The pelvic floor dysfunction associated lower urinary tract disease.It is women who often multiple diseases,is closely related to the perineum and urogenital diaphragm tissue of old injury and chronic inflammation caused by pregnancy,childbirth,surgical delivery,injection of pelvic trigger point and interventional treatment for the pelvic floor dysfunction associated lower urinary tract diseases is significance.

This paper reports a method for detecting circulating immune complexes (CIC) inmice with an enzyme-linked immunosorbent assay (Raji-ELISA). This method isspecific, sensitive and easy to perform, the reagents are safe and reliable, and it canbe used without much difficulty. It has a sensitivity of 5.5?g/ml, along with a goodspecificity and reproducibility. Good correlation was observed between the Raji-ELISA and polyethylene glycol (PEG) precipitation assay. Forty-six serum samplesfrom normal Kunming mice were determined by the Raji-ELISA assay, and theconcentration of CIC was 26.18?20.41?g/ml. Only 6.5% of normal Kunming miceshowed a value of CIC above + 2s. The mice allografted with spleen cells fromnormal mice had no elevation in the concentration of CIC. However, the CIC ofEhrlich ascite tumor bearing mice showed a great increase, reached a value of105.12 + 38.76?g/ml with a total positivity of 93%.

AIM: To study the change of glutamate (Glu) transport across blood brain barrier ( BBB ) in rat following forebrain ischemia/reperfusion. METHODS: BBB unidirectional transfer constant ( Ki ) for [3H] - Glu in rat hippocampus, cerebral cortex and striatum were determined after rats were subjected to cerebral ischemia 10 min ( two - carotid occlusion plus hypovolemic hypotension) followed by 0.17, 2, 6 and 24 h of reperfusion. The recovery of [3H] - Glu in cerebrum was also determined after intracerebral injection of [3H] - Glu in another experiment. RESULTS: Compared with control rat brain, Ki for [3H] -Glu significantly( P < 0.05) decreased at 10 ain cerebral ischemia followed by 0.17, 2 and 6 h of reperfusion. At 5 min after intracerebrally injecting [3H] - Glu , recovery of [3H] - Glu in control rat brain was 23.83%. The result indicted that there is a Glu efflux mechanism on BBB. This efflux was not significantly inhibited by pretreatment of 200 mg/L probenecid. After 10 ain cerebral ischemia followed by 2 h of reperfusion, the recovery( 13.13 % ) was significantly lower than contro( P < 0.05), its recovery was only 55 % of the control. The result indicated that cerebral ischemia/reperfusion may enhanced the effiux of [3H] -Glu from brain. CONCLUSION: Cerebral ischemia/reperfusion significantly reduced Glu BBB transport from plasma to brain and enhanced effiux of Glu from brain.

AIM: to study the change of glutamate(Glu) transport across blood brain barrier(BBB) in rat following forebrain ischemia/reperfusion. METHODS: BBB unidirectional transfer constant(K i) for [3H]-Glu in rat hippocampus, cerebral cortex and striatum were determined after rats were subjected to cerebral ischemia 10 min (two-carotid occlusion plus hypovolemic hypotension) followed by 0.17, 2, 6 and 24 h of reperfusion. The recovery of [3H]-Glu in cerebrum was also determined after intracerebral injection of [3H]-Glu in another experiment. RESULTS: Compared with control rat brain, K i for [3H]-Glu significantly(P

Aim To study the effects of 9-(4-ethoxycarbonylphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydro acridine (EDT) on free radical induced injury in primary cultured rat cortical neuron and cerebral ischemia in mice. Methods In primary rat cortical neuron, free radical injury model was established by 10 μmol*L-1 H2O2. The content of malondiadehyde (MDA) and activity of superoxide dismutase (SOD) in cells were investigated. Chronic cerebral ischemia model was produced by occlusion of one carotid artery and pneumogastric nerve in mice. The step down test was adopted to investigate the effect of EDT on the memory impairment. The cerebra morphology and MDA, NO content and SOD activity in mice cerebra were detected. Results In primary rat cortical culture, 0.01-3 μmol*L-1 EDT concentration-dependently inhibited the formation of MDA and reduction of SOD activity induced by 10 μmol*L-1 H2O2. In chronic cerebral ischemia, EDT 2.5, 5 and 10 mg*kg-1 ig for 5 d greatly improved the memory impairment, reduced NO efflux and MDA content, while increased SOD activity in mice cerebra. Conclusion EDT was found to protect neurons from H2O2-induced neurotoxicity and inhibit chronic cerebral ischemia mediated injury and memory impairment in mice.

The mdr 1-type P-glycoprotein can confer multidrug resistance to tumor cells by actively pumping a wide variety of drugs from the cells. To counteract this drug resistance, P-glycoprotein-blocking agents are currently administered to patient during chemotherapy. However, this may also affect the normal physiological functions of the mdr 1-type P-glycoprotein. The P-gp is a transmembrane efflux transporter found on the luminal side of the capillary cells that comprise the blood-brain barrier. Recent insights recognize P-glycoprotein, as an important element of the blood-brain barrier (BBB), play an important role for mdr 1a P-glycoprotein in the blood-brain barrier. Studies in mice, which lack P-gp in the BBB 〔mdr1a (-/-) mice〕, have contributed significantly to these insights. In addition, the potential of new therapeutic approaches in the near future as well as their limitations will be clearified.

AIM: To study the effects of 9 (4 Ethoxycarboxylyphenoxy) 6,7 dimethoxy 1,2,3,4 tetrahydro acridine (EDT) on learning and memory abilities. METHODS: The step down test and Y maze test were adopted in this study. RESULTS: EDT ( 2.5 , 5, 10 mg?kg -1 , ig? 5 d ) dose dependently improved the impairment of memory acquisition, memory consolidation and memory retrieval induced by scopolamine, NaNO 2 and alcohol in mice. CONCLUSION: EDT can improve learning and mermory ability in mice.

Multidrug resistance (MDR) is the phenomenon observed in tumor cells that describes the simultaneous emergence of cellular resistance to the cytotoxic attack by structurally and mechanism unrelated chemotherapeutic drugs. The mdr 1 gene was sufficient to confer the MDR phenotype, including the expression of the P Glycoprotein (P Gp). P Gp appears to play an important role in tumor cells by acting as an energy dependent efflux pump to remove various drugs from the cell before they have a chance to exert their cytotoxic effects. It is generally accepted that reversal or inhibition of P Gp function in tumor cells is an important way for modulating MDR. It has been demonstrated in the laboratory that MDR mediated by the P Gp may be modulated by a wide variety of compounds. These compounds , which include verapamil and cyclosporin, generally have little or no effect by themselves on the tumor cells, but when used in conjunction with antineoplastic agents, they decrease, and in some instances eliminate, MDR. This paper will introduce some new reversal agents and discuss their physical and chemical characteration and others.

Free radicals are highly reactive molecules generated predominantly during cellular respiration and normal metabolism. Imbalance between cellular production of free radicals and the ability of cells to defend against them is referred to oxidative stress (OS). OS has been implicated as a potential contributor to the pathogenesis of ischemic cerebrovascular diseases. After brain injury by ischemia, the production of reactive oxygen species (ROS) may increase, leading to tissues damage via several different cellular molecular pathways. Radicals can cause damage to cardinal cellular components such as lipids, proteins, and neucleic acids, leading to subsequent cell death by modes of necrosis or apoptosis. Treatment with antioxidants may prevent propagation of tissues damage and improve both the survival and neurological outcome. The present paper reviews the antioxidants therapy in ischemic cerebrovascular disease, discusses probable reasons of inconsistency between animal experiments and clinical trials on antioxidants, and puts forward strategies against oxidative stress in the treatment of ischemic cerebrovascular diseases.

Aim To identify the GABA transporter subtypes and to find its new associated member at the blood brain barrier.Methods Labeled by in vitro infusion of magnetic beads through carotid arteries,the brain microvessels without intact neural cells were sorted in magnetic fields,and identified by RT PCR.The homologous primer of GAT superfamily and the tRNA from isolated brain microvessels were used in the RT PCR to amplify target DNA.The PCR products were isolated by polyacrylamide gel electrophoresis(PAGE) and cloned, sequenced rospectively.The sequences were screened in dbEST of Genbank by Blast.Results Seven DNA bands were isolated from RT PCR products of isolated brain microvessels by PAGE. B3,B5 complete sequences were highly homologous with rat partial GAT 2 and BGT 1 respectively,B7 complete sequence was highly homologous with rat partial TAUT. The other 4 EST of B1(Accession No:CF358965), B2(CD568346), B4(CF358966) and B6(CD568347) were submitted to dbEST,they were homologous with some sequences in Genbank,but were not homologous with GAT members.Conclusion GAT 2 and BGT 1 of GAT and TAUT were localized at the blood brain barrier which might be responsible for the GABA transport across the blood brain barrier.The genes and their functions of 4 EST associated with GAT need to be clarified.