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Introduction: Evidence regarding the association between body mass index (BMI) and outcomes in non-cardiothoracic, non-obstetric surgery patients with pulmonary hypertension (PHTN) is limited. We aimed to investigate the association between BMI and 30-day mortality in non-cardiothoracic, non-obstetric surgery patients with pulmonary hypertension. Material and Methods: We performed a secondary analysis of non-cardiothoracic, non-obstetric procedures on patients with PHTN between 2007 and 2013 at a single institution. Multivariable logistic regression models were used to estimate the association between BMI and 30-day mortality. Interaction and stratified analyses were conducted according to age, sex, PHTN medical therapy, anticipated inpatient or outpatient post-procedure status, procedure length > 2 h, open surgical approach, and PHTN severity class. Results: A total of 513 participants were included, with men accounting for 55.8% of the sample; the 30-day mortality was 1.9%. In the multivariate regression models, BMI was significantly associated with 30-day mortality after adjusting for potential covariates. A 1 kg/m2 increase in BMI was associated with a 15% decrease in 30-day mortality (adjusted OR = 0.85, 95% CI: 0.73–0.98, P = 0.03). Stratified analyses indicated that this negative correlation was robust. Conclusions: In this study, we found that low BMI is associated with increased risk of death in patients undergoing non-cardiothoracic, non-obstetric surgery requiring general anesthesia. Further studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

In this paper, the authors establish the boundedness of parametrized Littlewood–Paley area integral and g λ ∗ -function, and their high-order commutators on Herz-type Hardy spaces with variable exponent. These results are also new even for classical Herz-type Hardy space. [ABSTRACT FROM AUTHOR]

Therefore, applying NH4+-N tp PHW-SA caused greater tolerance to Cd toxicity by higher biomass production, photosynthetic capacity, Ca and Cu accumulation, better root development and lower translocation factor of Cd as well as Cd concetration in organelle fraction. The Cd stress inhibited the growth performance of wheat seedlings, the mineral nutrient accumulation, and nitrogen uptake and distribution, and different forms of nitrogen have different protective effects on wheat. In PHW-SA, ANCd treatment caused lower reduction in biomass accumulation, photosynthesis, isotope stable N content, Ca and Cu accumulation, root development inhibition, tissue Cd concentration, and transfer factor, which even led to lower concentrations of Cd in Fco than those in Fcw and Fs in comparison with NNCd treatment. On the other hand, the converse growth performance was recorded in J-11 under ANCd treatment. Meanwhile, the nitrogen absorption preference in PHW-SA was altered along with the enhanced absorption efficiency of nitrogen. Therefore, applying NH4+-N to PHW-SA caused greater tolerance to Cd toxicity by higher biomass production, photosynthetic capacity, Ca and Cu accumulation, better root development and lower translocation factor of Cd as well as Cd concetration in organelle fraction.. [ABSTRACT FROM AUTHOR]

Betaine, a neutral zwitterionic compound, could regulate intramuscular fat (IMF) deposition and meat quality. However, the efficacy is controversial. Moreover, the regulatory mechanism of betaine on lipid metabolism in skeletal muscle cells remains unclear. Therefore, in this study, we examined the effects and regulatory mechanism of betaine on lipid accumulation in adipogenic-differentiated C2C12 cells. We found that adipogenic-induced C2C12 cells treated with 10 mM betaine for 24 and 48 h had more lipid accumulation than the control group. Real-time PCR and Western blot results revealed that betaine treatment did not alter the expression of lipolysis and lipid oxidation-related genes, but dramatically increased the expression of peroxisome proliferator-activated receptor γ (PPARγ) and its target genes such as fatty acid binding protein 4 (aP2), fatty acid synthase (FAS) and lipoprteinlipase (LPL). Furthermore, betaine combined with PPARγ inhibitor GW9662 treatment showed that betaine elevated C2C12 lipid accumulation through upregulation of PPARγ. Mechanistically, we found that betaine promoted PPARγ expression and lipid accumulation through inhibition of extracellular regulated protein kinases1/2 (ERK1/2) signalling pathway. These results demonstrate that betaine acts through ERK1/2-PPARγ signalling pathway to regulate lipid metabolism in adipogenic-differentiated skeletal muscle cells, which could provide some useful information for controlling muscle lipid accumulation by manipulating ERK1/2 and PPARγ signalling pathway. [ABSTRACT FROM AUTHOR]

Excessive intramyocellular triacylglycerols (IMTGs, muscle lipids) are associated with the abnormal energy metabolism and insulin resistance of skeletal muscle. AMP-activated protein kinase (AMPK), a crucial cellular energy sensor, consists of α, β and γ subunits. Researchers have not clearly determined whether Prkaa1 (also known as AMPKα1) affects IMTG accumulation in skeletal muscle. Here, we show an important role of Prkaa1 in skeletal muscle lipid metabolism. Deletion of muscle Prkaa1 leads to the delayed development of skeletal muscles but does not affect glucose tolerance or insulin sensitivity in animals fed a normal diet. Notably, when animals are fed a high-fat diet, the skeletal muscle of muscle-specific Prkaa1 knockout mice accumulates more lipids than the skeletal muscle of wild-type (WT) mice, with concomitant upregulation of adipogenic gene expressions and downregulation of the expression of genes associated with mitochondrial oxidation. Muscle-specific Prkaa1 ablation also results in hyperlipidemia, which may contribute to the increased IMTG levels. Furthermore, Prkaa1 deletion activates skeletal muscle mTOR signalling, which has a central role in lipid metabolism and mitochondrial oxidation. Collectively, our study provides new insights into the role of Prkaa1 in skeletal muscle. This knowledge may contribute to the treatment of related metabolic diseases. [ABSTRACT FROM AUTHOR]

N-methyladenosine (mA) is the most abundant and reversible internal modification ubiquitously occurring in eukaryotic mRNA, albeit the significant biological roles of mA methylation have remained largely unclear. The well-known DNA and histone methylations play crucial roles in epigenetic modification of biologic processes in eukaryotes. Analogously, the dynamic and reversible mA RNA modification, which is installed by methyltransferase (METTL3, METTL14, and WTAP), reversed by demethylases (FTO, ALKBH5) and mediated by mA-binding proteins (YTHDF1-3, YTHDC1), may also have a profound impact on gene expression regulation. Recent discoveries of the distributions, functions, and mechanisms of mA modification suggest that this methylation functionally modulates the eukaryotic transcriptome to influence mRNA transcription, splicing, nuclear export, localization, translation, and stability. This reversible mRNA methylation shed light on a new dimension of post-transcriptional regulation of gene expression at the RNA level. mA methylation also plays significant and broad roles in various physiological processes, such as development, fertility, carcinogenesis, stemness, early mortality, meiosis and circadian cycle, and links to obesity, cancer, and other human diseases. This review mainly describes the current knowledge of mA and perspectives on future investigations. [ABSTRACT FROM AUTHOR]

The past decade has witnessed a rapid surge of interest in the research and development of non-precious metal-based electrocatalysts for the oxygen reduction reaction (ORR). Until now, the best catalysts in acidic electrolytes have exclusively been Fe-N-C-type materials from high-temperature pyrolysis. Despite the ORR activities of metal phthalocyanine or porphyrin macrocycles having long been known, their durability remains poor. In this work, we use these macrocycles as a basis to develop a novel organic-carbon hybrid material from in-situ polymerization of iron phthalocyanine on conductive multiwalled carbon nanotube scaffolds using a low-temperature microwave heating method. At an optimal polymerto- carbon ratio, the hybrid electrocatalyst exhibits excellent ORR activity with a positive half-wave potential (0.80 V), large mass activity (up to 18.0 A/g at 0.80 V), and a low peroxide yield (<3%). In addition, strong electronic coupling between the polymer and carbon nanotubes is believed to suppress demetallization of the macrocycles, significantly improving cycling stability in acids. Our study represents a rare example of non-precious metal-based electrocatalysts prepared without high-temperature pyrolysis, while having ORR activity in acidic media with potential for practical applications. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease among children and adolescents in the developed world. Betaine, as a methyl donor, recently has been demonstrated to exert its hepatoprotective effects through rectifying the genomic DNA hypomethylation state. However, whether betaine supplementation affects N6-methyladenosine (mA) mRNA methylation in NAFLD is still unknown. We conducted the current study to investigate the effects of betaine supplementation during adolescence on high-fat diet-induced pathological changes in liver of mice, and we further identified the effects of betaine supplementation on expression of the fat mass and obesity-associated gene (FTO) and hepatic mA mRNA methylation. Our results showed that betaine supplementation across adolescence significantly alleviated high-fat-induced impairment of liver function and morphology as well as ectopic fat accumulation. Surprisingly, no significant effects on serum TG and NEFA level, as well as fat mass, were observed in mice supplemented with betaine. We also found that high-fat diet upregulated ACC1 and FAS gene expression and downregulated HSL and ATGL gene expression. However, these alterations were rectified by betaine supplementation. Moreover, an mA hypomethylation state and increased FTO expression were detected in mice fed with high-fat diet, while betaine supplementation prevented these changes. Our results suggested that betaine supplementation during adolescence could protect mice from high-fat-induced NAFLD by decreasing de novo lipogenesis and increasing lipolysis. Furthermore, a novel FTO-dependent function of mA may involve in the hepatoprotective effects of betaine. [ABSTRACT FROM AUTHOR]

Selenium-enriched exopolysaccharides (EPS) produced by Enterobacter cloacae Z0206 have been proven to possess effect on reducing blood glucose level in diabetic mice. To investigate the specific mechanism, we studied the effects of oral supply with EPS on skeletal muscle glucose transportation and consumption in high-fat-diet-induced diabetic KKAy mice. We found that EPS supplementation increased expressions of glucose transporter 4 (Glut4), hexokinase 2 (hk2), phosphorylation of AMP-activated kinase subunit α2 (pAMPKα2), and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), and increased expression of characteristic protein of oxidative fibers such as troponin I and cytochrome c (Cytc). Furthermore, we found that EPS increased glucose uptake and expressions of pAMPKα2 and PGC-1α in palmitic acid (PA)-induced C2C12 cells. However, while EPS inhibited AMPKα2 with interference RNA (iRNA), effects of EPS on the improvement of glucose uptake diminished. These results indicated that EPS may improve skeletal muscle glucose uptake of diabetic KKAy mice through AMPKα2-PGC-1α pathway. [ABSTRACT FROM AUTHOR]

Adipose triglyceride lipase (ATGL) was recently identified as a triglyceride (TG)-specific lipase. In this study, we first obtained from large yellow croaker fish a 1,820-bp (GenBank ID: HQ916211) ATGL cDNA fragment with a 141-bp 5′UTR, a 1,485-bp open reading frame, and a 194-bp 3′UTR. The predicted fish ATGL had 494 amino acids (GenBank ID: ADY89608) and a calculated molecular weight of 55.1 kDa. ATGL was highly expressed in liver and, to a lesser degree, in heart, muscle, and abdominal fat. ATGL gene expression was high at 4.5 g and then decreased at 157.9 g and increased again at 474.2 g. The effects of lipid levels and lipid sources on ATGL expression in vivo were also investigated. A high-lipid diet decreased ATGL expression in fish significantly ( P < 0.01). Fish in soybean oil group exhibited significantly lower ATGL expression than fish in the fish oil and beef tallow groups ( P < 0.01). These data enhance our understanding of ATGL in fish lipid metabolism. [ABSTRACT FROM AUTHOR]

A 13-day feeding trial was carried out to evaluate the effectiveness of a microbound diet for rearing the larvae of Chinese shrimp Fenneropenaeus chinensis in comparison with the live foods that consist of Isochrysis galbana, Chlorella vulgaris, Tetraselmis chuii, rotifer (Brachionus plicatilis) and Artemia sp. Larvae of 0 to 13d post-hatch (dph) were reared in a temperature-controlled semi-open culture system and stocked at a density of 100 larvae L−1 in tanks, each containing 50 L sterilized seawater with salinity 30–32. Larvae were manually fed either the live foods or the microbound diet 6 times per day. At 13dph, the growth of the larvae fed on the microbound diet was approximately 84% of that fed on the live foods. The survival rate of the larvae fed on the microbound diet was 44.29% at 13 dph, which was not significantly different from that of larvae fed on live foods (63.55% ). The body length and development index (DI) of the larvae fed on the microbound diet were always lower than those of larvae fed on live foods. However, the differences reached significant levels only at 11 and 13dph ( P<0.05). The mean dry weight loss of the microbound diet was 9.2% after 90min immersion in seawater, indicating that this diet has a good water stability. The microbound diet contains 5223% crude protein and 10.27% lipid and is easy to prepare. These characteristics of the diet suggest good potentials for its successful use in the larviculture of other penaeid and fish species. [ABSTRACT FROM AUTHOR]

Skeletal muscle plays important roles in whole-body energy homeostasis. Excessive skeletal muscle lipid accumulation is associated with some metabolic diseases such as obesity and Type 2 Diabetes. The energy sensor AMPK (AMP-activated protein kinase) is a key regulator of skeletal muscle lipid metabolism, but the precise regulatory mechanism remains to be elucidated. Here, we provide a novel mechanism by which AMPK regulates skeletal muscle lipid accumulation through fat mass and obesity-associated protein (FTO)-dependent demethylation of N6-methyladenosine (m6A). We confirmed an inverse correlation between AMPK and skeletal muscle lipid content. Moreover, inhibition of AMPK enhanced lipid accumulation, while activation of AMPK reduced lipid accumulation in skeletal muscle cells. Notably, we found that mRNA m6A methylation levels were inversely correlated with lipid content in skeletal muscle. Furthermore, AMPK positively regulated the m6A methylation levels of mRNA, which could negatively regulate lipid accumulation in C2C12. At the molecular level, we demonstrated that AMPK regulated lipid accumulation in skeletal muscle cells by regulating FTO expression and FTO-dependent demethylation of m6A. Together, these results provide a novel regulatory mechanism of AMPK on lipid metabolism in skeletal muscle cells and suggest the possibility of controlling skeletal muscle lipid deposition by targeting AMPK or using m6A related drugs. [ABSTRACT FROM AUTHOR]