Acute myocardial ischemia and reperfusion led to arrhythmias and increase of glutamic oxalacetic transaminase (GOT),lactate dehydrogenase (LDH),non-csterified fatty acid (FFA) and malondialdehyde (MDA) content, and decrease of superoxide dismutase (SOD) activity in rats. 3, 6-di-methylamino-dibenzopyri-odonium edetate (IHC-72) 5 mg?kg-1 iv significantly reduced the incidence of ventricular tachy-cardia (VT) and ventricular fibrillation(VF) ,shortened the duration of arrhythmias induced by reperfusion, decreased the release of GOT, LDH and FFA, obviously reduced the MDA content,and effectively protected SOD activity in ischemia-reperfused rat hearts. Our experimental results suggested that IHC-72 had protective effects on ischemia-reperfusion injury rat hearts in vivo. The mechanism of the protection might be associated with the inhibition of cellular lipid peroxidation.

Objective To investigate the effect of optimized radiological examination strategy on iatrogenic radiation exposure in severe trauma patients so as to provide scientific basis for standardized application of radiological examination.Methods A controlled, three-stage intervention study from April 2010 to November 2011 was carried out.From April 2010 to July 2010, a pre-intervention study was conducted and enrolled 60 patients [43 males, 17 females;age (50 ± 14)years, age range 23-78 years].From August 2010 to March 2011, optimized strategies of radiological examination were implemented, including improving clinicians' knowledge to the standardization of radiological examination and iatrogenic radiation injury and limiting frequency of CT scans through the electronic medical record.From April 2011 to November 2011, post-intervention study was conducted and enrolled 100 patients (81 males, 19 females;age (47 ± 14) years, age range 18-79 years].During this period, major trauma patients were analyzed with respect to the clinical information, radiation examination frequency, ionizing radiation dose and influencing factors.Radiation examination frequency and radiation dose were compared before and after the intervention.Results Radiological examinations were mainly X-ray and CT before the implication of optimized strategies.Of the 60 patients, median frequency of X-rays and CT scan was 6.0(3.0-11.0) and 10.0(8.0-13.8).Median frequency of CT scan was positively correlated with the injury severity score (ISS) and ICU length of stay (r =0.369 and 0.523, P ＜ 0.05).Of the 100 patients, median frequency of CT scan was significantly reduced after the optimization of radiological examination (8.0 vs.10.0, P ＜ 0.05).Total frequency of radiological examination was significantly reduced as well (13.6 vs.17.8, P ＜0.01).There was no significant difference in the treatment success rate before and after the optimization of radiological examination (85.0％ vs.88.3％, P ＞ 0.05).When the frequency of head and chest CT scan was limited, the frequency of radiological examination, radiation exposure and radiological examination expenses were greatly reduced.Conclusions Too much X-ray,CT or other radiological examinations are noted in major trauma patients during the treatment period.Improved understanding of radiation-induced injury, optimizing radiological examination and controlling the repeated radiological examinations of the same site contribute to reducing iatrogenic radiology exposure without affecting the outcome.

Objective To observe the release of glutamate (Glu)and γ-amino butyric acid (GABA) from PC 12 cells induced by aconitine,and to study the intervention of Shuanghuanglian on the injury of these cells. Methods The cell proliferation test agent in cell counting kit(CCK-8)was applied to assay the aconitine toxicity to PC12 cells and to establish the PC12 cell injury model induced by aconitine. The PC12 cells during logarithmic growing phase were randomly divided into the following groups:blank control group(complete medium containing 0.1% dimethyl sulfoxide was added), Shuanghuanglian control group (complete medium containing 50 μg/mL Shuanghuanglian),baicalin control group(complete medium containing 20 μmol/L baicalin),aconitine toxic group(complete medium containing 100 μmol/L aconitine),Shuanghuanglian intervention group(complete medium containing 100μmol/L aconitine and 50μg/mL Shuanghuanglian)and baicalin intervention group(complete medium containing 100 μmol/L aconitine and 20 μmol/L baicalin). The cells in all groups were incubated for 24 hours respectively. The changes of PC12 cell absorbance(A)values were detected by CCK-8 assay before and after intervention by Shuanghuanglian and baicalin. The PC12 cell apoptosis was determined by flow cytometry. Glu and GABA contents in cell culture medium were determined by chromatometry and enzyme-linked immunosorbent assay (ELISA). Results Compared with blank control group,after the PC12 cells treated with 100 μmol/L aconitine for 24 hours,their cytoactivity was decreased markedly(A value:1.003±0.042 vs. 1.685±0.030,P<0.05),then afterwards in the experiment,the incubation of 100 μmol/L aconitine with PC12 cells for 24 hours was considered as the intervention concentration. In blank control group,the normal PC12 cells accounted for 95.89%,while in the aconitine toxic group,the rate of injured PC12 cells reached 64.27% and early apoptosis rate reached 45.46%, and in Shuanghuanglian intervention group and baicalin intervention group,the early apoptosis rate was decreased to 33.24% and 28.22% respectively. Compared with blank control group,there were no significant differences in cytoactivities and the contents of Glu and GABA released by PC12 cells in Shuanghuanglian control group and baicalin control group(all P<0.05),while in the aconitine toxic group,the cytoactivity was significantly decreased(A value:1.056±0.039 vs. 1.722±0.083),and the contents of Glu and GABA were significantly increased〔Glu(μmol/L):5.295±0.137 vs. 3.433±0.138;GABA(μmol/L):0.769±0.020 vs. 0.528±0.012,both P<0.05〕. Compared with aconitine toxic group,the cytoactivities of PC12 were significantly elevated(1.202±0.059 and 1.180±0.032),the levels of Glu were significantly reduced(4.055±0.086 and 3.984±0.057),and the contents of GABA were obviously increased(0.809±0.016 and 0.930±0.021)in the cell culture medium of the Shuanghuanglian intervention group and baicalin intervention group(all P<0.05). The increase of cytoactivity in Shuanghuanglian intervention group was more marked than that of baicalin intervention group(P<0.05). There were no statistical significant differences in contents of Glu and GABA between Shuanghuanglian intervention group and baicalin intervention group(both P>0.05). Conclusions The changes of Glu and GABA may be one of the mechanisms of neural toxic effect of aconitine. Shuanghuanglian possibly can decrease Glu level and increase GABA content by way of its main component baicalin to antagonize the aconitine neurotoxicity.

Objective To investigate the interference effect of baicalin on acute brain injury induced by aconitine in rats and its mechanism. Methods A total of 200 Sprague-Dawley(SD)rats were randomly divided into five groups:normal control,baicalin control,aconitine poisoning,baicalin 15 mg/kg intervention and baicalin 30 mg/kg intervention groups(each,n=40). Aconitine(20μg/kg)was given via tail vein in aconitine poisoning group. The rats in the normal control group and baicalin control group were respectively injected with saline 2 mL/kg and baicalin 30 mg/kg via tail vein. The aconitine poisoning rats were given with baicalin at the dose of 15 mg/kg and 30 mg/kg respectively in the low and high dose baicalin intervention groups within 2-3 minutes after injection of aconitine. Rats in all groups in the study were anesthetized and sacrificed at 1,6,12,24 hours after various agents were respectively given in the groups,the rat cerebral cortex samples were collected,the histological changes in normal and baicalin control groups and pathological changes of the aconitine poisoning rats were observed,the levels of glutamate(Glu),aspartate(Asp),γ-aminobutyric acid(GABA),glycine(Gly)were detected and the apoptotic cells were determined at the above time points. Results Compared with the normal control group,the aconitine poisoning group had significantly higher levels of excitatory amino acids Glu and Asp and the number of apoptotic neurons. After exposure to aconitine for 1 hour, the levels of inhibitory amino acids of GABA and Gly were markedly decreased in the rat cortex in the poisoning group compared to the normal control group(both P<0.05),at 6 hours and 12 hours they were significantly increased and after 24 h,they began to decline,but still maintained at relatively high levels. Compared with the aconitine poisoning group, after baicalin intervention for 1 hour,in the 15 mg/kg and 30 mg/kg baicalin intervention groups,the levels of Glu and Asp were markedly decreased〔Glu(μmol/L):309.39±14.59,307.22±23.69 vs. 370.46±40.31,Asp(μmol/L):143.43±8.36,129.12±4.86 vs. 222.97±6.26〕,while the levels of GABA and Gly were increased〔GABA(μmol/L):55.91±4.76,59.61±13.11 vs. 32.05±2.20,Gly(μmol/L):32.33±1.85,33.90±0.66 vs. 21.96±4.75〕,and the number of neuronal apoptosis was obviously decreased(cell/mm2:18.65±4.10,14.80±1.89 vs. 58.15±3.68,both P<0.05). Under microscope and electron microscope,the pathological and ultrastructural changes indicated that the aconitine poisoning group had the most marked cerebral cortex damage at 12 hours after poisoning,while the two baicalin intervention groups showed milder damage than that in aconitine poisoning group. Conclusions The neural toxic effect of aconitine in rats may be related to the imbalance between the neurotransmitter contents of excitatory Glu. Asp and inhibitory GABA,Gly in the cerebral cortex. Baicalin can decrease the contents of excitatory amino acid and elevate the inhibitory amino acid,therefore it may ameliorate the cerebral injury of acute aconitine intoxication in rats.

Objective To evaluate the relationship between changes in B-type natriuretic peptide(BNP) and cardiac troponin I(cTnI)levels and prognosis of critically ill patients with sepsis. Methods This study retrospectively reviewed the clinical data of 75 patients with severe sepsis and septic shock admitted into Emergency Intensive Care Unit(EICU)of the First Affiliated Hospital of Wenzhou Medical University in Zhejiang Province. According to the severity of the cases,they were divided into two groups:severe sepsis group(34 cases)and septic shock group(41 cases),and based on the difference in prognosis,they were divide into survivor group(32 cases) and non-survivor group(43 cases). Electrocardiogram(ECG)was performed within 24 hours after admission in all the patients. Acute physiology and chronic health evaluation Ⅱ(APACHEⅡ)score and biochemical markers showing organ dysfunctions as BNP, cTnI, creatine kinase (CK), creatine kinase MB mass(CK-MB), and lactate were compared between severe sepsis and septic shock groups and between survivor and non-survivor groups. Results The septic shock group had significantly higher baseline BNP,cTnI,lactate and APACHE Ⅱscore and mortality rate than those in severe sepsis group〔BNP(μg/L):1.90(1.08,2.79)vs. 0.41(0.31,0.75),cTnI (μg/L):1.15(0.92,1.28)vs. 0.58(0.40,0.79),lactate(mmol/L):6.63±3.72 vs. 3.28±1.66,APACHEⅡscore:26.00(24.00,28.00)vs. 21.50(20.00,29.25),mortality rate:70.73%vs. 41.18%,P<0.05 or P<0.01〕. Compared with survivor group,the ages of non-survivor group were older with more males and higher BNP,cTnI,lactate and APACHEⅡscore〔males(cases):30 vs. 13,age(years old):66.49±14.97 vs. 58.19±17.05,BNP:1.60(0.62, 2.51)vs. 0.57(0.37,1.79),lactate:4.10(3.00,9.00)vs. 3.10(2.13,4.18),cTnI:1.02±0.49 vs. 0.62±0.37, APACHE Ⅱ score:28.00(25.00,30.00)vs. 21.00(20.00,25.75),P<0.05 or P<0.01〕. However,there were no statistically significant differences in the levels of CK and CK-MB between the above compared groups(both P>0.05). The patients' ECGs had no obvious changes. Conclusions High plasma BNP and cTnI levels in patients with sepsis may suggest myocardial damage and relatively bad prognosis. The examination of BNP and cTnI levels may help clinicians to early detect the high-risk patients with septic cardiac dysfunction and assess their prognoses.

Objective To investigate the effect of resveratrol (Res) on paraquat (PQ)-induced acute lung injury (ALI) and mortality in mice and the mechanism of nuclear factor-κB (NF-κB) inflammatory pathway. Methods Sixty-eight healthy male ICR mice with grade SPF were enrolled, among them 20 mice were used for mortality observation (n = 10), and other 48 were used for determination of related parameters (n = 6). The mice were randomly divided into four group s: normal saline (NS) control group, Res control group, PQ group and PQ + Res group. The mice in the latter two groups were subdivided into 6, 24, 72 hours subgroups. The PQ poisoning model of mice was reproduced by one injection of 30 mg/kg PQ intraperitoneally. The mice in PQ + Res group were given 60 mg/kg Res intraperitoneally on the contralateral side after PQ injection. The mice were sacrificed at 6, 24, 72 hours after PQ poisoning, and lung tissue was harvested. The serum levels of tumor necrosis factor-α (TNF-α), interleukins (IL-6 and IL-1β) were determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung tissue were observed with electron microscopy. Apoptosis cells in the lung were identified by terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) for the estimation of apoptosis rate. The protein expression of NF-κB p65 was determined by Western Blot. Results Compared with PQ group, the death number of mice at 48, 72, 96 hours in PQ + Res group was slightly decreased (0 vs. 2, 2 vs. 5, 4 vs. 6) but without statistically significant difference (all P > 0.05). Under electron microscope, the lung injury in PQ group was severer than that in NS control group, and Res was found to be able to alleviate the lung injury. Compared with NS control group [(2.45±0.61)%], the apoptosis rate at 6 hours in PQ group was significantly increased [(8.42±1.48)%], and peaked at 72 hours [(21.23±3.47)%]. Res could decrease the apoptosis rate after PQ poisoning [6 hours: (5.56±1.31)% vs. (8.42±1.48)%, 24 hours: (11.14±2.07)% vs. (16.88±2.96)%, 72 hours: (13.28±2.32)% vs. (21.23±3.47)%, all P < 0.05]. The serum levels of TNF-α, IL-6, and IL-1β, and NF-κB p65 in lung tissue were all markedly increased after PQ poisoning, and they were significantly decreased after Res intervention as compared with those of PQ group [TNF-α (ng/L): 2.62±0.29 vs. 4.06±0.74 at 6 hours, 3.98±0.41 vs. 6.79±0.80 at 24 hours, 5.06±0.75 vs. 11.00±0.75 at 72 hours; IL-6 (ng/L): 14.19±1.54 vs. 16.55±1.24 at 6 hours, 13.21±1.37 vs. 19.73±0.85 at 24 hours, 13.72±0.56 vs. 22.45±0.72 at 72 hours; IL-1β (ng/L): 8.54±1.64 vs. 12.59±0.66 at 6 hours, 10.15±0.29 vs. 16.24±1.03 at 24 hours, 16.14±0.70 vs. 19.55±0.56 at 72 hours; 6-hour NF-κB p65: (1.34±0.07) folds vs. (1.86±0.11) folds when the expression in NS control group was represented as 1, all P < 0.05]. Conclusions Res cannot lower the mortality in mice with PQ poisoning, but it seems to be able to attenuate PQ-induced ALI and cell apoptosis. The mechanism responsible for the latter maybe the inhibitive effect of Res on NF-κB p65 translocation and cytokines production.

Objective:To investigate the role of growth arrest specific protein 6 (Gas6) in regulating macrophage polarization in wound healing.Methods:Clean male B6 mice were randomly(random number) divided into the normal group, skin defect group, skin defect group + normal saline group (PBS group), skin defect + Gas6 (1 μg) group, skin defect + Gas6 (5 μg) group, and skin defect + Gas6 (10 μg) group. Ten mice in each group were used to observe the healing of skin wounds. Macrophages were isolated from the wound tissues of the remaining 6 mice on the fifth day after modeling. The levels of IL-6 and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA), the mRNA expression levels of arginase-1 (Arg-1) and inducible nitric oxide synthase (iNOS) were detected by RT-PCR, and flow cytometry was used to detect the expression of M1 marker CD197, M2 marker CD163 and F4/80. HE staining was used to detect the pathological changes of skin wounds. Masson staining was used to analyze the granulation tissue and collagen deposition.Results:Scab began to form on the surface of the wound on the third day after the skin defect model was established. The wound area of the Gas6 treatment group was smaller than that of the PBS group, and the wound healing was better than that of the PBS group. Compared with the normal group, the proportion of CD197 in macrophages of the skin defect group was significantly increased ( P=0.00 49), the proportion of CD163 and F4/80 double positive was significantly decreased ( P=0.00 86), the level of IL-6 was significantly increased ( P=0.00 13), the level of IL-10 was significantly increased ( P=0.00 14), the level of iNOS mRNA was significantly increased ( P=0.00 8), and Arg-1 was significantly increased in the skin defect group The mRNA level was significantly decreased ( P=0.01 21), and the inflammatory infiltration was aggravated. Compared with the PBS group, the proportion of CD197 in the Gas6 treatment group was significantly decreased ( P=0.00 0), the double positive rates of CD163 and F4/80 were significantly increased ( P = 0.00 0), the level of IL-6 was significantly decreased (P = 0.00 0), the level of IL-10 was significantly increased ( P=0.00 03), the level of iNOS mRNA was significantly decreased ( P=0.00 18), the level of Arg-1 mRNA was significantly increased ( P=0.00 1), and the number of inflammatory cells and the number of collagen fibers were increased. Conclusions:Gas6 can promote the transformation of macrophages from M1 to M2 in mice with skin defect, which is beneficial to the wound healing of skin defect.

Objective:To explore the prognostic factors of patients with Vibrio vulnificus sepsis. Methods:The clinical data of 67 patients with Vibrio vulnificus sepsis from January 2008 to December 2019 in the First Affiliated Hospital of Wenzhou Medical University were retrospectively analyzed. Univariate analysis was used to compare the differences in general information, clinical manifestations, admission laboratory indicators, antibiotics and surgery between the death group and the cured group. Then the factors with significant difference in univariate analysis were included in multivariate analysis, and the factors of prognosis were obtained. Results:Univariate analysis showed that there were significant difference in liver disease, admission with hypotension shock, multiple limb injuries; admission leukocytes, platelets, pH value, albumin, lactic acid, aspartate aminotransferase, creatinine, procalcitonin, creatine kinase, activated partial thromboplastin time, prothrombin time between the death group and the cured group (all P <0.05). Multivariate analysis showed that admission lactate ( OR=0.628, 95% CI: 0.461-0.855, P=0.003), albumin ( OR=1.330, 95% CI:1.062-1.667, P=0.013), creatine kinase ( OR=0.999, 95% CI: 0.998-1.000, P=0.016) and admission surgery time ( OR=0.118, 95% CI: 0.015-0.938, P=0.043) were risk factors of the prognosis. Patients with high lactate, creatine kinase and low albumin at admission indicate poor prognosis; patients with admission surgery time≤ 12 h have better prognosis. Conclusion:For the treatment of patients with Vibrio vulnificus sepsis, medical staff should dynamically evaluate these prognostic factors in the early stage, and early surgical treatment should be adopted to improve the prognosis of patients.

AIM:To investigate the effect of capsaicin on lipopolysaccharide ( LPS)-induced activation of cul-tured endothelial cells of mouse aorta in vitro.METHODS:The endothelial cells were isolated from mouse aorta and cul-tured in vitro, and the specific cell markers of the cells were identified by immunofluorescence staining.The cells were stimulated with LPS (100μg/L) combined with or without capsaicin, and the cells and supernatant were collected at 12 h, 24 h and 48 h.The levels of soluble intercellular adhesion molecule 1 ( sICAM-1) , soluble vascular cell adhesion molecule 1 (sVCAM-1) and soluble P-selectin (sP-selectin) in the supernatant were measured by ELISA.The levels of nuclear NF-κB p65 and cytopasmic p-IκBαand IκBαwere detected by Western blotting.RESULTS: Compared with control group, the levels of sP-selectin, sICAM-1 and sVCAM-1 in LPS group were significantly increased (P<0.05), and LPS promoted the expression of sICAM-1 and sVCAM-1 in a time-dependent manner.Compared with LPS group at the same time point, capsaicin inhibited the expression of sP-selectin, sICAM-1 and sVCAM-1 in a dose-dependent manner.Compared with con-trol group, the protein levels of NF-κB p65 and p-IκBαin LPS group at 24 h were significantly increased (P<0.05), while the protein level of IκBαin LPS group at 24 h were significantly decreased (P<0.05).Compared with LPS group, capsaicin decreased the protein levels of NF-κB p65 and p-IκBαand increased the protein level of IκBαin a dose-depend-ent manner.CONCLUSION:Capsaicin has a protective effect on LPS-induced vascular endothelial cell activation, which potentially contributes to the suppression of IκBαdegradation and NF-κB p65 nuclear translocation.

Accidents ; Acute Lung Injury ; chemically induced ; Administration, Oral ; Humans ; Mediastinal Emphysema ; complications ; Potassium Permanganate ; toxicity