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Osteoporotic osteoarthritis (OPOA) is a specific phenotype of OA with high incidence and severe cartilage damage. This study aimed to explore the protective efficacy of PEMF on the progression of OPOA and observed the effects of PEMF on PPARγ, autophagy- and apoptosis-related proteins in OPOA rats. Rats were randomly divided into three groups: control group, OPOA group, and PEMF group (n = 6). One week after surgery, the rats in PEMF group were subjected to PEMF (3.82 mT, 8 Hz, 40 min/day and 5 day/week) for 12 weeks. Results showed that PEMF retarded cartilage degeneration and bone loss, as evidenced by pathological staining image, decreased MMP-13 expression and increased bone mineral density. PEMF inhibited the serum levels of inflammatory cytokines, and the expressions of caspase-3 and caspase-8, while upregulated the expression of PPARγ. Moreover, PEMF significantly improved the autophagy disorders, represented by decrease expressions of Beclin-1, P62, and LC3B. The research demonstrates that PEMF can effectively prevent cartilage and subchondral bone destruction in OPOA rats. The potential mechanism may be related to upregulation of PPARγ, inhibition of chondrocyte apoptosis and inflammation, and improvement of autophagy disorder. PEMF therapy thus shows promising application prospects in the treatment of postmenopausal OA. Osteoporotic osteoarthritis (OPOA) is a very common combination disease, that characterized by chronic pain, swollen joints and susceptibility to fractures. It is particularly common in postmenopausal women. At present, drug therapy is the main treatment method, but the adverse reactions are serious and can not stop the progression of the disease. PEMF is a safe physical therapy that has been shown to increase bone density, reduce pain, and improve joints mobility. In this study, we aimed to explore the protective effect and potential mechanism of PEMF on OPOA. We found that PEMF significantly inhibited the inflammatory response, ameliorated the damaged cartilage and subchondral bone in OPOA rats, that maybe related to the regulation of chondrocyte autophagy and apoptosis. This study provided a new vision for PEMF' treatment on OPOA and has positive significance for the clinical promotion of PEMF. [ABSTRACT FROM AUTHOR]

Transition metal sulfides (TMSs) show the potential to be competitive candidates as next-generation anode materials for Li-ion batteries (LIBs) due to their high theoretical specific capacity. However, sluggish ionic/electronic transportation and huge volume change upon lithiation/delithiation remain major challenges in developing practical TMS anodes. We rationally combine structural design and interface engineering to fabricate a tubular-like nanocomposite with embedded crystalline Cu 9 S5 nanoparticles and amorphous MoS x in a carbon matrix (C/Cu 9 S 5 -MoS x NTs). On the one hand, the hybrid integrated the advantages of 1D hollow nanostructures and carbonaceous materials, whose high surface-to-volume ratios, inner void, flexibility, and high electronic conductivity not only enhance ion/electron transfer kinetics but also effectively buffer the volume changes of metal sulfides during charge/discharge. On the other hand, the formation of crystalline-amorphous heterostructures between Cu 9 S 5 and MoS x could further boost charge transfer due to an induced built-in electric field at the interface and the presence of a long-range disorder phase. In addition, amorphous MoS x offers an extra elastic buffer layer to release the fracture risk of Cu 9 S 5 crystalline nanoparticles during repetitive electrochemical reactions. Benefiting from the above synergistic effect, the C/Cu 9 S 5 -MoS x electrode as an LIB anode in an ether-based electrolyte achieves a high-rate capability (445 mAh g -1 at 6 A g -1 ) and superior ultralong-term cycling stability, which delivers an initial discharge capacity of 561 mAh g -1 at 2 A g -1 and its retention capacity after 3600 cycles (376 mAh g -1 ) remains higher than that of commercial graphite (372 mAh g -1 ).

As a male-specific chromosome, the structure of Y chromosome is complex and lacks of recombination, with numerous repeating, amplifying and palindromic sequences. The research of Y chromosome is difficult and slow since there are few protein coding genes and a large amount of heterochromatin which has caused extreme difficulty for sequencing. In recent years, an increasing number of studies have been focused on the Y chromosome. With the completion of the sequencing of human Y chromosome, the rapid development of sequencing technology, and the composition of DNA sequences in human Y chromosomes and the determination of gene content. This paper has summarized the structural composition and genes function of human Y chromosome, as well as the related hereditary diseases, with an aim to provide reference for Y chromosome-related genetic research.