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Epidemiological studies have linked fine dust pollution to depression, yet the underlying mechanisms remain unclear. Oxidative stress and endoplasmic reticulum (ER) stress are known contributors to depression, but their induction by particulate matter (PM), particularly PM2.5, in animal models has been limited. This study aimed to establish a rat model of PM2.5-induced depression-like behaviors and elucidate the underlying molecular mechanisms. Adult male Sprague–Dawley rats received daily intranasal PM2.5 for four weeks. Behavioral assessments, including the open field test (OFT), forced swim test (FST), and light-dark box (LDB) test, were conducted weekly. PM2.5-exposed rats displayed depressive-like behaviors, particularly in the FST, reflecting decreased motivation and learned helplessness. Molecular analyses indicated a specific increase in ER stress markers (CHOP, eIF2α, GRP78, and P16) and NOX4 in the hypothalamus, while other brain regions (striatum, cortex, and hippocampus) were not as pronounced. Additionally, PM2.5 exposure reduced tyrosine hydroxylase (TH) levels in the hypothalamus, suggesting impaired dopamine synthesis. These findings indicate that PM2.5 induces depressive-like behaviors via hypothalamic ER stress and oxidative stress pathways, leading to dopaminergic dysfunction. Targeting oxidative and ER stress within the hypothalamus may offer new therapeutic strategies for treating depression associated with environmental pollutants. [ABSTRACT FROM AUTHOR]

Trong bài báo này, sợi nano bạc đã được tổng hợp bằng phương pháp polyol dưới tác động của siêu âm. Đã xác định được nồng độ tối ưu của polyvinyl pyrrolidone cho quá trình chế tạo dung dịch. Sản phẩm sợi nano được khảo sát bằng kỹ thuật XRD, SEM và UV-Vis. Dung dịch dẫn điện có điện trở thấp, bám dính tốt, tính linh hoạt cao và ổn định nhiệt. Dung dịch này đã được sử dụng để chế tạo màng dẫn điện. Sản phẩm có thể mở ra một hướng mới cho các ứng dụng công nghệ sau này.

Vật liệu BaTiO3 nano hình cầu phân tán cao với kích thước đồng đều được tổng hợp bằng phương pháp thủy nhiệt. Ảnh hưởng của tỉ lệ mol Ba/Ti lên sự hình thành vật liệu được nghiên cứu bằng cách phân tích dữ liệu XRD và SEM. TiO2·nH2O tổng hợp bằng phương pháp axit sunfuric với sự hỗ trợ sóng siêu âm được sử dụng làm nguyên liệu ban đầu. Vật liệu nano BaTiO3 hình cầu với độ phân tán cao và kích thước trung bình khoảng 100 nm đã thu được tại 200 °C trong 12 giờ với tỉ lệ Ba/Ti = 1,5. Tỷ lệ Ba/Ti ảnh hưởng mạnh đến sự hình thành BaTiO3 nano hình cầu với quá trình chuyển pha. Khi tăng tỉ lệ Ba/Ti, kích thước hạt tăng và tính đồng nhất giảm.

ARG2 has been reported to inhibit autophagy in vascular endothelial cells and keratinocytes. However, studies of its mechanism of action, its role in skin fibroblasts, and the possibility of promoting autophagy and inhibiting cellular senescence through ARG2 inhibition are lacking. We induced cellular senescence in dermal fibroblasts by using H2O2. H2O2-induced fibroblast senescence was inhibited upon ARG2 knockdown and promoted upon ARG2 overexpression. The microRNA miR-1299 suppressed ARG2 expression, thereby inhibiting fibroblast senescence, and miR-1299 inhibitors promoted dermal fibroblast senescence by upregulating ARG2. Using yeast two-hybrid assay, we found that ARG2 binds to ARL1. ARL1 knockdown inhibited autophagy and ARL1 overexpression promoted it. Resolvin D1 (RvD1) suppressed ARG2 expression and cellular senescence. These data indicate that ARG2 stimulates dermal fibroblast cell senescence by inhibiting autophagy after interacting with ARL1. In addition, RvD1 appears to promote autophagy and inhibit dermal fibroblast senescence by inhibiting ARG2 expression. Taken together, the miR-1299/ARG2/ARL1 axis emerges as a novel mechanism of the ARG2-induced inhibition of autophagy. Furthermore, these results indicate that miR-1299 and pro-resolving lipids, including RvD1, are likely involved in inhibiting cellular senescence by inducing autophagy. [ABSTRACT FROM AUTHOR]

Simple Summary: CDK5 is a serine/threonine type kinase that is mainly found in nerves. It is a target that has been studied primarily in neurological disorders, but recently it has been newly recognised for its importance in cancer. In this review, we mentioned the role of CDK5 in normal cells and the latest findings that CDK5 contributes to ten hallmarks of cancer and cancer-nerve connections. Also, we introduced representative CDK5 inhibitors and suggested the possibility of CDK5 inhibitors as treatments for refractory cancer. Cyclin-dependent kinase 5 (CDK5), which belongs to the protein kinase family, regulates neuronal function but is also associated with cancer development and has been proposed as a target for cancer treatment. Indeed, CDK5 has roles in cell proliferation, apoptosis, angiogenesis, inflammation, and immune response. Aberrant CDK5 activation triggers tumour progression in numerous types of cancer. In this review, we summarise the role of CDK5 in cancer and neurons and CDK5 inhibitors. We expect that our review helps researchers to develop CDK5 inhibitors as treatments for refractory cancer. [ABSTRACT FROM AUTHOR]