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Excessive iodine intake can induce autoimmune thyroiditis (AIT), and the methylation of programmed death receptor 2 (PD-L2) may be involved in the development of iodine-induced AIT. Here, we investigated the immune role of methylation of the susceptibility gene PD-L2 in the occurrence of iodine-induced AIT using the DNA methyltransferase inhibitor Decitabine (Dec) in an experimental autoimmune thyroiditis (EAT) rat model. After injecting Dec intraperitoneally into EAT rats, we performed arsenic-cerium catalytic spectrophotometry, pathological hematoxylin and eosin staining, enzyme-linked immunosorbent assay, quantitative methylation-specific polymerase chain reaction (qMSP), and quantitative real-time polymerase chain reaction (qPCR) to determine the relevant indices. The results showed that compared with the control group, the urinary iodine, thyroid lymphocyte infiltration, thyroglobulin antibody (TgAb), interferon (IFN-γ), and interleukin (IL-23) levels of the EAT rats were significantly increased. The PD-L2 methylation levels were significantly decreased in EAT rats compared to control rats, and the mRNA expression of the PD-L2 was significantly increased. Following Dec intervention, the methylation level of the PD-L2 in rats increased and interferon and interleukin-23 levels decreased, albeit not significantly. However, the mRNA expression of PD-L2 decreased significantly after Dec intervention, and the thyroid function of EAT rats also showed a gradual improvement trend. In summary, hypomethylation of PD-L2 is closely related to the development of iodine-induced AIT. Pro-inflammatory cellular factors are also involved in iodine-induced AIT progression. Although Dec shows promise in the treatment of AIT, further evaluation of its safety is necessary.

ABSTRACT: Two trials were conducted to draw the phase-response curve of productive and immunological variables in heat-exposed layer chickens at different ages (71 to 130 d, and 211 to 270 d). Birds were acclimated to the following conditions for 60 d: constant optimal ambient temperature at 24°C and high ambient temperature at 34°C for 8 h/d (10:00–18:00). Data collection and biochemical measurements were performed every 10 d. In both age ranges, high temperature favored the innate immunity (P < 0.01) at the cost of performance (P < 0.05) during a given period, including the relative abundance of B and T-helper lymphocytes, lymphocyte proliferation ratio (B and T lymphocytes), and serum immunoglobulin contents (IgG and IgM) in the peripheral blood, as well as splenic expression of inflammation-related genes (iNOS, TLR-4, TNF-α, IL-6, and INF-γ). Compared with laying hens, growing pullets showed a time-delayed activation of immune response following heat challenge, and had no immunosuppression up to the end of exposure. Overall, the immune system of layer birds has a trade-off with production tissues in a hot environment, and exhibits distinct age-range-specific responses of acclimatization.

Abstract To provide a basis for further optimization of the polio sequential immunization schedule, this study evaluated the effectiveness of booster immunization with one dose of bivalent oral poliovirus vaccine (bOPV) at 48 months of age after different primary polio immunization schedules. At 48 months of age, one dose of bOPV was administered, and their poliovirus types 1–3 (PV1, PV2, and PV3, respectively)-specific neutralizing antibody levels were determined. Participants found to be negative for any type of PV-specific neutralizing antibody at 24, 36, or 48 months of age were re-vaccinated with inactivated polio vaccine (IPV). The 439 subjects who received a bOPV booster immunization at the age of 48 months had lower PV2-specific antibody levels compared with those who received IPV. One dose of IPV during basic polio immunization induced the lowest PV2-specific antibody levels. On the basis of our findings, to ensure that no less than 70% of the vaccinated have protection efficiency, we recommend the following: if basic immunization was conducted with 1IPV + 2bOPV (especially Sabin strain-based IPV), a booster immunization with IPV is recommended at 36 months of age, whereas if basic immunization was conducted with 2IPV + 1bOPV, a booster immunization with IPV is recommended at 48 months of age. A sequential immunization schedule of 2IPV + 1bOPV + 1IPV can not only maintain high levels of antibody against PV1 and PV3 but also increases immunity to PV2 and induces early intestinal mucosal immunity, with relatively good safety. Thus, this may be the best sequential immunization schedule for polio in countries or regions at high risk for polio.

ABSTRACT: Two trials were performed to evaluate the association of hypothalamic abundances of thermosensitive transient receptor potential (TRP) ion channels with thermoregulation in broiler chickens. In trial 1, temporal changes in body temperatures, and hypothalamic expression patterns of TRP channels and thermoregulatory neurotransmitter concentrations were assessed from 3 to 42 d of age. In trial 2, the same variables were compared at 2 age stages between 2 distinct types of birds with high or low rectal temperatures (HRT or LRT). The core-to-brain temperature difference exhibited a rapid increase after hatching, arriving at a steady state in the fourth week (P < 0.01). The hypothalamus saw a progressive decrease of TRPV4 protein expression through 28 d (P < 0.01), followed by a great increase in the abundance of other channels right up to the end (P < 0.05). Compared to LRT birds, a decline in hypothalamic content of TRPV4 (P < 0.05), together with a bigger core-to-brain temperature difference (P < 0.01), was evident in the HRT counterpart at 33 d. In both trials, the core-to-brain and core-to-surface temperature differences were controlled in a synchronous and coordinated manner. These results allow concluding that developmental changes in the thermal sensitivity of hypothalamic neurons, determined by brain cooling capacity, involve a neuro-genomic mechanism, which regulates the ratio between thermosensitive TRP ion channels to attain a lower proportion of TRPV4 in comparison with other channels.

To uncover the molecular mechanism underlying glucocorticoid-induced loss of mitochondrial integrity in skeletal muscles, studies were performed to investigate whether the peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1)-mediated pathway was involved in this process. In an in vivo trial, 3 groups of 30-d-old Arbor Acres male broilers were randomly subjected to one of the following treatments for 7 days: corticosterone (CORT, 30 mg/kg diet), control (blank), and pair-feeding (restricted to the same feed intake as for the CORT treatment), each with 6 replicates of 15 birds. Mitochondrial abundance, morphology, and function were determined in the pectoralis major and biceps femoris muscles. In an in vitro trial, a primary culture of embryonic chick myotubes was incubated with a serum-free medium for 24 h in the presence or absence of CORT (0, 200, and 1,000 nM). Results showed that CORT destroyed mitochondrial ultrastructure (p < 0.01), and decreased the enzymatic activity and protein expression of respiratory chain complexes (p < 0.05), leading to an inferior coupling efficiency (p < 0.05). As reflected by a decline in mitochondrial density (p < 0.01) and mitochondrial DNA copy number (p < 0.05), CORT reduced mitochondrial contents. Among all three PGC-1 family members, only PGC-1β was down-regulated by CORT at the protein level (p < 0.05). Some aspects of these responses were tissue-specific and seemed to result from the depressed feed intake. Overall, CORT may impair mitochondrial biogenesis and oxidative phosphorylation in a PGC-1β-dependent manner in chicken muscles.

Introduction: Renal cancer is one of the most common cancers in the world, but the effect of therapies on advanced renal cancer has not improved for decades. Ferroptosis is an emerging type of programmed cell death and has been proved to play a vital role in many kinds of cancers. However, the mechanisms of ferroptosis regulated by long noncoding RNA (lncRNA) in the context of renal cancer was still unknown. Methods: We used bioinformation analysis to identify SLC16A1-AS1 as a survival-related lncRNA in renal cancer. The expression levels of SLC16A1-AS1 and microRNA-143-3p (miR-143-3p) were detected by quantitative reverse transcription–polymerase chain reaction. Cell counting kit-8 assay, 5-bromo-2′-deoxyuridine proliferation assay, and colony-formation assay were performed to evaluate cell viability and proliferation. Wound-healing assay and transwell assay were used to examine cell invasive and migration capacity. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation were used to identify the interaction among SLC16A1-AS1, miR-143-3p, and the target protein solute carrier family 7 membrane 11 (SLC7A11). Reduced glutathione and glutathione and lipid peroxidation measurements were carried out to evaluate the level of ferroptosis, and the expression levels of ferroptosis-related proteins were analyzed by western blot. Results: Our study revealed that SLC16A1-AS1 has high expression and was associated with overall survival in renal cancer. Knockdown SLC16A1-AS1 inhibited cell viability, proliferation, and migration of renal cancer cells. Furthermore, it was demonstrated that SLC16A1-AS1 served as a sponge of miR-143-3p, and knockdown SLC16A1-AS1 significantly increased the enrichment of miR-143-3p. And then, SLC7A11 was identified as the target protein of miR-143-3p, and overexpression miR-143-3p remarkably inhibited the expression of SLC7A11. Moreover, knockdown SLC16A1-AS1 could aggravate this effect. Finally, through inhibiting SLC7A11 expression, silencing SLC16A1-AS1 induced ferroptosis via increasing miR-143-3p. Conclusion: The present results suggest that silencing lncRNA SLC16A1-AS1 can induce ferroptosis through miR-143-3p/SLC7A11 signaling in renal cancer. Our study provided a novel view into the pathogenesis and treatment strategy of RCC.

In the new stage of the new century, a new technological revolution is coming quietly. This revolution is represented by “data.” The application of “big data (B D A)” technology is causing changes in all walks of life, and the use of “B D A research methods” in the education field will inevitably become a trend. The purpose of this article is an innovative research on the teaching methods of Taekwondo based on the background of B D A in a college elective course. This paper first introduces the core technology of the database by summarizing the basic theory of the database. Based on the current situation of elective Taekwondo teaching in contemporary universities, analyze the current problems and deficiencies and conduct innovative research on college elective Taekwondo teaching methods combined with Beidou technology. This paper systematically expounds the practical connection, method innovation, and implementation path between BDA technology and college elective Taekwondo teaching methods and compares the traditional Taekwondo teaching methods based on BDA technology. Experimental research shows that compared with traditional Taekwondo teaching methods, the performance of university Taekwondo teaching based on data mining (D M I) in the context of B D A is more than 20% higher, which fully reflects its feasibility and the innovation of traditional Taekwondo teaching methods needs to be solved urgently.

Previous school bullying was associated with increased risk of depression in students. However, little was known about the role of the Big Five personality traits in this association. The purpose of this study was to investigate the possible mediation by the Big Five personality traits in this association in a large group of Chinese college students, and to provide help for educators to prevent students from serious psychological and mental diseases caused by school bullying. Random stratified cluster sampling was used to survey 2152 college students ranging from freshmen to seniors at three universities in Qiqihar city, Heilongjiang Province, China. The risk factors for previous school bullying included gender, living expenses per month, caregivers, parents often quarreling, and divorced parents. Males were more likely to be bullied at school than females. The influencing factors of depression include gender, caregivers, living expenses per month, frequent parents quarreling, and parental divorce. Females were more prone to depression than males. Depression was significantly correlated with all dimensions of school bullying and the Big Five personality traits (p < 0.05). The Big Five personality traits were found to play a significant mediating role between depression and school bullying in up to 45% of cases involving depression. Our major findings highlighted the promising role of personality-based intervention measures in reducing the risk of depression associated with school bullying in Chinese students.

Here, we show the strategies to strengthen Mg alloys through modifying the matrix by planar faults and optimizing the local lattice strain by solute atoms. The anomalous shifts of the local phonon density of state of stacking faults (SFs) and long periodic stacking-ordered structures (LPSOs) toward the high-frequency mode are revealed by HCP-FCC transformation, resulting in the increase of vibrational entropy and the decrease of free energy to stabilize the SFs and LPSOs. Through integrating bonding charge density and electronic density of states, electronic redistributions are applied to reveal the electronic basis for the ‘strengthening’ of Mg alloys.

Incomplete knowledge of the mechanisms at work continues to hamper efforts to maximize reprogramming efficiency. Here, we present a systematic genome-wide RNAi screen to determine the global regulators during the early stages of human reprogramming. Our screen identifies functional repressors and effectors that act to impede or promote the reprogramming process. Repressors and effectors form close interacting networks in pathways, including RNA processing, G protein signaling, protein ubiquitination, and chromatin modification. Combinatorial knockdown of five repressors (SMAD3, ZMYM2, SFRS11, SAE1, and ESET) synergistically resulted in ∼85% TRA-1-60-positive cells. Removal of the novel splicing factor SFRS11 during reprogramming is accompanied by rapid acquisition of pluripotency-specific spliced forms. Mechanistically, SFRS11 regulates exon skipping and mutually exclusive splicing of transcripts in genes involved in cell differentiation, mRNA splicing, and chromatin modification. Our study provides insights into the reprogramming process, which comprises comprehensive and multi-layered transcriptional, splicing, and epigenetic machineries.

Anti-aging effect of Radix polygoni multiflori preparata in aging mice model was examined by bioassay method and explore new model of quality control of Traditional Chinese Medicine. Model of aging mice induced by D-galactose were used. The activity of senescence associated molecular markers such as superoxide dismutase, malondialdehyde and glutathione peroxidase in serum or homogenate were determined to evaluate the anti-aging activity. The results showed that the polysaccharide content in the 0.4, 0.8 g/mL decoction were 80.1, 160.2 mg/mL respectively. The HPLC results showed that stibene glucoside content in the 0.4 and 0.8 g/mL decoction were 404 and 808 mg/mL respectively. Experimental results showed that 10 week-old mice were the most sensitive to SOD activity in homogenate. In conclusion, Radix polygoni multiflori preparata has anti-aging effect probably by removing ROS.

MicroRNAs have been implicated in the regulation of several cellular signaling pathways of colorectal cancer (CRC) cells. Although emerging evidence proves that microRNA (miR)-106a is expressed highly in primary tumor and stool samples of CRC patients; whether or not miR-106a mediates cancer metastasis is unknown. We show here that miR-106a is highly expressed in metastatic CRC cells, and regulates cancer cell migration and invasion positively in vitro and in vivo. These phenotypes do not involve confounding influences on cancer cell proliferation. MiR-106a inhibits the expression of transforming growth factor-β receptor 2 (TGFBR2), leading to increased CRC cell migration and invasion. Importantly, miR-106a expression levels in primary CRCs are correlated with clinical cancer progression. These observations indicate that miR-106a inhibits the anti-metastatic target directly and results in CRC cell migration and invasion.

BackgroundGlucocorticoid has an important effect on lipid metabolism in muscles, and the type of fatty acid likely affects mitochondrial utilization. Therefore, we hypothesize that the different fatty acid types treatment may affect the glucocorticoid induction of intramuscular lipid accumulation.Methodology/principal findingsThe effect of dexamethasone (DEX) on fatty acid metabolism and storage in skeletal muscle of broiler chickens (Gallus gallus domesticus) was investigated with and without fatty acid treatments. Male Arbor Acres chickens (31 d old) were treated with either palmitic acid (PA) or oleic acid (OA) for 7 days, followed by DEX administration for 3 days (35-37 d old). The DEX-induced lipid uptake and oxidation imbalance, which was estimated by increased fatty acid transport protein 1 (FATP1) expression and decreased carnitine palmitoyl transferase 1 activity, contributed to skeletal muscle lipid accumulation. More sensitive than glycolytic muscle, the oxidative muscle in DEX-treated chickens showed a decrease in the AMP to ATP ratio, a decrease in AMP-activated protein kinase (AMPK) alpha phosphorylation and its activity, as well as an increase in the phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal p70S6 kinase, without Akt activation. DEX-stimulated lipid deposition was augmented by PA, but alleviated by OA, in response to pathways that were regulated differently, including AMPK, mTOR and FATP1.ConclusionsDEX-induced intramuscular lipid accumulation was aggravated by SFA but alleviated by unsaturated fatty acid. The suppressed AMPK and augmented mTOR signaling pathways were involved in glucocortcoid-mediated enhanced intramuscular fat accumulation.