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Gene Therapy Leaves a Vicious Cycle
Reena Goswami1, Gayatri Subramanian2, Liliya Silayeva1, Isabelle Newkirk1, Deborah Doctor1, Karan Chawla2, Saurabh Chattopadhyay2, Dhyan Chandra3, Nageswararao Chilukuri1 and Venkaiah Betapudi1,4* 1Neuroscience Branch, Research Division, United States Army Medical Research Institute of Chemical Defense, Aberdeen, MD, United States 2Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, United States 3Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States 4Department of Physiology and Biophysics, Case Western Reserve University, Clev...
Source: Frontiers in Oncology - April 23, 2019 Category: Cancer & Oncology Source Type: research

Pro ‐inflammatory M1 Macrophage enhances metastatic potential of ovarian cancer cells through NF‐κB activation
This article is protected by copyright. All rights reserved
Source: Molecular Carcinogenesis - October 12, 2017 Category: Molecular Biology Authors: Untack Cho, Boyun Kim, Soochi Kim, Youngjin Han, Yong Sang Song Tags: RESEARCH ARTICLE Source Type: research

Silencing of tumor necrosis factor receptor-1 in human lung microvascular endothelial cells using particle platforms for siRNA delivery.
Abstract Acute lung injury (ALI) and its most severe manifestation, acute respiratory distress syndrome (ARDS), is a clinical syndrome defined by acute hypoxemic respiratory failure and bilateral pulmonary infiltrates consistent with edema. In-hospital mortality is 38.5% for ALI, and 41.1% for ARDS. Activation of alveolar macrophages in the donor lung causes the release of pro-inflammatory chemokines and cytokines, such as TNF-α. To determine the relevance of TNF-α in disrupting bronchial endothelial cell function, we stimulated human THP-1 macrophages with lipopolysaccharide (LPS) and used the cytokine-suppleme...
Source: Current Drug Targets - July 22, 2015 Category: Drugs & Pharmacology Authors: Bai L, Andersson HA, McConnell K, Chan D, Hernandez M, Gonzalez J, Liu X, La Francesca S, Sakamoto J, Serda RE Tags: Curr Drug Targets Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice
Publication date: Available online 24 June 2015 Source:Brain, Behavior, and Immunity Author(s): Norimitsu Morioka , Fang Fang Zhang , Yoki Nakamura , Tomoya Kitamura , Kazue Hisaoka-Nakashima , Yoshihiro Nakata Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3days ...
Source: Brain, Behavior, and Immunity - July 3, 2015 Category: Neurology Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice.
Abstract Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3 days after partial sciatic nerve ligation (PSNL), but a persistent downregulation of astrocytic Cx43 in ipsilateral lumbar spinal dorsal horn was not observed until 7 days post-PSNL, suggesting that ...
Source: Brain, Behavior, and Immunity - June 23, 2015 Category: Neurology Authors: Morioka N, Zhang FF, Nakamura Y, Kitamura T, Hisaoka-Nakashima K, Nakata Y Tags: Brain Behav Immun Source Type: research

TNF-{alpha} antagonism ameliorates myocardial ischemia-reperfusion injury in mice by upregulating adiponectin
This study was conducted to investigate whether TNF-α is responsible for the decrease of APN, and whether antagonizing TNF-α affects MI/R injury by increasing APN. Male adult wild-type (WT), APN knockout (APN KO) mice, and those with cardiac knockdowns of APN receptors via siRNA injection were subjected to 30 min of MI followed by reperfusion. The TNF-α antagonist etanercept or globular domain of APN (gAD) was injected 10 min before reperfusion. Etanercept ameliorated MI/R injury in WT mice as evidenced by improved cardiac function, and reduced infarct size and cardiomyocyte apoptosis. APN concentrations ...
Source: AJP: Heart and Circulatory Physiology - June 15, 2015 Category: Cardiology Authors: Gao, C., Liu, Y., Yu, Q., Yang, Q., Li, B., Sun, L., Yan, W., Cai, X., Gao, E., Xiong, L., Wang, H., Tao, L. Tags: INTEGRATIVE CARDIOVASCULAR PHYSIOLOGY AND PATHOPHYSIOLOGY Source Type: research

TNF-alpha antagonism ameliorates myocardial ischemia/reperfusion injury in mice by upregulating adiponectin.
CONCLUSION: TNF-α is responsible for the decrease in APN during MI/R. The cardioprotective effects of TNF-α neutralization are partially due to the upregulation of APN. The results provide more insight into the TNF-α-mediated signaling effects during MI/R, and support the need for clinical trials in order to validate the efficacy of acute TNF-α antagonism in the treatment of MI/R injury. PMID: 25888509 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Heart and Circulatory Physiology - April 17, 2015 Category: Physiology Authors: Gao C, Liu Y, Yu Q, Yang Q, Li B, Sun L, Yan W, Cai X, Gao E, Xiong L, Wang H, Tao L Tags: Am J Physiol Heart Circ Physiol Source Type: research

TNF-α inhibitor protects against myocardial ischemia/reperfusion injury via Notch1 mediated suppression of oxidative/nitrative stress.
This study aims to determine the involvement of TNF-a inhibitor with Notch1 in MI/R and delineate the related mechanism. Notch1 specific small interfering RNA (siRNA, 20μg) or Jagged1 (a Notch ligand, 12μg) was delivered through intramyocardial injection. 48h after injection, mice received 30min of myocardial ischemia followed by 3h (for cell apoptosis and oxidative/nitrative stress) and 24h (for infarct size and cardiac function) of reperfusion. 10min before reperfusion, mice randomly received intraperitoneal injection of vehicle, Etanercept, diphenyleneiodonium, 1400W or EUK134. Finally, downregulation of Notch1 signif...
Source: Free Radical Biology and Medicine - February 10, 2015 Category: Biology Authors: Pei H, Song X, Peng C, Tan Y, Li Y, Li X, Ma S, Wang Q, Huang R, Yang D, Li, Gao E, Yang Y Tags: Free Radic Biol Med Source Type: research