Global impact of particulate matter on ischemic stroke.

Objective: This study assesses the worldwide impact of ischemic stroke caused by ambient particulate matter pollution between 1990 and 2019, utilizing data from the Global Burden of Disease (GBD) 2019. Methods: An analysis was conducted across various subgroups, including region, Socio-demographic Index (SDI) level, country, age, and gender. The study primarily examined metrics such as death cases, death rate, Disability-Adjusted Life Years (DALYs), DALY rate, and age-standardized indicators. The Estimated Annual Percentage Change (EAPC) was calculated to assess trends over time. Results: The study found a moderate increase in the global burden of ischemic stroke attributed to ambient particulate matter, with the age-standardized DALY rate showing an EAPC of 0.41. Subgroup analyses indicated the most substantial increases in Western Sub-Saharan Africa (EAPC 2.64), East Asia (EAPC 2.77), and Eastern Sub-Saharan Africa (EAPC 3.80). Low and middle SDI countries displayed the most notable upward trends, with EAPC values of 3.36 and 3.58 for age-standardized death rate (ASDR) and DALY rate, respectively. Specifically, countries like Equatorial Guinea, Timor-Leste, and Yemen experienced the largest increases in ASDR and age-standardized DALY rate. Furthermore, both death and DALY rates from ischemic stroke due to particulate matter showed significant increases with age across all regions. Conclusion: The study highlights the increasing worldwide health consequences of ischemic stroke linked to particulate matter pollution, particularly in Asia and Africa. This emphasizes the critical necessity for tailored public health interventions in these regions.

Tumstatin attenuates the promotion effect of IL-17 secreted by Th17 cells on the stemness maintenance of glioma cells.

The presence and clinical significance of IL-17 and IL-17-expressing cells have been studied for several cancers, although their correlation with tumor development remains controversial. Peripheral blood was collected from healthy donors and glioma patients to isolate peripheral blood mononuclear cells (PBMCs). The percentage of IL-17-expressing cells and the production of inflammatory cytokines in PBMCs and tissues were measured. Human IL­17 cDNA was then inserted into the pEGFP­N1 plasmid and transfected into the glioma U87MG cell line, and tumstatin was used to block the effect of the IL-17 overexpression. Stem cell transcription factors were evaluated in each group using qRT-PCR and western blotting, and proliferation and migration were detected using colony formation and wound-healing assays. The cells were then subcutaneously inoculated into nude mice to evaluate the growth of glioma. Compared with healthy donors, the PBMCs from glioma patients showed a significant accumulation of IL-17-expressing T cells. Th17 cell differentiation-related cytokines (IL-23, TGF-ß and IL-6) were increased in the tumor microenvironment. IL­17 transfection increased the mRNA and protein expression of stem cell transcription factors in U87MG cells in vitro. The proliferation and migration of U87MG cells were also increased. Moreover, the pEGFP­N1­IL­17­U87MG cells grew more rapidly than other cells. However, tumstatin-treated U87MG cells showed significantly inhibited the effects of IL-17 overexpression. Tumstatin effectively suppressed IL-17-derived U87MG cell growth by downregulating stem cell maintenance factors and inducing proliferation and migration. These findings indicated that IL-17 represents a potential prognostic marker for glioma, while tumstatin has potential in the treatment for glioma.

Mechanism of miR-320 in Regulating Biological Characteristics of Ischemic Cerebral Neuron by Mediating Nox2/ROS Pathway.

This study aimed to explore the mechanism of miR-320 in regulating biological characteristics of ischemic cerebral neuron by mediating Nox2/ROS pathway. Primary neurons were cultured and grouped: normal group (normal primary neurons), negative control (NC) group (ischemic primary neurons, transfected with negative control plasmid), model group (ischemic primary neurons), miR-320 mimic group (ischemic primary neurons, transfected with miR-320-overexpressed plasmid), Nox2 vector group (ischemic primary neurons, transfected with Nox2-overexpressed plasmid), and miR-320 mimic + Nox2 vector group (ischemic primary neurons, co-transfected with miR-320- and Nox2-overexpressed plasmid). Dual-luciferase reporter assay showed that there was the target relationship between miR-320 and Nox2. miR-320 expression was significantly decreased, and Nox2 expression was significantly increased in the rest groups compared with normal group (both P < 0.05). There was a co-localization of miR-320 and Nox2 in the cytoplasm. Cell proliferation, contents of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX), and mRNA and protein expressions of Ki67, Bcl-2, and c-myc were significantly declined, and apoptosis rate, contents of malondialdehyde (MDA) and reactive oxygen species (ROS), and caspase-3 mRNA and protein expressions were significantly increased in the rest groups compared with normal group (all P < 0.05). miR-320 promoted cell proliferation; increased contents of SOD, CAT, and GSH-PX; and declined apoptosis and contents of MDA and ROS. Moreover, miR-320 could affect the regulation of Nox2/ROS pathway on ischemic cerebral neuron by negatively regulating Nox2 expression. Overexpressed miR-320 affects the proliferation, apoptosis, and oxidative stress injury of ischemic cerebral neuron by inhibiting Nox2/ROS pathway.