The relationship between metabolic rate and sociability is altered by food-deprivation

Individuals vary in the extent to which they associate with conspecifics, but little is known about the energetic underpinnings of this variation in sociability. Group-living allows individuals to find food more consistently, but within groups, there can be competition for food items. Individuals with an increased metabolic rate could display decreased sociability to reduce competition. Long-term food deprivation (FD) may alter any links between sociability and metabolic rate by affecting motivation to find food. We examined these issues in juvenile qingbo carp Spinibarbus sinensis, to understand how FD and metabolic rate affect sociability. Like many aquatic ectotherms, this species experiences seasonal bouts of FD. Individuals were either: (i) food-deprived for 21 days; or (ii) fed a maintenance ration (control). Fish from each treatment were measured for standard metabolic rate (SMR) and tested for sociability twice: once in the presence of a control stimulus shoal and once with a food-deprived stimulus shoal. Control individuals ventured further from stimulus shoals over a 30-min trial, while food-deprived fish did not change their distance from stimulus shoals as trials progressed. Control fish with a higher SMR were least sociable. Well-fed controls showed decreased sociability when exposed to food-deprived stimulus shoals, but there was evidence of consistency in relative sociability between exposures to different shoal types. Results contrast with previous findings that several days of fasting causes individuals to decrease associations with conspecifics. Prolonged FD may cause individuals to highly prioritize food acquisition, and the decreased vigilance that would accompany continuous foraging may heighten the need for the antipredator benefits of shoaling. Conversely, decreased sociability in well-fed fish with a high SMR probably minimizes intraspecific competition, allowing them to satisfy an increased energetic demand while foraging. Together, these results suggest that FD – a challenge common for many ectothermic species – can affect individual sociability as well as the attractiveness of groups towards conspecifics. In addition, the lack of a link between SMR and sociability in food-deprived fish suggests that, in situations where group membership is linked to fitness, the extent of correlated selection on metabolic traits may be context-dependent

HDAC6 Inhibition Prevents TNF-α-Induced Caspase 3 Activation in Lung Endothelial Cell and Maintains Cell-Cell Junctions

Pro-inflammatory mediators such as TNF-α induce caspase activation in endothelial cells, which leads to degradation of cellular proteins, induction of apoptotic signaling, and endothelial cell dysfunction. New therapeutic agents that can inhibit caspase activation may provide protection against inflammatory injury to endothelial cells. In the present study, we examined the effects of selective histone deacetylase 6 (HDAC6) inhibition on TNF-α induced caspase 3 activation and cell-cell junction dysfunction in lung endothelial cells. We also assessed the protective effects of HDAC6 inhibition against lung inflammatory injury in a mouse model of endotoxemia. We demonstrated that selective HDAC6 inhibition or knockdown of HDAC6 expression was able to prevent caspase 3 activation in lung endothelial cells and maintain lung endothelial cell-cell junctions. Mice pre-treated with HDAC6 inhibitors exhibited decreased endotoxin-induced caspase 3 activation and reduced lung vascular injury as indicated by the retention of cell-cell junction protein VE-Cadherin level and alleviated lung edema. Collectively, our data suggest that HDAC6 inhibition is a potent therapeutic strategy against inflammatory injury to endothelial cells

Low-energy Scattering of (D∗Dˉ∗)±(D^{*}\bar{D}^{*})^\pm System and the Resonance-like Structure Zc(4025)Z_c(4025)

In this paper, low-energy scattering of the $(D^{*}\bar{D}^{*})^\pm$ meson system is studied within L\"uscher's finite-size formalism using $N_{f}=2$ twisted mass gauge field configurations. With three different pion mass values, the $s$-wave threshold scattering parameters, namely the scattering length $a_0$ and the effective range $r_0$, are extracted in $J^P=1^+$ channel. Our results indicate that, in this particular channel, the interaction between the two vector charmed mesons is weakly repulsive in nature hence do not support the possibility of a shallow bound state for the two mesons, at least for the pion mass values being studied. This study provides some useful information on the nature of the newly discovered resonance-like structure $Z_c(4025)$ observed in various experiments.Comment: 11 pages, 6 figures. arXiv admin note: substantial text overlap with arXiv:1403.131

Estradiol regulates miR-135b and mismatch repair gene expressions via estrogen receptor-β in colorectal cells.

Estrogen has anti-colorectal cancer effects which are thought to be mediated by mismatch repair gene (MMR) activity. Estrogen receptor (ER) expression is associated with microRNA (miRNA) expression in ER-positive tumors. However, studies of direct link between estrogen (especially estradiol E2), miRNA expression, and MMR in colorectal cancer (CRC) have not been done. In this study, we first evaluated the effects of estradiol (E2) and its antagonist ICI182,780 on the expression of miRNAs (miR-31, miR-155 and miR-135b) using COLO205, SW480 and MCF-7 cell lines, followed by examining the association of tissue miRNA expression and serum E2 levels using samples collected from 18 colorectal cancer patients. E2 inhibited the expressions of miRNAs in COLO205 cells, which could be reversed by E2 antagonist ICI 182.780. The expression of miR-135b was inversely correlated with serum E2 level and ER-β mRNA expression in CRC patients' cancer tissues. There were significant correlations between serum E2 level and expression of ER-β, miR-135b, and MMR in colon cancer tissue. This study suggests that the effects of estrogen on MMR function may be related to regulating miRNA expression via ER-β, which may be the basis for the anti-cancer effect in colorectal cells