Magnetic resonance diffusion tensor imaging for detecting the cerebral microstructure changes in patients with CSVD-induced mild cognitive impairment.

Cerebral small vessel disease (CSVD)-induced mild cognitive impairment (MCI) has been linked to cognitive decline. Brain atrophy is considered the most common change in patients with MCI, which can be measured by diffusion tensor imaging (DTI). The study aimed to explore the relationship between DTI parameters and cognitive function in CSVD patients with MCI.

Observation on the aerosol and ozone precursors in suburban areas of Shenzhen and analysis of potential source based on MAX-DOAS.

Long-term stereoscopic observations of aerosol, NO, and HCHO were carried out at the Yangmeikeng (YMK) site in Shenzhen. Aerosol optical depths and NO vertical column concentration (NO VCD) derived from MAX-DOAS were found to be consistent with other datasets. The total NO VCD values of the site remained low, varying from 2 × 10 to 8 × 10 mol/cm, while the HCHO VCD was higher than NO VCD, varying from 7 × 10 to 11 × 10 mol/cm.

Evaluation and measurement of tropospheric glyoxal retrieved from MAX-DOAS in Shenzhen, China.

Glyoxal is one of the representative oxygenated volatile organic compounds in the atmosphere. Its accurate measurement has high significance for the determination of VOC emission sources and the calculation of the global budget of secondary organic aerosol. We investigated the spatio-temporal variation characteristics of glyoxal through observations over a 23-day period.

Emergomyces orientalis Emergomycosis Diagnosed by Metagenomic Next-Generation Sequencing.

Emergomyces is a newly described dimorphic fungus genus; it may cause fatal infections in immunocompromised patients, but diagnosis is often delayed. We report a case of disseminated emergomycosis caused by the novel species Emergomyces orientalis in a kidney transplant recipient from Tibet. Infection was diagnosed early by metagenomic next-generation sequencing.

MiR-489 aggravates H2O2-induced apoptosis of cardiomyocytes via inhibiting IGF1.

Myocardial infarction (MI) is a major type of cardiovascular disorder worldwide. In the present study, we established a new microRNA (miRNA)-mRNA cross-talk network by integrating data obtained from The National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO). In addition, functional assays, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses, were conducted using the Database for Annotation, Visualization, and Integration Discovery (DAVID).

Long-term atorvastatin or the combination of atorvastatin and nicotinamide ameliorate insulin resistance and left ventricular diastolic dysfunction in a murine model of obesity.

Current studies aimed at investigating the association between atorvastatin therapy and insulin resistance (IR) appear to be controversial. IR is considered to be an important contributor to inducing cardiac dysfunction through multiple signals. The paradoxical cardiotoxicity of atorvastatin reported under different conditions suggests that the association between atorvastatin treatment, insulin resistance and cardiac function should be clarified further.

The Antifibrotic Effect of A Adenosine Receptor Antagonism in a Mouse Model of Dermal Fibrosis.

Objective: Systemic sclerosis (SSc; scleroderma) is a chronic disease that affects the skin and various internal organs. Dermal fibrosis is a major component of this disease. The mechanisms that promote dermal fibrosis remain elusive.

Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment.

Interstitial fibrosis plays a key role in the development and progression of heart failure. Here, we show that an enzyme that crosslinks collagen-Lysyl oxidase-like 2 (Loxl2)-is essential for interstitial fibrosis and mechanical dysfunction of pathologically stressed hearts. In mice, cardiac stress activates fibroblasts to express and secrete Loxl2 into the interstitium, triggering fibrosis, systolic and diastolic dysfunction of stressed hearts.

Blockade of A2B adenosine receptor reduces left ventricular dysfunction and ventricular arrhythmias 1 week after myocardial infarction in the rat model.

Background: Remodeling occurs after myocardial infarction (MI), leading to fibrosis, dysfunction, and ventricular tachycardias (VTs). Adenosine via the A2B adenosine receptor (A2BAdoR) has been implicated in promoting fibrosis.

Objective: To determine the effects of GS-6201, a potent antagonist of the A2BAdoR, on arrhythmogenic and functional cardiac remodeling after MI.

Adenosine A2B receptor and hyaluronan modulate pulmonary hypertension associated with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide. The development of pulmonary hypertension (PH) in patients with COPD is strongly associated with increased mortality. Chronic inflammation and changes to the lung extracellular matrix (ECM) have been implicated in the pathogenesis of COPD, yet the mechanisms that lead to PH secondary to COPD remain unknown.

GS-6201, a selective blocker of the A2B adenosine receptor, attenuates cardiac remodeling after acute myocardial infarction in the mouse.

Adenosine (Ado) is released in response to tissue injury, promotes hyperemia, and modulates inflammation. The proinflammatory effects of Ado, which are mediated by the A(2B) Ado receptor (AdoR), may exacerbate tissue damage. We hypothesized that selective blockade of the A(2B) AdoR with 3-ethyl-1-propyl-8-(1-(3-trifluoromethylbenzyl)-1H-pyrazol-4-yl)-3,7-dihydropurine-2,6-dione (GS-6201) during acute myocardial infarction (AMI) would reduce adverse cardiac remodeling.

The A2B adenosine receptor modulates pulmonary hypertension associated with interstitial lung disease.

Development of pulmonary hypertension is a common and deadly complication of interstitial lung disease. Little is known regarding the cellular and molecular mechanisms that lead to pulmonary hypertension in patients with interstitial lung disease, and effective treatment options are lacking. The purpose of this study was to examine the adenosine 2B receptor (A(2B)R) as a regulator of vascular remodeling and pulmonary hypertension secondary to pulmonary fibrosis.

Effect of a specific and selective A(2B) adenosine receptor antagonist on adenosine agonist AMP and allergen-induced airway responsiveness and cellular influx in a mouse model of asthma.

It has been previously proposed that adenosine plays an important role in the pathogenesis of asthma. The proposed mechanism of action for nucleoside adenosine is to activate A(2B) adenosine receptors (AR) and to indirectly modulate levels of mediators in the lung. In vivo data supporting the role of A(2B) AR in airway reactivity and inflammation in allergic animal models are lacking.

Role of A2B adenosine receptor signaling in adenosine-dependent pulmonary inflammation and injury.

Adenosine has been implicated in the pathogenesis of chronic lung diseases such as asthma and chronic obstructive pulmonary disease. In vitro studies suggest that activation of the A2B adenosine receptor (A2BAR) results in proinflammatory and profibrotic effects relevant to the progression of lung diseases; however, in vivo data supporting these observations are lacking. Adenosine deaminase-deficient (ADA-deficient) mice develop pulmonary inflammation and injury that are dependent on increased lung adenosine levels.

A2B adenosine receptors induce IL-19 from bronchial epithelial cells, resulting in TNF-alpha increase.

Adenosine is a signaling nucleoside that has been proposed to contribute to the pathogenesis of asthma and chronic obstructive pulmonary disease. Previous studies suggest that adenosine might play an important role in modulating levels of inflammatory mediators in the lung. Because airway epithelium is an important cellular source of inflammatory mediators, the objective of the present study was to determine whether adenosine affects the expression and release of inflammatory cytokines from human bronchial epithelial cells (HBECs).

Synergy between A2B adenosine receptors and hypoxia in activating human lung fibroblasts.

Chronic inflammatory airway diseases, such as asthma, chronic obstructive pulmonary disease and pulmonary fibrosis, are associated with subepithelial fibroblast activation, myofibroblast hyperplasia, hypoxia, and increase in interstitial adenosine concentrations. The goal of this study was to determine the effect of adenosine and its receptors on activation of human lung fibroblasts under normoxia (21% O2) and hypoxia (5% O2). Under the normoxic condition, adenosine and its stable analog, 5'-(N-ethylcarboxamido)-adenosine, via activation of A2B adenosine receptors, increased the release of interleukin (IL)-6 by 14-fold and induced the differentiation of human lung fibroblasts to myofibroblasts.

Hypoxia modulates adenosine receptors in human endothelial and smooth muscle cells toward an A2B angiogenic phenotype.

We previously reported that adenosine A2B receptor activation stimulates angiogenesis. Because hypoxia is a potent stimulus for the release of both adenosine and angiogenic factors, we tested the hypothesis that hypoxia alters the expression of adenosine receptors toward an "angiogenic" phenotype. We used human umbilical vein endothelial cells (HUVECs) and bronchial smooth muscle cells (BSMCs) because, under normoxic conditions, adenosine does not release vascular endothelial growth factor (VEGF).

A3 adenosine receptor signaling contributes to airway inflammation and mucus production in adenosine deaminase-deficient mice.

Adenosine signaling has been implicated in chronic lung diseases such as asthma and chronic obstructive pulmonary disease; however, the specific roles of the various adenosine receptors in processes central to these disorders are not well understood. In this study, we have investigated the role(s) of the A(3) adenosine receptor in adenosine-dependent pulmonary inflammation observed in adenosine deaminase (ADA)-deficient mice. The A(3) receptor (A(3)R) was found to be expressed in eosinophils and mucus-producing cells in the airways of ADA-deficient mice.

A(2B) adenosine receptors increase cytokine release by bronchial smooth muscle cells.

Adenosine (Ado) has been suggested to play a role in inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease. The goal of this study was to determine the effect of Ado and its receptor subtypes on cytokine release by bronchial smooth muscle cells. The A2B Ado receptor (AdoR) was expressed at the highest level among the four AdoR subtypes.

Activation of murine lung mast cells by the adenosine A3 receptor.

Adenosine has been implicated to play a role in asthma in part through its ability to influence mediator release from mast cells. Most physiological roles of adenosine are mediated through adenosine receptors; however, the mechanisms by which adenosine influences mediator release from lung mast cells are not understood. We established primary murine lung mast cell cultures and used real-time RT-PCR and immunofluorescence to demonstrate that the A(2A), A(2B), and A(3) adenosine receptors are expressed on murine lung mast cells.