Experimental biology and medicine (Maywood, N.J.)最新文献

{"title":"Retraction Notice.","authors":"","doi":"10.1177/15353702221123254","DOIUrl":"https://doi.org/10.1177/15353702221123254","url":null,"abstract":"1. Reuse of multiple Western blot bands representing different experimental conditions in Figure 3a. Bands appear identical within CnA and Adapt78. 2. Tubulin loading control blots between Figures 3A and 4C appear to be identical despite representing different experimental conditions, and the bands in Figure 3A appear to be vertically stretched. In addition, tubulin blots appear identical to bands representing eEF2, Figure 2D, in J. Cell. Mol. Med. Vol 13, No 8A, 2009 pp. 1513–1525. 3. Tubulin loading control blots between Figure 1B and 4C appear identical and display unreported alterations in contrast and/or brightness. 1123254 EBM","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"1609"},"PeriodicalIF":3.2,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9554162/pdf/10.1177_15353702221123254.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33455527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum.","authors":"","doi":"10.1177/15353702221113896","DOIUrl":"https://doi.org/10.1177/15353702221113896","url":null,"abstract":"","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"NP1"},"PeriodicalIF":3.2,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265518/pdf/10.1177_15353702221113896.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40471089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Musashi-1 enhances chemotherapeutic sensitivity in gastric cancer patient-derived xenografts.","authors":"Fan Liu,&nbsp;Huan Yang,&nbsp;Xinyu Zhang,&nbsp;Xianglin Sun,&nbsp;Jiamin Zhou,&nbsp;Yuan Li,&nbsp;Yifei Liu,&nbsp;Zhixiang Zhuang,&nbsp;Guohua Wang","doi":"10.1177/15353702221076793","DOIUrl":"https://doi.org/10.1177/15353702221076793","url":null,"abstract":"<p><p>Musashi-1 (MSI1), a neural RNA-binding protein, is considered a gastric and intestinal stem cell marker. Although the function of MSI1 in gastric cancer has attracted increasing interest, it is not known whether MSI1 can be used as a biomarker to monitor gastric cancer development and response to treatment. Here, the role of MSI1 in the chemotherapeutic sensitivity of gastric cancer was investigated. Patients with high MSI1 levels had poor outcomes, implicating the gene in the development and progression of the disease. We overexpressed and silenced MSI1 in the human gastric cancer cell lines MKN45 and HGC27, finding that knockdown reduced proliferation, invasion, and migration, while promoting apoptosis. A patient-derived xenograft gastric cancer model was constructed in which mice received chemical drugs, si-MSI1, or a drug-si-MSI1 combination. It was found that blocking MSI1 expression reduced gastric cancer drug tolerance. The combination treatment with si-MSI1 was superior to 5F-dUMP and cisplatin, either separately or in combination, indicating that including si-MSI1 was better than drug therapy alone. Transcriptome sequencing analysis showed that MSI1 altered cell cycle regulation and growth signal transduction, including that of blood vessel epicardial substance (BVES). These results suggest that MSI1 reduces the tolerance of gastric cancer to chemical drugs through modulation of MSI1/BVES signaling.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"868-879"},"PeriodicalIF":3.2,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9160935/pdf/10.1177_15353702221076793.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39900638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin-10 regulates starvation-induced autophagy through the STAT3-mTOR-p70s6k axis in hepatic stellate cells.","authors":"Dongmei Chen,&nbsp;Jiabing Chen,&nbsp;Yizhen Chen,&nbsp;Fenglin Chen,&nbsp;Xiaozhong Wang,&nbsp;Yuehong Huang","doi":"10.1177/15353702221080435","DOIUrl":"https://doi.org/10.1177/15353702221080435","url":null,"abstract":"<p><p>The degree of activation of hepatic stellate cells (HSCs) is closely related to the level of autophagy in HSCs. We previously showed that interleukin-10 (IL-10) strongly inhibits HSC activation in rat fibrotic liver. However, little is known about the effect of IL-10 on HSC autophagy. For investigation of the effect of IL-10 on starvation-induced autophagy in immortal rat hepatic stellate cells (HSC-T6) and the molecular mechanism, HSC-T6 cells were incubated with serum-free DMEM for different periods and treated with IL-10 at different concentrations. Transmission electron microscopy (TEM), analysis of autophagic flux and Western blotting (WB) assays were used to observe changes in autophagosome morphology and number and autophagy-related protein expression in HSC-T6 cells and to evaluate the regulatory effect of IL-10 on starvation-induced autophagy. Cryptotanshinone (CPT) and rapamycin (Rapa) were used to block activation of the signal transducer and activator of transcription 3 (STAT3) and mTOR signaling pathways, respectively. STAT3-mTOR-p70s6k signaling pathway proteins were analyzed by WB to assess the signaling pathway by which IL-10 regulates autophagy. WB showed an increased LC3II/I ratio, increased Beclin1 expression, and decreased p62 expression in HSC-T6 cells starved for 3 h (<i>p</i> < 0.05). IL-10 inhibited the increases in the LC3II/I ratio and Beclin1 expression and upregulated p62 expression (<i>p</i> < 0.05), and the optimal IL-10 concentration was 20 ng/mL. TEM and double-labeled immunofluorescence analysis showed that IL-10 inhibited autophagosome formation and autophagic flux, as indicated by the decreased numbers of double-membrane autophagosomes and yellow autophagic puncta. Further examination of signaling pathway molecules showed that phosphorylation of the mTOR, STAT3, and p70s6k proteins was significantly decreased during starvation-induced autophagy, but IL-10 could increase mTOR, STAT3, and p70s6k protein phosphorylation (<i>p</i> < 0.05). Blocking either the mTOR or STAT3 pathway reversed the inhibitory effect of IL-10 on starvation-induced autophagy in HSC-T6 cells (<i>p</i> < 0.05). IL-10 suppresses starvation-induced autophagosome formation through activation of the STAT3-mTOR-p70s6k axis in HSC-T6 cells.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"832-841"},"PeriodicalIF":3.2,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9160934/pdf/10.1177_15353702221080435.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39946561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Returning to basic principles to develop more effective treatments for central nervous system disorders.","authors":"Bruce E Wexler","doi":"10.1177/15353702221078291","DOIUrl":"https://doi.org/10.1177/15353702221078291","url":null,"abstract":"<p><p>Development of new treatments for diseases of the central nervous system (CNS) is stalled. Of candidate drugs developed through costly preclinical research, 93% fail clinical trials. Hoped-for improvements in diagnosis or treatment from decades of positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) imaging have yet to materialize. To understand what we are doing wrong, I begin with recognition that all aspects of life, including the brain and mind, are physical phenomena consistent with processes described by physicists. Two processes, emergence and entropy, are of particular relevance in complex arrangements of matter that constitute life in general and the brain in particular. The human brain functions through dynamically reconfiguring and hierarchically organized neural functional systems with emergent properties of cognition, emotion, and conscious experience. These systems are shaped and maintained by negentropic environmental input transformed by sensory receptors into neural signals that trigger epigenetic neuroplastic processes. CNS diseases produce clinical disorders by disrupting these systems. As researchers seek appropriate levels of system organization at which to characterize and treat illness, focus has been on medications that impact processes at lower levels or transcranial electric or magnetic stimulation that impact broad contiguous swaths of tissue. Neither align with the brain's neurosystem organization and therefore lack specificity necessary to be effective and to limit side effects. Digital neurotherapies (DNTs), in contrast, align with neurosystem organization and achieve the needed specificity using the same input pathways and neuroplastic processes that created the neural systems organization to repair it. The omission of DNTs from major systems-based initiatives represents powerful residua of dualist thinking. Interventions based on perceptual and cognitive processes are not thought of as being as physical as drugs or electric or magnetic stimulation through the skull. In fact, they are examples of the most basic processes that create and support life itself.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"856-867"},"PeriodicalIF":3.2,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/56/10.1177_15353702221078291.PMC9158240.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39929505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ISGylation is increased in the peripheral blood mononuclear cells derived from symptomatic COVID-19 patients.","authors":"Joshua Schwartzenburg,&nbsp;Ryan Reed,&nbsp;Hari Koul,&nbsp;Arnold H Zea,&nbsp;Judd Shellito,&nbsp;Lucio Miele,&nbsp;Judy S Crabtree,&nbsp;Shyamal Desai","doi":"10.1177/15353702221075606","DOIUrl":"https://doi.org/10.1177/15353702221075606","url":null,"abstract":"<p><p>Cytokine-driven hyper inflammation has been identified as a critical factor behind poor outcomes in patients severely infected with SARS-CoV-2 virus. Notably, protein ISGylation, a protein conjugated form of Type 1 IFN-inducible ubiquitin-like protein ISG15 (<b>I</b>nterferon-<b>S</b>timulated <b>G</b>ene <b>15</b>), induces cytokine storm (CS) and augments colonic inflammation in colitis-associated colon cancers in mouse models. However, whether ISGylation is increased and causally responsible for CS and hyper inflammation in symptomatic COVID-19 patients is unknown. Here, we measured ISGylation levels in peripheral blood mononuclear cells (PBMCs) from 10 symptomatic (SARS-CoV-2-positive with symptoms) and asymptomatic (SARS-CoV-2-positive with no symptoms) COVID-19 patients, and 4 uninfected individuals (SARS-CoV-2-negative), using Wes^Tm assay. Strikingly, we note significant increases in protein ISGylation and MX-1 (myxovirus-resistance protein-1) protein levels, both induced by type-I IFN, in symptomatic but not in asymptomatic patients and uninfected individuals. Knowing that ISGylation augments CS and intestinal inflammation in colon cancers, we propose that increased ISGylation may be an underlying cause of CS and inflammation in symptomatic patients.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"842-847"},"PeriodicalIF":3.2,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9160937/pdf/10.1177_15353702221075606.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39773527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testing lncRNAs signature as clinical stage-related prognostic markers in gastric cancer progression using TCGA database.","authors":"Narasimha M Beeraka,&nbsp;Hao Gu,&nbsp;Nannan Xue,&nbsp;Yang Liu,&nbsp;Huiming Yu,&nbsp;Junqi Liu,&nbsp;Kuo Chen,&nbsp;Vladimir N Nikolenko,&nbsp;Ruitai Fan","doi":"10.1177/15353702211067173","DOIUrl":"https://doi.org/10.1177/15353702211067173","url":null,"abstract":"LncRNA expression can be conducive to gastric cancer (GC) prognosis. The objective of this study is to ascertain five specific lncRNAs involved in tumor progression of GC and their role as prognostic markers to diagnose clinical stage-wise GC. High-throughput RNA sequencing data were obtained from The Cancer Genome Atlas (TCGA) database and performed genome-wide lncRNA expression analysis using edgeR package, Bioconductor.org, and R-statistical computing to analyze differentially expressed lncRNA analysis. Cutoff parameters were FDR < 0.05 and |Log2FC| > 2. Total 351 tumor samples with differentially expressed lncRNAs were divided into group-1 lncRNAs such as AC019117.2 and LINC00941, and group-2 lncRNAs such as LINC02410, AC012317.2, and AC141273.1 by 2:1. The Spearman correlation coefficients (p < 0.05) and correlation test function (cor.test ()) were performed for lncRNAs as per clinical stage. Cytoscape software was used to construct lncRNA–mRNA interaction networks. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway (p < 0.05) analysis were conducted using the clusterProfiler package. Kaplan–Meier survival analysis was performed to determine the overall survival of patients based on the expression of five lncRNAs in different clinical stages of GC. AC019117.2 and LINC00941 of group 1 inferred a positive correlation with clinical stages of stage I to stage IV, and their expressions were higher in tumor tissues than normal tissues. On the contrary, LINC02410, AC012317.2, and AC141273.1 of group 2 exhibited a negative correlation with clinical stage, and they exhibited more expression in normal tissues compared to tumor tissues. GO and KEGG pathway analysis reported that AC019117.2 may interact with LINC00941 via ITGA3 and trophoblast glycoprotein (TPBG) to foster tumor progression. Tumor-specific group-1 lncRNAs were conducive to the poor overall survival and exhibited a positive correlation with the clinical stages of stage I to stage IV in GC as per the lncRNA–mRNA networking analysis. These five lncRNAs could be considered as clinically useful lncRNA-based prognostic markers to predict clinical stage-wise GC progression.","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"658-671"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9039491/pdf/10.1177_15353702211067173.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39713013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Photoacoustic imaging systems based on clinical ultrasound platform.","authors":"Eun-Yeong Park,&nbsp;Haeni Lee,&nbsp;Seongyi Han,&nbsp;Chulhong Kim,&nbsp;Jeesu Kim","doi":"10.1177/15353702211073684","DOIUrl":"https://doi.org/10.1177/15353702211073684","url":null,"abstract":"<p><p>Photoacoustic imaging has drawn a significant amount of attention due to its unique capacity for functional, metabolic, and molecular imaging, which is achieved by the combination of optical excitation and acoustic detection. With both strengths of light and ultrasound, photoacoustic images can provide strong optical contrast at high ultrasound resolution in deep tissue. As photoacoustic imaging can be used to visualize complementary information to ultrasound imaging using the same data acquisition process, several studies have been conducted on combining photoacoustic imaging with existing clinical ultrasound systems. This review highlights our development of a photoacoustic/ultrasound dual-modal imaging system, various features and functionalities implemented for clinical translation, and preclinical/clinical studies performed by using the systems.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"551-560"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014524/pdf/10.1177_15353702211073684.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39962558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethical and regulatory oversight of clinical research: The role of the Institutional Review Board.","authors":"Lindsay McNair","doi":"10.1177/15353702221078216","DOIUrl":"https://doi.org/10.1177/15353702221078216","url":null,"abstract":"<p><p>The history of clinical research is, unfortunately, filled with examples of research studies that took advantage of and harmed research participants, to fulfill the research goals of scientists. Over time, we have created a system of ethical codes, principles, and regulations that are designed to prevent these abuses and to ensure that the rights and welfare of research participants are protected and honored. This review article will provide a brief history of clinical research ethics and ethical codes, outlining how those codes developed into the current regulatory requirements for the ethical oversight of clinical research. Understanding the current human subject protection systems will allow researchers to use best practices for planning and conducting rigorous, scientifically valid and ethical clinical studies. Understanding the history, principles, and foundations of the development of this system will equip researchers to understand what resources are available to them and how to make the best decisions when confronted with unique ethical situations in the conduct of their research.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"561-566"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014527/pdf/10.1177_15353702221078216.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39929507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>In vitro</i> contractile studies within isolated tissue baths: Translational research from Visible Heart^® Laboratories.","authors":"Weston J Upchurch,&nbsp;Paul A Iaizzo","doi":"10.1177/15353702211070535","DOIUrl":"https://doi.org/10.1177/15353702211070535","url":null,"abstract":"<p><p>The isolated tissue bath research methodology was first developed in 1904. Since then, it has been recognized as an important tool in pharmacology and physiology research, including investigations into neuromuscular disorders. The tissue bath is still used routinely as the instrument for performing the \"gold standard\" test for clinical diagnosis of malignant hyperthermia susceptibility - the caffeine-halothane contracture test. Our research group has utilized this tool for several decades for a range of research studies, and we are currently one of four North American diagnostic centers for determining susceptibility for malignant hyperthermia. This review provides a brief summary of some of the historical uses of the tissue bath. Important experimental considerations for the operation of the tissue bath are further described. Finally, we discuss the different studies our group has performed using isolated tissue baths to highlight the broad potential applications.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"584-597"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014520/pdf/10.1177_15353702211070535.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39727712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}