SummaryIn this systematic review of 13 observational studies, we found that diabetes was associated with a small but statistically significant risk for latent tuberculosis infection (LTBI). Findings imply a limited incremental gain if diabetics are targeted for LTBI screening.

Non-small cell lung cancer (NSCLC) is one of the most common causes of cancer-related mortality worldwide. microRNAs (miRNAs) play critical roles in carcinogenesis. miR-205 has been shown to be upregulated in NSCLC. In the present study, we identified the promotive effects of miR-205 on various significant biological properties of NSCLC cells, and confirmed the regulation of PTEN by miR-205. The expression of miR-205 was examined by quantitative real-time PCR both in NSCLC cell lines and tissues. The effect of miR-205 on PTEN expression was assessed in NSCLC cell lines with miR-205 mimics/inhibitor to elevate/decrease miR-205 expression. Furthermore, the roles of miR-205 in regulating the biological properties of NSCLC cells, including growth, invasion and chemoresistance, were assayed using miR-205 mimic/inhibitor-transfected cells. The 3'-untranslated region (3'-UTR) of PTEN combined with miR-205 and this was confirmed by luciferase reporter assay and western blotting. miR-205 expression was increased in NSCLC cell lines as well as in tissues. Overexpression of miR-205 promoted growth, migration and invasion, and enhanced the chemoresistance of NSCLC cells. Luciferase activity and western blotting demonstrated that miR-205 negatively regulated PTEN at a posttranscriptional level. However, miR-205 knockdown suppressed these processes in A549 cells and increased the expression of PTEN protein. Furthermore, overexpression of PTEN exhibited effects identical with those of the miR-205 inhibitor in NSCLC cells. Our results demonstrated that miR-205 is involved in the tumorigenesis of NSCLC through modulation of the PTEN signaling pathway.

Purpose: Laryngeal carcinomas always resist to radiotherapy. Hypoxia is an important factor in radioresistance of laryngeal carcinoma. Glucose transporter-1 (GLUT-1) is considered to be a possible intrinsic marker of hypoxia in malignant tumors. We speculated that the inhibition of GLUT-1 expression might improve the radiosensitivity of laryngeal carcinoma. Methods: We assessed the effect of GLUT-1 expression on radioresistance of laryngeal carcinoma and the effect of GLUT-1 expressions by antisense oligodeoxynucleotides (AS-ODNs) on the radiosensitivity of laryngeal carcinoma in vitro and in vivo. Results: After transfection of GLUT-1 AS-ODNs: MTS assay showed the survival rates of radiation groups were reduced with the prolongation of culture time (p<0.05); Cell survival rates were significantly reduced along with the increasing of radiation dose (p<0.05). There was significant difference in the expression of GLUT-1mRNA and protein in the same X-ray dose between before and after X-ray radiation (p<0.05). In vivo, the expressions of GLUT-1 mRNA and protein after 8Gy radiation plus transfection of GLUT-1 AS-ODNs were significant decreased compared to 8Gy radiation alone (p<0.001). Conclusion: Radioresistance of laryngeal carcinoma may be associated with increased expression of GLUT-1 mRNA and protein. GLUT-1 AS-ODNs may enhance the radiosensitivity of laryngeal carcinoma mainly by inhibiting the expression of GLUT-1.

ObjectiveThe risk of stroke in patients with Parkinson’s disease (PD) remains controversial. The purpose of this population-based propensity score-matched longitudinal follow-up study was to determine whether there is an increased risk of ischemic stroke after PD.MethodsWe used a logistic regression model that includes age, sex, pre-existing comorbidities and socioeconomic status as covariates to compute the propensity score. A total of 2204 patients with at least two ambulatory visits with the principal diagnosis of PD in 2001 was enrolled in the PD group. The non- PD group consisted of 2204, propensity score-matched subjects without PD. The ischemic stroke-free survival rates of the two groups were estimated using the Kaplan-Meier method. Stratified Cox proportional hazard regression with patients matched on propensity score was used to estimate the effect of PD on the occurrence of ischemic stroke.ResultsDuring the three-year follow-up period, 328 subjects in the PD group and 156 subjects in the non-PD group developed ischemic stroke. The ischemic stroke-free survival rate of the PD group was significantly lower than that of the non-PD group (P<0.0001). The hazard ratio (HR) of stroke for the PD group was 2.37 (95% confidence interval [CI], 1.92 to 2.93, P<0.0001) compared to the non- PD group.ConclusionsThis study shows a significantly increased risk of ischemic stroke in PD patients. Further studies are required to investigate the underlying mechanism.

Hypoxia is an important factor in radioresistance of laryngeal carcinoma. Glucose transporter-1 (GLUT-1) is an important hypoxic marker in malignant tumors, including laryngeal carcinoma. Apigenin is a natural phytoestrogen flavonoid that has potential anticancer effects. Various studies have reported that the effects of apigenin on lowering GLUT-1 expression were involved in downregulation of the PI3K/Akt pathway. Thus, apigenin may improve the radiosensitivity of laryngeal carcinoma by suppressing the expression of GLUT-1 via the PI3K/Akt pathway. The effect of GLUT-1 and PI3K/Akt pathway-related factor expressions by apigenin or antisense oligonucleotides (AS-ODNs) on the radiosensitivity of laryngeal carcinoma in vivo was assessed. The xenograft volume, xenograft weight and apoptosis detection were performed to determine radiosensitivity. The results showed that apigenin or apigenin plus GLUT-1 AS-ODNs improved the radiosensitivity of xenografts. Apigenin or apigenin plus GLUT-1 reduced the expression of GLUT-1, Akt, and PI3K mRNA after X-ray radiation. We found similar results at the protein level. The results suggest that the effects of apigenin on inhibiting xenograft growth and enhancing xenograft radiosensitivity may be associated with suppressing the expression of GLUT-1 via the PI3K/Akt pathway. In addition, apigenin may enhance the effects of GLUT-1 AS-ODNs via the same mechanism.