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9,126 result(s) for "Shu Xu"
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Recent Advances in Marine Algae Polysaccharides: Isolation, Structure, and Activities
Marine algae have attracted a great deal of interest as excellent sources of nutrients. Polysaccharides are the main components in marine algae, hence a great deal of attention has been directed at isolation and characterization of marine algae polysaccharides because of their numerous health benefits. In this review, extraction and purification approaches and chemico-physical properties of marine algae polysaccharides (MAPs) are summarized. The biological activities, which include immunomodulatory, antitumor, antiviral, antioxidant, and hypolipidemic, are also discussed. Additionally, structure-function relationships are analyzed and summarized. MAPs’ biological activities are closely correlated with their monosaccharide composition, molecular weights, linkage types, and chain conformation. In order to promote further exploitation and utilization of polysaccharides from marine algae for functional food and pharmaceutical areas, high efficiency, and low-cost polysaccharide extraction and purification methods, quality control, structure-function activity relationships, and specific mechanisms of MAPs activation need to be extensively investigated.
Gut microbiota dysbiosis worsens the severity of acute pancreatitis in patients and mice
BackgroundThe gut is implicated in the pathogenesis of acute pancreatitis (AP) and the infectious complications of AP are commonly associated with enteric bacteria, yet whether gut microbiota dysbiosis participants in AP severity remains largely unknown.MethodsWe collected clinical information and fecal samples from 165 adult participants, including 41 with mild AP (MAP), 59 with moderately severe AP (MSAP), 30 with severe AP (SAP) and 35 healthy controls (HC). The serum inflammatory cytokines and gut barrier indexes were detected. Male C57BL/6 mice with AP were established and injuries of pancreas were evaluated in antibiotic-treated mice, germ-free mice as well as those transplanted with fecal microbiota. The gut microbiota was analyzed by 16S rRNA gene sequencing.ResultsThe structure of gut microbiota was significantly different between AP and HC, and the disturbed microbiota was closely correlated with systematic inflammation and gut barrier dysfunction. Notably, the microbial composition changed further with the worsening of AP and the abundance of beneficial bacteria such as Blautia was decreased in SAP compared with MAP and MSAP. The increased capacity for the inferred pathway, bacterial invasion of epithelial cells in AP, highly correlated with the abundance of Escherichia–Shigella. Furthermore, the antibiotic-treated mice and germ-free mice exhibited alleviated pancreatic injury after AP induction and subsequent fecal microbiota transplantation in turn exacerbated the disease.ConclusionsThis study identifies the gut microbiota as an important mediator during AP and its dysbiosis is associated with AP severity, which suggests its role as potential therapeutic target.
Unraveling the effects of DIP payment reform on inpatient healthcare: insights into impacts and challenges
Background The Diagnosis-Intervention Packet (DIP) payment system, initiated by China's National Healthcare Security Administration, is designed to enhance healthcare efficiency and manage rising healthcare costs. This study aims to evaluate the impact of the DIP payment reform on inpatient care in a specialized obstetrics and gynecology hospital, with a focus on its implications for various patient groups. Methods To assess the DIP policy's effects, we employed the Difference-in-Differences (DID) approach. This method was used to analyze changes in total hospital costs and Length of Stay (LOS) across different patient groups, particularly within select DIP categories. The study involved a comprehensive examination of the DIP policy's influence pre- and post-implementation. Results Our findings indicate that the implementation of the DIP policy led to a significant increase in both total costs and LOS for the insured group relative to the self-paying group. The study further identified variations within DIP groups both before and after the reform. In-depth analysis of specific disease groups revealed that the insured group experienced notably higher total costs and LOS compared to the self-paying group. Conclusions The DIP reform has led to several challenges, including upcoding and diagnostic ambiguity, because of the pursuit of higher reimbursements. These findings underscore the necessity for continuous improvement of the DIP payment system to effectively tackle these challenges and optimize healthcare delivery and cost management.
Multistaged discharge constructing heterostructure with enhanced solid-solution behavior for long-life lithium-oxygen batteries
Inferior charge transport in insulating and bulk discharge products is one of the main factors resulting in poor cycling stability of lithium–oxygen batteries with high overpotential and large capacity decay. Here we report a two-step oxygen reduction approach by pre-depositing a potassium carbonate layer on the cathode surface in a potassium–oxygen battery to direct the growth of defective film-like discharge products in the successive cycling of lithium–oxygen batteries. The formation of defective film with improved charge transport and large contact area with a catalyst plays a critical role in the facile decomposition of discharge products and the sustained stability of the battery. Multistaged discharge constructing lithium peroxide-based heterostructure with band discontinuities and a relatively low lithium diffusion barrier may be responsible for the growth of defective film-like discharge products. This strategy offers a promising route for future development of cathode catalysts that can be used to extend the cycling life of lithium–oxygen batteries. Li–O 2 batteries suffer from poor charge transport in the insulating discharge products. Here the authors tackle the issue by pre-depositing a K 2 CO 3 layer and then using this to grow Li 2 O 2 film on top, enabling enhanced electronic conduction properties and improved overall performance.
Shotgun metagenomics reveals both taxonomic and tryptophan pathway differences of gut microbiota in major depressive disorder patients
The microbiota-gut-brain axis, especially the microbial tryptophan (Trp) biosynthesis and metabolism pathway (MiTBamp), may play a critical role in the pathogenesis of major depressive disorder (MDD). However, studies on the MiTBamp in MDD are lacking. The aim of the present study was to analyze the gut microbiota composition and the MiTBamp in MDD patients. We performed shotgun metagenomic sequencing of stool samples from 26 MDD patients and 29 healthy controls (HCs). In addition to the microbiota community and the MiTBamp analyses, we also built a classification based on the Random Forests (RF) and Boruta algorithm to identify the gut microbiota as biomarkers for MDD. The Bacteroidetes abundance was strongly reduced whereas that of Actinobacteria was significantly increased in the MDD patients compared with the abundance in the HCs. Most noteworthy, the MDD patients had increased levels of Bifidobacterium, which is commonly used as a probiotic. Four Kyoto Encyclopedia of Genes and Genomes (KEGG) orthologies (KOs) (K01817, K11358, K01626, K01667) abundances in the MiTBamp were significantly lower in the MDD group. Furthermore, we found a negative correlation between the K01626 abundance and the HAMD scores in the MDD group. Finally, RF classification at the genus level can achieve an area under the receiver operating characteristic curve of 0.890. The present findings enabled a better understanding of the changes in gut microbiota and the related Trp pathway in MDD. Alterations of the gut microbiota may have the potential as biomarkers for distinguishing MDD patients form HCs.
The emerging role of ferroptosis in intestinal disease
Ferroptosis is a newly recognised type of regulated cell death (RCD) characterised by iron-dependent accumulation of lipid peroxidation. It is significantly distinct from other RCDs at the morphological, biochemical, and genetic levels. Recent reports have implicated ferroptosis in multiple diseases, including neurological disorders, kidney injury, liver diseases, and cancer. Ferroptotic cell death has also been associated with dysfunction of the intestinal epithelium, which contributes to several intestinal diseases. Research on ferroptosis may provide a new understanding of intestinal disease pathogenesis that benefits clinical treatment. In this review, we provide an overview of ferroptosis and its underlying mechanisms, then describe its emerging role in intestinal diseases, including intestinal ischaemia/reperfusion (I/R) injury, inflammatory bowel disease (IBD), and colorectal cancer (CRC).
The emerging role of pyroptosis-related inflammasome pathway in atherosclerosis
Atherosclerosis (AS), a chronic sterile inflammatory disorder, is one of the leading causes of mortality worldwide. The dysfunction and unnatural death of plaque cells, including vascular endothelial cells (VEC), macrophages, and vascular smooth muscle cells (VSMC), are crucial factors in the progression of AS. Pyroptosis was described as a form of cell death at least two decades ago. It is featured by plasma membrane swelling and rupture, cell lysis, and consequent robust release of cytosolic contents and pro-inflammatory mediators, including interleukin-1β (IL-1β), IL-18, and high mobility group box 1 (HMGB1). Pyroptosis of plaque cells is commonly observed in the initiation and development of AS, and the levels of pyroptosis-related proteins are positively correlated with plaque instability, indicating the crucial contribution of pyroptosis to atherogenesis. Furthermore, studies have also identified some candidate anti-atherogenic agents targeting plaque cell pyroptosis. Herein, we summarize the research progress in understating (1) the discovery and definition of pyroptosis; (2) the characterization and molecular mechanisms of pyroptosis; (3) the regulatory mechanisms of pyroptosis in VEC, macrophage, and VSMC, as well as their potential role in AS progression, aimed at providing therapeutic targets for the prevention and treatment of AS.
Risk factors for gastrointestinal bleeding in patients with cerebral infarction after dual antiplatelet therapy
To investigate the risk factors for gastrointestinal bleeding in patients with cerebral infarction after dual antiplatelet therapy. Cerebral infarction patients who received dual antiplatelet therapy during January 2019 and December 2021 in Nanchang University Affiliated Ganzhou Hospital were included. Patients were divided into a bleeding group and a nonbleeding group. Propensity score matching was used to match the data between the two groups. The risk factors for cerebral infarction with gastrointestinal bleeding after receiving dual antiplatelet therapy were analyzed by conditional logistic regression. There were 2370 cerebral infarction patients who received dual antiplatelet therapy included in the study. There were significant differences between the bleeding group and the nonbleeding group in terms of sex, age, smoking, drinking, hypertension, coronary heart disease, diabetes and peptic ulcer before matching. After matching, 85 patients were included in the bleeding group and nonbleeding group, and there was no significant difference between the two groups in terms of sex, age, smoking, drinking, previous cerebral infarction, hypertension, coronary heart disease, diabetes, gout or peptic ulcer. Conditional logistic regression analysis showed that long-term use of aspirin and severity of cerebral infarction were risk factors for gastrointestinal bleeding in cerebral infarction patients receiving dual antiplatelet therapy, whereas the use of PPI was a protective factor against gastrointestinal bleeding. Long-term use of aspirin and severity of cerebral infarction are risk factors for gastrointestinal bleeding in cerebral infarction patients receiving dual antiplatelet therapy. The use of PPIs could reduce the risk of gastrointestinal bleeding. •few scholars have investigated the risk factors for gastrointestinal bleeding in cerebral infarction patients receiving dual antiplatelet therapy.•Long-term use of aspirin and severity of cerebral infarction are risk factors for gastrointestinal bleeding.•The use of PPIs could reduce the risk of gastrointestinal bleeding.•Risk factors for gastrointestinal bleeding in cerebral infarction patients receiving dual antiplatelet therapy were unclear.
The role of the mTOR pathway in breast cancer stem cells (BCSCs): mechanisms and therapeutic potentials
Breast cancer remains the most frequently diagnosed cancer globally, exerting a profound impact on women’s health and healthcare systems. Central to its pathogenesis and therapeutic resistance are breast cancer stem cells (BCSCs), which possess unique properties such as self-renewal, differentiation, and resistance to conventional therapies, contributing to tumor initiation, metastasis, and recurrence. This comprehensive review elucidates the pivotal role of the mechanistic target of rapamycin (mTOR) pathway in regulating BCSCs and its implications for breast cancer progression and treatment resistance. We explore the cellular mechanisms by which mTOR influences metastasis, metabolism, autophagy, and ferroptosis in BCSCs, highlighting its contribution to epithelial-to-mesenchymal transition (EMT), metabolic reprogramming, and survival under therapeutic stress. On a molecular level, mTOR interacts with key signaling pathways including PI3K/Akt, Notch, IGF-1R, AMPK, and TGF-β, as well as regulatory proteins and non-coding RNAs, orchestrating a complex network that sustains BCSC properties and mediates chemoresistance and radioresistance. The review further examines various therapeutic strategies targeting the mTOR pathway in BCSCs, encompassing selective PI3K/Akt/mTOR inhibitors, monoclonal antibodies, natural products, and innovative approaches such as nanoparticle-mediated drug delivery. Clinical trials investigating mTOR inhibitors like sirolimus and combination therapies with agents such as everolimus and trastuzumab are discussed, underscoring their potential in eradicating BCSCs and improving patient outcomes. Additionally, natural compounds and repurposed drugs offer promising adjunctive therapies by modulating mTOR activity and targeting BCSC-specific vulnerabilities. In conclusion, targeting the mTOR pathway presents a viable and promising avenue for enhancing breast cancer treatment efficacy by effectively eliminating BCSCs, reducing tumor recurrence, and improving overall patient survival. Continued research and clinical validation of mTOR-targeted therapies are essential to translate these insights into effective clinical interventions, ultimately advancing personalized cancer management and therapeutic outcomes for breast cancer patients.