Biomechanical study on different lengths of PFNA fixation for unstable intertrochanteric femoral fractures.

OBJECTIVE: The aim of our study was to compare the biomechanical stability of the Proximal Femoral Nail Antirotation (PFNA) (with 200 mm, 240 mm and 280 mm-long main nails) for the management of unstable intertrochanteric femoral fractures. METHODS: Tronzo-Evans Type IV and V fractures were built by applying a three-dimensional finite element model. Further, PFNA-II with 200 mm, 240 mm and 280 mm-long main nails were applied for fixation. The above model is the creation of 3 researchers designed in order to obtain average values of numerical stress. Von Mises stress distribution and medial and lateral stress peak of the femur and PFNA were compared. RESULTS: 240 mm and 280 mm PFNA medial stress peak was reduced significantly in comparison to 200 mm PFNA (p⟨0.05). However, there was no difference between 240 mm and 280 mm PFN. Also, no statistical difference was observed with any of 3 lengths in both medial and lateral stress peak for Evans Type IV and V PFNA. CONCLUSION: 240 mm and 280 mm PFNA could reduce femur fixation medial stress peak. Further, they were more efficient in comparison to the 200 mm PFNA, and their biomechanical stability was similar to that of the 280 mm nail.

Ropivacaine- and bupivacaine-induced death of rabbit annulus fibrosus cells in vitro: involvement of the mitochondrial apoptotic pathway.

OBJECTIVE: The purposes of this study were to assess whether local anesthetics (LAs), such as ropivacaine and bupivacaine, could induce apoptosis of rabbit annulus fibrosus (AF) cells in vitro and further to explore the possible underlying mechanism. METHODS: Rabbit AF cells at second passage were treated with saline solution and various concentrations of LAs. Apoptosis of AF cells were examined by cell counting kit-8 (CCK-8), Annexin V assays, Hoechst 33342 staining, and Caspase-3, -9 activity assays. The expression of apoptosis-related markers was detected by real-time PCR (RT-PCR) and Western Blot. The JC-1 staining was used to evaluate the change of mitochondrial membrane potential (MMP). Moreover, the levels of reactive oxygen species (ROS) were determined with fluorescent probe DCFH-DA. RESULTS: The results of flow cytometry indicated that LAs could induce apoptosis of rabbit AF cells in a dose-dependent manner. Apoptosis was confirmed by cell morphology, condensed nuclei and activation of Caspase-3 and -9. In addition, the molecular data showed that LAs could significantly up-regulate the expression of Bax, accompanied by a significant down-regulation of Bcl-2 expression. Furthermore, we also observed that LAs resulted in alteration of MMP and accumulation of intracellular ROS in AF cells. Blockade of ROS production by N-acetyl-l-cysteine (NAC) inhibited LAs-induced apoptosis. CONCLUSIONS: These findings suggest that LAs in clinically relevant concentrations could induce apoptosis of rabbit AF cells in vitro, and the mitochondrial pathway was, at least in part, involved in the LAs-mediated apoptosis. Further investigations focusing on the potential cytotoxicity of LAs on IVD cells are needed.

Autophagy is activated in compression-induced cell degeneration and is mediated by reactive oxygen species in nucleus pulposus cells exposed to compression.

OBJECTIVE: To determine whether autophagy contributes to the pathogenesis of degenerative disc disease (DDD) or retards the intervertebral disc (IVD) degeneration, and investigate the possible relationship between compression-induced autophagy and intracellular reactive oxygen species (ROS) in nucleus pulposus (NP) cells in vitro. METHODS: The autophagosome and autophagy-related markers were used to explore the role of autophagy in rat NP cells under compressive stress, which were measured directly by electronic microscopy, monodansylcadaverine (MDC) staining, immunofluorescence, western blot, and indirectly by analyzing the impact of pharmacological inhibitors of autophagy such as 3-methyladenine (3-MA) and chloroquine (CQ). And the relationship between autophagy and apoptosis was investigated by Annexin-V/propidium iodide (PI)-fluorescein staining. In addition, ROS were measured to determine whether these factors are responsible for the development of compression-induced autophagy. RESULTS: Our results indicated that rat NP cells activated autophagy in response to the same strong apoptotic stimuli that triggered apoptosis by compression. Autophagy and apoptosis were interconnected and coordinated in rat NP cells exposed to compression stimuli. Compression-induced autophagy was closely related to intracellular ROS production. CONCLUSIONS: Enhanced degradation of damaged components of NP cells by autophagy may be a crucial survival response against mechanical overload, and extensive autophagy may trigger autophagic cell death. Regulating autophagy and reducing the generation of intracellular ROS may retard IVD degeneration.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6, by Y. Zhao, X.-P. Qin, Y.-P. Lang, D. Kou, Z.-W. Shao, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5603-5610-DOI: 10.26355/eurrev_201907_18294-PMID: 31298312" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18294.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

OBJECTIVE: Recently, the roles of circular RNAs (circRNAs) in tumor progression have attracted much attention. Currently, circ-SMAD7 has been identified as an oncogene in cancers. The aim of this study was to investigate the function of circ-SMAD7 in the progression of ovarian cancer. PATIENTS AND METHODS: Circ-SMAD7 expression in both ovarian cancer cells and tissue samples was detected by quantitative Real Time-Polymerase Chain reaction (qRT-PCR). Circ-SMAD7 shRNA was constructed and transfected into the ovarian cancer cells. To identify the function of circ-SMAD7 in ovarian cancer, cell proliferation assay, colony formation assay, transwell assay, and Matrigel assay were conducted, respectively. In addition, qRT-PCR and Western blot assays were performed to elucidate the underlying mechanism and, then, it was analyzed. RESULTS: Circ-SMAD7 expression was remarkably higher in ovarian cancer tissue samples than in corresponding normal tissues. The proliferation of the ovarian cancer cells was significantly inhibited after circ-SMAD7 downregulation. Meanwhile, the migration and invasion of ovarian cancer cells were significantly inhibited after circ-SMAD7 downregulation in vitro. Both the mRNA and the protein expressions of the Krüppel-like factor 6 (KLF6) were remarkably promoted after circ-SMAD7 was knocked down in ovarian cancer cells. Furthermore, the KLF6 expression level was negatively correlated with circ-SMAD7 expression level in ovarian cancer samples. CONCLUSIONS: Our study suggests that circ-SMAD7 promotes the progression of ovarian cancer and enhances cell metastasis and proliferation via suppressing KLF6. In addition, circ-SMAD7 may be a novel therapeutic strategy in ovarian cancer.

Research on the correlation between the polymorphism of the back-2 gene and osteoarthritis.

OBJECTIVE: The objective of the present study was to investigate the correlation between polymorphisms of the back-2 gene and osteoarthritis. PATIENTS AND METHODS: We enrolled 76 patients with osteoarthritis who were admitted to our hospital between February 2014 and February 2015 for treatment as the observation group, and 46 healthy subjects as the control group. The analysis of back-2 gene polymorphisms (rs28502) was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). mRNA expression of the different genotypes was measured with reverse transcriptase-polymerase chain reaction (RT-PCR), and the protein expression of back-2 of different genotypes was measured with enzyme-linked immunosorbent assay (ELISA) and Western blotting. RESULTS: At locus 173 of the back-2 gene, there were a total of three genotypes, i.e. CC, CT, and TT. The frequencies of these genotypes in healthy subjects and osteoarthritis patients were 9.5%, 82.2%, 8.3% and 47.4%, 7.5%, 45.1%, respectively. There was a significant difference (p<0.05). However, the frequency of C/T in healthy older subjects and osteoarthritis patients was 50.6%, 49.4%, 51.15%, 48.85%, respectively, and there was no significant difference (p>0.05). RT-PCR showed no significant difference in mRNA expressions of the back-2 gene between the control group and observation group (p>0.05), although ELISA indicated that the protein expression of back-2 (12.3±0.36 µg/L) in osteoarthritis patients was significantly higher than in healthy subjects (1.52±0.18 µg/L) (p<0.05). Moreover, Western blotting analysis indicated that the protein expression of back-2 in osteoarthritis patients was significantly higher than in healthy subjects. CONCLUSIONS: Genetic polymorphisms of back-2 are associated with the metabolic syndrome in older people, i.e. older people with the CC or TT genotypes may be at high risk for metabolic syndrome.