The efficacy and safety of low-molecular-weight heparin use for cancer treatment: a meta-analysis.

BACKGROUND: Low-molecular-weight heparin (LMWH) has an anti-tumour effect in-vitro and in animal models of malignancy; however, the evidence from clinical trials is controversial. Thus, we performed a meta-analysis from the results of randomised controlled trials (RCTs) to assess LMWH efficacy and safety in cancer patients who had no venous thromboembolism (VTE). METHODS: We searched the MEDLINE, EMBASE and CENTRAL (The Cochrane Central Register of Controlled Trails) databases covering all papers published up until April 2012. Two reviewers (D. H. Che and J. Y. Cao) extracted the data independently. The inclusion criteria used were patients with cancer who had no VTE and were treated with LMWH. The outcomes of interest included the 1-year mortality rate, VTE, bleeding and major bleeding complications. The results were presented as a relative risk (RR), and the STATA 11.0 package was used for comprehensive quantitative analysis. RESULTS: A total of 11 studies with 3835 cases and 3449 controls were included. The meta-analysis showed significant differences in the rates of bleeding with an RR: 1.32 [95% confidence interval (95% CI, 1.08-1.62)] and VTE with an RR: 0.53 (95% CI, 0.42-0.67) in cancer patients when LMWH was compared with placebo or no anticoagulant. There were no significant differences in the 1-year mortality rate with an RR: 0.97 (95% CI, 0.92-1.02) and major bleeding with an RR: 1.22 (95% CI, 0.87-1.71). CONCLUSION: LMWH does not significantly reduce the 1-year mortality rate for cancer patients. Although LMWH can prevent VTE, we should consider the risk-effect ratio (in case of an increased bleeding event) when we use LMWH in the patients with cancer. Thus, further research is still needed to confirm these results.

Expression of N-methyl-D-aspartate receptor and its effect on nitric oxide production of rat alveolar macrophages.

We early show that glutamate (Glu) mediate hyperoxia-induced newborn rat lung injury through N-methyl-D-aspartate receptor (NMDAR). In this study, we search for evidence of NMDAR expression on newborn rat alveolar macrophages (AMs) and the difference between newborn and adult rat AMs, and the possible effect on nitric oxide (NO) production of AMs by exogenous NMDA. The protein of NMDAR was showed by immunocytochemistry, and the mRNA was examined by RT-PCR and real-time PCR. The results show that: (i) both newborn and adult rat AMs express NMDAR1 and the four NMDAR2 subtypes and newborn rat AMs are higher expression. (ii) NMDA administration increase NO production, inducible nitric oxide synthase (iNOS) activity and iNOS mRNA expression of AMs. (iii) NMDAR activation elevates NO secretion of AMs, which suggests that AM may be one of the key cellular origin of the elevated NO secretion in hyperoxia-induced lung injury.

Mercury pollution in Asia: a review of the contaminated sites.

This article describes the mercury contaminated sites in Asia. Among the various regions, Asia has become the largest contributor of anthropogenic atmospheric mercury (Hg), responsible for over half of the global emission. Based on different emission source categories, the mercury contaminated sites in Asia were divided into various types, such as Hg pollution from Hg mining, gold mining, chemical industry, metal smelting, coal combustion, metropolitan cities, natural resources and agricultural sources. By the review of a large number of studies, serious Hg pollutions to the local environment were found in the area influenced by chemical industry, mercury mining and gold mining. With the probable effects of a unique combination of climatic (e.g. subtropical climate), environmental (e.g. acid rain), economic (e.g. swift growth) and social factors (e.g. high population density), more effort is still needed to understand the biogeochemistry cycle of Hg and associated health effects in Asia. Safer alternatives and cleaner technologies must be developed and effectively implemented to reduce mercury emission; remedial techniques are also required to restore the historical mercury pollution in Asia.

An extracellular factor regulates expression of sdiA, a transcriptional activator of cell division genes in Escherichia coli.

The sdiA gene codes for a protein that regulates expression of the ftsQAZ cluster of essential cell division genes of Escherichia coli. SdiA up-regulates the ftsQ2p promoter that initiates transcription into the ftsQAZ cluster. In this paper, we report that expression of sdiA is itself regulated by a factor that is released into the growth medium by E. coli. When medium that had previously supported growth of E. coli (conditioned medium) was used to support growth of an indicator E. coli strain that contained an sdiA-lacZ transcriptional reporter, there was a 50 to 80% decrease in sdiA expression as monitored by beta-galactosidase activity. The down-regulation of PsdiA was associated with a decrease in expression of the SdiA target promoter ftsQ2p, as monitored by expression of an ftsQ2p-lacZ transcriptional fusion. An effect of conditioned medium on ftsQ2p expression was not seen when the wild-type sdiA gene was disrupted by insertional mutagenesis, indicating that the effect on ftsQ2p expression was secondary to the down-regulation of PsdiA. Conditioned medium had no effect on expression of Plac, PrpoS, or several other promoters associated with the ftsQAZ gene cluster (ftsQ1p and ftsZ1-4p). This suggests that the response is specific for PsdiA and for promoters that are regulated by the sdiA gene product and that cell-to-cell signalling may play a role in regulating expression of this group of genes.