PubMed · 3317705
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R A Goldstein. 1987. Inotropic support in patients with left ventricular dysfunction.. https://pubmed.ncbi.nlm.nih.gov/3317705/
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Risk factors for equine laminitis were examined in a prospective case-control study of the 258 cases seen at six collaborating veterinary teaching hospitals over a 32-month period. Case-control pairs were matched on institution, clinician, and season of diagnosis. The 90% of case-control pairs (78 acute, 155 chronic) that had complete data for age, gender, and breed were used in separate conditional logistic-regression models for acute and chronic laminitis. There was an increase in risk for horses with acute laminitis from 5 to 7 years of age (OR 4.7, 95% CI 1.3-16) and from 13 to 31 years of age (OR 3.9, 95% CI 1.3-12) (both compared to <5 years); risk was increased for chronic laminitis from 10 to 14 years (OR 3, 95% CI 1.4-6.8) and from 15 to 38 years (OR 2.9, 95% CI 1.4-6.1) (both compared to <6 years). Mares - but not stallions - were more likely than geldings to develop acute laminitis (OR 2.6, 95% CI 1.1-6.2) and chronic laminitis (OR 2.0, 95% CI 1.1-3.6). In the small acute-laminitis data set, the breed variable was collapsed into three categories: Thoroughbred (THB, reference), the Quarter Horse (QH), and other (non-QH-THB). The non-QH-THB group was at increased risk of acute laminitis (OR 3.8, 95% CI 1.2-11.8). For the seven breed-group categories used in the chronic-laminitis model, however, all non-THB breed groups appeared significantly at risk as compared to the THB, with odds ratios ranging from 3.3 (95% CI 1.3-8.30) for the QH to 9.1 (95% CI 2.1-39.3) for ponies.
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Human T-cell leukemia virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia (ATL), although the precise mechanisms involved in the transformation process have not yet been defined. Deregulated inhibition of apoptosis may facilitate the insurgence of leukemia. Survivin is an inhibitor of apoptosis and considered to play a role in oncogenesis. We investigated the expression of survivin in HTLV-I-infected T-cell lines and primary ATL cells. Northern blot analysis showed expression of survivin transcript in all 9 HTLV-I-positive T-cell lines. High survivin expression levels were detected in primary cells of patients with acute-type ATL, but no such expression was noted in the cells of chronic-type ATL or normal peripheral blood mononuclear cells. Treatment of an HTLV-I-infected T-cell line, MT-1, with survivin specific antisense oligonucleotide resulted in reduced cell growth. Our results suggest that expression of survivin may play an important role in the development and pathogenesis of ATL.