Association of barium deficiency with Type 2 diabetes mellitus incident risk was mediated by mitochondrial DNA copy number (mtDNA-CN): a follow-up study.

Accumulating evidence indicates that plasma metal levels may be associated with Type 2 diabetes mellitus (T2DM) incident risk. Mitochondrial function such as mitochondrial DNA copy number (mtDNA-CN) might be linked to metal exposure and physiological metabolism. Mediation analysis was conducted to determine the mediating roles of mtDNA-CN in the association between plasma metals and diabetes risk. In the present study, we investigated associations between plasma metals levels, mtDNA-CN, and T2DM incident in the elderly population with a 6-year follow-up (two times) study. Ten plasma metals [i.e. manganese, aluminum, calcium, iron, barium (Ba), arsenic, copper, selenium, titanium, and strontium] were measured using inductively coupled plasma mass spectrometry. mtDNA-CN was measured by real-time polymerase chain reaction. Multivariable linear regression and logistic regression analyses were carried out to estimate the relationship between plasma metal concentrations, mtDNA-CN, and T2DM incident risk in the current work. Plasma Ba deficiency and mtDNA-CN decline were associated with T2DM incident risk during the aging process. Meanwhile, plasma Ba was found to be positively associated with mtDNA-CN. Mitochondrial function mtDNA-CN demonstrated mediating effects in the association between plasma Ba deficiency and T2DM incident risk, and 49.8% of the association was mediated by mtDNA-CN. These findings extend the knowledge of T2DM incident risk factors and highlight the point that mtDNA-CN may be linked to plasma metal elements and T2DM incident risk.

Investigation of the spatial effects on PM2.5 in relation to land use and ecological restoration in urban agglomerations.

Heavy pollution of particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) poses increasing threats to the living environment worldwide. Urban agglomerations often lead to regional rather than local air pollution problems. This study explored the underlying global and local spatial driving mechanisms of PM2.5 variations of the 195 county-level administrative units in the urban agglomeration in the middle reaches of the Yangtze River, China, in 2020, using the global spatial regression and geographically weighted regression methods. Results showed that (1) at the county level, there were spatial variations of PM2.5, fluctuating from 20.1263 µg/m3 to 44.8416 µg/m3. (2) The concentrations of PM2.5 presented a positive spatial autocorrelation with a remarkable direct spatial spillover effect. (3) Forestland, grassland, elevation and ecological restoration were negatively correlated with PM2.5 concentrations, the indirect spatial spillover effect of elevation was noticeable. (4) The indirect reduction effects of ecological restoration on PM2.5 concentrations were substantial in the Wuhan urban agglomeration. (5) The reduction effect of forestland, grassland, ecological restoration and elevation on PM2.5 showed a noticeable spatial heterogeneity. In the future, it is suggested regional variability and the spatial spillover effect of air pollution be taken into account in environmental governance. Simultaneously, utilization of the mitigation effect of ecological restoration on PM2.5 is anticipated for the concerted effort in air pollution governance.

Complete mechanochemical defluorination of perfluorooctanoic acid using Al2O3 and Al powders through matching electron-mediated reduction with decarboxylation.

This work reports a mechanochemical (MC) method for complete defluorination of perfluorooctanoic acid (PFOA) by using Al and Al2O3 as milling agents. Both the Al/Al2O3 molar ratio ( [Formula: see text] ) and the pre-thermal treatment of Al2O3 strongly influenced the defluorination of PFOA. When commercial γ-Al2O3 was pre-treated at 1200 °C, the use of Al and heat-treated γ-Al2O3 with [Formula: see text] of 1: 1 led to PFOA defluorination of 100% after ball milling for 26 min at 350 rpm, being much higher than those (8.3%-58.1%) for using singlet milling agents or binary milling agents containing γ-Al2O3 pre-heated at temperatures lower than 700 °C. It was clarified that the carboxylate-mediated adsorption of PFOA on Al2O3 was essential for the MC decarboxylation as a degradation initiation step, and the in-situ generated electron on milled Al consequently caused the reductive dissociation of C-F bonds in the decarboxylation intermediate. A larger [Formula: see text] increased the in-situ electron generation rate (re), and a higher heat-treatment temperature decreased OH-/H2O adsorbed on Al2O3 to low the PFOA decarboxylation rate (rdec). The re/rdec ratio determined defluorination pathways, and the percentage of the defluorination of PFOA in its total degradation including the generation of any degradation intermediates increased linearly with increasing re/rdec.

Profiling Total Viable Bacteria in a Hemodialysis Water Treatment System.

Culture-dependent methods, such as heterotrophic plate counting (HPC), are usually applied to evaluate the bacteriological quality of hemodialysis water. However, these methods cannot detect the uncultured or viable but non-culturable (VBNC) bacteria, both of which may be quantitatively predominant throughout the hemodialysis water treatment system. Therefore, propidium monoazide (PMA)-qPCR associated with HPC was used together to profile the distribution of the total viable bacteria in such a system. Moreover, high-throughput sequencing of 16S rRNA gene amplicons was utilized to analyze the microbial community structure and diversity. The HPC results indicated that the total bacterial counts conformed to the standards, yet the bacteria amounts were abruptly enhanced after carbon filter treatment. Nevertheless, the bacterial counts detected by PMA-qPCR, with the highest levels of 2.14 × 107 copies/100 ml in softener water, were much higher than the corresponding HPC results, which demonstrated the occurrence of numerous uncultured or VBNC bacteria among the entire system before reverse osmosis (RO). In addition, the microbial community structure was very different and the diversity was enhanced after the carbon filter. Although the diversity was minimized after RO treatment, pathogens such as Escherichia could still be detected in the RO effluent. In general, both the amounts of bacteria and the complexity of microbial community in the hemodialysis water treatment system revealed by molecular approaches were much higher than by traditional method. These results suggested the higher health risk potential for hemodialysis patients from the up-to-standard water. The treatment process could also be optimized, based on the results of this study.

Expression of the integrin-linked kinase in a rat kidney model of chronic allograft nephropathy.

The purpose of this study was to investigate the expression and significance of integrin-linked kinase (ILK) in the pathogenesis of chronic allograft nephropathy (CAN) in rats. For this, kidneys of Fisher (F344) rats were orthotopically transplanted into Lewis (LEW) rats. The animals were evaluated at 4, 8, 12, 16, and 24 weeks post-transplantation for renal function and histopathology. ILK protein expression was determined by Western-blot and immunohistological assays, and mRNA by RT-PCR. Our data show that 24-h urinary protein excretion in CAN rats increased significantly at week 16 as compared with F344/LEW controls. Allografts showed markedly increased mononuclear cells infiltration and presented with severe interstitial fibrosis and tubular atrophy at 16 and 24 weeks. ILK expression (protein/mRNA) was upregulated in rat kidneys with CAN, and the increase became more significant over time after transplantation. ILK expression correlated significantly with 24-h urinary protein excretion, serum creatinine levels, tubulointerstitial mononuclear cells infiltration, smooth muscle cells (SMCs) migration in vascular wall, and interstitial fibrosis. Therefore, it was concluded that ILK overexpression was the key event that involved mononuclear cells infiltration and vascular SMCs migration at early stage, and interstitial fibrosis and allograft nephroangiosclerosis at later stage of CAN pathogenesis in rats.

Detection of acute renal allograft rejection by analysis of renal tissue proteomics in rat models of renal transplantation.

At present, the diagnosis of renal allograft rejection requires a renal biopsy. Clinical management of renal transplant patients would be improved if rapid, noninvasive and reliable biomarkers of rejection were available. This study is designed to determine whether such protein biomarkers can be found in renal-graft tissue proteomic approach. Orthotopic kidney transplantations were performed using Fisher (F344) or Lewis rats as donors and Lewis rats as recipients. Hence, there were two groups of renal transplant models: one is allograft (from F344 to Lewis rats); another is syngrafts (from Lewis to Lewis rats) serving as control. Renal tissues were collected 3, 7 and 14 days after transplantation. As many as 18 samples were analyzed by 2-D Electrophoresis and mass spectrometry (MALDI-TOF-TOF-MS). Eleven differentially expressed proteins were identified between groups. In conclusion, proteomic technology can detect renal tissue proteins associated with acute renal allograft rejection. Identification of these proteins as diagnostic markers for rejection in patients' urine or sera may be useful and non-invasive, and these proteins might serve as novel therapeutic targets that also help to improve the understanding of mechanism of renal rejection.

Gene expression profiling on acute rejected transplant kidneys with microarray.

To investigate the gene expression profiles in acute allograft rejection of renal transplantation, and identify the markers for the early diagnosis of acute rejection, heterotopic kidney transplantation was performed by using F344 or Lewis donors and Lewis recipients. No immunosuppressant was used. Renal grafts were harvested on days 3, 7, and 14. A commercial microarray was used to measure gene expression levels in day-7 grafts. The expression levels of 48 genes were up-regulated in the allograft in comparison with the isograft control, and interferon-gamma-induced GTPase gene was most significantly up-regulated in allografts. It is concluded that a variety of pathways are involved in organ transplant rejection which is dynamic and non-balanced. IFN-inducible genes, such as IGTP, may play an important role in the rejection. A lot of important factors involved in acute rejection are unnecessary but sufficient conditions for the rejection. We are led to conclude that it is virtually impossible to make an early diagnosis based on a single gene marker, but it could be achieved on the basis of a set of markers.