Background Against the background of global warming, frequent heatwaves pose a major threat to public health. Objective To investigate the effects of heatwaves on outpatient visits for skin diseases in Urumqi, characterize the exposure–response relationship, identify the critical temperature threshold, and provide scientific evidence for targeted prevention and control of heat-related skin diseases. Methods Data on meteorological conditions, air quality, and dermatological outpatient visits from 10 hospitals in Urumqi were collected from January 1, 2016 to December 31, 2024. A time-stratified case-crossover design combined with a distributed lag model was adopted to construct a conditional logistic regression model, with adjustment for potential confounders, including relative humidity, air pollutants, and COVID-19 lockdown measures. With a maximum lag of 14 d, single-lag and cumulative-lag effects of heatwaves were examined, and the exposure–response relationship between temperature and the risk of dermatological outpatient visit was fitted. Results A total of 385 heatwave days were identified in Urumqi from January 1, 2016 to December 31, 2024. These days were concentrated between June and September and showed an increasing annual trend. The median daily number of dermatological outpatient visits during heatwave periods (165 cases) was significantly higher than that during control periods (114 cases) (Z=−5.108, P<0.001). After adjusting for confounders, the odds of dermatological outpatient visits during heatwaves were 1.088 times higher than those of the control period (OR=1.088, 95%CI: 1.069, 1.107). Single-lag effects were statistically significant from lag0 to lag11 (P<0.05), peaking at lag0 (OR=1.088, 95%CI: 1.069, 1.107), showing an acute and immediate effect. Cumulative-lag effects were statistically significant from 1 to 14 d (P<0.05), peaking at lag04 (OR=1.117, 95%CI: 1.099, 1.136). The exposure–response relationship indicated that the OR values increased steeply with increasing temperature when the daily mean temperature exceeded 24.2 ℃, peaking at approximately 28.1 ℃ (OR=1.400, 95%CI: 1.189, 1.649). Conclusions Heatwave exposure is significantly associated with an increased risk of dermatological outpatient visits among residents in Urumqi. The impact of high temperature on skin diseases is predominantly acute, with peak risks observed on the day of exposure and within the subsequent 4 d. A daily mean temperature of 24.2 ℃ can serve as the critical threshold for heightened dermatological consultation risk. Strengthened health education and early warning systems are recommended to mitigate heatwave-related adverse dermatological outcomes.

Increasing evidence has underscored the significance of post-stroke alterations along gut-brain axis, while its role in pathogenesis and treatment of ischemic stroke (IS) remains largely unexplored. This study aimed to elucidate the therapeutic effects and action targets of Panax notoginseng saponins (PNS) on IS and explore a novel pathogenesis and treatment strategy of IS via profiling the microbial community and metabolic characteristics along gut-brain axis. Our findings revealed for the first time that the therapeutic effect of PNS on IS was microbiota-dependent. Ischemia/reperfusion (I/R) modeling significantly down-regulated Lactobacilli in rats, and PNS markedly recovered Lactobacilli, particularly Lactobacillus reuteri (L.Reu). Metabolomics showed a significant reduction in serum histidine (HIS) in clinical obsolete IS patients and rehabilitation period I/R rats. Meanwhile, the L.Reu colonization in I/R rats exhibited significant neuroprotective activity and greatly increased HIS in serum, gut microbiota, and brain. Moreover, exogenous HIS demonstrated indirect neuroprotective effects through metabolizing to histamine. Notably, vagus nerve severance in I/R rats was performed to investigate HIS's neuroprotective mechanism. The results innovatively revealed that PNS could promote HIS synthesis in gut by enhancing L.Reu proportion, thereby increasing intracerebral HIS through peripheral pathway. Consequently, our data provided novel insights into HIS metabolism mediated by L.Reu in the pathogenesis and treatment of IS.

OBJECTIVES: To investigate the effect of curcumin on lipid metabolism in non-small cell lung cancer (NSCLC) and its molecular mechanism. METHODS: The inhibitory effect of curcumin (0-70 μmol/L) on proliferation of A549 and H1299 cells was assessed using MTT assay, and 20 and 40 μmol/L curcumin was used in the subsequent experiments. The effect of curcumin on lipid metabolism was evaluated using cellular uptake assay, wound healing assay, triglyceride (TG)/free fatty acid (NEFA) measurements, and Oil Red O staining. Western blotting was performed to detect the expressions of PGC-1α, PPAR-α, and HIF-1α in curcumin-treated cells. Network pharmacology was used to predict the metabolic pathways, and the results were validated by Western blotting. In a nude mouse model bearing A549 cell xenograft, the effects of curcumin (20 mg/kg) on tumor growth and lipid metabolism were assessed by measuring tumor weight and observing the changes in intracellular lipid droplets. RESULTS: Curcumin concentration-dependently inhibited the proliferation of A549 and H1299 cells and significantly reduced TG and NEFA levels and intracellular lipid droplets. Western blotting revealed that curcumin significantly upregulated PGC-1α and PPAR‑α expressions in the cells. KEGG pathway enrichment analysis predicted significant involvement of the HIF-1 signaling pathway in curcumin-treated NSCLC, suggesting a potential interaction between HIF-1α and PPAR‑α. Western blotting confirmed that curcumin downregulated the expression of HIF-1α. In the tumor-bearing mice, curcumin treatment caused significant reduction of the tumor weight and the number of lipid droplets in the tumor cells. CONCLUSIONS Curcumin inhibits NSCLC cell proliferation and lipid metabolism by downregulating the HIF-1α pathway.
Curcumin/pharmacology* ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Animals ; Lipid Metabolism/drug effects* ; Carcinoma, Non-Small-Cell Lung/pathology* ; Lung Neoplasms/pathology* ; Mice, Nude ; Down-Regulation ; Mice ; Cell Proliferation/drug effects* ; Cell Line, Tumor ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; PPAR alpha/metabolism* ; Signal Transduction/drug effects* ; A549 Cells