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Li X.,Soochow University of China | Zhou Z.-Y.,Huaiyin Hospital of Huaian City | Zhang Y.-Y.,Huaian First Peoples Hospital | Yang H.-L.,Soochow University of China

Osteoporosis is one of the most prevalent skeletal system diseases. It is characterized by a decrease in bone mass and microarchitectural changes in bone tissue that lead to an attenuation of bone resistance and susceptibility to fracture. Vertebral fracture is by far the most prevalent osteoporotic fracture. In the musculoskeletal system, osteoblasts, originated from bone marrow stromal cells (BMSC), are responsible for osteoid synthesis and mineralization. In osteoporosis, BMSC osteogenic differentiation is defective. However, to date, what leads to the defective BMSC osteogenesis in osteoporosis remains an open question. In the current study, we made attempts to answer this question. A mouse model of glucocorticoid-induced osteoporosis (GIO) was established and BMSC were isolated from vertebral body. The impairment of osteogenesis was observed in BMSC of osteoporotic vertebral body. The expression profiles of thirty-six factors, which play important roles in bone metabolisms, were compared through antibody array between normal and osteoporotic BMSC. Significantly higher secretion level of IL-6 was observed in osteoporotic BMSCs compared with normal control. We provided evidences that IL-6 over-secretion impaired osteogenesis of osteoporotic BMSC. Further, it was observed that β-catenin activity was inhibited in response to IL-6 over-secretion. More importantly, in vivo administration of IL-6 neutralizing antibody was found to be helpful to rescue the osteoporotic phenotype of mouse vertebral body. Our study provides a deeper insight into the pathophysiology of osteoporosis and identifies IL-6 as a promising target for osteoporosis therapy. © 2016 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source

Liu Y.-P.,Tengzhou Central Peoples Hospital | Hao Y.-D.,Huaian First Peoples Hospital
Pakistan Journal of Medical Sciences

Objective: To explore the restoration of femoral offset, rotation centers, limbs length equality of Chinese total hip arthroplasty patients with careful preoperative surgical planning, the appropriate prosthesis and skillful manipulation combined with a variety of verification tests during the operation. Methods: There were 92 hips (from 92 patients) surgery was performed by the same surgeon using the posterlateral approach by careful preoperative surgical planning. Appropriate prosthesis was chosen determining the reasonable femur osteotomy location, skillful manipulation and paying attention to every detail combined with a variety of verification tests and preoperative measurements during the operation. We evaluated the offset and rotation centers of the healthy (not performed) side and the operated side, the preoperative and postoperative limbs length discrepancy and analyzed the change of femoral offset, rotation centers and limbs length discrepancy of THA patients by self-control. Results: We found that the preoperative and postoperative femoral offset was basically not changed, the postoperative rotation centers had a tendency to the medial and inferior of the original rotation centers, the limbs length discrepancy and Harris Hip Score (HHS) were improved much more than before. Conclusions: Careful preoperative surgical planning, the appropriate prosthesis and skillful manipulation combined with a variety of verification tests during the operation is significantly correlated to the remarkable radiological and clinical results of THA patients. Source

Pu D.,Nanjing Medical University | Xing Y.,Nanjing Medical University | Gao Y.,Huaian First Peoples Hospital | Gu L.,Nanjing Medical University | Wu J.,Nanjing Medical University
European Journal of Obstetrics Gynecology and Reproductive Biology

Objective Premature ovarian failure (POF) is a complex, heterogeneous disorder that is influenced by multiple genetic components. This meta-analysis aimed to investigate the association between gene variants and susceptibility to POF. Study design MEDLINE and CNKI were searched for studies published from inception (1950) to June 2014. Meta-analysis was performed when three or more studies reported genetic data on the same polymorphism or mutation. Additive and dominant models were analyzed using RevMan Version 5.1. Results The literature search yielded 575 articles, of which 59 studies on the association between POF and gene variants were identified for meta-analysis. Five genes were selected for analysis, including 10 common gene polymorphisms [BMP15 (-9C>G, 788insTCT and 852C>T), ESR1 (-351A>G and -397C>T), FMR1 CGG repeat, FSHR (919A>G and 2039A>G), INHA (-16C>T and -124A>G)] and two mutations (BMP15 538G>A and INHA 769G>A). BMP15 538G>A was found to be significantly more common in patients with POF compared with controls. No significant associations were found between the other variants of BMP15 and POF. With respect to ESR1, the accumulative results were not significant, although the findings of the individual studies were controversial. The incidence of FMR1 premutation was significantly higher in patients with POF compared with controls [odds ratio (OR) 9.2, 95% confidence interval (CI) 5.42-15.61; p < 0.001] in the overall population, as well as in both Caucasian and Asian subgroups. Stratified analysis was applied for INHA 769G>A by ethnicity; a significant association with POF was only found in the Asian subgroup (allelic frequency: OR 8.89, 95% CI 2.1-5.52; p = 0.004). No significant associations were found between the other variants of INHA and POF. Conclusions BMP15 538A, FMR1 premutation and INHA 769A (in Asians alone) may indicate susceptibility to POF. Further well-designed studies and larger samples are required to confirm the association between gene variants and POF. © 2014 Elsevier Ltd. All rights reserved. Source

Fei Z.-H.,Wenzhou University | Yu X.-J.,Huaian First Peoples Hospital | Zhou M.,Yangzhou University | Su H.-F.,Wenzhou University | And 2 more authors.
Tumor Biology

Emerging evidences indicate that dysregulated long non-coding RNAs (lncRNAs) are implicated in cancer tumorigenesis and progression and might be used as diagnosis and prognosis biomarker or potential therapeutic targets. Therefore, identification of cancer-associated lncRNAs and investigation of their biological functions and molecular mechanisms are important for understanding the development and progression of cancer. In this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues (P < 0.001). Furthermore, decreased LINC00982 expression was negatively correlated with invasion depth (P < 0.001), advanced TNM stage (P = 0.004), and regional lymph node metastasis (P = 0.005). LINC00982 levels were robust in differentiating gastric cancer tissues from controls [area under the curve (AUC) = 0.742; 95 % confidence interval (CI) = 0.678–0.800, P < 0.01]. Kaplan–Meier analysis demonstrated that decreased LINC00982 expression contributed to poor overall survival (P < 0.01) and disease-free survival (P < 0.01) of patients. A multivariate survival analysis also indicated that LINC00982 could be an independent prognostic marker. The levels of LINC00982 in gastric juice from gastric patients were significantly lower than those from normal subjects (P = 0.026). Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions. Our findings present that decreased lncRNA LINC00982 could be identified as a poor prognostic biomarker in GC and regulate cell proliferation. © 2015 International Society of Oncology and BioMarkers (ISOBM) Source

Wang Q.,Louisville Veterans Administration Medical Center | Wang Q.,University of Louisville | Ren Y.,Huaian First Peoples Hospital | Mu J.,University of Louisville | And 8 more authors.
Cancer Research

Inflammation is a hallmark of cancer. Activated immune cells are intrinsically capable of homing to inflammatory sites. Using three inflammatory-driven disease mouse models, we show that grapefruit-derived nanovectors (GNV) coated with inflammatory-related receptor enriched membranes of activated leukocytes (IGNVs) are enhanced for homing to inflammatory tumor tissues. Blocking LFA-1 or CXCR1 and CXCR2 on the IGNVs significantly inhibits IGNV homing to the inflammatory tissue. The therapeutic potential of IGNVs was further demonstrated by enhancing the chemotherapeutic effect as shown by inhibition of tumor growth in two tumor models and inhibiting the inflammatory effects of dextran sulfate sodium-induced mouse colitis. The fact that IGNVs are capable of homing to inflammatory tissue and that chemokines are overexpressed in diseased human tissue provides the rationale for using IGNVs to more directly deliver therapeutic agents to inflammatory tumor sites and the rationale for the use of IGNVs as treatment for certain cancers in personalized medicine. © 2015 American Association for Cancer Research. Source

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