The curative effect of Shenfu-injection in the treatment of burn sepsis and its effect on the patient's immune function, HMGB, and vWF.

OBJECTIVE: To investigate and analyze the immune regulatory effect of Shenfu-Injection (SFI) on patients with burn-injured sepsis by monitoring the serum level of high mobility group box 1 (HMGB1) and von Willebrand factor (vWF). METHODS: In this retrospective study, the Acute Physiology and Chronic Health Evaluation (APACHE II) score, Marshall score, peripheral blood T lymphocyte count, and NK cell concentration, levels of cytokines such as HMGB-1, and vWF in peripheral blood before and after treatment in patients from the control group (convention treatments, n=51) and the observation group (convention treatments plus SFI treatment, n=57) were analyzed. The prognosis of the two groups of patients at 28 days was analyzed and compared. RESULTS: After treatment, APACHE II score, Marshall score, IL-6, CPR, HMGB-1, and vWF in patients from the two groups decreased greatly when compared with those before the treatment (P<0.05). The APACHE II score, Marshall score, IL-6, CPR, HMGB-1, and vWF in the group for observation were significantly lower (P<0.05) than those in the control group. Concentrations of CD3+, CD4+, and NK cells in these two groups after 7 days of treatment were greatly higher than those before the treatment (P<0.05). Concentrations of CD3+, CD4+, and NK cells in the observation group were higher than those in the control group after treatment (P<0.05). There was no significant difference in terms of mortality between these two groups after 28 days (P<0.05). The average survival time of the non-survivors in the observation group was significantly longer than that in the control group (P<0.05). CONCLUSION: SFI can effectively improve the immunity of patients with burn-injured sepsis, reduce the expression of cytokines such as HMGB and vWF, and is of great help for the improvement of clinical prognosis.

A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer.

Non-small-cell lung cancer (NSCLC) is one of the leading causes of cancer-related death worldwide, and the 5-year survival rate is still low despite advances in diagnosis and therapeutics. A long noncoding RNA (lncRNA) HOX antisense intergenic RNA (HOTAIR) has been revealed to play important roles in NSCLC carcinogenesis but the detailed mechanisms are still unclear. In the current study, we aimed to investigate the regulation between the lncRNA HOTAIR and p53 in the NSCLC patient samples and cell lines. Our results showed that HOTAIR expression was significantly higher in the cancer tissues than that in the adjacent normal tissue, and was negatively correlated with p53 functionality rather than expression. When p53 was overexpressed in A549 cells, the lncRNA HOTAIR expression was downregulated, and the cell proliferation rate and cell invasion capacity decreased as a consequence. We identified two binding sites of p53 on the promoter region of HOTAIR, where the p53 protein would bind to and suppress the HOTAIR mRNA transcription. Inversely, overexpression of lncRNA HOTAIR inhibited the expression of p53 in A549 cells. Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). These studies identified a specific negative regulation loop of lncRNA HOTAIR and p53 in NSCLC cells, which revealed a new understanding of tumorigenesis in p53 dysfunction NSCLC cells.

Association Between Angiopoietin-2 and Enterovirus 71 Induced Pulmonary Edema.

OBJECTIVE: To characterize pulmonary edema (PE) fluid induced by enterovirus 71 (EV71) infection, elucidate the relationship between angiopoietin-2 (Ang-2) and PE, and explore the pathogenesis of PE. METHODS: Clinical data were collected from critical infants with EV71 infection. The infants were grouped into PE, non-PE, and control groups. The control group included infants in the preoperative period of elective inguinal hernia surgery. Biochemical changes in PE fluid were evaluated, and Ang-2 levels in serum and PE fluid were measured. Human pulmonary microvascular endothelial cells (HPMECs) were incubated with serum from the control and PE groups and human recombinant Ang-2 or serum from the PE group and human recombinant Ang-1, and changes in the intercellular junctions were recorded via immunofluorescence. RESULTS: Of the 161 infants with critical EV71 infection admitted to the hospital, 39 had PE. PE fluid was collected from 18 of these infants. The PE fluid-to-serum (P/S) ratio of total protein was 0.9 ± 0.2, and all P/S ratios of albumin were 1.0 ± 0.3. The Ang-2 level was higher in the non-PE group (333.2 ± 79.7 pg/ml) than in the control group (199.9 ± 26.7 pg/ml), although without statistical significance (P = 0.115). The Ang-2 level in the PE group (2819.2 ± 908.7 pg/ml) was higher than those in both the non-PE and the control groups (both, P < 0.001). Serum samples from the PE group had damaged cell junctions of confluent HPMEC monolayers that were reversed by Ang-1. CONCLUSIONS: The PE fluid of infants with EV71-induced PE was protein-rich, and elevated Ang-2 expression was associated with PE. The mechanism through which PE develops may be related to Ang-2-induced cell junction damage.

[The significance of lactic acid in early diagnosis and goal-directed therapy of septic shock patients].

OBJECTIVE: To investigate the application of lactic acid in early diagnosis and goal-directed therapy of septic shock, and to provide reference for the early clinical diagnosis and treatment of septic shock. METHODS: A prospective observational study was conducted, in which patients satisfied with the criteria of septic shock diagnosis were enrolled. The patients were randomly divided into two groups. The lactic group was defined using blood lactic acid concentration < 2 mmol/L as treatment guide target. Control group was defined according to the traditional diagnostic criteria of shock which systolic blood pressure was less than 90 mmHg (1 mmHg= 0.133 kPa) or systolic blood pressure value fell > 40 mmHg baseline or oliguria ( < 0.5 ml. kg-1.h-1) et al traditional septic shock diagnosis criteria and bundle treatment was performed. Organ dysfunction index, the sequential organ failure score (SOFA), acute physiology and chronic health evaluation score II ( APACHE II) score, the time of mechanical ventilation, the time of stay in the intensive care unit ( ICU), and the 7-and 28-day mortality were recorded. RESULTS: There were 26 and 31 septic shock patients in lactic group and control group respectively. Organ dysfunction index had been improved in different degrees after treatment compared with that before treatment. Creatinine ( Cr) at 48 hours after treatment in lactic group was significantly lower than that in control group (µmol/L: 94.48 ± 6.68 vs. 107.44 ± 10.35, P < 0.05), and there was no statistical difference in other indexes. The SOFA score of lactic group at 24 hours and 48 hours after treatment was lower than that of control group (9.27 ± 4.62 vs. 9.79 ± 3.80, t=2.103, P=0.040; 8.54 ± 5.53 vs. 9.70 ± 4.30, t=2.302, P=0.023). APACHE II score of two group after treatment were lower than that before treatment, and lactic group decreased more obviously compared with control group ( 14.25 ± 5.29 vs. 20.00 ± 9.74, t=2.298, P=0.026; 13.60 ± 6.18 vs 18.15 ± 6.62, t=2.653, P=0.011). The time of stay in the ICU and the time of mechanical ventilation of lactic group were shorter that those of control group, but there was no statistical difference [ICU time (days): 8.95 ± 5.19 vs. 9.45 ± 6.18, t=0.605, P=0.652; mechanical ventilation time (hours): 101.15 ± 11.50 vs. 110.63 ±13.26, t= 0.631, P=0.564]. There was no statistical difference regarding 7-day mortality of lactic group was lower than that of control group [15.38% (4/26) vs. 16.13% ( 5/31), Χ2=0.000, P=1.000]. The 28-day mortality of lactic group was lower than that of control group [26.92 % (7/26) vs. 54.84% (17/31). Χ2=4.520, P=0.033]. CONCLUSION: By blood lactic acid monitoring, inadequacy of organization perfusion i.e. septic shock can be found in the early stage, thus early intervention can be performed and improve resuscitation result and reduce the mortality of septic shock patients. Blood lactic acid ≥ 4 mmol/L can be used as one of the criteria for the diagnosis of septic shock, and 6-hour blood lactic acid < 2 mmol/L as a goal to guide shock treatment with obvious prognosis improvement.