Objective To study the effect of high soluble oxygen fluid (HSOF) therapy on the expression of serum matrix metallop roteinases-9 (MMP-9) in patients with intracerebral hemorrhage (ICH). Methods 66 patients with ICH were randomized into routine therapy group and HSOF+ routine therapy group The levels of serum MMP-9 were detected by ELISA for at 1 d,3 d, 7d and 2 weeks after therapy. Results The expression of MMP-9 in both two groups was higher than that in the control group (P

Objective To explore the effect of behavioral training on the differentiation of neural stem cells in the dental gyrus (DG) in rats with hippocampus infarction. Methods Seventy-eight Sprague-Dawley rats were randomized into infarction plus behavior training group, infarction group and control group. Photochemistry method was used to induce hippocampal infarction in rats of the infarction plus behavioral training group and infarc-tion group. At 1 day after surgery, Morris water maze training was used for infarction plus behavioral training group, free-movement without training was performed for infarction group. Double staining immunofluorescence was used to detect the co-expression of bromodeoxyuridine (BrdU) with neuronal nuclei ( NeuN ) or glia fibrillary acidic protein (GFAP) in the DG at different time points. Results Few BrdU/NeuN and BrdU/GFAP double staining cells were observed in the DG of control rats. In the infarction group and infarction plus behavioral training group the number of BrdU/NeuN and BrdU/GFAP double-stained cells increased in the DG on the opposite side compared with the control group on 14th, 21st, 28th and 35th days after surgery (P < 0.05 ). There observed significantly more BrdU/NeuN and BrdU/GFAP double-stained cells in the infarction plus behavioral training group than that in the infarction group on the 14th, 21st, 28th and 35th days after surgery ( P < 0.05 ). Conclusion Behavioral training can accelerate the differentiation of neural stem cells to neuron and astrocyte, by which to promote the re-covery of neural functions.

The kinase domain of receptor tyrosine kinase(RTK) ErbB2 was expressed fused with GFP in Pichia pastoris. Recombinant expression vector pPIC3.5K was constructed in Escherichia coli TOP10. The right P. pastoris transformants were screened on his-deficient plates and YPD-G418 plates by turns after electroporation of recombinant vector, and then induced by methanol in baffled shake bottles. The strain with highest protein yield was scaled up in a 5 L fermentor. Recombinant protein was analyzed with tyrosine kinase assay after Ni2+ affinity chromatograph. Results showed that the 100 kD recombinant protein with tyrosine kinase activity was successfully expressed in P. pastoris.

AIM:To research the effects of lithium chloride on transforming growth factor beta (TGF-β) and connective tissue growth factor (CTGF) in cultured human Tenon capsule fibroblasts (HTFs) and explore its mechanism.METHODS:HTFs were cultured and identified by vimentin staining with immunofluorescence and the morphological characteristics.The experimental group was processed 48h with LiCl in concentration of 80mmol/L, the control group without LiCl.The mRNA expression of TGF-β and CTGF in two groups were analyzed with real-time fluorescent quantitative polymerase chain reaction (real time-qPCR) and the protein expression was detected with Western blot.RESULTS:The cultured HTFs expressed TGF-β and CTGF.The mRNA expression of TGF-β and CTGF significantly decreased compared with the control group(t=20.042, 14.995, P<0.05).the protein expression of TGF-β and CTGF also decreased significantly compared with the control group(t=46.058、12.452, P<0.05)CONCLUSION:The cultured HTFs can express TGF-β and CTGF in mRNA and proteins' level.LiCl can reduce the expression of TGF-β and CTGF both in gene and proteins' level.LiCl has the potential to modulate wound healing for glaucoma filtration surgery.

AIM: To determine the relevance of NADPH oxidase subunit p22hox and the expression of superoxide anion on ventricular remodeling in myocardial infarction (MI) rats. METHODS: MI of Sprague-Dawley rats were established by left anterior descenting coronary artery ligation. 8 weeks after MI, Doppler echocardiography, hemodynamic study and histomorphometry were performed to analyze the ventricular remodeling. The level of thiobarbituric acid reactive substance in plasma and myocardium were measured, and the distribution of superoxide anion was observed with laser scanning confocal microscope. The expression of p22phox mRNA and protein level was detected by RT-PCR and immunohistochemistry. RESULTS: The left ventricular remodeling was significant in MI rats, also the level of thiobarbituric acid reactive substance increased in the plasma and non-infarcted myocardium. The expressions of p22-phox mRNA and protein levels, and superoxide anion increased in infarcted and non-infarcted myocardium in MI rats. CONCLUSION: Our results suggest that the expression of NADPH oxidase and its derived superoxide anion may take part in left ventricular remodeling through oxidative stresss after MI.

AIM: To clarify the protective effect of long-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on ventricular remodeling after myocardial infarction (MI) in rats and its mechanisms. METHODS: Myocardial infarction were established by ligated left coronary anterior artery in SD rats, 24 hours after the operation, the survival rats were treated by gavage fluvastatin (20 mg?kg~(-1)?d~(-1)) or distilled water for 8 weeks. Doppler echocardiography, homodynamic and cardiac histomorphometry were used to assess the ventricular remodeling and cardiac function. The plasma levels of total cholesterol (Tch), creatinine (Cr), glutamic-oxal (o) acetic transaminase (AST), lipid peroxidation (LPO), glutathione perioxidase (GSH-PX), nitrogen monoxide (NO_2~-/NO_3~-) were detected. RESULTS: The Tch, Cr and AST were not significant difference in groups. Left ventricular end-diastole pressure, right relative weight, left ventricular posterior wall thickness, collagen volume fraction and the lung weight were decreased in AMI+fluvastatin group compared to AMI group (P

To study the influence of behavioral stress on hippocampal spatial learning and memory, we used the freely moving rats that had undergone chronic implantation of a recording electrode in the hippocampus CA1 region and a bipolar stimulating electrode in the ipsilateral Schaffer collateral-commissural pathway. The field excitatory postsynaptic potentials (fEPSPs) were recorded in the absence of exogenous induction of high-frequency stimulation (HFS) or low-frequency stimulation (LFS) and reflected the effect of stress on the hippocampal spatial learning. And we also investigated the change of hippocampal synaptic plasticity when rats were re-exposed to the same environment at 24 h after novelty acquisition. We found that exploration of a novel environment induced the hippocampal synaptic depression in the rats with stress-adaption, whereas exposure to the novel environment induced the hippocampal synaptic potentiation in the behavioral stress rats. Furthermore, re-exposure to the same environment no longer elicited the hippocampal synaptic potentiation or depression at 24 h after the first novel acquisition in the behavioral stress rats. These results demonstrate that behavioral stress induces the hippocampal synaptic potentiation under novelty acquisition and further damages the hippocampal spatial learning and memory. However, the stress can be adapted by re-exposure to the novelty and thus does not further damage the hippocampal spatial learning and memory.
Animals ; CA1 Region, Hippocampal ; physiology ; Electric Stimulation ; Electrodes, Implanted ; Excitatory Postsynaptic Potentials ; physiology ; Exploratory Behavior ; physiology ; Learning ; physiology ; Male ; Memory ; physiology ; Neuronal Plasticity ; physiology ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological ; physiology ; Synaptic Potentials ; physiology

Objeetive To observe the disease-causing gene mutation in Chinese patients with hypertrophic cardiomyopathy and to analyze the correlation between the genotype and the phenotype.Methods Specimens of peripheral blood were collected and the genome DNA was extracted in 65 unrelated patients with hypertrophic cardiomyopathy and 60 normal controls.The exon 7 and 8 of cardiac troponin?gene were screened with PCR and direct sequencing technique.Results A missense mutation in the exon 7 of the cardiac troponin?gene Was identified in a 40-year-old male patient with hypertrophic cardiomyopathy (Asp127Tyr)which was absent in the controls.Conclusion A novel missense mutation of cardiac troponin?was identified in a patient with hypertrophic cardiomyopathy,this mutation might be the disease-causing gene mutation in this Chinese patient.

BACKGROUNDThe benefits and safety of sirolimus-eluting stent (SES) have not been systematically quantified in different trials in ST-segment elevation myocardial infarction (STEMI) patients with primary or rescue percutaneous coronary intervention (PCI). A meta-analysis of randomised trials comparing SES and bare-metal stent (BMS) was performed.

METHODSA systematic literature search was conducted to identify all randomized clinical trials. The primary outcome was the rate of major adverse cardiac events (MACEs). The secondary outcomes included death, recurrent myocardial infarction, recurrent revascularization, and stent thrombosis.

RESULTSTotally, 1973 STEMI patients were enrolled in seven eligible randomized trials comparing SES with BMS. The pooled rate of major adverse cardiac events was significantly lower in the SES group than in the BMS group (9.7% vs 20.3%, OR 2.45, 95% CI 1.88-3.19, P < 0.00001). No significant difference in all causes of death was found between the SES and BMS groups, as well as in the pooled recurrent myocardial infarction rates. The pooled recurrent revascularization rate was significantly lower in the SES group than in the BMS group (5.1% vs 14.8%, OR 3.30, 95% CI 2.37-4.60, P < 0.00001). No significant difference was found between the pooled rates of stent thrombosis (1.2% in the SES group and 2.0% in the BMS group, OR 1.61, 95% CI 0.79-3.26, P = 0.19).

CONCLUSIONSSES is associated with a decreased risk of major adverse cardiac events compared with BMS by the greater reduction in repeat revascularization in STEMI patients. Larger trials with longer follow up are warranted to better define the role of SES in STEMI.

Drug-Eluting Stents ; adverse effects ; Humans ; Immunosuppressive Agents ; administration & dosage ; adverse effects ; chemistry ; Myocardial Infarction ; therapy ; Randomized Controlled Trials as Topic ; Sirolimus ; administration & dosage ; adverse effects ; chemistry ; Stents ; adverse effects ; Treatment Outcome

OBJECTIVETo investigate the effect of long-term administration of fluvastatin on improvement of ventricular remodeling of rats after myocardial infarction and its mechanism.

METHODSSprague-Dawley rats were subjected to ligation in anterior descending branch of coronary artery and treated with fluvastatin (20 mg.kg(-1) d(-1)) or distilled water for 8 weeks. Doppler echocardiography, hemodynamic study and cardiac histomorphometry were used to estimate the ventricular remodeling and cardiac function. Laser scanning confocal microscope was used to definite the distribution of superoxide anion (O(2)(*-)) and nitrogen monoxide. RT-PCR and immunohistochemistry were used to detect the expression of NOS2 and p22phox in mRNA and protein level. The level of lipid peroxidation, glutathione peroxidase, nitrogen monoxide and total cholesterol were detected too.

RESULTSAdministration of fluvastatin ameliorated left ventricular remodeling without affecting the infarct size [(40 +/- 6 vs 42 +/-5)%, P>0.05]. The level of left ventricular end-diastolic pressure [(18.24 +/-6.58 vs 10.74 +/-4.71) mmHg, P<0.05], right ventricular ameliorated relative weight [(0.92 +/-0.19 vs 0.71 +/-0.13) g/kg, P<0.05], the thickness of left ventricular posterior wall [(3.04 +/-0.28 vs 2.60 +/-0.36) mm, P<0.05] decreased after fluvastatin treatment. The left ventricular ejection fraction was not influenced, the relative lung weight and the left atrium diameter reduced [(5.79 +/-2.92 vs 3.69 +/-0.68) g/kg, (0.55 +/-0.12 vs 0.45 +/-0.04) mm, P<0.05]; the expressions of LPO in the plasma and myocardium [(8.64 +/-0.59 vs 7.71 +/-0.66) U/dl, P<0.05; (3.12 +/-0.38 vs 1.93 +/-0.40) ng/microg.pro, P<0.01] were reduced, and the overexpressed NO was inhibited [(436.87 +/-47.22 vs 313.78 +/-34.35) mg/dl, P<0.01], but the expression of GPx increased [(66.13 +/-8.31 vs 79.78 +/-2.38) mg/dl, P<0.01]. The expression of O(2)(*-) and the activity of NADPH oxidase subunit p22phox increased; NOS2 and its products NO were over-expressed too.

CONCLUSIONVentricular remodeling and hemodynamics are improved profoundly in MI rats treated with fluvastatin. The effect of antioxidative stress of fluvastatin might be involved in the mechanism.

Animals ; Antioxidants ; pharmacology ; Fatty Acids ; pharmacology ; Fatty Acids, Monounsaturated ; pharmacology ; Indoles ; pharmacology ; Male ; Myocardial Infarction ; metabolism ; pathology ; physiopathology ; Rats ; Ventricular Remodeling ; drug effects