Although exercise seems to be beneficial for type 2 diabetes mellitus (T2DM) patients, there is limited research elucidating the optimal accessible indices of adiposity and insulin resistance for identifying elderly T2DM patients with poor glycemic control, which could be improved by performing regular exercise. A community-based, cross-sectional study was conducted with 918 Chinese elderly individuals with T2DM in Zhejiang. Relevant risk factors for poor glycemic control, as determined using glycated haemoglobin A1c (HbA1c) > 7%, were explored using logistic regression analyses and included body mass index (BMI), waist circumference (WC), waist to height ratio (WHtR), fasting blood glucose (FBG), triglycerides (TGs), total cholesterol (TC), the product of fasting triglycerides and glucose (TyG), visceral adiposity index (VAI), lipid accumulation product (LAP), TyG-BMI, and TyG-WC. Comparisons of the risk factors’ ability to discriminate poor glycemic control as well as their optimal cutoff values were determined using receiver operating characteristic (ROC) analyses, and then the extent of poor glycemic control risk reduction through regular exercise was examined using multivariate logistic regression analyses. The overall poor glycemic control rate was 49.3%. The factors associated with poor glycemic control included FBG > 3.869, TyG > 8.73, TyG-BMI > 222.45, and TyG-WC > 713.48 in logistic regression analyses. The optimal cutoff points of FBG, TyG, TyG-WC, and TyG-BMI in discriminating poor glycemic control were 7.38, 9.22, 813.33, and 227.77, and their corresponding areas under the ROC curves were 0.864(0.840–0.886), 0.684(0.653–0.714), 0.604(0.571–0.635), and 0.574(0.541–0.606), respectively. Occasional and regular exercise reduced the odds ratios (95% confidence interval) of poor glycemic control to 0.187 (0.063–0.557) and 0.183 (0.059–0.571) for subjects with TyG-WC > 813.33 (p = 0.008), to 0.349 (0.156–0.782) and 0.284 (0.123–0.652) for subjects with TyG > 9.22 (p = 0.011), and to 0.390 (0.175–0.869) and 0.300(0.130–0.688) for subjects with TyG-BMI > 227.77 (p = 0.017), respectively, after adjusting for multiple confounding factors. Among elderly individuals with T2DM, poor glycemic control risk might be identified using indices calculated from FBG, TG, BMI, and WC measurements, which are indicative of adiposity and insulin resistance. TyG-WC seems to be an accessible and useful indicator to identify which elderly T2DM patients would benefit from performing regular exercise to achieve good glycemic control.

Asbestos is a known carcinogen and exposure can lead to lung cancer and malignant mesothelioma. To examine the effects of asbestos fibers on human immune cells, the human T cell leukemia/lymphoma virus (HTLV)-1 immortalized human T cell line MT-2 was employed. Following continuous exposure to asbestos fibers for more than eight months, MT-2 sublines showed acquisition of resistance to asbestos-induced apoptosis with decreased death signals and increased surviving signals. These sublines showed various characteristics that suggested a reduction in anti-tumor immunity. On the other hand, inflammatory changes such as expression of MMP7, CXCR5, CXCL13 and CD44 was found to be markedly higher in sublines continuously exposed to asbestos compared with original MT-2 cells. All of these molecules contribute to lung inflammation, T and B cell interactions and connections between mesothelial cells and T cells. Thus, further investigation focusing on these molecules may shed light on the role of chronic inflammation caused by asbestos exposure and the occurrence of malignant mesothelioma. Finally, regarding peripheral T cells from healthy donors (HD) and asbestos-exposed patients with pleural plaque (PP) or malignant pleural mesothelioma (MPM), following stimulation of CD4+ T cells, T cells from MPM patients showed reduced potential of interferon (IFN)-γ expression. Moreover, levels of interleukin (IL)-6, one of the most important cytokines in chronic inflammation, in cultured supernatants were higher in PP and MPM patients compared with HD. Overall, asbestos-induced chronic inflammation in the lung as well as the pleural cavity may facilitate the onset of asbestos-induced cancers due to alterations in the interactions among fibers, immune cells such as T and B cells and macrophages, and mesothelial and lung epithelial cells. Further investigations regarding chronic inflammation caused by asbestos fibers may assist in identifying molecular targets for preventive and therapeutic strategies related to the effects of asbestos exposure.

With improvements in care of at-risk neonates, more and more children survive. This makes it increasingly important to assess, soon after birth, the prognosis of children with hypoxic-ischemic encephalopathy. Computed tomography, ultrasound, and conventional magnetic resonance imaging are helpful to diagnose brain injury, but cannot quantify white matter damage. In this study, ten full-term infants without brain injury and twenty-two full-term neonates with hypoxic-ischemic encephalopathy (14 moderate cases and 8 severe cases) underwent diffusion tensor imaging to assess its feasibility in evaluating white matter damage in this condition. Results demonstrated that fractional anisotropy, voxel volume, and number of fiber bundles were different in some brain areas between infants with brain injury and those without brain injury. The correlation between fractional anisotropy values and neonatal behavioral neurological assessment scores was closest in the posterior limbs of the internal capsule. We conclude that diffusion tensor imaging can quantify white matter injury in neonates with hypoxic-ischemic encephalopathy.

Objectives This study investigated the mesothelin (MSLN) methylation and its relationship with soluble mesothelin-related protein (SMRP) levels in participants stratified by asbestos exposure scenarios and benign asbestos-related diseases (ARDs). Methods The presence of benign ARDs was confirmed through chest X-ray and the asbestos exposure history was obtained using a standardized questionnaire in this study, including 262 participants. Sera SMRP were measured using MESOMARK, and MSLN methylation in genomic DNA extracted from whole blood was detected by real-time methylation-specific PCR. Covariates were compared with SMRP concentrations using correlation analysis and the potential covariates affecting SMRP were determined by multiple linear regression analysis, and the distribution of methylation status was analyzed by Chi-square test. Results There was a trend toward elevation of SMRP values in healthy individuals exposed to asbestos as compared with those without asbestos exposure. The highest median level of SMRP was 1.3 nM in subjects with asbestosis, followed by cases with pleura plaque and asbestosis (1.2 nM), pleura plaque (0.9 nM), healthy subjects with occupational exposure (0.9 nM), non-occupational exposure (0.8 nM), and mixed exposure (0.8 nM). Within asbestosis cases, those with higher profusion scores had higher SMRP values than those with lower profusion scores (1.6 vs. 0.8 nM). Based on multi-regression analysis, the trend toward elevation of SMRP remained significant in subjects with occupational exposure or in those with asbestosis, as compared with healthy subjects without exposure (p < 0.01), although body mass index had an effect on SMRP (p < 0.0001). Regardless of the differences in SMRP levels among these subgroups, MSLN methylation ranged from 80.5 to 92.5 %, with no significant difference. The elevated level of SMRP in asbestosis with higher profusion scores could not be attributed to low MSLN methylation status. Conclusions Our findings suggest that the elevation of SMRP is related to asbestos exposure and benign ARDs especially for cases with high profusion scores, which is independent of MSLN methylation.

Although the growing development and application of iron oxide nanoparticles (IONPs) may pose exposure risk and adverse health outcomes, biological changes due to occupational exposure remain unexplored. This cross-sectional study recruited 23 workers at a plant that manufactures IONPs and 23 age- and sex-matched controls without metal-rich occupational hazards exposure. Exposure metrics at worksites were monitored, and iron status, oxidation markers, and methylation profiles of genomic DNA in peripheral blood were measured using corresponding enzyme-linked immunosorbent assays and methylation-specific polymerase chain reaction (PCR), respectively. The mass concentration, number counting, and surface area concentration of airborne particles at the worksite significantly increased during the work process of manufacturing/handling IONPs. Overall, compared to controls, workers exhibited increased 5-hydroxymethylcytosine (5hmC) levels without changes in 5-methylcytosine (5mC), hepcidin methylation, iron, soluble transferrin receptor (sTfR), ferritin, hepcidin, 8-hydroxydeoxyguanosine, and glutathione. A positive correlation was found between 5hmC and IONP exposure year with adjustment for age, sex, and cotinine using partial correlation analyses (r = 0.521, p < 0.001). After stratification of INOPs exposure and 5hmC levels, the univariate general linear model with adjustment for age, sex, and cotinine found that the estimated mean levels of 5mC and sTfR in subjects with low and high 5hmC levels among controls were 11% and 14.4% (p ≤ 0.01) and 80.9 nM and 70.3 nM (p < 0.05), respectively. The estimated mean levels of sTfR in workers and controls with low 5hmC levels were 88.3 nM and 68.7 nM (p ≤ 0.01). Multivariate linear regression analyses suggested an association between sTfR and 5hmC (standardized β = −0.420, p = 0.014) and female sex (standardized β = 0.672, p < 0.001) for subjects with low 5hmC levels. These findings suggest that increased 5hmC could be differentially employed to monitor an epigenetic signature with steady iron homeostasis for occupational IONP-exposed individuals who are likely to experience early but specific decreased sTfR, especially for females concurrent with the onset of increment in 5hmC at low level.