The experiments of rabbit mydriasis & isolated cat ciliare muscle paralysis of atropine Methobromide (AMB) have demonstrated that : AMB has much larger mydriasis effect. It effects faster than Atropine Sulfate, Homatropine & Tropinexamide in acetylcholin -induced ciliare muscle contraction. The combined-force of AMB on ciliare muscle is less than Atropine & Homatropine, but a little larger than Tropinexamide. There fore AMB is a rapid & short-time mydriasis agent & ciliare muscle paralysis agent.

Objective To investigate the effect of brain ischemic preconditioning (IP) combined with traditional Chinese medicine three seven three alcohol saponin (PTS) on proliferation of endogenous neural stem cells and the mRNA expressions of delta opioid receptor (DOR),Bax,Bcl-2 in hippocampus at 7d post middle cerebral artery occlusion (MCAO).Methods The focal-focal ischemic tolerance models were established with twice suture method.80 SD rats were included and randomly divided into 5 groups:sham group,MCAO group,sham+ MCAO group,IP+ MCAO group,PTS+MCAO group (n=16 each).We chose 10 SD rats from each group to evaluate their neurological status,and made BrdU fluorescent immunolabeling.In addition,we chose the other 6 SD rats to detect the expression levels of DOR,Bax and Bcl-2 mRNA in ischemic region in hippocampusby using RT-PCR.Animals were given one set of BrdU injections (on day 6,three times,4h apart,50mg/kg) to label the proliferating cells.The neurological status was assessed by using Zea Longa neurological deficit scores at 7 days following cerebral infarction.Results Zea longa neurologic deficit scores in MCAO group and sham+ MCAO) group had significantly differences with IP+ MCAO group and PTS+ MCAO group respectively at 7d post MCAO(P＜0.01).There was no significant differeuce in Zea-longa neurologic deficit scores between MCAO group versus sham+ MCAO group,and IP+ MCAO group versus PTS+ MCAO group(P＞0.05).The number of BrdU+ ceils in hippocampus had significant differences between IP+ MCAO and PTS+ MCAO groups at 7d post MCAOand three groups of sham,MCAO and sham+ MCAO respectively (P＜0.01).There was no difference in the number of BrdU+ cells between MCAO versus Sham + MCAO groups and IP + MCAO versus PTS+MCAO groups(P＞0.05).DOR and Bcl-2 mRNA expression levels were higher and Bax mRNA expression level was lower in IP+ MCAO group than in MCAO,Sham+ MCAO and PTS+MCAO groups (P＜0.01).There were no significant differences in DOR,Bcl-2 and Bax mRNA expressions among MCAO,Sham + MCAO and PTS + MCAO groups (P＞ 0.05).Conclusions Acute cerebral infarction can induce the proliferation of endogenous neural stem cells in hippocampus in SD rats.IPC can facilitate the proliferation of endogenous neural stem cells in hippocampus afteracute cerebral infarction,improve the symptoms of neurologic dysfunction,increase DOR and Bcl 2 mRNA expressions,and reduce Bax mRNA expression in SD rats.PTS can facilitate the proliferation of endogenous neural stem cells in hippocampus after acute cerebral infarction in SD rats,and improve the symptoms of neurologic dysfunction,but it has no influence on the expressions of DOR,Bcl-2 and Bax mRNA.

Objective To explore the effect of δ-opioid receptor (DOR)on ischemic tolerance of rat brain.Methods The focal ischemic tolerance models of Sprague Dawley rats were established using the twice suture method with the middle cerebral artery occlusion (MCAO).A total of 24 male Sprague Dawley rats were randomly divided into sham group,ischemia (MCAO) group,sham +ischemia (sham+ MCAO) group and ischemic preconditioning + ischemia (IP+ MCAO) group (n=6,each).The neurological status was assessed using Zea-Longa neurological deficit scores at 7 days after cerebral infarction.The mRNA expressions of DOR,Bax,Bcl-2 in hippocampus in ischemic rat brain were detected by RT-PCR method.Results The Zea-Longa neurological deficit scores were 0.0±0.0,2.6±0.5,2.8±0.6 and 1.5±0.6 in Sham group,MCAO group,Sham+MCAO group and IP+ MCAO group,respectively at 7 days after cerebral infarction.The scores had significant differences among MCAO group,Sham+ MCAO group and IP+ MCAO group (both P＜0.01),but no difference between MCAO group and Sham+MCAO group(P＞0.05).The mRNA expressions of DOR and Bcl-2 were higher and Bax mRNA expression was lower in IP+MCAO group than in MCAO and Sham+ MCAO groups (all P＜0.01).Conclusions Ischemic preconditioning may increase the mRNA expressions of DOR and Bcl-2,reduce Bax mRNA expression,and improve the neurological status in rats.

BACKGROUND:Cerebral ischemia tolerance can promote proliferation of autologous neural stem cells in the hippocampus of cerebral infarction rats, but panaxtrial saponins effects on the proliferation of autologous neural stem cells in the brain have not been reported. OBJECTIVE:To explore the relationship of panaxtrial saponins, ischemic preconditioning and proliferation of endogenous neural stem cells in the hippocampus of rats at 7 days after cerebral infarction, and to observe the effect on neurobehavioral scores of rats after cerebral infarction. METHODS:Fifty Sprague-Dawley rats were included and randomly divided into five groups:sham group, ischemia group, ischemic control group, ischemic preconditioning group, and panaxtrial saponins group. In the latter four groups, acute models of cerebral infarction were established using Zea-Longa method. In the sham group, only an incision was made on the neck. The focal-focal ischemic tolerance models were established with twice suture method in the ischemic preconditioning and panaxtrial saponins groups. Sham operation was instead of ischemic preconditioning in the ischemic control group. In the panaxtrial saponins group, rats were given intraperitoneal injection of 100 mg/kg panaxtrial saponins at 7 days before modeling. RESULTS AND CONCLUSION:After 7 days of cerebral infarction, the neurobehavioral score and the number of neural stem cells in the hippocampus were significantly increased in the ischemia group (P<0.01);compared with the ischemia group, the neurobehavioral scores were lowered in the ischemic preconditioning and panaxtrial saponins groups (P<0.01), while the number of neural stem cells in the hippocampus was increased (P<0.01). However, there was no difference between the ischemic preconditioning and panaxtrial saponins groups (P>0.05). In addition, differences in the neurobehavioral scores and the number of neural stem cells in the hippocampus were insignificant between the ischemic control group and ischemia group (P>0.05). These findings indicate that panaxtrial saponins can play a role similar to ischemic tolerance, and thus improve neurologic impairment in rats with cerebral infarction.

Objective To determine the effect of willed movement on the expression of Nogo-A and Rho-associated kinase (ROCK) in adult rats with cerebral ischemia.Methods Cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion (MCAO) for 2 h,followed by a 24 h reperfusion in 54 adult rats and the degree of their neurological deficit was evaluated using Longa scale.They were then divided randomly into 3 groups,namely the MCAO group,the environmental modification (EM) group,and the willed movement (WM) group.The rats of MCAO group were raised in a regular breeding box,where they could get food and water freely.Meanwhile,those of the other two groups were raised in a homemade box.For the WM group,the water bottle and food were located on the roof of the homemade box.In each group,six rats were killed on day 3,7 and 15 after reperfusion and their neurological deficits were evaluated respectively.Immunohistochemistry assay was employed to examine the expression of Nogo-A and ROCK in the brain tissue around the ischemic foci.Results The rats of the WM group showed lessened neurological deficits on day 15 compared with the model and EM group.Their expression of Nogo-A decreases from(28.92 ± 2.17)/hpf on day 7 to (24.38 ± 2.29)/hpf on day 15 and that of ROCK did from (40.03 ± 2.14)/hpf to (38.08 ± 2.07) / hpf,lower than those of the model and EM group.However,no significant differences were found in the expression of Nogo-A and ROCK between the model group and EM group at any time points.Conclusion Willed movement could promote the functional recovery of neurological deficits in rats with ischemia after reperfusion,which is probably in relation to restrained expression of Nogo-A and Rho-associated in the tissue around the brain ischemic foci.

Objective To observe the effect of Chinese medicine of Gukang(GK) on bone mineral density(BMD) in osteoporosis rats.Methods Seventy-two female SD rats were randomized into 6 groups: pseudo-operation group,model group,nilestriol group(in the dose of 1mg/kg),and high-,middle-and low-dose GK groups(9.6,4.8 and 2.4 g?kg-1?d-1 respectively).Rat models of osteoporosis were induced by removal of bilateral ovaries.Three months after operation,the rats were given the corresponding medicine according the experimental design.After treatment for 3 months,in-vivo BMD as well as the in-vitro BMD in the isolated left femur and tibia was detected with dual energy X-ray bone densitometer.Results The in-vivo general BMD and lumbar BMD of the model group were decreased(P

OBJECTIVE:To observe the preventive effect of Ca/Mg infusion combined with glutathione and carbamazepine on oxaliplatin-induced neurotoxicity.METHODS:65patients treated with oxaliplatin,5-fluorouracil and leucovorin for gas-trointestinal cancer were divided into treatment group undergoing treatment with Ca/Mg infusion combined with glutathione and carbamazepine,and control group without any preventive treatment.RESULTS:At the third cycle,7patients in the treat-ment group but17patients in the control group showed clinically evident neurotoxicity,which demonstrated the statistical difference between the two groups(P=0.036).After12cycles,neurotoxicity of grade2to3was observed in2patients in the treatment group but in9patients in the control group,which demonstrated the statistical difference between the two groups(P=0.022).CONCLUSION:Ca/Mg infusions combined with glutathione and carbamazepine can prevent oxaliplatin-induced neurotoxicity.

Objective To explore the effects of constraint-induced movement therapy (CIMT) on the expression of tyrosine hydroxylase (TH) and glial cell derived neurotrophic factor (GDNF) in Parkinson's disease (PD) model rats. MethodsPD models were established by microinjection of 6-hydroxydopamine (6-OHDA) solution into substantia nigra of rats' right cerebral hemisphere.Forty-two model rats were divided randomly into an exercise group and a control group 1 week after microinjection.The exercise group rats were forced to use their impaired limbs by placing their nonimpaired fore-limbs in casts.The control group rats were housed in the same environment without any special treatment.Two weeks after 6-OHDA infusion and exercise training,the behavioral changes of rats were examined after intraperitoneal injection apomorphine ( APO).The content of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) was measured by high performance liquid chromatography with electrochemistry ( HPLAEC) ; the expressions of TH and GDNF in striatum were detected by immunohistochemical methods and TH,GDNF mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR).Results After 2 weeks of training,the rotating laps of the rats in exercise group within 30 min after APO induction,reduced to a significantly greater extent when compared to the control group (P ＜ 0.05).The content of DA and it's metabolites DOPAC in striatum homogenate was significantly higher in exercise group than that in the control group ( P ＜ 0.05 ),and the expression levels,of TH and GDNF protein/ mRNA were also significantly higher in the exercise group than those in control group ( P ＜ 0.05 ).Conclusions CIMT can improve the behavioral performance of PD rats,probably through promoting the expressions of TH and GDNF protein/mRNA in striatum,and increasing DA and it's metabolites DOPAC level.

The detection and monitoring of life signals such as heartbeat, respir ation, bloodpressure and temperature are often used to determine the patient's death. On the basis of the theory of military medical service, this paper discus ses life signals detection and monitoring technologies in the field of military medicine. With the progress of sciences, technologies and informatization of Chi nese PLA, life signals detection and monitoring technologies, based on informati on technology, microelectronic technology, communication technology and etc, wil l be more and more important in the development of digital medical equipment.

Objective To design a wearable physiological monitoring system for acquiring and monitor-ing vital signs non-intrusively and concurrently.Methods All bio-sensors were embedded in an elastic shirt for detecting physiological parameters with wearable technology.A patented respiratory inductive plethysmography technology was used to measure respiratory function,two sensors were woven into the jerkin around the patient's chest and abdomen.A three-lead,single channel ECG measures heart rate,and a three-axis accelerometer records posture and activity level.An NTC thermometer embedded in the shirt measures the body temperature.Results An elastic jerkin with embedded sensors that collect and continuously monitor respiration,cardiac,temperature,posture and activity signals was fabricated.Conclusion This wearable physiological monitoring system can record multiple parameters non-intrusively and concurrently.It can act as an useful platform for further researches.