Secular trends in blood pressure (BP) and body mass index (BMI) in children and adolescents foreshadow trends in cardiovascular disease in adults. They are useful sentinels for population cardiovascular health. Changes in BP do not mirror changes in BMI, as factors determining trends in BP and BMI may be less evident in different settings. Understanding the concomitant trends in BP and BMI and delineating their potential driving forces would provide aetiological insights for prevention. Specifically, the discordant trends in children and adolescents, which could not be explained by adult lifestyle risk factors or medication, suggest the importance of identifying factors in the early life course.1 Age-period-cohort modelling decomposes temporal trends into the relative contribution of age, calendar period, and year of birth. This makes it possible to distinguish the impact of early life cohort-specific factors (cohort effect) and the impact of contemporaneous population-wide factors (period effect) from the physiological changes of BP and BMI with increasing age (age effect). We delineated the relative contribution of age, period, and birth cohort to the trends in BP in children and adolescents aged 9 to 18 years from 1999 to 2014 and BMI for those aged 6 to 18 years from 1996 to 2014 in Hong Kong.

The purpose of this study was to explore the risk factors for renal survival in patients with severe Lupus nephritis treated with continuous renal replacement therapy (CRRT). Two hundred and forty-seven SLE patients (male 54, female 193, median age 30.0(23-41) years requiring CRRT from January 2009 to December 2016 in Jinling Hospital were included in this study. 152(61.54%) patients achieved dialysis independence (dialysis independent group);95(38.46%) patients were on maintenance dialysis (dialysis dependent group). The multivariate COX regression analysis revealed that kidney damage course (P = 0.047, HR = 0.997),albumin level (P = 0.021, HR = 1.765), serum creatinine level (p=0.033, HR=0.684), oliguria or anuria(P=0.001, HR=0.460)were the prognostic factors for renal recovery in these patients. Renal biopsy was performed in 137patients, the CI>5 were the independent factors for the renal recovery in these patients. During a median follow-up time of 39.63(14.38,72.28) months，26(18.98%) patients in the dialysis independence group progressed into maintenance dialysis, the 1 ,5and 8 year renal survival were 94.6 % ,75.5%and 69.7%, respectively. Conclusion: About Forty percent of the patients still need renal replacement therapy, Kidney damage course,Albumin serum creatinine, Oliguria or anuria and CI>5 were the independent factor for renal survival.

Knee osteoarthritis (KOA) is a common degenerative joint disease with unsatisfactory treatment. Recently, non-pharmacological therapies, such as physical exercise and mind-body exercises, have received considerable attention for their implications in pain management in KOA. However, the mechanisms underlying the efficacy of different exercises on pain improvement remain unclear. In this study, we investigate the effect and underlying mechanisms of mind-body exercises (Tai Chi Chuan and Baduanjin) and physical exercise (stationary cycling) in patients with knee osteoarthritis (KOA). One hundred and forty patients were randomized into Tai Chi Chuan, Baduanjin, stationary cycling, and health education control groups for 12 weeks. The Knee injury and Osteoarthritis Outcome Score (KOOS), resting-state functional connectivity (rsFC) of the cognitive control network (CCN), and blood markers [serum Protectin D1 (PD1) and brain derived neurotrophic factor (BDNF) levels] were measured at the beginning and end of the experiment. We also applied support vector machines regression to predict the effectiveness of different exercises on KOA patients based on rsFC of CCN. We found: –KOOS pain subscores and serum PD1 levels significantly increased in all three exercise groups compared to the control group, and there were no significant differences among the three exercise groups; –rsFC between the bilateral dorsal lateral prefrontal cortex (DLPFC) and bilateral supplementary motor area (SMA) and temporoparietal junction (TPJ) was significantly decreased in all exercise groups compared to control group, and the decreased DLPFC-SMA rsFC was significantly associated with improvements in knee pain and serum PD1 levels across all subjects at baseline; –baseline DLPFC-SMA rsFC can significantly predict the effect of exercise on pain improvement in KOA patients. Conclusion: Our findings demonstrate different exercises may achieve clinical improvements through shared pathways and highlight the potential of neuroimaging biomarkers for predicting the therapeutic effect of exercises on KOA pain.

Objectives: Composites can be classified differently, according to manufacturer information, filler particle size, resin-monomer base, or viscosity, for example. Using clinical trial data, network meta-analyses aim to rank different composite material classes. Dentists then use these ranks to decide whether to use specific materials. Alternatively, annual failure rates (AFRs) of materials can be assessed, not requiring any classification for synthesis. It is unclear whether different classification systems lead to different rankings of the same material (ie, erroneous conclusions). We aimed to evaluate the agreement of material rankings between different classification systems. Methods: A systematic review was performed via MEDLINE, Cochrane Central Register of Controlled Trials, and EMBASE. Randomized controlled trials published from 2005-2015 that investigated composite restorations placed in load-bearing cavitated lesions in permanent teeth were included. Network meta-analyses were performed to rank combinations of composite classes (according to manufacturer, filler particle size, resin-monomers, viscosity) and adhesives. Material combinations were additionally ranked using AFRs. Results: A total of 42 studies (6088 restorations, 2325 patients) were included. The ranking of most material class combinations showed significant agreement between classifications (R-2 ranged between 0.03 and 0.56). Comparing material combinations using AFRs had low precision and agreement with other systems. AFRs were significantly correlated with follow-up periods of trials. Conclusion: There was high agreement between rankings of identical materials in different classification systems. Such rankings thus allow cautious deductions as to the performance of a specific material. Syntheses based on AFRs might lead to erroneous results because AFRs are determined by follow-up periods and have low precision.

Abstract Serum amyloid A (SAA) is an apolipoprotein transported within the high density lipoprotein (HDL) in plasma. The SAA plasma levels increase during inflammatory conditions, e.g., in patients with chronic renal failure (CRF). The SAA-dependent reduction in anti-inflammatory condition of HDL and its pro-inflammatory response in smooth muscle cells was shown previously. The aim of this study was to investigate the signaling pathways of SAA in macrophages and therefore its influence on inflammatory vascular disease. THP-1 (human) monocytes were activated via PMA to macrophages and used for monocyte chemoattractant protein-1 (MCP-1) experiments. Murine RAW264.7 monocytes/macrophages were used for nitrite experiments. MCP-1 production was detected by Luminex™ technology. Nitrite production were measured via Griess Assay. Cell viability was determined via MTS assay. SAA accumulates in plasma of patients during conditions of CRF. Whereas there is only a slight increase within CRF stage 1 and 2, the plasma level of SAA further increase during CRF stage 3 to 5. Beside the pro-inflammatory potential of SAA to induce MCP-1 in vascular smooth muscle cells, it also induces MCP-1 secretion in human THP-1 macrophages in a dose-dependent manner. In addition, the production of nitrite was dose-dependently increased in murine RAW264.7 cells. Both, MCP-1 and nitrite production induced by SAA were regulated via TLR and SR-BI receptor activation. The TLR2/4 antagonist oxPAPC and the SR-BI antagonist BLT-1 diminished the SAA-induced MCP-1 and nitrite production. The activation of FPR2 seems not to be involved in the signaling pathway in macrophages after SAA stimulation in that experimental condition. Stimulation with receptor agonists confirmed these findings. The concentration used for agonists/antagonists had no significant influence on cell viability of macrophages. In conclusion, the pro-inflammatory reaction of SAA in macrophages in vitro depends on TLR2/4 and SR-BI activation. The accumulation of SAA plasma levels during CRF may substantially contribute to the increased cardiovascular risk of these patients.

EBI2 (Epstein-Barr virus-induced gene 2) has recently been shown to control follicular B-cell migration and T-cell-dependent antibody production. In this study, we show that dendritic cell (DC) function is aberrant in EBI2 knockout mice. The results demonstrated that EBI2- deficiency did not interfere with DC maturation. However, functional analysis showed that spleen DCs from EBI2 knockout mice had reduced allostimulatory capacity and altered cytokine secretion, such as down-regulation of IL-10 and IL-12. Using 7α,25-dihydroxycholesterol (also called 7α,25-OHC, a ligand of EBI2), we found that the alloreactive CD4+CD25- effector T cells (Teffs) proliferation was enhanced by 7α,25-OHC when co-cultured with DCs from wild-type mice but not from EBI2 knockout mice. Furthermore, in the presence of IL-2, 7α,25-OHC reduced the proliferation of alloreactive CD4+CD25+ regulatory T cells (Tregs) stimulated by wild-type DCs in vitro. To address the relevance of EBI2-regulated alloimmune response between in vitro and in vivo, we used a mouse heterotopic cardiac transplant model and observed that EBI2-deficiency slightly prolonged allograft survival compared with wild-type controls (with median survival time of 9.5 days vs. 7 days). Interestingly, treatment with a 10-day suboptimal dose of rapamycin (0.1 mg/kg/day) induced a significant prolongation of allograft survival in EBI2-deficent mice as compared with wild-type mice (with median survival time of 19 days vs. 13.5 days). These data provide the first evidence that inhibition of EBI2 function exerts immunosuppressive effects on regulation of DC-stimulated Teffs and Tregs proliferation, leading to a significant improvement of allograft survival in mice.