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Background: The COVID-19 pandemic has brought a lot of working stress to medical workers and has a certain impact on their mental health. Working stress is closely related to the increase in anxiety, but few studies have explored whether their relationship will be affected by positive psychological factors in the special situation.Methods: 798 medical workers were investigated online after the outbreak of the COVID-19 (10 February to 1 March 2020) in China. The relevant questionnaires were used to evaluate working stress, anxiety, sense of control, and psychological capital. The moderated mediation model test was performed using the SPSS software and PROCESS macro program.Results: Working stress could directly affect anxiety, and indirectly affect anxiety through sense of control. In addition, psychological capital moderated the direct effect of working stress on anxiety, which is more effective at high level of psychological capital. Psychological capital also moderated the second half of the indirect effect of working stress on anxiety, at low level of psychological capital, sense of control was more effective in predicting anxiety.Limitations: All the data in this study was collected through online questionnaire. The anxiety response measured in this study cannot be specific to the viral epidemic.Conclusions: Under the COVID-19 epidemic situation, for medical workers, low sense of control and low level of psychological capital may be important risk factors of anxiety caused by working stress. Thus, strengthening the sense of control and psychological capital of medical workers would be helpful to reduce their anxiety and maintain their mental health. [ABSTRACT FROM AUTHOR]

This study was carried out to investigate the effects of N -acetylcysteine (NAC) on growth performance and intestinal function of heat-stressed broilers. A total of two hundred 1-d-old Cobb male chicks were allocated to 1 of 4 treatments, with 5 replicated pens per treatment and 10 birds per pen. The experiment consisted of 4 treatments in a 2 × 2 factorial arrangements with two diets (basal diet or 1 g/kg NAC diet) and two temperatures (thermoneutral or heat stress). From day 8–35 of age, broilers were raised at thermoneutral (26 ± 1 °C) or exposed to cyclic heat stress (36 ± 1 °C from 0800 to 1800 and 26 ± 1 °C from 1800 to 0800). The results showed that heat stress reduced ADFI, ADG, plasma concentrations of triiodothyronine (T 3 ) and thyroxine (T 4 ), intestinal villus height (VH), ratio of VH to crypt depth (CD), intestinal mucosal ATP level, adenylate energy charge (AEC), activities of alkaline phosphatase (AKP), antioxidative and digestive enzymes, and mRNA level for Bcl-2, whereas increased the feed/gain, mortality rate, plasma corticosterone level, intestinal CD, intestinal mucosal AMP and malondialdehyde (MDA) levels, and mRNA levels of heat shock protein (HSP70), caspase-3, AMP-activated protein kinase (AMPK), heme-oxigenase (HMOX), and xanthine oxidoreductase (XOR). Dietary supplementation with NAC decreased the feed/gain, mortality rate, plasma corticosterone level, MDA concentration and intestinal mucosal mRNA levels of HSP70, AMPK and HMOX, while elevated the ratio of VH to CD, ATP, catalase (CAT) and trypsine activity in the small intestine of heat-stressed broilers. Taken together, these results suggest that dietary supplementation of 1 g/kg NAC could improve growth performance and intestinal function of broilers exposed to heat stress. [ABSTRACT FROM AUTHOR]

Background: Skeletal muscle undergoes rapid loss in response to inflammation. α-Ketoglutarate (AKG) has been reported to enhance muscle growth in piglets, but the underlying mechanisms are largely unknown.Objectives: This study tested the hypothesis that dietary AKG supplementation activates mechanistic target of rapamycin (mTOR) signaling and improves skeletal muscle energy metabolism in lipopolysaccharide (LPS)-challenged piglets.Methods: Forty-eight male piglets (Duroc × Landrace × Yorkshire) were weaned at 21 d of age to a corn- and soybean meal-based diet. After a 3-d period of adaptation, piglets with a mean weight of 7.21 kg were randomly assigned to control, LPS (intraperitoneal administration of 80 μg LPS/kg body weight on days 10, 12, 14, and 16), or LPS plus 1% dietary AKG (LPS+AKG) groups. On day 16, blood samples were collected from 8 piglets/group 3 h after LPS administration. On day 17, piglets were killed to obtain gastrocnemius muscle from 8 piglets/group for biochemical analysis.Results: Compared with the control group, LPS administration increased (P < 0.05) plasma concentrations of globulin (by 14%) and tumor necrosis factor α (by 59%) and the intramuscular ratio of AMP to ATP (by 93%) and abundance of phosphorylated acetyl-coenzyme A carboxylase (ACC) β protein (by 64%). Compared with the control group, LPS administration reduced (P < 0.05) weight gain (by 15%); plasma concentrations of glutamine (by 20%), glucose (by 23%), insulin, insulin-like growth factor I, and epidermal growth factor; intramuscular concentrations of glutamine (by 27%), ATP (by 12%), ADP (by 22%), and total adenine nucleotides; and intramuscular ratios of phosphorylated mTOR to total mTOR (by 38%) and of phosphorylated 70-kDa ribosomal protein S6 kinase (p70S6K) to total p70S6K (by 39%). These adverse effects of LPS were ameliorated (P < 0.05) by AKG supplementation.Conclusions: Dietary AKG supplementation activated mTOR signaling, inhibited ACC-β, and improved energy status in skeletal muscle of LPS-challenged piglets. These results provide a biochemical basis for the use of AKG to enhance piglet growth under inflammatory or practical postweaning conditions. [ABSTRACT FROM AUTHOR]

Long-chain (n-3) PUFA exert beneficial effects on inflammatory bowel diseases in animal models and clinical trials. In addition, pattern recognition receptors such as toll-like receptors (TLR) and nucleotide-binding oligomerization domain proteins (NOD) play a critical role in Intestinal inflammation. We hypothesized that fish oil could alleviate Escherichia coli LPS-induced Intestinal Injury via modulation of TLR4 and NOD signaling pathways. Twenty-four weaned piglets were used in a 2 x 2 factorial design and the main factors included a dietary treatment (5% corn oil or 5% fish oil) and immunological challenge (LPS or saline). After feeding fish oil or corn oil diets for 21 d, pigs were Injected with LPS or saline. At 4 h postinjection, blood samples were collected and pigs were killed. EPA, DHA, and total (n-3) PUFA were enriched in intestinal mucosa through fish supplementation. Fish oil improved intestinal morphology, indicated by greater villus height and villus height:crypt depth ratio, and intestinal barrier function, indicated by decreased plasma diamine oxidase (DAO) activity and increased mucosal DAO activity as well as enhanced protein expression of intestinal tight junction proteins including occludin and claudin-1. Moreover, fish oil decreased intestinal TNFα and PGE2 concentrations and caspase-3 and heat shock protein 70 protein expression. Finally, fish oil downregulated the mRNA expression of intestinal TLR4 and its downstream signals myeloid differentiation factor 88, IL-1 receptor-associated kinase 1, TNFα receptor-associated factor 6, and NOD2, and its adaptor molecule, receptor-interacting serine/threonine-protein kinase 2. Fish oil decreased the protein expression of intestinal NFKB p65. These results Indicate that fish oil supplementation is associated with inhibition of TLR4 and NOD2 signaling pathways and concomitant improvement of intestinal integrity under an inflammatory condition. [ABSTRACT FROM AUTHOR]

Oleum cinnamomi (OCM, cinnamon oil), which is produced by aromatic cinnamon plants, is increasingly used as a feed additive to animal diets. OCM is a natural product rich in polyphenolic compounds that exhibit strong antioxidative property. However, the direct addition of OCM to the feed is questionable due to several limiting physical–chemical factors such as the high hydrophobicity, volatility, odor, fast decomposition, and poor availability in the lower gastrointestinal tract of animals. Therefore, the coated form of OCM (cOCM) is one of the ways to solve these concerns. We have demonstrated that dietary cOCM supplementation did not improve the growth performance of broiler chickens, but it showed beneficial effects on immunity and intestinal integrity. In the current study, we further investigated the intestinal cinnamaldehyde release and antioxidative capacity of chickens fed cOCM-supplemented diets. As cinnamaldehyde is a major constituent of OCM, we evaluated the release of cOCM in the intestine of birds by determining the contents of cinnamaldehyde in the digesta of small intestine and cecum. The increased availability of OCM in the lower intestine supplied a foundation for exerting its antioxidative effects. The activities of antioxidative enzymes were increased and superoxide levels were decreased in the plasma and intestinal mucosa of birds fed cOCM-supplemented diets. The improvement of antioxidative capacity was achieved by modulating the gene expression of nuclear factor erythroid 2-related factor 2 and downstream antioxidative enzymes. [ABSTRACT FROM AUTHOR]

Intestinal health is critical for the growth and development of humans and animals. Our previous study has demonstrated that indomethacin (IDMT) could induce intestinal injury in piglets, and N-acetylcysteine (NAC) supplementation contributed to alleviating intestinal injury induced by various stimuli. In this study, we investigated the mechanism of IDMT-induced cell death in IPEC-1 cell lines and explored the role of NAC by using transcriptomic and proteomic analyses. Results showed that cell viability was substantially reduced with the increasing concentrations of IDMT, whereas NAC significantly increased the survival rate of IPEC-1 cells regardless of its addition method. Transcriptomics and proteomics data indicated that terms, such as cell cycle, energy metabolism, and cell proliferation, were significantly enriched by Gene ontology and pathway analyses. Flow cytometer analysis showed that IDMT induced cell cycle arrest at G0/G1 phase. The expression of cell cycle regulatory proteins (CDK1, CCNA2, and CDC45) was decreased by IDMT stimulation. Importantly, NAC treatment repaired IDMT-induced mitochondrial dysfunction by increasing ATP production, decreasing oxygen consumption rate in non-mitochondrial O2 consumption, and increasing the red/green fluorescence ratio. IDMT stimulation significantly increased caspase-3 expression, which was partially reversed by NAC treatment. These results suggest that IDMT-induced cell death may be attributable to disturbance of the cell cycle processes, mitochondria dysfunction and apoptosis, and NAC could confer a protective effect by restoring the mitochondrial function and inhibiting the apoptosis pathway. This study provides a theoretical basis for the pathogenesis of IDMT-induced intestinal injury and guides the clinic application of NAC. [ABSTRACT FROM AUTHOR]

Obesity develops from an imbalance of energy homeostasis and is associated with chronic low-grade inflammation in white adipose tissues (WAT). Inflammation is involved in the pathophysiology of many obesity-induced disorders including insulin resistance and diabetes. Increasing evidence has shown that dietary leucine supplementation positively affects the parameters associated with obesity and obesity-related metabolic disorders. The beneficial effects include increased loss of body weight, reduced WAT inflammation, improved lipid and glucose metabolism, enhanced mitochondrial function, and preserved lean body mass. Although these beneficial effects have not been clearly established, dietary leucine supplementation, either alone or as part of a therapeutic regimen, may be a good nutritional tool in the prevention and management of obesity and obesity-induced metabolic disorders. [ABSTRACT FROM AUTHOR]

Abstract: Pro-inflammatory cytokines play a critical role in many models of liver injury. In addition, aspartate (Asp) plays an important role in many biological and physiological processes including liver physiology. We hypothesized that Asp could alleviate lipopolysaccharide (LPS)-induced liver injury. Forty-eight weanling pigs were assigned to four treatments including: (1) non-challenged control; (2) LPS challenged control; (3) LPS+0.5% Asp; (4) LPS+1.0% Asp. After 20-d feeding with control (0% Asp), 0.5% or 1.0% Asp supplemented diets, pigs were injected with saline or LPS. At 4 (early phase) and 24 h (late phase) post-injection, blood and liver samples were obtained. Asp attenuated liver injury indicated by reduced serum aspartate aminotransferase activity and increased ratio of serum alanine aminotransferase and aspartate aminotransferase at 24 h, and less severe histological liver damage induced by LPS challenge at 4 or 24 h. In addition, Asp supplementation to LPS challenged pigs decreased mRNA expressions of tumor necrosis factor (TNF)-α and cyclooxygenase-2 linearly and quadratically at 4 h, and increased mRNA expressions of these pro-inflammatory mediators linearly and quadratically at 24 h. Finally, Asp decreased mRNA expression of toll-like receptor 4 (TLR4) signaling related genes (TLR4, myeloid differentiation factor 88, IL-1 receptor-associated kinase 1, TNF-α receptor-associated factor (6), nucleotide-binding oligomerization domain protein (NOD) signaling related genes (NOD1, NOD2 and receptor-interacting serine/threonine-protein kinase 2) and nuclear factor-κB p65 linearly or quadratically at 4 h. However, Asp increased mRNA expressions of these signaling molecules linearly or quadratically at 24 h. These results indicate that, at early and late phases of LPS challenge, Asp exerts opposite regulatory effects on mRNA expression of hepatic pro-inflammatory cytokines and TLR4 and NOD signalling related genes, and improves liver integrity. [Copyright &y& Elsevier]

Abstract: The intestine has a high requirement for ATP to support its integrity, function and health, and thus, energy deficits in the intestinal mucosa may play a critical role in intestinal injury. Aspartate (Asp) is one of the major sources of ATP in mammalian enterocytes via mitochondrial oxidation. We hypothesized that dietary supplementation of Asp could attenuate lipopolysaccharide (LPS)-induced intestinal damage via modulation of intestinal energy status. Twenty-four weanling piglets were allotted to one of four treatments: (1) nonchallenged control, (2) LPS-challenged control, (3) LPS+0.5% Asp treatment, and (4) LPS+1.0% Asp treatment. On day 19, pigs were injected with saline or LPS. At 24 h postinjection, pigs were killed and intestinal samples were obtained. Asp attenuated LPS-induced intestinal damage indicated by greater villus height and villus height/crypt depth ratio as well as higher RNA/DNA and protein/DNA ratios. Asp improved intestinal function indicated by increased intestinal mucosal disaccharidase activities. Asp also improved intestinal energy status indicated by increased ATP, ADP and total adenine nucleotide contents, adenylate energy charge and decreased AMP/ATP ratio. In addition, Asp increased the activities of tricarboxylic acid cycle key enzymes including citrate synthase, isocitrate dehydrogenase and alpha-oxoglutarate dehydrogenase complex. Moreover, Asp down-regulated mRNA expression of intestinal AMP-activated protein kinase α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and peroxisome proliferator–activated receptor gamma coactivator-1α (PGC1α) and decreased intestinal AMPKα phosphorylation. These results indicate that Asp may alleviate LPS-induced intestinal damage and improve intestinal energy status. [Copyright &y& Elsevier]