Porcine skeletal muscle fibres are classified based on their different physiological and biochemical properties. Muscle fibre phenotype is regulated by several independent signalling pathways, including the mitogen-activated protein kinase (MAPK), nuclear factor of activated T cells (NFAT), myocyte enhancer factor 2 (MEF2) and peroxisome proliferator-activated receptor (PPAR) signalling pathways. MicroRNAs are non-coding small RNAs that regulate many biological processes. However, their function in muscle fibre type regulation remains unclear. The aim of our study was to identify miRNAs that regulate muscle fibre type during porcine growth to help understand the miRNA regulation mechanism of fibre differentiation. We performed Solexa/Illumina deep sequencing for the microRNAome during 3 muscle growth stages (63, 98 and 161 d). In this study, 271 mature miRNAs and 243 pre-miRNAs were identified. We detected 472 novel miRNAs in the muscle samples. Among the mature miRNAs, there are 23 highest expression miRNAs (over 10000 RPM), account for 85.3% of the total counts of mature miRNAs., including 10 (43.5%) muscle-related miRNAs (ssc-miR-133a-3p, ssc-miR-486, ssc-miR-1, ssc-miR-143-3p, ssc-miR-30a-5p, ssc-miR-181a, ssc-miR-148a-3p, ssc-miR-92a, ssc-miR-21, ssc-miR-126-5p). Particularly, both ssc-miR-1 and ssc-miR-133 belong to the MyomiRs, which control muscle myosin content, myofibre identity and muscle performance. The involvement of these miRNAs in muscle fibre phenotype provides new insight into the mechanism of muscle fibre regulation underlying muscle development. Furthermore, we performed cell transfection experiment. Overexpression/inhibition of ssc-miR-143-3p in porcine skeletal muscle satellite cell induced an/a increase/reduction of the slow muscle fibre gene and protein (MYH7), indicating that miR-143 activity regulated muscle fibre differentiate in skeletal muscle. And it regulate MYH7 through the HDAC4-MEF2 pathway. 相似文献
There is an increasing concern on cardiometabolic health in young professional athletes at heavy-weight class.
Objective
Our cross-sectional survey aimed to evaluate the prevalence of metabolic syndrome and clustering of metabolic risk factors in a population of young and active professional athletes of strength sports in China.
Methods
From July 2006 to December 2008, a total of 131 male and 130 female athletes of strength sports were enrolled. We used two criteria provided by the Chinese Diabetes Society (2004) and the National Cholesterol Education Program''s Adult Treatment Panel III (2002) to define the metabolic syndrome and its individual components, respectively.
Results
Regardless of their similar ages (mean: 21 years) and exercise levels, athletes in the heaviest-weight-class with unlimited maximum body weight (UBW) boundaries (mean weight and BMI: 130 kg and 38 kg/m2 for men, 110 kg and 37 kg/m2 for women) had significantly higher prevalence of metabolic syndrome than did those in all other body-weight-class with limited body weight (LBW) boundaries (mean weight and BMI: 105 kg and 32 kg/m2 for men, 70 kg and 26 kg/m2 for women). Prevalence of metabolic syndrome using CDS criteria (UBW vs. LBW: 89% vs. 18% for men, 47% vs. 0% for women) and its individual components, including central obesity, hypertension, hypertriglyceridemia, low high-density lipoprotein-cholesterol levels, and impaired fasting glucose, were all significantly higher in athletes at the heaviest weight group with UBW than all other weight groups with LBW.
Conclusions
Our study suggests that professional athletes of strength sports at the heaviest-weight-class are at a significant increased risk of cardiometabolic disease compared with those at all other weight categories. The findings support the importance of developing and implementing the strategy of early screening, awareness, and interventions for weight-related health among young athletes. 相似文献
Mercury (Hg) release and migration from municipal solid waste landfills has been an important issue to nearby ecosystems and human health. To completely understand the Hg biogeochemical cycle in landfills, this review presents the Hg emission processes via different pathways, related controlling mechanisms, and critical Hg transport and transformation processes involving the diffusion and advection of Hg, Hg volatilization, Hg adsorption and desorption, Hg redox reactions, and Hg methylation and demethylation. These critical physical, chemical, and biological processes result in the phase transfer of Hg and the distribution of different Hg species in landfill gas (LFG), leachates, and cover soils. In addition, key factors (e.g., LFG, meteorological conditions, cover soils, and vegetation) affecting Hg emission processes and their impacts are discussed here. This work provides a comprehensive picture of Hg behavior in landfills, and has positive implications for the development of a process-based model and the control of Hg emissions from landfills.
Ataxin-10 is a cytoplasmic protein that belongs to the family of armadillo repeat proteins and the ataxin proteins are ubiquitously expressed in nervous tissue. A loss of Ataxin-10 in primary neuronal cells causes increased apoptosis of cerebellar neurons. Knockdown of ATXN10 with siRNA in HeLa cells results in cytokinesis defects-multinucleation. Because of the essential role of Ataxin-10 in nervous system and cellular cytokinesis, we investigated the spatiotemporal expression of Ataxin-10 in a rat sciatic nerve crush (SNC) model. After never injury, we observed that Ataxin-10 had a significant up-regulation from 3d, peaked at day 5 and then gradually decreased to the normal level at 4 weeks. At its peak expression, Ataxin-10 expressed mainly in Schwann cells and macrophages of the distal sciatic nerve segment from injury, but had few co-localizations in axons. Besides, the peak expression of Ataxin-10 was in parallel with proliferating cell nuclear antigen (PCNA), and Ataxin-10 co-labeled with PCNA. Thus, all of our findings suggested that Ataxin-10 may be involved in the pathophysiology of sciatic nerve after SNC. 相似文献
Nuclear pore complex (NPC) shuttles cargo across the nuclear envelope. Here we present single-particle cryo-EM structure of the nuclear ring (NR) subunit from Xenopus laevis NPC at an average resolution of 5.6 Å. The NR subunit comprises two 10-membered Y complexes, each with the nucleoporin ELYS closely associating with Nup160 and Nup37 of the long arm. Unlike the cytoplasmic ring (CR) or inner ring (IR), the NR subunit contains only one molecule each of Nup205 and Nup93. Nup205 binds both arms of the Y complexes and interacts with the stem of inner Y complex from the neighboring subunit. Nup93 connects the stems of inner and outer Y complexes within the same NR subunit, and places its N-terminal extended helix into the axial groove of Nup205 from the neighboring subunit. Together with other structural information, we have generated a composite atomic model of the central ring scaffold that includes the NR, IR, and CR. The IR is connected to the two outer rings mainly through Nup155. This model facilitates functional understanding of vertebrate NPC.Subject terms: Cryoelectron microscopy, Nuclear envelope相似文献
The innate immune system is the first line of defense against many common microorganisms, which can initiate adaptive immune
responses to provide increased protection against subsequent re-infection by the same pathogen. As a major family of antimicrobial
peptides, defensins are widely expressed in a variety of epithelial cells and sometimes in leukocytes, playing an important
role in the innate immune system due to their antimicrobial, chemotactic and regulatory activities. This review introduces
their structure, classification, distribution, synthesis, and focuses on their biological activities and mechanisms, as well
as clinical relevance. These studies of defensins in the innate immune system have implications for the prevention and treatment
of a variety of infectious diseases, including bacterial ocular disease. 相似文献
Toll-like receptors (TLRs) play an important role in innate immunity against invading pathogens. Although TLR signaling has been indicated to protect cells from infection of several viruses, the role of TLRs in Dengue virus (DENV) replication is still unclear. In the present study, we examined the replication of DENV serotype 2 (DENV2) by challenging hepatoma cells HepG2 with different TLR ligands. Activation of TLR3 showed an antiviral effect, while pretreatment of other TLR ligands (including TLR1/2, TLR2/6, TLR4, TLR5 or TLR7/8) did not show a significant effect. TLR3 ligand poly(I:C) treatment prior to viral infection or simultaneously, but not post-treatment, significantly down-regulated virus replication. Pretreatment with poly(I:C) reduced viral mRNA expression and viral staining positive cells, accompanying an induction of the type I interferon (IFN-β) and type III IFN (IL-28A/B). Intriguingly, neutralization of IFN-β alone successfully restored the poly(I:C)-inhibited replication of DENV2. The poly(I:C)-mediated effects, including IFN induction and DENV2 suppression, were significantly reversed by IKK inhibitor, further suggesting that IFN-β is the dominant factor involved in the poly(I:C) mediated antiviral effect. Our study presented the first evidence to show that activation of TLR3 is effective in blocking DENV2 replication via IFN-β, providing an experimental clue that poly(I:C) may be a promising immunomodulatory agent against DENV infection and might be applicable for clinical prevention. 相似文献