Although Chinese herbal medicine (CHM) has been widely used as an adjunctive therapy for colorectal cancer in Asia, its efficacy is not well defined. The purpose of this systematic review is to assess the efficacy of CHM as an adjunctive therapy to chemotherapy for the patients with colorectal cancer. Randomized controlled trials with CHM to treat colorectal cancer were extensively searched in seven databases. Two researchers independently assessed the quality and validity of included trials and extracted outcome data for synthesis. 20 trials were included for analysis. Compared to using chemotherapy alone, CHM combined with chemotherapy significantly increased 1- and 3-year survival rate [odds ratio (OR) 2.41, 95% confidence interval (CI) 1.32-4.41; OR 2.40, 95% CI 1.49-3.87]. The combined therapy significantly slowed colorectal cancer progression (OR 0.50, 95% CI 0.32-0.77) and improved quality of life (OR 3.43, 95% CI 2.35-5.02). It had positive effects in immunoregulation. CHM as an adjunctive therapy also had significant advantages in reducing the adverse effects of chemotherapy. This systematic review suggests that CHM as an adjunctive therapy with chemotherapy versus chemotherapy alone has significant efficacy in terms of prolonging survival, enhancement of tumor response, improvement of quality of life, immunoregulation, and alleviation of acute adverse effects. However, a firm conclusion could not be reached because of the poor quality of the included trials. Further trials with higher quality are required and the efficacy in other forms of advantages remains to be further determined.

OBJECTIVE Elevated serum IL-6 level is a risk factor for coronary heart disease (CHD). The -174G>C and -572G>C polymorphisms in the IL-6 gene have previously been shown to modulate IL-6 levels. But the association between the -174G>C and -572G>C polymorphisms and the risk of CHD is still unclear. A meta-analysis of all eligible studies was carried out to clarify the role of IL-6 gene polymorphisms in CHD. METHODS AND RESULTS PubMed, EMBASE, Vip, CNKI and CBM-disc were searched for eligible articles in English and Chinese that were published before October 2010. 27 studies involving 11580 patients with CHD and 17103 controls were included. A meta-analysis was performed for the included articles using the RevMan 5.0 and Stata 10.0 softwares. Overall, the -174C allele was not significantly associated with CHD risk (ORs = 1.04, 95%CI = 0.98 to 1.10) when compared with the -174G allele in the additive model, and meta-analysis under other genetic models (dominant, recessive, CC versus GG, and GC versus GG) also did not reveal any significant association. On the contrary, the -572C allele was associated with a decreased risk of CHD when compared with the -572G allele (ORs = 0.79, 95%CI = 0.68 to 0.93). Furthermore, analyses under the recessive model (ORs = 0.69, 95% = 0.59 to 0.80) and the allele contrast model (genotype of CC versus GG, ORs = 0.49, 95% = 0.35 to 0.70) yielded similar results. However, statistical significance was not found when the meta-analysis was restricted to studies focusing on European populations, studies with large sample size, and cohort studies by using subgroup analysis. CONCLUSIONS The -174G>C polymorphism in the IL-6 gene is not significantly associated with increased risks of CHD. However, The -572G>C polymorphism may contribute to CHD development. Future investigations with better study design and large number of subjects are needed.

Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). In-stent restenosis after PCI remains a challenging clinical problem. In China, Chinese herbal medicines (CHMs) are widely used for preventing restenosis. This paper systematically reviewed the literature on the effectiveness and safety of CHMs in preventing restenosis after PCI in patients with CAD. Electronic databases were searched for randomized controlled trials that compared CHMs plus RWM with the same RWM plus placebo in preventing restenosis after PCI. A total of 52 trials (4905 patients) on 34 CHMs met the inclusion criteria and were analyzed. Ten trials had low risk of bias. Methodological quality of included trials was generally poor. Meta-analysis showed that at the end of at least 3 months' followup, CHMs plus RWM could significantly reduce restenosis rate, cardiac mortality, recurrence rate of angina, acute myocardial infarction, numbers of repeat PCI, and numbers of coronary artery bypass graft. Reported adverse events included gastrointestinal upset, granulocytopenia, and increased alanine transaminase (ALT). CHMs may help prevent restenosis, thus reducing cardiac mortality after PCI. Caution should be exercised in drawing a definitive conclusion due to the poor methodological quality of the trials reviewed.

High glucose-induced proliferation of vascular smooth muscle cells (VSMCs) plays an important role in the development of diabetic vascular diseases. However, molecular mediators responding for the proliferation of VSMCs remain to be determined. In this study, VSMCs were isolated from the rat thoracic aorta, and two cell models with Irf-1 knockdown and overexpression were established by transfecting cells with pGCsi-FU-Irf-1 and pGC-FU-Irf-1 respectively. Subsequently high glucose was added to cells to induce proliferation. Proliferation assays were performed to see whether Irf-1 was involved in high glucose-induced proliferation of VSMCs. In addition, the expression of Irf-1 was detected in VSMCs stimulated with high glucose and the thoracic aorta of diabetic rats to confirm the relationship between Irf-1 expression and the proliferation of hyperglycemia-dependent VSMCs. The results showed that Irf-1 expression was significantly higher in the thoracic aorta of diabetic rats and VSMCs stimulated with high glucose than that in non-diabetic rats and untreated cells. Overexpression of Irf-1 accelerated the proliferation of VSMCs, and down-regulation of Irf-1 expression significantly depressed the proliferative ability of VSMCs under high-glucose conditions, indicating that Irf-1 was a positive regulator for high glucose-induced proliferation of VSMCs. It could be presumed that Irf-1 is associated with the accelerated proliferation of VSMCs in diabetic vascular diseases and may prove to be a potential target gene for disease treatment. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc.

The purpose of the study was to explore the association between plasma platelet activating factor (PAF) and platelet activating factor acetylhydrolase (PAF-AH) levels and risk of coronary heart disease (CHD) or blood stasis syndrome (BSS) of CHD. Questionnaire, routine clinical assays and plasma levels of PAF, PAF-AH and inflammatory factors hs-CRP and IL-6 were investigated or measured for 120 controls and 150 CHD patients (66 non-BSS and 84 BSS). Plasma PAF levels were higher in CHD patients [49.7 (34.8-73.2 pg/mL)] than in controls [23.8 (14.9-42.3 pg/mL)](P < 0.001), and in BSS [56.0 (40.1-86.1 pg/mL)] than in non-BSS [47.4 (29.0-67.4 pg/mL)](P = 0.027). Similarly, plasma PAF-AH levels were higher in CHD patients [11.5 (7.5-15.6 μmol/L)] than in controls [8.1 (5.4-12.6 μmol/L)](P < 0.001), and in BSS [13.4 (8.7-18.5 μmol/L)] than in non-BSS [9.5 (7.3-14.3 μmol/L)](P = 0.014). After adjustment for the confounded effects of inflammatory factors or conventional risk factors, plasma PAF and PAF-AH levels still had a significant difference between CHD patients and controls, but plasma PAF-AH rather than PAF levels had a significant difference between BSS and non-BSS. Elevated plasma PAF level contributed to the risk of CHD rather than BSS, and elevated plasma PAF-AH level was an independent risk factor of CHD and BSS.

It is known that angiotensin (Ang)-converting enzyme (ACE) 2 catalyzes Ang II to Ang 1-7 to prevent the detrimental effect of Ang II on blood pressure, renal fibrosis, and inflammation. However, mechanisms of renoprotective role of Ace2 remain largely unclear. The present study tested the hypothesis that deficiency of Ace2 may accelerate intrarenal Ang II-mediated fibrosis and inflammation independent of blood pressure in a model of unilateral ureteral obstructive (UUO) nephropathy induced in Ace2(+/y) and Ace2(-/y) mice. Results showed that both Ace2(+/y) and Ace2(-/y) mice had normal levels of blood pressure and plasma Ang II/Ang 1-7. In contrast, deletion of ACE2 resulted in a fourfold increase in the ratio of intrarenal Ang II/Ang 1-7 in the UUO nephropathy. These changes were associated with the development of more intensive tubulointerstitial fibrosis (α-SMA, collagen I) and inflammation (TNF-α, IL-1β, MCP-1, F4/80(+) cells, and CD3(+)T cells) in Ace2(-/y) mice at day 3 (all P<0.05) after UUO, becoming more profound at day 7 (all P<0.01). Enhanced renal fibrosis and inflammation in the UUO kidney of Ace2(-/y) mice were largely attributed to a marked increase in the intrarenal Ang II signaling (AT1-ERK1/2 mitogen-activated protein kinase), TGF-β/Smad2/3, and NF-κB signaling pathways. Further studies revealed that enhanced TGF-β/Smad and NF-κB signaling in the UUO kidney of Ace2(-/y) mice was associated with upregulation of an E3 ligase Smurf2 and a loss of renal Smad7. In conclusion, enhanced Ang II-mediated TGF-β/Smad and NF-κB signaling may be the mechanisms by which loss of Ace2 enhances renal fibrosis and inflammation. Smad7 ubiquitin degradation mediated by Smurf2 may be a central mechanism by which Ace2(-/y) mice promote TGF-β/Smad2/3-mediated renal fibrosis and NF-κB-driven renal inflammation in a mouse model of UUO nephropathy.

This study was designed to investigate the function of 17β-estradiol (17β-E2) against oxidative stress on the cell death of mice bone marrow mesenchymal stem cells (BMSCs) induced by hydrogen peroxide (H₂O₂). BMSCs were treated with 17β-E2 for 24h and then treated with 100μM H₂O₂ for 1h. Cell viability, apoptosis, caspase-9 mRNA, JNKs (Jun N-terminal kinases) and c-Jun protein expression in BMSCs were evaluated. Cell apoptosis of BMSCs were increased in a dose-dependent manner after treated with H₂O₂ compared to control group. But pretreatment with 17β-E2 can inhibit apoptosis of BMSCs, preserve the mitochondrial transmembrane potential, decrease caspase-9 mRNA, JNK1/2 and c-Jun protein expression. In conclusion, 17β-E₂ exerts antiapoptotic effects in BMSCs which related to the mitochondria death pathway and JNKs pathway. The study revealed that 17β-E₂ can reduce the donor stem cells damage.

In this demonstration, we propose and demonstrate an adaptive long-reach passive optical network (LR-PON) using four-band orthogonal frequency division multiplexed (OFDM) channels. The downstream traffic rates from 6.25 to 40 Gb/s (using fixed quadrature amplitude modulation (QAM) level in the four OFDM bands) and from 9.37 to 40.3 Gb/s (using variable QAM levels in the four OFDM bands) can be achieved adaptively in the optical network units (ONUs) depending on different fiber transmission lengths from 0 to 100 km. For the upstream transmission, a 10 Gb/s 16-QAM OFDM signal with pre-emphasis is experimentally performed by using a 2.5 GHz directly modulated laser (DML). Based on the simulation and experimental results, the proposed adaptive four-band OFDM system could be a promising candidate for the future LR-PON.

This study investigates whether KMUP-1 protects soluble guanylate cyclase (sGC) and inhibits vascular endothelial growth factor (VEGF) expression in lung epithelial cells in hypoxia, therapeutically targeting epithelial proinflammation. H441 cells were used as a representative epithelial cell line to examine the role of sGC and VEGF in hypoxia and the anti-proinflammatory activity of KMUP-1 in normoxia. Human H441 cells were grown in hypoxia for 24-72 h. KMUP-1 (1, 10, 100 microM) arrested cells at the G0/G1 phase of the cell cycle, reduced cell survival and migration, increased p21/p27, restored eNOS, increased soluble guanylate cyclase (sGC) and PKG and inhibited Rho kinase II (ROCK-II). KMUP-1 (0.001-0.1 microM) concentration dependently increased eNOS in normoxia and did not inhibit phosphodiesterase-5A (PDE-5A) in hypoxic cells. Hypoxia-induced factor-1alpha (HIF-1alpha) and VEGF were suppressed by KMUP-1 but not by L-NAME (100 microM). The PKG inhibitor Rp-8-CPT-cGMPS (10 microM) blunted the inhibition of ROCK-II by KMUP-1. KMUP-1 inhibited thromboxane A2-mimetic agonist U46619-induced PDE-5A, TNF-alpha (100 ng/ml)-induced iNOS, and ROCK-II and associated phospho-p38 MAPK, suggesting multiple anti-proinflammatory activities. In addition, increased p21/p27 by KMUP-1 at higher concentrations might contribute to an increased Bax/Bcl-2 and active caspase-3/procaspase-3 ratio, concomitantly causing apoptosis. KMUP-1 inhibited ROCK-II/VEGF in hypoxia, indicating its anti-neoplastic and anti-inflammatory properties. KMUP-1 inhibited TNF-alpha-induced iNOS and U46619-induced PDE-5A and phospho-p38 MAPK in normoxia, confirming its anti-proinflammatory action. KMUP-1 could be used as an anti-proinflammatory to reduce epithelial inflammation.

First-line drug treatment for tuberculosis (TB) is frequently associated with liver toxicity. The goal of this study was to examine the association between UDP-glucuronosyl-transferase 1A1 (UGT1A1) genetic variations and anti-tuberculosis drug-induced hepatotoxicity (ATDH). A total of 98 patients, including 17 patients with ATDH, were enrolled; compound UGT1A1*27 and UGT1A1*28 were associated with an increased risk for developing ATDH after adjusting for age (OR 13.859; 95%CI 1.085-177.056). These findings require confirmation. However, screening for genetic variations prior to TB treatment may reduce the incidence of ATDH and improve treatment adherence.