Heart ; drug effects ; Heart Failure ; drug therapy ; Humans ; Hydrogen Bonding ; Nitrogen Oxides ; pharmacology ; therapeutic use

OBJECTIVES: To investigate the role of tetramethylpyrazine(TMP) nitrone in proliferation and differentiation of neural stem cells (NSCs). METHODS: We separated and cultivated the original generation of NSCs from cerebral cortex of 14 days rat embryo, and the phenotype characteristics of the third-generation NSCs was tested by immunofluorescence. The experiment was divided into control group, β-mercaptoethanol positive control group, tetramethylpyrazine nitrone group and tetramethylpyrazine nitrone + ethylene glycol tetraacetic acid(EGTA) group (=4). The third-generation cultivation of NSCs was used in the experiment. The effect of tetramethylpyrazine nitrone on the number of NSCs proliferation was determined by BrdU and MTT, and the differentiation of NSCs was determined by Western blot. RESULTS: The primary NSCs was isolated successfully, neurospheres with typical NSCs morphology and expressing nestin was formed at 3-5 days. As BrdU and MTT assay results shown, compared with the control group andβ-mercaptoethanol positive control group, the NSCs proliferation numbers of tetramethylpyrazine nitrone group increased significantly(<0.05). The results of Western blot showed that the neuronal differentiation rate of NSCs was increased significantly in both the tetramethylpyrazine nitrone group and tetramethylpyrazine nitrone + EGTA group, and the differentiation rate of NSCs in tetramethylpyrazine nitrone + EGTA group increased more significantly(<0.05). CONCLUSIONS Tetramethylpyrazine nitrone can significantly enhance the proliferation and neuronal differentiation rate of NSCs. Decrease in extracellular Ca can promote the differentiation of NSCs into neurons induced by tetramethylpyrazine nitrone. Ca signaling plays an important role in the differentiation of NSCs into neurons.
Animals ; Calcium Signaling ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Neural Stem Cells ; cytology ; drug effects ; Nitrogen Oxides ; pharmacology ; Pyrazines ; pharmacology ; Rats

OBJECTIVETo evaluate the disinfection of wastewater in China.

METHODSDuring the SARS epidemic occurred in Beijing, a study of different disinfection methods used in the main local wastewater plants including means of chlorine, chlorine dioxide, ozone, and ultraviolet was carried out in our laboratory. The residual coliform, bacteria and trihalomethanes, haloacetic acids were determined after disinfection.

RESULTSChlorine had fairly better efficiency on microorganism inactivation than chlorine dioxide with the same dosage. Formation of THMs and HAAs does not exceed the drinking water standard. UV irradiation had good efficiency on microorganism inactivation and good future of application in China. Organic material and ammonia nitrogen was found to be significant on inactivation and DBPs formation.

CONCLUSIONChlorine disinfection seems to be the best available technology for coliform and bacteria inactivation. And it is of fairly low toxicological hazard due to the transformation of monochloramine.

Acetates ; analysis ; metabolism ; Ammonia ; analysis ; metabolism ; Animals ; Bacteria ; drug effects ; isolation & purification ; China ; Chlorine ; pharmacology ; Chlorine Compounds ; pharmacology ; Disinfectants ; pharmacology ; Disinfection ; methods ; Dose-Response Relationship, Drug ; Enterobacteriaceae ; drug effects ; isolation & purification ; Environmental Exposure ; Humans ; Nitrogen ; analysis ; metabolism ; Organic Chemicals ; analysis ; metabolism ; Oxides ; pharmacology ; Ozone ; pharmacology ; SARS Virus ; drug effects ; isolation & purification ; Trihalomethanes ; analysis ; metabolism ; Ultraviolet Rays ; Waste Disposal, Fluid ; methods ; Water Microbiology

We sought to know whether a free radical spin trap agent, alpha-phenyl-N-tert-butyl nitrone (PBN) influences brain cell membrane function and energy metabolism during and after transient global hypoxia-ischemia (HI) in the newborn piglets. Cerebral HI was induced by temporary complete occlusion of bilateral common carotid arteries and simultaneous breathing with 8% oxygen for 30 min, followed by release of carotid occlusion and normoxic ventilation for 1 hr (reoxygenationreperfusion, RR). PBN (100 mg/kg) or vehicle was administered intravenously just before the induction of HI or RR. Brain cortex was harvested for the biochemical analyses at the end of HI or RR. The level of conjugated dienes significantly increased and the activity of Na+, K+-ATPase significantly decreased during HI, and they did not recover during RR. The levels of ATP and phosphocreatine (PCr) significantly decreased during HI, and recovered during RR. PBN significantly decreased the level of conjugated dienes both during HI and RR, but did not influence the activity of Na+, K+-ATPase and the levels of ATP and PCr. We demonstrated that PBN effectively reduced brain cell membrane lipid peroxidation, but did not reverse ongoing brain cell membrane dysfunction nor did restore brain cellular energy depletion, in our piglet model of global hypoxic-ischemic brain injury.
Adenosine Triphosphate/metabolism ; Animals ; Animals, Newborn ; *Anoxia ; Brain/*drug effects/metabolism/pathology ; Cell Membrane/*metabolism ; Cerebral Cortex ; *Ischemia ; Lipid Peroxidation ; Na(+)-K(+)-Exchanging ATPase/metabolism ; Neuroprotective Agents/*pharmacology ; Nitrogen Oxides/*pharmacology ; Phosphocreatine/*analogs & derivatives/metabolism ; Reperfusion Injury/*drug therapy ; Support, Non-U.S. Gov't ; Swine ; Time Factors

BACKGROUNDCoronary artery damage from Kawasaki disease (KD) is closely linked to the dysfunction of the endothelial progenitor cells (EPCs). The aim of the present study was to evaluate the modulatory effect of granulocyte colony-stimulating factor (G-CSF) on EPCs and elastin breakdown of coronary arteries in a KD mouse model.

METHODSA Lactobacillus casei cell wall extract (LCWE)-induced KD model was established in C57BL/6 mice that were subsequently administrated with recombinant human G-CSF (rhG-CSF). Nω-nitro-L-arginine methyl ester (L-NAME) was administrated for the negative intervention. Evaluations included coronary artery lesions, EPC number and functions, and the plasma concentration of nitric oxide (NO).

RESULTSElastin breakdown was found in the coronary arteries of model mice 56 days after injection of LCWE. The number of circulating EPCs, plasma concentration of NO, and functions of bone marrow EPCs, including proliferation, adhesion, and migration abilities, were all lower in the KD model group compared with those in the control group. After administration of rhG-CSF, the number of circulating EPCs and plasma concentration of NO were increased significantly compared with those in the KD model group. There were also increases in the functional indexes of EPCs. Furthermore, rhG-CSF administration improved the elastin breakdown effectively. However, these protective effects of rhG-CSF on coronary arteries were attenuated by L-NAME.

CONCLUSIONThe present study indicated that the administration of G-CSF prevents elastin breakdown of the coronary arteries by enhancing the number and functions of EPCs via the NO system, and then accelerates the repair of coronary artery lesions in the KD.

Animals ; Coronary Vessels ; cytology ; drug effects ; metabolism ; Disease Models, Animal ; Elastin ; metabolism ; Endothelial Progenitor Cells ; cytology ; Granulocyte Colony-Stimulating Factor ; therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Mucocutaneous Lymph Node Syndrome ; blood ; drug therapy ; metabolism ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitrogen Oxides ; blood

AIMTo determine the biochemical effect of di-(2-ethylhexyl) phthalate (DEHP) on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium.

METHODSDiets containing 2% DEHP were given to male Crlj:CD1(ICR) mice for 10 days. The dose of DEHP was 0.90 +/- 0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-(2-ethylhexyl) phthalate (MEHP), nitrogen oxides (NOx) produced by peroxidation of nitric oxide (NO) with free radicals, and lipid peroxidation induced by the chain reaction of free radicals.

RESULTSHistological observation and serum analysis showed the presence of severe spermatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver.

CONCLUSIONThe results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.

Animals ; Body Weight ; drug effects ; Copper ; metabolism ; Diethylhexyl Phthalate ; analogs & derivatives ; metabolism ; pharmacology ; Iron ; metabolism ; Kidney ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitrogen Oxides ; metabolism ; Pancreas ; drug effects ; metabolism ; Spermatogenesis ; drug effects ; Testis ; drug effects ; metabolism ; Testosterone ; blood ; Zinc ; metabolism