Objective To learn the plague's host animals and parasitic flea composition, and to investigate the natural foci of plague in Xiji county in order to provide basic information for plague prevention and control. Methods The Citellus alaschanicus density, nocturnal rodents, the body flea, the burrow track flea, the nest flea were investigated in 8 townships (town) of Xiji county from June 11 2007 to July 25 2007. Specimens of small mammalian, fleas were collected for bacteriological and serological testing. Results The average density of the main host Citellus alaschanicus was 0.85 per hectare. The nocturnal mouse capture rate was 0.80%(24/2987).The survey found 16 species of small mammals that belonging to 3 orders, 9 families and 16 species with Citellus alaschanicus the dominant species. The Citellus alaschanicus had 2.84 fleas per body. Four families and 16 species of fleas were identified in the areas. The Citellus alaschanicus and Citellophilus Tesquorum Mongolicus were the dominant species. Plague bacteriology and serology tests were negative. Conclusions The study shows that the area is suitable for the formation of natural foci of Citellus alaschanicus plague. Surveillance is an important measure for prevention and control of the plague.

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.

BACKGROUND: Nitric oxide (NO) plays an important role in the ischemic brain injury, and hyperbaric oxygen (HBO) can improve ischemia/reperfusion (I/R)-caused nerve injury. Whether the effect of HBO is associated with NO? Its mechanism needs to be further investigated.OBJECTIVE: To observe the changes of expression of nitric oxide synthase (NOS)-positive neurons of rats following acute focal cerebral I/R injury and HBO treatment.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.MATERIALS : Sixty-six healthy male Sprague-Dawley rats were chosen and randomized into 5 groups: sham-operation group (n =5), sham-operation +HBO treatment group (n =5), model group (n =28), modeling +HBO treatment group (n =28). Ischemia 5,12, 24 and 72 hours four time points were set in the later 2 groups, 7 rats at each time point.METHODS: ①Rats in the model group and modeling+ HBO treatment group were created into models of middle cerebral artery ischemia according to the method from Koizum. Then, an embolus was inserted for ischemia; One hour later, the embolus was drawn out. Inserting embolus was omitted in the other two groups.②Rats in the sham operation + HBO treatment group and modeling + HBO treatment group were placed in HBO chamber at ischemia 2, 9, 21, 45 and 69 hours, separately, and given HBO treatment for 1 hour (0.25 MPa absolute pressure).MAIN OUTCOME MEASURES: The rats in each group were sacrificed at corresponding time points, and their brains were harvested. The distribution and morphology of NOS positive cells in cortical area, preoptic area, lateral and medial corpora striata of infarct region at the level of optic chiasma were observed with nicotinamide-adenine dinucleotide phosphate -diaphorase (NADPH-d) histochemical method.RESULTS: After supplement, 66 rats were involved in the final analysis. ①After ischemia, NOS-positive neurons changed in morphology, mainly presenting prominences were reduced or disappeared, neurons changed from ellipse or triangle into global shape, and shrank; Body of neuron darkly dyed; Both nucleus and cytoplasm were deeply dyed into dark blue; NOS-positive neurons with changed morphology were mostly in lateral corpora striatum, followed by preoptic area and medial corpora striatum, and those in the cortical area were few. NOS-positive neurons with changed morphology were not found in the sham-operation group and sham-operation + HBO treatment group. ②In the model group, NOS-positive neurons with changed morphology were increased with elongation of I/R time. At each time point, NOS-positive neurons in cortical area, preoptic area and medial corpora striatum in modeling + HBO treatment group were less than those in model group, but NOS-positive neurons in two groups both reached their peaks at ischemia 72 hours [Cortical area: (15.46±3.02) vs.(30.52±4.73)/visual field; Preoptic area:(28.56±4.05) vs. (68.81±7.84)/visual field; medial corpora striatum:(21.09±3.83) vs.(45.71±5.24)/visual field; all P＜0.01].CONCLUSION: HBO obviously inhibits the degeneration of NOS-positive neurons in acute focal cerebral I/R injury regions of rats, such as cortical area, preoptic area, medial corpora striatum, and so on

Advances in mechanism and application of the heating effect in breeding of microorganism are reviewed in this paper. Heat produces mutagenesis effect and screening effect. Heating mutagenesis effect is occurred through the substitution of G-C base pair induced by heat, and heating screening effect produces higher forward mutation rate induced by other mutagens.

Background Experimental autoimmune uveoretinitis(EAU)is proved to be an organ-specific,T lymphocyte-mediated autoimmune and self-limited disease.Research showed that CD4+CD25+T cell may play important regulation on the course of events,but its mechanism is pending for further study. Objective Present study was to investigate the potential role of CD4+CD25+T cell in the pathogenesis of EAU. Methods Retinal Santigen(S-Ag)was isolated from bovine retinas according tO the procedure as Caspi's previously describe.0.1 ml Santigen(50μg)emulsified with complete Freund'S adjuvant was injected on footpad of 24 inbred adult female Lewis rats aged six to eight-week-old to induce EAU,and 4 normal Lewis rats were as normal control group.Slim-lamp examination was performed to observe the ocular manifestation.Retinal section was prepared in 7,12,15,21 days aher injection for the pathological examination.The pathological grading was on the lnoki'S method.The retinas,inguinal nodes and spleens of rats were obtained in 7,12,15,21 days after injection and the cellular suspension was prepared.Expression of CD4+CD25+T cells on cellular suspension was assayed using flow eytometry.This study complied with the Standard of Association for Research in Vision and Ophthalmology. ResuRs The obvious inflammatory response of the anterior segment was found in S-Ag injected eyes from 7 days through 21 days.The most serious inflammation was found in 12-15 days under the slim-lamp.The hemotoxylin and eosin staining showed the higher pathological grading from 12 to 15 days after injection,showing significant difference in comparison with 7 days and 14 days(P=0.000).In EAU model rats,expressions of CD4+CD25+T cells was significantly increased in retinas, inguinal nodes and spleens in 15 days after injection,showing evidently differences in comparison with control rats(P=0.000). Conclusion The expression level of CD4+CD25+T cells in inflammatory tissue is associated with the inflammation procedure in EAU model rats.This study indicates that CD4+CD25+T cells may play a role in the development of EAU.

BACKGROUND:Dexamethasone can improve the cellapoptosis and decrease the number of osteoblasts and bone cells through increasing the time of cellcycle. Protein kinase C is a kind of intraecellular singnal transduction pathways, and there are related reports on the relationship between protein kinase C and cellapoptosis. OBJECTIVE:To investigate the mechanism of dexamethasone-induced osteoblast apoptosis via protein kinase C intracellular signal transduction pathway. METHODS:Fetal rat bone marrow mesenchymal stem cells were col ected for osteogenic induction, and the cells were divided into dexamethasone group, phorbol group and star cytochalasin group. The cells in the dexamethasone group were added with 1×10-6 mol/L dexamethasone, the cells in the phorbol group were added with 1×10-6 mol/L dexamethasone and 1×10-7 mol/L phorbol, while the cells in the star cytochalasin group were added with 1×10-6 mol/L dexamethasone and 1×10-7 RESULTS AND CONCLUSION:Dexamethasone could induce apoptosis significantly, and after added with mol/L star cytochalasin. The proliferation and inhibition of the cells in different intervention groups were observed, and the content of protein kinase C in the cellmembrane and cytoplasm was measured. phorbol, the apoptosis was increased significantly;while after added with star cytochalasin, the apoptosis was decreased significantly. After added with dexamethasone, the content of protein kinase C in the cytoplasm was significantly decreased, while increased in the cellmembrane. At different time points after added with dexamethasone, the change of the content of protein kinase C in the cytoplasm and cellmembrane was most significant at 30 minutes. The results indicated that mechanism of dexamethasone-induced osteoblast apoptosis was correlated with protein kinase C, and dexamethasone was the agonist of protein kinase C. After the cells were stimulated, the protein kinase C in the cytoplasm wil moved to the cellmembrane, and then the content of protein kinase C in the cytoplasm was decreased, while increased in the cellmembrane.

OBJECTIVETo observe the effect of octyl-a-cyanoacrylate upon bone healing and its degradation in vitro after middle tibial transverse fracture in rabbitsì and to establish treatment of higher efficacy with the application of octyl-a-cyanoacrylate.

METHODSMiddle tibial transverse fracture model of New Zealand rabbits was established. In the experimental group, internal fixation with 2 mm Kirschner wires was performed and the broken ends were fixed with octyl-a-cyanoacrylate. In the control group, only internal fixation with 2 mm Kirschner wires was conducted. Animals were killed at preset time intervals of 2, 4, 6, 8, 10 and 12 weeks postoperatively and samples were harvested.

RESULTSTwo weeks after operation, clear fracture lines were observed in both the experimental and the control groups. Fibrous soft tissue connection was noted between the broken ends and there was soft tissue adhesion around the fracture site. There was no callus formation and the broken ends were surrounded by adhesive soft tissues. Obvious external callus formation was confirmed at 8 weeks after operation in both groups with partial disappearance of fracture lines. Ten and twelve weeks after the operation, fracture lines disappeared completely and there was obvious external callus formation and bone union. In the fourth week, fibrous cells and chondrocytes were found to grow into the colloid and surround it at the 6th week. The adhesive material was degraded and gradually absorbed at the 8th week. Chondrification was observed.

CONCLUSIONSTwo weeks after fixation for tibial fracture in rabbits, octyl-a-cyanoacrylate begins in vivo degradation. Chondrocytes and fibrocytes gradually grow into the degradation area and surround the adhesive material, which broke into pieces at 8 weeks. Complete degradation and disappearance of the adhesive material is present between 10 and 12 weeks. No barrier effect hampering fracture healing is noted.

Adhesives ; therapeutic use ; Animals ; Cyanoacrylates ; therapeutic use ; Rabbits ; Radiography ; Tibial Fractures ; diagnostic imaging ; pathology ; therapy

BACKGROUND: The effect of pituitary adenylate cyclase activating polypeptide (PACAP) during traumatic brain injury (TBI) and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI. METHODS: Male Sprague Dawley rats were randomly divided into 3 treatment groups (n=6, each): sham-operated, vehicle (normal saline)+TBI, and PACAP+TBI. Normal saline or PACAP (1g/5L) was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4+ and CD8+ T cells in blood and the spleen were detected via flow cytometry. RESULTS: In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4+ CD8– lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBI+vehicle, and CD4– CD8+ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4+, and decreased CD8+, T lymphocytes in blood and the spleen. CONCLUSION: Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.

OBJECTIVETo investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy.

METHODSA total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry.

RESULTSThe expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group.

CONCLUSIONAbnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.

Adolescent ; Adult ; Brain Diseases ; metabolism ; pathology ; Child, Preschool ; Epilepsy ; metabolism ; pathology ; Female ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Immunohistochemistry ; Male ; Malformations of Cortical Development ; metabolism ; pathology ; Malformations of Cortical Development, Group I ; Nestin ; metabolism ; Neurons ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; Ribosomal Protein S6 Kinases, 70-kDa ; metabolism ; TOR Serine-Threonine Kinases ; metabolism ; Young Adult