Objective Mechanism of cerebral edema following blast injury in rabbits through the study of the expression of aquapodins-4 ( AQP-4 ) introduced by HBO,and perfusion as well,after cerebral blast injury.Methods One hundred and fifty New Zealand rabbits were randomly divided into the treatment group,the non-treatment group and the control group ( 10 animals).The animal model of cerebral blast injury was developed by using paper detonator.The treatment and the non-treatment groups were randomly divided into the 1 h,6 h,12 h,24 h,72 h,7 d and 14 d sub-groups,each consisting of 10 animals.The expression of AQP-4 mRNA was measured with RT-PCR,and the perfusion of the brain tissue was detected with perfusion weighted imaging (PWI) at each time points,following cerebral injury.Results The expression of AQP-4 mRNA began to increase 1 h after injury,reached peak in 72 h,and then decreased at day 7.Following initial HBO treatment,the expression of AQP-4 mRNA significantly decreased at various time points after 6 hours (P ＜0.05).PWI test indicated that blood perfusion for the non-treatment group significantly decreased in the initial stage of injury,however,12 h after injury perfusion gradually increased,and the amount of perfusion (close to the control group) was maintained for 2 weeks.For the treatment group,perfusion decreased more significantly in the early stages of injury (1-6 h).Conclusions Early HBO therapy could enhance the partial pressure of oxygen in the affected brain tissue,increase blood oxygen content and alleviate secondary cerebral edema induced by cerebral ischemia.

Objective Mechanism of cerebral edema following blast injury in rabbits through the study of the expression of aquapodins-4 ( AQP-4 ) introduced by HBO,and perfusion as well,after cerebral blast injury.Methods One hundred and fifty New Zealand rabbits were randomly divided into the treatment group,the non-treatment group and the control group ( 10 animals).The animal model of cerebral blast injury was developed by using paper detonator.The treatment and the non-treatment groups were randomly divided into the 1 h,6 h,12 h,24 h,72 h,7 d and 14 d sub-groups,each consisting of 10 animals.The expression of AQP-4 mRNA was measured with RT-PCR,and the perfusion of the brain tissue was detected with perfusion weighted imaging (PWI) at each time points,following cerebral injury.Results The expression of AQP-4 mRNA began to increase 1 h after injury,reached peak in 72 h,and then decreased at day 7.Following initial HBO treatment,the expression of AQP-4 mRNA significantly decreased at various time points after 6 hours (P ＜0.05).PWI test indicated that blood perfusion for the non-treatment group significantly decreased in the initial stage of injury,however,12 h after injury perfusion gradually increased,and the amount of perfusion (close to the control group) was maintained for 2 weeks.For the treatment group,perfusion decreased more significantly in the early stages of injury (1-6 h).Conclusions Early HBO therapy could enhance the partial pressure of oxygen in the affected brain tissue,increase blood oxygen content and alleviate secondary cerebral edema induced by cerebral ischemia.

Objective To evaluate the role of magnetic resonance spectroscopy (MRS) and diffusion-weighted MRI (DWI) in detecting regional cerebral metabolic changes and changes of water molecular motion in rabbits after explosive brain injury at different time points of injury after being treated with hyperbaric oxygen therapy. Methods Ninety New Zealand white rabbits were divided into control group, trauma group and hyperbaric oxygen treatment group. The injured models in the later 2 groups were established using 600 mg TNT equivalent of paper detonators in the rabbit brain at the top of 6.5 cm vertical distance. Rabbits in the trauma group and hyperbaric oxygen treatment group were sub-divided into 1, 3, 7, 14 and 21 d treatment groups, respectively. The survival of these rabbits was observed at these time points. Hyperbaric oxygen treatments lasting for 1, 3, 7, 14 and 21 d were given to each hyperbaric oxygen treatment sub-groups, respectively. Performance under MRS was detected and dynamic changes of N-acetylaspartate (NAA)/creatine (Cr) ratio and NAA/choline(Cho)+Cr value were observed with MRS. DWI was employed to detect the dynamic changes of apparent diffusion coefficient (ADC) values. Results The NAA/Cr ratio in the trauma group markedly decreased right after the injury and slightly rose 7 d after the injury. Compared with that in the trauma group, the NAA/Cr ratio in the hyperbaric oxygen treatment group was significantly increased (P＜0.05). The NAA/Cho+Cr value in the trauma group was markedly decreased right after the injury, while that in the hyperbaric oxygen treatment group was obviously increased as compared with that in the trauma group (P＜0.05). ADC values in the region of interest of the trauma group was decreased after 1 d of treatment and gradually increased after 3 d of treatment; the ADC values in the hyperbaric oxygen treatment group was obviously higher than those in the trauma group (P＜0.05). Conclusion Hyperbaric oxygen might improve the prognosis by improving local metabolism of neurons, inhibiting brain edema, and enhancing local gliosis repair;, ultra-early intervention (within one week of injury) may be much favorable for animals/patients after explosive brain injury.

Objective To observe the changes of autophagy and apoptosis in the cerebral cortex in rats with brain explosive injury and received hyperbaric oxygen (HBO) treatment, and investigate the effect and significance of HBO on them. Methods Fifty-four SD rats were randomly divided into control group (n=6), explosive injury group (n=24) and explosive injury treated with HBO group (n=24).The control group was not injured and 600 mg TNT electric detonators were exploded over the brain of rats at a 12 cm distance in the explosive injury group and explosive injury treated with HBO group. HBO management was given to the explosive injury treated with HBO group 3 and 22 h after explosive injury and at the same time of the other 6 d. RT-PCR and Western blotting were used to detect the changes of Beclin-1 and caspase-3 in the cerebral cortex on the 6th and 24th h, 3rd and 7th d of injury. Results The expression levels of Beclin-1 and caspase-3 in the explosive injury group and explosive injury treated with HBO group were obviously higher than those in the control group (P＜0.05). The levels of Beclin-1and caspase-3 in the explosive injury treated with HBO group were significantly lower than those in the explosive injury group at the same time points (P＜0.05). Conclusion The decreased expressions of autophagy and apoptosis in brain cells by HBO treatment might be one of the possible mechanisms of treating craniocerebral injury.

OBJECTIVETo investigate the feasibility of constructing a skin tissue engineering covering on chitinous membrane using rat epidermal stem cells (ESCs).

METHODSRat ESCs were isolated and cultured by cold digestive method and collagen type IV adherent method. Cell colonies were observed with inverted microscope. Expressions of DNA and RNA of ESCs were detected with laser scanning confocal microscope. Growth curves of cells were determined with Alamar BlueTM colorimetric method. Expressions of surface markers of ESCs (CD29, CD71, CD49d, and CD34) were detected with flow cytometer. Positive expressions of CK15, CK19, and P63 of ESCs were determined by immunohistochemistry. Influence of original chitinous membrane leachate in different dilutions on ESCs was observed. Condition of growth of ESCs on the vehicle was observed.

RESULTSIsolated cultured cells were verified as ESCs, of which the doubling generation time was 48 hs. CD29 and CD49d were positive; CD71 and CD34 were negative; CK19, CK15, and P63 were positive. Compared with that of control group, ESCs cultured in chitinous membrane leachate showed slight cell proliferation when diluted to 1:8-1:512 dilutions, but there was no statistically significant difference (P > 0.05). The checkerboard-form cell colonies of ESCs could be visualized with naked eyes on the chitinous membrane in 2-4 weeks of culture. A multitude of ESCs were seen to grow on fibres under microscope.

CONCLUSIONSChitinous membrane may be used as ESCs culture vehicle, and biological compatibility is good.

Animals ; Cell Culture Techniques ; methods ; Cellular Structures ; Chitin ; Epithelial Cells ; cytology ; Female ; Male ; Rats ; Stem Cells ; cytology ; Tissue Engineering ; methods ; Tissue Scaffolds

Objective To explore the relationship between clinical ischemic events and carotid calcification detected by 64 slices CT angiography. Methods We retrospectively analyzed the carotid calcified plaques in 116 patients underwent the 64 slices CT angiography. The relatinnship between the carotid calcification and the clinical ischemic events was analyzed. Results A total of 377 plaques were detected and the incidence of carotid plaque calcification was 63.40%. Incidence of plaque calcification was significantly lower in patients with ages<50 years than that in patients with ages 51-59 years, 60-69 years and higher than 70 years (P=0.003, P=0.002, P=0.000, respectively). The incidence of plaque calcification in the common carotid artery was significantly lower than the carotid bifurcation (P=0.000) and the internal carotid artery (P=0.000). The incidences of calcification in the mild, moderate and severe degree of stenosis and occlusion were 46.54%, 33.33%, 26.67% and 0% respectively. The distribution of intraplaque calcium was similar between patients with ischemic event and non-isehemic event group. However, the incidence of calcification was significantly lower patients with ischemic event than that in patients without ischemie event (30.34% vs. 43.10%, P=0.013). Calcified plaque was negatively associated with ischemie event (β=-0.688, P=0.006). Conclusion 64 slices CT angiography can analyze the characterization of carotid plaque calcium.

ObjectiveTo observe the effect of Acupotomy on spastic cerebral palsy. Methods105 cases of spastic cerebral palsy were random divided into group A (35 cases with acupotomy), group B (34 cases with physical therapy) and group C (36 cases with acupotomy and physical therapy). Modified Ashworth Scale (MAS) was used to assess spasticity before and a month after therapy. ResultsEffective rate of group A was 65.71%, group B was 29.41%, group C was 77.78%, which of group B was significantly lower than those of group A of C. ConclusionAcupotomy can reduce muscular tension of spastic cerebral palsy, which seems more effective than physical therapy.