0.05).Except imipenem and ampicillin,there was significant difference between the resistance of non-ESBLs-producing strains from CAP and from HAP to other eleven kinds of antibiotics(?2 test,P

OBJECTIVE To investigate the prevalence of extended-spectrum ?-lactamases(ESBLs) and the resistance in Escherichia coli isolates from biliary tract and abdominal cavity.METHODS ESBLs-producers were detected by CLSI Phenotypic Confirmatory Test and susceptibilities were tested by agar dilution method.RESULTS 50.1% Of isolates were ESBLs producers in those isolates.ESBLs producers were highly resistant to ampicillin,cefazolin,cefuroxime,fluoroquinolones,and cefotaxime.The resistant rate to ceftazidime,cefepime,cefoperazone-sulbactam,amikacin,and cefmetazole was less than 40%.None was resistant to meropenem in ESBLs producers.In non-ESBLs producers the resistant rate to ampicillin,cefazolin,cefuroxime,fluoroquinolones was more than 40% and most were susceptible to other antimicrobial agents.The resistant rate to ampicillin,cefazolin,cefuroxime,and ciprofloxacin was significantly higher in ESBLs producers than non-ESBLs producers.CONCLUSIONS With resistance to most of antimicrobial agents,ESBLs-producers were highly prevalent in E.coli isolates from biliary tract and abdominal cavity,so more attention should be paid to survey and detect those strains.

Objective To investigate the changes of CD11b on neutrophils during myocardial ischemia-reperfusion injury. Methods 12 patients undergoing coronary bypass grafts under CPB were studied. Blood samples were obtained from the coronary (coronary sinus) and systemic circulation (central venous and CPB machine), respectively. Samples obtained from coronary and systemic circulation were taken before the beginning of CPB, during CPB and after cardiac reperfusion. Neutrophil CD11b expression and serum cTnI concentration were measured. Results (1)Expression of CD11b increased gradually in systemic circulation during CPB and after reperfusion (P

Hypertriglyceridemia, and the ectopic deposition of triglycerides, are the risk factors for insulin resistance. To clarify the mechanism of regulations in triglyceride metabolism is an approach to the elucidation of pathogenesis and effective treatment of insulin resistance-related diseases.

Objective To investigate and evaluate the changes of PYK2 expression in hippocampal neurons and microglial cells in Kainate acid-induced status epilepticus. Methods Kainate acid-induced status epilepticus was established in rats, and by using immunostaining, changes of PYK2 expression in hippocampal neurons and microglial cells was investigated. Results Expression of PYK2 in hippocampal pyramidal neurons was markedly decreased after kainate acid-induced status epilepticus. However, 24h after the epileptic onset, a pronounced up-regulation of PYK2 and phosphor-PYK2 immunoreactivities were evident in amoeboid microglial cells. The upregulation of PYK2 and phosphor-PYK2 was in accordance with the morphological changes of the activated microglial cells. Conclusion PYK2 was activated in microglial cells after seizure. Furthermore, the activation of PYK2 in microglial cells after seizure might be related to the morphological and behavioral changes of microglial cells after activation.

Objective To investigate and evaluate the changes of phospho PYK2 and phospho p38MAPK expression in neurons after focal cerebral ischemia. Methods Focal ischemia reperfusion model was established in rats, and by using immunostaining, the changes of phospho PYK2 and phospho p38MAPK expression in neurons was observed. Results Faint phospho PYK2 and phospho p38MAPK immunoreactivity were revealed in normal cortical neurons. Fifteen minutes after the ischemia onset, a pronounced upregulation of phospho PYK2 and phospho p38MAPK immunoreactivities were evident in these ischemia attacked neurons. The immunoreactivities of phospho PYK2 and phospho p38MAPK reached its peak at 30min after ischemia, and decreased 60min after ischemia. Conclusion Cerebral ischemia was able to induce neuronal PYK2 phosphorylation. The activation of PYK2 might link ischemia attack to the p38MAPK signaling pathway to initiate the neuronal response to the stress stimuli

Expression of apelin mRNA in the isolated mouse adipocytes was confirmed by Northern blot. The level of apelin mRNA increased during stage of differentiation of 3T3-L1 cells. Insulin up-regulated the apelin expression in 3T3-L1 adipocytes, suggesting that apelin expression in adipocyte may correlate with obesity, insulin resistance and hypertension.

Resistance is one of the most important reasons that restrict the clinical application of most chemotherapeutic medicines. Docetaxel is a very widely applicated antitumor medicine. Most of the researches on the mechanism of resistance against docetaxel focused on the drug transporters, changes in drug metabolism and pathway alteration of cell cycle and apoptnsis. The mechanism of docetaxel resistance and the predictive data based on clinical research to docetaxel therapy in cancer treatment were reviewed.

Animals ; Heparin ; pharmacology ; Humans ; Ligands ; Lymphatic Metastasis ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms ; metabolism ; pathology ; Oligosaccharides ; metabolism ; Selectins ; metabolism ; physiology ; Signal Transduction

Antigens, Neoplasm ; genetics ; metabolism ; Breast Neoplasms ; enzymology ; genetics ; metabolism ; DNA Topoisomerases, Type II ; genetics ; metabolism ; DNA-Binding Proteins ; genetics ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; physiology ; Humans