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Nowadays, various new communication technologies operating in different frequency bands emerge constantly. There is a trend to integrate more than one of them into single system, for optimizing whole system performance and volume. As an important circuit component for frequency selection, the research on multiband bandpass filter (MB-BPF) receives much attention. This paper proposes a novel synthesis method for MB-BPF. It applies two frequency transformations on the specifications of the MB-BPF to be synthesized, so that a rough prototype containing the information of transmission and reflection zeros is constructed first. Then, optimization is applied for fine tuning until equal ripples are achieved in each passband. For simplicity, it is called the Rough Prototype and Fine Tuning (RP-FT) method, which demonstrate great advantage in flexibly controlling the performance of a MB-BPF such as passband number, performance of each passband, transmission zeros, etc. Furthermore, the filtering polynomials derived by the RP-FT method could be transformed into specific coupling matrixes for physical realization. For illustration, this paper derives a specific coupling matrix form, and applies it in the design of a microstrip quad-band bandpass filter. The measurement well verifies the validity of design process.

Osteoarthritis (OA) is a multifactorial disease that affects the entire joint, often resulting in severe pain, disability, psychological distress, and a lower quality of life. Patient self-management is emphasized in OA clinical recommendations. Currently, the clinical treatment of OA mainly focuses on pain relief and the improvement of joint function, with few options for regenerating degenerative cartilage or slowing the progression of OA. Therefore, we first reviewed the current treatment of OA, and then summarized the research advances of nanotechnology in OA treatment, including nano drug delivery systems for small molecule drugs, nucleic acids and proteins, nano-scaffolds for cartilage regeneration, and nanoparticle lubricants. Finally, we discussed the opportunities and potential challenges of nanotechnology in OA treatment.

Osteoarthritis (OA) is the most common joint disease, usually occurring in middle-aged and elderly people. However, current treatment for OA in its early stages is ineffective, and drug therapy is often ineffective in slowing the progression of the disease. In fact, a deeper understanding of the underlying molecular mechanisms of OA could help us to better develop effective therapeutic measures. N6-methyladenosine (m6A) is a methylation that occurs at the adenosine N6-position, which is the most common internal modification on eukaryotic mRNAs. The role and mechanisms of m6A in mammalian gene regulation have been extensively studied. The “Writer”, “eraser”, and “reader” proteins are key proteins involved in the dynamic regulation of m6A modifications. Recent studies on post-transcriptional regulation alone have shown that m6a modification has an important role in the development of OA. This paper summarizes the specific regulatory processes of M6A in disease and reviews the role of m6A in OA, describing its pathophysiological role and molecular mechanisms, as well as its future research trends and potential clinical applications in OA.

Osteoporosis is one of the most frequent skeletal disorders and a major cause of morbidity and mortality in the expanding aging population. Evidence suggests that hesperidin may have a therapeutic impact on osteoporosis. Nevertheless, little is known about the role of hesperidin in the development of osteoporosis. Bioinformatics analyses were carried out to explore the functions and possible molecular mechanisms by which hesperidin regulates osteogenic differentiation. In the present study, we screened and harvested 12 KEGG pathways that were shared by hesperidin-targeted genes and osteoporosis. The p53 signaling pathway was considered to be a key mechanism. Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.