Analysis of Short-Term Clinical Outcomes and Influencing Factors in Patients with Acute Type B Aortic Intramural Hematoma Treated with Optimal Medical Therapy.

This study aimed to investigate the short-term predictors of aortic-related adverse events in patients with acute type B aortic intramural hematoma (IMH) initially treated with optimized medical therapy.A total of 157 patients with acute type B IMH were included in this study. These patients were divided into worsening group (n = 45) and stable group (n = 112) based on the incidence of aortic-related adverse events. The clinical data and imaging features of the two groups were compared. Multivariate logistic regression analysis of predictors of aortic-related adverse events in type B IMH was performed. Receiver operating characteristic (ROC) curve was applied to determine the optimal cutoff value for maximum descending aorta diameter (MDAD). Kaplan-Meier survival curve was used to analyze the incidence of aortic-related adverse events.Worsening and stable groups were statistically significant in diuretics, abnormal D-dimer level, observation endpoint systolic blood pressure (SBP), MDAD, aortic atherosclerosis, ulcer-like projection (ULP), and thickness of hematoma (P < 0.05). Multivariate logistic regression showed that abnormal D-dimer level (OR = 12.464, P = 0.025), MDAD (OR = 1.113, P = 0.030), and ULP (OR = 5.849, P = 0.022) were powerful independent risk factors for predicting aortic-related adverse events in type B IMH, and observation endpoint SBP within 100-120 mmHg (OR = 0.225, P = 0.014) was a protective factor for predicting aortic-related adverse events in type B IMH. The cutoff value of MDAD was 35.2 mm.Short-term imaging is recommended for type B IMH patients with abnormal D-dimer level, MDAD > 35.2 mm, and ULP. Blood pressure should also be strictly monitored and controlled during the acute phase of IMH.

The sex-specific influence of FTO genotype on exercise intervention for weight loss in adult with obesity.

The impact of exercise on weight loss varies significantly among individuals, and genes play a critical role. This study aims to explore whether the FTO gene variant (rs8050136) affects the influence of exercise on weight. The study initially recruited 240 Han Chinese adults with obesity, and 178 of them (101 men, 77 women, aged from 21 to 60) completed a 12-week moderate aerobic exercise programme. The participants were genotyped and obesity-related data were collected before and after the intervention. The intensity and the amount of exercise were precisely monitored. After the intervention, most obesity-related parameters of the participants showed a significant decrease. For muscle and lean body mass, significant change was only observed in males (P < 0.001) but not females (P = 0.205, P = 0.200 respectively). Importantly, for weight and BMI loss, we observed a genotype-by-gender interaction (P = 0.041, P = 0.042 respectively, adjusted for age, exercise time and baseline value). In the further analysis, after stratified for gender, the exercise-induced weight loss (P = 0.008), BMI loss (P = 0.010), muscle mass loss (P = 0.005) and lean body mass loss (P = 0.004) showed greater decrease in male subjects carrying at least one A allele compared to non-carriers. In conclusion, our study suggests that in Han Chinese population with obesity, carrying "obese risk gene" FTO (rs8050136) does not lead to the resistance to weight management intervention. More importantly, in male subjects, carrying FTO risk allele would even lose more weight than non-carriers after exercise intervention.HighlightsFor Han Chinese adults with obesity, carrying "obese risk gene" FTO could still achieve weight loss through exercise.Males carrying FTO risk allele would lose more weight than non-carriers after a 12-weeks exercise programme.

Gefitinib-Induced Cutaneous Toxicities in Brown Norway Rats Are Associated with Macrophage Infiltration.

Gefitinib (Iressa), is a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), used in the targeted treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC). Skin toxicity is the major adverse effect observed in patients treated with EGFR-targeted TKIs such as gefitinib and erlotinib. To date, a corresponding skin animal model has not been established to address the mechanisms of these effects. Therefore, we analyzed the skin rash phenotype and its pathological features in Brown Norway (BN) rats treated with gefitinib 2.5 mg, 5.0 mg, or 10 mg/100 g/day for 4 weeks. We found that treatment with gefitinib led to weight loss, rash, itching, and hair loss in a dose-dependent manner. We also investigated the skin pathology and found that the animal model showed thickening of the epidermis, loss of moisture, and apoptosis of keratinocytes. Immunohistochemistry, flow cytometry, and analysis of monocytes and leukocytes in the blood revealed increased macrophage infiltration was associated with the cutaneous toxicities induced by gefitinib in the BN rats. Finally, we found that gefitinib-induced cutaneous toxicity is significantly associated with three inflammatory cytokines known to be secreted by activated macrophages, TREM-1, CINC-2, and CINC-3.

Determination of the normal A2Π state in MgF with application to direct laser cooling of molecules.

We report high resolution electronic spectroscopy of cold magnesium monofluoride (MgF) molecules in the gas phase, which are created by a combination of laser ablation, chemical reaction, and 6 K helium buffer-gas cooling. Thanks to the sufficient population in the low-lying rotational states, the P, Q, and R branches in the electronic transition of the X2Σ+ to A2Π state are able to be measured unambiguously by in-cell absorption spectra. For the first time, we show that the A2Π state of MgF is actually a normal state, not an inverted one. The laser cooling relevant transitions X2Σ+v=0,1,N=1→A2Π1/2(v=0,J'=1/2) are also identified, along with the hyperfine structure of the X2Σ+(v = 0, N = 1) state. This study provides an important step for ongoing laser cooling experiments of MgF molecules.

Note: Sensitive fluorescence detection through minimizing the scattering light by anti-reflective nanostructured materials.

We demonstrate a new approach with fabrication of anti-reflective coating to substantially reduce the scattering light in an ultra-high vacuum during laser induced fluorescence (LIF) detection. To do so, the surface of the vacuum chamber in the detection region was blackened and coated with the special solar heat absorbing nanomaterials. We demonstrate that more than 97.5% of the stray light in the chamber spanning from near infrared to ultraviolet can be absorbed which effectively improves the signal to noise (S/N) ratio. With this technique, the LIF signal from the cold magnesium monofluoride molecules has been observed with an S/N ratio of ∼4 times better than without that.

Effects of omeprazole or pantoprazole on platelet function in non-ST-segment elevation acute coronary syndrome patients receiving clopidogrel.

BACKGROUND: This study evaluated the effect of omeprazole or pantoprazole on platelet reactivity in non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients receiving clopidogrel. METHODS: Consecutive patients with NSTE-ACS (n = 620) from general hospital of Shenyang Military Command were randomized to the omeprazole or pantoprazole (20 mg/d) group (1:1), and received routine dual antiplatelet treatment. Patients' reversion rate of adenosine diphosphate-induced platelet aggregation (ADP-PA) was assessed at baseline, 12 to 24 h after administration of medication, and after 72 h of percutaneous coronary intervention (PCI). The primary endpoint of the study was platelet reactivity assessed with ADP-PA at 30 days after PCI. Adverse events (AEs) were recorded for 30-day and 180-day follow-up periods. RESULTS: There were no significant differences between both the groups in platelet response to clopidogrel at 12-24 h after drug administration (54.09% ± 18.90% vs 51.62% ± 19.85%, P = 0.12), 72 h after PCI (52.15% ± 19.45% vs 49.66% ± 20.05%, P = 0.18), and 30 days after PCI (50.44% ± 14.54% vs 48.52% ± 15.08%, P = 0.17). The rate of AEs did not differ significantly between groups during the 30-day (15.2% vs 14.8%, P = 0.91) and 180-day (16.5% vs 14.5%, P = 0.50) follow-up periods after PCI. CONCLUSIONS: The addition of omeprazole or pantoprazole to clopidogrel did not restrict the effect of platelet aggregation by reducing the conversion of clopidogrel. Compared with clopidogrel alone, pantoprazole-clopidogrel and omeprazole-clopidogrel combinations did not increase the incidence of adverse clinical events during 30-day and 180-day follow-up periods after PCI. TRIAL REGISTRATION: The study is registered in the National Institutes of Health website with identifier NCT01735227. Registered 14 November 2012.

CXCL5 is associated with the increased risk of coronary artery disease.

OBJECTIVE: To investigate the relevant expression of CXCL5 and CXCR2 in human atherosclerotic coronary artery and to study the association between the CXCL5 variant and coronary artery disease (CAD) in a Chinese Han population. MATERIALS AND METHODS: CXCL5 and CXCR2 expression in human coronary arteries was detected by immunohistochemical staining and western blotting analysis. The association between the CXCL5 variant and CAD was determined in a community-based sample by PCR-direct sequence analysis in a Chinese Han population. Finally, plasma CXCL5 levels were measured in a case-control study of CAD patients. RESULTS: We found that CXCL5 and CXCR2 expressions were higher in atherosclerotic coronary arteries plaque than in the normal coronary arteries. CXCL5 and CXCR2 expression levels increased in line with coronary artery lesion stages. A functional nonsynonymous -156 G/C in the CXCL5 promoter region was associated with CAD and plasma CXCL5 levels were significantly increased in CAD patients compared with control subjects (3891.21±1403.08 vs. 2812.39±840.62 pg/ml, P<0.05). Individuals with the CXCL5 promoter -156 G/C variant C/C and G/C carriers had higher plasma CXCL5 levels than those with the G/G genotype carriers in both CAD patients and control participants. CONCLUSION: CXCL5 and CXCR2 are enriched in human atherosclerotic coronary artery. Our findings show that the CXCL5 variant might be a genetic risk factor for the susceptibility of CAD and the CXCL5 promoter -156 G/C C allele might be an independent predictor for CAD. CXCL5 may be a useful molecular marker and a possible target for the treatment of CAD.

Impact of matrix metalloproteinase-8 gene variations on the risk of thoracic aortic dissection in a Chinese Han population.

The importance of matrix metalloproteinase 8 (MMP8) expression during the progression of thoracic aortic dissection (TAD) has been recently emphasized. Genetic variations that affect proteinase expression or activity might contribute to the pathogenesis of TAD. In this study, we investigated whether the MMP8 C-799T genotype is associated with TAD. The frequency distributions of the MMP8 C-799T polymorphism were determined by direct sequencing. Associations between the polymorphism and disease progression in TAD were investigated. The level of plasma and tissue MMP8 was measured by enzyme-linked immunosorbent assay and western blotting. The MMP8 C-799T polymorphism was significantly associated with susceptibility to disease progression in TAD patients (n = 152) than in controls (n = 147) (P = 0.004, OR = 0.62, 95 % CI 0.45-0.86). The TT homozygotes had a significantly higher risk of TAD compared to C allele carriers in a logistic regression model, after adjustment for the conventional risk factors for TAD. The plasma MMP8 concentration was significantly higher in TAD patients compared to control patients (P < 0.05). TT genotypes had increased MMP8 levels compared to CC and CT genotype carriers in both TAD and control subjects (P < 0.05). The C-799T polymorphism in the MMP8 promoter is part of the genetic variation underlying the susceptibility of individuals to the progression of TAD.