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Search Results for all work with filters:

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Work 1-10 of 514

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Article

Enteric Nervous System in the Small Intestine: Pathophysiology and Clinical Implications

by Behtash Ghazi Nezami; Shanthi Srinivasan

2010

Subjects
  • Health Sciences, General
  • Biology, General
  • Biology, Physiology
  • File Download
  • View on PubMed Central
  • View Abstract

Abstract:Close

The digestive system is endowed with its own, local nervous system, referred to as the enteric nervous system (ENS). Given the varied functions of small intestine, its ENS has developed individualized characteristics relating to motility, secretion, digestion, and inflammation. The ENS regulates the major enteric processes such as immune response, detecting nutrients, motility, microvascular circulation, intestinal barrier function, and epithelial secretion of fluids, ions, and bioactive peptides. Remarkable progress has been made in understanding the signaling pathways in this complex system and how they work. In this article, we focus on recent advances that have led to new insights into small intestinal ENS function and the development of new therapies.

Article

Exosomes derived from endometriotic stromal cells have enhanced angiogenic effects in vitro

by Djana Harp; Adel Driss; Sharifeh Mehrabi; Indrajit Chowdhury; Wei Xu; Dong Liu; Minerva Garcia-Barrio; Robert N. Taylor; Bert Gold; Samantha Jefferson; Neil Sidell; Winston Thompson

2016

Subjects
  • Biology, Cell
  • Biology, Physiology
  • Health Sciences, Obstetrics and Gynecology
  • File Download
  • View Abstract

Abstract:Close

Our objective has been to establish a pro-angiogenic role for exosomes in endometriosis and to determine whether a differential expression profile of cellular and exosomal microRNAs (miRNAs) exists in endometriosis. We performed an in vitro study of human primary endometrial stromal cells (ESCs) and human umbilical vein endothelial cells (HUVECs). We isolated and characterized exosomes from ESCs from five endometriosis patients and five phase-matched controls. Exosomes were characterized by transmission electron microscopy and NanoSight technology. MiRNA was assessed by deep sequencing and reverse transcription with quantitative polymerase chain reaction. Exosome uptake studies were achieved by means of confocal microscopy. The pro-angiogenic experiments were executed by treating HUVECs with ESC-derived exosomes. We observed differential profiles of exosomal miRNA expression between exosomes derived from endometriosis lesion cells and diseased eutopic stromal cells compared with exosomes derived from control ESCs. We also demonstrated autocrine cellular uptake of exosomes and paracrine functional angiogenic effects of exosomes on HUVECs. The results of this study support the hypothesis that exosomes derived from ESCs play autocrine/paracrine roles in the development of endometriosis, potentially modulating angiogenesis. The broader clinical implications are that Sampson’s theory of retrograde menstruation possibly encompasses the finding that exosomes work as intercellular communication modulators in endometriosis.

Article

Bioelectrical understanding and engineering of cell biology

by Zoe Schofield; Gabriel N. Meloni; Peter Tran; Christian Zerfass; Giovanni Sena; Yoshikatsu Hayashi; Murray Grant; Sonia A. Contera; Shelley D. Minteer; Minsu Kim; Arthur Prindle; Paulo Rocha; Mustafa B. A. Djamgoz; Teuta Pilizota; Patrick R. Unwin; Munehiro Asally; Orkun S. Soyer

2020

Subjects
  • Biology, Cell
  • Biology, Physiology
  • Biophysics, Medical
  • Physics, Electricity and Magnetism
  • File Download
  • View Abstract

Abstract:Close

The last five decades of molecular and systems biology research have provided unprecedented insights into the molecular and genetic basis of many cellular processes. Despite these insights, however, it is arguable that there is still only limited predictive understanding of cell behaviours. In particular, the basis of heterogeneity in single-cell behaviour and the initiation of many different metabolic, transcriptional or mechanical responses to environmental stimuli remain largely unexplained. To go beyond the status quo, the understanding of cell behaviours emerging from molecular genetics must be complemented with physical and physiological ones, focusing on the intracellular and extracellular conditions within and around cells. Here, we argue that such a combination of genetics, physics and physiology can be grounded on a bioelectrical conceptualization of cells. We motivate the reasoning behind such a proposal and describe examples where a bioelectrical view has been shown to, or can, provide predictive biological understanding. In addition, we discuss how this view opens up novel ways to control cell behaviours by electrical and electrochemical means, setting the stage for the emergence of bioelectrical engineering.

Article

ARF-Like (ARL) Proteins

by Richard Kahn; Michael P. East; Joshua W. Francis

2014

Subjects
  • Physics, Molecular
  • Biology, Physiology
  • Biology, Molecular
  • File Download
  • View Abstract

Abstract:Close

The ARF-like (ARL) proteins, within the ARF family, are a collection of functionally diverse GTPases that share extensive (>40 %) identity with the ARFs and each other and are assumed to share basic mechanisms of regulation and a very incompletely documented degree of overlapping regulators. At least four ARLs were already present in the last eukaryotic common ancestor, along with one ARF, and these have been expanded to >20 members in mammals. We know little about the majority of these proteins so our review will focus on those about which the most is known, including ARL1, ARL2, ARL3, ARL4s, ARL6, ARL13s, and ARFRP1. From this fragmentary information we extract some generalizations and conclusions regarding the sources and extent of specificity and functions of the ARLs.

Article

Preconditioning of bone marrow mesenchymal stem cells by prolyl hydroxylase inhibition enhances cell survival and angiogenesis in vitro and after transplantation into the ischemic heart of rats

by Xian-Bao Liu; Jian-An Wang; Xiao-Ya Ji; Shan Yu; Ling Wei

2014

Subjects
  • Biology, Physiology
  • Biology, Cell
  • Health Sciences, Medicine and Surgery
  • File Download
  • View Abstract

Abstract:Close

Introduction: Poor cell survival and limited functional benefits have restricted the efficacy of bone marrow mesenchymal stem cells (BMSCs) in the treatment of myocardial infarction. We showed recently that hypoxia preconditioning of BMSCs and neural progenitor cells before transplantation can enhance the survival and therapeutic properties of these cells in the ischemic brain and heart. The present investigation explores a novel strategy of preconditioning BMSCs using the Hypoxia-inducible factor 1α (HIF-α) prolyl hydroxylase inhibitor dimethyloxalylglycine (DMOG) to enhance their survival and therapeutic efficacy after transplantation into infarcted myocardium. Methods: BMSCs from green fluorescent protein transgenic rats were cultured with or without 1 mM DMOG for 24 hours in complete culture medium before transplantation. Survival and angiogenic factors were evaluated in vitro by trypan blue staining, Western blotting, and tube formation test. In an ischemic heart model of rats, BMSCs with and without DMOG preconditioning were intramyocardially transplanted into the peri-infarct region 30 minutes after permanent myocardial ischemia. Cell death was measured 24 hours after engraftment. Heart function, angiogenesis and infarct size were measured 4 weeks later. Results: In DMOG preconditioned BMSCs (DMOG-BMSCs), the expression of survival and angiogenic factors including HIF-1α, vascular endothelial growth factor, glucose transporter 1 and phospho-Akt were significantly increased. In comparison with control cells, DMOG-BMSCs showed higher viability and enhanced angiogenesis in both in vitro and in vivo assays. Transplantation of DMOG-BMSCs reduced heart infarct size and promoted functional benefits of the cell therapy. Conclusions: We suggest that DMOG preconditioning enhances the survival capability of BMSCs and paracrine effects with increased differentiation potential. Prolyl hydroxylase inhibition is an effective and feasible strategy to enhance therapeutic efficacy and efficiency of BMSC transplantation therapy after heart ischemia.

Article

Osteopontin and Disease Activity in Patients with Recent-onset Systemic Lupus Erythematosus: Results from the SLICC Inception Cohort

by Lina Wirestam; Helena Enocsson; Thomas Skogh; Leonid Padyukov; Andreas Jonsen; Murray B. Urowitz; Dafna Gladman; Juanita Romero-Diaz; Sang-Cheol Bae; Paul R. Fortin; Jorge Sanchez-Guerrero; Ann Clarke; Sasha Bernatsky; Caroline Gordon; John G. Hanly; Daniel Wallace; David Isenberg; Anisur Rahman; Joan Merrill; Ellen Ginzler; Graciela S. Alarcon; W. Winn Chatham; Michelle Petri; Munther Khamashta; Cynthia Aranow; Meggan Mackay; Mary Anne Dooley; Susan Manzi; Rosalind Ramsey-Goldman; Ola Nived; Kristjan Steinsson; Asad Zoma; Guillermo Ruiz-Irastorza; Sung Lim; Ken Kalunian; Murat Inanc; Ronald van Vollenhoven; Manuel Ramos-Casals; Diane L. Kamen; Soren Jacobsen; Christine Peschken; Anca Askanase; Thomas Stoll; Ian N. Bruce; Jonas Wettero; Christopher Sjowall

2019

Subjects
  • Biology, Neuroscience
  • Health Sciences, Immunology
  • Biology, Physiology
  • Health Sciences, Rehabilitation and Therapy
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Objective In cross-sectional studies, elevated osteopontin (OPN) has been proposed to reflect, and/or precede, progressive organ damage and severity in systemic lupus erythematosus (SLE). We aimed, in a prospective cohort of recent-onset SLE to determine whether raised serum OPN associates with disease activity and/or precedes organ damage. Methods We included 345 patients from the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort who had 5-years of follow-up data available. All patients fulfilled the 1982 American College of Rheumatology (ACR) criteria. Baseline sera from patients and from age- and sex-matched controls were analyzed for OPN using ELISA. Disease activity and damage were assessed at each annual follow-up visit using the SLE Disease Activity Index 2000 (SLEDAI-2K) and the SLICC/ACR damage index (SDI), respectively. Results Compared to controls, baseline OPN was raised fourfold in SLE cases (p<0.0001). A weak correlation was found between baseline OPN and accrual of global damage (r=0.16, p=0.004) at 5 years. OPN levels predicted damage when defined as SDI≥1 (p=0.024), but the damage-predictive value was lost when adjusting damage cut-off to SDI≥2. Baseline OPN correlated with disease activity at inclusion (r=0.27, p<0.0001). Patients with high disease activity (SLEDAI-2K≥5) had raised serum OPN (p<0.0001). Higher OPN levels were also found in patients with persistently raised disease activity (p=0.0005). Conclusions Raised OPN at SLE onset was associated with higher disease activity and more severe disease and may as a biomarker help to guide more targeted attempts to control disease activity over time.

Article

Notch3 Modulates Cardiac Fibroblast Proliferation, Apoptosis, and Fibroblast to Myofibroblast Transition via Negative Regulation of the RhoA/ROCK/Hif1α Axis

by Jianli Shi; Peilin Xiao; Xiaoli Liu; Yunlin Chen; Yanping Xu; Jinqi Fan; Yuehui Yin

2020

Subjects
  • Engineering, Biomedical
  • Chemistry, Biochemistry
  • Biology, Physiology
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Cardiac fibrosis is a common pathological process in multiple cardiovascular diseases, including myocardial infarction (MI). Abnormal cardiac fibroblast (CF) activity is a key event in cardiac fibrosis. Although the Notch signaling pathway has been reported to play a vital role in protection from cardiac fibrosis, the exact mechanisms underlying cardiac fibrosis and protection from it have not yet been elucidated. Similarly, Hif1α and the RhoA/ROCK signaling pathway have been shown to participate in cardiac fibrosis. The RhoA/ROCK signaling pathway has been reported to be an upstream pathway of Hif1α in several pathophysiological processes. In the present study, we aimed to determine the effects of notch3 on CF activity and its relationship with the RhoA/ROCK/Hif1α signaling pathway. Using in vitro experiments, we demonstrated that notch3 inhibited CF proliferation and fibroblast to myofibroblast transition (FMT) and promoted CF apoptosis. A knockdown of notch3 using siRNAs had the exact opposite effect. Next, we found that notch3 regulated CF activity by negative regulation of the RhoA/ROCK/Hif1α signaling pathway. Extending CF-based studies to an in vivo rat MI model, we showed that overexpression of notch3 by the Ad-N3ICD injection attenuated the increase of RhoA, ROCK1, ROCK2, and Hif1α levels following MI and further prevented MI-induced cardiac fibrosis. On the basis of these results, we conclude that notch3 is involved in the regulation of several aspects of CF activity, including proliferation, FMT, and apoptosis, by inhibiting the RhoA/ROCK/Hif1α signaling pathway. These findings are significant to further our understanding of the pathogenesis of cardiac fibrosis and to ultimately identify new therapeutic targets for cardiac fibrosis, potentially based on the RhoA/ROCK/Hif1α signaling pathway.

Article

Gut-seeded alpha-synuclein fibrils promote gut dysfunction and brain pathology specifically in aged mice

by Collin Challis; Acacia Hori; Timothy Sampson; Bryan B. Yoo; Rosemary C. Challis; Adam M. Hamilton; Sarkis M. Mazmanian; Laura A. Volpicelli-Daley; Viviana Gradinaru

2020

Subjects
  • Biology, Genetics
  • Biology, Neuroscience
  • Biology, Physiology
  • Health Sciences, Rehabilitation and Therapy
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Parkinson’s disease is a synucleinopathy that is characterized by motor dysfunction, death of midbrain dopaminergic neurons and accumulation of α-synuclein (α-Syn) aggregates. Evidence suggests that α-Syn aggregation can originate in peripheral tissues and progress to the brain via autonomic fibers. We tested this by inoculating the duodenal wall of mice with α-Syn preformed fibrils. Following inoculation, we observed gastrointestinal deficits and physiological changes to the enteric nervous system. Using the AAV-PHP.S capsid to target the lysosomal enzyme glucocerebrosidase for peripheral gene transfer, we found that α-Syn pathology is reduced due to the increased expression of this protein. Lastly, inoculation of α-Syn fibrils in aged mice, but not younger mice, resulted in progression of α-Syn histopathology to the midbrain and subsequent motor defects. Our results characterize peripheral synucleinopathy in prodromal Parkinson’s disease and explore cellular mechanisms for the gut-to-brain progression of α-Syn pathology.

Article

Heart rate variability and heart rate recovery in lung cancer survivors eligible for long-term cure

by Duc Ha; Atul Malhotra; Andrew L. Ries; Wesley T. O'Neal; Mark M. Fuster

2019

Subjects
  • Biology, Physiology
  • Health Sciences, Public Health
  • Health Sciences, Oncology
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Lung cancer survivors are at risk for physical fitness and autonomic function impairments. In a cross-sectional study of consecutive lung cancer survivors post-curative intent therapy, we assessed and identified predictors of resting heart rate variability (HRV) and heart rate recovery (HRR), defined as standard deviation of normal-to-normal-R-to-R intervals (SDNN) and root-mean-square-of-successive-differences (rMSSD) from routine outpatient single 10-s electrocardiographs (ECGs) and difference in heart rate (HR) at 1-minute following and the end of the six-minute-walk-test (6MWT), respectively. In 69 participants, the mean (SD) HRR was -10.6 (6.7) beats. Significant independent predictors of HRR were age and HR change associated with the 6MWT. In a subset of 41 participants with available ECGs, the mean (SD) SDNN and rMSSD were 19.1 (15.6) and rMSSD 18.2 (14.6) ms, respectively. Significant independent predictors of HRV were supine HR, HRR, and total lung capacity. HRV/HRR may be useful physiological measures in studies aimed at improving physical fitness and/or autonomic function in lung cancer survivors.

Article

Reduction of neuromuscular redundancy for postural force generation using an intrinsic stability criterion

by Nathan E. Bunderson; Thomas J. Burkholder; Lena Ting

2008

Subjects
  • Engineering, Biomedical
  • Biology, Physiology
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Postural control requires the coordination of multiple muscles to achieve both endpoint force production and postural stability. Multiple muscle activation patterns can produce the required force for standing, but the mechanical stability associated with any given pattern may vary, and has implications for the degree of delayed neural feedback necessary for postural stability. We hypothesized that muscular redundancy is reduced when muscle activation patterns are chosen with respect to intrinsic musculoskeletal stability as well as endpoint force production. We used a three-dimensional musculoskeletal model of the cat hindlimb with 31 muscles to determine the possible contributions of intrinsic muscle properties to limb stability during isometric force generation. Using dynamic stability analysis we demonstrate that within the large set of activation patterns that satisfy the force requirement for posture, only a reduced subset produce a mechanically stable limb configuration. Greater stability in the frontal-plane suggests that neural control mechanisms are more highly active for sagittal-plane and for ankle joint control. Even when the limb was unstable, the time-constants of instability were sufficiently great to allow long-latency neural feedback mechanisms to intervene, which may be preferential for movements requiring maneuverability versus stability. Local joint stiffness of muscles was determined by the stabilizing or destabilizing effects of moment-arm versus joint angle relationships. By preferentially activating muscles with high local stiffness, muscle activation patterns with feedforward stabilizing properties could be selected. Such a strategy may increase intrinsic postural stability without co-contraction, and may be useful criteria in the force-sharing problem.
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