Objective To ensure the quality of field operation materials, and enhance rescue ability of medical corps in field condition. Methods Materials for package and sterilization were tested and selected for new way of package and sterilization instead of the traditional cotton. Results Sheet package was preserved in normal condition. Every month the microorgarism in sheet package was sampled. There were no bacteria in the operation items in the half-year sampling. So the period of validity was prolonged from one week to half year. Conclusion With the new package sterilization method, the work load of nurses is alleviated and the expenses on repeated sterilization due to short term of validity are also reduced. At the same time, operation infection rate and death rate are decreased so that the battle injury rescue level was raised.

Objective To study the pharmacokinetics of aristolochic acid A in Radix Aristolochiae and the compound preparation of Guanxinsuhe Capsule in mice in vivo after single-dose oral administration and observe the difference of aristolochic acid A absorption and distribution. Methods Aristolochic acid A assay was performed by RP-HPLC on a Waters apparatus with a DiamonsilTM C18 column (250 mm × 4.6mm, 5 μm), a mobil phase: a mixture of methanol-water-acetic acid (72: 27 : 1), flow rate: 1.0 mL/min, detection wavelength: 315 nm, and column temperature: 20 ℃. Results Mice were given Radix Aristolochiae and Guanxinsuhe Capsule by ig at the same level of 2. 5 mg/kg of aristolochic acid A, respectively, which were suspended in 0. 3% CMC-Na solution. Plasma concentrations were determined by RPHPLC. After single-dose ig administration of Radix Aristolochiae or Guanxinsuhe Capsule to mice, the mean plasma concentration-time courses of aristolochic acid A obtained fitted the one-compartment model.The main pharmacokinetic parameters of aristolochic acid A in Radix Aristolochiae, t1/2ka, t1/2 ke, tmax,AUC, Cmax are 5. 103 min, 43. 63 min, 17.89 min, 80. 45 (μg · min)/mL, and 0. 916 8 μg/mL; the rela tive pharmacokinetic parameters in Guanxinsuhe Capsule are 5. 294 min, 43.50 min, 18. 32 min, 33.08(μg · min)/mL, and 0. 381 8 μg/mL. Conclusion The Cmax of aristolochic acid A in Guanxinsuhe Capsule is significantly less than that in Radix Aristolochiae, which indicates that the compound compability could decrease the absorption of aristolochiae acid A.

Objective To investigate the changes of excitatory amino acids (EAAs) of cerebrospinalfluid (CSF) in patients with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Method The EAAs levels of CSF including glutamate (Glu) and aspartate (Asp) in 24 patients with DEACMP and 20 controls with migraine were measured by high performance liquid chromatography( HPLC ).Results Glu and Asp levels in patients with DEACMP were significantly higher than those of the controls [(3.76 ± 1.52) μmol/L vs ( 1.55 ± 1.03 ) μmol/L, (0.73 ± 0.44) μmol/L vs (0.38 ± 0.33 ) μmol/L, P all <0.01]. Glu and Asp levels in moderate and severe DEACMP patients were higher than those in mild DEACMP patients. Conclusion It suggests that EAAs participated in the pathogenesis of DEACMP. The Glu and Asp levels in CSF may be regarded as indicator of DEACMP.

Objective To study the clinical feature of ciguatera fish poisoning.Methods Thirty-nine patients with ciguatera fish poisoning were observed.Results The clinical symlptoms of ciguatera poisoning usually began to appear 2～10 hours after eating a poisonous fish and could be classified into three broad groups:neurological,gastrointestinal cardiovascular symptoms.Gastrointes tinal symptoms were the most common complaint.Neurological symptoms generally stayed for 1～2 weeks.The clinical picture was characterized by temperature reversal.Conclusion Ciguatera poisoning can be differentiated by unique features affecting the neurological system.

Objective To investigate the role of Nrf2 on hydrogen treatment for intestinal injury caused by severe sepsis.Methods 152 male ICR mice were randomly divided into four groups:sham operation group,hydrogen control group,sepsis group,and hydrogen treatment group,each n=38.Sepsis model was reproduced by cecal ligation and puncture (CLP).The mice in sham operation group and hydrogen control group did not receive CLP,and the operative procedure was the same as follows.The mice in hydrogen control group and hydrogen treatment group received 1-hour inhalation of 2％ hydrogen 1 hour and 6 hours after sham operation or CLP.Twenty animals in each group were selected and observed for 7-day survival rate.Eighteen animals in each group were selected and sacrificed at 6,12 and 24 hours after CLP.The intestinal tissues were obtained to determine the expression of Nrf2 and high mobility group B1 (HMGB1) protein by Western Blot,and the expression of Nrf2 mRNA by reverse transcription-polymerase chain reaction (RT-PCR).The middle portion of jejunum was obtained to evaluate the degree of septic injury by light microscope after hematoxylin and eosin (HE) staining.Results There was no statistical signifieance in variables between sham operation group and hydrogen control group.Compared with sham operation group,the 7-day survival rate was significantly decreased in sepsis group (0 vs.100％,P＜0.05); compared with sepsis group,the 7-day survival rate was significantly increased in hydrogen treatment group (55％ vs.0,P＜0.05).Compared with sham operation group,the expression of Nrf2 protein (gray value) and Nrf2 mRNA were up-regulated in sepsis group at 6,12 and 24 hours after CLP (Nrf2 protein 6 hours:1.973 ± 0.350 vs.1.000 ± 0.000,t=4.411,P=0.002; 12 hours:2.367 ± 0.186 vs.1.000 ±0.000,t=10.210,P=0.000; 24 hours:2.517 ±0.280 vs.1.000 ±0.000,t=9.521,P=0.000; Nrf2 mRNA 6 hours:1.606 ± 0.271 vs.1.000 ± 0.000,t=3.631,P=0.002; 12 hours:1.692 ± 0.399 vs.1.000 ± 0.000,t=3.233,P=0.005; 24 hours:1.784 ± 0.341 vs.1.000 ± 0.000,t=3.894,P=0.001),and it was also the expression of HMGB1 (gray value) at 24 hours after CLP operation (1.507 ± 0.220 vs.1.000 ± 0.000,t=3.948,P=0.004).Compared with sepsis group,the expression of Nrf2 protein and Nrf2 mRNA in intestines were up-regulated at 6,12 and 24 hours after CLP in hydrogen treatment group (Nrf2 protein 6 hours:2.583 ± 0.395 vs.1.973 ± 0.350,t=2.765,P=0.024; 12 hours:2.725 ± 0.235 vs.2.367 ± 0.186,t=2.674,P=0.028; 24 hours:2.930 ± 0.212 vs.2.517 ± 0.280,t=2.595,P=0.032; Nrf2 mRNA 6 hours:2.008 ± 0.400 vs.1.606 ± 0.271,t=2.405,P=0.029; 12 hours:2.188 ± 0.475 vs.1.692 ±0.399,t=2.317,P=0.034; 24 hours:2.333 ±0.406 vs.1.784 ±0.341,t=2.728,P=0.015).Compared with sepsis group,the expression of HMGB1 was down-regulated significantly at 24 hours after CLP in hydrogen treatment group (1.147 ± 0.152 vs.1.507 ± 0.220,t=2.805,P=0.023).HE staining showed that there was significantly aggravated intestinal pathological injury in the mice of sepsis group; compared with sepsis group,the pathology was significantly less marked in hydrogen treatment group.Conclusion Through activation of Nrf2-antioxidant response element (ARE) pathway,hydrogen may increase the level of Nrf2,which is a kind of protective protein,in the intestine of mice,thus decreases the level of late pro-inflammatory factor,HMGB1,and it may protect the intestinal tissues in septic mice and increase the survival rate significantly.

Objective To evaluate the effects of hydrogen (H2) on nuclear factorE2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway in lung tissues in septic mice.Methods Seventy-two male ICR mice,weighing 20-25 g,aged 6 weeks,were randomly divided into 4 groups (n =18 each) using a random number table:sham operation group (group SH),group H2,sepsis group (group S),and sepsis + H2 group (group S + H2).Sepsis was produced by cecal ligation and puncture (CLP).H2 and S + H2 groups inhaled 2％ H2 for 1 h starting from 1 and 6 h after CLP.Six mice in each group were chosen and sacrificed at 7,12 and 24 h after CLP (T1-3).The pulmonary specimens were obtained to determine the expression of Nrf2 and HO-1 protein (by Western blot) and Nrf2 mRNA (by RT-PCR).At 24 h after CLP,the pathological changes of lungs were scored,wet/dry lung weight ratio (W/D ratio) was determined,and the expression of high mobility group box-1 (HMGB-1) in lung tissues was measured (by Western blot).Results Compared with group SH,the pathological scores and W/D ratio were significantly increased,and the expression of Nrf2 protein and mRNA,HO-1 and HMGB1 was up-regulated in S and S + H2 groups,while no significant change was found in the indexes mentioned above in group H2.Compared with group S,the pathological scores and W/D ratio were significantly decreased,the expression of Nrf2 protein and mRNA and HO-1 was up-regulated and HMGB1 expression was down-regulated in group S + H2.Conclusion The mechanism by which H2 reduces acute lung injury in septic mice is related to activation of Nrf2/ARE pathway.

Objective:To investigate the incidence of sarcopenia in maintenance hemodialysis (MHD) patients and analyze its influencing factors.Methods:Totally 441 non-hospitalized MHD patients in stable condition were selected,by bioelectrical impedance analysis (BIA) to test appendicular skeletal muscle mass(ASM), by testing grip strength of MHD patients, to assess Muscle strength, by gait speed test to measure the 4-m usual walking speed, to assess physical performance of MHD patients.Risk factors of sarcopenia were identified by Logistic regression analysis.Results:The total incidence of sarcopenia in 441 MHD patients was 16.55% (73/441) and the incidence of sarcopenia in patients over 60 years old was 28.91% (61/211).The results showed older age ( OR=0.213, 95% CI 0.099-0.458, P<0.01), Karnofsky ( OR=9.661, 95% CI 3.850-24.244, P<0.01), subjective global assessment ( OR=0.491, 95% CI 0.250-0.965, P=0.039), serum phosphorus ( OR=0.422, 95% CI 0.204-0.875, P=0.020) and body mass index ( OR=0.754, 95% CI 0.609-0.935, P=0.010) were risk factors of sacopenia. Conclusions:The incidence of sarcopenia in elder, performed less physical activity, malnutrition predisposed MHD patients was high, so to those patients we should be paid more attention and gave active interventions to reduce sarcopenia.

ObjectiveTo investigate the correlation of hippocampal synaptic plasticity with spatial learning and memory under normal and pathological condition,and provide experimental evidence for the coincidence of hippocampal late-phase long-term potentiation (L-LTP) and behavioral experiments.Methods 38 SD rats were randomly divided into two groups,control and AD model.First,Morris water maze was used to test the ability of spatial learning and memory of rats.The escape latencies for rats to search for an underwater platform in 5 days of navigation tests and the swimming time percentage in target qtuadrant on the 6th day after withdrawing the platform in probe trails were recorded.Then,in vivo hippocampus L-LTP of field excitatory postsynaptic potential (fEPSP)in CA1 region was recorded after delivering high frequency stimulation (HFS).ResultsBilateral intrahippocampal injection of 4 nmol amyloid β peptide ( Aβ 25-35 ) significantly impaired spatial learning and memory of rats in water maze tests,as well as in vivo hippocampal L-LTP.In control group,there was a significant negative correlation between the amplitude of fEPSP and the escape latency ( r =-0.8306,P ＜ 0.01 ) and a significant positive correlation between the amplitude of fEPSP and the swimming time percentage in target quadrant ( r=0.7709,P＜0.01 ).In AD model group,similar correlations were found,with a correlation coefficient of r =-0.7675 (P ＜0.01 ) and r =0.8049 (P ＜ 0.01 ),respectively.When putting all data from the two groups together,the hippocampal L-LTP was more correlated with escape latency ( r =-0.9124,P ＜ 0.01 ) and swimming time percentage ( r=0.9745,P＜0.01).ConclusionThere is very close correlation between the hippocampal L-LTP and the spatial learning and memory behavior in rats,suggesting that the hippocampal L-LTP may be involved in the electrophysiological mechanism of spatial learning and memory in rats,and the impairment of L-LTP could partly represent the deficits in cognitive function of animals.

Objective To explore the subcellular localization of Galectin-9 and its effect on allogeneic immune response.Methods The plasmid pEGFP-N1 was inserted with Galectin-9 fragment which was amplified from pBKCMV-Galectin-9 by PCR.The recombinant plagmid wag then transfected into CHO cells using JetPEI in vitro.The cells were cultured in G418 selecting mediam to obtain the stably-transfected cells.The transcription and expression of Galectin-9 gene were verified by immunohistochemical staining and RT-PCR.The solid-phase transgenic CHO cells or freshly-cultured supernatant wag added into the mixed lymphocyte response system to detect the inhibitory effect of Galectin-9.Galectin-9 protein wag administered intraperitoneally for 7d consecutively.Results The expression of Galectin-9 wag localized in the cytosol of CHO.The allogeneic mix lymphocyte proliferation was dose-dependently inhibited by the freshly-cultured supernatant from stably-transfected CHO cells.Furthermore,the supernatant from stably-transfected CHO cells dose-dependently inhibited the level of IL-2.The inhibitory effect could be reversed by Tim-3-Fc blocking.Administration of Galectin-9 significantly prolonged the survival of allogeneic cardiac transplants[(22.7±1.2)d vs(7.2±0.4)d)].Conclusion Galectin-9 may be secreted in physical situation to exert its immunomodulatory function on allogeneic immune response.Furthermore.Galectin-9 may be a novel therapeutic drug in transplant medicine.

Objective To evaluate the effect of penehyelidine hydrochloride(PHCD)on tumor necrosis factor α-induced protein 8-like-2(TIPE2)-Toll-like receptor 4(TLR4)-myeloid differentiation fac-tor 88(MyD88)signaling pathway in a rat model of traumatic acute lung injury(ALI).Methods Thirty SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 190-210 g,were divided into 3 groups(n＝15 each)by a random number table method: sham operation group(group Sham),traumatic ALI group(group ALI)and group PHCD.ALI was induced by blunt chest trauma in ALI and PHCD groups.PHCD 2 mg/kg was intraperitoneally injected immediately after blunt chest trauma in group PHCD.The rats were sacrificed and lung tissues were removed at 8 h after the model was successfully established for exami-nation of the pathological changes and ultrastructure of lung tissues(with a light microscope or an electron microscope)and for determination of the wet to dry weight ratio(W/D ratio)and expression of TLR4 and MyD88 in lung tissues.Results Compared with group Sham,the W/D ratio was significantly increased,TIPE2 expression was down-regulated,and the expression of TLR4 and MyD88 was up-regulated in ALI and PHCD groups(P＜0.05).Compared with group ALI,the W/D ratio was significantly decreased,TIPE2 expression was up-regulated,and the expression of TLR4 and MyD88 was down-regulated(P＜0.05),and the pathological changes of lung tissues and ultrastructure were significantly attenuated in group PHCD.Conclusion The mechanism by which PHCD reduces traumatic AIL is related to activating TIPE2-TLR4-MyD88 signaling pathway in rats.