We studied 39 patients with thromboangiitis obliterans to determine their cellular and humoral immune responses to native human collagen Type I and Type III, which are constituents of blood vessels. Cell-mediated sensitivity to these collagens was measured by an antigen-sensitive thymidine-incorporation assay. The mean stimulation index--the ratio of thymidine incorporation in the presence of antigen to that in its absence--with both Type I and Type III collagens used as antigens was significantly higher in patients with thromboangiitis obliterans than in patients with arteriosclerosis obliterans or in healthy male controls. Lymphocytes from 77 per cent of the patients with thromboangiitis obliterans exhibited cellular sensitivity to human Type I or Type III collagens (or both). Furthermore, in 17 of 39 serum samples from the patients with thromboangiitis obliterans a low but significant level of anticollagen antibody activity was detected, whereas there was no antibody activity in serum samples from controls. These results suggest that there is a distinct etiologic factor in this disease and also raise the possibility of differentiating between thromboangiitis obliterans and arteriosclerosis obliterans by immunologic means.

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Pulmonary fibrosis is a disorder causing a high mortality rate for which therapeutic options are limited. Therefore, the effect of halofuginone, a novel inhibitor of collagen type I synthesis, on bleomycin-induced pulmonary fibrosis was studied in rats. Pulmonary fibrosis was induced by intraperitoneal injections of bleomycin for seven consecutive days, and halofuginone was administered intraperitoneally every second day during the entire experimental period of 42 d. Collagen determination in the lungs and the examination of histologic sections showed that halofuginone significantly reduced fibrosis relative to the untreated control rats. We conclude that halofuginone is a potent in vivo inhibitor of bleomycin-induced pulmonary fibrosis, and that it may potentially be used as a novel therapeutic agent for the treatment of this dysfunction.

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Three wall intrabony defects were produced in 11 dogs using a round bur followed by curettes and hoes. A copper band was fixed to the tooth with stainless steel ligature wire. Six weeks later, the copper band was removed and the defect was treated with an enriched collagen solution (ECS) prepared from acid-extracted dog skin collagen. Thirty-three defects were treated with ECS and 33 defects were controls. Healing was assessed histologically 4 and 6 weeks after treatment for the presence of new cementum, periodontal ligament and alveolar bone, as well as arrested epithelial downgrowth along the dental root. Unlike the controls, treatment with ECS resulted in restoration of periodontal attachment after 4 weeks. This included formation of new cementum, new alveolar bone and dense connective tissue fiber running between bone and cementum. Control sections showed epithelial migration along the root, separating it from the adjacent connective tissue and thus preventing new attachment.