Microarray technology are being performed more widely than ever before on many areas in lifescience,although the technology is still evolving,the challenge of performing a microarray experiment is no longer in the data generation,but in extracting useful information and utilizing it to get the results with biological meanings.Some methods and tools used for expressional microarray data mining based on previous work were summarized.These methods include gene clustering,GO analysis,regulating pathway analysis,and related algorithm.We hope this can be helpful for those researchers who are implementing expressional microarray for biological analysis.

OBJECTIVEEndothelial apoptosis plays an important role in the initiation of atherosclerosis. It would be useful to clarify whether activation of non-neuronal muscarinic receptor (NNMR) could prevent endothelial apoptosis and atherosclerosis. We investigated the effects of NNMR activation on regulating rat aortic endothelial cells (RAECs) apoptosis induced by homocysteine, an independent risk factor of atherosclerosis, and further studied its molecular mechanism.

METHODSRAECs were incubated using homocysteine at the concentration of 2.7 mmol/L for 36 h. RAECs were also pre-treated with carbachol or arecoline to examine their effects. RT-PCR was used to assess changes in the gene expression related to cell apoptosis.

RESULTSIncubation of RAECs with homocysteine at the concentration of 2.7 mmol/L resulted in morphologic changes, such as cellular shrinkage, membrane blebbing, chromatin condensation and margination. These could be attenuated by pretreatment with carbachol and arecoline at the concentration of 10 micromol/L for 12 h. Homocysteine induced apoptosis in RAECs and the molecular mechanisms were associated with the regulation of fas, fas-L and caspase-8 in the death receptor pathway, bcl-2, bcl-xL and bax in the mitochondrial pathway, caspase-12 in the endoplasmic reticulum pathway and caspase-3, caspase-6 and p53 as downstream effectors. Carbachol and arecoline attenuated the effects of homocysteine on genes in the death receptor pathway, in the mitochondrial pathway and in the downstream pathway. Atropine could reverse all of the effects of arecoline.

CONCLUSIONActivation of NNMR by carbacol and arecoline inhibits homocysteine-induced endothelial cell apoptosis mainly through regulation of death receptor pathway, mitochondrial pathway and downstream effectors.

Animals ; Aorta ; cytology ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Arecoline ; Carbachol ; Cell Cycle ; Endoplasmic Reticulum ; metabolism ; Endothelial Cells ; cytology ; drug effects ; Homocysteine ; adverse effects ; Mitochondria ; metabolism ; Rats ; Receptors, Muscarinic ; metabolism

Adult ; Amides ; adverse effects ; Benzene ; adverse effects ; Burns, Chemical ; pathology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Nitro Compounds ; adverse effects ; Young Adult

Animals ; Antibiotics, Antineoplastic ; pharmacology ; Blotting, Northern ; Cells, Cultured ; Dexamethasone ; pharmacology ; Doxorubicin ; pharmacology ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation ; drug effects ; Glucocorticoids ; pharmacology ; Kidney Glomerulus ; cytology ; drug effects ; metabolism ; Mice ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Vascular Endothelial Growth Factor A ; genetics ; metabolism

Altitude ; Animals ; Astrocytes ; cytology ; Brain ; cytology ; Hypoxia ; Male ; Microglia ; cytology ; Rats ; Rats, Wistar

Objective To explore the application value of DOSE index score in the peitients with chronic obstructive pulmonary disease.Methods 122 cases of plateau COPD patients were followed up for 12 months,and we recorded and analyzed the patient's health and life.We also recorde FEV 1 and DOSE scores of the patients with COPD,and record the COPD risk events,including the number of respiratory failure and death,and the times of hospitalization,total such confinement,outpatient expenses,hospitalization expenses,mMRC,and scored in the number of exacerbations,etc.Results The DOSE index score was negatively correlated with FEV1％ pred (r=0.73,P ＜ 0.05) for 122 COPD patients,and were positively correlated with mMRC (r=085,P ＜ 0.01),the annual number of exacerbations (r=0.71,P ＜ 0.01),respiratory failure (r=0.65,P ＜ 0.01),heart failure (r=0.50,P ＜ 0.01),number of outpatient service (r=0.12,P＜0.01),hospitalization time (r=0.70,P＜0.01),the totalsuchconfinement (r=0.66,P＜0.01),outpatient expenses (r=0.13,P＞ 0.13),hospitalization expenses (r=0.65,P＜0.01).ROC curve was used to analyzed the cut-off point and curve area of COPD DOSE index.Conclusion The DOSE index is a simple COPD assessment tools,and is closely related to the prognosis of patients and health.

AIM:To observe the expression and tissue localization of matrix metalloproteinase 9 (MMP-9) and transforming growth factor beta 1 ( TGF-β1 ) in the rat acute cerebral ischemia model.METHODS:Male Wistar rats were used to establish acute cerebral ischemia model by a suturing method.The rats were divided into normal control group, sham group and ischemia 6 h, 12 h, 1 d, 2 d, 6 d and 14 d groups.The rat cerebral cortex and hippocampus of the brain were collected at different time points.The mRNA and protein levels of MMP-9 and TGF-β1 in the brain tissues were detec-ted by real-time PCR and in situ histochemistry staining, respectively.The levels of MMP-9 and TGF-β1 in the plasma were also measured by ELISA.RESULTS:The results of real-time PCR showed that the mRNA levels of MMP-9 began to in-crease 6 h after acute ischemia and reached to a peak 2 d after acute ischemia.Similarly, the mRNA level of TGF-β1 began to rise 12 h after acute ischemia and reached to the highest level 6 d after acute ischemia.Compared with the sham rats, the mRNA levels of MMP-9 and TGF-β1 in the rat brains that collected at ischemic time of 12 h, 1 d, 2 d, 6 d and 14 d were significantly increased.Moreover, results of in situ histochemical staining showed that the expression of MMP-9 was detected at cerebral cortex and hippocampus 1 d after acute cerebral ischemia.Further studies showed that MMP-9 dyeing of the rat cerebral cortex was most obvious 2 d after the acute cerebral ischemia.Similarly, the rat cortex and hippocampus began to express TGF-β1 2 d after acute ischemia and TGF-β1 staining at rat cerebral cortex was most obvious 6 d after the acute cerebral ischemia.In addition, ELISA showed that the increase in MMP-9 and TGF-β1 was detected in the plasma 12 h after ischemia.Compared with the sham rats, the level of these 2 factors significantly upregulated since 1 d after ischemia. CONCLUSION:The brain tissue itself contributes to the upregulation of MMP-9 and TGF-β1 post acute cerebral ischemia, which shed light on the related research in the field.

ObjectiveTostudy the value of color Doppler sonography in diagnosisof rhabdomyolysis.Methods The color Doppler sonography images of twenty-one patients with diagnosed rhabdomyolysis were retrospective analyzed.The pathological changes of the muscle were observed.Results The appearance of ultrasound was cloundness and rough-cast glass change in the diseased area of rhabdomyolysis.The diseased region can be found by ultrasound,and location and scope can be displayed clearly.There were major differences in the location of rhabdomyolysis because of etiological factor.The muscle volume and tension of rhabdomyolysis were increased for trauma,the individual patients will lead to the osteofascial compartment syndrome.There was no blood flow signal or little blood flow signal in the diseased area of rhabdomyolysis.Conclusions The color Doppler sonography is an efficient method for diagnosis of rhabdomyolysis.

Whether M3 cholinergic receptor signal transduction pathway is involved in regulation of the activation of NF-kappaB and the expression of chemokine MOB-1, MCP-lgenes in pancreatic acinar cells was investigated. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, atropine and PDTC in vitro. The MOB-1 and MCP-1 mRNA expression was detected by using RT-PCR. The activation of NF-kappaB was monitored by using electrophoretic mobility shift assay. The results showed that as compared with control group, M3 cholinergic receptor agonist (10(-3) mol/L, 10(-4) mol/L carbachol) could induce a concentration-dependent and time-dependent increase in the expression of MOB-1, MCP-1 mRNA in pancreatic acinar cells. After treatment with 10(-3) mol/L carbachol for 2 h, the expression of MOB-1, MCP-1 mRNA was strongest. The activity of NF-kappaB in pancreatic acinar cells was significantly increased (P<0.01) after treated with M3 cholinergic receptor agonist (10(-3) mol/L carbachol) in vitro for 30 min. Either M3 cholinergic receptor antagonist (10(-5) mol/L atropine) or NF-kappaB inhibitor (10(-2) mol/L PDTC) could obviously inhibit the activation of NF-kappaB and the chemokine MOB-1, MCP-1 mRNA expression induced by carbachol (P<0.05). This inhibitory effect was significantly increased by atropine plus PDTC (P<0.01). The results of these studies indicated that M3 cholinergic receptor signal transduction pathway was likely involved in regulation of the expression of chemokine MOB-1 and MCP-lgenes in pancreatic acinar cells in vitro through the activation of NF-kappaB.

Objective To investigate the osteoclast′s function levels in infants and toddlers and the relationship between the osteoclast function and sex,age,body length,body weight and body mass index(BMI).Methods Sixty-eight children(37 boys and 31 girls,aged from 1 to 36 months) were studied.All of the children were in good health.These children were divided as infants group and toddlers group according to their age.Just before the samples were collected,the children′s body weight,body length were measured and the BMI were calculated.Two biochemical markers,such as serum tartrate-resistant acid phosphatase 5b(TRAP5b) and urine deoxypyridinoline(DPD) were measured.Results The difference of serum TRAP5b concentration between infants and toddlers was significant at the level of P