The application of modified functional movement screen as predictor of training injury in athletes.

Background: The Functional Movement Screen (FMS) is widely recognized by clinicians and trainers as a valuable tool for the prediction and prevention of training injuries in sports population. However, some studies suggested that FMS may not fully meet the needs of professional athletes. To address this, the Modified Functional Movement Screen (MFMS) has been specifically developed for athletes. Methods: A total of 527 male athletes in active service without prior training injuries 18.5 ± 1.2 years old) underwent the MFMS test, and their training injuries were monitored during a 2-year follow-up period. The ability of the MFMS to predict the risk of training injury was evaluated based on the receiver operating characteristic (ROC) curve of the total MFMS score. Binary logistic analysis was employed to examine the correlation between the 10 MFMS tests and the risk of training injury. Results: The injured group of athletes had significantly lower total MFMS scores compared to the healthy group (P < 0.001). The total MFMS score demonstrated a strong predictive ability for training injury risk, with an area under the ROC curve of 0.97 (P < 0.001). The calculated cut-off point was set at 22, yielding an odds ratio of 25.63, sensitivity of 0.94, and specificity of 0.88. Binary logistic regression analysis revealed a negative correlation between 6 MFMS tests and the risk of training injury. Conclusion: The MFMS can effectively predict the risk of training injuries. Athletes with a total MFMS score below 22 are more susceptible to experiencing injuries during training.

Clinical characteristics of the adaptive phenomenon of antituberculosis drug-induced liver injury / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the clinical characteristics of the adaptation phenomenon occurring in antituberculosis drug-induced liver injury.</p><p><b>METHODS</b>Our department's clinical records were searched using the standardized diagnostic criteria and monitoring programs parameters of drug-induced liver injury to identify cases with the adaptation phenomenon. The 32 identified cases were classified according to whether or not the drug was discontinued after development of the drug-induced liver injury: withdrawal group (n = 11) and continuing group (n = 21). The types of patients with adaptation phenomenon were assessed to determine the relationship between liver injury and development time, and between the severity grade of liver injury (determined by biomarker expression) and symptoms.</p><p><b>RESULTS</b>All of the 32 cases of drug-induced liver injury with the adaptation phenomenon were classified as the hepatocellular injury type. The average overall incubation period was 16.59+/-13.05 days (range: 6-60 days), while that of the continuing group was 17.05 +/-13.71 days (6-60 days) and that of the withdrawal group was 16.46+/-12.09 days (6-43 days). The average overall time for peak transaminase levels to decrease to the normal range was 11.34 +/-5.97 days (6-30 days), while that of the continuing group was 11.20+/-5.92 days (6-30 days) and that of the withdrawal group was 11.91/-6.20 days (7-30 days). Thirty of the overall patients showed grade 1 degree of liver injury and only two showed grade 2.</p><p><b>CONCLUSION</b>The clinical characteristics of the adaptation phenomenon include a transient increase in biochemical indicators of the antituberculosis drug-induced liver injury. It is important to understand the clinical variations in the adaptation phenomenon to formulate feasible and appropriate programs for monitoring and prevention.</p>

Midkine confers Adriamycin resistance in human gastric cancer cells.

Midkine (MDK) is a heparin-binding molecule involved in the regulation of growth and differentiation during embryogenesis, which is overexpressed in most of human malignant tumors and may act as an oncoprotein. The aim of the current study was to investigate the mechanism of MDK involved in the Adriamycin (ADR) resistance in human gastric cancer cells in vitro. We found that Adriamycin-resistant SGC7901 (SGC7901/ADR) exhibited 58.6-fold greater resistance to ADR compared with Adriamycin-sensitive SGC7901 cell line. MDK mRNA and protein expression levels were significantly higher in SGC7901/ADR than in SGC7901. To gain a deeper insight into the role of MDK in SGC7901/ADR, we stably transfected Adriamycin-sensitive SGC7901 with viral vector expressing MDK. Our result showed that multidrug resistance type I (MDR1) was found in SGC7901/ADR, not in SGC7901 by RT-PCR regardless of MDK transfection. P-Glycoprotein, which is the MDR1-coded protein, was found in SGC7901/ADR, not in SGC7901 by Western blot regardless of MDK transfection. We investigated whether an activation of the tyrosine kinase pathway would change the drug resistance phenotype with MDK transfection. Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Understanding the molecular mechanisms, driving MDK-induced ADR resistance, will provide benefits in developing new therapies for gastric cancer.

Myrislignan attenuates lipopolysaccharide-induced inflammation reaction in murine macrophage cells through inhibition of NF-κB signalling pathway activation.

Myrislignan is a new kind of lignan isolated from Myristica fragrans Houtt. Its antiinflammatory effects have not yet been reported. In the present study, the antiinflammatory effects and the underlying mechanisms of myrislignan in lipopolysaccharide (LPS)-induced inflammation in murine RAW 264.7 macrophage cells were investigated. Myrislignan significantly inhibited LPS-induced production of nitric oxide (NO) in a dose-dependent manner. It inhibited mRNA expression and release of interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α). This compound significantly inhibited mRNA and protein expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) dose-dependently in LPS-stimulated macrophage cells. Further study showed that myrislignan decreased the cytoplasmic loss of inhibitor κB-α (IκB-α) protein and the translocation of NF-κB from cytoplasm to the nucleus. Our results suggest that myrislignan may exert its antiinflammatory effects in LPS-stimulated macrophages cells by inhibiting the NF-κB signalling pathway activation.