Search

Objective: Well-conducted meta-analyses (MAs) are considered as one of the best sources of clinical evidence for treatment decision. MA with methodological flaws may introduce bias and mislead evidence users. The aim of this study is to investigate the characteristics and methodological quality of MAs on diabetes mellitus (DM) treatments., Design: Systematic review., Methods: Cochrane Database of Systematic Review and Database of Abstract of Reviews of Effects were searched for relevant MAs. Assessing methodological quality of systematic reviews (AMSTAR) tool was used to evaluate the methodological quality of included MAs. Logistic regression analysis was used to identify association between characteristics of MA and AMSTAR results., Results: A total of 252 MAs including 4999 primary studies and 13,577,025 patients were included. Over half of the MAs (65.1%) only included type 2 DM patients and 160 MAs (63.5%) focused on pharmacological treatments. About 89.7% MAs performed comprehensive literature search and 89.3% provided characteristics of included studies. Included MAs generally had poor performance on the remaining AMSTAR items, especially in assessing publication bias (39.3%), providing lists of studies (19.0%) and declaring source of support comprehensively (7.5%). Only 62.7% MAs mentioned about harm of interventions. MAs with corresponding author from Asia performed less well in providing MA protocol than those from Europe., Conclusions: Methodological quality of MA on DM treatments was unsatisfactory. There is considerable room for improvement, especially in assessing publication bias, providing lists of studies and declaring source of support comprehensively. Also, there is an urgent need for MA authors to report treatment harm comprehensively., (© 2016 European Society of Endocrinology.)

The influence of bacille Calmette-Guérin (BCG) on the pathogenesis of experimental airborne tuberculosis was studied. In a model that approximates the conditions under which man is vaccinated and infected, BCG-vaccinated and unvaccinated guinea pigs were infected by the respiratory route with an inoculum that resulted in the inhalation and retention (by each animal) of approximately three virulent tubercle bacilli (Mycobacterium tuberculosis strain H37Rv). Hematogenous seeding of the lungs occurred in unvaccinated animals about three weeks after aerosol infection but did not occur in BCG-vaccinated animals. Furthermore, the lungs of BCG-vaccinated animals failed to kill H37Rv that was introduced intravenously; however, evidence of mycobacteriostatic activity was found throughout the lungs. In view of the importance of hematogenous dissemination to the apex of the lungs in the establishment of pulmonary tuberculosis in man, the foregoing observations suggest a means by which vaccination with BCG may confer acquired resistance to tuberculosis.

Reverse triiodothyronine (rT3) was measured in cord serum from 5 infants with congenital hypothyroidism and compared with normal values in 70 euthyroid control infants. The mean (and SEM) value in the affected infants (135 +/- 12 ng/dl) was significantly lower than that in the control population (270 +/- 9 ng/dl). However, the large overlap in range of concentrations in affected and control infants indicates that newborn screening based on the determination of rT3 in cord blood specimens offers no advantage over present screening methods.

The glucose absorption inhibitors, Phenformin and 3-phenylpropylaminoguanide HCl (SaH 43-522) have different effects on hepatic gluconeogenesis. Unlike phenformin, 43--522 in vivo does not inhibit hepatic gluconeogenesis; inhibition occurred only when 43--522 was added directly to a liver perfusion system. This suggests that when 43--522 is administered in vivo it is metabolized to an agent that does not inhibit hepatic gluconeogenesis whereas phenformin is not metabolized, and does inhibit gluconeogenesis. This is an advantage of 43--522 since it thereby specifically inhibits intestinal glucose absorption without a potential hypoglycaemic effect due to the suppression of gluconeogenesis.

Evidence suggests that in humans tuberculous disease usually arises at apical or subapical sites in the lungs seeded as a consequence of an early bacillemic phase of the infection. This study examined the fate of bacilli transported via the bloodstream to metastatic sites in the lungs of guinea pigs after aerosol infection with approximately two viable virulent Mycobacterium tuberculosis. The results revealed that, even after logarithmic-phase multiplication of bacilli in primary lesions had been terminated, bacilli seeded via the bloodstream to metastatic sites in the lung were able to multiply. These observations, made in an animal model that mimics the conditions under which tuberculosis develops in human subjects, challenge the relevance of systemic macrophage activation in experimental airborne tuberculosis in guinea pigs.