K Channel Blocker Glibenclamide Prevents Radiation-Induced Lung Injury and Inhibits Radiation-Induced Apoptosis of Vascular Endothelial Cells by Increased Ca Influx and Subsequent PKC Activation.

Radiation-induced lung injury (RILI) is a common and severe side effect of thoracic radiotherapy, which compromises patients' quality of life. Recent studies revealed that early vascular injury, especially microvascular damage, played a central role in the development of RILI. For this reason, early vascular protection is essential for RILI therapy.

Omega-6 fatty acids down-regulate matrix metalloproteinase expression in a coronary heart disease-induced rat model.

The present study investigated the therapeutic potential of omega-6 fatty acids, according to their effects on antioxidant markers and matrix metalloproteinases (MMPs), in coronary heart disease-induced rats. Rats were grouped into group I (sham control), group II (control), group III (0.5 g/kg bwt of omega-6 fatty acids) and group IV (1 g/kg bwt of omega-6 fatty acids).

TRIF Regulates BIC/miR-155 via the ERK Signaling Pathway to Control the ox-LDL-Induced Macrophage Inflammatory Response.

Toll/IL-1R-domain-containing adaptor-inducing IFN- (TRIF) is an important adaptor for TLR3- and TLR4-mediated inflammatory signaling pathways. Recent studies have shown that TRIF plays a key role in vessel inflammation and atherosclerosis; however, the precise mechanisms are unclear. We investigated the mechanisms of the TRIF-regulated inflammatory response in RAW264.

Yunnanterpene G, a spiro-triterpene from the roots of , downregulates the expression of CD147 and MMPs in PMA differentiated THP-1 cells.

A new cycloartane triterpene, yunnanterpene G (1), containing an oxaspiro[5.4]decane moiety, was purified from the roots of . The new structure was determined from spectroscopic data and the X-ray diffraction method.

The feedback loop of "EMMPRIN/NF-κB" worsens atherosclerotic plaque via suppressing autophagy in macrophage.

This study examined the significance of macrophage autophagy in extracellular matrix metalloproteinase inducer (EMMPRIN)-mediated atherosclerosis (AS). Apolipoprotein E-deficient (ApoE-/-) mice were fed a western diet to establish an AS model. EMMPRIN and p62/Sequestosome-1(SQSTM1) expression were evaluated in plaque macrophages from the AS mice using immunofluorescence.

Ox-LDL-Induced MicroRNA-155 Promotes Autophagy in Human Endothelial Cells via Repressing the Rheb/ mTOR Pathway.

Background/aims: Autophagy, an evolutionary conserved biological process, is activated in cells to cope with various types of stress. MicroRNAs control several activities related to autophagy. However, the role of autophagy-related microRNAs during atherosclerosis is far from known.

[Effect of microRNA-155 on inflammatory response and lipid uptake of macrophages and its mechanism].

Objective To investigate the effect of microRNA-155 on inflammatory response and lipid uptake of macrophages after the cells are stimulated by ox-LDL and its potential mechanism. Methods Macrophage RAW264.7 cells were treated with 0, 25, 50 and 100 μg/mL ox-LDL for 24 hours or with 50 μg/mL ox-LDL for 0, 6, 12, 24 hours.

Effects of fenofibrate on inflammatory cytokines in diabetic retinopathy patients.

The role of cytokines in diabetic retinopathy (DR) and effects of fenofibrate on cytokines were explored by observing changes in serum IL-1β, TNF-α, VEGF, and Lp-PLA2 in different stages of DR and the intervention effect of oral fenofibrate on cytokines.In total, 190 patients with type 2 DR were enrolled and divided into 3 groups: diabetic without retinopathy (NDR) group (n = 30), nonproliferative diabetic retinopathy (NPDR) group (n = 80), and proliferative diabetic retinopathy (PDR) group (n = 80). According to whether or not to accept fenofibrate treatment, NPDR and PDR groups were further divided into the NPDR control (NPDR1) group (n = 40) and the NPDR treatment (NPDR2) group (n = 40), and the proliferative diabetic retinopathy control (PDR1, n = 40) group and the proliferative diabetic retinopathy treatment (PDR2) group (n = 40).

Atorvastatin attenuates plaque vulnerability by downregulation of EMMPRIN expression via COX-2/PGE2 pathway.

Extracellular matrix metalloproteinase inducer (EMMPRIN) reportedly has a key regulatory role in matrix metalloproteinase (MMP) activities and the progression of atherosclerosis. Statins, which are anti-atherosclerotic pharmacological agents, are widely applied in clinical settings. The aim of the present study was to investigate the pharmaceutical effect of atorvastatin on EMMPRIN expression in atherosclerotic plaques.

MicroRNA-99a inhibits insulin-induced proliferation, migration, dedifferentiation, and rapamycin resistance of vascular smooth muscle cells by inhibiting insulin-like growth factor-1 receptor and mammalian target of rapamycin.

Patients with type 2 diabetes mellitus (T2DM) are characterized by insulin resistance and are subsequently at high risk for atherosclerosis. Hyperinsulinemia has been associated with proliferation, migration, and dedifferentiation of vascular smooth muscle cells (VSMCs) during the pathogenesis of atherosclerosis. Moreover, insulin-like growth factor-1 receptor (IGF-1R) and mammalian target of rapamycin (mTOR) have been demonstrated to be the underlying signaling pathways.

Overexpression of Jagged1 Ameliorates Aged Rat-Derived Endothelial Progenitor Cell Functions and Improves Its Transfusion Efficiency for Rat Balloon-Induced Arterial Injury.

Background: Endothelial progenitor cell (EPC) has significant age-dependent alterations in properties, but the role of Jagged1 in aging-induced decline of EPC functions remains unclear.

Methods: 2- and 20-month old healthy male Sprague-Dawley rats were used in present study. Jagged1 gene transfection was performed in EPC isolated from aged (AEPC) and young rats (YEPC), respectively.

miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis.

Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS.

Suppression of TRPV4 channels ameliorates anti-dipsogenic effects under hypoxia in the subfornical organ of rats.

The phenomenon of water intake reduction during the 1(st) day of hypobaric hypoxia has been known for a long time. However, the reason for the same is yet unknown. The transient receptor potential vanilloid (TRPV) channels, including TRPV1 and TRPV4, are located in the subfornical organ (SFO).

Inhibitor of DNA binding 1 regulates cell cycle progression of endothelial progenitor cells through induction of Wnt2 expression.

Endothelial injury is a risk factor for atherosclerosis. Endothelial progenitor cell (EPC) proliferation contributes to vascular injury repair. Overexpression of inhibitor of DNA binding 1 (Id1) significantly promotes EPC proliferation; however, the underlying molecular mechanism remains to be fully elucidated.

Transcription factor E2-2 inhibits the proliferation of endothelial progenitor cells by suppressing autophagy.

Endothelial progenitor cells (EPCs) play a key role in repairing the injured vascular endothelium by differentiating into mature endothelial cells (ECs) or secreting cytokines in a paracrine manner to promote proliferation of existing ECs. However, the mechanisms underlying the proliferation of EPCs were not fully understood. In order to investigate the mechanisms of EPC proliferation, we isolated EPCs from mononuclear cells of mouse spleens.

Percutaneous Coronary Intervention after Fibrinolysis for ST-Segment Elevation Myocardial Infarction Patients: An Updated Systematic Review and Meta-Analysis.

Background: Percutaneous coronary intervention (PCI), fibrinolysis and the combination of both methods are current therapeutic options for patients with ST-segment elevation myocardial infarction (STEMI).

Methods: We searched PubMed, EMBASE, Google scholar and Cochrane Controlled Trials Register for randomized controlled trials (RCTs) evaluating the efficacy and safety of PCI after fibrinolysis within 24 hours, which was compared with primary PCI alone and ischemia-guided or delayed PCI. Meta-analysis was conducted using Review Manager 5.

Identification of Rab6a as a New Target of microRNA-155 Involved in Regulating Lipopolysaccharide-Induced TNF Secretion.

This study aims to provide experimental proof that Rab6a is an efficient target of microRNA-155 in regulating pro-inflammatory tumor necrosis factor (TNF) secretion stimulated by lipopolysaccharide (LPS) in macrophages. We identified Rab6a as a new target of microRNA-155 (miR-155) and found that overexpression of miR-155 decreased Rab6a expression at both protein and mRNA levels, which resulted in a significant reduction of TNF secretion induced by lipopolysaccharide stimulation. We have demonstrated that miR-155 can negatively regulate inflammatory TNF secretion in lipopolysaccharide stimulated macrophages, partly by targeting Rab6a, thereby providing new insights into the role of miR-155 in cytokine secretion in inflammatory macrophages.

A novel patient-specific navigational template for anatomical reconstruction of the lateral ankle ligaments.

Purpose: We discuss the clinical effects of anatomical reconstruction of the lateral ankle ligaments to treat chronic lateral ankle instability (CAI) by creating fibular channels with a patient-specific navigational template.

Methods: From August 2010 to February 2014, 15 patients presenting with CAI were treated by creating fibular channels with a patient-specific navigational template for anatomical reconstruction of the lateral ankle ligaments.

Results: All patients were followed up for nine to 24 months postoperatively (15 months on average); no recurrent CAI was found.

Median effective effect-site concentration of sufentanil for wake-up test in adolescents undergoing surgery: a randomized trial.

Background: To determine the median effective concentration of sufentanil as an analgesic during wake-up tests after sevoflurane anesthesia during surgery for adolescent idiopathic scoliosis (AIS).

Methods: This is a randomised controlled trial. Sixty patients aged 13-18 years scheduled for AIS surgery were randomized into six groups of 10 patients each to receive target effect-site concentrations of sufentanil of 0.

MicroRNA-155 inhibits angiotensin II-induced vascular smooth muscle cell proliferation.

Background: MicroRNA-155 (miR-155) is a multifunctional signal microRNA that participates in a variety of cardiovascular diseases and is involved in physiological and pathological processes in different cell types.

Objective: The objective of this article is to examine the effect of miR-155 on angiotensin II (Ang II)-induced primary mice vascular smooth muscle cell (VSMC) proliferation.

Methods: Primary cultured VSMCs from the aorta of C57/BL6 mice were incubated with Ang II and miR-155.

microRNA-155 is inversely associated with severity of coronary stenotic lesions calculated by the Gensini score.

Objectives: This study aimed to investigate the association between microRNA-155 (miR-155) and the severity and extent of coronary stenotic lesions.

Patients And Methods: We measured the miR-155 expression by real-time PCR in 110 consecutive patients undergoing coronary angiography for suspected coronary artery disease. The severity and extent of coronary stenotic lesions were evaluated on the basis of coronary angiography findings by the Gensini score.

Tumor necrosis factor-α-induced a disintegrin and metalloprotease 10 increases apoptosis resistance in prostate cancer cells.

In developed countries, prostate cancer (PCa) is the second most frequently diagnosed type of cancer and the third most common cause of cancer-related mortality in males. Compared with western countries, the morbidity rate of PCa in China is markedly lower, however, it is rising annually. The etiology of PCa is unclear, therefore, to investigate how a disintegrin and metalloprotease 10 (ADAM10) functions in PCa, ADAM10 mRNA and protein levels induced by tumor necrosis factor (TNF)-α were identified using polymerase chain reaction and flow cytometry, respectively.

Tumor vasculature-targeted recombinant mutated human TNF-α enhanced the antitumor activity of doxorubicin by increasing tumor vessel permeability in mouse xenograft models.

Objective: Increasing evidence suggests that, when used in combination, tumor necrosis factor-α (TNF-α) synergizes with traditional chemotherapeutic drugs to exert a heightened antitumor effect. The present study investigated the antitumor efficacy of recombinant mutated human TNF-α specifically targeted to the tumor vasculature (RGD-rmhTNF-α) combined with the chemotherapeutic agent doxorubicin in 2 murine allografted tumor models.

Methods: Mice bearing hepatoma or sarcoma allografted tumors were treated with various doses of RGD-rmhTNF-α alone or in combination with doxorubicin (2 mg/kg).

Effect of the intraoperative wake-up test in sevoflurane-sufentanil combined anesthesia during adolescent idiopathic scoliosis surgery: a randomized study.

Study Objective: To investigate the effect of the intraoperative wake-up test on sevoflurane-sufentanil anesthesia for adolescent idiopathic scoliosis (AIS) surgery.

Design: Randomized, double-blind, parallel trial.

Setting: Operating room.

Stim1- and Orai1-mediated store-operated calcium entry is critical for angiotensin II-induced vascular smooth muscle cell proliferation.

Aim: Despite the fact that angiotensin (Ang) II is a critical regulator of the proliferation and migration of vascular smooth muscle cells (VSMCs), the effect of Ang II on VSMC proliferation has remained unclear. In this study, we determined whether Stim1- and Orai1-mediated store-operated calcium (Ca(2+)) entry (SOCE) plays a critical role in Ang II-induced VSMC proliferation and Ang II-accelerated neointimal growth after balloon injury of rat carotid arteries.

Methods And Results: Knockdown of Stim1 and Orai1, putative calcium sensors/modulators, suppressed Ang II-mediated Ca(2+) entry and cell proliferation in synthetic VSMCs.