Mechanistic studies indicated that mBMPR1A-mFc administration promoted osteoblastogenesis by activating Wnt/Lrp5/β-catenin signaling while decreasing osteoclastogenesis by inhibiting the RANKL/RANK/OPG pathway. Our novel findings provide solid evidence for the application of mBMPR1A-mFc as a therapeutic treatment for radiation-induced osteoporosis. check details AJTR Copyright © 2020.Oxidative stress can trigger DNA damage response and activation of cellular senescence. Accumulating studies have demonstrated that senescent cells can produce senescence-associated secretory phenotype that leads to increased bone resorption and decreased bone formation. And elimination of senescent cells or inhibition of SASP secretion has been shown to prevent bone loss in mice. N-acetylcysteine (NAC) is a strong antioxidant. However, it is unclear whether reversed estrogen deficiency-induced bone loss by antioxidant NAC was associated with the inhibition of oxidative stress, DNA damage, osteocyte senescence and SASP. In this study, OVX mice were supplemented with/without E2 or NAC, and were compared with each other. Our results showed that oxidative stress, DNA damage, osteocyte senescence and the secretion of senescence-associated inflammatory cytokines were increased in OVX mice compared with sham-operated mice. However, these parameters were obviously rescued in OVX mice supplemented with E2 or NAC. Data from this study suggest that NAC can prevent OVX-induced bone loss by inhibiting oxidative stress, DNA damage, cell senescence and the secretion of the senescence-associated secretory phenotype. AJTR Copyright © 2020.Reportedly, several long non-coding RNAs (lncRNAs) have been involved in the regulation of cardiac hypertrophy induced by diabetic cardiomyopathy (DCM), causing cardiac dysfunction and subsequent failure. Although lncRNA taurine upregulated gene 1 (TUG1) is associated with myocardial injury, the expression profile and potential role of TUG1 in DCM-related cardiac hypertrophy remain unknown. This study elucidated the functions of TUG1 in DCM and its underlying mechanisms. Our results demonstrated that the expression of TUG1 was upregulated in db/db mice cardiomyocytes. Inhibition of TUG1 by lentivirus si-TUG1 indicated no effect on systolic function; however, it effectively improved DCM-induced diastolic dysfunction in db/db mice. TUG1 silencing demonstrated no influence on the metabolic characteristics of DCM, including blood glucose and lipid levels. Notably, TUG1 knockdown significantly decreased cardiac hypertrophy and reduced the fibrotic area, in vivo. To further investigate the underlying mechanism, miR-499-5p was predicted as the targeted TUG1 microRNA. The RT-qPCR and luciferase activity results confirmed that TUG1 negatively regulated miR-499-5p in cardiomyocytes. Furthermore, the overexpression of miR-499-5p abated the inhibitory effects of TUG1 silencing on high glucose-mediated cardiac hypertrophy, in vitro. Collectively, our study suggested that TUG1 knockdown attenuated DCM-induced cardiac hypertrophy and diastolic dysfunction by upregulating miR-499-5p. lncRNA TUG1 may be a novel potential target for DCM therapy. AJTR Copyright © 2020.We herein report a case of well-differentiated small hepatocellular carcinoma (HCC) with severe lymphocytic infiltrate (SLI) in a 55-year-old male patient with HCV-related cirrhosis. The patient had been followed-up because of HCV-related cirrhosis. He was found to have two small nodules in S8 by imaging techniques, and he underwent S8 segmentectomy. The resected liver showed two small nodules. Both were encapsulated, well-defined, solid, reddish and expansive nodules with fibrous septa. They measured 8 × 8 mm and 15 × 10 mm, respectively. Histologically, both tumours were pure HCC; the smaller showed SLI with lymphocytes/HCC cells ratio over 20, while the larger showed mild lymphocytic infiltration with lymphocytes/HCC cells ratio of 0.8. The smaller HCC was well-differentiated (trabecular thickness I). Extremely well-differentiated Edmondson I HCC or adenomatous hyperplasia areas were seen in the periphery of both HCCs. The patterns of SLI could be classified into the following three sinusoids (S) type, porxpressed macrophage antigens aside from myofibroblastic antigens. These data suggest that, in the present case, pan-B-cells, pan-T-cells, helper T-cells, cytotoxic T-cells, plasma cells, macrophages, Kupffer cells, stellate cells, myofibroblasts, fibroblasts, endothelial cells, dendritic cells, Langerhans cells, and toxic molecules may play roles in tumour immunology. IJCEP Copyright © 2020.Cartilage degeneration is considered the main pathologic feature of osteoarthritis (OA). Cumulative evidence indicates that chondrocyte apoptosis is associated with cartilage degradation. However, the underlying molecular mechanism of chondrocyte apoptosis remains unclear. Growth factor receptor-bound protein 2 (GAB2), an adaptor protein, belongs to the Gab family and is involved in various biologic processes. Here, we explored the role of GAB2 in the pathogenesis of osteoarthritis (OA). GAB2 expression was markedly increased in OA articular cartilage. GAB2 expression was also increased in an in vitro model of TNFα-induced apoptosis. GAB2 depletion by siRNA promoted expression of the apoptosis markers, PARP and caspase-3, and increased the number of apoptotic cells, indicating that GAB2 might have an anti-apoptotic effect in chondrocytes. Moreover, GAB2 knockdown inhibited AKT phosphorylation, increased BAX expression, and decreased BCL2 expression, which indicated that GAB2 regulates chondrocyte apoptosis through PI3K-AKT signaling. Taken together, our study indicates that GAB2 plays a vital role in chondrocyte apoptosis and provides a new therapeutic target for OA. IJCEP Copyright © 2020.Cervical cancer is one of the most common cancers in women worldwide. Metastasis in cancer has been a Gordian knot due to unsatisfactory clinical treatments. KIN17, a highly conserved gene from yeast to human, up-regulation is associated with the pathogenesis and development of several common cancers. Our previous works revealed that elevated expression of kin17 observed in cervical cancer tissues showed a close association with lymph node metastasis. This study aimed to explore roles and mechanisms of kin17 in the migration and invasion of cervical cancer cells. Cervical cancer cell lines HeLa and SiHa with kin17 knockdown were constructed by using recombinant lentiviral vector that carry specific siRNA targeting KIN17 gene. The mRNA and protein levels of kin17 in cells were determined by RT-qPCR and western blotting, respectively. Wound healing assay and transwell assays were performed to assess the migration and invasion abilities of the cancer cells, respectively. The expression of signaling proteins involved in the NF-κB-Snail pathway was analyzed by western blotting.check details