Metalloendoprotease inhibitors that block fusion also prevent biochemical differentiation in L6 myoblasts.

The effect of metalloendoprotease inhibitors on the biochemical differentiation of the rat skeletal muscle line, L6, was investigated. Confluent unfused L6 cells exposed briefly to 1,10-phenanthroline, a chelator of divalent metal cations, or continuously to dipeptide amide metalloendoprotease substrates that are blocked at the NH2-terminals, N-carbobenzyloxyserylleucyl amide and N-carbobenzyloxyglycylleucyl amide, did not fuse or express creatine kinase, myosin heavy chain, or alpha-actin. These effects were reversible and dose-dependent. Exposure to N-carbobenzyloxylglycylglycyl amide, which is not a metalloendoprotease inhibitor, had no effect. As the differentiation in a culture progressed, 1,10-phenanthroline became less effective in blocking the accumulation of creatine kinase and myosin heavy chain. Exposure of partially fused cultures to N-carbobenzyloxyserylleucyl amide prevented any further accumulation of muscle-specific proteins. In confluent cultures where cell division was blocked before the onset of differentiation, N-carbobenzyloxyserylleucyl amide still prevented fusion and the induction of creatine kinase. This indicates that these inhibitors do not act by interfering with the cell cycle. Experiments that measured DNA synthesis rates, plating efficiencies, and the effects of sequential dipeptide and dimethyl sulfoxide treatments indicate that L6 myoblasts do not irreversibly withdraw from the cell cycle when exposed to N-carbobenzyloxyserylleucyl amide. These results are consistent with the role of a metalloendoprotease in initiating the terminal differentiation of cultured muscle cells

Lung adenocarcinoma with peculiar growth to the pulmonary artery and thrombus formation: report of a case

<p>Abstract</p> <p>Background</p> <p>Cases of pulmonary artery masses have only rarely been reported, and the optimal type of the diagnosis and treatment is controversial.</p> <p>Case Presentation</p> <p>An 81-year-old woman was found to have an abnormal shadow on chest X-ray film. Computed tomography showed an irregularly bordered tumor centered in the hilar region extending from segment 6 to the middle lobe of the right lung. Pulmonary angiography showed complete occlusion of the trunk at the periphery proximal to the bifurcation of the posterior ascending branch. Based on bronchoscopic biopsy of the tumor, an adenocarcinoma was diagnosed. Middle and lower lobectomy was performed. Histopathologically, the adenocarcinoma had invaded the tunica intima of the pulmonary artery and also replaced the endothelium in the same region. Although a large thrombus was found at the vessel invasion site of the adenocarcinoma in the pulmonary artery, there were no malignant findings in the thrombus itself.</p> <p>Conclusions</p> <p>This is the first reported case of radical resection of a lung cancer with invasion along the pulmonary artery wherein a benign thrombus had formed. In general, surgery would be the treatment of choice for a pulmonary artery mass.</p

Role of anatomical sites and correlated risk factors on the survival of orthodontic miniscrew implants:a systematic review and meta-analysis

Abstract Objectives The aim of this review was to systematically evaluate the failure rates of miniscrews related to their specific insertion site and explore the insertion site dependent risk factors contributing to their failure. Search methods An electronic search was conducted in the Cochrane Central Register of Controlled Trials (CENTRAL), Web of Knowledge, Scopus, MEDLINE and PubMed up to October 2017. A comprehensive manual search was also performed. Eligibility criteria Randomised clinical trials and prospective non-randomised studies, reporting a minimum of 20 inserted miniscrews in a specific insertion site and reporting the miniscrews’ failure rate in that insertion site, were included. Data collection and analysis Study selection, data extraction and quality assessment were performed independently by two reviewers. Studies were sub-grouped according to the insertion site, and the failure rates for every individual insertion site were analysed using a random-effects model with corresponding 95% confidence interval. Sensitivity analyses were performed in order to test the robustness of the reported results. Results Overall, 61 studies were included in the quantitative synthesis. Palatal sites had failure rates of 1.3% (95% CI 0.3–6), 4.8% (95% CI 1.6–13.4) and 5.5% (95% CI 2.8–10.7) for the midpalatal, paramedian and parapalatal insertion sites, respectively. The failure rates for the maxillary buccal sites were 9.2% (95% CI 7.4–11.4), 9.7% (95% CI 5.1–17.6) and 16.4% (95% CI 4.9–42.5) for the interradicular miniscrews inserted between maxillary first molars and second premolars and between maxillary canines and lateral incisors, and those inserted in the zygomatic buttress respectively. The failure rates for the mandibular buccal insertion sites were 13.5% (95% CI 7.3–23.6) and 9.9% (95% CI 4.9–19.1) for the interradicular miniscrews inserted between mandibular first molars and second premolars and between mandibular canines and first premolars, respectively. The risk of failure increased when the miniscrews contacted the roots, with a risk ratio of 8.7 (95% CI 5.1–14.7). Conclusions Orthodontic miniscrew implants provide acceptable success rates that vary among the explored insertion sites. Very low to low quality of evidence suggests that miniscrews inserted in midpalatal locations have a failure rate of 1.3% and those inserted in the zygomatic buttress have a failure rate of 16.4%. Moderate quality of evidence indicates that root contact significantly contributes to the failure of interradicular miniscrews placed between the first molars and second premolars. Results should be interpreted with caution due to methodological drawbacks in some of the included studies

Metalloendoprotease inhibitors that block fusion also prevent biochemical differentiation in L6 myoblasts.

The effect of metalloendoprotease inhibitors on the biochemical differentiation of the rat skeletal muscle line, L6, was investigated. Confluent unfused L6 cells exposed briefly to 1,10-phenanthroline, a chelator of divalent metal cations, or continuously to dipeptide amide metalloendoprotease substrates that are blocked at the NH2-terminals, N-carbobenzyloxyserylleucyl amide and N-carbobenzyloxyglycylleucyl amide, did not fuse or express creatine kinase, myosin heavy chain, or alpha-actin. These effects were reversible and dose-dependent. Exposure to N-carbobenzyloxylglycylglycyl amide, which is not a metalloendoprotease inhibitor, had no effect. As the differentiation in a culture progressed, 1,10-phenanthroline became less effective in blocking the accumulation of creatine kinase and myosin heavy chain. Exposure of partially fused cultures to N-carbobenzyloxyserylleucyl amide prevented any further accumulation of muscle-specific proteins. In confluent cultures where cell division was blocked before the onset of differentiation, N-carbobenzyloxyserylleucyl amide still prevented fusion and the induction of creatine kinase. This indicates that these inhibitors do not act by interfering with the cell cycle. Experiments that measured DNA synthesis rates, plating efficiencies, and the effects of sequential dipeptide and dimethyl sulfoxide treatments indicate that L6 myoblasts do not irreversibly withdraw from the cell cycle when exposed to N-carbobenzyloxyserylleucyl amide. These results are consistent with the role of a metalloendoprotease in initiating the terminal differentiation of cultured muscle cells