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Ulcerative colitis (UC) is a complex inflammatory disease of colorectum that induces abnormal immune responses and severely affects the quality of life of the patients. Grape seed proanthocyanidin extract (GSPE) exerts anti‐inflammatory and antioxidant functions in many inflammatory diseases. The objective of this study was to investigate the potential therapeutic effects and underlying mechanisms of GSPE in UC using a dextran sodium sulfate (DSS)‐induced mouse UC model and a lipopolysaccharide (LPS)‐stimulated RAW264.7 macrophage model. In this study, we found that the GSPE markedly prevented DSS‐induced weight loss and colon length shortening in UC mice. Further investigations showed that GSPE significantly attenuated the expression of pro‐inflammatory cytokines TNF‐α, IL‐6, and IL‐1β, and elevated the expression of anti‐inflammatory cytokine IL‐10 in the colon tissues and serum of DSS‐induced colitis mice by suppressing NF‐κB signaling pathway. Furthermore, LPS‐induced inflammation in RAW264.7 cells was also reversed by GSPE. Taken together, our results confirm that GSPE can ameliorate inflammatory response in experimental colitis via inhibiting NF‐κB signaling pathway. This study advances the research progress on a potentially effective therapeutic strategy for inflammatory bowel diseases. [ABSTRACT FROM AUTHOR]

Sarcoidosis is a systemic granulomatous disease associated with Th1/ regulatory T cells (Treg) paradigm. PI3K/Akt signaling, critical for maintaining Treg's homeostasis, is aberrantly activated in sarcoidosis patients. Here we tested the role of the PI3K inhibitors, LY294002 and BKM120, in immune modulation in experimental pulmonary sarcoidosis, concerning Th1/Th17/Treg immune profile detected by fluorescence‐activated cell sorting analysis or quantitative polymerase chain reaction, as well as the effect on Treg's suppressive functions. Our investigation showed abnormal activation of PI3K/Akt signaling both in lung and Treg in pulmonary sarcoidosis, along with decreased frequency and damaged function of Treg. Blockage of PI3K suppressed this signaling in Treg, rebalanced Th1/Treg, inhibited the production of inflammatory cytokines, and enhanced Treg's function. These results demonstrate the key role of the PI3K/Akt signaling in regulating Th1/Th2 rebalances and indicates that PI3K/Akt signaling is critical for the optimal Treg responses in pulmonary sarcoidosis. Thus, PI3K inhibitors have potential for therapeutic translation, and can be candidate for add‐on drugs to treat pulmonary sarcoidosis. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The therapeutic effects of bone marrow‐derived mononuclear cells (BMMNCs) transplantation in patients with nonischaemic dilated cardiomyopathy (DCM) are still under debate. Current randomized controlled trials (RCTs) reported conflicting results. The aim of this study was to assess the effects of BMMNCs transplantation on left ventricular ejection fraction (LVEF) in patients with nonischaemic DCM. Methods: A comprehensive search of PubMed, EMBASE and Cochrane Controlled Trials Register was performed. We included RCTs reporting data on LVEF in patients with nonischaemic DCM after BMMNCs transplantation. Results: Seven RCTs including 463 patients were included. BMMNCs transplantation significantly improved LVEF by 3.79% (95% CI: 0.56%‐7.03%; P = .007) and LVESV by −24.36 mL (95% CI: −46.36 to −2.36 mL; P = .03), while had no impact on the risk of all‐cause death (OR 0.92; 95% CI: 0.41 to 2.08%; P = .84). Subgroup analysis demonstrated a more significant improvement of LVEF in patients with longer follow‐up (~15 months to 5 years) than shorter ones (12 months). Moreover, using bone marrow mononuclear cells was more effective than using G‐CSF‐stimulated bone marrow/peripheral blood stem cells in the improvement of LVEF in patients with nonischaemic DCM. Conclusions: Bone marrow‐derived mononuclear cells transplantation is associated with a moderate, but significant, improvement in LVEF in patients with nonischaemic DCM. This meta‐analysis supports further RCT conductions using BMMNCs transplantation with larger patient's population and longer term follow‐up. [ABSTRACT FROM AUTHOR]

Background and objective Short telomere is a crucial risk factor for idiopathic pulmonary fibrosis ( IPF). However, little is known about the association between baseline telomere length and survival in IPF. We aimed to determine whether telomere length is associated with survival of IPF. Methods Leukocyte telomere lengths were measured by quantitative polymerase chain reaction in IPF patients at the time of the initial enrolment assessment in Nanjing Drum Tower Hospital Affiliated to Medical School of Nanjing University. The primary endpoint was the survival of the IPF patients since their initial enrolment assessment. Results Ninety-four IPF patients were enrolled between 1 January 2012 and 30 June 2014. The mean age-adjusted telomere length of IPF patients (0.85 ± 0.60) was significantly shorter than age-matched controls (1.15 ± 0.60, P = 0.001). During the follow-up period, 43 IPF patients died. The mean age-adjusted telomere length of the non-survivors (0.61 ± 0.53) was significantly shorter than that of the survivors (1.03 ± 0.59, P = 0.005). The association between telomere length (hazard ratio ( HR) 0.470 (95% confidence interval ( CI): 0.25-0. 89); P = 0·019) and survival in patients with IPF was independent of age, sex, forced vital capacity or diffusing capacity of carbon monoxide. After excluding the six patients with telomerase gene mutations, telomere length ( HR 0.46 (95% CI: 0.24-0.88); P = 0·018) remained an independent predictor of survival time in patients with IPF. Conclusions Short telomere length is independently associated with worse survival in IPF. Future research should focus on the molecular mechanism underlying the shortening of telomere length in IPF. [ABSTRACT FROM AUTHOR]

The sonographic and histopathologic features of a rare case of left ventricular aneurysm are reported, detailing the method of prenatal diagnosis and suggesting possible etiology of congenital ventricular aneurysm. [ABSTRACT FROM AUTHOR]