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To assess the role of the kynurenine pathway in the pathology of Alzheimer's disease (AD), the expression and localization of key components of the kynurenine pathway including the key regulatory enzyme tryptophan 2,3 dioxygenase (TDO), and the metabolites tryptophan, kynurenine, kynurenic acid, quinolinic acid and picolinic acid were assessed in different brain regions of triple transgenic AD mice. The expression and cell distribution of TDO and quinolinic acid, and their co-localization with neurofibrillary tangles and senile β amyloid deposition were also determined in hippocampal sections from human AD brains. The expression of TDO mRNA was significantly increased in the cerebellum of AD mouse brain. Immunohistochemistry demonstrated that the density of TDO immuno-positive cells was significantly higher in the AD mice. The production of the excitotoxin quinolinic acid strongly increased in the hippocampus in a progressive and age-dependent manner in AD mice. Significantly higher TDO and indoleamine 2,3 dioxygenase 1 immunoreactivity was observed in the hippocampus of AD patients. Furthermore, TDO co-localizes with quinolinic acid, neurofibrillary tangles-tau and amyloid deposits in the hippocampus of AD. These results show that the kynurenine pathway is over-activated in AD mice. This is the first report demonstrating that TDO is highly expressed in the brains of AD mice and in AD patients, suggesting that TDO-mediated activation of the kynurenine pathway could be involved in neurofibrillary tangles formation and associated with senile plaque. Our study adds to the evidence that the kynurenine pathway may play important roles in the neurodegenerative processes of AD.

To assess the role of the kynurenine pathway in the pathology of Alzheimer's disease (AD), the expression and localization of key components of the kynurenine pathway including the key regulatory enzyme tryptophan 2,3 dioxygenase (TDO), and the metabolites tryptophan, kynurenine, kynurenic acid, quinolinic acid and picolinic acid were assessed in different brain regions of triple transgenic AD mice. The expression and cell distribution of TDO and quinolinic acid, and their co-localization with neurofibrillary tangles and senile beta amyloid deposition were also determined in hippocampal sections from human AD brains. The expression of TDO mRNA was significantly increased in the cerebellum of AD mouse brain. Immunohistochemistry demonstrated that the density of TDO immuno-positive cells was significantly higher in the AD mice. The production of the excitotoxin quinolinic acid strongly increased in the hippocampus in a progressive and age-dependent manner in AD mice. Significantly higher TDO and indoleamine 2,3 dioxygenase 1 immunoreactivity was observed in the hippocampus of AD patients. Furthermore, TDO co-localizes with quinolinic acid, neurofibrillary tangles-tau and amyloid deposits in the hippocampus of AD. These results show that the kynurenine pathway is over-activated in AD mice. This is the first report demonstrating that TDO is highly expressed in the brains of AD mice and in AD patients, suggesting that TDO-mediated activation of the kynurenine pathway could be involved in neurofibrillary tangles formation and associated with senile plaque. Our study adds to the evidence that the kynurenine pathway may play important roles in the neurodegenerative processes of AD.

Vaccination expanded central memory T cell populations and provided long-term protection, underscoring its potential in prophylactic lung cancer vaccination. From biomarker identification to mechanistic investigations, and from immune microenvironment analysis to innovative therapies and vaccines, these contributions demonstrate how molecular, cellular, and clinical perspectives converge to advance patient care. Conflict of interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

To determine the epidemiology of coronavirus disease (COVID-19) in a remote region of China, far from Wuhan, we analyzed the epidemiology of COVID-19 in Gansu Province. From January 23 through February 3, 2020, a total of 35 (64.8%) of 54 reported cases were imported from COVID-19-epidemic areas. Characteristics that differed significantly during the first and second waves of illness in Gansu Province were mean patient age, occupation, having visited epidemic areas, and mode of transportation. Time from infection to illness onset for family clusters was shorter in Gansu Province than in Wuhan, consistent with shortened durations from onset to first medical visit or hospitalization. Spatial distribution pattern analysis indicated hot spots and spatial outliers in Gansu Province. As a result of adequate interventions, transmission of the COVID-19 virus in Gansu Province is decreasing.

Members of the interleukin-1 (IL-1) superfamily play crucial roles in orchestrating inflammation and immune responses. Among them, IL-36 and IL-38 have emerged as cytokines with contrasting roles in cardiovascular disease (CVD). IL-36 typically promotes inflammation, contributing to endothelial dysfunction, atherogenesis, and myocardial injury. In contrast, IL-38 exerts predominantly anti-inflammatory effects, modulating immune responses and promoting tissue repair. This mini-review provides a critical synthesis of current findings on IL-36 and IL-38 in the context of atherosclerosis, myocardial ischaemia–reperfusion (I/R) injury, and post-percutaneous coronary intervention (PCI) outcomes. We discuss their molecular mechanisms, potential as biomarkers, and therapeutic implications, while identifying key gaps in knowledge that merit further investigation.

[...]Jiao et al.present a sobering case of immune-related haemophagocytic lymphohistiocytosis following tislelizumab treatment in a patient with microsatellite instability-high colorectal cancer and systemic lupus erythematosus (https://doi.org/10.3389/fonc.2025.1585133). Acknowledgments Gansu Provincial Science and Technology Program Sponsorship (24RCKD001), China, The deep integration of medical and health care advances clinical rehabilitation and fosters the high-quality development of health services. Conflict of interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Prostate cancer (PCa) is still as a major cause of morbidity and mortality in men at the global level, highlighting the necessity for improved diagnostic and therapeutic strategies beyond current PSA screening limitations. This mini-review focuses on the complex and often opposing roles of two key cytokines, IL-33 and IL-38, within the tumour microenvironment and their implications for host immunosurveillance in PCa. Intra-tumoral IL-33 expression is significantly reduced in PCa tissues and correlates with aggressive disease features such as higher Gleason scores and lymphatic metastasis, suggesting an inherent anti-tumour function. Such a protective role may be mediated via the ST2/NF-κB signalling pathway and the recruitment of lymphocytes into the tumour microenvironment. However, a paradoxical increase in circulating IL-33 levels in PCa patients hints at complex systemic compensatory mechanisms or differential compartmental regulation. In contrast, intra-tumoral IL-38 exhibits markedly elevated expression in PCa compared to benign prostatic hyperplasia and non-cancerous tissues. This increased IL-38 correlates with tumour severity, advanced TNM stages, and poorer overall survival, indicating a pro-tumoral role. Mechanistically, IL-38 appears to inhibit CD8 + cytotoxic T cell infiltration and potentially promotes immunosuppression through the upregulation of regulatory T cells (Tregs), thereby facilitating tumour progression. The contrasting expression patterns and clinicopathological associations of IL-33 and IL-38 highlight their potential as novel biomarkers for PCa diagnosis and prognosis. Further comprehensive investigation, including multi-centre studies across diverse populations, functional in vitro and in vivo analyses, and exploration of their therapeutic targetability, is crucial to translate these findings into effective precision medicine strategies for PCa patients.

With advancements in medical care and improved public health in China, the incidence of hookworm infections has significantly decreased, particularly in first-tier cities. We report a case of severe microcytic hypochromic anaemia caused by hookworm disease. The patient received multiple blood transfusions for unexplained anaemia, with negative faecal smear results. GI endoscopic examination revealed hookworms in the pyloric ring, antrum, and duodenum, which were removed using biopsy forceps. Morphological analysis identified the worms as Ancylostoma duodenale . The patient was treated with a single dose of 400 mg albendazole and hematinics. Follow-up haemoglobin testing 3 months later showed an improvement to 126 g/L (115–150 g/L). This case highlights the importance of GI endoscopy diagnostics in identifying a typical presentations of hookworm disease, particularly in first-tier cities. Timely and accurate diagnosis of hookworm infections is essential for preventing long-term health consequences and reducing associated healthcare costs.