In this paper is proved a weighted inequality for Riesz potential similar to the classical one by D. Adams. Here the gain of integrability is not always algebraic, as in the classical case, but depends on the growth properties of a certain function measuring some local potential of the weight.
Alkali stress is an important agricultural problem that affects plant metabolism, specifically root physiology. In this study, using two rice cultivars differing in alkali resistance, we investigated the physiological and molecular responses of rice plants to alkali stress. Compared to the alkali-sensitive cultivar (SC), the alkali-tolerant cultivar (TC) maintained higher photosynthesis and root system activity under alkali stress. Correspondingly, the Na+ content in its shoots was much lower, and the contents of mineral ions (e.g., K+, NO3-, and H2PO4-) in its roots was higher than those of the SC. These data showed that the metabolic regulation of roots might play a central role in rice alkali tolerance. Gene expression differences between the cultivars were much greater in roots than in shoots. In roots, 46.5% (20 of 43) of selected genes indicated over fivefold expression differences between cultivars under alkali stress. The TC had higher root system activity that might protect shoots from Na+ injury and maintain normal metabolic processes. During adaptation of TC to alkali stress, OsSOS1 (salt overly sensitive protein 1) may mediate Na+ exclusion from shoots or roots. Under alkali stress, SC could accumulate Na+ up to toxic concentrations due to relatively low expression of OsSOS1 in shoots. It possibly harmed chloroplasts and influenced photorespiration processes, thus reducing NH4+ production from photorespiration. Under alkali stress, TC was able to maintain normal nitrogen metabolism, which might be important for resisting alkali stress., H. Wang, X. Lin, S. Cao, Z. Wu., and Obsahuje bibliografii
This study aimed to examine the effect of eicosapentaenoic acid (EPA) on skeletal muscle hypertrophy induced by muscle overload and the associated intracellular signaling pathways. Male C57BL/6J mice were randomly assigned to oral treatment with either EPA or corn oil for 6 weeks. After 4 weeks of treatment, the gastrocnemius muscle of the right hindlimb was surgically removed to overload the plantaris and soleus muscles for 1 or 2 weeks. We examined the effect of EPA on the signaling pathway associated with protein synthesis using the soleus muscles. According to our analysis of the compensatory muscle growth, EPA administration enhanced hypertrophy of the soleus muscle but not hypertrophy of the plantaris muscle. Nevertheless, EPA administration did not enhance the expression or phosphorylation of Akt, mechanistic target of rapamycin (mTOR), or S6 kinase (S6K) in the soleus muscle. In conclusion, EPA enhances skeletal muscle hypertrophy, which can be independent of changes in the AKT-mTOR-S6K pathway.
Acute myocardial infarction (AMI) represents the acute manifestation of coronary artery disease. In recent years, microRNAs (miRNAs) have been extensively studied in AMI. This study focused on the role of miR-431-5p in AMI and its effect on cardiomyocyte apoptosis after AMI. The expression of miR-431-5p was analyzed by quantitative real-time PCR (qRT-PCR). By interfering with miR-431-5p in hypoxiareoxygenation (H/R)-induced HL-1 cardiomyocytes, the effect of miR-431-5p on cardiomyocyte apoptosis after AMI was examined. The interaction between miR-431-5p and selenoprotein T (SELT) mRNA was verified by dual-luciferase reporter assay. Cell apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and flow cytometry. Cell viability was examined by 3-(4,5)- dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay. The results of qRT-PCR showed that the expression of miR-431-5p in AMI myocardial tissues and H/R-induced HL-1 cardiomyocytes was significantly increased. After interfering with miR-431-5p, the expression of SELT in HL-1 cells was up-regulated, cell apoptosis was decreased, cell viability was increased, and lactate dehydrogenase (LDH) activity was decreased. The dual-luciferase reporter assay confirmed the targeting relationship between miR-431-5p and SELT1 3’ untranslated region (UTR). In H/R-induced HL-1 cells, the simultaneous silencing of SELT and miR-431-5p resulted in a decrease of Bcl-2 expression, an increase of Bax expression, and an increase of cleaved-caspase 3 expression compared with silencing miR-431-5p alone. Also, cell viability was decreased, while LDH activity was increased by the simultaneous silencing of SELT and miR-431-5p. Interfering miR-431-5p protected cardiomyocytes from AMI injury via restoring the expression of SELT, providing new ideas for the treatment of AMI.