Objective To study the expression and its significance of bcl-2 associated death (bad) gene in human optic nerves from traumatic atrophic eyeballs. Methods The optic nerves from 8 normal human donor eyes and 31 traumatic atrophic eyes were studied by immunohistochemistry technique. Results Bad protein was positively expressed in the normal optic nerve myelin sheath and residual myelin portions of optic nerve tissues from traumatic atrophic eyes. The expression of bad protein in the residual portions of myelin sheath was stained significantly stronger than that in normal optic nerves (P0 05). Conclusion Bad might possess the function of promoting the optic nerve atrophy processes in traumatic atrophic eyes.

Amino Acids ; metabolism ; Animals ; Brain ; metabolism ; Electromagnetic Fields ; Electrophysiological Phenomena ; Glutamates ; metabolism ; Male ; Neurotransmitter Agents ; metabolism ; Pain ; physiopathology ; Pain Threshold ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid ; metabolism

砄bjective:To purify and characterize human high molecular eight salivary mucin(MG1).Methods: MG1 was purified by 10%(w/v) cetyltrimethylammonium bromid precipitation, CM Sephadex ion exchange chromatography and sephadax G 200 gel filtration chromatography. The protein content was studied with Folinin Lowrys analysis and characterized by PAGE and SDS PAGE electrophoresis.Results:The data of PAGE showed that the purified glycoprotein was free of contaminating proteins;those SDS PAGE showed that the melocular weight of the glycoprotein was between Mr 500 000 and 1 000 000.Protein quantitative analysis showed that it contained 14.17% of protein.Amino acid analysis revealed that it contained 17 kinds of amino acid;Thr,Ser,Pro and ALa were the dominant amino acid(45.6% of the total).Conclusion: The data indicate the applied technique is reliable for purification MG1 from saliva.

This study was performed for the output of nitrous oxide (N_2O) after N_2O cessation. The breathing bag with the volume of 3000 ml served as the simulator lung,and 5 patients, ASA grade Ⅰ,aged 18-48 years scheduled for elective surgery,acted as the clinical subiects. After the equilibration of end-expiratory N_2O concentration of 50% was developed,the N_2O administration was cut off,then was expelled with oxygen flow rate at 3L/min or 6L/min. The inspiration-expiration N_2O concentration difference of simulator or patient lung (SC_(I-E) N_2O or PC_(I-E) N_2O)was recorded with an infra-red gas analyser. The N_2O dilution induced by the anesthesia circuit volume and the functional residual capacity, was similar to that by simulator lung,so the clinical output of N_2O in one minute was calculated as followed: N_2O output=(PC_(I-E) N_2O-SC_(I-E) N_2O)?minute volume of ventilation. The results showed that in the first minute after N_2O termination,there was no N_2O output,but from the second to the tenth minute the N_2O output increased gradually and was kept at the high level,additionally,the levels of N_2O output at the oxygen flow rate of 6L/min were higher than those at 3L/min in the corresponding times, respectively. It is suggested that following the withdrawal of 1:1 N_2O-O_2 anesthesia ,the N_2O output is related to the oxygen flow rate,and there is not the occurance of diffusion hypoxia.

Objective To investigate the protective effect of desflurane on the brain against ischemia-reperfusion (I/R) injury and the underlying mechanism. Methods Ninety-six male Wistar rats weighing 250-300 g were randomly divided into 4 groups (n = 24 each) : group A sham operation; group B I/R; group C desflurane + I/R and group D 5-HD + desflurane + I/R. I/R was induced by occlusion of bilateral common carotid arteries combined with controlled hypotension for 10 min. In C group 1 MAC desflurane (5.9% ) was inhaled for 60 min before I/R. In group D 5-HD 5 mg?kg-1 was given i.v. before desflurane inhalation. The animals recovered from anesthesia at 30 min of reperfusion. The neurological behavior was evaluated by the clambering test, the overhanging test, the inclined plane test and the beam balance test. Animals were killed at 6, 24 and 48 h ( n = 8 each) of reperfusion in each group and the brains were removed for microscopic examination of area CA1 of hippocampus for the number of normal pyramidal neurons surviving I/R. Results Neurological behavior was greatly compromised by I/R at 6, 24 and 48 h of reperfusion. The animals behaved significantly better at 6,24 and 48h in C group but only at 6 h in D group than in B group. The number of normal pyramidal neurons in CA1 of hippocampus was significantly decreased by I/R at 6, 24 and 48 h of reperfusion. The number was significantly larger at 6, 24 and 48 h in C group but only at 6h in D group than in B group. Conclusion Desflurane preconditioning has protective effect on the brain against I/R injury. Activation of KATP channel is involved in the mechanism.

Objective To investigate the effects of aerosolized prostaglandin E1 (PGE1) inhalation on oxygenation and intrapulmonary shunt in acute lung injury (ALI) .Methods Eighteen healthy male pigs weighing 14-18 kg were anesthetized with intraperitoneal pentobarbital 50 mg?kg-1, intubated and mechanically ventilated (VT=10-15 ml?kg-1, RR= 16 bpm, FiO2=100%) . PaCO2 was maintained at 34-45 mm Hg. Anesthesia was maintained with intravenous infusion of ketamine-procaine-succinyl-choline. Swan-Ganz catheter was placed via right femoral vein. Right femoral artery was cannulated for BP monitoring and blood sampling. ALI was induced by intratracheal instillation of HCl (0.1 mol?L-1) until PaO2 was

Objective To observe the effect of Salvia TMP on the therapeutic, blood lipids, inflammatory cytokines and cardiac function in treatment of patients with unstable angina pectoris ( UAP) .Methods Eighty cases of patients with UAP treated in the hospital from May 2013 to May 2015 were selected and randomly divided into control group and observation group ,40 patients in each group.The control group received routine medical treatment,observation group supplemented Salvia TMP injection on the basis of conventional therapy.After two weeks for a course of treatment, the difference between the two groups of patients on therapeutic,blood lipid,inflammatory cytokines and cardiac function related indicators were compared. Results Compared with control group post-treatment, the symptom control and ECG effective rate of observation group were significantly higher (χ2 =8.658,P=0.026), the levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C),TC/high-density lipoprotein cholesterol(HDL-C) and LDL-C /HDL-C in observation group were lower(P<0.05),the level of HDL-C was higher(P<0.05), the levels of interleukin-6(IL-6), high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-α(TNF-α) in observation group were significantly lower (P<0.05), the levels of stroke volume (SV), left ventricular systolic pressure (LVSP) and left ventricular ejection fraction (LVEF)were higher(P<0.05), the levels of N-terminal pro-brain natriurelic peptide (NT-proBNP) and cardiac troponin I (cTnI) were lower (P<0.05).Conclusion Salvia TMP injection could effectively regulate blood lipids in patients with UAP,control inflammation cytokines and promote the recovery of cardiac function , which has a good role in improving the symptoms of angina patients,promoting the recovery of disease.

BACKGROUND: Typically antiepileptic drugs, such as phenobarbital, fenitoina sodica and diazepam, can inhibit amygdala kindling effect in rats. However, whether midazolam has the same effect is still unclear.OBJECTIVE: To investigate the inhibitory effect of midazolam on amygdala kindling onset in rats and maximal electroshock seizure (MES) in mice and effeots of antiepileptic drugs.DESIGN: This study was divided into three subexperiments, including the effects of midazolam on amygdala kindling onset, independent activities and incidence convulsion. All the three subexperiments were completely randomized,infra-group control or self-control studies.SETTING: Medical College of Qingdao University.MATERIALS: The experiment was carried out in the Comprehensive Experimental Room, Affiliated Hospital of Medical College of Qingdao University from August 2004 to March 2005. Nine Wistar rats weighing (250±10) g and 120 Kunming mice weighing (20±5) g and either gender were provided by Animal Center of Qingdao Institute of Drug Control.Midazolam (5 g/L) was provided by Xuzhou Enhua Drugs Co., Ltd. (batch number: 20030706).METHODS: ① Establishment of amygdala kindling models: Nine kindled rats were randomly selected and intraperitoneally injected with 0.25, 0.5 and 1 mg/kg midazolam, respectively. Quadri-pathway biological signal processing system (SMUP-PC) was used to measure discharge duration (ADD) and Racine's stage. ② Sixty mice were randomly divided into 5 groups, including saline group, 40 mg/kg phenobarbital group, 0.5, 1.0 and 1.5 mg/kg midazolam groups with 12 mice in each group. And then, numbers of activities in a unit time (times per 5 minutes) were determined by XZC-4A mini-animals independent activity instrument. ③ MES models were established to calculate incidence of convulsion.MATN OUTCOME MEASURES: Effects of midazolam on ADD, Racine's stage, numbers of independent activities and incidence of convulsion.RESULTS: All the 9 rats and the 120 mice were involved in the final analysis. ① Effect of midazolam on amygdala kindling onset: After intraperitoneal injection of 0.5 and 1.0 mg/kg midazolam, ADD and Racine's stage were obviously lower than those before administration (P ＜ 0.05-0.01). After intraperitoneal injection of 0.25 mg/kg midazolam, ADD was obviously lower than that before administration (P ＜ 0.05), but there was no significant difference in Racine's stage. ②Effect of midazolam on independent activities of mice: Numbers of independent activities were lower in the phenobarbital group and 0.5, 1.0 and 1.5 mg/kg midazolam groups than those in the saline group (P ＜ 0.01), while numbers of independent activities were higher in 0.5 mg/kg midazolam group than those in the phenobarbital group (P ＜ 0.05). ③Effect of midazolam on maximal electroshock seizure: Incidence of convulsion was lower in the phenobarbital group and 0.5, 1.0 and 1.5 mg/kg midazolam groups than that in the saline group (P ＜ 0.05-0.01), while Incidence of convulsion was higher in 0.5 mg/kg midazolam group than that in the phenobarbital group (P＜ 0.05).CONCLUSION: Midazolam can significantly inhibit amygdala kindling onset, reduce numbers of independent activities,and antagonist MES in mice.

Adolescent ; Adult ; Aged ; Burns ; etiology ; microbiology ; Child ; Child, Preschool ; Drug Resistance, Bacterial ; Explosions ; Female ; Humans ; Male ; Middle Aged ; Wound Infection ; microbiology ; Young Adult

Adult ; Blast Injuries ; etiology ; therapy ; Burns ; etiology ; therapy ; Explosions ; Humans ; Male ; Young Adult