• FindZebra
  • About
  • Contact
  • Help
  • Login
Advanced
  • Psittacine Beak And Feather Disease Wikipedia
    Scientific Reports . 5 : 14511. doi : 10.1038/srep14511 . ^ a b c d Sarker, S.; Lloyd, C.; Forwood, J.; Raidal, S.R. (2016). ... Emu . 118 (1): 80–93. doi : 10.1080/01584197.2017.1387029 . ^ Portas, T.; Jackson, B.; Das, S.; Shamsi, S.; Raidal, S. R. (2017). ... Australian Veterinary Journal . 93 (12): 471–475. doi : 10.1111/avj.12389 . ^ a b Das, S.; Sarker, S.; Ghorashi, S.A.; Forwood, J.K.; Raidal, S.R. (2016). ... Australian Veterinary Journal . 70 (4): 133–137. doi : 10.1111/j.1751-0813.1993.tb06104.x . ^ Das, S.; Sarker, S.; Peters, A.; Ghorashi, S.A.; Phalen, D.; Forwood, J.K.; Raidal, S.R. (2016). ... Molecular Phylogenetics and Evolution . 100 : 281–291. doi : 10.1016/j.ympev.2016.04.024 . ^ Sarker, S.; Das, S.; Ghorashi, S.A.; Forwood, J.K.; Raidal, S.R. (2014).
  • Sexual Fetishism Wikipedia
    New York: Guilford. ^ a b c d Scorolli, C., Ghirlanda, S., Enquist, M., Zattoni, S., & Jannini, E. ... A.; Lenzi, A.; Isidori, A. M.; Sante, S. Di; Ciocca, G.; Carosa, E.; Gravina, G. ... The Guilford Press. pp. 112 –113. ^ Darcangelo, S. (2008). "Fetishism: Psychopathology and Theory". ... J., Schaefer, G. A., Mundt, I. A., Roll, S., Englert, H., Willich, S. N., & Beier, K. ... CS1 maint: multiple names: authors list ( link ) ^ Dawson, S. J., Bannerman, B. A., & Lalumière, M.
  • Perifolliculitis Capitis Abscedens Et Suffodiens, Familial Omim
    In both patients, the only microorganism isolated was S. epidermidis. Treatment with oral isotretinoin was successful in both. INHERITANCE - Isolated cases SKIN, NAILS, & HAIR Skin - Suppurative scalp nodules - Scalp sinus formation - Small areas of alopecia - Scalp itching - S. epidermidis only microorganism isolated MISCELLANEOUS - Successful treatment with oral isotretinoin ▲ Close
    TNF
    • Dissecting Cellulitis Of The Scalp Orphanet
      Dissecting cellulitis of the scalp is a rare chronic suppurative dermatosis of the scalp that mainly affects black men and that is characterized by multiple painful inflammatory follicular and perifollicular nodules, pustules, and abscesses that interconnect via sinus tracts and eventually result in scarring alopecia.
    • Dissecting Cellulitis Of The Scalp Gard
      Dissecting cellulitis of the scalp is a rare and severe form of scalp folliculitis. It is sometimes associated with acne conglobata , hidradenitis suppurativa and spinal arthritis. Signs and symptoms of this condition include lardge nodules and cysts as well as smaller follicular papules. Hair loss occurs over the affected region and permanent scarring and bald patches appear. Treatment options for dissecting cellulitis of the scalp includes steroids and antibiotics but the condition does not typically improve even after treatment.
    • Dissecting Cellulitis Of The Scalp Wikipedia
      Dissecting cellulitis of the scalp Boggy, suppurative nodule with patchy hair loss typical of dissecting cellulitis of the scalp. Specialty Dermatology Medication Isotretinoin Dissecting cellulitis of the scalp , also known as dissecting folliculitis of the scalp , perifolliculitis capitis abscedens et suffodiens of Hoffman , perifolliculitis abscedens et suffodiens , or folliculitis abscedens et suffodiens , is an inflammatory condition of the scalp that can lead to scarring alopecia , which begins with deep inflammatory nodules , primarily over occiput , that progresses to coalescing regions of boggy scalp. Boggy tissue has a high fluid level that results in a spongy feeling. Isotretinoin proves to be the medicine of choice for the treatment of the disease. [1] [2] [3] [4] : 649 [5] : 761 [6] See also [ edit ] List of cutaneous conditions References [ edit ] ^ Alexis, Andew F. "Dissecting cellulitis of the scalp" . uptodate.com . Archived from the original on 2020-11-12 .
  • Idiopathic Facial Aseptic Granuloma Wikipedia
    . ^ Boralevi, F.; Léauté-Labrèze, C.; Lepreux, S.; Barbarot, S.; Mazereeuw-Hautier, J.; Eschard, C.; Taïeb, A.
  • Paratyphoid Fever Wikipedia
    Some very rare symptoms are psychosis (mental disorder), confusion, and seizures. [ citation needed ] Cause [ edit ] Paratyphoid fever is caused by any of three serovars of Salmonella enterica subsp. enterica : S. Paratyphi A, S. Paratyphi B (invalid alias S. schottmuelleri ), S. ... S2CID 13689184 . ^ a b Bhan MK, Bahl R, Bhatnagar S (2005). "Typhoid and paratyphoid fever". ... M.; Ferreccio, C.; Black, R. E.; Lagos, R.; Martin, O. S.; Blackwelder, W. C. (2007). "Ty21a Live Oral Typhoid Vaccine and Prevention of Paratyphoid Fever Caused by Salmonella enterica Serovar Paratyphi B" . ... A.; Franco-Paredes, C.; Del Rio, C.; Edupuganti, S. (2009). "Rethinking Typhoid Fever Vaccines: Implications for Travelers and People Living in Highly Endemic Areas" . ... CS1 maint: archived copy as title ( link ) >. ^ Rubin, Raphael., David S. Strayer., Emanuel Rubin., Jay M.
    CRP, PRKN, ABCB1, PACRG
    • Paratyphoid Fever Orphanet
      A rare form of salmonellosis caused by Salmonella enterica serovar Paratyphi A, characterized by typical symptoms of enteric fever including high fever, headache, abdominal pain and intestinal symptoms, dry cough, chills, and rashes, followed by a long period of recovery. The infection can be complicated by intestinal hemorrhage and perforation, as well as cardiac involvement, and may even be fatal. Transmission of the pathogen is via the fecal-oral route, with humans as the sole reservoir of infection.
  • Anosognosia Wikipedia
    Unawareness of one's own illness, symptoms or impairments Anosognosia Pronunciation / æ ˌ n ɒ s ɒ ɡ ˈ n oʊ z i ə / , / æ ˌ n ɒ s ɒ ɡ ˈ n oʊ ʒ ə / Specialty Psychiatry , Neurology Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. ... S2CID 34463285 . ^ a b Starkstein, S. E.; Fedoroff, J. P.; Price, T. R.; Leiguarda, R.; Robinson, R. ... Stroke . 23 (10): 1446–53. doi : 10.1161/01.STR.23.10.1446 . PMID 1412582 . ^ Chapman S, Colvin LE, Vuorre M, Cocchini G, Metcalfe J, Huey ED, Cosentino S (April 2018). ... ISBN 978-0-19-508497-9 . ^ David, Anthony S.; Amador, Xavier Francisco (2004). ... ISBN 978-0-19-852568-4 . ^ a b McEvoy, Joseph P.; Applebaum, Paul S.; Apperson, L. Joy; Geller, Jeffrey L.; Freter, Susan (1989).
    APOE, CDR1, CDR2, BRD2, MCIDAS
  • Cerebellar Cognitive Affective Syndrome Wikipedia
    Learning & Memory, 4, 1-35. ^ Hokkanen, L. S. K., Kauranen, V., Roine, R. O., Salonen, O., & Kotila, M. (2006). ... Lancet, 2, 700-701. ^ a b Tran, K. D., Smutzer, G. S., Doty, R. L., & Arnold, S. E. (1998). ... C., Giedd, J. N., Jacobsen, L. K., Hamburger, S. D., Krain, A. L., Rapoport, J. L., & Castellanos, F. ... Basel: Karger. ^ Konarski, J. Z., McIntyre, R. S., Grupp, L. A., & Kennedy, S. H. (2005). ... R., Safar, L., Ongur, D., Stone, W. S., Seidman L.J., Schmahmann, J.D., Pascual-Leone, A. (2010).
    STUB1, ERBB2
  • Fibrous Dysplasia Of Bone Wikipedia
    PMID 25719192 . ^ Cole DE; Fraser FC; Glorieux FH; Jequier S; Marie PJ; Reade TM; Scriver CR (14 Apr 1983). ... S2CID 21276747 . ^ Hart, Elizabeth S.; Kelly, Marilyn H.; Brillante, Beth; Chen, Clara C.; Ziran, Navid; Lee, Janice S.; Feuillan, Penelope; Leet, Arabella I.; Kushner, Harvey (2007-09-01). ... PMID 15005844 . S2CID 37760051 . ^ Weinstein, L. S.; Shenker, A.; Gejman, P. V.; Merino, M. ... ISSN 0021-9355 . PMID 14996879 . ^ Lee, J. S.; FitzGibbon, E. J.; Chen, Y. R.; Kim, H. J.; Lustig, L. R.; Akintoye, S. O.; Collins, M. T.; Kaban, L. B. (2012-05-24).
    GNAS, FGF23, COASY, FOLH1, GH1, IL6, TNFSF11, CREB1, MDM2, POSTN, MFAP1, CDK4, RUNX2, APRT, AR, HDAC8, DLEU7, S100A1, S100B, SH3BP2, SSTR4, LEPQTL1, ANBC, B3GAT1, LPAR2, ADAMTS2, ACKR3, PTH, CXCR6, SMUG1, PTGS2, ADRA1A, PRKAR1A, GHR, BGLAP, BMP2, BRS3, CAMP, COL1A1, CTNNB1, CFD, EDNRA, GPR42, CFP, IGF1, IGFBP3, SMAD6, MAS1, ADRA2B, COX2, NF1, FURIN, MTCO2P12
    • Fibrous Dysplasia Gard
      Fibrous dysplasia is a skeletal disorder that is characterized by the replacement of normal bone with fibrous bone tissue. It may involve one bone ( monostotic ) or multiple bones ( polyostotic ). Fibrous dysplasia can affect any bone in the body. The most common sites are the bones in the skull and face, the long bones in the arms and legs, the pelvis, and the ribs. Though many people with this disorder do not have any symptoms, others may have bone pain, abnormally shaped bones (deformities), or an increased risk of fractures (broken bones). The problems a person experiences depend on which bones are affected, and may arise from compression and displacement of adjacent structures to the lesions.
    • Fibrous Dysplasia Of Bone Orphanet
      Initial symptoms are usually pain in the involved limb(s), associated with a limp if the lower extremity is involved, and spontaneous fracture.
  • Oat Sensitivity Wikipedia
    They had the following amino acid sequences: Antibody recognition sites on three avenins CIP1 (γ-avenin) P S E Q Y Q P Y P E Q Q Q P F CIP2 (γ-avenin) T T T V Q Y D P S E Q Y Q P Y P E Q Q Q P F V Q Q Q P P F CIP3 (α-avenin) T T T V Q Y N P S E Q Y Q P Y Within the same study, three other proteins were identified, one of them an α- amylase inhibitor as identified by protein homology. ... PMID 10871113 . ^ Baldo BA, Krilis S, Wrigley CW (January 1980). "Hypersensitivity to inhaled flour allergens. ... PMID 25922672 . ^ Haboubi NY, Taylor S, Jones S (Oct 2006). "Coeliac disease and oats: a systematic review" . ... PMID 17068278 . ^ de Souza MC, Deschênes ME, Laurencelle S, Godet P, Roy CC, Djilali-Saiah I (2016). ... S2CID 3421741 . ^ Kilmartin C, Lynch S, Abuzakouk M, Wieser H, Feighery C (January 2003).
  • Currarino Syndrome Wikipedia
    Eur J Pediatr Surg . 17 (3): 214–6. doi : 10.1055/s-2007-965121 . PMID 17638164 . ^ Ashcraft KW; Holder TM (October 1974). ... CS1 maint: multiple names: authors list ( link ) ^ Emoto S, Kaneko M, Murono K, Sasaki K, Otani K, Nishikawa T, Tanaka T, Hata K, Kawai K, Imai H, Saito N, Kobayashi H, Tanaka S, Ikemura M, Ushiku T, Nozawa H (2018). ... CS1 maint: multiple names: authors list ( link ) ^ Crétolle C, Zérah M, Jaubert F, Sarnacki S, Révillon Y, Lyonnet S, Nihoul-Fékété C (2006). ... CS1 maint: multiple names: authors list ( link ) ^ Emoto S, Kaneko M, Murono K, Sasaki K, Otani K, Nishikawa T, Tanaka T, Hata K, Kawai K, Imai H, Saito N, Kobayashi H, Tanaka S, Ikemura M, Ushiku T, Nozawa H (2018). ... CS1 maint: multiple names: authors list ( link ) ^ Duru S, Karabagli H, Turkoglu E, Erşahin Y (2014).
    MNX1, PCSK5, HPGD, MNX1-AS2, HTC2, AKR1A1, ARMC9
    • Hypertrophic Osteoarthropathy, Primary, Autosomal Recessive, 1 Omim
      A number sign (#) is used with this entry because of evidence that autosomal recessive primary hypertrophic osteoathropathy-1 (PHOAR1) is caused by homozygous mutation in the HPGD gene (601688) on chromosome 4q34. Isolated digital clubbing (119900) as well as cranioosteoarthropathy can also be caused by homozygous mutation in the HPGD gene. Description Primary hypertrophic osteoarthropathy is a familial disorder characterized by digital clubbing and osteoarthropathy, with variable features of pachydermia, delayed closure of the fontanels, and congenital heart disease. Secondary hypertrophic osteoarthropathy, or pulmonary hypertrophic osteoarthropathy, is a different disorder characterized by digital clubbing secondary to acquired diseases, most commonly intrathoracic neoplasm (Uppal et al., 2008). Touraine et al. (1935) recognized pachydermoperiostosis as a familial disorder with 3 clinical presentations or forms: a complete form characterized by periostosis and pachydermia; an incomplete form with bone changes but without pachydermia; and a 'forme fruste' with pachydermia and minimal skeletal changes.
    • Currarino Syndrome Omim
      A number sign (#) is used with this entry because of evidence that at least some cases of the Currarino syndrome are caused by heterozygous mutation in the HLXB9 homeobox gene (MNX1; 142994) on chromosome 7q36. Clinical Features The Currarino triad involves the association of partial sacral agenesis with intact first sacral vertebra ('sickle-shaped sacrum'), a presacral mass, and anorectal malformation (Currarino et al., 1981). The specific sacral anomaly is distinct to this syndrome. Of 10 affected members in the family reported by O'Riordain et al. (1991), only 4 were symptomatic, 3 of these had the full Currarino syndrome (sacral agenesis, presacral mass, and anorectal malformation), and the fourth had an anterior meningocele with no anorectal problems. All 10 had evidence of partial sacral agenesis on x-ray. Constipation and perianal sepsis are common complaints. Ascending infection resulting in E. coli bacterial meningitis has been reported.
    • Currarino Syndrome Orphanet
      Currarino syndrome (CS) is a rare congenital disease characterized by the triad of anorectal malformations (ARMs) (usually anal stenosis), presacral mass (commonly anterior sacral meningocele (ASM) or teratoma) and sacral anomalies (i.e. total or partial agenesis of the sacrum and coccyx or deformity of the sacral vertebrae).
    • Currarino Triad Gard
      Currarino triad or syndrome is an autosomal dominant hereditary condition which is characterized by the triad of sacral agenesis abnormalities (abnormally developed lower spine), anorectal malformation (most commonly in the form of anorectal stenosis ) and presacral mass consisting of a teratoma , anterior sacral meningocele or both. However only 1 out of 5 cases of Currarino triad has all three abnormalities present. Currarino triad is considered a spectrum disorder with a wide variation in severity. Up to one-third of the patients are asymptomatic and may only be diagnosed during adulthood only on X-rays and ultrasound examinations that are performed for different reasons. Currarino triad is most often caused by mutations in the MNX1 gene . Treatment depends on the type and severity of abnormalities present, but may involve surgery.
    • Cranio-Osteoarthropathy Orphanet
      Cranio-osteoarthropathy (COA) is a form of primary hypertrophic osteoarthropathy (see this term) characterized by delayed closure of the cranial sutures and fontanels, digital clubbing, arthropathy, and periostosis. Epidemiology Prevalence is unknown. To date, about 30 cases have been reported. Clinical description COA presents in childhood with features of primary hypertrophic osteoarthropathy including digital clubbing and clinodactyly of the fingers, eczematous skin eruption, arthropathy and periosteal new bone formation as well as poor neurocranium ossification with delayed closure of the cranial sutures and fontanels, resulting in wide fontanels, and an increased number of wormian bones. COA may also be associated with congenital heart disease. Etiology It is caused by mutations in the HPGD gene (4q33-q34) and is inherited as an autosomal recessive trait; however, heterozygous carriers can have a mild phenotype.
  • Post-Thrombotic Syndrome Wikipedia
    . ^ Roumen-Klappe EM, Janssen MC, Van Rossum J, Holewijn S, Van Bokhoven MM, Kaasjager K, et al. ... Dermatology Online Journal . 14 (3): 13. PMID 18627714 . ^ Vedantham S (2009). "Valvular dysfunction and venous obstruction in the post-thrombotic syndrome". ... PMID 18983518 . ^ Prandoni P, Lensing AW, Cogo A, Cuppini S, Villalta S, Carta M, et al. (July 1996). ... PMID 9685132 . ^ Kahn SR, Partsch H, Vedantham S, Prandoni P, Kearon C (May 2009). ... PMID 12535239 . ^ Bergqvist D, Jendteg S, Johansen L, Persson U, Odegaard K (March 1997).
    F5, F2, F10, PECAM1
  • Filariasis Wikipedia
    . ^ Macfarlane CL, Budhathoki SS, Johnson S, Richardson M, Garner P (January 2019). ... PMC 6354574 . PMID 30620051 . ^ Adinarayanan S, Critchley J, Das PK, Gelband H, et al. ... PMC 6532694 . PMID 17253495 . ^ Gaur RL, Dixit S, Sahoo MK, Khanna M, Singh S, Murthy PK (April 2007). ... Parasitology . 134 (Pt 4): 537–44. doi : 10.1017/S0031182006001612 . PMID 17078904 . ^ Hoerauf A, Mand S, Fischer K, Kruppa T, Marfo-Debrekyei Y, Debrah AY, Pfarr KM, Adjei O, Buttner DW (2003), "Doxycycline as a novel strategy against bancroftian filariasis-depletion of Wolbachia endosymbionts from Wuchereria bancrofti and stop of microfilaria production", Med Microbiol Immunol (Berl) , 192 (4): 211–6, doi : 10.1007/s00430-002-0174-6 , PMID 12684759 , S2CID 23349595 ^ Taylor MJ, Makunde WH, McGarry HF, Turner JD, Mand S, Hoerauf A (2005), "Macrofilaricidal activity after doxycycline treatment of Wuchereria bancrofti: a double-blind, randomised placebo-controlled trial", Lancet , 365 (9477): 2116–21, doi : 10.1016/S0140-6736(05)66591-9 , PMID 15964448 , S2CID 21382828 ^ a b Andersson J, Forssberg H, Zierath JR (5 October 2015), "Avermectin and Artemisinin - Revolutionary Therapies against Parasitic Diseases" (PDF) , The Nobel Assembly at Karolinska Institutet , retrieved 5 October 2015 ^ Ndeffo-Mbah ML, Galvani AP (April 2017). ... Page from the "Merck Veterinary Manual" on "Parafilaria multipapillosa" in horses v t e Parasitic disease caused by helminthiases Flatworm/ platyhelminth infection Fluke/trematode ( Trematode infection ) Blood fluke Schistosoma mansoni / S. japonicum / S. mekongi / S. haematobium / S. intercalatum Schistosomiasis Trichobilharzia regenti Swimmer's itch Liver fluke Clonorchis sinensis Clonorchiasis Dicrocoelium dendriticum / D. hospes Dicrocoeliasis Fasciola hepatica / F. gigantica Fasciolosis Opisthorchis viverrini / O. felineus Opisthorchiasis Lung fluke Paragonimus westermani / P. kellicotti Paragonimiasis Intestinal fluke Fasciolopsis buski Fasciolopsiasis Metagonimus yokogawai Metagonimiasis Heterophyes heterophyes Heterophyiasis Cestoda ( Tapeworm infection ) Cyclophyllidea Echinococcus granulosus / E. multilocularis Echinococcosis Taenia saginata / T. asiatica / T. solium (pork) Taeniasis / Cysticercosis Hymenolepis nana / H. diminuta Hymenolepiasis Pseudophyllidea Diphyllobothrium latum Diphyllobothriasis Spirometra erinaceieuropaei Sparganosis Diphyllobothrium mansonoides Sparganosis Roundworm/ Nematode infection Secernentea Spiruria Camallanida Dracunculus medinensis Dracunculiasis Spirurida Filarioidea ( Filariasis ) Onchocerca volvulus Onchocerciasis Loa loa Loa loa filariasis Mansonella Mansonelliasis Dirofilaria repens D. immitis Dirofilariasis Wuchereria bancrofti / Brugia malayi / | B. timori Lymphatic filariasis Thelazioidea Gnathostoma spinigerum / G. hispidum Gnathostomiasis Thelazia Thelaziasis Spiruroidea Gongylonema Strongylida ( hookworm ) Hookworm infection Ancylostoma duodenale / A. braziliense Ancylostomiasis / Cutaneous larva migrans Necator americanus Necatoriasis Angiostrongylus cantonensis Angiostrongyliasis Metastrongylus Metastrongylosis Ascaridida Ascaris lumbricoides Ascariasis Anisakis Anisakiasis Toxocara canis / T. cati Visceral larva migrans / Toxocariasis Baylisascaris Dioctophyme renale Dioctophymosis Parascaris equorum Rhabditida Strongyloides stercoralis Strongyloidiasis Trichostrongylus spp.
    IL10, IFNG, SLCO6A1, GPT2, MBL2, IL5, IL4, IGHG3, GSTK1, CHIT1, EDN1, HLA-A, TLR2, DTYMK, PRDX5, DLEU2, ALKBH1, TNFRSF18, TTR, TNF, TLR4, TGM1, HSPA8, LGALS2, IL13, CALU, F13A1, F13B, IL2, GLB1, GPT, ABO
    • Filariasis Orphanet
      A parasitic disease caused by tissue-invasive, vector-borne nematodes which can be found anywhere in the human body and that are transmitted to humans through the bite of an infected mosquito or fly or by consumption of unsafe drinking water and which, depending on the subtype can manifest with lymphedema, dermatitis, subcutaneous edema and eye involvement. The disorder is a major public health problem in many tropical and subtropical countries. Six subtypes have been described in the literature: lymphatic filariasis, onchocerciasis, loiasis, mansonelliasis, dirofilariasis and dracunculiasis caused by Wuchereria bancrofti and filarioidea of the genus Brugia ; Onchocerca volvulus ; Loa loa ; Mansonella ; Dirofilaria ; and Dracunculus medinensis , respectively. Tropical eosinophilia is considered a frequent manifestation.
  • Chronic Deciduitis Wikipedia
    .; Machin, G.; Rizek, R.; Watson, C.; Keating, S. (2009). "The prevalence of chronic deciduitis in cases of preterm labor without clinical chorioamnionitis". ... S2CID 25693917 . ^ Khong, TY.; Bendon, RW.; Qureshi, F.; Redline, RW.; Gould, S.; Stallmach, T.; Lipsett, J.; Staples, A.
  • Embryocardia Wikipedia
    Please introduce links to this page from related articles ; try the Find link tool for suggestions. ( February 2017 ) Embryocardia Specialty Neonatology Embryocardia is a condition in which S 1 and S 2 ( the two heart sounds that produce the typical " lubb-dubb " sound of the heart) become indistinguishable and equally spaced. [1] Thus the normal "lubb-dubb" rhythm of the heart becomes a "tic-toc" rhythm resembling the heart sounds of a fetus .
  • Neurotrophic Keratitis Wikipedia
    Clin Ophthalmol 8 (2014) 571-9. ^ Bonini S, Rama P, Olzi D, Lambiase A, Neurotrophic keratitis. Eye 17 (2003) 989-995. ^ B.S. Shaheen, M. Bakir, and S. Jain, Corneal nerves in health and disease. ... Liesegang, Corneal complications from herpes zoster ophthalmicus. Ophthalmology 92 (1985) 316-24. ^ S. Bonini, P. Rama, D. Olzi, and A. ... Hyndiuk, E. L. Kazarian, R. O. Schultz, and S. Seideman, Neurotrophic corneal ulcers in diabetes mellitus. Arch Ophthalmol 95 (1977) 2193-6. ^ S. Bonini, P. Rama, D. Olzi, and A.
    NGF, TAC1, TMSB4X, TYRP1, NRP1, TBPL1, SEMA3C
    • Neurotrophic Keratopathy Orphanet
      Neurotrophic keratopathy is a rare degenerative disease of the cornea characterized by reduction or loss of corneal sensitivity that can be asymptomatic or present with red-eye and, during the early stages of the disease, a minor decrease in visual acuity. It eventually leads to loss of vision. Epidemiology No epidemiological data are available. However, prevalence can be estimated at around 1/2,380 in Europe. Clinical description Neurotrophic keratopathy (NK) most commonly occurs in adults, and rarely presents in children. It is often asymptomatic, but early signs can include red-eye, blurred vision, and decreased visual acuity. As the disease progresses, epithelial defects and corneal ulcers may develop; corneal scarring and astigmatism can lead to further reduction of visual function.
  • Subareolar Abscess Wikipedia
    ISSN 0007-1323 . ^ Rizzo M, Gabram S, Staley C, Peng L, Frisch A, Jurado M, Umpierrez G (March 2010). ... Geburtshilfe Frauenheilkd (in German). 51 (2): 109–16. doi : 10.1055/s-2007-1023685 . PMID 2040409 . ^ a b Michael S. ... Radiographics (review). 31 (6): 1683–99. doi : 10.1148/rg.316115521 . PMID 21997989 . ^ a b Hanavadi S, Pereira G, Mansel RE (2005). "How mammillary fistulas should be managed". ... Thieme Georg Verlag. ISBN 3-13-722904-9 . ^ Michael S. Sabel (2009). Essentials of Breast Surgery . ... Further reading [ edit ] Kasales CJ, Han B, Smith JS, Chetlen AL, Kaneda HJ, Shereef S (February 2014). "Nonpuerperal mastitis and subareolar abscess of the breast".
  • Neuro-Behçet's Disease Wikipedia
    References [ edit ] ^ Serdaroflu P, Yazici H, Ozdemir C, Yurdakul S, Bahar S, Aktin E (1989). "Neurologic involvement in Behçet's syndrome. ... PMID 2919979 . ^ Yazici H, Fresko I, Yurdakul S (2007). "Behçet's syndrome: disease manifestations, management, and advances in treatment". ... PMID 17334337 . S2CID 21869670 . ^ Farah S, Al-Shubaili A, Montaser A (1998). ... Brain . 122 : 2171–82. doi : 10.1093/brain/122.11.2171 . PMID 10545401 . ^ Al-Fahad S, Al-Araji A (1999). "Neuro-Behçet's disease in Iraq: a study of 40 patients". ... Koçer, N; Islak, C; Siva, A; Saip, S; Akman, C; Kantarci, O; Hamuryudan, V (Jun–Jul 1999).
  • Phaeohyphomycosis Wikipedia
    See also [ edit ] Skin lesion References [ edit ] ^ Naggie S, Perfect JR (June 2009). "Molds: hyalohyphomycosis, phaeohyphomycosis, and zygomycosis" . ... Clinical Infectious Disease 34:467-476. ^ a b c d e f g Seyedmousavi, S., J. Guillot and G. S. de Hoog. 2013. ... Journal of Dermatology 40:638-640. ^ a b Cai, Q., G. Lv, Y. Jiang, H. Mei, S. Hu, H. Xu, X. Wu, Y. Shen, and W. ... Mycopathologia 176:101-105. ^ Bossler, A. D., S. S. Richter, A. J. Chavez, S. A. Vogelgesang, D. ... Sutton, A. M. Grooters, M. G. Rinaldi, G. S. de Hoog, and M. A. Pfaller. 2003.
    CARD9, CRK, MAPK14, MAPK1, AIMP2, GRAP2, AHSA1, RNF19A, POLDIP2
    • Phaeohyphomycosis Gard
      Phaeohyphomycosis refers to fungal infections caused by dematiaceous (darkly pigmented) fungi. It can be associated with a variety of clinical syndromes including invasive sinusitis ; nodules or abscesses beneath the skin; keratitis ; lung masses; osteomyelitis ; mycotic arthritis ; endocarditis ; brain abscess; and wide-spread infection. Although the condition can affect anyone, it is most commonly diagnosed in people with suppressed immune systems (like those who have undergone an organ transplant) and can even be life-threatening in these populations. Treatment depends on the signs and symptoms present in each person but may include surgery and/or various antifungal medications.
  • Dental Subluxation Wikipedia
    See also [ edit ] Subluxation Dental trauma References [ edit ] ^ a b c Paediatric dentistry . Welbury, Richard., Duggal, Monty S., Hosey, Marie Thérèse. (4th ed.). ... Retrieved 2018-11-12 . ^ Lecky F, Russell W, Fuller G, McClelland G, Pennington E, Goodacre S, Han K, Curran A, Holliman D, Freeman J, Chapman N, Stevenson M, Byers S, Mason S, Potter H, Coats T, Mackway-Jones K, Peters M, Shewan J, Strong M (January 2016). ... Retrieved 2018-11-12 . ^ Azami-Aghdash S, Ebadifard Azar F, Pournaghi Azar F, Rezapour A, Moradi-Joo M, Moosavi A, Ghertasi Oskouei S (2015).
  • Aplasia Cutis Congenita Wikipedia
    Naevi and other developmental defects. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology. 8th ed. ... Naevi and other developmental defects. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology. 8th ed. United Kingdom (UK): Wiley-Blackwell Publication; 2010. p. 18, 18.98-18. 106. ^ Meena N, Saxena AK, Sinha S, Dixit N. Aplasia cutis congenita with fetus papyraceus. ... Naevi and other developmental defects. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology. 8th ed. United Kingdom (UK): Wiley-Blackwell Publication; 2010. p. 18, 18.98-18. 106. ^ Meena N, Saxena AK, Sinha S, Dixit N. Aplasia cutis congenita with fetus papyraceus.
    BMS1, ITGB4, DLL4, PLEC, GJB6, RHOA, NOTCH1, DOCK6, ARHGAP31, COL7A1, KCTD1, EOGT, TFAP2A, NFIB, GLI3, IGF2, ITGA6, KRAS, LAMA3, HSPA9, COL17A1, COX7B, CTNNB1, TP53, LAMB3, LAMC2, MYB, TAF1, DSP, B9D1, ACACA, RBPJ, ATRX, ATP6V1B2, KIT, MYBL1, MIR483, EGFR, PRKAB1, PRKAA1, PRKAA2, ERBB2, IGF1, CDKN2A, NR5A1, IGF1R, CXCR4, ESR1, VEGFA, SOX10, ELAVL2, ZNRF3, HTC2, CCND1, BCL2A1, LOC110806263, RUNX3, ACACB, PIK3CA, MDM2, RASSF1, SLC12A7, APC, ZEB2, PGR, SST, MC2R, TERT, TWIST1, HIF1A, POMC, BRCA1, VIM, MTOR, ERCC1, MIR210, INHA, ABCB1, PECAM1, MIR195, POTEM, POTEKP, MSH2, MRC1, MIR503, MEN1, SMAD4, STMN1, PIK3CB, MIR335, SCARNA22, MIR497, MET, DKK3, PIM1, ARMC5, TYMS, VAV2, GEMIN2, BECN1, PROM1, SCAF11, PTTG1, IL6, SLC9A3R2, LONP1, FHL5, CD274, ACOT7, SMUG1, TOP2A, ACTBL2, PIK3CD, RARRES2, PIK3CG, MIR184, PPARG, PRKAR1A, MIR139, PTEN, BBC3, STK11, SKP2, SLC2A1, SMARCA2, FSCN1, SOX2, MALAT1, SERPINA3, MAPK8, ATM, ACTG1, BCL2, EZH2, FABP7, FOXM1, FOXO1, FN1, AQP1, XIAP, BUB1B, GNAS, CYP19A1, JAG1, ACTG2, ESRRA, HSP90AA1, CDK2, UBA2, HCN2, SLC40A1, NEUROG3, PDE11A, TMED7, CDH1, LEF1, SIRT6, MED27, NBAS, DDX23, DCUN1D1, DIABLO, PBK, PCYT1B, ACKR3, NDRG2, BCL9, CDKN1B, CGA, GAS5, NDRG4, PINK1, BIRC7, CORO7, OBP2A, BNIP3, GLYAT, MAT2B, ZNRD2, AKT3, DCTN6, CD44, CDA, CD36, MELK, LILRB1, SDS, CD14, HRH3, CCNB1, MMRN1, SPEN, TBC1D9, CDK1, NNT, CASP3, LIN28A, PELP1, CAD, B3GAT1, PCLAF, BRCA2, APOBEC3B, LY96, IL2, BARD1, MIR205, ALCAM, MIR214, MIR222, MIR34A, MIR17HG, AKT1, AGT, MIR431, MIR511, ADK, SNORA21, UCA1, ASIC2, SCARNA4, SNORA51, MIR675, ZGLP1, FCGR1CP, PRINS, AOS, MIR1275, MIR1202, TMED7-TICAM2, MYB-AS1, MTCO2P12, ACADVL, H3P23, MIR21, ALOX15B, EHMT1, BIRC2, PDCD1LG2, SESN2, KREMEN1, BCL10, MINDY4, MAML2, FATE1, ZNF160, MRAP2, AZIN2, TXNRD3, TWIST2, AMER1, KCTD11, SKA1, ARSA, HMSD, AQP3, GADL1, CYP26C1, TICAM2, SBSN, MIRLET7D, BIRC3, MIR150, MIR155, MIR183, CP, DGKZ, SPHK1, FOSB, MYC, NAGA, NAGLU, GHSR, NOS1, NOS2, GFAP, NUMA1, PA2G4, PCNA, GCG, GATA6, GAA, FOS, MUC1, FOLH1, FOXO3, PLAG1, PMAIP1, FGFR3, FGFR1, FCGR1B, FCGR1A, PRKACA, PRKD1, MAPK1, PSMD9, ETV6, GLP1R, COX2, CREBBP, HLA-G, IL13, IGF2R, IFNB1, ITGAV, IFI27, JUN, JUNB, JUND, ID1, KIF22, HSPD1, KRT15, HSD17B4, HGF, SFN, LHCGR, EPCAM, MARCKS, HDC, GUSB, MCAM, GSTP1, NR3C1, GRIN2B, MGMT, KMT2A, MMP9, GPX4, PTGS2, PTK7, PTPRC, CYP11B1, TCF21, DHCR24, TIMM8A, TFAP2C, TGFA, TLR4, DECR1, DDT, TSC1, DAPK1, UBC, KDM6A, CYP17A1, VEGFC, NECTIN1, CTLA4, SF1, CTBS, GHS, NR4A3, MLRL, AXIN1, AXIN2, VCAN, PPM1D, CXCL8, NCOA1, CRH, TBX1, SARDH, SULT2A1, DNAH8, RASGRF1, RPS6KB1, RRM1, RRM2, S100A1, S100B, SCN7A, SDHB, SFPQ, SGTA, EPHB2, EN1, SMARCA1, CTTN, EIF4EBP1, SOAT1, SORD, SOS1, EIF4E, SOX4, EGF, SPN, SPP1, SRC, E2F1, STAR, STAT3, H3P10
    • Aplasia Cutis Congenita Gard
      Aplasia cutis congenita is a condition in which there is congenital (present from birth) absence of skin, with or without the absence of underlying structures such as bone. It most commonly affects the scalp, but any location of the body can be affected. While most people with aplasia cutis congenita have no other abnormalities, some people have congenital malformations involving the cardiovascular (heart), gastrointestinal, genitourinary, and central nervous systems. The cause of this condition is unclear and appears to be multifactorial (many different factors appear to play a role); contributing factors may include teratogens, genes, trauma, and compromised blood flow to the skin.
    • Aplasia Cutis Congenita Orphanet
      A rare skin disorder characterized by localized absence of skin that is usually located on the scalp but can occur anywhere on the body including the face, trunk and extremities. Aplasia cutis congenita (ACC) may occasionally be associated with other anomalies. Epidemiology Worldwide ACC prevalence is approximately 1/10,000 live births. Clinical description ACC is noticed immediately at birth and usually presents as a solitary lesion on or near the vertex. There may also be multiple lesions occurring on the scalp or elsewhere.
    • Aplasia Cutis Congenita, Nonsyndromic Omim
      A number sign (#) is used with this entry because of evidence that nonsyndromic aplasia cutis congenita (ACC) is caused by heterozygous mutation in the BMS1 gene (611448) on chromosome 10q11. One such family has been reported. Description Aplasia cutis congenita (ACC) is defined as congenital localized absence of skin. The skin appears as a thin, transparent membrane through which the underlying structures are visible. The location is usually on the scalp (Evers et al., 1995). Approximately 20 to 30% of cases have underlying osseous involvement (Elliott and Teebi, 1997). Autosomal dominant inheritance is most common, but recessive inheritance has also been reported.
    • Aplasia Cutis Congenita Of Limbs, Autosomal Recessive Omim
      Clinical Features Freire-Maia et al. (1980) described congenital absence of skin in the upper or lower limbs or both in 6 members (5 males and 1 female) of 3 inbred sibships of the same kindred. The lesions usually healed spontaneously leaving a clinical appearance like that of the hypotrichotic scar of an old burn. In 6 instances, an affected father married to a relative had an affected child (pseudodominance). There was no trunk or scalp involvement. Portnoy and Metzker (1981) described a disorder affecting a brother and sister with Yemenite parents who were presumed to be unrelated. Clinically, the disorder resembled the Bart type of epidermolysis bullosa dystrophica (132000), which is inherited as an autosomal dominant, but may, in fact, represent prenatal manifestation of epidermolysis bullosa of either the Koebner type (131900), due to a keratin defect, or epidermolysis bullosa dystrophica, due to a defect in COL7A1 (120120).
    • Nonsyndromic Aplasia Cutis Congenita Medlineplus
      Nonsyndromic aplasia cutis congenita is a condition in which babies are born with localized areas of missing skin (lesions). These areas resemble ulcers or open wounds, although they are sometimes already healed at birth. Lesions most commonly occur on the top of the head (skull vertex), although they can be found on the torso or limbs. In some cases, the bone and other tissues under the skin defect are also underdeveloped. Most affected babies have a single lesion. The lesions vary in size and can be differently shaped: some are round or oval, others rectangular, and still others star-shaped.
  • ←
  • 1
  • 2
    • ...
  • 15
  • 16
  • 17
  • 18
  • 19
  • 20
  • 21
    • ...
  • 321
  • 322
  • →

FindZebra

contact@findzebra.com