Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin-dependent diabetes (IDDM) results from autoimmune destruction of pancreatic beta cells mediated predominantly by cellular effector mechanisms. To date, investigators have studied a limited number of islet cell proteins stimulatory to T cells. However, before development of clinical IDDM, the majority of the beta cells are impaired or destroyed. Thus, numerous proteins from lysed beta cells would be accessible to the immune system of the patient. Our goal was to investigate the PBMC reactivity of IDDM patients to the full spectrum of fractionated human pancreatic islet cell proteins to determine whether numerous islet cell proteins or a select few would be recognized. We observed that PBMCs from IDDM patients responded reproducibly (mean stimulation index, >2.0) to the proteins in all m.w. regions, whereas the mean stimulation index for controls from all m.w. regions was <2.0. Using three different islet protein preparations, PBMC responses of IDDM patients (n = 30) and controls (n = 39) to the islet cell proteins were significantly different. Dose responses were also demonstrated for the lymphocyte reactivity of the IDDM patients (n = 29) vs controls (n = 56) to the islet cell preparations. Proteins, presumably irrelevant to the IDDM disease process, from a human osteosarcoma cell line and normal human spleen cells did not stimulate PBMCs from IDDM patients or controls. Moreover, IDDM patients and controls responded similarly to mitogens and tetanus toxoid. These studies show that at the time of diagnosis of IDDM, PBMCs from IDDM patients are stimulated by a wide array of islet cell proteins.
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PMID:Peripheral blood mononuclear cells of insulin-dependent diabetic patients respond to multiple islet cell proteins. 895 20

A consecutive series of cases of dogs and cats with locked jaw syndrome (inability to open or close the mouth) are reported in this study. Dogs were significantly overrepresented (84.0%) and adult dogs were more frequently affected (81.0%). Temporomandibular joint ankylosis due to fracture was the most common cause (54.0%) of locked jaw syndrome. Additional potential causes of locked jaw syndrome are masticatory muscle myositis, neoplasia, trigeminal nerve paralysis and central neurological lesions, temporomandibular joint luxation and dysplasia, osteoarthritis, retrobulbar abscess, tetanus, and severe ear disease. Treatment of locked jaw is directed towards the primary cause. It is important to treat the tonic spasm in order to minimize periarticular fibrosis. Surgical intervention is recommended for temporomandibular joint ankylosis. Masticatory muscle myositis treatment is initiated by gradually opening the mouth, with medical treatment based on immunosuppressive therapy. Fracture and masticatory muscle myositis are associated with a relatively good prognosis in regard to short-term outcome as compared to animals with central neurologic lesions or osteosarcoma which have a poor prognosis.
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PMID:Locked jaw syndrome in dogs and cats: 37 cases (1998-2005). 1875 57