Objective To compare the effects of sedation induced with dexmedetomidine and propofol on intracranial pressure and cerebral oxygen metabolism in patients with permissive hypercapnia. Methods Twentyfour patients with acute respiratory distress syndrome (ARDS) were randomly divided into 2 groups ( n = 12 each) :dexmedetomidine group (group D) and propofol group (group P) . Their APACHE Ⅱ scores were 11-18. The patients were mechanically ventilated (VT 5-7 ml/kg, RR 12-17 bpm, PEEP 6-10 cm H2O, FiO2 40-60%). PaCO2 was maintained at 50-65 mm Hg. Radial artery was cannulated for direct BP monitoring and blood sampling. Right internal jugular vein was cannulated and the catheter was advanced cephalad until jugular bulb. Continuous infusion of dexmedetomidine was started at 0.5 μg· kg-1· h-1 and TCI of propofol was started at target plasma concentration (Cp) of 0.4 μg/ml. The infusion of both drugs was gradually increased until Ramsay score (1= fully awake, 6 =asleep, unresponsive to loud verbal stimulus) reached 3,4,5. Transcranial Doppler monitoring was used to determine cerebral blood flow velocity (CBFV), pulsatility index (PI) and resistance index (RI) before administration of dexmedetomidine and propofol (T0 ) and at 30 min after the 3 levels of sedation were reached (T1-3) . Meanwhile blood samples were taken from radial artery and jugular bulb for blood gas analyses. Cerebral O2 metabolic rate (CMRO2), cerebral A-V O2 content differences (Da-jvO2) and cerebral O2 extraction rate (CERO2) were calculated .ResultsCBFV, PI, RI and CMRO2 were significantly decreased at T1-3 as compared with the baseline values at T0 in both groups. CBFV was positively correlated with CMRO2 in both group D (r = 0.80) and group P ( r = 0.76) . CBFV, PI and RI were significantly lower at T1-3 in group D than in group P. There was no significant change in Da-jvO2 and CERO2 at T1-3 as compared with the baseline values at T0 in both groups. Conclusion At different sedation levels, dexmedetomidine results in lower intracranial pressure than propofol and maintains the balance between cerebral O2 supply and demand in patients with permissive hypercapnia.

Objective To investigate the changes in auditory evoked potential index(AAI)value and bispectral index(BIS)value produced by treatment of hypotension with ephedrine or phenylephrine during induction of general anesthesia.Methods Seventy-five ASA Ⅰ or Ⅱ patients of both sexes aged 30-50 yr with body mass index ＜ 30 kg/m2 underwent elective abdominal surgery under general anesthesia.Anesthesia was induced with 8%sevoflurane,midazolam 0.1 mg/kg and fentanyl 3 μg/kg.Tracheal intubation was facilitated with succinylcholine 2 mg/kg.Anesthesia was maintained with sevoflurane inhalation.BIS value was maintained at 40-50 and AAI value at 20-30 by adjusting the concentration of sevoflurane.When the desired level of BIS value and AAI value was reached during induction of anesthesia,hypotension(MAP ＜ 80 % of the baseline)was treated with intravenous ephedrine 0.1 mg/kg(group E,n = 25)or phenylephrine 2 mg/kg(group P,n = 25)or 6% HES(130/0.4)10 ml/kg(group C,n = 25)at random.MAP,HR,BIS value and AAI value value were recorded before(T0)and at 2,5,7,10 min after fluid or vasoactive agent administration(T1-4).Results MAP significantly increased after treatment at T1-4 as compared with MAP at To in all 3 groups.BIS and AAI values were significantly increased after administration of ephedrine at T3,4 as compared with MAP at To in group E.There were no significant differences in BIS and AAI values before and after administration of phenylephrine and 6% HES in group P and C.Con-clusion Treatment of hypotension with ephedrine during induction of general anesthesia can increase BIS and AAI and decrease the depth of anesthesia but phenylephrine cannot.

Objective To understand the current status of overall management and treatment of garbage and waste water in rural areas of Fujian,and to provide scientific evidence for governments at all levels to make policies in rural sanitation. Methods From September to December,2006,215 villages in 21 counties in Fujian rural areas were selected,and 10 families were sampled and investigated for garbage collection and waste water treatment from each village. Results In the investigated villages,the production of garbage amounted to 40 837.4 tons per month;and domestic and productive garbage accounted for 32.2% and 67.8% of the total,respectively. Among the domestic garbage,23.7% was randomly discharged or stacked,and only 8.5% went through harmless treatment (incineration,composting under high temperature or direct reuse). However,30.7% productive garbage was randomly discharged or stacked,and 37.1% went through harmless treatment. Every month,948 195 tons of waste water was produced in the investigated villages;57.5% of them were domestic and 42.5% were productive. Only 0.6% of the domestic waste water and 33.0% of the productive waste water were treated. Conclusion The rural public health infrastructure building is far lagged,with low rate of harmless treatment of garbage and waste water. Random littering and piling (discharging) garbage are common phenomena in rural areas. Thus,it is urgent to improve rural sanitation development.

This paper has reviewed the basic characteristics of algae toxins. The effects of several water purification processes on removal of algae toxins from drinking water have been compared and discussed. The processes such as the enhanced pretreatment+conventional treatment, the conventional treatment+activated carbon filter, the conventional treatment+membrane filter are effective in the removal of algae toxins.

BACKGROUND: Gene chip of expression spectrum is used to make contrastive analysis of the changes of gene expression of histocytes derived from different individuals, tissues, cell cycles, developmental stages, differentiating stages, physiological and pathological status, and stimulating conditions.OBJECTIVE: To investigate gene expression changes of cerebral tissues of mice at different phases after ischemia/reperfusion injury, and screen out and understand genes related to cerebral ischemic/reperfusion injury.DESIGN: A randomized and controlled animal study.SETTING: Laboratory of the Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital affiliated to Capital University of Medical Sciences;Laboratory of Shanghai Biostar Gene Chip Co., Ltd.MATERIALS: The experiment was performed in the Laboratory of Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital affiliated to Capital University Medical Sciences, and the Laboratory of Shanghai Biostar Gene Chip Co., Ltd. from September 2002 to October 2003. Totally 20 male mice of C57BL/6 species were selected and randomized into 4 groups with 5 in each group: 48-hour and 10-day sham-operation groups and 48-hour and 10-day cerebral ischemia-reperfusion groups.METHODS: The bilateral common carotid arteries of mice in cerebral ischemia/reperfusion group were blocked with clamp for 20 minutes to establish models of cerebral ischemia/perfusion injury. The bilateral common carotid arteries of mice in sham-operation group were separated without clamp. We killed the mice by breaking off their necks at the 48th hour and 10th day after operation. Expression changes of cerebral tissues of mice were detected with BiostarM-20 s gene chip of expression spectrum.MAIN OUTCOME MEASURES: Changes of gene expression of cerebral tissues of mice in each group.RESULTS: A total of 20 mice were involved in the result analysis. ①Differential expression gene in 48-hour sham-operation group and 48-hour cerebral ischemia/reperfusion group showed that the number of up-regulated expression genes was 30. Among them the most obvious up-regulated gene was related to DNA synthesis, repair and transcription. The number of down-regulated expression genes was 119. Among them the most obvious down-regulated gene was protein phosphatase 1 (PP1) gene related to cellular signal and transferrin protein. ② Differential expression gene between 10-day sham-operation group and 10-day cerebral ischemia/reperfusion group showed no up-regulated gene, but 7 down-regulated genes, and the most obvious down-regulated gene was the one that related to cell apoptosis.CONCLUSION: At the 48th hour after cerebral ischemia/reperfusion, upregulated gene is the one that related to DNA synthesis, repair and transcription, which is helpful for cerebral tissue repair after cerebral ischemia/reperfusion. Genes related to cell signal and transferrin are down-regulated, and can level off barrier of endothelial cells and relieve cerebral ischemia/reperfusion injury. At the 10th day after cerebral ischemia/reperfusion, cell apoptosis-related gene is down-regulated, and can accelerate apoptosis and aggravate injury of cerebral cells, which may be related to delayed neuronal necrosis.

Objective To investigate the effect and significance of hyperbaric oxygenation in down-regulation of platelet membrane glycoproteins CD31 and CD62p in rats of traumatic brain injury (TBI).Methods Fifty-six SD rats were randomly distributed into TBI group,hyperbaric oxygenation group,and sham group by the lottery method.Furthermore,TBI group and hyperbaric oxygenation group were subgrouped at 6,48,and 96 hours.There were 8 rats per group.The rat models of severe TBI were induced by lateral fluid percussion.Levels of CD31 and CD62p were measured in all groups by flow cytometry.Results At 6,48 and 96 hours,expressions of CD31 (30.8 ± 8.9,32.5 ± 9.2 and 29.0 ±5.0) and CD62p (34.5 ±9.1,33.9 ±7.5 and 30.4 ±6.4) in TBI group were significantly higher than those (18.9-± 5.5,19.5 ± 6.1) in sham group (P ＜ 0.05).At 96 hours,expression of CD31 (22.7 ±5.5) in hyperbaric oxygenation group was significantly lower than 29.0 ± 5.0 in the TBI group (P ＜0.05).At 48 and 96 hours,expressions of CD62p (26.1 ± 5.8,23.6 ± 5.7) in hyperbaric oxygenation group were significantly lower than 33.9 ± 7.5 and 30.4 ± 6.4 in TBI group (P ＜ 0.05).Conclusions Platelet activation is enhanced in the acute phase after TBI.But platelet activation may be relieved with hyperbaric oxygenation,which is conducive to inhibiting microthrombosis and mitigating secondary brain injury after TBI.

Objective: To investigate the relationship between the plasma concentration of nitric oxide (NO) and prognosis of the hemorrhagic shock. Method:The blood levels of NO and Lactate (LA) were measured with fluorophotometry and colorimetry in 30 hemorrhagic shock patients,and another 30 patients for elective surgery served as a control. Result :Concentration of NO was significantly lower and that of LA was significantly higher in hemorrhagic shock group than that of control group. NO level had a negative correlation with LA level and injury index. NO level in the patients complicated by sepsis were still lower than the control. Conclusion:Decrease of NO level may result in disturbance of microcirculation and increase of LA. So nitroglycerin should be used as early as possible in the hemorrhagic shock patients.

To investigate the inhibiting effects of ketamine on arterial plasma TNF-? concentration and lung injury in septic shock rat. Method: 40 Wister rats were divided into five groups. 15mg?kg~(-1) endotoxin (LPS) was intravenously injected alone (group Ⅰ)or ip ketamine 50,100 and 200mg?kg~(-1) before LPS, then ketamine was infused at 10mg?kg~(-1)?min~(-1) (Ⅱ, Ⅲ and Ⅳgroup). TNF-? was assessed with ELISA, and at the same time the arterial blood oxygen tension and lung water content were measured. Result: In contrast to normal control level, arterial plasma TNF-? levels and lung water content increased and arterial oxygen tension decreased after LPS in group Ⅰ, but in the rats of giving ketamine, plasma TNF-? level decreased more than that in the rats of giving LPS alone (group Ⅰ), change of arterial blood oxygen tension and lung water content in former groups were better than that of later, in dosage-dependent way. Conclusion: Ketamine can dose-relatedly decrease TNF-? concentration and lung injury degree induced by endotoxin.

Objective To compare the influences of propofol and ketamine on mean pulmonary arterial pressure (MPAP), Ca 2+ content and the ultrastrcture of lung tissues during acute hypoxia Methods Twenty one Wistar rats were randomly divided into 3 group: infusion with propofol 8mg kg -1 h -1 in P group and ketamine 8 mg kg -1 h -1 in K group ,21% O 2 gas was inhaled in 15 min followed by inhalation of mixture gas of 10% O 2 and 90% N 2 for 20 min in the both groups ; continuous infusion with normal saline with 21% O 2 inhalation for 35 min in C group Carotid blood gas was analysed, pulmonary Ca 2+ content was measured with absorption spectrophotometry and the lung ultrastructure was detected with electron microscopy at the end of the experiment Results Compared with those in C group, MAP and PaO 2 decreased significantly and MPAP increased markedly in P and K groups , with MPAP in P group being lower than that in K group (P

Objective To investigate the roles of reactive oxygen species (ROS) and phosphatidyl-inositol 3-kinase-Akt (PI3K-Akt) in neuroprotection against spinal cord ischemia-reperfusion (I/R) injury by ischemic postconditioning (IP) or controlled low perfusion pressure (LR). Methods One hundred and twenty-six adult male SD rats weighing 300-350 g were randomly divided into 7 groups (n = 18 each): group Ⅰ I/R; group ⅡIP; group Ⅲ LR; group Ⅳ IP + LY-294002 (IP + LY); group Ⅴ LR + LY-294002 (LR + LY); group Ⅵ IP +N-acetylcysteine (IP+ N) and group Ⅶ LR+ N-acetyl-cysteine (LR+ N). Spinal cord ischemia was induced by 9 min occlusion of the thoracic aorta combined with controlled hypotension (MAP = 40 mm Hg). In IP group the animals were subjected to 3 cycles of 30 s reperfusion interspersed with 30 s ischemia immediately after release of aortic occlusion. In LR group MAP was maintained at 40 mm Hg for another 5 min immediately after release of aortic occlusion, then increased to 100 mm Hg. In group Ⅳ-Ⅶ LY-294002 (PI3K inhibitor) 25 mg/kg or N-acetylcysteine (ROS scavenger) 100 mg/kg were administered at the onset of reperfusion. Twelve animals in each group were killed at 2 h of reperfusion. The lumbar segment of the spinal cord was removed for determination of the level of Akt phosphorylation and opening of mitochondrial permeability transition pore (mPTP). Neurological function was assessed and scored (15 = normal function, 0 = unable to move hind limb) at 4, 12, 24 and 48 h of reperfusion in another 6 animals in each group. The animals were then killed after last assessment and the lumbar segment of the spinal cord was removed for detection of apoptotic neurons. Results Compared with I/R group,both IP and LR significantly enhanced the level of Akt phosphorylation in the spinal cord, inhibited mPTP opening and neuronal apoptosis and increased neurological function scores. There was no significant difference in the protective effects exerted by IP and LR. The neuroprotective effects exerted by IP and LR were abolished by LY-294002 and N-acetylcysteine. Conclusion Ischemic postconditioning or controlled low perfusion pressure can protect the spinal cord from I/R injury by activating PI3K-Akt and inhibiting mitochondrial permeability.