Comparing Augmentative Plating and Exchange Nailing for the Treatment of Nonunion of Femoral Shaft Fracture after Intramedullary Nailing: A Meta-analysis.

OBJECTIVE: The aim of this meta-analysis was to systematically evaluate the efficacy of augmentative plating (AP) and exchange nailing (EN) in the treatment of nonunion of femoral shaft fracture. METHODS: For the present meta-analysis, PubMed, EMBASE, and the Cochrane Library were searched to identify relevant articles up to April 2019. Two investigators independently evaluated the quality of original publications following the guidelines proposed by the Cochrane Handbook. Data were extracted from the studies and analyzed using Review Manager 5.3. RESULTS: Five studies were included in this meta-analysis, with a total of 506 patients. There were 232 patients in the AP group and 276 patients in the EN group. The AP group was associated with higher union rate (OR, 11.66; 95% CI, 4.31-31.50; P < 0.01), shorter union time (SMD, -1.10; 95% CI, -2.09 to -0.11; P = 0.03), shorter operation time (SMD, -0.55; 95% CI, -0.88 to -0.21; P < 0.01), less blood loss (SMD, -1.72; 95% CI, -3.33 to -0.11; P < 0.01), and fewer complications (OR, -0.11; 95% CI, -0.16 to -0.07; P < 0.01) than the EN group. CONCLUSION: The results of the meta-analysis showed that AP is found to be superior for nonunion of femoral shaft fractures in both intraoperatively (ie, shorter operation time and less blood loss) and postoperatively (ie, higher union rate, shorter union time, and lower complication rate). Overall, AP was superior to EN in the treatment of nonunion of femoral shaft fractures after intramedullary nailing (IMN).

Inhibitory effects of methamphetamine on mast cell activation and cytokine/chemokine production stimulated by lipopolysaccharide in C57BL/6J mice.

Previous studies have demonstrated that methamphetamine (MA) influences host immunity; however, the effect of MA on lipopolysaccharide (LPS)-induced immune responses remains unknown. Mast cells (MCs) are considered to serve an important role in the innate and acquired immune response, but it remains unknown whether MA modulates MC activation and LPS-stimulated cytokine production. The present study aimed to investigate the effect of MA on LPS-induced MC activation and the production of MC-derived cytokines in mice. Markers for MC activation, including cluster of differentiation 117 and the type I high affinity immunoglobulin E receptor, were assessed in mouse intestines. Levels of MC-derived cytokines in the lungs and thymus were also examined. The results demonstrated that cytokines were produced in the bone marrow-derived mast cells (BMMCs) of mice. The present study demonstrated that MA suppressed the LPS-mediated MC activation in mouse intestines. MA also altered the release of MC cytokines in the lung and thymus following LPS stimulation. In addition, LPS-stimulated cytokines were decreased in the BMMCs of mice following treatment with MA. The present study demonstrated that MA may regulate LPS-stimulated MC activation and cytokine production.

Radiographic findings of hemolymphangioma in four patients: A case report.

Due to the rarity of hemolymphangioma, a limited number of cases of the disease have been reported in the literature thus far. The present case report describes the cases of 4 patients with hemolymphangioma that were diagnosed and treated at the Second Affiliated Hospital of Xi'an Jiaotong University (Xi'an, China). All patients were female, with a mean age of 44.7 years and a mean duration of symptoms prior to diagnosis of 2.7 years. The diagnosis of hemolymphangioma was determined by postoperative histopathology in all patients. A total of 2 patients were diagnosed with tumors that exhibited cystic characteristics (one in the mediastinum and the other in the neck), which was determined by computed tomography and magnetic resonance imaging. Another of the patients' tumors was located in the left forearm, and 1 patient had multifocal hemolymphangioma in the mediastinum and spleen. All patients underwent surgery and were asymptomatic during the follow-up periods (range, 8-15 months). In the present case report, the radiographic findings of the 4 cases are presented, including the unusual imaging characteristics that were observed, and relevant reports in the literature are discussed.

[Oestrogen inhibits invasion and metastasis of hepatocellular carcinoma MHCC97H cells by regulating the activity of AKT signaling pathway].

OBJECTIVE: To explore the inhibitory effect of estrogen against metastasis of human hepatocellular carcinoma MHCC97H cells and explore the molecular mechanism. METHODS: The inhibitory effect of estrogen on the migration and invasion of MHCC97H cells was evaluated with wound healing assay and Transwell assay. Western blotting was used for investigating the expression of MMP-2, MMP-9, AKT and p-AKT in the cells treated with estrogen. RESULTS: Estrogen treatment significantly inhibited the migration and invasion of MHCC97H cells in a dose-dependent manner. Estrogen significantly down-regulated the protein expressions of MMP-2 and MMP-9 and lowered the phosphorylation level of AKT. CONCLUSION: The anti-metastatic effect of estrogen involves inhibition of MMP-2 and MMP-9 in MHCC97H cells probably by regulating AKT signal pathway.

[p16INK4a protein is a specific molecular biomarker of breast cancer].

OBJECTIVE: To investigate the expression of p16INK4a protein in breast cancer and analyze its clinical significance. METHODS: A total of 132 surgical specimens of primary breast cancer obtained between 2014 and 2015 were examined for expressions of ER, PR, CK5/6, Her-2 and p16INK4a proteins using immunohistochemistry. RESULTS: The breast cancer samples were classified into 5 molecular subtypes, namely Luminal A (58 cases), Luminal B (32 cases), Her-2-positive (21 cases), basal-like (12 cases) and normal-like (9 cases) types. p16INK4a expression was negative in 7/132 (5.30%) cases, weakly positive in 15/132 (11.36%) cases, positive in 40/132 (30.30%) cases, and strongly positive in 70/132 (53.03%) cases. When categorizing negative and weakly positive cases into negative group and the positive and strongly positive cases into positive group, the total negative and positive expression rates of p16INK4a were 16.67% (22/132) and 83.33% (110/132) in the carcinoma tissues. Statistical analysis showed the expression intensity of p16INK4a differed significantly between the age groups (P<0.05) but was not significantly correlated with ER, PR, Her-2, molecular subtypes or metastasis of the tumors. CONCLUSION: The compensatory high expression of p16INK4a is the main mechanism of cell cycle deregulation in invasive breast cancer and can be an important specific molecular marker for invasive breast cancer.

The effects of D3R on TLR4 signaling involved in the regulation of METH-mediated mast cells activation.

Accumulating studies have revealed that the dopamine D3 receptor (D3R) plays an important role in methamphetamine (METH) addiction. However, the action of D3R on METH-mediated immune response and the underlying mechanism remain unclear. Mast cells (MCs) are currently identified as effector cells in many processes of immune responses, and MC activation is induced by various stimuli such as lipopolysaccharide (LPS). Moreover, CD117 and FcεRI are known as MC markers due to their specific expression in MCs. To investigate the effects of D3R on METH-mediated alteration of LPS-induced MCs activation and the underlying mechanism, in this study, we examined the expression of CD117 and FcεRI in the intestines of wild-type (D3R(+/+)) and D3R-deficient (D3R(-/-)) mice. We also measured the production of MC-derived cytokines, including TNF-α, IL-6, IL-4, IL-13 and CCL-5, in the bone marrow-derived mast cells (BMMCs) of WT and D3R(-/-) mice. Furthermore, we explored the effects of D3R on METH-mediated TLR4 and downstream MAPK and NF-κB signaling induced by LPS in mouse BMMCs. We found that METH suppressed MC activation induced by LPS in the intestines of D3R(+/)mice. In contrast, LPS-induced MC activation was less affected by METH in D3R(-/-) mice. Furthermore, METH altered LPS-induced cytokine production in BMMCs of D3R(+/+) mice but not D3R(-/-) mice. D3R was also involved in METH-mediated modulation of LPS-induced expression of TLR4 and downstream MAPK and NF-κB signaling molecules in mouse BMMCs. Taken together, our findings demonstrate that the effect of D3R on TLR4 signaling may be implicated in the regulation of METH-mediated MCs activation induced by LPS.