Objective To investigate the effect of the transplantation of autologous marrow mesenchymal stem cells transfected by angiogenin gene in a porcine chronic ischemic beart model.Methods Methods Mesenchymal stem cells were trnsfected byAd/Ang.The pigs underwent placement of amerold occluder around LCx and 4 weeks later sujected to transplantation of the trandected mesenchymal stem cells.The animals were evaluated by coronary angiography,echocardiography,mannetic resonance imaging end pathologic observation.Results All animal showed 95%occlusion fo LCx.4 weeks after treatment ,the perfusion of LCx,left ventricular ejection fracton were greatly evhanced.A large number of labeled mesenchymal stem cells were successfully uncorporated into blood vessels in the ischemic myocardial regions with increased vessels countin and survival of implanted cell.Conclusion Transplantaton of autologous mesenchymal stem cells trendected by angiogenin gene offere obvious advsntases of great improvement of blood supply and the heart funcition.

Objective:To study the effect of compound Biejiaruangan tablets on the expression of liver AngiotensionII and its receptor in rats with hepatic fibrosis,and to explore the mechanism of its anti-hepatic fibrosis.Methods: Thirty male SD rats were randomly divided into three groups as followings: the normal group,the model group and the compound Biejiaruangan tablets group,all rats in the two latter groups were given subcutaneous injection of 40%carbon tetrachloride(twice every week for 6 weeks),the rats in the compound Biejiaruangan tablets group were given 1g?kg-1?d-1 of the compound Biejiaruangan tablets by daily gavage,the rats in normal control group and the model group were given distilled water according to the same volume,the histopathological changes in liver were observed through HE and Massion staining.The serum ALT,AST and ALP were evaluated by antomatic biochemistry analysator,the serum levels of hyaluronic acid (HA),Laminin(LN) and plasm AngiotensionII(Ang-Ⅱ) were determined by radio immunoassay.The expressions of AngⅡ,AT1R mRNA were examined by RT-PCR.Results:The severity of inflammation scoring,hepatic fibrosis scoring,the amounts of serum ALT,AST,ALP,HA,LN and plasma AngⅡ in the liver tissues of hepatic fibrosis model group were higher than those in the normal group(P

Background An ethylnitrosourea(ENU)-induced mutant strain C57BL/6 mouse model has been established by our research group.This model is proved to have the spontaneous phenotype of corneal opacity and the typical pathological process similar to human keratitis.Therefore,this model is expected to be a good animal model in the research of the mechanism,hereditary property,and development of drugs for corneal infectious diseases.Objective The present study is to investigate the biological features of opportunistic pathogens using a mouse Staphylococcus-infected corneal model(C57BL/6 mouse) induced by N-ethyl-N-nitrosourea(ENU),and offers an evidence of stability in this animal model.Methods Ten-week-old male C57BL/6 mice were treated with ENU at 150mg/kg by intraperitoneal injection,and then mated with female mice after 60 days.Corneal opacity mutant mice in the F1 generation were selected to backcross with C57BL/6 mice.The bacteria were isolated from the eyeballs of the mutants and cultivated,purified and identified.Drug sensitivity assay was carried out to screen for effective antibiotics for clinic medical care.Results The staphylococcus-infected corneal mouse model(B6-Co) was established successfully,and the Staphylococcus sciuri strain was separated and purified,and then the sensitive antibiotics were distinguished from resistant ones.The sensitive drugs for Staphylococcus sciuri included azithromycin,clindamycin,chloramphenicol,gentamicin,rifampicin,tetracycline,amikacin,sulfamethoxazole compound sinomin,minocycline,levofloxacin,cephalothin,cefotaxime,and furazolidone;whereas this Staphylococcal strain was resistant to cefoxitin,penicillin,ampicillin,novobiocin.Nitrofurantoin showed an intermediate sensitivity.Conclusion The C57BL/6 mouse model is a spontaneous-derived animal model that is infected by coagulase-negative staphylococci,among which the most abundant strain is Staphylococcus sciuri.

BACKGROUND: It has been found that xenogenic extracellular matrix (ECM) may cause a strong inflammatory response in humans during clinical application of decellularized porcine heart valve (synergraft valves). An early inflammatory reaction severely weakens matrix structure of valve wall, leading to structural rupture and decay of grafts. From Synergraft's event, the decellularized porcine heart valves still had immunogenicity, especially for pediatric patients. The mechanisms by which the ECM triggers this immune process need to be further evaluated. OBJECTIVE: To find the difference of gene sequence between human and porcine ECM and to identify the ECM immunogenicity based on bioinformatics. DESIGN, TIME AND SETTING: A contrast study between human and porcine ECM based on type IV collagen was performed at the Laboratory of Cardiothoracic Surgery, Changhai Hospital, the Second Military Medical University of Chinese PLA from June 2008 to February May.MATERIALS: The fresh porcine heart valves were obtained from Shanghai Wufengshangshi Slaughter House. Decellularized porcine aortic valves, hybridoma cells, and monoclonal antibodies were provided by our laboratory. METHODS: Similar region and conservative site of gene sequence among human, porcine, and rat were compared so as to look for common similar region, site, and sequence difference and investigate the segment which caused common and different gene sequence. Type IV collagen monoclonal antibody was used to evaluate the persistence of ECM of decellularized porcine heart valve following immunohistochemical staining. MAIN OUTCOME MEASURES: Type IV collagen gene sequence; efficacy of self-made antibody using immunohistochemistry; effect of self-made antibody on type IV collage of decellularized porcine heart valve. RESULTS: The differential gene serial in type IV collagen protein was found out by bioinformatics method. Monoclonal antibodies were successfully produced by human-mouse hybridoma technique. Residual porcine ECM was observed on decellularized porcine heart valve. CONCLUSION: Residual porcine ECM was observed on decellularized porcine heart valve and had immunogenicity.

Objective To observe the effect of early rehabilitation treatment at different time point on the motor function and activity of daily living (ADL) and emotion in acute stroke patients. Methods 120 patients with acute stroke were randomly assigned to three reha-bilitation groups and one control group according to the disease course (3 days, 5 days, 8 days when the disease is steady). Each group con-sisted of 30 eases. The patients in each group were treated with the regular medication therapy, rehabilitation groups were treated with com-prehensive rehabilitation treatment including Bobath technique therapy. Neurological deficit, motor function, balance function, ADL, emo-tion of all the patients were assessed before and 21 days after rehabilitation intervention. Results After treatment, the motor function, bal-ance function, ADL and emotion of each rehabilitation group were improved. The patients'rehabilitation scores in FMA, Fugl-Meyer balance function, MBI and HRSD got much better than that in control group. The difference was statistic significant. The effect of rehabilitation treat-ment did not show difference among rehabilitation groups. Conclusion Early rehabilitation treatment for acute stroke does benefit for stroke patients. Effect does not show vary with the start time of rehabilitation treatment within 8 days after acute stroke.

OBJECTIVE: To demonstrate the mechanism of mechanical ventilation (MV) induced endoplasmic reticulum stress (ERS) promoting mechanical ventilation-induced pulmonary fibrosis (MVPF), and to clarify the role of angiotensin receptor 1 (AT1R) during the process. METHODS: The C57BL/6 mice were randomly divided into four groups: Sham group, MV group, AT1R-shRNA group and MV+AT1R-shRNA group, with 6 mice in each group. The MV group and MV+AT1R-shRNA group mechanically ventilated for 2 hours after endotracheal intubation to establish MVPF animal model (parameter settings: respiratory rate 70 times/minutes, tidal volume 20 mL/kg, inhated oxygen concentration 0.21). The Sham group and AT1R-shRNA group only underwent intubation after anesthesia and maintained spontaneous breathing. AT1R-shRNA group and MV+AT1R-shRNA group were airway injected with the adeno-associated virus one month before modeling to inhibit AT1R gene expression in lung tissue. The expressions of AT1R, ERS signature proteins [immunoglobulin heavy chain-binding protein (BIP), protein disulfide isomerase (PDI)], fibrosis signature proteins [collagen I (COL1A1), α-smooth muscle actin (α-SMA)] in lung tissues were detected by immunofluorescence and Western blotting. Hematoxylin-eosin (HE) staining was used to evaluate lung injury and Masson staining was used to evaluate pulmonary fibrosis. RESULTS: Compared with the Sham group, the degree of pulmonary fibrosis and lung injury were more significant in the MV group. In the MV group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were increased (AT1R/β-actin: 1.40±0.02 vs. 1, BIP/β-actin: 2.79±0.07 vs. 1, PDI/β-actin: 2.07±0.02 vs. 1, COL1A1/α-Tubulin: 2.60±0.15 vs. 1, α-SMA/α-Tubulin: 2.80±0.25 vs. 1, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue increased, and the fluorescence intensity of COL1A1 and α-SMA increased. Compared with the MV group, the degree of pulmonary fibrosis and lung injury were significantly relieved in the MV+AT1R-shRNA group. In the MV+AT1R-shRNA group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were decreased (AT1R/β-actin: 0.53±0.03 vs. 1.40±0.02, BIP/β-actin: 1.73±0.15 vs. 2.79±0.07, PDI/β-actin: 1.04±0.07 vs. 2.07±0.02, COL1A1/α-Tubulin: 1.29±0.11 vs. 2.60±0.15, α-SMA/α-Tubulin: 1.27±0.10 vs. 2.80±0.25, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue decreased, and the fluorescence intensity of COL1A1 and α-SMA decreased. There was no statistically significant difference in the indicators between AT1R-shRNA group and Sham group. CONCLUSIONS MV up-regulate the expression of AT1R in alveolar epithelial cells, activate the AT1R pathway, induce ERS and promote the progression of MVPF.
Mice ; Animals ; Pulmonary Fibrosis/chemically induced* ; Lung Injury ; Respiration, Artificial/adverse effects* ; Actins/metabolism* ; Tubulin ; Mice, Inbred C57BL ; Endoplasmic Reticulum Stress ; RNA, Small Interfering

Objective:To explore the disturbance of metal element balance in mice after exposure to radon.Methods:Mice were randomly divided into control group, radon exposure of 30 WLM group, 60 WLM group and 120 WLM groups, with 10 mice in each group. After radon exposure with the cumulative dose, the lung function of mice was detected by a non-invasive pulmonary function testing instrument. Mice blood was taken from eyeballs. The lungs, heart, liver, kidney and spleen were also collected. HE staining was used to observe the pathological changes of lung tissue. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect the content of metal elements, including essential trace elements in the body: chromium (Cr), molybdenum (Mo), cobalt (Co), selenium (Se), copper (Cu), zinc (Zn), manganese (Mn), nickel (Ni), and potentially toxic elements: arsenic (As), tin (Sn), lead (Pb), aluminum (Al), mercury (Hg), cadmium (Cd), and silver (Ag).Results:Compared with the control group, lung ventilation function of the radon-exposed mice was decreased, alveolar structure was destroyed, and the contents of pulmonary metal elements Cr, Al, Pb, Sn( F=0.34, 0.66, 3.14, 1.16, P<0.05) and essential trace elements Mn, Cr, Zn, and Mo in the blood were decreased( F=0.65, 1.44, 0.97, 2.08, P<0.05), while the elements of Cu, Mo, Se and As in the lungs were increased( F=1.31, 1.26, 0.81, 2.04, P<0.05), and the element contents in other tissues also fluctuated. Conclusions:Inhalation of a certain cumulative dose of radon can reduce the lung ventilation function of mice and induce lung inflammation, as well reduce the content of essential trace elements in the lung and blood so that the content of metal elements in the body fluctuates.