Animals ; Astrocytes ; metabolism ; Brain Ischemia ; metabolism ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Neuroprotective Agents ; pharmacology ; Propofol ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; prevention & control

Animals ; Disease Models, Animal ; Electric Stimulation ; Neurons ; metabolism ; Nitric Oxide Synthase ; metabolism ; Parkinson Disease ; metabolism ; Rats ; Subthalamic Nucleus ; metabolism

Objective To investigate the role of intestinal fatty acid binding protein (IFABP) and blood procalcitonin (PCT) in diagnosis of traumatic Intestinal rupture in early stage.Methods The clinical data of 58 patients with abdominal injuries admitted from May 2012 to April 2016 were retrospectively analyzed.All 58 patients were divided into intestinal rupture group (n =21) and nonintestinal rupture group (n =37).The concentrations of IFABP and PCT were detected,analyzed and compared between two groups at different intervals.Results The IFABP and PCT in intestinal rupture group were significantly higher than those in non-intestinal rupture group.The IFABP and PCT in intestinal rupture group significantly decreased after operations.There were significantly differences in IFABP and PCT between two groups at admission,4 hours after admission,preoperative period,and 24 hours after operation.However,these differences disappeared at 72 hours after operation.At the same time,the accuracy rate 92.4％,sensitivity 96.3％,specificity 72.8％ found in combination of these two biomarkers were significantly higher than those of IFABP and PCT measured separately.Conclusions The combination of IFABP and PCT detection can be used as an indicator for the diagnosis of traumatic intestinal rupture in the early stage.

AIMTo observe the change of STR neuronal firing rates with high frequency stimulation of subthalamic nucleus in PD rats.

METHODSA model of Parkinson's disease was induced by unilateral administration of 6-hydroxydopamine into right substantia nigra in rats. After the high-frequency stimulation to STN, the spontaneous firing rates of STR on normal and PD rats were recorded by using extracellular recordings.

RESULTSStimulation caused a direct excited effect of STR neurons in normal rats whereas a excited and inhibited effect in PD rats. The inhibited effect was correlated with the stimulation period (r = 0.94).

CONCLUSIONStimulation to STN may inhibit the spontaneous firing rates of STR neurons in PD rats. These results also give some clues that high-frequency stimulation to STN may be a effective therapy to the clinical treatment of Parkinson's disease.

Action Potentials ; Animals ; Corpus Striatum ; physiopathology ; Disease Models, Animal ; Electric Stimulation Therapy ; Male ; Neurons ; physiology ; Parkinson Disease ; physiopathology ; therapy ; Rats ; Rats, Sprague-Dawley ; Subthalamic Nucleus

Animals ; Dentate Gyrus ; metabolism ; Epilepsy ; chemically induced ; metabolism ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; Kainic Acid ; Male ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins ; metabolism ; Neurons ; metabolism ; Neuropeptides ; metabolism

Objective To investigate the utilization of damage control surgery (DCS) in treatment of the severe abdominal traumas.Methods The clinical data of 56 patients with severe abdominal traumas treated by DCS (Emergency operation,fluid resuscitation and definitive operation were used gradually.)from January 2011 to January 2013 in Department of General Surgery,Taizhou People's Hospital were retrospectively analyzed.Results Of the 56 patients,52 were cured and discharged from hospital,the clinical curative rate was 92.9％; 4 patients dead.Conclusions Abdominal traumas under going operations by applying the damage control surgery significantly increased the clinical curative rate.

BACKGROUND: A great quantity of cell loss in early stage following stem cell transplantation can significantly affect transplantation effect. Presently, it is confirmed that overexpression of AKT1 gene significantly inhibit cell apoptosis. OBJECTIVE: To explore whether AKT1 gene overexpression can block stem cell apoptosis under hypoxic condition following pig autologous bone marrow mesenchymal stem cell (BMSC) transplantation, and the effect of repairing damaged myocardium. DESIGN, TIME AND SETTING: The randomized controlled animal study was performed at the Soochow University from August 2005 to February 2007.MATERIALS: A total of 24 healthy male Meishan pigs were supplied by the Animal Experimental Center of Soochow University. METHODS: The CDS (regulation domin of AKT1) AKT1-cDNA fragment was amplified. Lentivector Packaging Kit was used to transfect BMSCs after synthesized with pCDH1-AKT1 shuttling plasmid. Following BrdU labeling, models of myocardial infarction were constructed by occluding the distal left anterior descending coronary artery in pigs with gelatin sponge. 4 weeks later, pigs were randomly divided into four groups: the model control group, the DMEM group, the BMSCs group, and the AKT-transfected group. In model control group, there was no other injection after occluding the left anterior descending coronary artery. In the DMEM group, 5 mL DMEM was injected into the coronary artery. 5 mL BMSCs (1×10~7 cells) were infused into the coronary artery in the BMSCs group. 5 mL BMSCs transfected with the AKT1 gene were injected in the AKT-transfected group MAIN OUTCOME MEASURES: Western blot analysis and real time RT-PCR were used to test the plasmid. The cardiac function was evaluated by magnetic resonance image. Histological characteristics of the myocardium were observed using immunohistochemistry. Serum vascular endothelial growth factor and transforming growth factor β1 levels were determined by ELISA. RESULTS: AKT1-cDNA was cloned into pCDH1-MCS1-EF1-copGFP and the sequence was confirmed in comparison with the published one. AKT mRNA expression could be detected distinctly 24 and 48 hours after transfecting cells. The expression of AKT1 intensity in MSCs remained strong 2 weeks later with detected by real time RT-PCR and Western blot analysis. AKT1-mRNA transcriptional levels were 120 times of primary cells. Before the cell implantation, the left ventricular end-diastolic dimension increased and the stroke volume decreased in the myocardial infarction hearts. The cardiac function was significantly improved after cell implantation, and the implanted MSCs prevented the infarct region from thinning and expanding, improved contraction and increased perfusion in all groups relative to the control hearts. The left ventricular chamber size was smaller in the hearts with being transplanted cells than that in the control hearts. Moreover, the improvement was even markedly greater in AKT-transfected group (P < 0.05). Hematoxylin-eosin staining results showed that fibering was significant in the model control group and DMEM group. Island-like myocardium was observed in the infarct zone of the BMSCs group and AKT-transfected group, and plenty of small vessels-shape structure was detected in the AKT-transfected group. Immunohistochemistry demonstrated that Von Willebrand Factor (vWF) and Cx-43 expression was determined in the myocardium in the BMSCs group and AKT-transfected group, and the proportion of BrdU and Cx-43-positive cells to BrdU-positive cells was significantly greater in the AKT-transfected group compared with the BMSCs group 4 weeks following transplantation (P < 0.05). Following cell transplantation, vascular endothelial growth factor levels were gradually increased, peaked at 1 week, gradually decreased, and reached a normal level at 4 weeks. Transforming growth factor p1 levels were gradually reduced, and significantly less than the model control group, DMEM group 4 weeks later (P < 0.05), and significantly lower than that pretransplantation (P < 0.05).CONCLUSION: Using lentiviral vector to construct with AKT1 gene could stably make BMSCs overexpress AKT1. The BMSCs engraftment in host myocardium might improve the left ventricle function by attenuating the contractile dysfunction and pathologic thinning in this model of left ventricular wall infarction. AKT1 overexpression can significantly improve cardiac function following infarction.

BACKGROUNDCathepsin S and its endogenous inhibitor cystatin C are implicated in the pathogenesis of atherosclerosis, especially in the plaque destabilization and rupture leading to acute coronary syndrome. However, whether circulating cathepsin S and cystatin C also change in association with coronary plaque morphology is unknown yet.

METHODSWe recruited 98 patients with unstable angina (UA, n = 6) or stable angina (SA, n = 2) who had a segmental stenosis resulting in > 20% and < 70% diameter reduction in one major coronary artery on coronary angiography. Thirty-one healthy subjects served as controls. Intravascular ultrasound (IVUS) was used to evaluate plaque morphology. Plasma cathepsin S and cystatin C were measured as well.

RESULTSAt the culprit lesion site, plaque area ((7.85 +/- 2.83) mm(2) vs (6.53 +/- 2.92) mm(2), P = 0.027), plaque burden ((60.92 +/- 11.04)% vs (53.87 +/- 17.52)%, P = 0.025), remodeling index (0.93 +/- 0.16 vs 0.86 +/- 0.10, P = 0.004) and eccentricity index (0.74 +/- 0.17 vs 0.66 +/- 0.21, P = 0.038) were bigger in UA group than in SA group. Plasma cathepsin S and cystatin C were significantly higher in patients than in controls (P < 0.01). Plasma cathepsin S was higher in UA group ((0.411 +/- 0.121) nmol/L) than in SA group ((0.355 +/- 0.099) nmol/L, P = 0.007), so did the plasma cystatin C ((0.95 +/- 0.23) mg/L in UA group, (0.84 +/- 0.22) mg/L in SA group; P = 0.009). Plasma cathepsin S positively correlated with remodeling index (r = 0.402, P = 0.002) and eccentricity index (r = 0.441, P = 0.001), and plasma cystatin C positively correlated with plaque area (r = 0.467, P < 0.001) and plaque burden (r = 0.395, P = 0.003) in UA group but not in SA group.

CONCLUSIONSPlasma cathepsin S and cystatin C increased significantly in UA patients. In angina patients, higher plasma cathepsin S may suggest the presence of vulnerable plaque, and higher plasma cystatin C may be a clue for larger atherosclerotic coronary plaque.

Adult ; Aged ; Aged, 80 and over ; Cathepsins ; blood ; Coronary Artery Disease ; blood ; diagnostic imaging ; pathology ; Cystatin C ; blood ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Ultrasonography, Interventional ; methods

OBJECTIVETo compare the differences in uptake of 2-deoxy-D-glucose (2-DG)-conjugated nanoparticles between breast carcinoma MDA-MB-231 cells with high metabolism and breast fibroblasts with normal metabolism, and investigate the feasibility of using the coated nanoparticles as a MRI-targeted contrast agent for highly metabolic carcinoma cells.

METHODSThe γ-Fe2O3@DMSA-DG was prepared. The glucose metabolism level of both cell lines was determined. The targeting efficacy of γ-Fe2O3@DMSA-DG and γ-Fe2O3@DMSA NPs to breast carcinoma MDA-MB-231 cells and breast fibroblasts at 10 min, 30 min, 1 h and 2 h was measured with Prussian blue staining and UV colorimetric assay. MRI was performed to visualize the changes of T2WI signal intensity.

RESULTSPrussian blue staining showed more intracellular blue granules in the MDA-MB-231 cells of γ-Fe2O3@DMSA-DG NPs group than that in the γ-Fe2O3@DMSA NPs group, and the γ-Fe2O3@DMSA-DG uptake was greatly competed by free D-glucose. As revealed by UV colorimetric assay, MDA-MB-231 cells also showed that the cellular iron amount of γ-Fe2O3@DMSA-DG group was significantly higher than that of the γ-Fe2O3@DMSA group and γ-Fe2O3@DMSA-DG + D-glucose group, statistically with a significant difference between them. MRI showed that the signal intensity of γ-Fe2O3@DMSA-DG group was decrease significantly, the T2 signal intensity was decreased by 10.5%, 37.5%, 72.9%, 92.0% for 10 min, 30 min, 1 h and 2 h, respectively. In contrast, the signal intensity did not show obvious decrease in the γ-Fe2O3@DMSA-DG group, the T2 signal intensity was decreased by 8.5%, 11.4%, 32.0%, 76.7% for 10 min, 30 min, 1 h and 2 h, respectively. However, HUM-CELL-0056 cells did not produce apparent difference for positive staining in the γ-Fe2O3@DMSA-DG group, γ-Fe2O3@DMSA group and γ-Fe2O3@DMSA-DG+D-glucose group, and the signal intensity also did not produce apparent difference.

CONCLUSIONSγ-Fe2O3@DMSA-DG has good targeting ability to highly metabolic breast carcinoma (MDA-MB-231) cells. It is feasible to serve as a specific MRI-targeted contrast agent for highly metabolic carcinoma cells, and deserves further studies in vivo.

Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cells, Cultured ; Colorimetry ; methods ; Contrast Media ; pharmacokinetics ; Deoxyglucose ; chemistry ; pharmacokinetics ; Female ; Ferric Compounds ; chemistry ; pharmacokinetics ; Fibroblasts ; cytology ; metabolism ; Glucose ; metabolism ; Humans ; Iron ; metabolism ; Magnetic Resonance Imaging ; methods ; Nanoconjugates ; chemistry ; Particle Size ; Succimer ; chemistry ; pharmacokinetics

OBJECTIVETo investigate the effect of penehyclidine hydrochloride on glutamate (Glu)release and N-methyl-D-aspartate receptor (NMDAR)1 expression in hippocampus CA1 with global cerebral ischemia/reperfusion rats.

METHODSSixty male Wistar rats were randomly allocated into three groups; group A received sham operation; group B received ischemia/reperfusion; group C received penehyclidine hydrochloride treatment (2 mg/kg) before ischemia/reperfusion (n=20). Global cerebral ischemia was induced according to Pulsinelli-Brierley method. All animals were divided into two experiments: (I) Microdialysis plus HPLC/FD were used to detect Glu level after reperfusion 1 h, 3 h, 6 h. (II) After reperfusion 3 h, the animals were decapitated on ice and the brains were immediately removed to detect NMDAR1 expression in CA1 area by immunohistochemistry.

RESULTSAfter penehyclidine hydrochloride treatment, extracellular Glu level in CA1 were significantly decreased compared with those of control group (P < 0.05 or 0.01); Total integrated OD, average gray value and positive-cell area of NMDAR1 in CA1 were also significantly decreased compared with those of control group (P < 0.05 or 0.01).

CONCLUSIONPenehyclidine hydrochloride might has protective effect in hippocampus CA1 on global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting Glu release and NMDAR1 expression.

Animals ; Brain Ischemia ; metabolism ; physiopathology ; CA1 Region, Hippocampal ; metabolism ; Cholinergic Antagonists ; pharmacology ; Glutamic Acid ; metabolism ; Male ; Quinuclidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Reperfusion Injury ; metabolism ; prevention & control