742 results match your criteria: "Xi'an Jiaotong University School of Medicine.[Affiliation]"

BCL6 attenuates renal inflammation via negative regulation of NLRP3 transcription.

Cell Death Dis

October 2017

Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

Renal inflammation contributes to the pathogeneses of hypertension. This study was designed to determine whether B-cell lymphoma 6 (BCL6) attenuates renal NLRP3 inflammasome activation and inflammation and its underlying mechanism. Male spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were used in the present study.

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NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension.

Cell Death Dis

October 2017

Department of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.

Inflammation is involved in pathogenesis of hypertension. NLRP3 inflammasome activation is a powerful mediator of inflammatory response via caspase-1 activation. The present study was designed to determine the roles and mechanisms of NLRP3 inflammasome in phenotypic modulation and proliferation of vascular smooth muscle cells (VSMCs) in hypertension.

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There have been no reports describing the effects of cancer cell-derived extracellular vesicles (EVs) on three-dimensional organoids. In this study, we delineated the proneoplastic effects of esophageal adenocarcinoma (EAC)-derived EVs on gastric organoids (gastroids) and elucidated molecular mechanisms underlying these effects. EVs were identified using PKH-67 staining.

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Suppression of Sirt1 sensitizes lung cancer cells to WEE1 inhibitor MK-1775-induced DNA damage and apoptosis.

Oncogene

December 2017

Engineering Research Center of Molecular and Neuro Imaging, Ministry of Education, School of Life Science and Technology, Xidian University, Xi'an, China.

Lung cancer treatment remains a challenge for clinical practice and new therapeutic approaches are urgently needed. Loss of functional WEE1 kinase causes DNA replication stress, DNA damage and unscheduled mitotic entry due to elevated CDK activity. The selective WEE1 inhibitor MK-1775 synergize with DNA-damaging agent to inhibit cancer cell growth.

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Evidence indicates that after brain injury, neurogenesis is enhanced in regions such as hippocampus, striatum, and cortex. To study the role of hypoxia-inducible factor-1 (HIF‑1α) and Wnt signaling in cerebral ischemia/hypoxia-induced proliferation of neural stem cells (NSCs), we investigated the proliferation of NSCs, expression of HIF‑1α, and activation of Wnt signaling under conditions of pathologic hypoxia in vitro. NSCs were isolated from 30-day-old Sprague-Dawley rats and subjected to 0.

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Background: A wide range of pesticides is applied for crop protection in vegetable cultivation in China. Regulation of pesticide maximum residue limits (MRLs) in vegetables is established but not fully enforced. And pesticide residues in vegetables were not well monitored.

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microRNA-33a (miR-33a) belongs to the miR-33 family that is implicated in the progression of various types of cancers. Aberrant expression of miR-33a has been detected in several human cancers, and has been shown to regulate the migration and invasion as well as proliferation and apoptosis of tumor cells. However, the clinical significance and precise mechanisms underlying the dysfunction of miR-33a in glioma have not been well investigated in previous studies.

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Fibrous sheath interacting protein 1 (FSIP1), a spermatogenesis-related testicular antigen, is expressed in abundance in breast cancers, particularly in those overexpressing human epidermal growth factor receptor 2 (HER2); however, little is known about its role in regulating the growth and metastasis of breast cancer cells. We and others have shown previously that FSIP1 expression in breast cancer correlates positively with HER2-positivity, recurrence, and metastases and negatively with survival. Here, using coimmunoprecipitation and microscale thermophoresis, we find that FSIP1 binds to the intracellular domain of HER2 directly.

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The orexin system is involved in arginine vasopressin (AVP) regulation, and its overactivation has been implicated in hypertension. However, its role in salt-sensitive hypertension (SSHTN) is unknown. Here, we tested the hypothesis that hyperactivity of the orexin system in the paraventricular nucleus (PVN) contributes to SSHTN via enhancing AVP signaling.

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Background: Our previous studies demonstrated that the class IA PI3K/p110β is critical in castration-resistant progression of prostate cancer (CRPC) and that targeting prostate cancer with nanomicelle-loaded p110β-specific inhibitor TGX221 blocked xenograft tumor growth in nude mice, confirming the feasibility of p110β-targeted therapy for CRPCs. To improve TGX221's aqueous solubility, in this study, we characterized four recently synthesized TGX221 analogs.

Methods: TGX221 analog efficacy were examined in multiple prostate cancer cell lines with the SRB cell growth assay, Western blot assay for AKT phosphorylation and cell cycle protein levels.

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Resveratrol (RSV) has been shown to have a renoprotective effect against diabetic nephropathy, but the underlying mechanisms of this have not been fully elucidated. The aim of the current study was to explore the mechanisms responsible for the therapeutic effects of RSV in rat mesangial cells and in a rat model of diabetic nephropathy. The viability of CRL-2573 rat mesangial cells and their expression levels of p38, phosphorylated (p)-p38, transforming growth factor beta 1 (TGF-β1) and fibronectin were assessed in response to treatment with high glucose, with or without RSV.

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Sirtuin 1 (Sirt1) is a longevity gene that has protective effects in cardiovascular diseases (CVDs). The endothelin type A (ET) receptor is involved in pathogenesis of CVDs. The extracellular signal related kinases 1 and 2 (ERK1/2) signaling pathway is involved in regulation of the ET receptor induced by some CVD risk factors in vascular smooth muscle cells (VSMCs).

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Increased Hepatic Expression of Endothelial Lipase Inhibits Cholesterol Diet-Induced Hypercholesterolemia and Atherosclerosis in Transgenic Rabbits.

Arterioscler Thromb Vasc Biol

July 2017

From the Department of Molecular Pathology, Faculty of Medicine, Graduate Faculty of Interdisciplinary Research, Graduate School, University of Yamanashi, Japan (C.W., M.N., B.N., H.Y., Y.C., J.F.); Department of Pathology, Xi'an Medical University, China (B.N., J.F.); Animal Research Laboratory, Bioscience Education-Research Support Center, Akita University, Japan (K.N.); Analytical Research Center for Experimental Sciences, Saga University, Japan (S.K., F.M.); Research Institute of Atherosclerotic Disease and Laboratory Animal Center, Xi'an Jiaotong University School of Medicine, China (E.L.); and Center for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor (J.Z., Y.E.C.).

Objective: Endothelial lipase (EL) is a key determinant in plasma high-density lipoprotein-cholesterol. However, functional roles of EL on the development of atherosclerosis have not been clarified. We investigated whether hepatic expression of EL affects plasma lipoprotein metabolism and cholesterol diet-induced atherosclerosis.

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Melanocortin neurons: Multiple routes to regulation of metabolism.

Biochim Biophys Acta Mol Basis Dis

October 2017

Department of Intensive Care Unit, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, Heilongjiang 150081, China; Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai 200433, China; Division of Hypothalamic Research, the University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390, USA. Electronic address:

The burden of disability, premature death, escalating health care costs and lost economic productivity due to obesity and its associated complications including hypertension, stroke, cardiovascular disease and type 2 diabetes is staggering [1,2]. A better understanding of metabolic homeostatic pathways will provide us with insights into the biological mechanisms of obesity and how to fundamentally address this epidemic [3-6]. In mammals, energy balance is maintained via a homeostatic system involving both peripheral and central melanocortin systems; changes in body weight reflect an unbalance of the energetic state [7-9].

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The aim of this study was to profile somatic mutation spectrum in gallbladder cancers (GBCs), and determine the role of MAP kinase pathway in GBC by a series of in vitro and in vivo studies. We performed targeted massively parallel sequencing of DNA isolated from GBCs and matched blood from 14 GBC patients to search for mutations in 504 genes commonly altered in human cancers. We identified recurrent mutations enriched in several major signaling pathways including MAP kinase, Wnt/β-catenin and NF-κB pathways.

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Background: Improving islet graft revascularization has become a crucial task for prolonging islet graft survival. Endothelial cells (ECs) are the basis of new microvessels in an isolated islet, and EC coating has been demonstrated to improve the vascularization and survival of an islet. However, the traditional method of EC coating of islets has low efficiency in vitro.

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Salusin-β contributes to oxidative stress and inflammation in diabetic cardiomyopathy.

Cell Death Dis

March 2017

Department of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.

Salusin-β accelerates inflammatory responses in vascular endothelial cells, and increases oxidative stress in vascular smooth muscle cells. Plasma salusin-β levels were increased in diabetic patients. This study was designed to determine whether salusin-β is involved in the pathogenesis of diabetic cardiomyopathy (DCM), and whether knockdown of salusin-β attenuates cardiac inflammation and oxidative stress in rats with DCM.

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Autophagy is activated during nutritionally depleted or hypoxic conditions to facilitate cell survival. Because growth plate is an avascular and hypoxic tissue, autophagy may have a crucial role during chondrogenesis; however, the functional role and underlying mechanism of autophagy in regulation of growth plate remains elusive. In this study, we generated Atg7 (Atg7cKO) mice to explore the role of autophagy during endochondral ossification.

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Purpose: Antithyroid drug (ATD)-induced agranulocytosis is a rare but life-threatening adverse drug reaction that occurs in patients during the treatment of Graves' disease. We aimed to comprehensively examine data for patients with this rare complication and to improve the clinical safety of ATDs.

Methods: We retrospectively reviewed the medical records of 64 hospitalized patients diagnosed with ATD-induced agranulocytosis between 2000 and 2015.

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Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.

Sci Rep

February 2017

Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

Salusin-β is a bioactive peptide involved in vascular smooth muscle cell proliferation, vascular fibrosis and hypertension. The present study was designed to determine the effects of silencing salusin-β on hypertension and cardiovascular remodeling in spontaneously hypertensive rats (SHR). Thirteen-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were subjected to intravenous injection of PBS, adenoviral vectors encoding salusin-β shRNA (Ad-Sal-shRNA) or a scramble shRNA.

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Clinical outcomes of patients with and without diabetes mellitus after hepatectomy: A systematic review and meta-analysis.

PLoS One

August 2017

Shaanxi Center for Regenerative Medicine and Surgical Engineering, Institute of Advanced Surgical Technology and Engineering, Department of Hepatobiliary Surgery, First Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi Province, China.

Background: Clinical data regarding the influence of diabetes mellitus (DM) on the outcomes of patients undergoing hepatectomy are conflicting. To determine the impact of DM on the clinical outcomes of patients undergoing hepatectomy, we systematically reviewed published studies and carried out a meta-analysis.

Methods: A systematic literature search of Pubmed, Sciencedirect, Web of Science, and Chinese Biomedical Database was conducted from their inception through February 2, 2016.

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Curcumin is a biologically active ingredient abundantly present in the ground rhizomes of Curcuma longa with a wide range of bioactive properties, including antitumor effects. Hypoxia is a common characteristic of solid tumors, including osteosarcoma. However, whether curcumin has antitumor effects on osteosarcoma under hypoxic conditions, and its underlying molecular mechanisms, remain unclear.

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Inhibition of Drp1 attenuates mitochondrial damage and myocardial injury in Coxsackievirus B3 induced myocarditis.

Biochem Biophys Res Commun

March 2017

Department of Cardiology, The Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710004, China. Electronic address:

Viral myocarditis (VMC) is closely related to apoptosis, oxidative stress, innate immunity, and energy metabolism, which are all linked to mitochondrial dysfunction. A close nexus between mitochondrial dynamics and cardiovascular disease with mitochondrial dysfunction has been deeply researched, but there is still no relevant report in viral myocarditis. In this study, we aimed to explore the role of Dynamin-related protein 1 (Drp1)-linked mitochondrial fission in VMC.

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Objectives: We sought to study whether the level of completeness of revascularization as measured by the SYNTAX revascularization index (SRI) independently predicts adverse ischemic events after percutaneous coronary intervention (PCI) with second-generation drug-eluting stents (DES).

Background: The SRI quantifies the proportion of revascularized myocardium. It has been shown to independently predict adverse ischemic events after PCI with first-generation DES.

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Neuroglobin (Ngb) has been reported to be upregulated by hypoxia and plays an anti-apoptotic function. Previous studies have reported that Ngb is expressed in human glioblastoma cells and up-regulated in hypoxic microregions of glioblastoma tumor xenografts. While, the clinical significance of Ngb and its function in human glioma keep unknown.

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