Interannual characteristics and driving mechanism of CO2 fluxes during the growing season in an alpine wetland ecosystem at the southern foot of the Qilian Mountains.

The carbon process of the alpine ecosystem is complex and sensitive in the face of continuous global warming. However, the long-term dynamics of carbon budget and its driving mechanism of alpine ecosystem remain unclear. Using the eddy covariance (EC) technique-a fast and direct method of measuring carbon dioxide (CO2) fluxes, we analyzed the dynamics of CO2 fluxes and their driving mechanism in an alpine wetland in the northeastern Qinghai-Tibet Plateau (QTP) during the growing season (May-September) from 2004-2016. The results show that the monthly gross primary productivity (GPP) and ecosystem respiration (Re) showed a unimodal pattern, and the monthly net ecosystem CO2 exchange (NEE) showed a V-shaped trend. With the alpine wetland ecosystem being a carbon sink during the growing season, that is, a reservoir that absorbs more atmospheric carbon than it releases, the annual NEE, GPP, and Re reached -67.5 ± 10.2, 473.4 ± 19.1, and 405.9 ± 8.9 gCm-2, respectively. At the monthly scale, the classification and regression tree (CART) analysis revealed air temperature (Ta) to be the main determinant of variations in the monthly NEE and GPP. Soil temperature (Ts) largely determined the changes in the monthly Re. The linear regression analysis confirmed that thermal conditions (Ta, Ts) were crucial determinants of the dynamics of monthly CO2 fluxes during the growing season. At the interannual scale, the variations of CO2 fluxes were affected mainly by precipitation and thermal conditions. The annual GPP and Re were positively correlated with Ta and Ts, and were negatively correlated with precipitation. However, hydrothermal conditions (Ta, Ts, and precipitation) had no significant effect on annual NEE. Our results indicated that climate warming would be beneficial to the improvement of GPP and Re in the alpine wetland, while the increase of precipitation can weaken this effect.

Transcriptome Profiling Reveals PHLDA1 as a Novel Molecular Marker for Ischemic Cardiomyopathy.

Ischemic cardiomyopathy (ICM) represents a worldwide health issue owning to its high sudden death rate. Easy diagnosis and effective treatment of ICM are still lacking. Identification of novel molecular markers will help illustrate the pathophysiology of ICM and facilitate its diagnosis and targeted treatment. Transcription profiling could be an easy and efficient way for identifying new markers. However, the mega data in the available database may contain a large number of false-positive hits. To identify the true marker for ICM, we systematically compared available microarray datasets in the GEO database and identified 26 genes that are shared by all datasets. We further verified the expression pattern of these 26 genes in ICM rat model. Only 12 genes show significant differential expression in our animal model. Among them, we focused on PHLDA1, a well-documented pro-apoptotic factor. Expression of PHLDA1 was elevated in both ischemic cardiac cell lines and in rat model. Overexpression of PHLDA1 promotes apoptosis of cardiac muscle cell. Meanwhile, PHLDA1 not only inhibited AKT pathway, but also activated p53 pathway. We thus confirmed PHLDA1 as a true molecular marker for ICM.

Inhibition of Cardiomyocytes Hypertrophy by Resveratrol Is Associated with Amelioration of Endoplasmic Reticulum Stress.

BACKGROUND/AIMS: Resveratrol (Res), a polyphenol antioxidant found in red wine, has been shown to play a cardioprotective role. This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress. METHODS: Cardiomyocytes were randomly assigned to the control group, ISO group (100 nM ISO for 48 h), Res + ISO group (50 µM Res and 100 nM ISO for 48 h) and Res group (50 µM Res for 48h only). Hypertrophy was estimated by measuring the cell surface area and the atrial natriuretic peptide (ANP) gene expression. Apoptosis was measured using Hoechst 33258 staining and transmission electron microscopy. Protein expression of ER stress and apoptosis factors was analyzed using Western Blot analysis. RESULTS: Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. CONCLUSION: In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress.