PurposeTo evaluate the clinical effects of magnesium sulfate in the treatment of diffuse axonal injury (DAI).Patients and methodsThis study was a randomized, double-blind, placebo-controlled trial conducted in the First Affiliated Hospital of Sun Yat-sen University, Guangzhou and Zhuhai People’s Hospital, Zhuhai, two trauma center hospitals. A total of 128 patients suffered from DAI, with initial Glasgow coma scale (GCS) scores of 3–8. They were randomly divided into two groups: magnesium sulfate treatment (MST) group (n=64) and control group (n=64). The MST group received 250 μmol/kg magnesium sulfate intravenously 20 minutes after admission, followed by 750 μmol/kg magnesium sulfate intravenously daily for 5 days. The control group received standard management without MST. GCS scores and serum neuron-specific enolase values were measured and recorded at admission, and on days 3 and 7 after injury. Outcomes were determined by Glasgow outcome scale scores at discharge and at 3 months’ follow-up, respectively.ResultsAfter the 7-day treatment, patients in the MST group, compared with those in the control group, had a lower serum neuron-specific enolase level (25.40±6.66 vs 29.58±7.32, respectively, P=0.001) and higher GCS score (8.23±2.72 vs 7.05±2.64, respectively, P=0.016). Although the length of stay and mortality did not differ between the groups in the intensive care unit, Glasgow outcome scale score was significantly lower in the MST group at discharge (3.30±1.35 vs 3.90±1.10, P=0.004) and 3 months after discharge (2.95±1.48 vs 3.66±1.44, P=0.009).ConclusionEarly treatment with magnesium sulfate resulted in a significant improvement in DAI outcome. Further studies are needed to confirm the clinical significance of treatment of DAI patients with magnesium sulfate.
PurposeTo investigate the possible associations between serum levels of soluble receptor for advanced glycation end products (sRAGE) and specific clinical markers and prognosis in critically ill patients diagnosed with stress hyperglycemia.Patients and methodsA total of 70 critically ill patients and 25 normal controls were recruited for this study. Serum levels of sRAGE and advanced glycation end products (AGEs) were determined using enzyme-linked immunosorbent assay. Additional data on other clinical markers were obtained from patient records in the intensive care unit. Comparisons of sRAGE and AGEs levels between groups were assessed by t-test. The relationships between sRAGE and other clinical markers were assessed by Pearson’s correlation analyses and multiple linear regression analyses. Risk factors for prognosis, such as 28-day mortality were analyzed using logistic regression analysis.ResultsSerum sRAGE and AGEs levels were significantly higher in critically ill patients, compared to normal controls (P<0.05). The increase in serum sRAGE levels was significantly correlated with AGEs levels, interleukin-6 levels, and the sequential organ failure assessment score (P<0.01). Using multiple linear regression analysis, the association between AGEs and sRAGE remained significant after adjustment of other clinical factors. However, there were no significant correlations between sRAGE levels and patient outcome in these critically ill patients.ConclusionSerum sRAGE levels were significantly elevated in critically ill patients and positively correlated with higher AGEs levels, but sRAGE levels were not associated with increased mortality, suggesting sRAGE levels are not a predictor of prognosis in critically ill patients.
Purpose: To identify natural chemiome that inhibits matrix-metalloproteinases (MMPs) with a view to discovering novel disease-modifying osteoarthritis drugs (DMOADs). Methods: Computer-aided drug design (CADD) with virtual screening, ADME/Tox, molecular docking, molecular dynamics simulation, and MM-PBSA calculations were used in search of novel natural compounds that inhibit MMPs. Results: From more than fifty thousand compounds, a single lead compound (IBS ID: 77312) was shortlisted using bias based on binding energy and drug-likeness. This lead compound synergistically bound to the S1 domain of MMP-13 protein through five hydrogen bonds. The interactions became stable within 100-nanosecond molecular dynamics simulation run. The in vitro data for the lead compound showed that its minimal non-lethal dose increased collagen content but decreased aggrecan level in chondrocytes. Conclusion: This study has identified a natural lead compound that may pave the way for a novel DMOAD of natural origin against OA.
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