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Background Myocardial infarction (MI) is an acute and fatal condition that threatens human health. Dl-3-n-butylphthalide (NBP) has been used for the treatment of acute ischemic stroke. Mitochondria may play a protective role in MI injury. However, there are few reports on the cardioprotective effect of NBP or the potential mitochondrial mechanism for the NBP-induced protection against cardiac ischemia injury. We investigated the therapeutic effects of NBP in an in vivo MI model and an in vitro oxidative stress model, as well as the potential mitochondrial mechanism. Methods This study comprised two different experiments. The aim of experiment 1 was to determine the protective effects of NBP on MI and the underlying mechanisms in vivo. In part 1, myocardial infarct size was measured by staining with 2,3,5-triphenyltetrazoliumchloride (TTC). Myocardial enzymes and mitochondrial enzymes were assayed. The aim of experiment 2 was to investigate the role of NBP in H 2 O 2 -induced myocardial ischemic injury in H9c2 cells and to determine the potential mechanism. In part 2, H9c2 cell viability was evaluated. ROS levels, mitochondrial morphology, and mitochondrial membrane potential of H9c2 cells were measured. ATP levels were evaluated using an assay kit; mitochondrial DNA (mtDNA), the expressions of NRF-1 and TFAM, and mitochondrial biogenesis factors were determined. Results NBP treatment significantly reduced the infarct ratio, as observed by TTC staining, decreased serum myocardial enzymes in MI, and restored heart mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and a-ketoglutarate dehydrogenase (a-KGDH) activities after MI. Moreover, in in vitro studies, NBP significantly increased the viability of H9c2 cells in a dose-dependent manner, reduced cell apoptosis, protected mitochondrial functions, elevated the cellular ATP levels, and promoted H 2 O 2 -induced mitochondrial biogenesis in H9c2 cardiomyoblasts. Conclusion Collectively, the results from both the in vivo and in vitro experiments suggested that NBP exerted a cardioprotective effect on cardiac ischemic injury via the regulation of mitochondrial function and biogenesis.

Pancreatic cancer (PC) is a highly lethal malignancy, with pancreatic ductal adenocarcinoma (PDAC) being the most common and aggressive subtype, characterized by late diagnosis, aggressive progression, and resistance to conventional therapies. Despite advances in understanding its pathogenesis, including the identification of common genetic mutations (e.g., KRAS, TP53, CDKN2A, SMAD4) and dysregulated signaling pathways (e.g., KRAS–MAPK, PI3K–AKT, and TGF‐β pathways), effective therapeutic strategies remain limited. Current treatment modalities including chemotherapy, targeted therapy, immunotherapy, radiotherapy, and emerging therapies such as antibody–drug conjugates (ADCs), chimeric antigen receptor T (CAR‐T) cells, oncolytic viruses (OVs), cancer vaccines, and bispecific antibodies (BsAbs), face significant challenges. This review comprehensively summarizes these treatment approaches, emphasizing their mechanisms, limitations, and potential solutions, to overcome these bottlenecks. By integrating recent advancements and outlining critical challenges, this review aims to provide insights into future directions and guide the development of more effective treatment strategies for PC, with a specific focus on PDAC. Our work underscores the urgency of addressing the unmet needs in PDAC therapy and highlights promising areas for innovation in this field. Although the treatment landscape for cancer has evolved rapidly in recent years, progress has stagnated for pancreatic cancer (PC). PC includes multiple types, but pancreatic ductal adenocarcinoma (PDAC) accounts for >90% of cases. This review focuses on the molecular pathogenesis and different treatments for PDAC, hoping to propose future directions for optimizing treatment modalities and improving clinical outcomes of PDAC (created with BioRender.com).

The \"food desert\" problem has been treated under a national strategy in the United States and other countries. At present, there is little research on the phenomenon of \"food desert\" in China. This study takes Shanghai as the research area and proposes a multiscale analysis method using a linear tessellation model that splits the street network into homogeneous linear units. Firstly, the network kernel density estimation using a linear tessellation model is used to measure the travel-mode-based food accessibility. Considering the actual travel constraints, the GPS trajectory data of four travel modes (walking, bicycle, metro and taxi) are applied to calculate the speed of each linear unit. Secondly, the “food desert” phenomenon in Shanghai are identified combing with the results of the network K-function. Finally, the resident income conditions in different modes are fitted based on the housing price data and the spatial distribution of four \"food desert\" patterns are detected by the overlay analysis of food accessibility and resident income conditions. The experimental results show that fifty percent of Shanghai is characterized by low food accessibility, and half of these areas are disadvantaged and low-income areas in suburbs, which are the locations experiencing the “food desert” phenomenon. Comparing the results of the proposed method and that of the traditional planar method, the identification results for all modes based on the traditional planar method underestimate the severity of the “food desert”, especially for the bicycle and taxi modes. This study also provides corresponding decision-making reference for the alleviation and resolution of “food desert” issues. Moreover, the proposed method provides a new research perspective for urban research under the street network space.

Insomnia is one of the main symptoms of sleep disorders. Previous studies have suggested that alcohol intake is associated with several adverse health outcomes. The association between alcohol consumption and insomnia has been addressed in several studies with different results. However, whether gender may modify the association between alcohol consumption and insomnia is not clear. This study will focus on gender differences in the relationship between alcohol consumption and insomnia. The final study includes 8081 subjects aged between 18 and 65 years from the Jidong cohort. The data on alcohol consumption is collected by questionnaires, and insomnia problems are assessed using the entire 8-item Athens Insomnia Scale (AIS-8). Logistic analysis is used to evaluate the association between alcohol consumption and insomnia. Among the 8081 participants in this study, 2618 (32.4%) are alcohol drinkers, including 2424 males and 194 females. The prevalence of insomnia is 9.6% in the male and 10.6% in the female. The adjusted odds ratios (ORs) with 95% confidence interval (CI) of mild-to-moderate drinkers and heavy drinkers for insomnia are 1.27 (1.02-1.58) and 1.02 (0.79-1.32), respectively. Heavy alcohol consumption is significantly correlated with insomnia in the female, after controlling for potential confounding factors (OR: 2.11, 95% CI: 1.28-3.49, p for interaction = 0.002). A significant association between alcohol consumption and insomnia is found in females, but not in males from the northern Chinese population.

Neurogenesis, especially neurite outgrowth is an essential element of neuroplasticity after cerebral ischemic injury. Mitochondria may supply ATP to power fundamental developmental processes including neuroplasticity. Although rosuvastatin (RSV) displays a potential protective effect against cerebral ischemia, it remains unknown whether it modulates mitochondrial biogenesis and function during neurite outgrowth. Here, the oxygen-glucose deprivation (OGD) model was used to induce ischemic injury. We demonstrate that RSV treatment significantly increases neurite outgrowth in cortical neurons after OGD-induced damage. Moreover, we show that RSV reduces the generation of reactive oxygen species (ROS), protects mitochondrial function, and elevates the ATP levels in cortical neurons injured by OGD. In addition, we found that, under these conditions, RSV treatment increases the mitochondrial DNA (mtDNA) content and the mRNA levels of mitochondrial transcription factor A (TFAM) and nuclear respiratory factor 1 (NRF-1). Furthermore, blocking Notch1, which is expressed in primary cortical neurons, reverses the RSV-dependent induction of mitochondrial biogenesis and function under OGD conditions. Collectively, these results suggest that RSV could restore neurite outgrowth in cortical neurons damaged by OGD , by preserving mitochondrial function and improving mitochondrial biogenesis, possibly through the Notch1 pathway.

Soil residual concentration of organochlorine pesticides (OCPs) were determined in 245 agricultural surface soil samples collected from Chengdu Economic Region, Sichuan Province, Southwest China, in order to investigate their spatial distribution and the controlling environmental factors. Results showed that detectable ratios of hexachlorocyclohexane (HCH) and dichlorodiphenyltrichloroethane (DDT) were very high, ranging from 88.16 (for δ -HCH) to 97.96% (for p , p ′-DDE). The concentrations of DDTs were higher than HCHs, which were consistent with their historical usage in China. OCPs concentrations in the economically developed regions (Chengdu Plain) were higher than in the less developed, mountainous region around Chengdu Plain. The metabolite to parent ratio analysis of HCHs and DDTs indicated there were new pesticide inputs, possibly from the use of lindane ( γ -HCH) and dicofol in some regions although they have banned for agricultural use since 1983. Also, the distribution of OCP congeners in soil was mainly governed by their individual physical and chemical characteristic, historical usage amount and patterns, and the environmental conditions, such as, temperature, landform, soil type, etc.

Spatial interpolation is a crucial aspect of soil toxic element pollution research, serving as a vital foundation for pollution assessment, treatment, and sustainability efforts. The selection and adjustment of interpolation methods directly influences the accuracy of spatial distribution maps and data results, thereby indirectly impacting related research. This paper conducts a comparative study of different interpolation methods and analyses the sources of soil toxic elements in the study area of Cangxi County, aiming to provide a scientific foundation for future soil management, remediation, and enhanced local sustainability. The spatial correlation of As, Cd, Hg, Mn, Pb, and Mo in 228 surface soil samples in the study area of Cangxi County is analyzed. The interpolation results, spatial distribution of OK (ordinary Kriging), IDW (inverse distance weighting), RBF (radial basis function) and the changes of pollution area after interpolation are compared. The smoothing effect is assessed based on the comparison results, interpolation accuracy, and impact on pollution assessment of OK, IDW, and RBF. The interpolation method most suitable for each metal in the study area is selected. It can be concluded that the optimal interpolation method for As, Hg, and Mn is IDW; for Cd and Mo, it is RBF; and for Pb, it is OK. After the correlation analysis of toxic elements in the soil of the study area, the PMF (positive matrix factorization) model and hotspot analysis is applied to analyzing the source of toxic elements. The analysis indicates that the predominant sources of pollution are anthropogenic, categorized into industrial activities (30.8%), atmospheric deposition caused by coal combustion and traffic exhaust (21.5%) and agricultural activities (19.5%). Natural sources, such as soil parent material, contribute to 28.2% of the pollution on average.

Cerebral artery stenosis (CAS) is the most important causes of ischaemic stroke. Lipoprotein‐associated phospholipase A2 (Lp‐PLA2) plays 2 diverse roles in atherosclerosis (pro‐inflammatory and anti‐inflammatory), and the association between Lp‐PLA2 mass and cardiovascular or cerebrovascular events is inconsistent among previous studies. A cross‐sectional study including 2012 North Chinese adults aged ≥40 years was performed in 2010‐2011 to investigate whether Lp‐PLA2 mass is associated with asymptomatic cerebral artery stenosis (ACAS). Serum Lp‐PLA2 mass was determined by enzyme‐linked immunosorbent assay (ELISA). All participants underwent transcranial Doppler (TCD) and bilateral carotid duplex ultrasound to evaluate intracranial artery stenosis (ICAS) and extracranial arterial stenosis (ECAS). The median serum Lp‐PLA2 mass of the participants was 140.74 ng/mL (interquartile range: 131.79‐158.07 ng/mL). The adjusted odds ratio (OR) when comparing the 4th quartile to the 1st quartile of Lp‐PLA2 was 1.98 (95% confidence interval (CI): 1.42‐2.78), 1.79 (95% CI: 1.08‐2.94) and 1.87 (95% CI: 1.28‐2.73) for the occurrence of ACAS, asymptomatic ECAS and asymptomatic ICAS, respectively, after controlling for vascular risk factors. These independently significant associations remained statistically significant in the male or elderly subgroups, but not in females or middle‐aged participants. Lp‐PLA2 mass is positively correlated with subclinical atherosclerosis determined by ACAS, ICAS and ECAS in North Chinese, particularly in male and older participants, suggesting that serum Lp‐PLA2 mass might be potential biomarker for the detection of ACAS in the adults.

Transforming growth factor beta (TGF-β) is suggestive of a molecular target for cancer therapy due to its involvement in cell cycle, differentiation, and morphogenesis. Meanwhile, survivin is identified as an apoptosis inhibitor and involved in tumorgenesis. Here, we aimed to investigate the potential associations between TGF-β and survivin in glioblastoma U87 cell line. Survivin small interfering RNA (siRNA), Western blotting, and cell cycle analysis were introduced to detect relevant proteins in TGF-β pathways. In this study, we observed a concentration- and time-dependent increase of survivin expression after treatment with TGF-β1. However, the kinase inhibitors U0126 and LY294002 inhibited the upregulation of survivin in comparison with DMSO. In addition, survivin siRNA effectively abrogated survivin expression in U87 cells, therefore affected cells' entry into the S phase of cell cycle, and then repressed the expression of epidermal growth factor receptor (EGFR) and matrix metalloproteinase 9 (MMP9) in comparison with non-transfection. In conclusion, the present study shows that TGF-β upregulates survivin expression via ERK and PI3K/AKT pathway, leading to glioblastoma cell cycle progression. Thus, the blockade of survivin will allow for the treatment of glioblastoma, partially attributing to the inhibition of EGFR and MMP9 expression.

This study investigated optimal pathways for preeclampsia (PE) utilizing the network-based guilt by association (GBA) algorithm. The inference method consisted of four steps: preparing differentially expressed genes (DEGs) between PE patients and normal controls from gene expression data; constructing co-expression network (CEN) for DEGs utilizing Spearman's correlation coefficient (SCC) method; and predicting optimal pathways by network-based GBA algorithm of which the area under the receiver operating characteristics curve (AUROC) was gained for each pathway. There were 351 DEGs and 61,425 edges in the CEN for PE. Subsequently, 53 pathways were obtained with a good classification performance (AUROC >0.5). AUROC for 9 was >0.9 and defined as optimal pathways, especially microRNAs in cancer (AUROC=0.9966), gap junction (AUROC=0.9922), and pathogenic infection (AUROC=0.9888). Nine optimal pathways were identified through comprehensive analysis of data from PE patients, which might shed new light on uncovering molecular and pathological mechanism of PE.