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.

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 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 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.

Objective To evaluate the role of autophagy in survival of hypoxia-preconditioned bone marrow mesenchymal stem cells (BMSCs) in damaged tissues resulting from spinal cord ischemiareperfusion (I/R) injury in rats.Methods In vitro experiment Rat BMSCs were seeded in 12-well plates at a density of 1× 106 cells/ml (1 ml/well) , and randomly divided into 6 groups (n =30 wells each) : control group (group C) , normoxia-incubated group (group N) , hypoxic preconditioning (HP) group (group H), HP + AMP-activated protein kinase (AMPK) inhibitor Compound C group (group HC), HP + autophagy inhibitor 3-methyladenine group (group HM) and HP + mammalian target of rapamycin (mTOR) inhibitor rapamycin group (group HR).In HC, HM and HR groups, 10 mmol/L Compound C, 5 mmol/L 3-methyladenine and 10 nmol/L rapamycin were added to the culture medium, respectively, at 3 h before HP.Twelve wells in each group were selected, and the expression of phosphorylated AMPK (p-AMPK) , phosphorylated mTOR (p-mTOR), microtubule-associated protein 1 light chain 3 Ⅰ (LC3 Ⅰ), and LC3 Ⅱ in BMSCs was determined.Eighteen wells in each group were selected, and BMSCs were co-cultured with 500 μ mmol/L H2O2 for 24 h, the survival and apoptotic rate of BMSCs were measured, and the activities of caspase-9 and caspase-3 were detected.In vivo experiment Adult male Sprague-Dawley rats, weighing 300-350 g, aged 3 months, underwent spinal cord I/R.A total of 192 rats with spinal cord I/R injury were randomly divided into C, N, H, HC, HM and HR groups (n =32 each) using a random number table.At 30 min of reperfusion, BMSC suspension 5 μ l (1×106 cells/ml) processed in N, H, HC, HM and HR groups of in vitro experiment was implanted into the lumbar segment (L1-5) of the spinal cord in N, H, HC, HM and HR groups, respectively.Neurological function was scored at 4, 12, 24 and 48 h of reperfusion.The lumbar segment of spinal cord was removed for detection of apoptosis in BMSCs.Results In vitro experiment Compared with group N, the p-AMPK expression, LC3 Ⅱ/LC3 Ⅰ and survival rate were significantly increased, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were decreased in group H (P＜0.05).Compared with group H, the p-AMPK expression, LC3 Ⅱ/LC3 Ⅰ and survival rate were significantly decreased, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were increased in group HC, LC3 Ⅱ/LC3 Ⅰ and survival rate were decreased, and apoptotic rate and activities of caspase-9 and caspase-3 were increased in group HM, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were decreased, and LC3 Ⅱ/LC3 Ⅰ and survival rate were increased in group HR (P＜0.05).In vivo experiment Compared with group N, the neurological function scores were significantly increased, and the number of apoptotic BMSCs was decreased in group H (P＜0.05).Compared with group H, neurological function scores were significantly decreased,and the number of apoptotic BMSCs was increased in HC and HM groups (P＜O.05).Conclusion Enhanced autophagy is involved in survival of hypoxia-preconditioned BMSCs in damaged tissues resulting from spinal cord I/R injury, and the mechanism is associated with activated AMPK/mTOR pathway in rats.

Objective To evaluate the effect of lactulose on spinal cord ischemia-reperfusion (I/R) injury in rats.Methods One hundred forty-four male Sprague-Dawley rats, aged 3 months, weighing 300-350 g, in which gastric tube was successfully inserted, were randomly divided into 4 groups (n=36 each) using a random number table: sham operation group (group S), spinal cord I/R group (group I/R), lactulose group (group L), and lactulose + antibiotics group (group LA).Spinal cord ischemia was induced by occlusion of the thoracic aorta combined with controlled hypotension for 9 min, followed by reperfusion.Lactulose 0.5 g/kg was administered intragastrically immediately after onset of reperfusion in group L.Metronidazole 30 mg/kg and gentamicin 40 mg/kg were administered intragastrically three times a day during 1-3 days before operation in group LA, and the other procedures were similar to those previously described in group L.Hydrogen concentration in cerebrospinal fluid was detected before ischemia and at 10, 30, 60, 90, 120, 150 and 180 min after reperfusion.At 12, 24 and 48 h of reperfusion, 8 rats in each group were sacrificed, and the L3-5 segment of the spinal cord was isolated for determination of nuclear factor E2-related factor 2 (Nrf2) expression (by Western blot), superoxide dismutase (SOD) activity (by using xanthine oxidase method), catalase (CAT) activity (ammonium molybdate method), and 8-hydroxy-2'-deoxyguanosine (8-OHdG), 3-nitrotyrosine (3-NT) and malondialdehyde (MDA) contents (by ELISA).Neurological function was assessed and scored at 48 h of reperfusion.Six animals in each group were then sacrificed after assessment of neurological function, and the L3-5 segment of the spinal cord was removed for detection of apoptotic neurons.The cell survival rate and apoptotic rate were calculated.Results Compared with group S, no significant change was found in the hydrogen concentration in the cerebrospinal fluid at each time point, and in the level of Nrf2, CAT and SOD at 12, 24 and 48 h of reperfusion, the contents of 8-OHdG, 3-NT and MDA were significantly increased, the neurological scores and cell survival rate were decreased, and the apoptotic rate was increased in group I/R, and the hydrogen concentration in the cerebrospinal fluid at 30-180 min of reperfusion was increased, the level of Nrf2, CAT and SOD was increased at 12, 24 and 48 h of reperfusion, and no significant change was found in the contents of 8-OHdG, 3-NT and MDA, neurological scores, cell survival rate, and apoptotic rate in group L.Compared with group I/R, the hydrogen concentration in the cerebrospinal fluid at 30-180 min of reperfusion was increased, the level of Nrf2, CAT and SOD was increased, the contents of 8-OHdG, 3-NT and MDA were decreased, the neurological scores and cell survival rate were increased, and the apoptotic rate was decreased in group L, and no significant change was found in the parameters mentioned above in group LA.Conclusion Lactulose can reduce spinal cord I/R injury in rats.

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 The purpose of this study was to assess the effects of heat stress response (HSR) on i of pulmonary arterial endothelium cells (PAEC)incubated with TNF-?. We tried to illustrate the mechanism of injury to PAEC caused by TNF-? and the effects of HSR.Methods The study consisted of four groups.In group Ⅰ confluent monolayer of calf PAEC were directly incubated with TNF-? at final concentrations of 500, 1 000 and 2 000 u/ml for 24 h.In group Ⅱ PAEC were first bathed in 42℃ water for 20 min and then allowed to recover for 24 h.In turn they were incubated with TNF-? at the same concentrations.In group Ⅲ PAEC were not heated and incubated with TNF-?.In group Ⅳ PAEC were heated but not incubated with TNF-?.i of PAEC was assayed by fluorospectrophotometry and i of four groups were compared.The change in i before and after incubation of PAEC with TNF-?(?i) was calculated.Results (1) i was considerably higher in group Ⅰ than that in group Ⅲ at different concentrations in dose-dependent way.(2) Although i was higher in group Ⅳ than that in group Ⅲ, HSR could inhibit the further increase in i of PAEC incubated with TNF-?.Conclusions HSR may decrease the i in PAEC incubated with TNF-?.It indicates that HSR can prevent PAEC from calcium overload and provide protection on PAEC against injuries.

ve When a new drug is introduced for intrathecal (IT) administration, its effect on spinal cord should be studied for safety reason. The aim of this study was to determine the ultra-microstructure of spinal cord and Ca2+ content in spinal cord after IT administration of ropivacaine in dogs. Methods Eighteen mongrel dogs of either sex weighing about 10kg were randomly assigned to one of three groups according to the dose of ropivacaine administered IT: group A received normal saline 2ml IT and served as control; group B received 0.5% ropivacaine 2ml(10mg) IT; group C received 1% ropivacaine 2ml(20mg) IT. Anesthesia was induced with intramuscular ketamine 20mg.kg-1 and atropine 0.05mg?kg-1 and maintained with intermittent iv boluses of ketamine 3mg?kg-1 and fentanyl 5?g?kg-1 Left internal jugular artery was cannulated for intra-arterial pressure monitoring. An incision was made in the back at L3-4 and lumbar puncture was confirmed by aspiration of cerebral-spinal fluid (CSF). Normal saline or ropivacaine was then injected over 20 seconds. 3 hours after IT administration the animals were sacrificed and L1-2 segment of spinal cord and nerve roots were immediately removed for Ca content determination and electron microscopic examination. Results The Ca2+ content of spinal cord was significantly higher in group C than that in group A and B. Electron microscope revealed that in group A and B neurolemma of the nerve root and mitochondria and endoplasmic reticulum of the neurons in spinal cord were intact, while in group C neurolemma was stratified and partly disrupted and mitochondria and endoplasmic reticulum underwent swelling and there was vacuole degeneration. Conclusions Ropivacaine of high concentration or at high dose may be injurious to spinal cord.