Abstract. Worldwide research contributions have allowed the field of fracture surgery to progress. However, to the best of our knowledge, no studies have documented the main characteristics of publications from different countries. The present study aimed to determine the quantity and quality of worldwide research in fracture surgery. The Web of Science database was searched to identify fracture articles published between 2005 and 2014. The contributions of countries were evaluated based on paper and citation numbers, and the research output of each country was adjusted according to population size.

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Activation of the proinflammatory-associated cytokine, tumor necrosis factor-α (TNF-α), in nucleus pulposus (NP) cells is essential for the pathogenesis of intervertebral disc degeneration (IDD). Restoring autophagic flux has been shown to effectively protect against IDD and is a potential target for treatment. The goal of this study was to explore particular autophagic signalings responsible for the protective effects of naringin, a known autophagy activator, on human NP cells. The results showed that significantly increased autophagic flux was observed in NP cells treated with naringin, with pronounced decreases in the inflammatory response and oxidative stress, which rescued the disturbed cellular homeostasis induced by TNF-α activation. Autophagic flux inhibition was detectable in NP cells cotreated with 3-methyladenine (3-MA, an autophagy inhibitor), partially offsetting naringin-induced beneficial effects. Naringin promoted the expressions of autophagy-associated markers via SIRT1 (silent information regulator-1) activation by AMPK (AMP-activated protein kinase) phosphorylation. Either AMPK inhibition by BML-275 or SIRT1 silencing partially counteracted naringin-induced autophagic flux enhancement. These findings indicate that naringin boosts autophagic flux through SIRT1 upregulation via AMPK activation, thus protecting NP cells against inflammatory response, oxidative stress, and impaired cellular homeostasis. Naringin can be a promising inducer of restoration autophagic flux restoration for IDD.

It is well known that glucocorticoid (GC)-induced bone loss is caused primarily by hypofunction and apoptosis of osteoblasts. However, the precise molecular events underlying the effect of GC on osteoblast apoptosis are not fully understood. Recent studies implicated an important role of E4BP4 in the regulation of osteoblast apoptosis and differentiation. Furthermore, E4BP4 is a GC-regulated gene required for GC-induced apoptosis in many cells. Therefore, we hypothesize that E4BP4 may be implicated in the process of GC-induced osteoblast apoptosis. Western blot, reverse-transcription-PCR, flow cytometry, and Hoechst 33258 staining were employed to investigate the role of E4BP4 in dexamethasone (DEX)-induced osteoblast apoptosis. We found that the expression of E4BP4 is significantly up-regulated in osteoblasts exposed to DEX. Furthermore, the depletion of E4BP4 significantly decreased DEX-induced osteoblast apoptosis. In addition, E4BP4 plays a crucial role in GC-evoked apoptosis of osteoblasts by enabling induction of Bim. On the basis of these results above, we can draw the conclusion that E4BP4 may contribute to the process of DEX-induced osteoblast apoptosis.

Background This study aimed to explore the relationship among different cervical sagittal parameters in asymptomatic volunteers and the correlation between surgical efficacy and difference of presumed and actual postoperative C2–7 Cobbs’s angle (C2–7COBB), which was calculated based on preoperative T1 slope (T1S) in patients undergoing cervical reconstruction. Methods In total, 158 inpatients with cervical spondylosis and 274 asymptomatic volunteers were retrospectively reviewed. Cervical sagittal parameters, such as C2–7COBB, T1S, thoracic inlet angle (TIA), and neck tilt (NT), were compared. Then, the correlation among these parameters was analyzed in asymptomatic volunteers, and a regression equation between T1S and C2–7COBB was established and used to analyze the correlation among the Japanese Orthopaedic Association (JOA) score improvement, the sagittal parameters, and the difference between presumed and actual postoperative C2–7COBB in patients after cervical reconstruction. Results The mean T1S, C2–7COBB, and TIA were significantly decreased in patients (P < 0.01). T1S and NT had a strong correlation with TIA (P < 0.01). T1S demonstrated a moderate correlation with C2–7COBB in asymptomatic volunteers (r = 0.569, P < 0.01). A regression equation had been established as C2–7COBB = 0.742 × T1S − 0.866. The mean C2–7COBB and JOA score improved significantly (P < 0.05) postoperatively. Moreover, the JOA improvement rate showed a significant negative correlation with the difference in the presumed and actual postoperative C2–7COBB (r = − 0.696, P < 0.01). Conclusion Our study successfully established a regression equation for calculating postsurgical C2–7COBB based on the correlation between T1S and C2–7COBB in asymptomatic volunteers. The regression equation could be used for guiding surgeons to accomplish an ideal postsurgical C2–7COBB for patients with cervical spondylosis.

Intralesional pingyangmycin is a cheap, effective, and safe treatment for xanthelasma, which has been well accepted by patients.

CDH in most patients with SCIWORET likely occurred before rather than after trauma. CDH caused more severe cord compression but did not aggravate the neurologic injury. The extent of MSCC had no association with the initial neurologic deficit or final recovery.

PAARNF restricted atlantoaxial flexion-extension but preserved axial rotation and lateral bending at the atlantoaxial joint in a type II odontoid fracture model. However, it should not be used clinically until further studies have been performed to test the long-term effects of this procedure.