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Infant sex ratios that differ from the biological norm provide a measure of gender status inequality that is not susceptible to social desirability bias. Ratios may become less biased with educational expansion through reduced preference for male children. Alternatively, bias could increase with education through more access to sex-selective medical technologies. Using National Vital Statistics data on the population of live births in the United States for 1969–2018, we examine trends in infant sex ratios by parental race/ethnicity, education, and birth parity over five decades. We find son-biased infant sex ratios among Chinese and Asian Indian births that have persisted in recent years, and regressions suggest son-biased ratios among births to Filipino and Japanese mothers with less than a high school education. Infant sex ratios are more balanced at higher levels of maternal education, particularly when both parents are college educated. Results suggest greater equality of gender status with higher education in the United States.

In the United States, high marital instability calls for more research on union transitions after marital dissolution. Previous studies focus on remarriage and pay little attention to rising post-dissolution cohabitation. In this study, I apply marital search theory to examine the level, pace, and differentials of repartnering (remarriage or cohabitation vs. staying single) and the exit from cohabitation (remarriage or dissolution vs. staying cohabiting). Adopting union history data from the pooled National Survey of Family Growth (2011–2017), I track union transitions among a sample of N = 2129 women. Analyses based on life tables and discrete-time event history analyses reveal important findings. First, most women repartner after marital dissolution. Compared to remarriage, cohabitation occurs more frequently and shows a quicker pace. Second, post-dissolution cohabitation is short-lived, and its transition to remarriage is more common than to dissolution. Third, these union transitions differ by demographic and socioeconomic predictors, including age, race and ethnicity, and education. Overall, I reveal that post-dissolution union transition is a divergent and unequal process, and I further discuss the implications on theory and family inequality.

Objective. To investigate the diagnostic value of circulating integrins β1, 2, and 3 in venous thrombosis (VTE). Materials and Methods. A total of 474 VTE patients and 306 patients with nonhigh risk for VTE as the control group were studied. Levels of adhering integrins β1, 2, and 3 were detected by flow cytometry. Levels of circulating integrins β1, 2, and 3 in serum were measured by enzyme-linked immunosorbent assay. Results. We found that integrins β1, 2, and 3 were expressed highly both in serum and on the surface of leukocytes and platelets in venous thromboembolism. The levels of circulating integrins β1, 2, and 3 are positively correlated with adhering integrins. It showed excellent clinical diagnostic performance of circulating integrins β1, 2, and 3 in venous thromboembolism. Conclusions. Integrin subunit β can be used as a diagnostic marker with high sensitivity and specificity for venous thromboembolism.

BACKGROUND The study aimed to investigate the relationship between the aerobic exercise intensity determined by 6-minute walking distance (6MWD) and its counterpart based on anaerobic threshold (AT) in chronic heart failure (CHF) individuals for exploring suitable means for CHF exercise rehabilitation. METHODS We retrospectively analyzed data in patient with CHF, who performed cardiopulmonary exercise test (CPET) and 6-minute walking test (6MWT) uniformly. Anthropometric characteristics, left ventricular ejection fraction (LVEF), and multiple parameters of 6MWT and AT were collected. RESULTS The results of the analysis revealed that the 6MWD was correlated with the AT positively [CHF group: r=0.433, heart failure with reduced ejection fraction (HFrEF) group: r=0.395, heart failure with intermediate ejection fraction (HFmEF) group: r=0.477, heart failure with preserved ejection fraction (HFpEF) group: r=0.445; all P

With the development and improvement of new techniques in cell biology, molecular biology and biostatistics, increasing studies have been conducted to investigate the mechanism of venous thromboembolism (VTE). Some studies have found that the pathogenesis of VTE is largely related to the abnormality of the immune system as demonstrated by the thrombosis in mice infected with H1N1 influenza and the changes in the expression of genes related to immune system. According to the protein-protein interaction analysis of the differential expression of the immune system in VTE patients, the presence of venous thrombosis was related to the abnormal expression of molecules in JAK/STAT signaling pathway. We discussed the mechanism of VTE and provided two novel therapeutic targets for venous thrombosis: AKT1 and AOX1. Our review may be helpful for better understanding of the current research status of VTE, and provide evidence on the molecular mechanism of VTE.

Context: The pathogenesis of cardiomyocyte death is closely associated with mitochondrial homeostasis via poorly understood mechanisms.Objective: The aim of our study is to explore the contribution of large tumor suppressor kinase 2 (LATS2) to the apoptosis of cardiomyocyte H9C2 cells.Materials and Methods: Adenovirus-mediated LATS2 overexpression was carried out in H9C2 cells. The cell viability and apoptosis rate were measured via an MTT assay, TUNEL staining, western blotting, an ELISA, and an LDH release assay. Mitophagy was quantified using immunofluorescence and western blotting.Results: The overexpression of LATS2 in H9C2 cells drastically promoted cell death. Molecular investigations showed that LATS2 overexpression was associated with mitochondrial injury, as evidenced by increased mitochondrial ROS production, reduced antioxidant factor levels, increased cyt-c liberation into the nucleus and activated mitochondrial caspase-9-dependent apoptotic pathway activity. Furthermore, our results demonstrated that LATS2-mediated mitochondrial malfunction by repressing mitophagy and that the reactivation of mitophagy could sustain mitochondrial integrity and homeostasis in response to LATS2 overexpression. Furthermore, we found that LATS2 inhibited mitophagy by inactivating the Prx3-Mfn2 axis. The reactivation of Prx3-Mfn2 pathways abrogated the LATS2-mediated inhibition of mitochondrial apoptosis in H9C2 cells.Conclusions: The overexpression of LATS2 induces mitochondrial stress by repressing protective mitophagy in a manner dependent on Prx3-Mfn2 pathways, thus reducing the survival of H9C2 cells.

Background Long noncoding RNA urothelial cancer‐associated 1 (lnc‐UCA1) targets microRNA‐26a (miR‐26a) and microRNA‐195 (miR‐195) to participate in coronary heart disease (CHD) progression via regulation of vascular smooth muscle cell and microvascular endothelial cell viability and mobility. Therefore, this study set out to further explore the relationship between lnc‐UCA1 and miR‐26a and miR‐195, along with their roles in the management of patients with CHD. Methods One hundred and thirty‐six CHD patients and 70 age‐/gender‐matched controls were recruited in this case‐control study. Their peripheral blood mononuclear cell samples were collected for lnc‐UCA1, miR‐26a, and miR‐195 measurement. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecules measurement. The Gensini score was used to evaluate the stenosis severity in CHD patients. Results Lnc‐UCA1 expression tend to be increased, while miR‐26a and miR‐195 expressions were reduced in patients with CHD compared to that of controls (all p, There were 136 coronary heart disease (CHD) patients and 70 age‐/gender‐matched controls constitutively recruited. Their peripheral blood mononuclear cell samples were collected for long noncoding RNA urothelial cancer‐associated 1 (lnc‐UCA1), microRNA‐26a (miR‐26a), and microRNA‐195 (miR‐195) measurement. Besides, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecules measurement. Lnc‐UCA1 expression was increased, while miR‐26a and miR‐195 expressions were reduced in CHD patients compared to controls. In CHD patients, lnc‐UCA1 negatively correlated with miR‐26a and miR‐195. Besides, lnc‐UCA1 positively correlated, while miR‐26a and miR‐195 negatively correlated with Gensini score. Moreover, lnc‐UCA1 positively correlated with total cholesterol (TC), low‐density lipoprotein cholesterol (LDL‐C), C‐reactive protein (CRP), tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, vascular cell adhesion molecule‐1 (VCAM‐1), and intercellular adhesion molecule‐1 (ICAM‐1), while miR‐26a negatively correlated with TNF‐α, IL‐6, VCAM‐1, and ICAM‐1. Also, miR‐195 negatively correlated with IL‐1β and ICAM‐1. These findings suggest that lnc‐UCA1, miR‐26a, and miR‐195 may serve as potential biomarkers for CHD patients’ management.

Purpose To develop a weakly supervised deep learning (WSDL) method that could utilize incomplete/missing survival data to predict the prognosis of extranodal natural killer/T cell lymphoma, nasal type (ENKTL) based on pretreatment 18F-FDG PET/CT results. Methods One hundred and sixty-seven patients with ENKTL who underwent pretreatment 18F-FDG PET/CT were retrospectively collected. Eighty-four patients were followed up for at least 2 years (training set = 64, test set = 20). A WSDL method was developed to enable the integration of the remaining 83 patients with incomplete/missing follow-up information in the training set. To test generalization, these data were derived from three types of scanners. Prediction similarity index (PSI) was derived from deep learning features of images. Its discriminative ability was calculated and compared with that of a conventional deep learning (CDL) method. Univariate and multivariate analyses helped explore the significance of PSI and clinical features. Results PSI achieved area under the curve scores of 0.9858 and 0.9946 (training set) and 0.8750 and 0.7344 (test set) in the prediction of progression-free survival (PFS) with the WSDL and CDL methods, respectively. PSI threshold of 1.0 could significantly differentiate the prognosis. In the test set, WSDL and CDL achieved prediction sensitivity, specificity, and accuracy of 87.50% and 62.50%, 83.33% and 83.33%, and 85.00% and 75.00%, respectively. Multivariate analysis confirmed PSI to be an independent significant predictor of PFS in both the methods. Conclusion The WSDL-based framework was more effective for extracting 18F-FDG PET/CT features and predicting the prognosis of ENKTL than the CDL method.

Learning with game-based interactive strategies becomes a popular trend in this mobile era. Especially for young children to acquire linguistic awareness, practicing through games can be more light-hearted and engaging. This study investigates the effectiveness of hand-eye coordination training with game-based interactive learning and multi-touch technology on orthographic awareness in an online study environment for preschool children. Field experiments in real online teaching scenarios were conducted with a large sample size of 1712 K5 preschool students in total. Our results showed a significant improvement in the orthographic awareness performance for the group which participated in the hand-eye coordination training. We conclude that the practice of visual-motor integration skills with the interactive game approach has a positive effect on orthographic awareness cultivation.

Systemic vasculitis is a heterogeneous group of multisystem autoimmune disorders characterized by inflammation of blood vessels. Although many progresses in diagnosis and immunotherapies have been achieved over the past decades, there are still many unanswered questions about vasculitis from pathological understanding to more advanced therapeutics. Extracellular vesicles (EVs) are double-layer phospholipid membrane vesicles harboring various cargoes. EVs can be classified into exosomes, microvesicles (MVs), and apoptotic bodies depending on their size and origin of cellular compartment. EVs can be released by almost all cell types and may be involved in physical and pathological processes including, inflammation and autoimmune responses. In systemic vasculitis, EVs may have pathogenic involvement in inflammation, autoimmune responses, thrombosis, endothelium injury, angiogenesis and intimal hyperplasia. EV-associated redox reaction may also be involved in vasculitis pathogenesis by inducing inflammation, endothelial injury and thrombosis. Additionally, EVs may serve as specific biomarkers for diagnosis or monitoring of disease activity and therapeutic efficacy, i.e. AAV-associated renal involvement. In this review, we have discussed the recent advances of EVs, especially their roles in pathogenesis and clinical involvements in vasculitis.

Objective Atrial fibrillation (AF) and sinus node dysfunction (SND) have common underlying pathophysiological mechanisms. As an index of SND, corrected sinus node recovery time (CSNRT) may also reflect atrial function. The aim of the present study was to determine whether CSNRT predicts AF recurrence in patients undergoing AF ablation. Methods Consecutive patients with paroxysmal atrial fibrillation (PAF) who underwent radiofrequency catheter ablation between January 2017 and December 2018 were enrolled. Clinical data, CSNRT, and other electrophysiology indices were collected and analysed between patients with or without AF recurrence. Results A total of 159 patients with PAF who underwent the same radiofrequency catheter ablation procedure were enrolled, including 25 patients with SND. During the one-year follow-up period, 22 patients experienced AF recurrence. Patients with recurrence had a significantly longer CSNRT and a larger left atrial volume index (LAVI) than patients without AF recurrence. SND (CSNRT > 550 ms) and a larger LAVI were independently associated with AF recurrence after ablation. A statistically significant CSNRT cut-off value of 550 ms predicted AF recurrence with 73% sensitivity and 85% specificity. Conclusion CSNRT and LAVI are independent predictors of PAF recurrence following ablation.

Repeated practice is fundamental to the acquisition of skills, which is typically accompanied by increasing reliability of neural representations that manifested as more stable activation patterns for the trained stimuli. However, large-scale neural pattern induced by learning has been rarely studied. Here, we investigated whether global connectivity patterns became more reliable as a result of motor learning using a novel analysis of the multivariate pattern of functional connectivity (MVPC). Human participants were trained with a finger-tapping motor task for five consecutive days and went through Functional magnetic resonance imaging (fMRI) scanning before and after training. We found that motor learning increased the whole-brain MVPC stability of the primary motor cortex (M1) when participants performed the trained sequence, while no similar effects were observed for the untrained sequence. Moreover, the increase of MVPC stability correlated with participants’ improvement in behavioral performance. These findings suggested that the acquisition of motor skills was supported by the increased connectivity pattern stability between the M1 and the rest of the brain. In summary, our study not only suggests global neural pattern stabilization as a neural signature for effective learning but also advocates applying the MVPC analysis to reveal mechanisms of distributed network reorganization supporting various types of learning.

Purpose To develop a weakly supervised deep learning (WSDL) method that could utilize incomplete/missing survival data to predict the prognosis of extranodal natural killer/T cell lymphoma, nasal type (ENKTL) based on pretreatment 18F-FDG PET/CT results. Methods One hundred and sixty-seven patients with ENKTL who underwent pretreatment 18F-FDG PET/CT were retrospectively collected. Eighty-four patients were followed up for at least 2 years (training set = 64, test set = 20). A WSDL method was developed to enable the integration of the remaining 83 patients with incomplete/missing follow-up information in the training set. To test generalization, these data were derived from three types of scanners. Prediction similarity index (PSI) was derived from deep learning features of images. Its discriminative ability was calculated and compared with that of a conventional deep learning (CDL) method. Univariate and multivariate analyses helped explore the significance of PSI and clinical features. Results PSI achieved area under the curve scores of 0.9858 and 0.9946 (training set) and 0.8750 and 0.7344 (test set) in the prediction of progression-free survival (PFS) with the WSDL and CDL methods, respectively. PSI threshold of 1.0 could significantly differentiate the prognosis. In the test set, WSDL and CDL achieved prediction sensitivity, specificity, and accuracy of 87.50% and 62.50%, 83.33% and 83.33%, and 85.00% and 75.00%, respectively. Multivariate analysis confirmed PSI to be an independent significant predictor of PFS in both the methods. Conclusion The WSDL-based framework was more effective for extracting 18F-FDG PET/CT features and predicting the prognosis of ENKTL than the CDL method. Supplementary Information The online version contains supplementary material available at 10.1007/s00259-021-05232-3.

Rapid changes in American families have reshaped inequalities in child well-being. This paper examines the unequal consequences of family structures for infant health, focusing on birthweight. Existing studies mainly address the average association between marriage (versus singlehood) and birthweight. I extend the literature by 1) explicitly considering cohabitation and 2) exploring the heterogeneous associations based on mother's likelihood of union formation at conception. Pooling nationally representative data from the National Survey of Family Growth 2011-17, I analyze a sample of recent births (N = 4,376) born to mothers aged between 20 and 49 years. Propensity score methods are used to address selections. Results show that 1) compared to single mothers, married mothers reap birthweight benefits, while cohabiting mothers do not; 2) married mothers with a higher likelihood to marry at conception (i.e., more advantaged) reap even larger birthweight benefits than their low-likelihood counterparts (i.e., less advantaged). Overall, the findings reveal important and nuanced roles of family structure in the reproduction of intergenerational inequality through infant health.

Background: To evaluate the natural innate and adaptive immunity through gene expression and cytology levels in peripheral blood mononuclear cells in patients with acute myocardial infarction (AMI), stable angina pectoris (SAP) and controls. Methods: 210 patients with AMI, 210 with SAP, and 250 clinical controls were recruited. Whole human genome microarray analysis was performed in 20 randomly chosen subjects per group were examined to detect the expressions of complement markers, natural killer cells, T cells and B cells. The quantity of these cells and related cytokines as well as immunoglobulin levels were measured in all subjects. Results: In AMI group, the mRNA expressions of late complement component, markers of natural killer cells, CD3+, CD8+ T cells and B cells were down-regulated, while those of early complement component and CD4+T cells were up-regulated (p

Yb3+–Er3+ and Yb3+–Tm3+ activated novel garnet structure Ca2LaZr2Ga3O12 phosphors were synthesized by solid state reaction and its upconversion luminescence properties were investigated. X-ray diffraction patterns confirmed the synthesized samples were indexed to the garnet structure. The upconversion emission spectra revealed that under 980 nm laser excitation, bright green and blue light had been achieved in Ca2LaZr2Ga3O12:Yb3+,Er3+ and Ca2LaZr2Ga3O12:Yb3+,Tm3+ phosphors, respectively. Yb3+ acted as sensitizers in the upconversion process and did not show its characteristic emission peak. Strong Er3+ and Tm3+ emission peaks were obtained via energy transfer from Yb3+. The possible energy transfer processes of Yb3+ to Er3+ and Tm3+ were discussed. The results indicated that Yb3+–Er3+ and Yb3+–Tm3+ activated Ca2LaZr2Ga3O12 phosphors exhibited excellent upconversion luminescence properties.

The aim of the present study was to evaluate differences in the expression of complement system genes, and serum levels of CH50, C3 and C4 in peripheral blood mononuclear cells from patients with myocardial infarction (AMI), stable angina pectoris (SA) and controls. A total of 100 patients with AMI, 100 with SA and 100 clinical controls were recruited in the present study. In each group, 20 randomly selected individuals were examined using whole human genome microarray analysis to detect the expression of genes of the complement system. The serum levels of CH50, C3 and C4 were measured in all 300 subjects. In the patients with AMI, the expression levels of genes encoding C1qα, C1qβ, C1qγ, C1r, Factor P, C5a (complement component), CR1, integrin αM, integrin αX, integrin β2, C5aR, CRIg (complement receptors) and CD46, CD55 and CD59 (complement regulators) were significantly higher, compared with the respective genes in the SA patients and controls (P

Aims Previously we identified four Tocilizumab mimotopes and antibodies induced by these mimotopes could bind to IL-6R (interleukin-6 receptor) and regulate the downstream signaling pathways. On the basis of obtained research data, we sought to investigate whether the therapeutic strategies by Tocilizumab mimotope vaccination could be effective in the renal fibrosis model and show the desired activity by inhibiting IL-6 signaling in current study. Main methods We immunized the mice with the Tocilizumab mimotope and then performed the unilateral ureteric obstruction (UUO) surgery. Masson-trichrome staining and immunohistochemistry were performed to evaluate the renal fibrosis. The activations and differentiations of F4/80+ cells in the spleens and kidneys were detected by flow cytometry, immunohistochemistry and immunofluorescence. Signaling pathways involved IL-6, pro-fibrotic and ferroptosis were analyzed by immunoblot assay. The free iron and lipid oxidation end product were performed by Prussian blue staining and immunohistochemistry. The injury and apoptosis in the kidneys were evaluated by immunofluorescence. Key findings The results showed the mimotope vaccination could reduce the level of fibrosis, injury and apoptosis by down-regulating the pro-fibrotic proteins, alleviating the activations and differentiations of macrophage F4/80+ cells in UUO models. IL-6/ERK signaling pathway was inhibited with the mimotope vaccination. The ferroptosis inhibited proteins significantly increased after the mimotope vaccination. On the contrary, the levels of free iron and lipid oxidation end product were observed to decrease in the mimotope treatment group. Significance Our results suggested that the Tocilizumab mimotope vaccination might be an alternative therapy to against renal fibrosis.

The current study aimed to identify differentially expressed B cell‑associated genes in peripheral blood mononuclear cells and observe the changes in B cell activation at different stages of coronary artery disease. Groups of patients with acute myocardial infarction (AMI) and stable angina (SA), as well as healthy volunteers, were recruited into the study (n=20 per group). Whole human genome microarray analysis was performed to examine the expression of B cell‑associated genes among these three groups. The mRNA expression levels of 60 genes associated with B cell activity and regulation were measured using reverse transcription‑quantitative polymerase chain reaction. The mRNA expression of the B cell antigen receptor (BCR)‑associated genes, CD45, NFAM, SYK and LYN, were significantly upregulated in patients with AMI; however, FCRL3, CD79B, CD19, CD81, FYN, BLK, CD22 and CD5 mRNA expression levels were significantly downregulated, compared with patients in the SA and control group. The mRNA levels of the T‑independent B cell‑associated genes, CD16, CD32, LILRA1 and TLR9, were significantly increased in AMI patients compared with SA and control patients. The mRNA expression of genes associated with T‑dependent B cells were also measured: EMR2 and CD97 were statistically upregulated, whereas SLAMF1, LY9, CD28, CD43, CD72, ICOSL, PD1, CD40 and CD20 mRNAs were significantly downregulated in AMI group patients compared with the two other groups. Additionally the gene expression levels of B cell regulatory genes were measured. In patients with AMI, CR1, LILRB2, LILRB3 and VAV1 mRNA expression levels were statistically increased, whereas, CS1 and IL4I1 mRNAs were significantly reduced compared with the SA and control groups. There was no statistically significant difference in B cell‑associated gene expression levels between patients with SA and the control group. The present study identified the downregulation of genes associated with BCRs, B2 cells and B cell regulators in patients with AMI, indicating a weakened T cell‑B cell interaction and reduced B2 cell activation during AMI. Thus, improving B2 cell‑mediated humoral immunity may be a potential target for medical intervention in patients with AMI.

Immune activation and inflammation participate in the progression of chronic heart failure (CHF). Th17 cells and CD4+CD25+ regulatory T (Treg) cells both come from naive Th cells and share reciprocal development pathways but exhibit opposite effects. We hypothesized that the Th17/Treg balance was impaired in patients with CHF, and exercise can improve it. Rats with ischemic cardiomyopathy were prepared by ligaturing the left anterior descending branch of the left coronary artery. Rats in training group were trained with treadmill; Th17 cells increased significantly while Treg cells significantly decreased in s by flow cytometry, and the peripheral blood level of IL-6, IL-17, and TNF-α was obviously elevated by ELISA assay. We found that Th17/Treg balance is impaired in CHF rats, suggesting Th17/Treg imbalance potentially plays a role in the pathogenesis of CHF. Exercise can improve Th17/Treg imbalance, which also improves cardiac function of CHF.

The minute ventilation/carbon dioxide production (VE/VCO2) slope has been widely demonstrated to have strong prognostic value in patients with chronic heart failure (CHF), and the risk of mortality is believed to increase when the VE/VCO2 slope is >32.8; however, there is little evidence concerning the prognostic value of the VE/VCO2 slope in Chinese patients. In the present study, the prognostic value of the VE/VCO2 slope was investigated in patients with CHF. A total of 258 subjects underwent symptom-limited cardiopulmonary exercise testing (CPET) and were divided into CHF (113 males and 16 females; LVEF

The aim of the present study was to explore the function and interaction of differentially expressed genes (DEGs) in pulmonary embolism (PE). The gene expression profile GSE13535, was downloaded from the Gene Expression Omnibus database. The DEGs 2 and 18 h post‑PE initiation were identified using the affy package in R software. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the DEGs were analyzed using Database for Annotation Visualization and Integrated Discovery (DAVID) online analytical tools. In addition, protein‑protein interaction (PPI) networks of the DEGs were constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins. The PPI network at 18 h was modularized using Clusterone, and a functional enrichment analysis of the DEGs in the top three modules was performed with DAVID. Overall, 80 and 346 DEGs were identified 2 and 18 h after PE initiation, respectively. The KEGG pathways, including chemokine signaling and toll‑like receptor signaling, were shown to be significantly enriched. The five highest degree nodes in the PPI networks at 2 or 18 h were screened. The module analysis of the PPI network at 18 h revealed 11 hub nodes. A Gene Ontology terms analysis demonstrated that the DEGs in the top three modules were associated with the inflammatory, defense and immune responses. The results of the present study suggest that the DEGs identified, including chemokine‑related genes TFPI2 and TNF, may be potential target genes for the treatment of PE. The chemokine signaling pathway, inflammatory response and immune response were explored, and it may be suggested that these pathways have important roles in PE.

Objectives: This study's aim was to evaluate the protective effects of salvianolate on contrast-induced nephropathy after primary percutaneous coronary intervention (PPCI) compared with normal saline (NS) hydration. Methods: We enrolled patients with acute myocardial infarction who underwent PPCI in 3 centers in Shanghai. The patients were randomly assigned to the salvianolate group or the NS group. The incidence of CIN, the changes in renal function parameters, and the occurrence of adverse events after the procedure were compared between the 2 groups. We used a multivariate logistic regression analysis to determine the independent correlates of CIN after PPCI. Results: A total of 484 patients were finally included in the statistical analysis. Compared with the control group, salvianolate reduced the incidence of CIN (9.1 vs. 16.3%, p = 0.018) after PPCI. The renal function parameters after PPCI in the salvianolate group were superior to those of the control group (p < 0.05). The composite adverse events rate was significantly lower in the salvianolate group within 1 month after the procedure (9.5 vs. 15.5%, p = 0.046). A higher peak of troponin I and loop diuretic therapy were the independent correlates of CIN after PPCI. Conclusions: Salvianolate reduces the incidence of CIN and protects renal function after PPCI, and the effects were superior to those of NS hydration.

We demonstrate a strong enhancement of second harmonic generation based on a three-layered super absorbing metasurface consisting of a dielectric spacer layer sandwiched by an array of random metallic nanoparticles and a metal ground plate.

Introduction and Objectives: Recent studies have shown that the major risk factors for arterial thrombotic diseases are closely associated with venous thromboembolism (VTE). This study aimed to investigate the expression of CD3, CD4 and CD8 in T lymphocytes, the CD4/CD8 ratio and high-sensitivity C-reactive protein (hs-CRP) levels in patients with VTE, coronary artery atherosclerosis (CAA) and healthy subjects. Methods: A total of 82 healthy subjects, 51 VTE patients and 114 CAA patients were recruited, and the expression of CD3, CD4 and CD8 in T lymphocytes and the CD4/CD8 ratio were determined. Serum hs-CRP was also measured. Results: Compared to healthy subjects, VTE patients had significantly reduced CD3 expression (p=0.019), comparable CD4 expression (p=0.868), significantly reduced CD8 expression (p

Background Atherosclerosis is a chronic inflammatory process, in which oxidative stress is the key event. Gamma-glutamyl transferase (GGT) is a cellular production of oxidants. We aimed to elucidate the relationship of serum GGT levels and coronary artery disease (CAD) in a Chinese population. Material/Methods A total of 513 adult subjects who had undergone coronary angiography were enrolled in the study. Clinical characteristics, coronary angiography, and serum samples were collected from all the patients and analyzed for the serum GGT, blood lipids, and cardiovascular risk factors. Results Subjects with CAD had significantly increased activity of serum GGT (p=0.003). Serum GGT levels exhibited positive correlations with alcohol intake (β=0.177, p

This article summarized our recent progress in theoretical designs for achieving super absorption in ultra-thin organic photovoltaic (OPV) films based on various planar OPV-on-metal and metal-OPV-metal structures. Three different structures were numerically simulated to demonstrate strongly enhanced optical absorption in ultra-thin OPV layers, which is polarization-independent and occurs over a wide range of incident angles in visible regime. Physical mechanisms associated with these super absorptive ultra-thin layers are analyzed and validated using numerical and analytical modeling.

Atrial fibrillation (AF) is the most common form of sustained cardiac arrhythmia in humans and is responsible for substantial morbidity and mortality worldwide. Emerging evidence indicates that abnormal cardiovascular development is involved in the pathogenesis of AF. In this study, the coding exons and splice sites of the NKX2-5 gene, which encodes a homeodomain-containing transcription factor essential for cardiovascular genesis, were sequenced in 146 unrelated patients with lone AF as well as the available relatives of the mutation carriers. A total of 700 unrelated ethnically matched healthy individuals used as controls were genotyped. The disease-causing potential of the identified NKX2-5 variations was predicted by MutationTaster and PolyPhen-2. The functional characteristics of the mutant NKX2-5 proteins were analyzed using a dual-luciferase reporter assay system. As a result, two heterozygous NKX2-5 mutations, including a previously reported p.E21Q and a novel p.T180A mutation, were identified in two families with AF transmitted in an autosomal dominant pattern. The mutations co-segregated with AF in the families with complete penetrance. The detected substitutions, which altered the amino acids highly conserved evolutionarily across species, were absent in 700 control individuals and were both predicted to be causative. Functional analyses demonstrated that the NKX2-5 mutants were associated with significantly decreased transcriptional activity compared with their wild-type counterpart. The findings expand the spectrum of NKX2-5 mutations linked to AF and provide additional evidence that dysfunctional NKX2-5 may confer vulnerability to AF, suggesting the potential benefit for the early prophylaxis and personalized treatment of AF.

Introduction We aim to compare the midterm outcomes between coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) in diabetic patients who had multivessel coronary artery diseases (CAD).

Introduction Pulmonary embolism (PE) is a disease with a high mortality and morbidity rate, and the pathogenesis of PE remains still unclear. We aimed to investigate the gene expression differences of the complement system in peripheral blood mononuclear cells (PBMCs) from patients with symptomatic PE and controls. Methods Twenty cases of PE patients and twenty sex and age matched controls were recruited into the study. Human cDNA microarray analysis was used to detect the gene expression difference of the complement system between the two groups. Results 1). Expression of twenty-one genes encoding complement components was detected. In PE patients, expression of the genes encoding C1qα, C1qβ, C4b, C5 and Factor P was significantly greater (P

We proposed a dielectric grating that can launch surface plasmon resonance mode efficiently on the other side of flat metal films with normal incident light, which is suitable for the integration with optical fiber tips.

BACKGROUND: In the present study, the whole human genome oligo microarray was employed to investigate the gene expression profile in symptomatic pulmonary embolism (PE). METHODS: Twenty patients with PE and 20 age and gender matched patients without PE as controls were enrolled into the present study in the same period. The diagnosis of PE was based on the clinical manifestations and findings on imaging examinations. Acute arterial and/or venous thrombosis was excluded in controls. The whole human genome oligo microarray was employed for detection. Statistical analysis was performed with t test following analysis of very small samples of repeated measurements and Gene Ontology (GO) analysis. RESULTS: Genomic data showed no damage to vascular endothelial cells in PE patients. Genomic data only found increased mRNA expression of a small amount of coagulation factors in PE patients. In the PE group, anticoagulant proteins, Fibrinolytic system and proteins related to platelet functions only played partial roles in the pathogenesis of PE. In addition, the mRNA expressions of a fraction of adhesion molecules were markedly up-regulated. Gene Ontology analysis showed the genes with down-regulated expressions mainly explain the compromised T cell immunity. Symptomatic VTE patients have compromised T cell immunity. CONCLUSION: The damage to vascular endothelial cells is not necessary in the pathogenesis of VTE, and only a fraction of factors involved in the shared coagulation cascade are activated. Genomic results may provide a new clue for clinical diagnosis, treatment and prevention of VTE.

The aim of this study was to identify the differences in the expression of cell adhesion molecule-related mRNAs between symptomatic pulmonary embolism (PE) and a control group, and to investigate the interactions among activated leukocytes, platelets and endothelial cells. Whole human gene chip was applied to detect the expression of cell adhesion molecule-related mRNAs in symptomatic PE and in the control group, and statistical analysis was performed. In patients with PE, the expression of the majority of integrin mRNAs located on leukocytes and platelets was significantly upregulated. The expression of mRNAs related to L-selectin and P-selectin glycoprotein ligand was significantly upregulated, while the expression of mRNA related to E-selectin was significantly downregulated. The expression of mRNAs related to classic cadherins and protocadherins was downregulated, and the expression of mRNAs related to vascular endothelial cadherin was significantly downregulated; the expression of mRNAs related to the immunoglobulin superfamily had no obvious difference between the 2 groups. In conclusion, we demonstrated that, in symptomatic PE patients, the adhesion of leukocytes and platelets was enhanced; the activation of endothelial cells was obviously weakened; the adherens junctions among endothelial cells were weakened, with the endothelium becoming more permeable.