BACKGROUND: The goal of this study was to evaluate the effects of resistance training on subjects with COPD. METHODS: We performed a systematic search in MEDLINE, PubMed, Embase, CINAHL, Elsevier ScienceDirect, EBM Reviews, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov and also of leading respiratory journals for randomized controlled trials on COPD treatment for > 4 weeks with resistance training compared with non-exercise control or with combined resistance and endurance training compared with endurance training alone. Data from these studies were pooled to calculate odds ratio and weighted mean differences (WMDs) with 95% CI. RESULTS: Eighteen trials with 750 subjects with advanced COPD met the inclusion criteria. There were 2 primary and 5 secondary outcomes. Compared with non-exercise control, resistance training led to significant improvements in the dyspnea domain of the Chronic Respiratory Disease Questionnaire (WMD of 0.59, 95% CI 0.26 -0.93, I2 ‫؍‬ 0%, P < .001), skeletal muscle strength, and percent-of-predicted FEV 1 (WMD of 6.88%, 95% CI 0.41-13.35%, I2 ‫؍‬ 0%, P ‫؍‬ .04). The combination of resistance and endurance training significantly improved the St George Respiratory Questionnaire total score (WMD of ؊7.44, 95% CI ؊12.62 to ؊2.25, I2 ‫؍‬ 0%, P ‫؍‬ .005), each domain score, and skeletal muscle strength. There were no significant differences in 6-min walk distance, 6-min pegboard and ring test, maximum exercise work load, and maximum oxygen consumption between the 2 groups. There were no reports of adverse events related to resistancetraining intervention. CONCLUSIONS: Resistance training can be successfully performed alone or in conjunction with endurance training without increased adverse events during pulmonary rehabilitation in COPD.

Natural pathogens, such as viruses, often induce T-dependent and T-independent Ab responses. However, the activation and differentiation of Ag-specific B cells under these conditions had not been examined in detail. In this study, we used bacterial phage Qβ-derived virus-like particles (Qβ-VLPs) as an immunogen to examine the T-independent and T-dependent phases of the response in mice. Using Qβ-specific cell labeling and enrichment methods developed in this study, we were able to characterize the rare Ag-specific B cells in detail. Surprisingly, we found that Qβ-VLPs could induce Bcl-6 expression in pregerminal center B cells independently of T cell help. In addition, Qβ-VLP-induced T-independent responses could lead to isotype-switched and somatically mutated memory B cells. Finally, in contrast to what has been reported with several other Ags, long-lived IgG memory cells were induced by Qβ-VLPs, with IgM memory B cells being produced but only evident for a limited time, suggesting that different types of immunogens may preferentially generate or maintain IgM versus IgG memory B cells.

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MicroRNAs have become pivotal modulators in the pathogenesis of Alzheimer’s disease. MiR-338-5p is associated with neuronal differentiation and neurogenesis, and expressed aberrantly in patients with cognitive dysfunction. However, its role and potential mechanism involved in Alzheimer’s disease remain to be elucidated. Herein, we showed that the expression of miR-338-5p decreased in APP/PS1 mice, accompanied by the elevation in the expression level of amyloid β, which indicated a reverse relationship between Alzheimer’s disease progression and miR-338-5p. In addition, lentiviral overexpression of miR-338-5p through intrahippocampal injection mitigated the amyloid plaque deposition and cognitive dysfunction in APP/PS1 mice, suggesting a protecting role of miR-338-5p against the development of Alzheimer’s disease. Moreover, miR-338-5p decelerated apoptotic loss of neurons in APP/PS1 mice. MiR-338-5p decreased neuronal apoptosis in vitro induced by amyloid β accumulation, which was attributed to the negative regulation of BCL2L11 by miR-338-5p, since the restoration of BCL2L11 eliminated the protective role of miR-338-5p against neuronal apoptosis. Taken together, all of these results may indicate miR-338-5p as an innovative modulator in the pathogenesis of Alzheimer’s disease, and also suggest that the protective effect of miR-338-5p on neuronal apoptosis may underlie its beneficial effect on APP/PS1 mice.