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Coxsackie B virus-induced myocarditis in a patient with a history of lymphoma: A case report and review of literature.
Zhang, Q, Yuan, J, Zhao, W, Ouyang, W, Chen, B, Li, Y, Tao, J, Chen, X, Li, G, Guo, Z, et al
Medicine. 2024;(10):e37248
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Abstract
INTRODUCTION In rare occasions, coxsackievirus infections can cause serious illness, such as encephalitis and myocarditis. The immunotherapies of cancer could increase the risk of myocarditis, especially when applying immune checkpoint inhibitors. Herein, we report a rare case of Coxsackie B virus-induced myocarditis in a patient with a history of lymphoma. CASE PRESENTATION A 32-year-old woman was admitted to the hospital with recurrent fever for more than 20 days, and she had a history of lymphoma. Before admission, the positron emission tomography/computed tomography result indicated that the patient had no tumor progression, and she was not considered the cancer-related fever upon arriving at our hospital. Patient's red blood cell, platelet count, and blood pressure were decreased. In addition, she had sinus bradycardia and 3 branch blocks, which was consistent with acute high lateral and anterior wall myocardial infarction. During hospitalization, the patient had recurrent arrhythmia, repeated sweating, poor mentation, dyspnea, and Coxsackie B virus were detected in patient's blood samples by pathogen-targeted next-generation sequencing. The creatine kinase, creatine kinase MB, and N-terminal pro-brain natriuretic peptide were persistently elevated. Consequently, the patient was diagnosed with viral myocarditis induced by Coxsackie B virus, and treated with acyclovir, gamma globulin combined with methylprednisolone shock therapy, trimetazidine, levosimendan, sildenan, continuous pump pressors with m-hydroxylamine, entecavir, adefovir, glutathione, pantoprazole, and low-molecular-weight heparin. Her symptoms worsened and died. CONCLUSION We reported a case with a history of lymphoma presented with fever, myocardial injury, who was ultimately diagnosed with Coxsackie B virus-induced myocarditis. Moreover, pathogen-targeted next-generation sequencing indeed exhibited higher sensitivity compared to mNGS in detecting Coxsackie B virus.
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High frequency electrocoagulation resection effect analysis and prognosis observation in the treatment of patients with gastric polyps under painless gastroscopy.
Chen, X, Zhang, D, Chen, M
Medicine. 2024;(6):e37027
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Abstract
To explore high frequency electrocoagulation resection effect in treatment of patients with gastric polyps under painless gastroscopy. Sixty-four patients with gastric polyps were randomly divided into experimental group (32 cases) and control group (32 cases). Experimental group received basic treatment drugs for 8 weeks, and then treated with painless gastroscope high-frequency electrocoagulation resection. Control group was also given basic treatment drugs for 8 weeks, and then received high-frequency electrocoagulation resection under ordinary gastroscope. The patients in both groups were given rabeprazole sodium enteric coated capsules for 4 weeks. The improvement of symptom score, postoperative gastric mucosal healing and comprehensive curative effect of the 2 groups were observed after treatment. The patients with polyps cured under gastroscopy were subjected to a 6-month follow-up period during which gastroscopy was performed to assess the recurrence of polyps. Symptom scores comparison after treatment showed that experimental group had obvious advantages in improving epigastric fullness, fatigue and loose stool in patients with gastric polyps (P < .01 or P < .05). Gastric mucosa healing in experimental group was better at 2 weeks after operation (P < .05), showing no difference 4 weeks after operation (P > .05). Comprehensive curative effect comparison showed that the experimental group was better (P < .01), showing no difference in long-term efficacy (P > .05). In treating patients with gastric polyps, painless endoscopic high-frequency electrocoagulation resection effect is better, which not only promotes postoperative rehabilitation in patients but also reduces complications incidence, demonstrating a high level of safety. Therefore, it is highly recommended for widespread adoption and application.
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Ferroptosis in cancer: From molecular mechanisms to therapeutic strategies.
Zhou, Q, Meng, Y, Li, D, Yao, L, Le, J, Liu, Y, Sun, Y, Zeng, F, Chen, X, Deng, G
Signal transduction and targeted therapy. 2024;(1):55
Abstract
Ferroptosis is a non-apoptotic form of regulated cell death characterized by the lethal accumulation of iron-dependent membrane-localized lipid peroxides. It acts as an innate tumor suppressor mechanism and participates in the biological processes of tumors. Intriguingly, mesenchymal and dedifferentiated cancer cells, which are usually resistant to apoptosis and traditional therapies, are exquisitely vulnerable to ferroptosis, further underscoring its potential as a treatment approach for cancers, especially for refractory cancers. However, the impact of ferroptosis on cancer extends beyond its direct cytotoxic effect on tumor cells. Ferroptosis induction not only inhibits cancer but also promotes cancer development due to its potential negative impact on anticancer immunity. Thus, a comprehensive understanding of the role of ferroptosis in cancer is crucial for the successful translation of ferroptosis therapy from the laboratory to clinical applications. In this review, we provide an overview of the recent advancements in understanding ferroptosis in cancer, covering molecular mechanisms, biological functions, regulatory pathways, and interactions with the tumor microenvironment. We also summarize the potential applications of ferroptosis induction in immunotherapy, radiotherapy, and systemic therapy, as well as ferroptosis inhibition for cancer treatment in various conditions. We finally discuss ferroptosis markers, the current challenges and future directions of ferroptosis in the treatment of cancer.
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Heartache and Heartbreak: An Observational and Mendelian Randomization Study.
Cai, D, Xia, M, Chen, X, Yagi, K, Xu, L, Wang, B, Wang, Y, Zhou, Y, Liu, J
Global heart. 2024;(1):19
Abstract
BACKGROUND Depression has a significant effect on cardiovascular disease (CVD), but uncertainties persist regarding which modifiable risk factors mediate the causal effects. We aim to determine whether depression is causally linked to CVD and which modifiable risk factors play potential mediating roles. METHODS We used a two-sample Mendelian randomization (MR) approach and NHANES 2007-2018 data to estimate the effects of depression on various CVD cases and investigated 28 potential mediators of the association between depression and CVD. RESULTS The results of our MR analysis indicated that genetically determined depression was associated with increased risk of several CVD, including coronary heart disease (odds ratio (OR) = 1.14; 95% confidence interval (CI): 1.05,1.22), myocardial infarction (OR = 1.19; 95% CI, 1.09,1.31), atrial fibrillation (OR = 1.14; 95% CI, 1.06,1.22), and stroke (OR = 1.13; 95% CI, 1.05,1.22). However, there was no causal association between depression and heart failure. Four out of 28 cardiometabolic risk factors, including hyperlipidemia, hypertension, diabetes, and prescription opioid use, were identified as mediators of the association between depression and various CVDs. Observational association analyses from NHANES data yielded consistent results. CONCLUSION Our findings demonstrated that depression has a causal detrimental effect on various CVDs. Four causal mediators (hyperlipidemia, hypertension, diabetes, and prescription opioid use) were screened to explain the causal effect. Implementing targeted management strategies for these risk factors may be warranted to mitigate the public health burden of CVD among individuals with depression.
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A genome-wide cross-trait analysis identifies shared loci and causal relationships of obesity and lipidemic traits with psoriasis.
Wu, Y, Huang, M, Chen, X, Wu, J, Li, L, Wei, J, Lu, C, Han, L, Lu, Y
Frontiers in immunology. 2024;:1328297
Abstract
BACKGROUND Obesity and dyslipidemia, major global health concerns, have been linked to psoriasis, but previous studies faced methodological limitations and their shared genetic basis remains unclear. This study examines various obesity-related and lipidemic traits as potential contributors to psoriasis development, aiming to clarify their genetic associations and potential causal links. METHODS Summary statistics from genome-wide association studies (GWAS) conducted for obesity-related traits (body mass index (BMI), waist-to-hip ratio (WHR), and waist-to-hip ratio adjusted for the body mass index (WHRadjBMI)) and lipidemic traits (high-density lipoprotein (HDL), LDL, triglyceride (TG), total Cholesterol (TC), apolipoprotein A1 (apoA1), apolipoprotein B (apoB), and apolipoprotein E (apoE)) and psoriasis, all in populations of European ancestry, were used. We quantified genetic correlations, identified shared loci and explored causal relationship across traits. RESULTS We found positive genetic correlation between BMI and psoriasis (rg=0.22, p=2.44×10-18), and between WHR and psoriasis (rg=0.19, p=1.41×10-12). We further found the positive genetic correlation between psoriasis and WHRadjBMI(rg=0.07, p=1.81×10-2) the genetic correlation, in while the effect of BMI was controlled for. We identified 14 shared loci underlying psoriasis and obesity-related traits and 43 shared loci between psoriasis and lipidemic traits via cross-trait meta-analysis. Mendelian randomization (MR) supported the causal roles of BMI (IVW OR=1.483, 95%CI=1.333-1.649), WHR (IVW OR=1.393, 95%CI=1.207-1.608) and WHRadjBMI (IVW OR=1.18, 95%CI=1.047-1.329) in psoriasis, but not observe any significant association between lipidemic traits and the risk of psoriasis. Genetic predisposition to psoriasis did not appear to affect the risk of obesity and lipidemic traits. CONCLUSIONS An intrinsic link between obesity-related traits and psoriasis has been demonstrated. The genetic correlation and causal role of obesity-related traits in psoriasis highlight the significance of weight management in both the prevention and treatment of this condition.
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So close, yet so far away: the relationship between MAM and cardiac disease.
Lu, B, Chen, X, Ma, Y, Gui, M, Yao, L, Li, J, Wang, M, Zhou, X, Fu, D
Frontiers in cardiovascular medicine. 2024;:1353533
Abstract
Mitochondria-associated membrane (MAM) serve as crucial contact sites between mitochondria and the endoplasmic reticulum (ER). Recent research has highlighted the significance of MAM, which serve as a platform for various protein molecules, in processes such as calcium signaling, ATP production, mitochondrial structure and function, and autophagy. Cardiac diseases caused by any reason can lead to changes in myocardial structure and function, significantly impacting human health. Notably, MAM exhibits various regulatory effects to maintain cellular balance in several cardiac diseases conditions, such as obesity, diabetes mellitus, and cardiotoxicity. MAM proteins independently or interact with their counterparts, forming essential tethers between the ER and mitochondria in cardiomyocytes. This review provides an overview of key MAM regulators, detailing their structure and functions. Additionally, it explores the connection between MAM and various cardiac injuries, suggesting that precise genetic, pharmacological, and physical regulation of MAM may be a promising strategy for preventing and treating heart failure.
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Effect of metabolic reprogramming on the immune microenvironment in gastric cancer.
Shang, Z, Ma, Z, Wu, E, Chen, X, Tuo, B, Li, T, Liu, X
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2024;:116030
Abstract
Gastric cancer (GC) is a malignant tumor of the gastrointestinal tract with a high mortality rate worldwide, a low early detection rate and a poor prognosis. The rise of metabolomics has facilitated the early detection and treatment of GC. Metabolism in the GC tumor microenvironment (TME) mainly includes glucose metabolism, lipid metabolism and amino acid metabolism, which provide energy and nutrients for GC cell proliferation and migration. Abnormal tumor metabolism can influence tumor progression by regulating the functions of immune cells and immune molecules in the TME, thereby contributing to tumor immune escape. Thus, in this review, we summarize the impact of metabolism on the TME during GC progression. We also propose novel strategies to modulate antitumor immune responses by targeting metabolism.
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Unraveling two decades of phyllosphere endophytes: tracing research trends and insights through visualized knowledge maps, with emphasis on microbial interactions as emerging frontiers.
Muneer, MA, Chen, X, Wang, H, Munir, MZ, Afridi, MS, Yan, X, Ji, B, Li, W, Wu, L, Zheng, C
Stress biology. 2024;(1):12
Abstract
Phyllosphere endophytes play a critical role in a myriad of biological functions, such as maintaining plant health and overall fitness. They play a determinative role in crop yield and quality by regulating vital processes, such as leaf functionality and longevity, seed mass, apical growth, flowering, and fruit development. This study conducted a comprehensive bibliometric analysis aiming to review the prevailing research trajectories in phyllosphere endophytes and harness both primary areas of interest and emerging challenges. A total of 156 research articles on phyllosphere endophytes, published between 2002 and 2022, were retrieved from the Web of Science Core Collection (WoSCC). A systematic analysis was conducted using CiteSpace to visualize the evolution of publication frequency, the collaboration network, the co-citation network, and keywords co-occurrence. The findings indicated that initially, there were few publications on the topic of phyllosphere endophytes. However, from 2011 onwards, there was a notable increase in the number of publications on phyllosphere endophytes, gaining worldwide attention. Among authors, Arnold, A Elizabeth is widely recognized as a leading author in this research area. In terms of countries, the USA and China hold the highest rankings. As for institutional ranking, the University of Arizona is the most prevalent and leading institute in this particular subject. Collaborative efforts among the authors and institutions tend to be confined to small groups, and a large-scale collaborative network needs to be established. This study identified the influential journals, literature, and hot research topics. These findings also highlight the interconnected nature of key themes, e.g., phyllosphere endophyte research revolves around the four pillars: diversity, fungal endophytes, growth, and endophytic fungi. This study provides an in-depth perspective on phyllosphere endophytes studies, revealing the identification of biodiversity and microbial interaction of phyllosphere endophytes as the principal research frontiers. These analytical findings not only elucidate the recent trajectory of phyllosphere endophyte research but also provide invaluable insights for similar studies and their potential applications on a global scale.
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Gut microbiome and serum amino acid metabolome alterations in autism spectrum disorder.
Chang, X, Zhang, Y, Chen, X, Li, S, Mei, H, Xiao, H, Ma, X, Liu, Z, Li, R
Scientific reports. 2024;(1):4037
Abstract
Gut microbiota and their metabolic products might play important roles in regulating the pathogenesis of autism spectrum disorder (ASD). The purpose of this study was to characterize gut microbiota and serum amino acid metabolome profiles in children with ASD. A non-randomized controlled study was carried out to analyze the alterations in the intestinal microbiota and their metabolites in patients with ASD (n = 30) compared with neurotypical controls (NC) (n = 30) by metagenomic sequencing to define the gut microbiota community and liquid chromatography/mass spectrometry (LC/MS) analysis to characterize the metabolite profiles. Compared with children in the NC group, those in the ASD group showed lower richness, higher evenness, and an altered microbial community structure. At the class level, Deinococci and Holophagae were significantly lower in children with ASD compared with TD. At the phylum level, Deinococcus-Thermus was significantly lower in children with ASD compared with TD. In addition, the functional properties (such as galactose metabolism) displayed significant differences between the ASD and NC groups. Five dominant altered species were identified and analyzed (LDA score > 2.0, P < 0.05), including Subdoligranulum, Faecalibacterium_praushitzii, Faecalibacterium, Veillonellaceae, and Rumminococcaceae. The peptides/nickel transport system was the main metabolic pathway involved in the differential species in the ASD group. Decreased ornithine levels and elevated valine levels may increase the risk of ASD through a metabolic pathway known as the nickel transport system. The microbial metabolism in diverse environments was negatively correlated with phascolarctobacterium succinatutens. Our study provides novel insights into compositional and functional alterations in the gut microbiome and metabolite profiles in ASD and the underlying mechanisms between metabolite and ASD.
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Cholesterol metabolism: physiological regulation and diseases.
Guo, J, Chen, S, Zhang, Y, Liu, J, Jiang, L, Hu, L, Yao, K, Yu, Y, Chen, X
MedComm. 2024;(2):e476
Abstract
Cholesterol homeostasis is crucial for cellular and systemic function. The disorder of cholesterol metabolism not only accelerates the onset of cardiovascular disease (CVD) but is also the fundamental cause of other ailments. The regulation of cholesterol metabolism in the human is an extremely complex process. Due to the dynamic balance between cholesterol synthesis, intake, efflux and storage, cholesterol metabolism generally remains secure. Disruption of any of these links is likely to have adverse effects on the body. At present, increasing evidence suggests that abnormal cholesterol metabolism is closely related to various systemic diseases. However, the exact mechanism by which cholesterol metabolism contributes to disease pathogenesis remains unclear, and there are still unknown factors. In this review, we outline the metabolic process of cholesterol in the human body, especially reverse cholesterol transport (RCT). Then, we discuss separately the impact of abnormal cholesterol metabolism on common diseases and potential therapeutic targets for each disease, including CVD, tumors, neurological diseases, and immune system diseases. At the end of this review, we focus on the effect of cholesterol metabolism on eye diseases. In short, we hope to provide more new ideas for the pathogenesis and treatment of diseases from the perspective of cholesterol.