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Background: The T cell-mediated delayed-type hypersensitivity (DTH) response is critical for elucidating cellular immune mechanisms, especially the role of memory T cells upon antigen re-exposure. This study aimed to investigate the specific effects of the immunosuppressive drugs Cyclophosphamide (CY) and Dexamethasone (DEX) on intestinal immunity and microbiota in a DTH mouse model, contributing to a more nuanced understanding of their immunomodulatory mechanisms. Methods: Female BALB/c mice were sensitized to 2,4-dinitrofluorobenzene (DNFB) and randomly allocated into control, CY, and DEX groups. The impact of CY and DEX on immune function was assessed through measurement of thymus and spleen indices, lymphocyte proliferation in mesenteric lymph nodes (MLNs) using MTT assay, and flow cytometric analysis of T cell subsets and TCR expression. Intestinal secretory IgA (sIgA) was quantified by ELISA, and gut microbiota diversity was evaluated using 16S rRNA gene sequencing. Results: CY and DEX significantly reduced the immune function in DNFB-induced sensitized mice, as indicated by decreased thymus and spleen indices, MLN enlargement, intestinal sIgA content, and ear swelling degree. Flow cytometry revealed that CY increased the proportion of total CD3+ T cells but reduced CD3+CD69+ activated T cells and CD3+TCRγ/δ+ T cells, while DEX increased CD3+CD4+ helper T cells. Both drugs induced distinct changes in gut microbiota diversity and structure, with CY enhancing α diversity and DEX reducing it. Conclusions: The study demonstrates that CY and DEX have distinct regulatory effects on the immune organ index, distribution of T cell subsets, and diversity and structure of gut microbiota on DTH-induced immune responses mice, suggesting their differential influence on intestinal mucosal immunity. These findings have implications for the development of targeted immunotherapies and understanding the interplay between immunosuppressive drugs and gut microbiota. [ABSTRACT FROM AUTHOR]

Aim: Chemosensory anhedonia refers to the lack of hedonic ability to experience pleasure through the senses of smell and taste, which reduces the pleasure and comfort of food, and increases the risk of nutritional and immune deficiencies. However, there is no direct scientific evidence regarding chemosensory anhedonia in patients with late‐life depression (LLD). The aim of this study was to investigate chemosensory anhedonia in patients with LLD, and its potential association with depressive symptoms and cognitive function. Methods: A total of 114 patients with LLD and 92 normal controls were included in this study. They experienced clinical assessment, Chemosensory Pleasure Scale assessment, 17‐item Hamilton Depression Rating Scale assessment and cognitive assessments, which contain the Verbal Fluency Test. The associations between chemosensory pleasure and depressive symptoms or cognitive function in patients with LLD were explored using partial correlation analysis and mediation analysis. Results: The Chemosensory Pleasure Scale scores were lower in the LLD group than in the normal control group, and were negatively correlated with the total scores and factors' scores (retardation, cognitive bias and anxiety/somatization) of the 17‐item Hamilton Depression Rating Scale, and positively correlated with the Verbal Fluency Test scores. The scores for the Food and Imagination dimensions of the Chemosensory Pleasure Scale showed partial mediating effects on the differences in Cognitive bias (a factor of the 17‐item Hamilton Depression Rating Scale) between patients with LLD and normal controls. Conclusions: Patients with LLD showed significant chemosensory anhedonia, and both depressive symptoms and cognitive impairment were associated with the severity of chemosensory anhedonia. Enhancing chemosensory pleasure in patients with LLD could potentially ameliorate their depressive symptoms. Geriatr Gerontol Int 2024; 24: 1022–1029. [ABSTRACT FROM AUTHOR]

The Proton Exchange Membrane Fuel Cell (PEMFC) is a fast-developing battery technology, and the key to its reliability and lifespan improvement lies in the accurate assessment of durability. However, the degradation mechanism of the PEMFC is hard to determine and its internal parameters are highly coupled. Thus, the development of a more accurate life prediction model that meets the actual scenarios is to be investigated urgently. To solve this problem, a multi-feature fusion life prediction method based on the Temporal Convolutional Network-Gated Recurrent Unit (TCN-GRU) is proposed. A TCN algorithm is used as the prediction base model, and two GRU modules are included with the model to strengthen the model's expression ability and improve its predictive accuracy. Two widely recognized datasets and two operating conditions are utilized for model training and prediction, respectively. Comparisons are made with single-feature parameter models in terms of Root Mean Square Error (RMSE) and the Determination Coefficient (R2). The results show that the prediction accuracy of the TCN-GRU multi-feature fusion model is higher than that of the single-feature models in terms of stability and anti-interference under both operating conditions. The accuracy of the TCN-GRU (three-feature) model is the most optimal in a steady-state condition at 80% of the training set ratio (RMSE = 3.27 × 10−3, R2 = 0.965). Furthermore, with the increase in the input feature parameter, the TCN-GRU model is closer to the real value, which proves once again that the proposed model can meet the accuracy requirements of the life prediction of the PEMFC. [ABSTRACT FROM AUTHOR]

Background and Objectives: Spontaneous massive foetomaternal haemorrhage (SM‐FMH) is a rare yet critical condition that poses substantial risk to foetal health and survival. Existing data indicate that many cases may be undiagnosed. The current study aimed to investigate and validate the utility of identifying mixed field red blood cell (RBC) agglutination during maternal blood typing as a diagnostic aid for SM‐FMH. Materials and Methods: Retrospective analysis of medical records from neonates born at our tertiary, university‐affiliated medical centre between 2016 and 2023 was performed. Diagnosis of SM‐FMH was based on neonates born with severe anaemia (haematocrit [HCT] <15%) within the first 24 h post‐delivery with positive maternal Kleihauer–Betke (KB) test. Maternal ABO/Rhesus D (RhD) blood typing results were scrutinized with the primary objective of assessing the ability to identify dual RBC populations in cases clinically diagnosed with SM‐FMH. Results: Among 29,192 neonates studied, a mere 0.02% (5 cases) exhibited severe SM‐FMH. Notably, a mixed field RBC agglutination was discerned in 80% (4/5) of these cases. Conclusion: This study underscores the significance of detecting mixed field RBC agglutination during antepartum maternal ABO/RhD blood typing as a potential indicator for SM‐FMH. Increased awareness among blood bank technology specialists and obstetricians regarding these laboratory findings could prove instrumental in saving foetal lives. [ABSTRACT FROM AUTHOR]

Introduction: Gestational vascular complications (GVCs), including gestational hypertension and preeclampsia, are leading causes of maternal morbidity and mortality. Elevated levels of extracellular vesicles (EVs), in GVC have been linked to vascular injury. This study aims to characterize placental and circulating EV miRNA in GVCs, and explores the involvement of EV-miRNA in GVC, and whether they may be used to distinguish between placental and maternal pathologies.Methods: Blood samples were obtained from 15 non-pregnant (NP), 18 healthy-pregnant (HP), and 23 women with GVC during the third trimester. Placental sections were obtained after caesarian section. Platelet-poor-plasma (PPP) and EV pellets were characterized: EV size/concentration, protein content and miRNA expression were measured by nanoparticle tracking analysis, western blot, nano-string technology and RT-PCR. The effects of EVs on trophoblasts and EC miRNA expression were evaluated.Results: Higher EVs concentrations were observed in HP-PPP and GVC-PPP (p < 0.0001) compared to the NP-PPP. The concentration of large EVs (>100 nm) was higher in PPP and EV pellets of HP and GVC compared to the NP group. EV pellets of pregnant women demonstrated lower expression of exosomal markers CD63/CD81 compared to NP-EVs. GVC-EVs expressed more human placental lactogen (hPL) hormone than HP-EVs, reflecting their placental origin. Screening of miRNAs in EV pellets and in PPP identified certain miRNAs that were highly expressed only in EVs pellets of the HP (13%) and GVC groups (15%), but not in the NP group. Differences were detected in the expression of hsa-miR-16-5p, hsa-miR-210, and hsa-miR-29b-3p. The expression of hsa-miR-16-5p and hsa-miR-210 was low in EV pellets obtained from NP, higher in HP-EVs, and significantly lower in GVC-EVs. Except for hsa-miR-29b-3p, which was upregulated in GVC, no significant differences were found in the levels of other miRNAs in placental sections. Exposure to GVC-EVs resulted in higher expression of hsa-miR-29b-3p compared to cells exposed to HP-EVs in villous trophoblasts, but not in EC.Conclusion: Expression of hsa-miR-16-5p and hsa-miR-210 reflects maternal pathophysiological status, while hsa-miR-29b-3p reflects placental status. These findings suggest that EV-miRNA are involved in GVC, and that they may be used to distinguish between pathologies of placental and maternal origins in preeclampsia.

Increasing scientific evidence demonstrates that the gut microbiota influences normal physiological homeostasis and contributes to pathogenesis, ranging from obesity to neurodegenerative diseases, such as Alzheimer’s disease (AD). Gut microbiota can interact with the central nervous system (CNS) through the microbiota-gut-brain axis. The interaction is mediated by microbial secretions, metabolic interventions, and neural stimulation. Here, we review and summarize the regulatory pathways (immune, neural, neuroendocrine, or metabolic systems) in the microbiota-gut-brain axis in AD pathogenesis. Besides, we highlight the significant roles of the intestinal epithelial barrier and blood–brain barrier (BBB) in the microbiota-gut-brain axis. During the progression of AD, there is a gradual shift in the gut microbiota and host co-metabolic relationship, leading to gut dysbiosis, and the imbalance of microbial secretions and metabolites, such as lipopolysaccharides (LPS) and short-chain fatty acids (SCFAs). These products may affect the CNS metabolic state and immune balance through the microbiota-gut-brain axis. Further, we summarize the potential microbiota-gut-brain axis-targeted therapy including carbohydrates, probiotics, dietary measures, and propose new strategies toward the development of anti-AD drugs. Taken together, the data in this review suggest that remodeling the gut microbiota may present a tractable strategy in the management and development of new therapeutics against AD and other neurodegenerative diseases.