HiMul-LGG: A hierarchical decision fusion-based local-global graph neural network for multimodal emotion recognition in conversation.

Emotion recognition in conversation (ERC) is a vital task that requires deciphering human emotions through analysis of contextual and multimodal information. However, extant research on ERC concentrates predominantly on investigating multimodal fusion while overlooking the model's constraints in dealing with unimodal representation discrepancy and speaker dependencies. To address the aforementioned problems, this paper proposes a Hierarchical decision fusion-based Local-Global Graph Neural Network for multimodal ERC (HiMul-LGG). HiMul-LGG employs a hierarchical decision fusion strategy to ensure feature alignment across modalities. Moreover, HiMul-LGG also adopts a local-global graph neural network architecture to reinforce inter-modality and intra-modality speaker dependency. Additionally, HiMul-LGG utilizes a cross-modal multi-head attention mechanism to promote interplay between modalities. We evaluate HiMul-LGG on two emotion recognition datasets, IEMOCAP and MELD, where HiMul-LGG outperforms existing methods. The results of the ablation study also imply the effectiveness of the proposed hierarchical decision fusion strategy and local-global structure of Graph construction.

Sudden Blast Crisis in a chronic myeloid leukemia patient in Treatment Free Remission: A case report and literature review.

Introduction：Treatment-free remission (TFR) has emerged as a new goal in the treatment of chronic myeloid leukemia (CML). TFR is considered a safe intervention because patients who experienced molecular relapse usually responded well to tyrosine kinase inhibitors resumption and regained molecular response quite efficiently. Nevertheless, there have been reports of occurrence of blast crisis during TFR. Case Presentation: We report a case of sudden lymphoid blast crisis in a CML patient who had been in TFR for 21 months without any prior molecular loss. Whole-exon sequencing identified a frameshift mutation of SETD2. In addition, we reviewed the current literature on cases of blast crisis in TFR. Only eleven cases of blast crisis have been reported among thousands of patients who discontinued tyrosine kinase inhibitor (TKI) therapy, including our patient. Of these cases, nine presented with lymphoid blast crisis. Additional gene mutations are frequently observed. Conclusion: This case, along with others, emphasizes the necessity of implementing a long-term monitoring strategy following TKI discontinuation due to the potential for late onset of blast crisis. Systematic genetic studies in patients failing TFR should be properly carried out to further understand the mechanism and eventually, to predict or prevent such adverse event in patients in TFR.

Methionine restriction alleviates diabetes-associated cognitive impairment via activation of FGF21.

Glucose metabolism disturbances may result in diabetes-associated cognitive decline (DACI). Methionine restriction (MR) diet has emerged as a potential dietary strategy for managing glucose homeostasis. However, the effects and underlying mechanisms of MR on DACI have not been fully elucidated. Here, we found that a 13-week MR (0.17 % methionine, w/w) intervention starting at 8 weeks of age improved peripheral insulin sensitivity in male db/db mice, a model for type 2 diabetes. Notably, MR significantly improved working as well as long-term memory in db/db mice, accompanied by increased PSD-95 level and reduced neuroinflammatory factors, malondialdehyde (MDA), and 8-hydroxy-2'-deoxyguanosine (8-OHdG). We speculate that this effect may be mediated by MR activating hepatic fibroblast growth factor 21 (FGF21) and the brain FGFR1/AMPK/GLUT4 signaling pathway to enhance brain glucose metabolism. To further delineate the mechanism, we used intracerebroventricular injection of adeno-associated virus to specifically knock down FGFR1 in the brain to verify the role of FGFR1 in MR-mediated DACI. It was found that the positive effects of MR on DACI were offset, reflected in decreased cognitive function, impaired synaptic plasticity, upregulated neuroinflammation, and balanced enzymes regulating reactive oxygen species (Sod1, Sod2, Nox4). Of note, the FGFR1/AMPK/GLUT4 signaling pathway and brain glucose metabolism were inhibited. In summary, our study demonstrated that MR increased peripheral insulin sensitivity, activated brain FGFR1/AMPK/GLUT4 signaling through FGF21, maintained normal glucose metabolism and redox balance in the brain, and thereby alleviated DACI. These results provide new insights into the effects of MR diet on cognitive dysfunction caused by impaired brain energy metabolism.

Zanubrutinib ameliorates experimental idiopathic inflammatory myopathy-associated interstitial lung disease by BTK/NF-κB signaling pathway.

Idiopathic inflammatory myopathy, abbreviated as myositis, is a heterogeneous disease characterized by proximal muscle involvement and chronic inflammation, primarily affecting the lungs. The aim of this study was to establish a stable idiopathic inflammatory myopathy (IIM)-associated interstitial lung disease (ILD) mouse model and evaluate the effects of zanubrutinib on IIM-ILD. We induced an IIM lung involvement model in balb/c mice through subcutaneous injection of skeletal muscle homogenate and intraperitoneal injection of pertussis toxin. We observed that the combination of skeletal muscle protein and pertussis toxin in balb/c mice could establish a stable IIM lung involvement model, characterized by muscle inflammation and pulmonary interstitial changes similar to clinical pathology. Zanubrutinib alleviated IIM and ILD, and its anti-inflammatory properties were demonstrated by a reduction in inflammatory cells and inflammatory factors in bronchoalveolar lavage fluid and bronchial inflammation. Its anti-inflammatory and anti-fibrotic effects were mainly achieved through the inhibition of BTK and NF-κB phosphorylation. This study established a stable IIM-ILD animal model and demonstrated for the first time that the BTK inhibitor zanubrutinib effectively attenuates experimental IIM-ILD in this model.

Risk Factors of Postoperative Atrial Fibrillation After Isolated Coronary Artery Bypass Grafting Surgery in the Recent 10 Years: Clinical Analysis of 6229 Patients.

BACKGROUND: Postoperative atrial fibrillation (POAF) is a common complication after coronary artery bypass grafting (CABG) that prolongs hospitalization and increases expenses. HYPOTHESIS: Perioperative risk factors may predict POAF. METHODS: From March 2015 to January 2023, 6229 patients who underwent isolated CABG and were in sinus rhythm before CABG were included in this retrospective study. The preoperative and postoperative variants of patients were collected and analyzed by univariate analyses between the patients with and without POAF. Multivariate logistic regression analysis was then used to study the independent risk factors for POAF. RESULTS: The incidence of POAF in this group of patients was 30.94%. Univariate analyses demonstrated that age (p < 0.001), hypertension (p < 0.001), smoking (p < 0.05), cardiopulmonary bypass (CPB) time (p < 0.01), and ejection fraction (EF, p < 0.01) were the risk factors for POAF. Multivariate logistic regression analysis determined the independent risk factors associated with POAF were old age (odds ratio [OR] = 1.062, p = 0.000) and low EF (OR = 0.980; p = 0.008). CONCLUSIONS: In the current era, after isolated CABG surgery, there is still a quite high incidence of POAF (30.94% in this group of CABG patients). The main risk factors correlating to POAF include age, hypertension, smoking, CPB time, and EF. Among these factors, multivariate analysis identified old age and low EF as the independent risk factors associated with POAF. Particular care should be taken in the perioperative period for these patients in the prevention of POAF.

Nerandomilast Improves Bleomycin-Induced Systemic Sclerosis-Associated Interstitial Lung Disease in Mice by Regulating the TGF-ß1 Pathway.

Systemic sclerosis (SSc) is a rare connective tissue disease with a heterogeneous clinical course. Interstitial lung disease (ILD) is a common complication of SSc and a major contributor to SSc-related deaths. Besides nintedanib and tocilizumab, there are currently no clinically approved drugs for SSc-ILD, highlighting the urgent need for new treatment strategies. Previous studies have shown that cyclic adenosine monophosphate (cAMP) plays a crucial role in the pathogenesis of SSc and lung fibrosis. Phosphodiesterases (PDEs) are enzymes that specifically hydrolyze cAMP, making PDE inhibitors promising candidates for SSc-ILD treatment. Nerandomilast, a preferential phosphodiesterase 4B (PDE4B) inhibitor currently undergoing phase III clinical trials for idiopathic pulmonary fibrosis and progressive fibrosing interstitial lung diseases (PF-ILD), has good preference for PDE4B but lacks studies for SSc-ILD. Our research demonstrates that nerandomilast effectively inhibits skin and lung fibrosis in a bleomycin-induced mouse model of SSc-ILD. For lung fibrosis, we found that nerandomilast could improve bleomycin-induced SSc-ILD through inhibiting PDE4B and the TGF-ß1-Smads/non-Smads signaling pathways, which provides a theoretical basis for potential therapeutic drug development for SSc-ILD.

Myelin oligodendrocyte glycoprotein-associated transverse myelitis after SARS-CoV-2 infection: A case report.

BACKGROUND: Cases of myelin oligodendrocyte glycoprotein (MOG) antibody-related disease have a history of coronavirus disease 2019 infection or its vaccination before disease onset. Severe acute respiratory syndrome virus 2 (SARS-CoV-2) infection has been considered to be a trigger of central nervous system autoimmune diseases. CASE SUMMARY: Here we report a 20-year male with MOG-associated transverse myelitis after a SARS-CoV-2 infection. The patient received a near-complete recovery after standard immunological treatments. CONCLUSION: Attention should be paid to the evaluation of typical or atypical neurological symptoms that may be triggered by SARS-CoV-2 infection.

Baricitinib alleviates cardiac fibrosis and inflammation induced by chronic sympathetic activation.

Cardiac fibrosis is characterized by the over-proliferation, over-transdifferentiation and over-deposition of extracellular matrix (ECM) of cardiac fibroblasts (CFs). Cardiac sympathetic activation is one of the leading causes of myocardial fibrosis. Meanwhile, cardiac fibrosis is often together with cardiac inflammation, which accelerates fibrosis by mediating inflammatory cytokines secretion. Recently, the Janus kinase/signal transducer and activator of transcription (JAK/STAT3) signaling pathway has been confirmed by its vital role during the progression of cardiac fibrosis. Thus, JAK/STAT3 signaling pathway is thought to be a potential therapeutic target for cardiac fibrosis. Baricitinib (BR), a novel JAK1/2 inhibitor, has been reported excellent effects of anti-fibrosis in multiple fibrotic diseases. However, little is known about whether and how BR ameliorates cardiac fibrosis caused by chronic sympathetic activation. Isoproterenol (ISO), a ß-Adrenergic receptor (ß-AR) nonselective agonist, was used to modulate chronic sympathetic activation in mice. As expected, our results proved that BR ameliorated ISO-induced cardiac dysfunction. Meanwhile, BR attenuated ISO-induced cardiac fibrosis and cardiac inflammation in mice. Moreover, BR also inhibited ISO-induced cardiac fibroblasts activation and macrophages pro-inflammatory secretion. As for mechanism studies, BR reduced ISO-induced cardiac fibroblasts by JAK2/STAT3 and PI3K/Akt signaling, while reduced ISO-induced macrophages pro-inflammatory secretion by JAK1/STAT3 and NF-κB signaling. In summary, BR alleviates cardiac fibrosis and inflammation caused by chronic sympathetic activation. The underlying mechanism involves BR-mediated suppression of JAK1/2/STAT3, PI3K/Akt and NF-κB signaling.

Discovery of delayed gas production after implantation of a continuous-flow left ventricular assist device and a preliminary exploration of the mechanisms of its occurrence.

Objective: To characterize the gas production phenomenon in the animal model of left ventricular assist device (LVAD), and study its mechanism. Methods: An in vitro bubble precipitation experiment was conducted, and the blood samples of Parma spp. animals were divided into ordinary group and oxygen-enriched group according to whether they were oxygenated or not at the time of blood collection, and a static control group was set up respectively. Blood gases were drawn and analyzed before and after the experiment. Activate the pump, and the number of air bubbles in the loop was measured by ultrasound at different rotational speeds; CFD was applied to simulate the flow field in the blood pump, and pressure, fluid velocity vector and shear force diagrams were plotted, and a thrombus model was constructed and the flow field was simulated and plotted as a cloud diagram. Results: There was a statistical difference in the number of bubbles in the inflow and outflow tubes of the blood pump (P values of 0.04 and 0.023, respectively), and the number of bubbles in the outflow tubes of both groups was significantly higher than the number of bubbles in the inflow tubes. The number of bubbles in the tubes of both the oxygen-enriched and normal groups was significantly higher than that in the inflow group. In both the normal and oxygen-enriched groups, more gas was produced at higher speeds than at lower speeds. Blood gas analysis showed that the reduced gas composition in the blood was mainly oxygen. Flow field simulation results: the high rotation speed group had lower central pressure and greater scalar shear. The thrombus simulation group was more prone to turbulence, sudden pressure changes, and greater shear than the normal group. Conclusion: Blood gas production is associated with higher partial pressures of blood oxygen, higher rotation speed, and intrapump thrombosis, and the mechanism of pump gas production is degassing of dissolved gases rather than cavitation of water, and the gas released is most likely to have oxygen. The degassing phenomenon is an warning factor for pump thrombosis.

The architecture of functional brain network modulated by driving under train running noise exposure.

A noisy environment can considerably impact drivers' attention and fatigue, endangering driving safety. Consequently, this study designed a simulated driving experimental scenario to analyse the effects of noise generated during urban rail transit train operation on drivers' functional brain networks. The experiment recruited 16 participants, and the simulated driving scenario was conducted at noise levels of 50, 60, 70, and 80 dB. Functional connectivity between all electrode pairs across various frequency bands was evaluated using the weighted phase lag index (WPLI), and a brain network based on this was constructed. Graph theoretic analysis employed network global efficiency, degree, and clustering coefficient as metrics. Significant increases in the WPLI values of theta and alpha frequency bands were observed in high noise environments (70 dB, 80 dB), as well as enhanced brain synchronisation. Furthermore, concerning the topological metrics of brain networks, it was observed that the global efficiency of brain networks in theta and alpha frequency ranges, as well as the node degree and clustering coefficients, experienced substantial growth in high noise environments (70 dB, 80 dB) as opposed to 50 dB and 60 dB. This finding indicates that high-noise environments impact the reorganisation of functional brain networks, leading to a preference for network structures with improved global efficiency. Such findings may improve our understanding of the neural mechanisms of driving under noise exposure, and thus potentially reduce road accidents to some extent.

MHC-I-presented non-canonical antigens expand the cancer immunotherapy targets in acute myeloid leukemia.

Identification of tumor neoantigens is indispensable for the development of cancer immunotherapies. However, we are still lacking knowledge about the potential neoantigens derived from sequences outside protein-coding regions. Here, we comprehensively characterized the immunopeptidome landscape by integrating multi-omics data in acute myeloid leukemia (AML). Both canonical and non-canonical MHC-associated peptides (MAPs) in AML were identified. We found that the quality and characteristics of ncMAPs are comparable or superior to cMAPs, suggesting ncMAPs are indispensable sources for tumor neoantigens. We further proposed a computational framework to prioritize the neoantigens by integrating additional transcriptome and immunopeptidome in normal tissues. Notably, 6 of prioritized 13 neoantigens were derived from ncMAPs. The expressions of corresponding source genes are highly related to infiltrations of immune cells. Finally, a risk model was developed, which exhibited good performance for clinical prognosis in AML. Our findings expand potential cancer immunotherapy targets and provide in-depth insights into AML treatment, laying a new foundation for precision therapies in AML.

Behavioral dysregulation in Nile tilapia (Oreochromis niloticus, GIFT) post-Streptococcus agalactia infection: Role of the microbiota-gut-brain axis.

In the aquatic farming industry, understanding the factors affecting fish behavior is crucial, particularly in response to infections that compromise welfare and productivity. Swimming performance is a key life history trait critical to their ecology. This study explores the swimming behavior imbalance in Nile tilapia (Oreochromis niloticus, GIFT) post-infection with Streptococcus agalactiae (GBS), a common pathogen responsible for significant losses in aquaculture. We focused on how the microbiota-gut-brain axis influences the behavioral response of tilapia to GBS infection. Behavioral changes were quantified by measuring collision times and swimming speeds, which decreased significantly following infection. This behavioral downturn is mediated by alterations in the microbiota-gut-brain axis, evidenced by increased levels of monoamine neurotransmitters (serotonin, norepinephrine, and dopamine) in the brain and intestinal tissues. The study utilized pharmacological agents, the 5-HT1A receptor agonist (8-OH-DPAT) and antagonist (WAY-100635), to investigate their efficacy in mitigating these behavioral and biochemical changes. Both agents partially restored normal behavior by adjusting neurotransmitter concentrations disrupted by GBS infection. Additionally, a notable increase in the relative abundance of Streptococcus within the gut microbiota of infected fish highlights the potential role of specific bacterial populations in influencing host behavior. This research provides novel insights into the complex interactions between pathogen-induced gut microbiota changes and Nile tilapia's behavioral outcomes, highlighting potential avenues for improving fish health management through microbiota-targeted interventions.

Secoisolariciresinol diglucoside attenuates neuroinflammation and cognitive impairment in female Alzheimer's disease mice via modulating gut microbiota metabolism and GPER/CREB/BDNF pathway.

BACKGROUND: Gender is a significant risk factor for late-onset Alzheimer's disease (AD), often attributed to the decline of estrogen. The plant estrogen secoisolariciresinol diglucoside (SDG) has demonstrated anti-inflammatory and neuroprotective effects. However, the protective effects and mechanisms of SDG in female AD remain unclear. METHODS: Ten-month-old female APPswe/PSEN1dE9 (APP/PS1) transgenic mice were treated with SDG to assess its potential ameliorative effects on cognitive impairments in a female AD model through a series of behavioral and biochemical experiments. Serum levels of gut microbial metabolites enterodiol (END) and enterolactone (ENL) were quantified using HPLC-MS. Correlation analysis and broad-spectrum antibiotic cocktail (ABx) treatment were employed to demonstrate the involvement of END and ENL in SDG's cognitive improvement effects in female APP/PS1 mice. Additionally, an acute neuroinflammation model was constructed in three-month-old C57BL/6J mice treated with lipopolysaccharide (LPS) and subjected to i.c.v. injection of G15, an inhibitor of G protein-coupled estrogen receptor (GPER), to investigate the mediating role of the estrogen receptor GPER in the cognitive benefits conferred by SDG. RESULTS: SDG administration resulted in significant improvements in spatial, recognition, and working memory in female APP/PS1 mice. Neuroprotective effects were observed, including enhanced expression of CREB/BDNF and PSD-95, reduced ß-amyloid (Aß) deposition, and decreased levels of TNF-α, IL-6, and IL-10. SDG also altered gut microbiota composition, increasing serum levels of END and ENL. Correlation analysis indicated significant associations between END, ENL, cognitive performance, hippocampal Aß-related protein mRNA expression, and cortical neuroinflammatory cytokine levels. The removal of gut microbiota inhibited END and ENL production and eliminated the neuroprotective effects of SDG. Furthermore, GPER was found to mediate the inhibitory effects of SDG on neuroinflammatory responses. CONCLUSION: These findings suggest that SDG promotes the production of gut microbial metabolites END and ENL, which inhibit cerebral ß-amyloid deposition, activate GPER to enhance CREB/BDNF signaling pathways, and suppress neuroinflammatory responses. Consequently, SDG exerts neuroprotective effects and ameliorates cognitive impairments associated with AD in female mice.

Liquid Biopsy-Based Accurate Diagnosis and Genomic Profiling of Hard-to-Biopsy Tumors via Parallel Single-Cell Genomic Sequencing of Exfoliated Tumor Cells.

Liquid biopsy provides a convenient and safer procedure for the diagnosis and genomic profiling of tumors that are inaccessible to biopsy by analyzing exfoliated tumor cells (ETCs) or tumor-derived cell-free DNA (cfDNA). However, its primary challenge lies in its limited accuracy in comparison to tissue-based approaches. We report a parallel single-ETC genomic sequencing (Past-Seq) method for the accurate diagnosis and genomic profiling of hard-to-biopsy tumors such as cholangiocarcinoma (CCA) and upper tract urothelial carcinoma (UTUC). For CCA, a prospective cohort of patients with suspicious biliary strictures (n = 36) was studied. Parallel single-cell whole genome sequencing and whole exome sequencing were performed on bile ETCs for CCA diagnosis and resolving mutational profiles, respectively, along with bile cfDNA sequenced for comparison. Concordant single-cell copy number alteration (CNA) profiles in multiple ETCs provided compelling evidence for generating a malignant diagnosis. Past-Seq yielded bile-based accurate CCA diagnosis (96% sensitivity, 100% specificity, and positive predictive value), surpassing pathological evaluation (56% sensitivity) and bile cfDNA CNA analysis (13% sensitivity), and generated the best performance in the retrieval tissue mutations. To further explore the applicability of Past-Seq, 10 suspicious UTUC patients were investigated with urine specimens, and Past-Seq exhibited 90% sensitivity in diagnosing UTUC, demonstrating its broad applicability across various liquid biopsies and cancer types.

Cobalt and nitrogen co-doped hollow periodic mesoporous organosilica spheres activated by potassium chloride for selective oxidation of ethylbenzene.

Enhancing the exposure of metal active sites and maximizing metal atom utilization are critical challenges in heterogeneous catalysis. To solve these issues, heterogeneous catalysts are usually activated by chemicals. Herein, potassium chloride (KCl) was used as an activator to prepare cobalt-nitrogen co-doped (Co-Nx) hollow periodic mesoporous organosilica spheres (Co-Nx/HPMOs-KCl). Co-Nx/HPMOs-KCl showed outstanding catalytic activity for the selective oxidation of ethylbenzene to acetophenone, with a conversion of up to 94.0% for ethylbenzene and a high selectivity of 98.4% towards acetophenone. Additionally, Co-Nx/HPMOs-KCl maintained excellent catalytic performance for the oxidation of ethylbenzene after six cycles. The excellent performance of Co-Nx/HPMOs-KCl was attributed to the activation of KCl, which increased the specific surface area of the catalyst and thus facilitated the exposure of more metal active sites. After the removal of unstable metal species through further acid treatment, the remaining metal active sites were thus fully exposed and stably embedded in the framework of the hollow periodic mesoporous organosilica spheres (HMPOs). This work presents an efficient catalyst and offers new insights for the improvement of heterogeneous catalysts.

Chidamide represses MYC expression and might improve survival for patients with double expressor lymphoma.

Double expressor lymphoma (DEL), characterized by high expressions of both MYC and BCL-2, displays poor prognosis after current therapies. The HDAC inhibitor chidamide has been approved for treatment of T cell lymphoma, but its efficacy on B cell lymphoma is unclear. Here, by combining inhibition screening and transcriptomic analyses, we found that the sensitivity of B lymphoma cells to chidamide was positively correlated with the expression levels of MYC. Chidamide treatment reduced MYC protein levels and repressed MYC pathway in B lymphoma cells with high MYC expressions. Ectopic expression of MYC in chidamide-insensitive B lymphoma cells increased their response to chidamide. Thus, we proposed that adding chidamide into R-CHOP (CR-CHOP) might be effective for DEL, and retrospectively analyzed 185 DEL patients treated in West China Hospital. 80% of patients showed response to CR-CHOP treatment. In the median follow-up of 42 months, CR-CHOP significantly improve the survival for DEL patients with R-IPI ≤2. Totally 35 patients underwent autologous stem cell transplantation (ASCT) in remission and demonstrated a trend for better survival. Combining CR-CHOP with ASCT resulted in the most superior PFS and OS above all. For response patients, CR-CHOP reduced relapse with better PFS than R-CHOP-like regimens with or without ASCT. Taken together, our data indicated that chidamide repressed the MYC pathway in B lymphoma and is potentially efficacious to treat DEL.

Synbiotic therapy with Clostridium sporogenes and xylan promotes gut-derived indole-3-propionic acid and improves cognitive impairments in an Alzheimer's disease mouse model.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized primarily by cognitive impairment. Recent investigations have highlighted the potential of nutritional interventions that target the gut-brain axis, such as probiotics and prebiotics, in forestalling the onset of AD. In this study, whole-genome sequencing was employed to identify xylan as the optimal carbon source for the tryptophan metabolism regulating probiotic Clostridium sporogenes (C. sporogenes). Subsequent in vivo studies demonstrated that administration of a synbiotic formulation comprising C. sporogenes (1 × 1010 CFU per day) and xylan (1%, w/w) over a duration of 30 days markedly enhanced cognitive performance and spatial memory faculties in the 5xFAD transgenic AD mouse model. The synbiotic treatment significantly reduced amyloid-ß (Aß) accumulation in the cortex and hippocampus of the brain. Importantly, synbiotic therapy substantially restored the synaptic ultrastructure in AD mice and suppressed neuroinflammatory responses. Moreover, the intervention escalated levels of the microbial metabolite indole-3-propionic acid (IPA) and augmented the relative prevalence of IPA-synthesizing bacteria, Lachnospira and Clostridium, while reducing the dominant bacteria in AD, such as Aquabacterium, Corynebacterium, and Romboutsia. Notably, synbiotic treatment also prevented the disruption of gut barrier integrity. Correlation analysis indicated a strong positive association between gut microbiota-generated IPA levels and behavioral changes. In conclusion, this study demonstrates that synbiotic supplementation significantly improves cognitive and intellectual deficits in 5xFAD mice, which could be partly attributed to enhanced IPA production by gut microbiota. These findings provide a theoretical basis for considering synbiotic therapy as a novel microbiota-targeted approach for the treatment of metabolic and neurodegenerative diseases.

Effect of Pond-Based Rice Floating Bed on the Microbial Community Structure and Quality of Water in Pond of Mandarin Fish Fed Using Artificial Diet.

The culture of mandarin fish using artificial feed has been gaining increasing attention in China. Ensuring good water quality in the ponds is crucial for successful aquaculture. Recently, the trial of pond-based rice floating beds (PRFBs) in aquaculture ponds has shown promising results. This research assessed the impact of PRFBs on the microbial community structure and overall quality of the aquaculture pond, thereby enhancing our understanding of its functions. The results revealed that the PRFB group exhibited lower levels of NH4+-N, NO2--N, NO3--N, TN, TP, and Alk in pond water compared to the control group. The microbial diversity indices in the PRFB group showed a declining trend, while these indices were increasing in the control group. At the phylum level, there was a considerable increase in Proteobacteria abundance in the PRFB group throughout the culture period, suggesting that PRFBs may promote the proliferation of Proteobacteria. In the PRFB group, there was a remarkable decrease in bacterial populations related to carbon, nitrogen, and phosphorus metabolism, including genera Rhodobacter, Rhizorhapis, Dinghuibacter, Candidatus Aquiluna, and Chryseomicrobium as well as the CL500_29_marine_group. Overall, the research findings will provide a basis for the application of aquaculture of mandarin fish fed an artificial diet and rice floating beds.

Long-term outcomes of the BalMedic bovine pericardial bioprosthetic valve in female patients ≤50 years: a multicenter retrospective study.

Background: A bioprosthetic valve is recommended for women of childbearing age who require cardiac valve replacement in order to minimize the risk of blood clot formation. However, it should be noted that compared to mechanical valves, bioprosthetic valves have a shorter lifespan and a higher likelihood of requiring reoperation during follow-up. To assess the long-term postoperative results, including the incidence of structural valve deterioration (SVD) and other clinical outcomes, in female patients aged 50 years and younger who underwent BalMedic bovine pericardial bioprosthetic valve replacement, a multicenter retrospective study was implemented in China. Methods: Between 2004 and 2015, a cohort of 86 female patients across three medical centers underwent the implantation of 97 bioprosthetic valves. The primary outcome measure was overall survival (OS), while the secondary outcome measures were preliminary evidence of reoperation, SVD incidence, and bioprosthetic valve-related complications. Results: In this cohort study, 21 patients (24.4%, 21/86) died, while 37 patients (43.0%, 37/86) underwent a second valve replacement. The OS rates at 5 and 10 years were 97.56% and 71.93%, respectively. Additionally, the reoperation-free rates at 5 and 10 years were 92.83% and 80.68%, respectively. Similarly, the rates of freedom from SVD at 5 and 10 years were 95.65% and 51.82%, respectively, and the average duration of bioprosthetic valve replacement in our study was 9.34±3.31 years. Conclusions: Despite the recruitment of younger female patients of child-bearing age in our cohort, the OS, reoperation-free survival, and SVD-free rates of the BalMedic bovine pericardial bioprosthetic valve were not inferior to those of the other age groups in the study or those reported in the literature.