ... Gene-targeted testing requires that the clinician determine which gene(s) are likely involved, whereas genomic testing does not. ... Option 2 When the phenotype is indistinguishable from many other inherited disorders characterized by stroke and/or dementia, comprehensive genomic testing (which does not require the clinician to determine which gene[s] are likely involved) is the best option. ... CARASIL = c erebral a utosomal r ecessive a rteriopathy with s ubcortical i nfarcts and l eukoencephalopathy 2.
    • Cerebral Autosomal Dominant Arteriopathy-Subcortical Infarcts-Leukoencephalopathy Orphanet
      CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a hereditary cerebrovascular disorder characterized by mid-adult onset of recurrent subcortical ischemic stroke and cognitive impairment progressing to dementia in addition to migraines with aura and mood disturbances seen in about a third of patients. Epidemiology In Europe, the prevalence of CADASIL has been estimated to range between 1/50 000- 1/25 000. Clinical description The first manifestation of the disease occurs at a mean age of 45-50, usually in the form of ischemic stroke or cognitive decline. The disease onset and course is variable, but more than two thirds of patients suffer from (recurrent) stroke or dementia. Migraine, usually with aura, occurs in about a third of patients and often precedes stroke and dementia symptoms, with a mean age of onset of about 30 years.
    • Cerebral Arteriopathy, Autosomal Dominant, With Subcortical Infarcts And Leukoencephalopathy, Type 1 OMIM
      A number sign (#) is used with this entry because of evidence that autosomal dominant cerebral arteriopathy with subcortical infarcts and leukoencephalopathy type 1 (CADASIL1) is caused by heterozygous mutation in the NOTCH3 gene (600276) on chromosome 19p13. Description Autosomal dominant cerebral arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a progressive disorder of the small arterial vessels of the brain manifest by migraine, strokes, and white matter lesions, with resultant cognitive impairment in some patients (review by Kalimo et al., 1999). Clinical Features Stevens et al. (1977) reported an English family with onset of recurrent cerebral ischemic strokes between 39 and 57 years resulting in progressive neurologic dysfunction and eventual dementia. Affected individuals did not have hypertension, diabetes, or increased cholesterol, but neuropathologic investigation showed abnormalities of the cerebral vasculature; the authors suggested that it was a form of 'vascular encephalopathy.' Low et al. (2007) provided a follow-up of the family reported by Stevens et al. (1977), including confirmation of the CADASIL diagnosis by identification of a pathogenic mutation in the NOTCH3 gene (see MOLECULAR GENETICS).
    • Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts And Leukoencephalopathy MedlinePlus
      Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, usually called CADASIL, is an inherited condition that causes stroke and other impairments. This condition affects blood flow in small blood vessels , particularly cerebral vessels within the brain. The muscle cells surrounding these blood vessels (vascular smooth muscle cells ) are abnormal and gradually die. In the brain, the resulting blood vessel damage (arteriopathy) can cause migraines, often with visual sensations or auras, or recurrent seizures (epilepsy). Damaged blood vessels reduce blood flow and can cause areas of tissue death (infarcts) throughout the body.
    • Cadasil GARD
      CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy) is an inherited disease of the blood vessels that occurs when the thickening of blood vessel walls blocks the flow of blood to the brain. The disease primarily affects the small blood vessels in the white matter of the brain. CADASIL is characterized by migraine headaches and multiple strokes , which progresses to dementia. Other symptoms include white matter lesions throughout the brain, cognitive deterioration, seizures, vision problems, and psychiatric problems such as severe depression and changes in behavior and personality. Individuals may also be at higher risk of heart attack. Symptoms and disease onset vary widely, with signs typically appearing in the mid-30s.
  • Cavitary Myiasis Orphanet
    Clinical presentation is variable depending on the affected site(s) and degree of infestation and include foreign-body sensation (with or without movement sensation), hemorrhage, pain, edema, sensory loss, malodor, and pruritus, among others.
  • Leukoplakia GARD
    Removing the source of irritation may cause the condition to go away, but surgery to remove the sore(s) may be necessary in some cases.
    CTTN, TP53, MDM2, GSTT1, GSTM1, XRCC1, EGFR, BCL2, GSTM3, ERBB2, CYP1A1, DEFB4A, CDKN1A, CCND1, TGFB1, POLRMT, CIB2, PAX5, ABCB6, DLEC1, TP63, PABPN1, MFAP5, PRKDC, TFAM, PTGS2, RPE65, UVRAG, TP73, S100A4, PDPN, TLR4, TGM3, NAT1, RRAS2, CKAP4, POLG2, SIK1B, DEFB4B, MIR31, MIR29A, MIR21, GSTK1, LTO1, SIK1, SLCO6A1, DERL3, ARHGAP24, MTUS1, SLC12A9, EIF5A2, PIWIL2, TLR9, CD274, HPGDS, NOTCH1, NRAS, MMP13, NOS2, NELL2, FHIT, FGFR2, FGFR3, FGF2, ERCC2, ECT2, DNMT3B, DES, DEFB1, CYP2E1, COL4A1, CDKN2A, CDKN1C, CASP10, CASP7, CASP1, BSG, BRCA1, BAG1, GFAP, GSTP1, HOXC9, MCC, COX2, MSH2, MRE11, ATM, MMP9, MMP2, MLH1, MCL1, MAL, HOXC13, LCN2, LAMC2, KRT19, KRT13, KRT4, KRAS, IL10, IL6, MTCO2P12
    • Leukoplakia Mayo Clinic
      Overview With leukoplakia (loo-koh-PLAY-key-uh), thickened, white patches form on your gums, the insides of your cheeks, the bottom of your mouth and, sometimes, your tongue. These patches can't be scraped off. Doctors don't know what causes leukoplakia but consider chronic irritation from tobacco — whether smoked, dipped or chewed — to be the main culprit in its development. Most leukoplakia patches are noncancerous (benign), though some show early signs of cancer. Cancers on the bottom of the mouth can occur next to areas of leukoplakia. And white areas mixed in with red areas (speckled leukoplakia) may indicate the potential for cancer.
    • Leukoplakia Wikipedia
      ISBN 978-1-55009-186-1 . ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af Odell W (2010). ... PMID 27865803 . ^ a b c d e f Scully C, Porter S (July 2000). "ABC of oral health. ... Endoscopy . 33 (5): 469. doi : 10.1055/s-2001-14256 . PMID 11396772 . ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab Soames, JV; Southam, J.C. (1999). ... Page accessed on December 19, 2006. ^ Warnakulasuriya S, Johnson NW, van der Waal I (November 2007). ... PMID 17944749 . ^ a b c Cawson RA, Odell EW, Porter S (2002). Cawsonś essentials of oral pathology and oral medicine (7th ed.).
  • Griscelli Syndrome Wikipedia
    . ^ Rath, Sanjeev; Jain, Vivek; Marwaha, R. K.; Trehan, Amita; Rajesh, L. S.; Kumar, Vijay (February 2004). "Griscelli syndrome". ... External links [ edit ] Classification D ICD - 10 : E70.3 OMIM : 214450 607624 609227 DiseasesDB : 32776 External resources eMedicine : derm/926 Orphanet : 381 Griscelli syndrome type 1 at NIH 's Office of Rare Diseases OMIM: 214450 Griscelli syndrome type 2 at NIH 's Office of Rare Diseases OMIM: 607624 Griscelli syndrome type 3 at NIH 's Office of Rare Diseases OMIM: 609227 v t e Pigmentation disorders / Dyschromia Hypo- / leucism Loss of melanocytes Vitiligo Quadrichrome vitiligo Vitiligo ponctué Syndromic Alezzandrini syndrome Vogt–Koyanagi–Harada syndrome Melanocyte development Piebaldism Waardenburg syndrome Tietz syndrome Loss of melanin / amelanism Albinism Oculocutaneous albinism Ocular albinism Melanosome transfer Hermansky–Pudlak syndrome Chédiak–Higashi syndrome Griscelli syndrome Elejalde syndrome Griscelli syndrome type 2 Griscelli syndrome type 3 Other Cross syndrome ABCD syndrome Albinism–deafness syndrome Idiopathic guttate hypomelanosis Phylloid hypomelanosis Progressive macular hypomelanosis Leukoderma w/o hypomelanosis Vasospastic macule Woronoff's ring Nevus anemicus Ungrouped Nevus depigmentosus Postinflammatory hypopigmentation Pityriasis alba Vagabond's leukomelanoderma Yemenite deaf-blind hypopigmentation syndrome Wende–Bauckus syndrome Hyper- Melanin / Melanosis / Melanism Reticulated Dermatopathia pigmentosa reticularis Pigmentatio reticularis faciei et colli Reticulate acropigmentation of Kitamura Reticular pigmented anomaly of the flexures Naegeli–Franceschetti–Jadassohn syndrome Dyskeratosis congenita X-linked reticulate pigmentary disorder Galli–Galli disease Revesz syndrome Diffuse/ circumscribed Lentigo / Lentiginosis : Lentigo simplex Liver spot Centrofacial lentiginosis Generalized lentiginosis Inherited patterned lentiginosis in black persons Ink spot lentigo Lentigo maligna Mucosal lentigines Partial unilateral lentiginosis PUVA lentigines Melasma Erythema dyschromicum perstans Lichen planus pigmentosus Café au lait spot Poikiloderma ( Poikiloderma of Civatte Poikiloderma vasculare atrophicans ) Riehl melanosis Linear Incontinentia pigmenti Scratch dermatitis Shiitake mushroom dermatitis Other/ ungrouped Acanthosis nigricans Freckle Familial progressive hyperpigmentation Pallister–Killian syndrome Periorbital hyperpigmentation Photoleukomelanodermatitis of Kobori Postinflammatory hyperpigmentation Transient neonatal pustular melanosis Other pigments Iron Hemochromatosis Iron metallic discoloration Pigmented purpuric dermatosis Schamberg disease Majocchi's disease Gougerot–Blum syndrome Doucas and Kapetanakis pigmented purpura / Eczematid-like purpura of Doucas and Kapetanakis Lichen aureus Angioma serpiginosum Hemosiderin hyperpigmentation Other metals Argyria Chrysiasis Arsenic poisoning Lead poisoning Titanium metallic discoloration Other Carotenosis Tar melanosis Dyschromia Dyschromatosis symmetrica hereditaria Dyschromatosis universalis hereditaria See also Skin color Skin whitening Tanning Sunless Tattoo removal Depigmentation v t e Inherited disorders of trafficking / vesicular transport proteins Vesicle formation Lysosome / Melanosome : HPS1 – HPS7 Hermansky–Pudlak syndrome LYST Chédiak–Higashi syndrome COPII : SEC23A Cranio-lenticulo-sutural dysplasia COG7 CDOG IIE APC: AP1S2 X-linked intellectual disability AP3B1 Hermansky–Pudlak syndrome 2 AP4M1 CPSQ3 Rab ARL6 BBS3 RAB27A Griscelli syndrome 2 CHM Choroideremia MLPH Griscelli syndrome 3 Cytoskeleton Myosin : MYO5A Griscelli syndrome 1 Microtubule : SPG4 Hereditary spastic paraplegia 4 Kinesin : KIF5A Hereditary spastic paraplegia 10 Spectrin : SPTBN2 Spinocerebellar ataxia 5 Vesicle fusion Synaptic vesicle : SNAP29 CEDNIK syndrome STX11 Hemophagocytic lymphohistiocytosis 4 Caveolae : CAV1 Congenital generalized lipodystrophy 3 CAV3 Limb-girdle muscular dystrophy 2B , Long QT syndrome 9 Vacuolar protein sorting : VPS33B ARC syndrome VPS13B Cohen syndrome DYSF Distal muscular dystrophy See also vesicular transport proteins
    RAB27A, MYO5A, MLPH, FCGR3A, FCGR3B, FGL1, HPS1, RAB27B, AP3B1, VPS39, SBF2, ORAI1, DNAJC21, NCR3
  • Canine Degenerative Myelopathy Wikipedia
    Retrieved 2008-07-25 . ^ Awano, T.; Johnson, G. S.; Wade, C. M.; Katz, M. L.; Johnson, G. ... F.; Perloski, M.; Biagi, T.; Baranowska, I.; Long, S.; March, P. A.; Olby, N. J.; Shelton, G. D.; Khan, S.; O'Brien, D. P.; Lindblad-Toh, K.; Coates, J. ... Saunders Company, 2004, pp 147-9. ^ Kathmann I, I; Cizinauskas S; Doherr MG; Steffen F; Jaggy A. (July–August 2006).
  • Long Face Syndrome Wikipedia
    Therefore, individual variations in response should be expected from the alteration of a long face syndrome patient's breathing mode." [6] References [ edit ] ^ Carano, Aldo; Siciliani, Giuseppe; Bowman, S. Jay (September 2005). "Treatment of skeletal open bite with a device for rapid molar intrusion: a preliminary report" . ... CS1 maint: DOI inactive as of January 2021 ( link ) ^ Schendel, S. A.; Eisenfeld, J.; Bell, W. H.; Epker, B. ... PMID 1067758 . ^ Taub, Daniel I.; Jacobs, Jordan M. S.; Jacobs, Jonathan S. (2013). "Chapter 16: Anthropometry, cephalometry, and orthognathic surgery" .
  • ←
  • 1
  • 2
    • ...
  • 50
  • 51
  • 52
  • 53
  • 54
  • 55
  • 56
    • ...
  • 321
  • 322
  • →

FindZebra

contact@findzebra.com