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A sustainable, heat-resistant and flame-retardant cellulose-based composite nonwoven has been successfully fabricated and explored its potential application for promising separator of high-performance lithium ion battery. It was demonstrated that this flame-retardant cellulose-based composite separator possessed good flame retardancy, superior heat tolerance and proper mechanical strength. As compared to the commercialized polypropylene (PP) separator, such composite separator presented improved electrolyte uptake, better interface stability and enhanced ionic conductivity. In addition, the lithium cobalt oxide (LiCoO 2 )/graphite cell using this composite separator exhibited better rate capability and cycling retention than that for PP separator owing to its facile ion transport and excellent interfacial compatibility. Furthermore, the lithium iron phosphate (LiFePO 4 )/lithium cell with such composite separator delivered stable cycling performance and thermal dimensional stability even at an elevated temperature of 120°C. All these fascinating characteristics would boost the application of this composite separator for high-performance lithium ion battery.

Heat stress in dairy cows is aggravated by Global warming, which negatively affects their performance and health, especially high yielding cows are more susceptible to high temperature and humidity in summer. Besides increasing body temperature and reducing feed intake, heat stress also compromises mammary gland function by inducing apoptosis in bovine mammary epithelial cells (BMECs). UFBP1 (Ufm1-binding protein 1) serves as an essential component of ufmylation, is crucial for the preservation of cellular homeostasis. However, little is known about its contribution to heat stress-induced apoptosis in BMECs. Therefore, the present study aimed to elucidate the effect of UFBP1 on heat stress-induced apoptosis through knockdown and overexpression of UFBP1 in BMECs. The results showed that heat stress triggered cell apoptosis (increased apoptosis rate and Bax/Bcl-2 protein expression) and decreased the expression of genes associated with the production of milk fat and protein both in vivo and in vitro studies. Furthermore, UFBP1 silencing aggravated the high-temperature-induced cell damage, and overexpression of UFBP1 attenuated heat stress-induced mitochondrial dysfunction, as evidenced by increased mitochondrial membrane potential (MMP), ATP synthesis and NAD+/NADH ratio, as well as the reduced reactive oxygen species (ROS) generation. Importantly, the mitochondrial apoptosis pathway triggered by heat stress was blocked by UFBP1, as indicated by the reduced apoptosis rate and Bax/Bcl-2 protein expression. In addition, UFBP1 restored the expression of milk fat and protein-related genes in heat-stressed BMECs. In conclusion, these findings indicate that UFBP1 may serve as a promising therapeutic target for ameliorating heat stress in dairy cows, thereby providing novel theoretical insights into the mitigation of adverse thermal stress effects on livestock productivity.

Backgroud This study aimed to determine the effects of early antibiotic intervention (EAI) on subsequent blood parameters, apparent nutrient digestibility, and fecal fermentation profile in pigs with different dietary crude protein (CP) levels. Eighteen litters of piglets (total 212) were randomly allocated to 2 groups and were fed a creep feed diet with or without in-feed antibiotics (olaquindox, oxytetracycline calcium and kitasamycin) from postnatal d 7 to d 42. On d 42, the piglets within the control or antibiotic group were mixed, respectively, and then further randomly assigned to a normal- (20%, 18%, and 14% CP from d 42 to d 77, d 77 to d 120, and d 120 to d 185, respectively) or a low-CP diet (16%, 14%, and 10% CP from d 42 to d 77, d 77 to d 120, and d 120 to d 185, respectively), generating 4 groups. On d 77 (short-term) and d 185 (long-term), serum and fecal samples were obtained for blood parameters, microbial composition and microbial metabolism analysis. Results EAI increased ( P  < 0.05) albumin and glucose concentrations in low-CP diet on d 77, and increased ( P  < 0.05) urea concentration in normal-CP diet. On d 185, EAI increased ( P  < 0.05) globulin concentration in normal-CP diets, but decreased glucose concentration. For nutrient digestibility, EAI increased ( P  < 0.05) digestibility of CP on d 77. For fecal microbiota, the EAI as well as low-CP diet decreased ( P  < 0.05) E. coli count on d 77. For fecal metabolites, on d 77, EAI decreased ( P  < 0.05) total amines concentration but increased skatole concentration in low-CP diet. On d 185, the EAI increased ( P  < 0.05) putrescine and total amines concentrations in low-CP diets but reduced ( P  < 0.05) in the normal-CP diets. The low-CP diet decreased the concentrations of these compounds. Conclusions Collectively, these results indicate that EAI has short-term effects on the blood parameters and fecal microbial fermentation profile. The effects of EAI varied between CP levels, which was characterized by the significant alteration of glucose and putrescine concentration.

Pseudorabies virus (PRV) variants broke out in china since 2011, causing high fever, respiratory distress, systemic neurological symptoms, and diarrhea in piglets. This study investigated the effect of intranasal PRV variant (AH02LA) infection on ileal and colonic bacterial communities and immune status in piglets. Ten piglets (free of PRV) were assigned to PRV variant and control groups (uninfected). At day 5 after inoculation, all piglets were euthanized. No PRV was detected in the ileal and colonic mucosa. In the PRV group, we observed up-regulation of specific cytokines gene expression, down-regulation of intestinal barrier-related gene expression, and reduction of secretory immunoglobulin A (sIgA) concentration in the ileum and colon. PRV infection increased the diversity of ileal bacterial community composition. PRV infection reduced the abundance of some beneficial bacteria (Lactobacillus species in the ileum and colon; butyrate-producing bacteria species in the colon) and increased the abundance of potentially pathogenic Fusobacterium nucleatum in the ileum and Sphingomonas paucimobilis in the colon. Moreover, PRV infection decreased concentrations of the beneficial lactate in the ileum and butyrate in the colon. However, this study does not allow to evaluate whether the observed changes are directly due to the PRV infection or rather to indirect effects (fever, clinical signs and changes in diet), and will be our next research content. In summary, our findings provide evidence that intranasal PRV infection directly or indirectly brings gut health risks and implications, although no PRV was detected in the ileum and colon.

In this study, we applied bacterial artificial chromosome (BAC) technology with PRVΔTK/gE/gI as the base material to replace the first, central, and terminal segments of the US3 gene with codon-deoptimized fragments via two-step Red-mediated recombination in E. coli GS1783 cells. The three constructed BACs were co-transfected with gI and part of gE fragments carrying homologous sequences (gI+gE’), respectively, in swine testicular cells. These three recombinant viruses with US3 codon de-optimization ((PRVΔTK&gE-US3deop−1, PRVΔTK&gE-US3deop−2, and PRVΔTK&gE-US3deop−3) were obtained and purified. These three recombinant viruses exhibited similar growth kinetics to the parental AH02LA strain, stably retained the deletion of TK and gE gene fragments, and stably inherited the recoded US3. Mice were inoculated intraperitoneally with the three recombinant viruses or control virus PRVΔTK&gEAH02 at a 107.0 TCID50 dose. Mice immunized with PRVΔTK&gE-US3deop−1 did not develop clinical signs and had a decreased virus load and attenuated pathological changes in the lungs and brain compared to the control group. Moreover, immunized mice were challenged with 100 LD50 of the AH02LA strain, and PRVΔTK&gE-US3deop−1 provided similar protection to that of the control virus PRVΔTK&gEAH02. Finally, PRVΔTK&gE-US3deop−1 was injected intramuscularly into 1-day-old PRV-negative piglets at a dose of 106.0 TCID50. Immunized piglets showed only slight temperature reactions and mild clinical signs. However, high levels of seroneutralizing antibody were produced at 14 and 21 days post-immunization. In addition, the immunization of PRVΔTK&gE-US3deop−1 at a dose of 105.0 TCID50 provided complete clinical protection and prevented virus shedding in piglets challenged by 106.5 TCID50 of the PRV AH02LA variant at 1 week post immunization. Together, these findings suggest that PRVΔTK&gE-US3deop−1 displays great potential as a vaccine candidate.

Background Pseudorabies virus (PRV) is a preferred vector for recombinant vaccine construction. Previously, we generated a TK&gE-deleted PRV (PRV Δ TK&gE−AH02 ) based on a virulent PRV AH02LA strain. It was shown to be safe for 1-day-old piglets with maternal PRV antibodies and 4 ~ 5 week-old PRV antibody negative piglets and provide rapid and 100 % protection in weaned pigs against lethal challenge with the PRV variant strain. It suggests that PRV TK&gE−AH02 may be a promising live vaccine vector for construction of recombinant vaccine in pigs. However, insertion site, as a main factor, may affect foreign gene expression. Results In this study, we constructed four recombinant PRV-S bacterial artificial chromosomes (BACs) carrying the same spike (S) expression cassette of a variant porcine epidemic diarrhea virus strain in different noncoding regions (UL11-10, UL35-36, UL46-27 or US2-1) from AH02LA BAC with TK, gE and gI deletion. The successful expression of S gene (UL11-10, UL35-36 and UL46-27) in recombinant viruses was confirmed by virus rescue, PCR, real-time PCR and indirect immunofluorescence. We observed higher S gene mRNA expression level in swine testicular cells infected with PRV-S(UL11-10)ΔTK/gE and PRV-S(UL35-36)ΔTK/gE compared to that of PRV-S(UL46-27)ΔTK/gE at 6 h post infection ( P  < 0.05). Moreover, at 12 h post infection, cells infected with PRV-S(UL11-10)ΔTK/gE exhibited higher S gene mRNA expression than those infected with PRV-S(UL35-36)ΔTK/gE ( P  = 0.097) and PRV-S(UL46-27)ΔTK/gE ( P  < 0.05). Recovered vectored mutant PRV-S (UL11-10, UL35-36 and UL46-27) exhibited similar growth kinetics to the parental virus (PRV Δ TK&gE−AH02 ). Conclusions This study focuses on identification of suitable sites for insertion of foreign genes in PRV genome, which laids a foundation for future development of recombinant PRV vaccines.

The increased virulence of infectious bursal disease virus (IBDV) is a threat to the chicken industry. The construction of novel herpesvirus of turkey-vectored (HVT) vaccines expressing VP2 of virulent IBDV may be a promising vaccine candidate for controlling this serious disease in chickens. We generated a novel infectious clone of HVT Fc-126 by inserting mini-F sequences in lieu of the glycoprotein C (gC) gene. Based on this bacterial artificial chromosome (BAC), a VP2 expression cassette containing the pMCMV IE promoter and a VP2 sequence from the virulent IBDV NJ09 strain was inserted into the noncoding area between the UL55 and UL56 genes to generate the HVT vector VP2 recombinant, named HVT-VP2-09. The recovered vectored mutant HVT-VP2-09 exhibited higher titers (p = 0.0202 at 36 h) or similar growth kinetics to the parental virus HVT Fc-126 (p = 0.1181 at 48 h and p = 0.1296 at 64 h). The high reactivation ability and strong expression of VP2 by HVT-VP2-09 in chicken embryo fibroblasts (CEFs) were confirmed by indirect immunofluorescence (IFA) and Western blotting. The AGP antibodies against IBDV were detected beginning at 3 weeks post-inoculation (P.I.) of HVT-VP2-09 in 1-day-old SPF chickens. Seven of ten chickens immunized with HVT-VP2-09 were protected post-challenge (P.C.) with the virulent IBDV NJ09 strain. In contrast, all chickens in the challenge control group showed typical IBD lesions in bursals, and eight of ten died P.C. In this study, we demonstrated that (i) a novel HVT BAC with the whole genome of the Fc-126 strain was obtained with the insertion of mini-F sequences in lieu of the gC gene; (ii) HVT-VP2-09 harboring the VP2 expression cassette from virulent IBDV exhibited in vitro growth properties similar to those of the parental HVT virus in CEF cells; and (iii) HVT-VP2-09 can provide efficient protection against the IBDV NJ09 strain.

Background Compared with oral antibiotics (primarily disrupt foregut microbiota), the present study used antibiotics with ileum terminal infusion to disrupt the hindgut microbiota, and investigated the changes in specific bacterial composition and immune indexes in the jejunum and colon, and serum of growing pigs. Twelve barrows (45 d of age, 12.08 ± 0.28 kg) fitted with a T-cannula at the terminal ileum, were randomly assigned to two groups and infused either saline without antibiotics (Control) or with antibiotics (Antibiotic) at the terminal ileum. After 25 d experiment, all pigs were euthanized for analyzing bacterial composition and immune status. Results Ileum terminal antibiotic infusion (ITAI) altered dominant bacteria counts, with a decrease in Bifidobacterium , Clostridium cluster IV and Clostridium cluster IV in the colon ( P  < 0.05), and an increase in Escherichia coli in the jejunum ( P  < 0.05). ITAI decreased ( P  < 0.05) short-chain fatty acids concentrations in the colon. ITAI decreased interleukin-8 (IL-8), IL-10 and secretory immunoglobulin A (sIgA) concentrations, and down-regulated IL-10 , Mucin-1 ( MUC1 ), Mucin-2 ( MUC2 ) and zonula occludens-1 ( ZO-1 ) mRNA expression in the colonic mucosa ( P  < 0.05). In the jejunal mucosa, ITAI decreased interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), sIgA and IgG levels together with down-regulation of IFN-γ , TNF-α , MUC2 and ZO-1 mRNA expression ( P  < 0.05). Furthermore, ITAI decreased IL-10, INF-γ, TNF-α, IgA and IgG concentrations in serum ( P  < 0.05). Correlation analysis revealed that the change in intestinal microbiota was correlated with alterations of Ig and cytokines. Conclusions ITAI affected jejunal and colonic specific bacteria counts, and altered some immune markers levels in the jejunal and colonic mucosa and serum. These findings implicate the potential contribution of hindgut bacteria to immune response in the intestinal mucosa and serum of growing pigs.

The study aimed to evaluate the effects of early antibiotic intervention (EAI) on bacterial fermentation patterns and mucosal immune markers in the colon of pigs with different protein level diets. Eighteen litters of piglets at day (d) 7 were fed creep feed without or with growth promoting antibiotics until d 42. At d 42, pigs within each group were further randomly assigned to a normal- or low-crude protein (CP) diet. At d 77 and d 120, five pigs per group were slaughtered for analyzing colonic bacteria, metabolites, and mucosal gene expressions. Results showed that low-CP diet increased propionate and butyrate concentrations at d 77 but reduced ammonia and phenol concentrations ( P  < 0.05). EAI increased p -cresol and indole concentrations under normal-CP diet at d 77 ( P  < 0.05). Low-CP diet significantly affected ( P  < 0.05) some bacteria groups ( Firmicutes , Clostridium cluster IV, Clostridium cluster XIVa, Escherichia coli , and Lactobacillus ), but EAI showed limited effects. Low-CP diet down-regulated gene expressions of pro-inflammatory cytokines, toll-like receptor (TLR4), myeloid differentiating factor 88 (MyD88), and nuclear factor-κB p65 (NF-κB p65) ( P  < 0.05). EAI up-regulated mRNA expressions of interleukin-8 (IL-8) and interferon-γ (IFN-γ) under normal-CP diet at d 77 ( P  < 0.05). Furthermore, reductions of E. coli and ammonia under low-CP diet were positively correlated with down-regulated gene expressions of pro-inflammatory cytokines, which were positively correlated with the down-regulated TLR4-MyD88-NF-κB signaling pathway. In conclusion, EAI had short-term effects under normal-CP diet with increased aromatic amino acid fermentation and gene expressions of pro-inflammatory cytokines. Low-CP diet markedly reduced protein fermentation, modified microbial communities, and down-regulated gene expressions of pro-inflammatory cytokines possibly via down-regulating TLR4-MyD88-NF-κB signaling pathway.