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The primary productivity of seasonal ice-covered water bodies is an important variable for understanding how temperate lake ecosystems are changing due to global warming. But there have been few studies on the complete change process of primary productivity during the ice-covered period, and the connection between ice physical and associated biological production has not been fully understood. In this study, a Vertically Generalized Production Model (VGPM) suitable for the ice-covered period was used to calculate the primary productivity of a temperate lake, and the key physical controlling factor was analyzed in the process of primary productivity change in the ice-covered period. The results showed that there was a high level of primary productivity, (189.1 ± 112.6) mg C·m−2·d−1, under the ice in the study site, Hanzhang Lake. The phytoplankton production under the ice was not as severely restricted by light as commonly thought. The water temperature played a more crucial role in the changes of primary productivity than the light beneath the ice. The study highlighted the variability in primary productivity covering the whole ice-covered age, and provided a better understanding of how the aquatic environment of lakes in seasonal ice-covered areas was affected by warmer temperatures. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Yb-Er and Yb-Tm activated novel garnet structure CaLaZrGaO 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 CaLaZrGaO:Yb,Er and CaLaZrGaO:Yb,Tm phosphors, respectively. Yb acted as sensitizers in the upconversion process and did not show its characteristic emission peak. Strong Er and Tm emission peaks were obtained via energy transfer from Yb. The possible energy transfer processes of Yb to Er and Tm were discussed. The results indicated that Yb-Er and Yb-Tm activated CaLaZrGaO phosphors exhibited excellent upconversion luminescence properties. [ABSTRACT FROM AUTHOR]

Intracranial hemorrhage remains the most feared complication in tissue plasminogen activator (tPA) thrombolysis for ischemic stroke. However, the underlying molecular mechanisms are still poorly elucidated. In this study, we reported an important role of caveolin-1 (Cav-1) s-nitrosylation in matrix metalloproteinase (MMP)-2 and 9 secretion from tPA-treated ischemic endothelial cells. Brain vascular endothelial cells (bEND3) were exposed to oxygen-glucose deprivation (OGD) for 2 h before adding recombinant human tPA for 6 h. This treatment induced a significant increase of MMP2 and 9 in the media of bEND3 cells and a simultaneous degradation of fibronectin and laminin β-1, the two main components of extracellular matrix (ECM). Inhibition of MMP2 and 9 with SB-3CT completely blocked the degradation of fibronectin and laminin β-1. ODG+tPA treatment led to Cav-1 shedding from bEND3 cells into the media. Notably, OGD triggered nitric oxide (NO) production and S-nitrosylationof Cav-1 (SNCav-1). Meanwhile tPA induced activation of ERK signal pathway and stimulates the secretion of SNCav-1. Pretreatment of bEND3 cells with C-PTIO (a NO scavenger) or U0126 (a specific ERK inhibitor) significantly reduced OGD-induced S-nitrosylation of Cav-1 in cells and blocked the secretion of Cav-1 and MMP2 and 9 into the media as well as the degradation of fibronectin and laminin β-1 in OGD and tPA-treated cells. These data indicate that OGD-triggered Cav-1 S-nitrosylation interacts with tPA-induced ERK activation to augment MMP2 and 9 secretion and subsequent ECM degradation, which may account for the exacerbation of ischemic blood brain barrier damage following tPA thrombolysis for ischemic stroke. [ABSTRACT FROM AUTHOR]

Background: Cardiopulmonary exercise testing has been widely used to risk stratify patients with chronic heart failure (CHF). Peak oxygen consumption (peakVO2) was regarded as a powerful predictor of survival, as it is a surrogate for peak cardiac output (CO), which by most is considered the “true” measure of heart failure. Therefore, it is reasonable to hypothesize that CO is an even stronger predictor than peak VO2. The present study is aimed to investigate the prognostic value of peak cardiac power output (peak CPO) in comparison with peakVO2 in Chinese patients with CHF. Methods: Participants provided written informed consent to participate in this study. Totally 129 patients with CHF underwent symptom-limited cardiopulmonary exercise testing (CPET), with mean age 59.1±11.4 years, 87.6% male, 57.4% ischemic etiology, body mass index (BMI) 24.7±3.7 kg/m2 and LVEF 38±9%. CO was measured using an inert gas rebreathing method. The primary endpoints are cardiac deaths. Results: Over median 33.7-month follow-up, 19 cardiac deaths were reported. Among peak VO2,VE/VCO2 slope and Peak CPO, their area under ROC were 0.64, 0.67, 0.68, respectively (Ρ<0.05).The optimal thresholds for predicting cardiac deaths were peak VO2≤13.4 ml.kg-1.min-1, and VE/VCO2 slope≥39.3 and peak CPO≤ 1.1 respectively by ROC analysis. Finally, in patients with a peak VO2≤13.4 ml.kg-1.min-1 those with peak CPO>1.1W had better survival than those with peak CPO ≤ 1.1W. However, by multivariate analysis adjusted for age, sex, BMI, resting heart rate, LVMI, LVEF, Peak CPO was not an independent predictor of cardiac deaths (P> 0.05). Conclusions: Peak CPO was not a predictor of cardiac death in Chinese CHF patients. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Mimotope, a kind of peptide vaccine, is developed to bind natural receptor and inhibit the downstream signaling. We have demonstrated that the vaccination of Tocilizumab mimotopes could alleviate the renal fibrosis by interfering with both IL-6 and ferroptosis signaling. However, the effect of the vaccination of Tocilizumab mimotopes on the fibroblast was not investigated in previous study. Thus, we sought to explore the changes in the fibroblast induced by the Tocilizumab mimotopes vaccination. Bleomycin instillation was performed to construct the pulmonary fibrosis model after the immunization of Tocilizumab mimotopes. Lung histological analysis showed that the Tocilizumab mimotopes could significantly reduce the maladaptive repairment and abnormal remodeling. Immunoblotting assay and fluorescence staining showed that Immunization with the Tocilizumab mimotopes reduces the accumulation of fibrosis-related proteins. High level of lipid peroxidation product was observed in the animal model, while the Tocilizumab mimotopes vaccination could reduce the generation of lipid peroxidation product. Mechanism analysis further showed that Nrf-2 signaling, but not GPX-4 and FSP-1 signaling, was upregulated, and reduced the lipid peroxidation. Our results revealed that in the BLM-induced pulmonary fibrosis, high level of lipid peroxidation product was significantly accumulation in the lung tissues, which might lead to the occurrence of ferroptosis. The IL-6 pathway block therapy could inhibit lipid peroxidation product generation in the lung tissues by upregulating the Nrf-2 signaling, and further alleviate the pulmonary fibrosis.

Background: To investigate the protective efficacy of miR-155 on down regulating NADPH oxidase isoform subunit A1 (NoxA1) gene expression, resulting in inhibition of VSMC migration and over proliferation and thus ameliorating the progression of arterial atherosclerosis in AS mouse model. Therefore, to further explore the regulatory effect of miR-155 on neointima formation in AS and locate potential anti-atherosclerosis target., Methods: The mouse vascular aorta smooth muscle cell (MOVAS) was cultured and transfected with recombinant Pad2YFG adenovirus fluorescent vector with miR-155 fragment into 4 groups. Western blotting and RT-PCR were performed to identify the expression of NoxA1 under different circumstances. Fluorescence microscope was applied to observe the transfection rate of miR-155 into adenovirus. Twelve-week fatty food induced atherosclerotic ApoE -/- mouse model was established as host to accept miR-155 transfected adenovirus transplantation to observe its effect on VSMC in AS progression. Carotid and thoracic artery were extracted at 1 month after dosing. Distribution of miR-155 was quantified via expression levels of protein and RNA to detect NoxA1, Nox1, p47phox and NADPH expression. Immunohistochemistry, fluorescence imaging and other methods were performed in arteries section to compare the thickness of neointima and assess the severity of AS in each group., Results: Luciferase reporter gene assay showed significant expression of miR-155 in mimic group indicating that miR-155 had target binding effect with NoxA1 gene. Western blotting and RT-PCR results both showed significantly decreased NoxA1 expression in miR-155 mimic group while increased with its inhibitor. The miR-155 distribution was observed varied at 1 month after in control, miR-155 mimic and inhibitor groups. The NoxA1, NADPH, Nox1 and pp47phox protein expression in VSMC was decreased in mimic group vs control and inhibitor groups (P<0.05); no significant difference of NADPH expression was observed in all groups. The NoxA1, Nox1 and p47phox gene expression in VSMC were both found reduced compared with those of control group at week 4 (P<0.05). Immunohistochemistry staining of artery frozen sections figured out that the thickness of neointima of carotid artery in miR-155 mimic group was significantly lower vs control and inhibitor groups (P<0.01) at week 4., Conclusions: miR-155 played an important role in NoxA1-related signaling pathway. miR-155 transfection into VSMC may have anti-inflammatory regulatory effect on NoxA1 expression in vivo and resulting in amelioration of atherosclerotic lesion in AS mouse model. In summary, miR-155 specifically plays in a negative feedback loop and demonstrates a protective role during atherosclerosis-associated VSMC proliferation and neointima formation through the miR-155-NoxA1-p47phox complex signaling pathway., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/cdt-20-518). The authors have no conflicts of interest to declare., (2021 Cardiovascular Diagnosis and Therapy. All rights reserved.)

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<0.05). In both AMI and SAP patients, the quantity of natural killer cells, CD3+, CD8+ T cells, B cells, IgM and IgG were significantly lower than those of the controls. CD4+ T cells, CH50, C3, C4, IL-2, IL-4, IL-6 and IFN-γ were significantly higher (p<0.05). Conclusions : In AMI patients, both of gene expressions related to complement, natural killer cells, CD3+, CD8+ T cells, B cells and the quantity of these immune cells decreased while cell number reduced in SAP patients. Immune function in both AMI and SAP patients decreased especially in AMI patients with declined gene and protein levels. To improve the immune system is a potential target for medical interventions and prevention in AMI., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.

The minute ventilation/carbon dioxide production (VE/VCO 2 ) 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/VCO 2 slope is >32.8; however, there is little evidence concerning the prognostic value of the VE/VCO 2 slope in Chinese patients. In the present study, the prognostic value of the VE/VCO 2 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 <0.49) and control (106 males and 23 females) groups. The cardiac-related events over a median 33.7-month follow-up period subsequent to the CPET were evaluated using receiver operating characteristic curve analysis. The VE/VCO 2 slope was significantly different between the CHF and control groups (P<0.001). The area under the curve (AUC) for the VE/VCO 2 slope in predicting cardiac-related mortalities in the patients with CHF was 0.670 (P<0.05), and the sensitivity and specificity of the VE/VCO 2 slope were 0.667 and 0.620, respectively. The optimal threshold of the VE/VCO 2 slope for predicting cardiac-related mortalities in patients with CHF was ≥39.3. The AUC for the VE/VCO 2 slope in predicting cardiac-related hospitalizations in patients with CHF was 0.682 (P<0.05), and the sensitivity and specificity of the VE/VCO 2 slope were 0.631 and 0.778, respectively. The optimal threshold of the VE/VCO 2 slope for predicting cardiac-related hospitalizations in patients with CHF was ≥32.9. In conclusion, ventilatory efficiency decreases in patients with CHF. The VE/VCO 2 slope is a strong predictor of cardiac-related mortalities in the patients with CHF analyzed.

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 and 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<0.001), coronary complexity (β=0.068, p<0.001), and triacylglycerol (β=0.058, p<0.001). High-density lipoprotein cholesterol levels (β=0.157, p=0.008) and age (β=0.004, p=0.002) were negatively correlated with serum GGT in the CAD group. The coronary complexity presented a negative correlation with Ig-apolipoprotein AI (β=-2.517, p=0.001) and positive correlations with smoking (β=0.640, p<0.001), Ig-GGT (β=0.613, p=0.004), Ig high sensitivity-C reactive protein (β=0.320, p<0.001), and hypertension (β=0.286, p<0.026)., Conclusions: The study showed a positive correlation between serum GGT and CAD in a Chinese population. Serum GGT levels may be a potential biomarker for CAD.

The characteristics of human genomics and cellular immune function between clinically symptomatic venous thromboembolism (VTE) and controls were systematically compared to explore the immunologic pathogenesis of VTE. Microarray assay showed the mRNA expressions of genes related to non-specific cellarer immune and cytokines were significantly down-regulated. Abnormal expressions of CD3+, CD4+, CD8+, NK marker CD16+56+, CD19 and aberrant CD4+/CD8+ ratio were detected in 54 among 56 patients. In PE patients, microarray assay revealed the imbalance in the expressions of genes related to the immune system. The expressions of genes related to non-specific immune cells and cytokines were markedly up-regulated and those associated with cellular immune were dramatically down-regulated. In VTE patients, cytological examination indicated the functions of NK cells were significantly compromised, and the antigen recognition and killing function of T cells markedly decreased. The consistence between genomic and cytological examination suggests the symptomatic VTE is closely associated with the infection and immune dysfunction.

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.