In recent years, lithium/sulfur (Li/S) cells have attracted great attention as a candidate for the next generation of rechargeable batteries due to their high theoretical specific energy of 2600 W·h kg(-1), which is much higher than that of Li ion cells (400-600 W·h kg(-1)). However, problems of the S cathode such as highly soluble intermediate species (polysulfides Li2Sn, n = 4-8) and the insulating nature of S cause poor cycle life and low utilization of S, which prevents the practical use of Li/S cells. Here, a high-rate and long-life Li/S cell is proposed, which has a cathode material with a core-shell nanostructure comprising Li2S nanospheres with an embedded graphene oxide (GO) sheet as a core material and a conformal carbon layer as a shell. The conformal carbon coating is easily obtained by a unique CVD coating process using a lab-designed rotating furnace without any repetitive steps. The Li2S/GO@C cathode exhibits a high initial discharge capacity of 650 mA·h g(-1) of Li2S (corresponding to the 942 mA·h g(-1) of S) and very low capacity decay rate of only 0.046% per cycle with a high Coulombic efficiency of up to 99.7% for 1500 cycles when cycled at the 2 C discharge rate.

The objective of the current study was to investigate the effects of feed restriction on whole-organism upper thermal tolerance and the heat shock response of green and white sturgeon to determine how changes in food amount might influence physiological performance of each species when faced with temperature stress. Two parallel feed restriction trials were carried out for juvenile green (202g; 222-day post hatch: dph) and white sturgeon (205g; 197-dph) to manipulate nutritional status at 12.5%, 25%, 50%, or 100% of optimum feeding rate (100% OFR were 1.6% and 1.8% body weight/day, respectively) for four weeks. Following the trials, the critical thermal maximum (CTMax, 0.3°C/min) of sturgeon (N=12/treatment/species) was assessed as an indicator of whole-organism upper thermal tolerance. To assess temperature sensitivity, sturgeon (N=9/treatment/species) were acutely transferred to two temperature treatments (28°C and 18°C as a handling control) for 2h followed by 2h of recovery at 18°C before being sacrificed, and gill, brain, and mucus sampled for measurements of 70-kDa heat shock protein levels (Hsc/Hsp70). Feeding rate had species-specific effects on CTMax in green and white sturgeon such that CTMax of green sturgeon decreased as the magnitude of feed restriction increased; whereas, CTMax of white sturgeon did not change with feed restriction. Elevated temperature (28°C) and feed restriction increased Hsc/Hsp70 levels in the gill tissue of green sturgeon, while heat shock increased Hsc/Hsp70 levels in the mucus of white sturgeon. Our results suggest that green sturgeon may be more susceptible to temperature stress under food-limited conditions.

Berberine (BBR), which is an active component of Coptis chinensis Franch, has been reported to improve glucose metabolism and insulin resistance in animal and human studies, predominantly via activation of the 5'-adenosine monophosphate kinase (AMPK) pathway and suppression of the inflammation response. However, the mechanisms underlying the effects of BBR on AMPK and inflammation remain unclear. In this present study, we found that BBR upregulated SIRT1 expression in 3T3L-1 adipocytes and adipose tissue. Inhibition of SIRT1 blunted the BBR-induced increase in glucose consumption and uptake in adipocytes. The BBR-induced activation of the AMPK pathway and AKT phosphorylation in adipocytes and adipose tissue were also attenuated by inhibition or knockout of Sirt1. The BBR-induced improvement of systemic insulin sensitivity was impaired by Sirt1 knockout in HFD-induced obese mice. The suppressing effects of BBR on systemic and local inflammatory responses, such as serum concentrations and expression of inflammatory cytokines, phosphorylation of c-Jun N-terminal kinase (JNK) and IKKβ, and the accumulation of F4/80-positive macrophages in adipose tissue were also attenuated in Sirt1 knockout mice. The BBR-induced decrease in PGC-1α acetylation was reversed by inhibition or knockout of Sirt1 in adipocytes and adipose tissue. Together, these results indicate that adipose tissue SIRT1 is a key regulator of the insulin sensitizing and anti-inflammatory effects of BBR, which contributes to the improvement of metabolic dysregulation.

Background

Breeding for genes controlling key agronomic traits is an important goal of rice genetic improvement. To gain insight into genes controlling grain morphology, we screened M₃ plants derived from 1,000 whole-genome sequenced (WGS) M₂ Kitaake mutants to identify lines with altered grain size.

Results

In this study, we isolated a mutant, named fast-neutron (FN) 60-4, which exhibits a significant reduction in grain size. We crossed FN60-4 with the parental line Kitaake and analyzed the resulting backcross population. Segregation analysis of 113 lines from the BC₂F₂ population revealed that the mutant phenotype is controlled by a single semi-dominant locus. Mutant FN60-4 is reduced 20% in plant height and 8.8% in 1000-grain weight compared with Kitaake. FN60-4 also exhibits an 8% reduction in cell number and a 9% reduction in cell length along the vertical axis of the glume. We carried out whole-genome sequencing of DNA pools extracted from segregants with long grains or short grains, and revealed that one gene, LOC_Os09g02650, cosegregated with the grain size phenotype in the BC₁F₂ and BC₂F₂ populations. This mutant allele was named grain shape 9-1 (gs9-1). gs9-1 carries a 3-bp deletion that affects two amino acids. This locus is a new allele of the BC12/GDD1/MTD1 gene that encodes a kinesin-like protein involved in cell-cycle progression, cellulose microfibril deposition and gibberellic acid (GA) biosynthesis. The GA biosynthesis-related gene KO2 is down-regulated in gs9-1. The dwarf phenotype of gs9-1 can be rescued by adding exogenous GA₃. In contrast to the phenotypes for the other alleles, the gs9-1 is less severe, consistent with the nature of the mutation, which does not disrupt the open reading frame as observed for the other alleles.

Conclusions

In this study, we isolated a mutant, which exhibits altered grain shape and identified the mutated gene, gs9-1. Our study reveals that gs9-1 is a semi-dominant gene that carries a two-amino acid mutation. gs9-1 is allelic to the BC12/GDD1/MTD1 gene involved in GA biosynthesis. These results demonstrate the efficiency and convenience of cloning genes from the whole-genome sequenced Kitaake mutant population to advance investigations into genes controlling key agronomic traits in rice.

Rhein, a component derived from rhubarb, has been proven to possess anti-inflammatory properties. Here, we show that rhein mitigates obesity by promoting adipose tissue thermogenesis in diet-induced obese mice. We construct a macrophage-adipocyte co-culture system and demonstrate that rhein promotes adipocyte thermogenesis through inhibiting NLRP3 inflammasome activation in macrophages. Moreover, clues from acetylome analysis identify SIRT2 as a potential drug target of rhein. We further verify that rhein directly interacts with SIRT2 and inhibits NLRP3 inflammasome activation in a SIRT2-dependent way. Myeloid knockdown of SIRT2 abrogates adipose tissue thermogenesis and metabolic benefits in obese mice induced by rhein. Together, our findings elucidate that rhein inhibits NLRP3 inflammasome activation in macrophages by regulating SIRT2, and thus promotes white adipose tissue thermogenesis during obesity. These findings uncover the molecular mechanism underlying the anti-inflammatory and anti-obesity effects of rhein, and suggest that rhein may become a potential drug for treating obesity.

Palmitic acid hydroxystearic acids (PAHSAs) are endogenous lipids with anti-diabetic and anti-inflammatory effects. PAHSA levels are reduced in serum and adipose tissue of insulin-resistant people and high-fat diet (HFD)-fed mice. Here, we investigated whether chronic PAHSA treatment enhances insulin sensitivity and which receptors mediate PAHSA effects. Chronic PAHSA administration in chow- and HFD-fed mice raises serum and tissue PAHSA levels ∼1.4- to 3-fold. This improves insulin sensitivity and glucose tolerance without altering body weight. PAHSA administration in chow-fed, but not HFD-fed, mice augments insulin and glucagon-like peptide (GLP-1) secretion. PAHSAs are selective agonists for GPR40, increasing Ca⁺² flux, but not intracellular cyclic AMP. Blocking GPR40 reverses improvements in glucose tolerance and insulin sensitivity in PAHSA-treated chow- and HFD-fed mice and directly inhibits PAHSA augmentation of glucose-stimulated insulin secretion in human islets. In contrast, GLP-1 receptor blockade in PAHSA-treated chow-fed mice reduces PAHSA effects on glucose tolerance, but not on insulin sensitivity. Thus, PAHSAs activate GPR40, which is involved in their beneficial metabolic effects.