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Objective To evaluate the effect of miacalcic on bone mineral density (BMD) and cytokines in the osteoporotic patients. Methods Sixty patients with osteoporosis were equally randomly assigned into 2 groups. Patients in control group (30 cases) received 600mg Caltratc per day. Patients in observation group (30 cases) received miacalcic besides Caltrate. The BMD of L2-4 lumbar spine and the femoral neck, insulin-like growth factor-1 (IGF-1), intcrleukin-6 (IL-6), and tumor necrosis factor-a TNF-α were determined before and after the treatment. Clinical symptoms were observed. Results BMD of the L2A lumbar spine and the femoral neck were higher in observation group than in control group (P < 0.05). The scrum levels of IGF-1, IL-6, and TNF-α were lower in observation group than in control group (P < 0.01). Pain was significantly relieved in the treatment group compared to control group (P < 0.05). BMD change was positively correlated to IGF-1 but negatively correlated to IL-6 and TNF-α in both groups. Conclusion Miacalcic is effective to improve BMD and to relieve pain in patients with osteoporosis. It can improve the levels of IGF-1, IL-6, and TNF-α. It can effectively relieve pain. [ABSTRACT FROM AUTHOR]

Although various antibacterial strategies have been developed, antibiotic chemotherapy remains the primary clinical treatment for bacterial infections. To address the limitations associated with the traditional antibiotic therapy, like burst drug release, rapid drug clearance, and the emergence of drug resistance, it is highly desirable to develop drug release systems that can realize controlled and sustained drug release to enhance the therapeutic efficacy. Herein, we present a novel drug release system, CIP@SU-102, which shows superior and long-lasting antibacterial activity. CIP@SU-102 was readily fabricated by the encapsulation of ciprofloxacin (CIP), a cationic broad-spectrum antibiotic, into an anionic Zr-based metal-organic framework SU-102 through ion-exchange. Notably, the loading capacity and efficiency of CIP were impressively high, reaching 33.3% and 66.8%, respectively. In vitro assays demonstrated that CIP@SU-102 has superior and prolonged antimicrobial activity against Gram-negative ( Escherichia coli ) and Gram-positive ( Staphylococcus aureus ) bacteria, including the methicillin-resistant Staphylococcus aureus (MRSA). Remarkably, CIP@SU-102 could retain its antibacterial efficacy even after continuous drug release for 20 days. In vivo assays verified that CIP@SU-102 could significantly accelerate infected wound healing because of its sustained drug release properties. Due to the low cost and biocompatibility of SU-102 as well as the affordability of ciprofloxacin, CIP@SU-102 is a very promising antibacterial agent for long-lasting bacterial disinfection and boosting infected wound healing in actual clinical applications. This work highlights the potential of the metal-organic framework-based drug release systems for sustained antimicrobial therapy.

Melittin (Mel), a natural detergent, is a major component of bee venom. Mel exhibits favorable clinical effects on the treatment of rheumatoid osteoarthritis, myositis, lumbar muscle strain, and peripheral neurological disorders. Interleukin-1β (IL-1β) contributes to the progression of osteoarthritis and is one of the key proinflammatory cytokines. However, the effect of Mel on IL-1β-induced osteoarthritis has not been reported. We examined the effects of Mel on the expressions of inducible NO synthase (iNOS), nuclear transcription factor κB (NF-κB), and I kappa B (I-κB) in the knee joint cells of C518 rats induced by IL-1β. Western blot and qPCR results showed that Mel at 0.1µg/mL or higher significantly inhibited iNOS expression. Similarly, 1µg/mL of Mel prevented IL-β-induced I-κB degradation in the cytoplasm and NF-κB migration from cytoplasm to nucleus. Mel exerts an inhibitory effect on IL-β-induced NF-κB activation by inhibiting both I-κB degradation and NF-κB migration and can potentially be developed as a new anti-osteoarthritis drug. Further research is needed to clarify the detailed mechanism.

Autosomal dominant polycystic kidney disease (ADPKD) is the common hereditary kidney disease, resulting from mutations in polycystic kidney disease 1 ( PKD1 ) and polycystic kidney disease 2 ( PKD2 ). Clinical data and genetic features of six Chinese families including ADPKD patients were analyzed via Next generation sequencing (NGS), Sanger sequencing, and multiplex ligation-dependent probe amplification. In family A, the proband (II5) with polycystic kidney (PK), hypertension, left ventricular hypertrophy, and valvular heart disease exhibited a heterozygous nonsense mutation, c.5086C>T (p.Gln1696Ter), in PKD1 (NM&#95;001009944). In family B, the proband (II3) with PK, polycystic liver (PL), hypertension, hypertrophy of the left ventricle and septum, valvular heart disease, chronic kidney disease (CKD) stage 5, bilateral renal calculi, and right inguinal hernia exhibited a heterozygous missense mutation, c.6695T>C (p.Phe2232Ser), in PKD1 . In family C, the proband (III1) with PK, PL, seminal vesicle cyst, hypertension, CKD stage 3, hypertrophy of the left ventricle and septum, and valvular heart disease harbored a heterozygous nonsense mutation, c.662T>G (p.Leu221Ter), in PKD2 (NM&#95;000297). In family D, the proband (III3) with PK, hypertension, and CKD stage 5 harbored a heterozygous missense mutation, c.8311G>A (p.Glu2771Lys), in PKD1 . In family E, the proband (II1) with PK, PL, hypertension, and CKD stage 5 exhibited a heterozygous deletion mutation, exon15-22, in PKD1 . In family F, the proband (II2) with PK, PL, CKD stage 3, hypertension, thickened interventricular septum, and valvular heart disease carried a heterozygous missense mutation, c.1649A>G (p.His550Arg), in PKD2 . Thus, three novel mutation sites which are responsible for ADPKD were discovered in this study., Competing Interests: None., (AJTR Copyright © 2020.)