Exposure to Secondhand Smoke and Risk of Cancer in Never Smokers: A Meta-Analysis of Epidemiologic Studies.

This is first meta-analysis to evaluate cancer risk associated with secondhand smoking across all cancers. A literature search was conducted for articles published before June 2014 on Pubmed, SCOPUS, Cochrane library, and CINAHL, and 40 articles on secondhand smoke and the prevalence of cancer among never smokers were selected for final analysis as per the inclusion criteria. Of the 40 articles, 27 were case-control studies and 13 were prospective cohort studies. With respect to overall cancer risk, odds ratio (OR) involving never smokers with significant exposure to secondhand smoke compared to never smokers without such exposure was 1.163 (95%CI 1.058⁻1.279). Subgroup meta-analyses by study design showed significant positive associations for both case-control studies and prospective cohort studies (OR 1.165, 95%CI 1.029⁻1.320; and OR 1.160, 95%CI 1.002⁻1.343, respectively). The association was stronger in the case of females (OR 1.253, 95%CI 1.142⁻1.374), lung cancer (OR 1.245, 95%CI 1.026⁻1.511), and breast cancer (OR 1.235, 95%CI 1.102⁻1.385). Secondhand smoking may increase the overall risk of cancer for never smokers, particularly lung and breast cancer, and especially in women. Strict implementation of smoking cessation programs should be encouraged, not only to reduce active smoking but also to limit exposure to secondhand smoke.

Identifying lysophosphatidic acid receptor subtype 1 (LPA1) as a novel factor to modulate microglial activation and their TNF-α production by activating ERK1/2.

Microglia regulate immune responses in the brain, and their activation is key to the pathogenesis of diverse neurological diseases. Receptor-mediated lysophosphatidic acid (LPA) signaling has been known to regulate microglial biology, but it is still unclear which receptor subtypes guide the biology, particularly, microglial activation. Here, we investigated the pathogenic aspects of LPA receptor subtype 1 (LPA1) in microglial activation using a systemic lipopolysaccharide (LPS) administration-induced septic mouse model in vivo and LPS-stimulated rat primary microglia in vitro. LPA1 knockdown in the brain with its specific shRNA lentivirus attenuated the sepsis-induced microglia activation, morphological transformation, and proliferation. LPA1 knockdown also resulted in the downregulation of TNF-α, at both mRNA and protein levels in septic brains, but not IL-1ß or IL-6. In rat primary microglia, genetic or pharmacological blockade of LPA1 attenuated gene upregulation and secretion of TNF-α in LPS-stimulated cells. In particular, the latter was associated with the suppressed TNF-α converting enzyme (TACE) activity. We reaffirmed these biological aspects using a BV2 microglial cell line in which LPA1 expression was negligible. LPA1 overexpression in BV2 cells led to significant increments in TNF-α production upon stimulation with LPS, whereas inhibiting LPA1 reversed the production. We further identified ERK1/2, but not p38 MAPK or Akt, as the underlying effector pathway after LPA1 activation in both septic brains and stimulated microglia. The current findings of the novel role of LPA1 in microglial activation along with its mechanistic aspects could be applied to understanding the pathogenesis of diverse neurological diseases that involve microglial activation.

Obesity Markers as Predictors for Colorectal Neoplasia.

BACKGROUND: The goal of this study was to determine the relations between the risk of colorectal neoplasia and obesity markers: body mass index (BMI), waist circumference (WC), and waist-to-height ratio (WHtR). METHODS: The subjects who underwent screening colonoscopies at a Kyungpook National University Hospital in Daegu from July to December 2010 were enrolled. We defined colorectal neoplasia as tubular adenoma, advanced adenoma, or cancer. We performed a logistic regression analysis to investigate the correlations between obesity and colorectal neoplasia and a receiver operating characteristic (ROC) curve analysis to determine the cut-off obesity marker values for detecting colorectal neoplasia. RESULTS: Among the total of 268 subjects, 83 (31.0%) subjects had colorectal neoplasia. Subjects with neoplasia had higher BMI, WC, and WHtR than the subjects without any neoplasia. The adjusted odds ratio (aOR) of WHtR ≥0.5 with the association of neoplasia was 1.927 (95% confidence interval [CI], 1.041-3.569) in the total subjects. In women, the obesity markers of WC ≥85 cm (aOR 4.611; 95% CI, 10.166-18.240) and WHtR ≥0.5 (aOR 1.747; 95% CI, 1.149-19.617) were significantly related to neoplasia; however, there was no significant result in men. The ROC analysis showed the optimal cut-off values of BMI as >23.14 kg/m2 (P=0.002), WHtR as >0.50 (P<0.001), and WC as>82.5 cm (P=0.650) in men and >77 cm in women (P<0.001). CONCLUSION: Obesity is significantly associated with the increased risk of colorectal neoplasia. WC and WHtR have more significant correlations with neoplasia; thus, obese people should undergo regular colonoscopy screenings to detect colorectal neoplasia.

The glycemic status of diabetes in an urban area of Cambodia.

Recently the Korea Diabetes Association participated in the 'Cambodia-Korea Twinning Project' to help Cambodia establish its own modernized diabetes center and to raise awareness of the seriousness of diabetes. Here we report the status of diabetes in an urban area of Cambodia as obtained through this project.