No abstract

We investigated the effects of dietary supplementation with Bacillus subtilis PB6 ( B. subtilis PB6) during late gestation and lactation on sow reproductive performance, antioxidant indices, and gut microbiota. A total of 32 healthy Landrace × Yorkshire sows on d 90 of gestation were randomly assigned to 2 groups, with 16 replicates per group, receiving basal diet (CON) or the basal diet + 0.2% B. subtilis PB6, containing 4.0 × 10 8 CFU/kg of feed (BS). The litter sizes (total born) and numbers of piglets born alive were larger in the BS group ( P < 0.01), whereas the weights of piglets born alive and the piglet birth intervals were lower in the BS group ( P < 0.05). Although the litter weights and piglet bodyweights (after cross-fostering) were lower after BS treatment ( P < 0.05), the litter sizes, litter weights, lactation survival rate, and litter weight gains at weaning were higher in BS group ( P < 0.05). The concentrations of malondialdehyde (MDA) in the sow sera at parturition were lower in the BS group ( P < 0.01). The serum total antioxidant capacity (T-AOC) at parturition and the serum catalase (CAT) concentrations on d 21 of lactation were higher in the BS group ( P < 0.05). Dietary supplementation with B. subtilis PB6 ( P < 0.05) reduced the serum endotoxin concentrations in the sows and the serum cortisol concentrations of the piglets at d 14 of lactation. The α-diversity indices of microbial were higher in the CON group ( P < 0.05). At the phylum level, B. subtilis PB6 supplementation increased the relative abundances of Gemmatimonadete and Acidobacteria (both P < 0.01) and reduced those of Proteobacteria, and Actinobacteria (both P < 0.05). At the genus level, B. subtilis PB6 supplementation increased the relative abundance of Ruminococcaceae_UCG-013 cc ( P < 0.05) and reduced that of Streptococcus ( P < 0.05). This study demonstrated that adding 4.0 × 10 8 CFU/kg B. subtilis PB6 to sows’ feed during late gestation and lactation could shorten piglet birth intervals, enhance the growth performance of suckling piglets, and improve the gut health of sows during late gestation.

We aim to investigate the preventive and therapeutic effects of ghrelin on a rat NAFLD model and possible underlying mechanism. Sprague-Dawley rats were fed with high-fat diet for 8 weeks to induce NAFLD. A group of rats were also treated with ghrelin throughout the NAFLD induction. After 8 weeks, rats were sacrificed for liver injury measurements. Rats with NAFLD showed obvious histological changes including necrosis and inflammation foci, elevated serum enzyme (ALT and AST) levels, dysregulated hepatic lipid metabolism, increased formation of oxidative stress, and lipid peroxidation markers, up-regulated levels of pro-inflammatory cytokines and apoptotic cells in the liver. Treatment of ghrelin improved liver injury through counter-acting those events. The improvement of ghrelin was accompanied with a restoration of LKB1/AMPK and PI3 K/Akt pathways. Ghrelin treatment alone did not influence the healthy rat liver. In addition, "therapeutic" ghrelin administration (2 weeks) after the establishment of early NAFLD symptoms (4 weeks) in rats further proved the beneficial effects of ghrelin. In conclusion, administration of ghrelin could attenuate NAFLD-induced liver injury, oxidative stress, inflammation, and apoptosis partly through the action of LKB1/AMPK and PI3 K/Akt pathways.

This work aims to explore the roles and mechanisms of long non coding RNA (lncRNA) THOR in regulating the stemness of gastric cancer cells. RNA-sequencing combined with quantitative real-time PCR (qRT-PCR) indicated that lncRNA THOR level was significantly upregulated in gastric cancer tissues compared with that in normal adjacent tissues. Knockdown of THOR attenuated the stemnness of gastric cancer cells, evident by the decrease of stemness markers expression and capacity of cells spheroid formation. Further RNA-sequencing combined with qRT-PCR and western blot analysis demonstrated that expression of transcriptional factor SOX9 was remarkably decreased in gastric cancer cells with THOR stable knockdown. Additionally, RNA immunoprecipitation (RIP) combined with luciferase reporter assay revealed that THOR directly bound to SOX9 3' untranslated region (3'UTR), but not its 5'UTR or coding area. Notably, overexpression of SOX9 rescued THOR knockdown-mediated inhibition on the stemness of gastric cancer cells. Thus, our results suggest that THOR could potentiate the stemness of gastric cancer cells via directly binding to SOX9 3'UTR.

No abstract

Although systemic bone loss accompanying estrogen deficiency has been proposed as a risk factor for periodontal disease in post-menopausal women, the mechanisms involved remain unclear. The objective of this study was to elucidate the potential bone-sparing effect of estrogen (17beta-estradiol, E(2)) via modulation of inflammatory cytokine production in human periodontal ligament (hPDL) cells. E. coli lipopolysaccharide (LPS) increased the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and receptor activator of NF- B ligand (RANKL) by hPDL cells at both mRNA and protein levels. E(2) treatment reversed the stimulatory effects of LPS on pro-inflammatory cytokine expression by hPDL cells. Moreover, E(2) up-regulated osteoprotegerin (OPG) expression and therefore attenuated the reduction of the OPG vs. RANKL ratio. Our results suggested that estrogen may play a significant role in modulating periodontal tissue responses to LPS, and may exert its bone-sparing effects on periodontal tissues via altering the expression of inflammatory cytokines in hPDL cells.

Doctors and patients attempt to accelerate orthodontic tooth movement with a minimally invasive surgery approach. The purpose of this systematic review was to evaluate the evidence of accelerated tooth movement in minimally invasive surgery and the adverse effects from it. A systematic search of the literature was performed in the electronic databases of PubMed, CENTRAL (Cochrane Central Register of Controlled Trials), Embase, Scopus, Web of Science, Science Direct, and Medline and was complemented by a manual search until February 2019. The inclusion criteria were prospective clinical studies of patients treated with a fixed appliance, and the intervention was accelerated orthodontic treatment with minimally invasive surgery. Nineteen articles (538 participants) were included in the review: 9 studies assessed the rate of upper canine movement; 5 considered the treatment time; 1 evaluated the en masse retraction time; and 4 studied adverse effects. We performed a meta-analysis for the rate of canine movement and treatment time and described the results for the adverse effects in a systematic review. The results of the subgroup analysis according to micro-osteoperforation and piezocision were included in the study. No accelerated tooth movement was found in the micro-osteoperforation group. After flapless corticotomy procedures, increased tooth movement rates were identified by weighted mean differences of 0.63 (95%CI = 0.22, 1.03, P = 0.003) and 0.64 (95% CI, −25 to 1.53; P = 0.16) for 1 and 2 mo, respectively. The mean treatment time was 68.42 d (95% CI, −113.19 to −23.65; P = 0.003) less that than for minimally invasive surgery. Moreover, no significant adverse effect was found. Because of the high heterogeneity of the meta-analysis, the results must be validated by additional large-sample multicenter clinical trials. There is not sufficient evidence to support that the single use of micro-osteoperforation could accelerate tooth movement, and there is only low-quality evidence to prove that flapless corticotomy could accelerate tooth movement.

Osteoporotic women exhibit high frequency of alveolar bone loss and low bone density. Estrogen deficiency, which is vital in the pathogenesis of postmenopausal osteoporosis, has received increasing attention in the studies related to the periodontal diseases. Similar to most hormones, estrogen exerts its influence by binding to specific receptors, estrogen receptor (ER)-alpha and -beta. The periodontal ligament cells (PDLcs) are very important in maintaining the integrity of the periodontal tissue, which is the connective tissue located between the alveolar bone and the root surface of tooth. In this study, we evaluated the effects of estrogen deficiency on the alveolar bone in ovariectomized rats by histometric measurement of attachment level in vivo. Using the reverse transcriptase polymerase chain reaction (RT-PCR) and Western-blot procedure, we also detected mRNA and protein products of ERs and investigated the effects of estrogen on bone-forming capability by monitoring alkaline phosphatase (ALP) activity and osteocalcin production in cultured human PDLcs. Our results demonstrated that both ER-alpha and -beta were expressed in PDLcs. Moreover, when exposed to 17-beta estradiol, PDLcs exhibited positive modulation on ALP activity and osteocalcin production. The study suggests that estrogen and ERs may play an important role in periodontal diseases.