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Objectives: Muscle wasting and exercise intolerance are common in heart transplant recipients. Most studies on the effects of exercise training have used relatively small sample sizes and are heterogeneous in nature. The purpose of this meta-analysis was to systematically review the relevant studies and investigate the effects of exercise training on exercise capacity and muscle strength in heart transplant recipients. Methods: A systematic search was adopted from electronic databases and relevant references, using medical subject heading key words related to heart transplantation and exercise. Only randomized controlled trials with exercise intervention versus usual care were included. The data were expressed as the weighted mean differences with 95% confidence intervals (CIs). Results: Altogether 6 studies were included. Peak oxygen consumption (VO₂) was reported in 4 trials (117 patients), and muscle strength was reported in 3 trials (67 patients). Peak VO₂ was significantly increased by 2.34 ml/kg/min (95% CI 0.63–4.05). One-repetition maxima of the chest press (23.28 kg, 95% CI 0.64–45.91) and leg press (28.84 kg, 95% CI 5.70–51.98) were significantly improved by exercise training. Conclusion: Exercise training is recommended for heart transplant recipients to improve peak VO₂ and muscle strength despite the small number of trials included in this meta-analysis.

ObjectiveWe assessed blood pentraxin 3 (PTX3) and macrophage chemotactic factor-1 (MCP-1) levels as indicators of disease activity in rheumatoid arthritis (RA) patients, because data on disease activity score 28 (DAS28)-erythrocyte sedimentation rate (ESR) and DAS28-C-reactive protein (CRP) are still imperfect.MethodsIn 111 patients with RA, we examined longitudinal and cross-sectional correlations of blood PTX3, MCP-1, CRP, and ESR levels with measures of clinical arthritic activity, namely, swollen joint count (SJC), tender joint count (TJC), visual analog scale for general health (GH), DAS28, and adapted DAS28-MCP-1.ResultsBlood MCP-1, but not PTX3, was significantly correlated with SJC, TJC, DAS28, and DAS28-CRP. DAS28-MCP-1 was strongly correlated with DAS28 (r  = 0.984, P<0.001) and DAS28-CRP (r  = 0.971, P<0.001), and modestly correlated with CRP (r  = 0.350, P<0.001), and ESR (r  = 0.386, P<0.001). Similarly, the duration of arthritic symptoms, but not sex, was significantly correlated with variables of arthritic activity. In particular, DAS28-MCP-1 significantly correlated with DAS28 during a 6-month period (r  = 0.944, P<0.001; r  = 0.951, P<0.001; r  = 0.862, P<0.001; and r  = 0.865, P<0.001 for month 0, 1, 3, and 6, respectively).ConclusionBlood MCP-1 and adapted DAS28-MCP-1, but not blood PTX3, may be useful in monitoring RA activity.

Our earlier results indicate that peritoneal B cells (PEB cells) were not hyporesponsive to in vitro crosslinking of the immunoglobulin (Ig) with a secondary anti‐IgG reagent. In this study, the response of PEB cells was reduced by the same treatment given i.p. PEB cells were only sensitive to anti‐IgM hyper‐crosslinking in the presence of peritoneal macrophages. This sensitivity was partially reversed by anti‐interferon‐β antibody. Elevated BCL‐6 with c‐MYC gene expression in NZB/W F1 splenic B cells after anti‐IgM treatment correlated well with reduction of IgM secretion. On the contrary, PEB cells not sensitive to induction of hyporesponsiveness cause abnormal BCL‐6/c‐MYC gene expression after challenges. A bigger change of increased BCL‐6 gene expression after anti‐IgM treatment was seen in PEB cells than in splenic B cells. Higher BCL‐2 gene expression in NZB/W splenic B cells than those in NZB/W PEB cells do not prevent hyporesponsiveness in the former. In conclusion, the relationship between BCL‐6/c‐MYC gene expression and IgM secretion in NZB/W F1 splenic B cells is similar to that of conventional B2 cells. Although PEB cells from wild type strain can be rendered hyporesponsive in vivo in the presence of macrophages, the resistance to hyporesponsiveness of challenged autoimmune NZB/W PEB cells in vivo is probably related to abnormal BCL‐6/c‐MYC gene expression. These combined findings suggest that autoimmune B1 cells violate the accepted paradigm for expression of differentiation‐associated transcription factors in B2 cells.