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Previous research has demonstrated that ferredoxin 1 (FDX1) contributes to the accumulation of toxic lipoylated dihydrolipoamide S-acetyltransferase (DLAT) and results in cuproptotic cell death. However, the role that FDX1 plays in human cancer prognosis and immunology is still not well understood. The original data was obtained from TCGA and GEO databases and integrated using R 4.1.0. The TIMER2.0, GEPIA, and BioGPS databases were used to explore FDX1 expression. The impact of FDX1 on prognosis was analyzed using the GEPIA and Kaplan–Meier Plotter databases. External validation will be performed using the PrognoScan database. FDX1 expression in different immune and molecular subtypes of human cancers was evaluated using the TISIDB database. The correlation between FDX1 expression and immune checkpoints (ICP), microsatellite instability (MSI), and tumor mutational burden (TMB) in human cancers was analyzed using R 4.1.0. The TIMER2.0 and GEPIA databases were used to study the relationship between FDX1 expression and tumor-infiltrating immune cells. With the c-BioPortal database, we investigated the genomic alterations of FDX1. Pathway analysis and assessment of the sensitivity potential of FDX1-related drugs were also performed. Using the UALCAN database, we analyzed the differential expression of FDX1 in KIRC (kidney renal clear cell carcinoma) with different clinical features. Coexpression networks of FDX1 were analyzed using LinkedOmics. In general, FDX1 was expressed differently in different types of cancer in humans. Expression of FDX1 was strongly correlated with patient prognosis, ICP, MSI, and TMB. FDX1 was also participated in immune regulation and the tumor microenvironment. Coexpression networks of FDX1 were primarily involved in oxidative phosphorylation regulation. Pathway analysis revealed that the expression of FDX1 was correlated to cancer-related and immune-related pathways. FDX1 has the potential to serve as a biomarker for pan-cancer prognosis and immunology, as well as a novel target for tumor therapy.

In the context of rural revitalization, scientific and efficient improvement of the human settlement environment is of great practical significance to improve the quality of life of farmers as well as to promote modern rural construction. To understand the research status and trends of human settlement environment improvement, the paper visually analyzed the relevant literature from 2012 to 2022 based on CNKI and the Web of Science database with the help of CiteSpace software(developed by Chaomei Chen, Drexel University, Philadelphia, PA, USA) (v6.2.r2). The results show the following: (1) the research literature on human settlement environment improvement has undergone three stages of slow growth, steady growth, and explosive growth; (2) many countries and institutions have published research on the improvement of human settlement environment, forming a close cooperative relationship; (3) three research hotspots have been formed: the concept and classification of the human settlement environment, the improvement path of the human settlement environment, and the evaluation method of the human settlement environment; and (4) waste management and green space are the frontier issues in the field of human settlement environment improvement. The subsequent research on the improvement of human settlement environments should strengthen the breadth and depth of research, improve the evaluation index system, innovate research methods, and build interdisciplinary integration, to provide a perfect research paradigm for research on the improvement of human settlement environments in the future.

Zero-shot stance detection is pivotal for autonomously discerning user stances on novel emerging topics. This task hinges on effective feature alignment transfer from known to unseen targets. To address this, we introduce a zero-shot stance detection framework utilizing multi-expert cooperative learning. This framework comprises two core components: a multi-expert feature extraction module and a gating mechanism for stance feature selection. Our approach involves a unique learning strategy tailored to decompose complex semantic features. This strategy harnesses the expertise of multiple specialists to unravel and learn diverse, intrinsic textual features, enhancing transferability. Furthermore, we employ a gating-based mechanism to selectively filter and fuse these intricate features, optimizing them for stance classification. Extensive experiments on standard benchmark datasets demonstrate that our model significantly surpasses existing baseline models in performance.

Macrophages play a pivotal role in the inflammatory response to the zoonotic pathogen E. coli , responsible for causing enteric infections. While considerable research has been conducted to comprehend the pathogenesis of this disease, scant attention devoted to host-derived H 2 S. Herein, we reported that E. coli infection enhanced the expression of CSE in macrophages, accompanied by a significantly increased inflammatory response. This process may be mediated by the involvement of excessive autophagy. Inhibition of AMPK or autophagy with pharmacological inhibitors could alleviate the inflammation. Additionally, cell model showed that the mRNA expression of classic inflammatory factors (Il-1β, Il-6), macrophage polarization markers (iNOS, Arg1) and ROS production was significantly down-regulated after employing CSE specific inhibitor PAG. And PAG is capable of inhibiting excessive autophagy through the LKB1-AMPK-ULK1 axis. Interestingly, exogenous H 2 S could suppress inflammation response. Our study emphasizes the importance of CSE in regulating the macrophage-mediated response to E. coli . Increased CSE in macrophages leads to excessive inflammation, which should be considered a new target for drug development to treat intestinal infection.

An aptamer based assay is presented for the determination of the antibiotics oxytetracycline (OTC) and kanamycin (KAN). Magnetic beads were applied for separation, and gold nanoparticles (AuNPs) for signal amplification. DNA aptamers against OTC and KAN were firstly designed. After specific recognition events, the aptamer sequences were released from the surface of magnetic beads and the remaining DNA probes captured horseradish peroxidase (HRP) modified AuNPs. Subsequently, 3,3′,5,5′-tetramethylbenzidine and o-phenylenediamine are catalytically oxidized by HRP, and the generated colorimetric responses can reflect the concentrations of OTC (at 370 nm) and KAN (at 450 nm), respectively. Experimental results demonstrate that the method is highly sensitive with the detection limit as low as 1 ag mL −1 for OTC and KAN. An extremely wide linear range (over 11 orders of magnitude) is achieved. The high selectivity is attributed to the high affinity between aptamer and the substrate. The results of real sample tests also verify that the method is promising for antibiotics analysis in the applications of food monitoring and clinical diagnosis. Graphical abstract Schematic presentation of a colorimetric assay for antibiotics based on aptamer-modified magnetic beads and horseradish peroxidase modified gold nanoparticles. Colorimetric responses result from the enzymatic oxidation of 3,3′,5,5′-tetramethylbenzidine (TMB) and o-phenylenediamine (OPD), respectively.

Streptococcus uberis infection can cause serious inflammation and damage to mammary epithelial cells and tissues that can be significantly alleviated by taurine. Autophagy plays an important role in regulating immunity and clearing invasive pathogens and may be regulated by taurine. However, the relationships between taurine, autophagy, and S. uberis infection remain unclear. Herein, we demonstrate that taurine augments PTEN activity and inhibits Akt/mTOR signaling, which decreases phosphorylation of ULK1 and ATG13 by mTOR and activates autophagy. Activating autophagy accelerates the degradation of intracellular S. uberis, reduces intracellular bacterial load, inhibits over-activation of the NF-κB pathway, and alleviates the inflammation and damage caused by S. uberis infection. This study increases our understanding of the mechanism through which taurine regulates autophagy and is the first to demonstrate the role of autophagy in S. uberis infected MAC-T cells. Our study also provides a theoretical basis for employing nutritional elements (taurine) to regulate innate immunity and control S. uberis infection. It also provides theoretical support for the development of prophylactic strategies for this important pathogen.

Background China has experienced rapid socioeconomic, and health transitions over the last four decades, and urban–rural disparities are becoming increasingly apparent. Research on depression among rural and urban students can provide evidence on the relationship between sociodemographic characteristics and adolescent depression. Methods We examined the association between sociodemographic characteristics and adolescent depression among 3605 students from Wuhan city and Jianli county that was recruited from the local junior middle school via a cross-sectional study. Univariate and multivariate logistic regression models were used to explore the sociodemographic characteristics of adolescent depression in urban and rural areas, respectively. Nomograms were constructed to calculate individual depression risk of junior middle school students. Results 32.47% of rural students and 35.11% of urban students display depressive symptoms. The protective factors of depression in urban students are exercise habit, younger, key class, better academic achievement and males, while Left-behind children (LBC), poor academic achievement and females had higher depression risk in rural area. Two nomograms were constructed to screen the adolescent depression in urban and rural junior middle school students, respectively. The clinical tools were well calibrated. Conclusion The field-based research examined sociodemographic characteristics potentially associated with adolescent depression and offered an effective and convenient tool of individualized depression risk evaluation for junior middle school students. Future longitudinal epidemiologic research on adolescent depression may help to further validate the discovery of present study, which will support developing policies and practices to minimize the factors of adolescent depression.

Oxidative stress is implicated in the pathogenesis of diabetic nephropathy. The present study aimed to investigate the effect of β-casomorphin-7 (BCM7) on the oxidative stress occurring in kidney tissue in streptozotocin (STZ)-induced diabetic rats and proximal tubular epithelial cells (NRK-52E) exposure to high glucose (HG) by using biochemical methods. There is a significant decrease in plasma insulin and a significant increase in plasma glucagon in the rats of diabetic group. Oral administration of BCM7 for 30 days to rats with STZ-induced diabetes resulted in a significant increase in serum level of insulin, and a decrease in the level of glucagon. Moreover, rats with STZ-induced diabetes had lower levels of superoxide dismutase (SOD), glutathione peroxidase (GPx) and total antioxidative capacity (T-AOC), higher levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) in the kidney than that in the control rats. The administration of BCM7 altered the changes of SOD, GPx, T-AOC, MDA and H2O2 in the kidney of diabetic rats. Furthermore, BCM7 alleviated high glucose-induced decreasement in SOD and GPx activity, increasement in MDA contents in the NRK-52E cells. BCM7 ameliorated the changes of angiotensin converting enzyme (ACE) and ACE2 levels in the kidney of diabetic rats and BCM7 lowered the levels of angiotensin (Ang)II in the kidney of diabetic rats and culture medium for cells. Moreover losartan (antagonist of angiotensin II type I receptor) lowered the high glucose-induced oxidative stress in the NRK-52E cells. Our results suggest that administration of BCM7 would alleviate high glucose-induced renal oxidative stress in vivo and in vitro, which may be associated with down regulation of the concentration of Ang II partly.

Neutrophil extracellular traps (NETs) are produced by neutrophil activation and usually have both anti-infective and pro-damage effects. Streptococcus uberis ( S. uberis ), one of the common causative organisms of mastitis, can lead to the production of NETs. Taurine, a free amino acid abundant in the organism, has been shown to have immunomodulatory effects. In this study, we investigated the molecular mechanisms of S. uberis -induced NETs formation and the regulatory role of taurine. The results showed that NETs had a disruptive effect on mammary epithelial cells and barriers, but do not significantly inhibit the proliferation of S. uberis . S. uberis induced NADPH oxidase-dependent NETs. TLR2-mediated activation of the MAPK signaling pathway was involved in this process. Taurine could inhibit the activation of MAPK signaling pathway and NADPH oxidase by modulating the activity of TAK1, thereby inhibiting the production of ROS and NETs. The effects of taurine on NADPH oxidase and NETs in S. uberis infection were also demonstrated in vivo . These results suggest that taurine can protect mammary epithelial cells and barriers from damage by reducing S. uberis -induced NETs. These data provide new insights and strategies for the prevention and control of mastitis.

Foamy macrophages containing prominent cytoplasmic lipid droplets (LDs) are found in a variety of infectious diseases. However, their role in Streptococcus uberis -induced mastitis is unknown. Herein, we report that S. uberis infection enhances the fatty acid synthesis pathway in macrophages, resulting in a sharp increase in LD levels, accompanied by a significantly enhanced inflammatory response. This process is mediated by the involvement of fatty acid binding protein 4 (FABP4), a subtype of the fatty acid-binding protein family that plays critical roles in metabolism and inflammation. In addition, FABP4 siRNA inhibitor cell models showed that the deposition of LDs decreased, and the mRNA expression of Tnf , Il1b and Il6 was significantly downregulated after gene silencing. As a result, the bacterial load in macrophages increased. Taken together, these data demonstrate that macrophage LD formation is a host-driven component of the immune response to S. uberis . FABP4 contributes to promoting inflammation via LDs, which should be considered a new target for drug development to treat infections.