The impact of ulinastatin on wound infection and healing in patients with burn wounds: A meta-analysis.

Burn injuries result in localised tissue damage and precipitate systemic responses; routine clinical treatments, which typically include metabolic nutritional support and anti-infection therapies, do not yield optimal outcomes. Therefore, we aimed to systematically evaluate the effects of ulinastatin on wound infection and healing in patients with burns to provide reliable evidence-based recommendations for burn treatment. An electronic search of the Web of Science, PubMed, Cochrane Library, Embase, Wanfang, Chinese Biomedical Literature Database, and China National Knowledge Infrastructure databases, supplemented by manual searches, was conducted from database inception to October 2023 to collect randomised controlled trials (RCTs) assessing the efficacy of ulinastatin for the treatment of burns. Two researchers screened all retrieved articles according to the inclusion and exclusion criteria; the included studies were evaluated for quality, and the relevant data were extracted. Stata 17.0 software was employed for data analysis. Overall, 8 RCTs with 803 patients were included, with 404 and 399 in the ulinastatin and conventional treatment groups, respectively. The analysis revealed that wound infections (odds ratio [OR] = 0.08, 95% CI: 0.02-0.35, p = 0.001) and complications (OR = 0.21, 95% CI: 0.10-0.42, p < 0.001) were significantly lower, and wound healing time (standardised mean differences [SMD] = -1.31, 95% CI: -2.05 to -0.57, p = 0.001) was significantly shorter, in the ulinastatin groups than in the control group. This meta-analysis revealed that ulinastatin can effectively reduce the incidence of wound infections and complications and significantly shorten the duration of wound healing in patients with burns, thereby promoting early recovery in these patients.

Removal of biofilm is essential for long-term ventilation tube retention.

BACKGROUND: Although long-term retention of a ventilation tube is required in many ear diseases, spontaneous removal of conventional ventilation tube is observed in patients within 3 to 12 mo. To address this issue, we aimed to determine a new method for long-term retention of the ventilation tube. AIM: To explore the value of removing the biofilm for long-term retention of tympanostomy ventilation tubes. METHODS: A case-control study design was used to evaluate the safety and effectiveness of long-term tube retention by directly removing the biofilm (via surgical exfoliation) in patients who underwent myringotomy with ventilation tube placement. The patients were randomly divided into two groups: Control group and treatment group. Patients in the treatment group underwent regular biofilm exfoliation surgery in the clinic, whereas those in the control group did not have their biofilm removed. Only conventional ventilation tubes were placed in this study. Outcome measures were tube position and patency. Tube retention time and any complications were documented. RESULTS: Eight patients with biofilm removal and eight patients without biofilm removal as a control group were enrolled in the study. The tympanostomy tube retention time was significantly longer in the treatment group (43.5 ± 26.4 mo) than in the control group (9.5 ± 6.9 mo) (P = 0.003). More tympanostomy tubes were found to be patent and in correct position in the treatment group during the follow-up intervals than in the control group (P = 0.01). CONCLUSION: Despite the use of short-term ventilation tubes, direct biofilm removal can be a well-tolerated and effective treatment for long-term tube retention of tympanostomy ventilation tubes in patients who underwent myringotomy.

Effect of ginkgolide B on brain metabolism and tissue oxygenation in severe haemorrhagic stroke.

Ginkgolide B, a diterpene, is an herbal constituent isolated from the leaves of Ginkgo biloba tree. The present study demonstrates the effect of ginkgolide B in osmotherapy on brain metabolism and tissue oxygenation. Multimodality monitoring including intracranial pressure (ICP), cerebral perfusion pressure (CPP), partial pressure of brain tissue oxygen (PbtO2), lactate/pyruvate ratio (LPR) and microdialysis were employed to study the effect of ginkgolide B osmotherapy. The results demonstrated that administration of 15% solution of ginkgolide B to the comatose patients with raised ICP (> 20 mm Hg) and resistant to standard therapy led to a significant decrease in ICP. The cerebral microdialysis was used to compare mean arterial blood pressure (MAP), ICP, CPP, PbtO2, brain lactate, pyruvate and glucose level after hourly intervals starting 3 h before and up to 4 h after hyperosmolar therapy. There was a decrease in ICP in 45 min from 23 ± 14 mm Hg (P < 0.001) to 18 ± 24 mm Hg and increase in CPP after 1 h of gingkolide B infusion from 74 ± 18 to 85 ± 22 mm Hg (P < 0.002). However there was no significant effect on MAP but PbtO2 was maintained in the range of 22-26. The peak lactate/pyruvate ratio was recorded at the time of initiation of osmotherapy (44 ± 20) with an 18% decrease over 2 h following gingkolide B therapy. Also the brain glucose remained unaffected.

[Adsorption of phenanthrene from aqueous solution on cetylpyridinium bromide (CPB) -modified zeolite].

Surfactant-modified zeolites (SMZs) with different coverage types were prepared by loading of different amounts of cetylpyridinium bromide (CPB) onto natural zeolites and were used as adsorbents to remove phenanthrene from aqueous solution. The adsorption of phenanthrene from aqueous solution on monolayer and bilayer SMZs as a function of adsorbent dosage, initial phenanthrene concentration, contact time, and temperature was investigated using batch experiments. Results showed monolayer and bilayer SMZs were effective for the removal of phenanthrene from aqueous solution. The phenanthrene removal efficiency of SMZs increased with increasing adsorbent dosage, but the amount of phenanthrene adsorbed on SMZs decreased with increasing adsorbent dosage. The adsorption kinetics of phenanthrene on SMZs well followed a pseudo-second-order kinetic model. The equilibrium adsorption data of phenanthrene on SMZs at a low concentration of phenanthrene in solution could be described by the Linear equation and Freundlich equation. The main mechanism for phenanthrene adsorption onto monolayer SMZ is hydrophobic interaction, and the main mechanism for phenanthrene adsorption onto bilayer SMZ is organic partitioning. The calculated thermodynamic parameters such as Gibbs free energy change (deltaG(theta)), enthalpy changes (deltaH(theta)), and entropy change (deltaS(theta)) showed that the adsorption process of phenanthrene on SMZs is spontaneous and exothermic in nature. When the CPB loading amount of bilayer SMZ was twice as much as that of monolayer SMZ, the phenanthrene adsorption capacity for bilayer SMZ was slightly higher than that for monolayer SMZ. In a conclusion, both monolayer and bilayer SMZs are promising adsorbents for the removal of phenanthrene from water and wastewater, and monolayer SMZ is a more cost-effective adsorbent for phenanthrene removal than bilayer SMZ.

[Changes in plasma content of matrix metallo proteinase-9 in acute cerebral infarction patients before and after thrombolytic therapy and its significance].

OBJECTIVE: To investigate the changes in the content of plasma matrix metallo proteinase-9 (MMP-9) in patients with acute cerebral infarction before and after thrombolytic therapy and its clinical significance. METHODS: The levels of MMP-9 were determined in 34 patients with acute cerebral infarction before and after thrombolytic therapy, and 34 healthy individuals served as healthy control. RESULTS: Compared with the healthy controls, the levels of plasma MMP-9 before thrombolytic therapy were not significantly increased [(13.47±3.09) ng/L vs. (12.89±10.22) ng/L, P >0.05]. In contrast, MMP-9 values were significantly increased after thrombolytic therapy [(22.06±12.53) ng/L] compared with that in either before or healthy control group (both P<0.05). MMP-9 values were significantly higher in patients with hemorrhage after thrombolytic therapy (incidence rate was 26.5%, 9/34) compared with before treatment [(24.02±15.41) ng/L vs. (14.28±2.33) ng/L, P<0.05], and the values of MMP-9 were higher than those of patients without hemorrhage [(20.42±9.57) ng/L], but there was no statistically significant difference ( P >0.05). In patients with complete revascularization (revascularization rate was 58.8%, 20/34), MMP-9 level was markedly higher than before thrombolytic therapy after thrombolytic therapy [(19.26±7.94) ng/L vs. (13.63±3.02) ng/L, P<0.05], and the values of MMP-9 were higher than the no-revascularization patients [(18.97±4.23) ng/L], but there was no statistically significant difference ( P >0.05). CONCLUSION: Thrombolytic therapy activated MMP-9, and MMP-9 increased the risk of hemorrhage after thrombolytic therapy, and it participated in the mechanisms of hemorrhagic tendency after thrombolysis.

[Study of the protection and mechanism of IGF-1 on tau protein hyperphosphorylation in PC12 cells induced by Abeta(1-40)].

OBJECTIVE: To investigate the effect and the molecular mechanism of insulin-like growth factor 1 (IGF-1) on the level of tau protein phosphorylation in PC12 cells induced by aggregated beta-amyloid protein(1-40) (Abeta(1-40)). METHODS: MTT assay was used to measure the survival rate of PC12 cells, Western blot was applied to detect tau phosphorylation level, total tau, glycogen synthase kinase-3beta (GSK-3beta), and phosphorylation of GSK-3beta Ser9 for observing the effect of IGF-1 or LiCl, a specific inhibitor of GSK-3beta, on Abeta-induced tau protein phosphorylation in PC12 cells. RESULTS: Different concentrations of IGF-1 could improve the survival rate of PC12 cells compared with that of Abeta(1-40) group (P < 0.05), and the best protective effect was observed in 1 microg/mL IGF-1 group. The levels of tau protein phosphorylation in the sites of Ser396, Ser(199/202) and the amount of whole tau increased after 3 h exposure and reached the maximum level after 12 h exposure to Abeta(1-40), meanwhile, the expressions of the amount of whole GSK-3beta was also increased (P < 0.05), but a decreased phosphorylation of GSK-3betaSer9 was observed (P < 0.05). Pretreatment with several dose of IGF-1 or LiCl, markedly reduced Abeta(1-40)-induced tau hyperphosphorylation and the expression of GSK-3beta (P < 0.05), but the expression of phosphorylation of GSK-3betaSer9 was increased (P < 0.05). CONCLUSION: The levels of tau protein phosphorylation in the sites of Ser396, Ser(199/202) and the amount of whole tau increased by Abeta(1-40) in PC12 cells, GSK-3beta activation by Abeta(1-40) may lead to extensive tau phosphorylation. IGF-1 could attenuate Abeta(1-40)-induced tau protein hyperphosphorylation by inhibiting the activation of GSK-3beta.