Gap junctions(GJ) form the chemical signal channels between cardiocytes.The core proteins of these channels are the connexins(Cx).The quantity or distribution of Cx will lead to the remodeling of GJ, which contributed to arrhythmia and remodeling following the acute myocardial infarction.GJ remodeling is the key reason and pathological basis of arrhythmia following acute myocardial infarction.How to increase the number of myocardial cells and lighten or reverse the heart reconstitution have become a focal point.In the acute myocardial infarction cell transplantation treatment, stem cells are characterized by self-renewal and multi-directional differentiation have been paid great attention.This study summarized the basis and clinical research of GJ structure, function, distribution, remodeling and stem cell transplantation treatment following myocardial infarction.

Biological performances of Ni-Cr porcelain alloy are highly correlated with released metallic ions. Released metal ions from Ni-Cr porcelain alloy, particularly Ni, Be can induce inflammation of the adjacent periodontal tissue and oral mucosa. In vitro evidence has indicated that the immune response can be altered by various metal ions. Allergic reactions due to metallic dental restorations have been documented. Ni has especially been identified as being highly allergenic. The cytotoxicity and corrosion level of Ni-Cr porcelain alloy is increased after recasting. The Ni-Cr porcelain alloy produced according to technology requirements has good biological safety. Ni-Cr porcelain alloy released a few of metal ions which might induce allergy and density of adjacent periodontal tissues, for the stimulation effect of these metal ions. There is no evidence to suggest that Ni-Cr porcelain alloy restorations has systemic toxicity or carcinogenic/genotoxic effect to human.

Smooth muscle cell (SMC) proliferation, platelet free calcium level and aggregation of experimental atherosclerotic rabbits were investigated in this study. Aortic SMC ofhyperlipidemic rabbits in vitro showed higher growth activity than did normal rabbit SMC. And also hyperlipidemic serum stimulated SMC to proliferate at a significantly greater rate than control serum. Moreover, the level of platelet free calcium and the platelet aggregation was also higher in hyperlipidemic rabbits, indicating that activitated platelets possibly release more PDGF to act as a stimulator to SMC proliferation and calcium is an important factor to activate platelets. Furthermore, SMC from 8501-treated rabbits appeared lower proliferative rate than thecells from hyperlipidemic rabbits. And serum from those rabbits inhibited SMC proliferation compared with hyperlipidemic serum, the inhibitory effect was even stronger than that of normal serum. It may be relevant to the favorable effects of 8501 to TXA2/PGI2 balance.

Objective To evaluate the value of cranial MRI on diagnosing nonalcoholic Wernickes encephalopathy (WE). Methods The clinical characters, cranial MRI features, and outcomes materials in six cases of nonalcoholic Wernickes encephalopathy were analyzed.Results Cranial MR and Flair imaging of the patients exhibited areas of increased T 2W and flair signals symmetrically surrounding the aqueduct and third ventricle and within the medial thalamus. One patient who became persistent vegetative state coexistenced increased T 2W and flair signal of the cortex. According to the follow-up results, the alterations of four patients in T 2W and Flair signals showed to resolve being consistent with the clinical recovery. One patient with persistent vegetative state had no change within two years of the follow-up.Conclusions Cranial MRI is of great value in diagnosing nonalcoholic Wernickes encephalopathy and reflects appropriately the pathological evolution of this disease.

Objective To study the effect of Tongxinluo on the plasma C-reactive protein(CRP)and endothelin-1(ET-1)in acute coronary syndrome(ACS) patients.Methods 100 patients with ACS were randomly divided into conventional therapy group and treatment group(conventional therapy+Tongxinluo gelatin capsule).The changes of CRP and ET-1 in the first day,7th and 14th day were observed.Results In the treatment group,CRP and ET-1 were significantly decreased in the 7th and 14th day(P＜0.05,P＜0.01),and there was significant decrease only in the 14th day(P＜0.05)in the conventional therapy group.CRP and ET-1 levels in the treatment group were significantly different as compared with conventional thereapy group(P＜0.01).Conclusion Tongxinluo capsule may protect blood vessel endothelium through inhibiting CRP and ET-1 to decrease the inflammatory response of endangium.

Objective To investigate the effect of microRNA-101 (miRNA-101) on atrial fibrosis in human chronic atrial fibrillation (AF). Methods Right atrial appendages were obtained from 59 patients (30 with AF) undergoing cardiac surgery, including 47 patients with valve heart disease and 12 patients with congenital heart disease. The expression of miRNA-101 was determined by quantitative real-time PCR in the right atrial appendages of patients with and without AF. The cell-specific localization of miRNA-101 was detected by in situ hybridization assay. The mRNA and protein expression levels of transforming growth factor β typeⅠreceptor (TGFβRⅠ) and collagen type I (COL1) were determined by quantitative real-time PCR and Western-blot assay, respectively. Collagen in the right atrial appendages was observed by Masson staining assay. Results The expression of miRNA-101 was found to be significantly down-regulated in AF patients compared with patients with sinus rhythm (SR) (P < 0.05). The result of miRNA-ISH showed that miRNA-101, which was highly distributed within the connective tissues of heart, was down-regulated at about 24.9% in patients with AF compared with patients with SR. No significant differences at the mRNA expression level of TGFβRI was found between patients with AF and patients with SR (P > 0.05). But the protein expression of TGFβRI in patients with AF was significantly higher than that of patients with SR (P < 0.05). The mRNA and protein expressionsl of COL1 were significantly higher in patients with AF than thoset of patients with SR (P < 0.05). The collagen was significantly increased in patients with AF than that of patients with SR (P < 0.05). Conclusions Downregulation of miRNA-101 may contribute to atrial fibrosis in human atrial fibrillation by targeting TGFβRⅠ.

Objective:To explore the effect of endothelin-1 on atrial ifbrosis in patients with atrial ifbrillation (AF).
Methods: A total of 72 patients with thoracotomy were studied, the patients were divided into 2 groups:AF group, n=39 and Sinus rhythm (SR) group, n=33. The mRNA and protein expressions of endothelin-1 (ET-1), platelet derived growth factor-B (PDGF-B) and collagen I (COL1) in right atrial appendage (RAA) tissue were measured by RT-PCR and Western blot analysis;meanwhile, the impact of ET-1 stimulation and non-selective ET-1 receptor antagonist (sulfafurazole SIZ) on PDGF-B mRNA and protein expressions in H9c2 cells were measured.
Results: ①The RAA tissue mRNA and protein expressions in AF group were higher than those in SR group, as for ET-1 (2.830 ± 2.276) vs (1.220 ± 0.887) and (0.835 ± 0.241) vs (0.286 ± 0.083), both P<0.01;for PDGF-B (2.568 ± 2.348) vs (1.567 ± 0.831) and (0.807±0.241) vs (0.381 ± 0.105), both P<0.05;for COL1α1 (3.376 ± 1.598) vs (1.629 ± 0.833) and (0.652 ± 0.210) vs (0.312 ± 0.12), both P<0.05.②The protein expressions of ET-1 and COL1 had positive correlation (r=0.580, P<0.01).③ET-1 promoted PDGF-B secretion in H9c2 cells in a concentration and time-dependent manner;SIZ could reduce such promotion.
Conclusion: ET-1 plays an important role in AF occurrence which might be related to PDGF-B regulation.

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