Objective To summarize the experience on imaging diagnosis and surgical treatment for popliteal artery entrapment syndrome (PAES). Methods From 2004 to 2010, 11 patients (12 limbs) diagnosed as PAES by CTA and MR ( A) underwent surgery. There were 11 patients with a mean age of (28 ±19) years, eight patients were male, three patients were female. Two patients were found to have bilateral involvement. Intermittent claudication was the most frequent presenting symptom. Six limbs were type Ⅰ , three limbs were type Ⅱ , three limbs were type Ⅲ , one limb was type Ⅳ. The preoperative mean ABI was 0.47 ± 0. 27. Results Popliteal artery exploration surgery or peripopliteal artery lysis was performed in 12 limbs, and this procedure was combined with a great saphenous vein bypass graft in seven limb because of arterial occlusion or aneurysm. After a median follow-up of ( 19 ± 20) months (0 month to 6 years) , the mean ABI improved to 0. 81 ±0. 30, which was significantly higher than that of preoperation( P ＜ 0.05),one patient died of pulmonary embolism one day after operation, one patient (one limb) had popliteal artery thrombosis after operation. Intermittent claudication symptoms disappeared in all other patients. Conclusions Timely imaging diagnosis and surgical intervention is very important for patients of PAES.

AIM:To evaluate the effects of pilocarpine, brinzolamide and the preservatives of them on corneal epithelial cells and the histopathology of rabbit conjunctiva. METHODS: Fifteen New Zealand white rabbits weighing 1.5 kg to 2.5 kg were randomly divided into three groups. One group with three rabbits served as untreated controls. Pilocarpine 1% and brinzolamide 1% each were administered to the right eyes in one treated group, and the preservatives (chlorobutanol 0.01% in pilocarpine, benzalkonium chloride 0.01% in brinzolamide) to the left eyes. Corneal epithelial damage was evaluated by scanning electron microscopy, and conjunctival specimens were examined under light microscopy. RESULTS: Compared with normal controls, brinzolamide and BAC caused corneal epithelium damage and increased number of inflammatory cells in the conjunctiva, while pilocarpine and the preservative chlorobutanol mainly influenced the corneal epithelium. Brinzolamide produced significantly more damage than pilocarpine (P

This paper was aim to optimize the purification technology of Rehmanniae Radix Praeparata extract with macroporous adsorption resin. With the content of manninotriose as index, the absorptive flow and time were investigated, as well as kinds, amount, flow of eluent. D-101 type macroporous adsorption resin was the best choice for the purification of manninotriose. The optimized parameters were as follows: the content of manninotriose at 161.16-53.72 mg x g(-1), absorption time 240 min, eluting solvent of purified water, volume flow at 1.5 BV x h(-1), and eluant volume at 6 BV. D-101 type macroporous adsorption resin could significantly increase the purity of Rehmanniae Radix Praeparata extract with the advantage of high absorption, remove most part of impurity, and the effect of semi-works production was better.
Adsorption ; Chemical Fractionation ; Chromatography, Liquid ; instrumentation ; methods ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; Rehmannia ; chemistry ; Resins, Synthetic ; chemistry

Objective To assess the value of ultrasound examination in transvaginal diagnosis of normal fetal heart with 11-14 weeks of gestation.Methods Totally 158 cases of normal fetal heart with high risk pregnancy and nuchal translucency thickness were examined by two ultrasoud approaches:transvaginal(TVS) and tranabdomina(TAS) in 11-14 weeks of gestation.Results The group of TVS was obviously clearer than TAS by displaying the normal fetal cardiac structural in 12 week of gestation and 13-14 weeks of gestation with significant difference between the two groups (P<0.05),respectively.No significant difference between the two groups in 11 week of gestation was observed.Conclusion The transvaginal echocardiogram is of clinical value in the high risk gravida during the late first and the early second trimester.

Objective To summarize the epidemiological feature of plague cases oceuwed in China.Methods The epidemiological and clinical data from 1981 to 2006 year in China were analyzed with descriptive study method.Result Nine hundred and seveneteen human plague cases were diagnosed in 9 provinces(regions) from 1981 to 2006 years,105 cases died,the mortality rate being 11.45%,and they distributed in 69 counties (cities or banners).In Qinghai Province 108 cases were diagnosed,the mortality rate was 46.30%(50/108),the cases distributed in 17 counties(cities);137 cans in Guizhou,distributing in 2 counties(cities);517 cases in Yunnan,distributing in 26 counties(cities).Plague cases peaked separately in 1983,1990,1996 and 2000 years,they were 25,75,98 and 254 separately.The principal spreading ways were breathing flying particles,touching,skinning and eating marmot in Qinghai;750 cases were of bubonic plague,among whom 4 cases in Tibet died,the fatality rate was 0.53(4/750);121 cases were of pneumonic prague,among whom 65 cases died,was accounting for 53.72%(65/121);31 cases were of septieaemic plague,and 30 cases died(one cases was cured in Inner Mongolia),accounting for 96.77%(30/31).Others were brain plague,intestinal plague,tonsil plague and plague cellulites,which were cured.Conclusion From 1990,human plague epidemical scope and intensity is enlarging continuously compared with 1980-1990 and there is a trend of going up gradually in China.

Objective To explore the alterations of protein phosphatase-2A (PP-2A) in lymphocytes in mild cognition impairment (MCI) and Alzheimer's disease (AD).Methods The activity PP-2A of was measured by ~(32)p liquid seintillography for incorporated radioactivity in control group(n=11) , the MCI group(n=11),and the AD group(n=11).The expression of PP-2A was determined by Western blot.Results In the control group,the activity of PP-2A (1.01?0.09) and the expression of PP-2A (0.96?0.07) were high while in the MCI group,the activity of PP-2A (0.71?0.12) and the expression of PP-2A (0.80?0.05) were decreased (both P

Objective To investigate the role of plasmid pYC on proteome of Yersinia pestis. Methods Two dimensional electrophoresis was performed to strains of Yersinia pestis with and without the pYC plasmid, and differential proteins were identified by mass spectrometry. Results More than 500 protein spots of Yersinia pestis with and without plasmid pYC were recognized,and their protein profiles were generally similar. The chaperone GroEL was highly expressed in strains with plasmid pYC, whereas the protein GroEL was not encoded by plasmid pYC. ConclusionsPlasmid pYC has an impact on proteome of Yersiniapestis. The proteins of pYC-p10 and pYC-p11 encoded by plasmid pYC may regulate the expression of GroEL.

Objective To express the plasminogen activator(Pla) of Yersinia pestis and one of its gene fragments,and to detect their immunological reactivity.Methods The pla gene and its specific gene fragment pla-c were amplified by PCR using the EV76 strain as a template.PCR products were then ligated with the plasmid pET32a (+).The recombinant plasmids pET32a (+)-pla and pET32a (+)-pla-c were subsequently trausformed into E.coli BL21 (DE3).The expressed products were purified by HIS affinity chromatography,and their immunological reactivity was detected by Western blotting.Results The recombinant Pla(52.8 × 103) was expressed as inclusion bodies,and the recombinant Pla-c protein (24.0 × 103) was expressed in the soluble form.These two recombinant proteins reacted with anti-Yersinia pestis EV76 rabbit sera.Conclusions The recombinant Pla and its specific fragments have displayed immunological reactivity,and can be served as an alternative diagnosis method for Yersinia pestis.

BACKGROUND:Hyperbaric oxygen (HBO) can increase oxygen diffusing capacity, thereby, improve hypoxic state of brain edema and brain tissue and promote the recovery of physiological function of brain cells in focal zone, the establishment of bypass circuit, and regeneration and repair of brain cells.OBJECTIVE: To observe the effect of hyperbaric oxygen on c-fos oncogene expression of rats at different time points following acute focal cerebral ischemia/reperfusion(I/R) injury.DESIGN : Randomized grouping animal experiment.SETTING: Department of Emergency, Tangdu Hospital, Fourth Military Medical University of Chinese PLA; Department of Laboratory Medicine, Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA; Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out in the Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA in April 2002. Sixty-five 2-month-old healthy male SD rats.METHODS: The involved rats were randomized into: model group (n =20), normal control group (n =5), pure oxygen treatment group (n =20) and HBO treatment group (n =20). In the model group, following the method of Koizumi et al, rat models of middle cerebral artery (MCA) ischemia were developed. In the normal control group, only occlusion of arterial blood flow was omitted; In the pure oxygen treatment group, the operation procedure was the same as that of model group, and embolus being drawn out at ischemia for 1 hour, rats were placed in the hyperbaric cabin at 2,9,21, 45 and 69 hours after embolus being inserted, and they inhaled pure oxygen under the normal pressure; In the HBO treatment group, the operation procedure was the same as that of model group, and rats inhaled pure oxygen for 1 hour under 0.25 MPa pressure. MAIN OUTCOME MEASURES: By means of immunohistochemical and pathohistological methods, neutrophilic infiltration,c-fos oncogene protein and positive cell expression in cerebral cortex, preoptic area and corpora striatum of rats in each group were observed at cerebral I/R 5, 12, 24 and 72 hours; Neuronal necrosis degree in cerebral cortex, medial area of corpora striatum and preoptic area, and cerebrovascular leakage area of left cerebral hemisphere of rats were calculated.RESULTS: Sixty-five rats were involved in the final analysis. ① c-fos positive products mainly focused in the center of the preoptic area, but they were occasionally seen in the contralateral cortex, slightly expressed in the preoptic area and moderately expressed in the corpora striatum, c-fos positive products began to reduce in the above-mentioned area at ischemia 12 hours, and were obviously reduced at ischemia 24 hours; c-fos positive products in the cerebral cortex and preoptic area were obviously weakened in the HBO treatment group than in the simple ischemia group; At I/R 12 hours,neutrophils in the preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group, respectively(P ＜ 0.05); At I/R 24 hours, neutrophils in the cerebral cortex, preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group (P ＜ 0.05). ② Cerebrovascular leakage area was more significantly contracted in the HBO treatment group than in the model group (P＜ 0.05); At I/R 72 hours, the number of injured nerve cells in the optic chiasm cortex, medial area of corpora striatum and preoptic area was significantly smaller in the HBO treatment group than in the model group (P＜0.05). Neuronal damage was not found in the sham-operation group.CONCLUSION: HBO can markedly contract cerebrovascular leakage area of rats with acute focal cerebral ischemia/reperfusion injury, alleviate the symptoms of nervous system, inhibit neutrophilic infiltration and c-fos oncogene protein expression in the infarct area, and reduce neuronal necrosis in the "penumbral region".

BACKGROUND:Acute carbon monoxide (CO) poisoning may lead to delayed amnesia in rats,and which is similar to delayed neurologic syndrome caused by acute CO in human.So,this experiment is to investigate the pathogenesis of delayed neurologic syndrome by studying acute CO poisoning in the rats.OBJECTIVE:To observe the changes in delayed neuronal damage and memory after acute CO poisoning in the rats,and analyze their correlation.DESIGN:Randomized controlled animal experiment.SETTING:Department of Emergency,Tangdu Hospital,Fourth Military Medical University of Chinese PLA;Department of Laboratory Medicine,Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA,Center for Hyperbaric Oxygen Treatment,Department of Aerospace Medicine,Fourth Military Medical University of Chinese PLA.MATERIALS:This experiment was carried out in the Laboratory of Aviation Pathology and Molecular Biology,Department of Aerospace Medicine.Fourth Military Medical University of Chinese PLA from July to November 2005.Fiftyhealthy male Sprague-Dawley(SD)rats were randomized into control group and CO poisoning group,with 25 rats each.METHODS:The awake rats in the CO poisoning group were placed in self-made jar for poisoning,then which was pumped with 0.999 volume fraction of CO.Rats in the jar inhaled the mixture of CO and air for 60 minutes.The average volume fraction of CO in the jar was 3.451×10-3.Rats in the control group were untouched.MAIN OUTCOME MEASURES:①The step down test was carried out in the rats before and 1,3,5 and 7 days after Coexposure.Escape latency was used as an index for evaluating the ability of memory retention.Shorter escape latencyindicated poor memory ability.②Pathological changes of brain tissue:After step down test was carried out following 1,3,5 and 7 days of CO exposure,6 rats were separately sacrificed in each group,and their brains were harvested.The brain tissue sections were performed haematoxylin & eosin (HE) staining for observing pathological injury degree and the amount of pyramidal neurons in hippocampal CA1 region.③SPSS 10.0 software was used to analyze the relationship of the amount of pyramidal neurons in hippocampal CA1 region and escape latency.RESULTS:Forty-eight rats were involved in the final analysis.①There were no significant differences in escape latencyon the 1"and 3"days after CO exposure between two groups. but escape latency in the CO poisoning group was significantly shorter than that in the control group on the 5th and 7th days after CO exposure(P＜0.05,0.01).②There were no significant changes in the amount of pyramidal neurons in hippocampal CA1 region on the 1st day after CO exposure between CO poisoning group and control group,but pyramidal neurons in hippocampal CA1 region in the CO poisoning group were significantly reduced on the 3rd,5th and 7th days after CO exposure,and 1 5%dead pyramidal neurons were found on the 7th day after CO exposure.③Decrease of pyramidal neurons in hippocampal CA1 region was significantly correlated with shortening of escape latency of rats in the CO poisoning group(r=0.270,P＜0.01).CONCLUSION:Acute CO poisoning leads to delayed neuronal damage,which causes delayed amnesia.