Celiac Artery Compression Syndrome Evaluated with 3-D Contrast-Enhanced Ultrasonography: a New Approach.

This study was performed to estimate the value of 3-D contrast-enhanced ultrasonography (3-D-CEUS) in the diagnosis of celiac artery compression syndrome (CACS). Patients suspected of having CACS were assessed with 3-D-CEUS and contrasted with computed tomography angiography. Diagnostic accuracy was evaluated with a receiver operating characteristic curve. Three-dimensional CEUS revealed 19 positive and 9 negative cases. In the negative group, the contrast agent did not change with respiration. In the positive group, the contrast agent exhibited a hook-shaped stenosis on expiration and returned to normal on inspiration. Computed tomography angiography indicated 1 false-positive case and 1 false-negative case. The sensitivity and specificity of 3-D-CEUS were 95% and 89%, respectively. The area under the receiver operating characteristic curve was 0.982 (p <0.01). In conclusion, 3-D-CEUS can accurately reveal the characteristic hooked appearance and dynamic nature of CACS with respiration, and thus, it represents a new, non-invasive approach to CACS diagnosis.

miR-155 functions downstream of angiotensin II receptor subtype 1 and calcineurin to regulate cardiac hypertrophy.

Cardiac hypertrophy is characterized by maladaptive tissue remodeling that may lead to heart failure or sudden death. MicroRNAs (miRs) are negative regulators of angiotensin II and the angiotensin II receptor subtype 1 (AGTR1), which are two components involved in cardiac hypertrophy. In the present study, the interaction between angiotensin II receptor subtype 1 (AGTR1) signaling and miR-155 was investigated. Rat H9C2 (2-1) cardiomyocytes were transfected with miR-155 analogues or inhibitors, then stimulated with angiotensin II to induce cardiac hypertrophy. miR-155 expression was revealed to be altered following transfection with chemically-modified miR-155 analogues and inhibitors in rat cardiomyocytes. In cell cardiac hypertrophy models, the cell surface area, AGTR1, atrial natriuretic peptide and myosin heavy chain-ß mRNA expression levels were revealed to be lower in cells stimulated with miR-155 analogue-transfected cells treated with angiotensin II compared with cells stimulated with angiotensin alone (P<0.05), as determined using reverse transcription-polymerase chain reaction (PCR), quantitative PCR and western blot analyses. Furthermore, calcineurin mRNA and protein, intracellular free calcium and nuclear factor of activated T-cells-4 proteins were downregulated in miR-155 analogue-transfected cells treated with angiotensin II, as compared with cells stimulated with angiotensin II alone (P<0.05). In conclusion, the current study indicates that miR-155 may improve cardiac hypertrophy by downregulating AGTR1 and suppressing the calcium signaling pathways activated by AGTR1.

Tumor necrosis factor-alpha G-238A polymorphism and coronary artery disease risk: a meta-analysis of 4,222 patients and 4,832 controls.

BACKGROUND: The aim of the present study was to investigate the association between tumor necrosis factor-alpha (TNF-α) gene G-238A polymorphism and risk of coronary artery disease (CAD) using a meta-analytical approach. METHODS: The PubMed and Embase databases were searched for relevant publications up to January 13, 2015. Four authors (XPH, XDZ, XTZ, and ZJZ) independently selected the studies, extracted, and analyzed the data using the Comprehensive Meta-Analysis software. The sensitivity and subgroups analyses were also performed. Either a fixed effects or a random effects model was used to estimate pooled odds ratios (ORs) and their 95% confidence intervals (CIs). RESULTS: Finally, ten articles including eleven case-control studies involving 4,222 patients and 4,832 controls were yielded. The results indicated no significant association between G-238A polymorphism and CAD risk (A vs G: OR =1.08, 95% CI =0.89-1.30; AA vs GG: OR =1.15, 95% CI =0.59-2.25; GA vs GG: OR =1.14, 95% CI =0.88-1.48; AA vs [GG + GA]: OR =1.09, 95% CI =0.56-2.14; (GA + AA) vs GG: OR =1.11, 95% CI =0.90-1.38). In the subgroup analyses, similar results were obtained with overall populations. The sensitivity analyses showed that the overall results were robust. No publication bias was detected. CONCLUSION: Based on current evidence, we can conclude that TNF-α G-238A polymorphism might not be associated with CAD risk.