Acetyltransferases ; genetics ; Breast Neoplasms ; genetics ; Female ; GPI-Linked Proteins ; Gene Expression Regulation, Neoplastic ; genetics ; Humans ; Membrane Glycoproteins ; genetics ; Neoplasm Metastasis ; genetics ; physiopathology ; S100 Proteins ; genetics ; Transcription Factors ; genetics

Cell Movement ; drug effects ; Chemokine CXCL12 ; genetics ; metabolism ; pharmacology ; physiology ; Humans ; Neoplasm Invasiveness ; physiopathology ; Neoplasm Metastasis ; physiopathology ; Neoplasms ; metabolism ; Neovascularization, Pathologic ; physiopathology

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

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

Objective To investigate the effects of ?-lipoic acid on the proliferation and activation of NF-?B induced by high glucose (HG) in rat mesenteric cells (MCs). Methods The rat mesenteric cells were cultured in the medium with normal glucose (5.6mmol/L, NG), high glucose (25mmol/L, HG), HG+100 ?mol/L ?-lipoic acid, or HG+200?mol/L ?-lipoic acid and HG+PDTC (a NF-?B inhibitor). Activation of nuclear factor-?B (NF-?B) of rat mesenteric cells were measured by electrophoretic mobility shift assay (EMSA). The cell proliferation was assessed by MTT. Results ?-lipoic acid (50~300?mol/L) can inhibit the proliferation of MCs. The NF-?B binding activity was 2.2 -fold higher in MCs exposed to HG compared to NG (P

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

ObjectiveTo investigate the feasibility and effectiveness of low central venous pressure (LCVP) in the operation of major hepatic resection.MethodsFourty-eight patients underwent major hepatic resection were randomized into two groups: LCVP and control group.In the LCVP group,CVP was maintained ≤5 cm H2O during the hepatic resection and then returned to normal after resection.In the control group,CVP was maintained normal between 6 -12 cm H20.The duration of hepatectomy,volume of blood loss,volume of blood transfused and renal function were compared between the two groups.ResultsFor the LCVP and control group,the time for hepatectomy was (45 ± 8 ) and ( 35 ± 5 ) min,respectively; the volumes of blood loss were ( 850 ± 160) and (436 ±280)ml,respectively; the blood loss during operation was (490 ± 130) and (270 ± 105 ) ml respectively.The differences were statistically significant (t values were 15.53,7.69 and 17.89 separately,P ＜0.05 ).No significant difference in the renal function was observed before and after the operation ( P ＞ 0.05 ).Conclusion Using LCVP technique during liver resection significantly reduced the operation time,blood loss and blood infusion.And there wa.s no obvious adverse effect on renal function.

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.

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.