Pathophysiology of Angiotensin II-Mediated Hypertension, Cardiac Hypertrophy, and Failure: A Perspective from Macrophages.

Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among the various regulatory systems that impact on these heterogeneous pathological processes, angiotensin II (Ang II)-activated macrophages play a pivotal role in the induction of subcellular defects and cardiac adverse remodeling during the progression of heart failure.

Ferroptosis: A potential target of macrophages in plaque vulnerability.

Plaque vulnerability has been the subject of several recent studies aimed at reducing the risk of stroke and carotid artery stenosis. Atherosclerotic plaque development is a complex process involving inflammation mediated by macrophages. Plaques become more vulnerable when the equilibrium between macrophage recruitment and clearance is disturbed.

Cardiovascular Protection with a Long-Acting GLP-1 Receptor Agonist Liraglutide: An Experimental Update.

Angiotensin II (Ang II), a peptide hormone generated as part of the renin-angiotensin system, has been implicated in the pathophysiology of many cardiovascular diseases such as peripheral artery disease, heart failure, hypertension, coronary artery disease and other conditions. Liraglutide, known as an incretin mimetic, is one of the glucagon-like peptide-1 (GLP-1) receptor agonists, and has been proven to be effective in the treatment of cardiovascular disorders beyond adequate glycemic control. The objective of this review is to compile our recent experimental outcomes-based studies, and provide an overview the cardiovascular protection from liraglutide against Ang II- and pressure overload-mediated deleterious effects on the heart.

Nickel Foam Coated by Ni Nanoparticle-Decorated 3D Nanocarbons as a Freestanding Host for High-Performance Lithium-Sulfur Batteries.

Nanocarbons (NCs) consisting of carbon nanotubes (CNTs) and carbon nanofibers (CNFs) were coated on the surface of nickel foam (NF) via a chemical vapor deposition method. The CNFs formed conductive networks on NF, while the CNTs grew perpendicular to the surface of the CNFs, accompanied with the formation of Ni nanoparticles (Ni NPs) at the end of CNTs. The unique Ni-NCs-coated NF with a porous structure was applied as the three-dimensional (3D) current collector of lithium-sulfur (Li-S) batteries, which provided enough space to accommodate the electrode materials inside itself.

Suppression of angiotensin II-activated NOX4/NADPH oxidase and mitochondrial dysfunction by preserving glucagon-like peptide-1 attenuates myocardial fibrosis and hypertension.

This study aims to investigate whether stabilization of glucagon-like peptide-1 (GLP-1) level reduces angiotensin II (Ang II)-induced cardiac fibrosis and -elevated blood pressure accompanying with inhibition of NADPH oxidase (NOX) expression and preservation of mitochondrial integrity. The study was performed in Sprague-Dawley rat model of Ang II infusion (500 ng/kg/min) using osmotic minipumps for 4 weeks. GLP-1 receptor agonist liraglutide (0.

A Novel Mitochondrial Complex of Aldosterone Synthase, Steroidogenic Acute Regulatory Protein, and Tom22 Synthesizes Aldosterone in the Rat Heart.

Aldosterone, which regulates renal salt retention, is synthesized in adrenocortical mitochondria in response to angiotensin II. Excess aldosterone causes myocardial injury and heart failure, but potential intracardiac aldosterone synthesis has been controversial. We hypothesized that the stressed heart might produce aldosterone.

Aerobic degradation of 4-fluoroaniline and 2,4-difluoroaniline: performance and microbial community in response to the inocula.

In this study, a distinct inoculum was investigated as an isolated variable within sequencing batch reactors via a comparison of the 4-fluoroaniline (4-FA) or 2,4-difluoroaniline (2,4-DFA) removal amounts. The inocula were derived from a treatment plant for treating pharmaceutical wastewater plus a small amount of municipal sewage (PMS), a treatment plant for treating fluoridated hydrocarbon wastewater (FHS), and a treatment plant for treating the comprehensive wastewater in an industrial park (CIS). There were slight differences among the degradation patterns of the 4-FA for the three inocula, whether during the enrichment period or the high concentration shock period.

Glucagon-Like Peptide-1 Analog Liraglutide Attenuates Pressure-Overload Induced Cardiac Hypertrophy and Apoptosis through Activating ATP Sensitive Potassium Channels.

Purpose: This study aimed to investigate whether inhibition of glucagon-like peptide-1 (GLP-1) on pressure overload induced cardiac hypertrophy and apoptosis is related to activation of ATP sensitive potassium (KATP) channels.

Methods: Male SD rats were randomly divided into five groups: sham, control (abdominal aortic constriction), GLP-1 analog liraglutide (0.3 mg/kg/twice day), KATP channel blocker glibenclamide (5 mg/kg/day), and liraglutide plus glibenclamide.

Exogenous supplement of glucagon like peptide-1 protects the heart against aortic banding induced myocardial fibrosis and dysfunction through inhibiting mTOR/p70S6K signaling and promoting autophagy.

Mammalian target of rapamycin (mTOR) and a ribosomal protein S6 kinase (p70S6K) mediate tissue fibrosis and negatively regulate autophagy. This study aims to investigate whether glucagon-like peptide-1 (GLP-1) analog liraglutide protects the heart against aortic banding-induced cardiac fibrosis and dysfunction through inhibiting mTOR/p70S6K signaling and promoting autophagy activity. Male SD rats were randomly divided into four groups (n = 6/each group): sham operated control; abdominal aortic constriction (AAC); liraglutide treatment during AAC (0.

Steroidogenic acute regulatory protein/aldosterone synthase mediates angiotensin II-induced cardiac fibrosis and hypertrophy.

Aldosterone produced in adrenal glands by angiotensin II (Ang II) is known to elicit myocardial fibrosis and hypertrophy. This study was designed to test the hypothesis that Ang II causes cardiac morphological changes through the steroidogenic acute regulatory protein (StAR)/aldosterone synthase (AS)-dependent aldosterone synthesis primarily initiated in the heart. Sprague-Dawley rats were randomized to following groups: Ang II infusion for a 4-week period, treatment with telmisartan, spironolactone or adrenalectomy during Ang II infusion.

Conservation of glucagon like peptide-1 level with liraglutide and linagilptin protects the kidney against angiotensin II-induced tissue fibrosis in rats.

This study tested the hypothesis that the enhancement of glucagon-like peptide-1 (GLP-1) level through either exogenous supply of GLP-1 agonist, liraglutide or prevention of endogenous GLP-1 degradation with dipeptidyl peptidease-4 inhibitor, lingaliptin ameliorates angiotensin II (Ang II)-induced renal fibrosis. Sprague-Dawley rats were randomly divided into four groups: 0.9% saline or Ang II (500 ng/kg/min) was infused with osmotic minipumps for 4 weeks, defined as sham and Ang II groups.

Aerobic degradation of 2- and 3-fluoroaniline in mixed culture systems and microbial community analysis.

Among three monofluoroanilines, 2-fluoroaniline (2-FA) and 3-fluoroaniline (3-FA) exhibit relatively poor biodegradability. This work examined their degradation characteristics in a mixed culture system and also analyzed the microorganism community. After acclimation for 58 d and 43 d, the high removal efficiency of 100% of 2-FA and 95.

Liraglutide attenuates cardiac remodeling and improves heart function after abdominal aortic constriction through blocking angiotensin II type 1 receptor in rats.

Objective: Angiotensin II (Ang II) is known to contribute to the pathogenesis of heart failure by eliciting cardiac remodeling and dysfunction. The glucagon-like peptide-1 (GLP-1) has been shown to exert cardioprotective effects in animals and patients. This study investigates whether GLP-1 receptor agonist liraglutide inhibits abdominal aortic constriction (AAC)-induced cardiac fibrosis and dysfunction through blocking Ang II type 1 receptor (AT1R) signaling.

Degradation of 3-fluoroanilne by Rhizobium sp. JF-3.

The interest of fluoroanilines in the environment is due to their extensive applications in industry and their low natural biodegradability. A pure bacterial strain capable of degrading 3-fluoroaniline (3-FA) as the sole source of carbon and energy was isolated from a sequencing batch reactor operating for the treatment of 3-FA. The strain (designated as JF-3) was identified by 16S rRNA gene analysis as a member of the genus Rhizobium.

CD44 Deficiency in Mice Protects the Heart Against Angiotensin Ii-Induced Cardiac Fibrosis.

This study tested the hypothesis that CD44 is involved in the development of cardiac fibrosis via angiotensin II (Ang II) AT1 receptor-stimulated TNFα/NFκB/IκB signaling pathways. Study was conducted in C57BL/6 wild type and CD44 knockout mice subjected to Ang II infusion (1,000 ng/kg/min) using osmotic minipumps up to 4 weeks or with gastric gavage administration of the AT1 receptor blocker, telmisartan at a dose of 10 mg/kg/d. Results indicated that Ang II enhances expression of the AT1 receptor, TNFα, NFκB, and CD44 as well as downregulates IκB.

Curcumin inhibits cardiac hypertrophy and improves cardiovascular function via enhanced Na/Ca exchanger expression after transverse abdominal aortic constriction in rats.

Background: This study tested the hypothesis that inhibition of cardiac hypertrophy and preservation of cardiac/endothelial function by the natural yellow pigment curcumin are associated with upregulated expression of Na/Ca exchanger (NCX) after transverse aortic constriction (TAC).

Methods: Male Wistar rats were subjected to TAC for 10 weeks and curcumin (50 mg/kg/day) was fed by gastric gavage during TAC. Expression of NCX and endothelial nitric oxide synthase (eNOS) was analyzed by Western blot and immunohistochemistry.

Edaravone inhibits pressure overload-induced cardiac fibrosis and dysfunction by reducing expression of angiotensin II AT1 receptor.

Angiotensin II (Ang II) is known to be involved in the progression of ventricular dysfunction and heart failure by eliciting cardiac fibrosis. The purpose of this study was to demonstrate whether treatment with an antioxidant compound, edaravone, reduces cardiac fibrosis and improves ventricular function by inhibiting Ang II AT1 receptor. The study was conducted in a rat model of transverse aortic constriction (TAC).

Postconditioning attenuates coronary perivascular and interstitial fibrosis through modulating angiotensin II receptors and angiotensin-converting enzyme 2 after myocardial infarction.

Background: Postconditioning (Postcon) is known to reduce infarct size. This study tested the hypothesis that Postcon attenuates the perivascular and interstitial fibrosis after myocardial infarction through modulating angiotensin II-activated fibrotic cascade.

Materials And Methods: Male Sprague-Dawley rats were subjected to 45-min coronary occlusion followed by 1 and 6 wk of reperfusion.

Recruitment of macrophages from the spleen contributes to myocardial fibrosis and hypertension induced by angiotensin II.

Introduction: The purpose of this study was to determine whether macrophages migrated from the spleen are associated with angiotensin II-induced cardiac fibrosis and hypertension.

Methods: Sprague-Dawley rats were subjected to angiotensin II infusion in vehicle (500 ng/kg/min) for up to four weeks. In splenectomy, the spleen was removed before angiotensin II infusion.

Biological phosphorus removal in an extended ASM2 model: Roles of extracellular polymeric substances and kinetic modeling.

This paper presents the results of an extended ASM2 model for the modeling and calibration of the role of extracellular polymeric substances (EPS) in phosphorus (P) removal in an anaerobic-aerobic process. In this extended ASM2 model, two new components, the bound EPS (X) and the soluble EPS (S), are introduced. Compared with the ASM2, 7.

Overexpression of miR-223 Tips the Balance of Pro- and Anti-hypertrophic Signaling Cascades toward Physiologic Cardiac Hypertrophy.

MicroRNAs (miRNAs) have been extensively examined in pathological cardiac hypertrophy. However, few studies focused on profiling the miRNA alterations in physiological hypertrophic hearts. In this study we generated a transgenic mouse model with cardiac-specific overexpression of miR-223.

The Sex Difference in Basic Surgical Skills Learning: A Comparative Study.

Background: Very little is known of sex-related differences among medical students in the acquisition of basic surgical skills at an undergraduate level. The aim of this study was to investigate the sex differences in basic surgical skills learning and the possible explanations for sex disparities within basic surgical skills education.

Methods: A didactic description of 10 surgical skills was performed, including knot tying, basic suture I, basic suture II, sterile technique, preoperative preparation, phlebotomy, debridement, laparotomy, cecectomy, and small bowel resection with hand-sewn anastomosis.

Angiotensin II AT1 receptor alters ACE2 activity, eNOS expression and CD44-hyaluronan interaction in rats with hypertension and myocardial fibrosis.

Aim: This study tested the hypothesis that angiotensin II (Ang II) AT1 receptor is involved in development of hypertension and cardiac fibrosis via modifying ACE2 activity, eNOS expression and CD44-hyaluronan interaction.

Main Methods: Male Sprague-Dawley rats were subjected to Ang II infusion (500ng/kg/min) using osmotic minipumps up to 4weeks and the AT1 receptor blocker, telmisartan was administered by gastric gavage (10mg/kg/day) during Ang II infusion.

Key Findings: Our results indicated that Ang II enhances AT1 receptor, downregulates AT2 receptor, ACE2 activity and eNOS expression, and increases CD44 expression and hyaluronidase activity, an enzyme for hyaluronan degradation.

Attenuation of myocardial fibrosis with curcumin is mediated by modulating expression of angiotensin II AT1/AT2 receptors and ACE2 in rats.

Curcumin is known to improve cardiac function by balancing degradation and synthesis of collagens after myocardial infarction. This study tested the hypothesis that inhibition of myocardial fibrosis by curcumin is associated with modulating expression of angiotensin II (Ang II) receptors and angiotensin-converting enzyme 2 (ACE2). Male Sprague Dawley rats were subjected to Ang II infusion (500 ng/kg/min) using osmotic minipumps for 2 and 4 weeks, respectively, and curcumin (150 mg/kg/day) was fed by gastric gavage during Ang II infusion.