Adolescent ; Antigens, CD34 ; metabolism ; Bone Neoplasms ; diagnostic imaging ; metabolism ; pathology ; Chondrosarcoma, Mesenchymal ; metabolism ; pathology ; Diagnosis, Differential ; Hemangiopericytoma ; diagnostic imaging ; metabolism ; pathology ; Humans ; Male ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Sarcoma, Synovial ; metabolism ; pathology ; Tomography, X-Ray Computed ; Vimentin ; metabolism

Cardiomyopathies ; diagnosis ; pathology ; Echocardiography ; Heart Ventricles ; pathology ; Humans ; Magnetic Resonance Imaging ; Young Adult

Objectives To explore the effects of enhanced external counterpulsation(EECP)on the serum level of C-reactive protein and endothelin-1 in patients with cerebral ischemic stroke,to provide clinical evidence for the treat?ment and secondary prevention of patients with cerebral ischemic stroke. Methods Total 187 patients with ischemic stroke were enrolled measure the serum level of C-reactive protein and endothelin-1, before EECP, after36 hours EECP, and one-month after EECP. Then contrast the difference of these indicators. Result After treatment, the serum levels of C-reactive protein and endothelin-1 in EECP group were obviously decrease and the difference was statistically signifi?cant(hs-CRP 60.1%vs. ET-1 40.9%,P<0.05). After treatment, the serum levels of C-reactive protein and endothelin-1 in EECP group were obviously decrease than that in the control group and the difference was statistically significant ( hs-CRP 41.3%vs. ET-1 24.3%,P<0.05). One-month after EECP, the serum level of endothelin-1 in EECP group was obviously decrease than that in the control group(43.8%vs. 31.8%,P<0.05). One-month after EECP, there was no signif?icant difference in the serum levels of C-reactive protein between the two groups (P>0.05). Conclusion EECP can obvi?ously reduce the serum levels of C-reactive protein and endothelin-1 in the patients with ischemic stroke, which indi?cates that EECP can slow atherosclerotic process.

Medical ethics is correlated with further development of affiliated teaching hospital.Our hospital took ‘ Bethune spirit’ and philosophy of forgiveness and kindheartedness as guidance and became the first batch of Bethune spirit model hospital of Chongqing.Teaching quality was improved by providing lectures about ‘ Bethune spirit’ for medical students and equally emphasizing medical knowledge and medical ethics education.Anti-corruption and academy governing movements with the subject of ‘ Bethune spirit’ were carried out to repel academic misdeed,with the result that clinical,teaching and scientific works were promoted and advanced.

?ig-h_3 was first identified as a transforming growth factor-beta1-inducible gene in human lung adenocarcinoma cell line. It encodes for a secreted extracellular matrix (ECM) protein, which is thought to act on cell attachment and ECM composition. Previous study showed that ?ig-h_3 were highly expressed in human hepatoma cell lines and lowly expressed in human normal hepatic cells. The present study aimed to transfect ?ig-h_3 into 7721 cells to investigate its effect on secretion of MMPs in the transfected human hepatoma cells. Full-length ?ig-h_3 gene,cloned by reverse transcription polymerase chain reaction (RT-PCR) was inserted into the eukaryotic expression vector pEGFP-C_2. The recombinant plasmid was transfected into 7721 cells with Lipofectamine2000 and Gelatin-Zymography were adopted to detect the production of MMPs in the transfected cells. Results showed that ?ig-h_3/pEGFP-C_2 recombinant expression plasmid was successfully constructed and achieved high transfection efficiency. MMPs expression of the transfected cells was promoted significantly. These results suggest that overexpression of ?ig-h_3 promoted the production of MMPs, indicating that ?ig-h_3 may play roles in the invasive and metastatic processes of hepatoma.

BACKGROUND: Paraquat (PQ) is an effective herbicide and is widely used in agricultural production, but PQ poisoning is frequently seen in humans with the lung as the target organ. Clinically pulmonary pathological changes are often used to predict the severity and prognosis of the patients. In this study, we observed the expression of heat shock protein 70 (HSP70) in rat lung after PQ poisoning and to investigate the therapeutic effects of ulinastatin. METHODS: Seventy-two adult healthy SD rats were randomly divided into a control group (group A, n=24), a poisoning group (group B, n=24), and an ulinastatin group (group C, n=24). The rat models of acute PQ poisoning were established by intra-gastric administration of 80 mg/kg PQ to rats of groups B and C, and the rats of group C were intra-peritoneally injected with 100000 IU/kg ulinastatin 30 minutes after poisoning. The expression of HSP70 in lung tissue was observed, and W/D and histopathological changes in the lung tissue were compared 12, 24, 48 and 72 hours after poisoning. The expression of HSP70 in the lung tissue was assayed by using RT-PCR. All quantitative data were processed with one-way analysis of variance to compare multiple sample means. RESULTS: Compared to group A, the expression of HSP70 in the lung of rats in groups B and C increased significantly at all intervals (P<0.05). The pathological changes in lung tissue of rats with PQ poisoning included congestion, leukocytes infiltration and local hemorrhage, whereas those of group C were significantly lessened. CONCLUSION: Ulinastatin may ameliorate acute lung injury to some extent after PQ poisoning in rats by enhancing the expression of HSP70.

BACKGROUND: Paraquat (PQ) is an effective herbicide and is widely used in agricultural production, but PQ poisoning is frequently seen in humans with the lung as the target organ. Currently, there are many studies on lung injury after PQ poisoning. But the kidney as the main excretory organ after PQ poisoning is rarely studied and the mechanisms of this poisoning is not very clear. In this study, we observed the expression of caspase-3 and livin protein in rat renal tissue after PQ poisoning as well as the therapeutic effects of ulinastatin. METHODS: Fifty-four Sprague-Dawley (SD) rats were randomly divided into three experimental groups: control group (group A), paraquat poisoning group (group B) and ulinastatin group (group C), with 18 rats in each group. Rats in group B and group C were administered intragastrically with 80 mg/kg PQ, rats in group C were injected peritoneally with 100000 U/kg ulinastatin once a day, while rats in group A were administered intragastrically with the same volume of saline as PQ. At 24, 48, 72 hours after poisoning, the expression of livin in renal tissue was detected by Westen blotting, the expression of caspase-3 was detected by immunohistochemistry, and the rate of renal cell apoptosis was tested by TUNEL detection. The histopathological changes were observed at the same time. RESULTS: Compared to group A, the expression of caspase-3 in the renal tissue of rats in groups B and C increased significantly at any time point. Compared with group B, the expression of caspase-3 in renal tissue of rats in group C decreased. Compared with group A, the expression of livin in renal tissue in rats of groups B and C increased significantly at any time point (P<0.01), especially in group C (P<0.01). TUNEL method showed that the rate of renal cell apoptosis index was higher in group B at corresponding time points than in group A (P<0.01), and was lower in group C at corresponding time points than in group B (P<0.01). CONCLUSION: UTI has a protective effect on the renal tissue of rats after paraquat poisoning through up-regulating the expression of livin and down-regulating the expression of caspase-3, but the regulation path still needs a further research.

Aged ; Coronary Disease ; etiology ; Female ; Humans ; Male ; Middle Aged ; Sleep Apnea, Obstructive ; complications

OBJECTIVETo study the pathogens, drug sensitivity and risk factors for ventilator-associated pneumonia (VAP) in neonates.

METHODSRetrospective analysis was performed on the clinical data of 401 neonates who were admitted to the neonatal intensive care unit and received mechanical ventilation for 48 hours or longer from January 2008 to February 2012. Eighty-five of the 401 neonates suffered VAP.

RESULTSThe main pathogens for VAP were Gram-negative bacteria (97%), including Klebsiella pneumoniae (51%), Acinetobacter baumannii (17%) and Escherichia coli (12%) as the three most frequent ones. The drug sensitivity test showed that these pathogens developed resistance to amoxicillin, amoxicillin/clavulanic acid, piperacillin, ceftazidime, cefazolin, and cefotaxime, with a susceptibility rate of below 15%, and demonstrated decreased sensitivity to imipenem and meropenem, with a susceptibility rate of below 75%. The independent risk factors for neonatal VAP included birth weight (OR=1.399, P<0.05), duration of mechanical ventilation (OR=1.966, P<0.01), length of hospital stay (OR=1.812, P<0.01), times of tracheal intubation (OR=2.056, P<0.01), and 1 min Apgar score (OR=2.146, P<0.01).

CONCLUSIONSThe incidence of neonatal VAP is influenced by many factors. The main pathogens for neonatal VAP are Gram-negative bacteria and antibacterial agents should be properly used according to drug sensitivity test results. Comprehensive prevention and control measures should be taken to reduce the incidence of VAP.

Female ; Gram-Negative Bacteria ; drug effects ; isolation & purification ; Humans ; Infant, Newborn ; Logistic Models ; Male ; Microbial Sensitivity Tests ; Pneumonia, Ventilator-Associated ; etiology ; microbiology ; Risk Factors

OBJECTIVETo investigate the sequence-dependent effect of combined use of gemcitabine and pemetrexed on the proliferation of human pancreatic carcinoma cell lines BXPC-3 and PANC-1 in vitro and explore the cellular mechanism.

METHODSMTT assay was used to determine the proliferation of the two cells after addition of the two drugs in different sequences, and the cell cycle changes were analyzed by flow cytometry.

RESULTSBoth gemcitabine (10(-7)-10 mg/ml) and pemetrexed (10(-7)-10 mg/ml) significantly inhibited the proliferation of BXPC-3 and PANC-1 cells in a dose- and time-dependent manner. The effect of combined administration of gemcitabine and pemetrexed on the cell proliferation varied with the order of the drug delivery, and addition of gemcitabine 24 h after pemetrexed administration produced a significant enhancement of the inhibitory effect as compared with simultaneous drug administration (P<0.05) or the administration of the two drugs in a reverse order (P<0.05). Compared with the control group, combined administration of gemcitabine and pemetrexed caused obvious cell cycle arrest at G1 and S phases (P<0.05). Simultaneous administration of the two drugs resulted in significantly reduced G2-phase cells (P<0.05); addition of gemcitabine prior to pemetrexed caused cell cycle arrest in G1 phase (P<0.05), while the reverse caused cell cycle in S phase (P<0.05).

CONCLUSIONBoth gemcitabine and pemetrexed can inhibit the proliferation of BXPC-3 and PANC-1 cells, and their synergetic effect depends on the sequence of their administration. The sequential administration of pemetrexed followed by gemcitabine produces significant synergetic effects against the cell proliferation, which might not be associated with their influence of the cell cycle.

Antimetabolites, Antineoplastic ; pharmacology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Glutamates ; pharmacology ; Guanine ; analogs & derivatives ; pharmacology ; Humans ; Pancreatic Neoplasms ; pathology ; Pemetrexed