Objective To evaluate the clinical value of serum MUC1(sMUC1)in the patients with multiple myeloma.Methods The enzyme linked immunosorbent assay(ELISA)was used to compare the sMUC1 levels in the 12 cases of newly diagnosed multiple myeloma.15 cases of post-chemotherapy and 46 healthy donors.Results The mean concentration of sMUC1 in the newly diagnosed patients with multiple myeloma was 33.44 U/ml(10.86～88.80 U/ml).In the patients of post-chemotherapy the mean concentration was 11.6U/ml(3.92～22.22 U/ml),and in the healthy donors the concentration was 12.81 U/ml(3.84～30.45 U/ml).The level of sMUC1 in the new diagnosed patients was significandy higher than that in the patients of post-chemotherapy(P=0.001)and healthy donors(P=0.000).There was no significant difference between post-chemotherapy and healthy donors(P=0.461).Conclusion sMUC1 may be one of the tumor markers for the diagnosis of multiple myeloma.sMUC1 could also be used as one of the indicators of prognosis and the evaluation of the chemotherapy efficacy.sMUC1 might be a potential target for the immunotherapy to the patients with multiple myeloma.

AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis in-duced by CoCl 2 .METHODS:NSCs were exposed to CoCl 2 at different doses (200~600μmol/L) for 24 h.The cell via-bility and apoptosis were measured by CCK-8 assay and TUNEL method.The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR.The protein levels of Bcl-2 and Bax were detected by Western blotting .RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05).CoCl2 at concentration of 400μmol/L for 24 h was used to induce apopto-sis and the expression of miR-26a was down-regulated compared with control (P<0.05).Exposure to CoCl2 at concentra-tion of 400μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax , down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05).CONCLUSION:CoCl2 at concentration of 400μmol/L induces the apoptosis of NSCs obviously . CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway .Declining miR-26a may be related to NSC apopto-sis.

Objective To evaluate the effects of Ulinastatin (UTI) on the expressions of TNF-α,IL-6 and neurons apoptosis in cerebral cortex of rats after cardiopulmonary resuscitation (CPR).Methods Thirty-six healthy male adult Wistar rats were induced ventricular fibrillation untreated for 7 min and then received CPR.The animals were infused UTI 100 000 U/kg or phosphate-buffered solution (PBS) at once after ROSC.At 2,4 and 8 h after ROSC,cerebral cortex were removed to determine the mRNA expressions and levels of TNF-α protein and IL-6 protein,the translocation ratio of NF-κB p65 from cytoplasm to nucleus and the apoptotic neurons.Results The plasma levels of TNF-α (ng/mL) in animals of UTI group were (17.7 ± 1.4),(21.9 ± 2.1) and (17.1 ± 0.6) at 2,4 and 8 h after ROSC respectively,and significantly lower than those in PBS group at the given intervals.Mean while,the levels of IL-6 (ng/mL) were (208.9 ± 14.1),(281.5 ±25.9) and (251.8 ± 15.3) at 2,4 and 8 h after ROSC respectivèly in animals of UTI group,and lower than those in PBS group.The expressions of TNF-α mRNA and IL-6 mRNA and protein levels of TNF-α and IL-6 in UTI group were both lower than those in PBS group at given intervals,respectively.The translocation ratio of NF-κB p65 from plasma to nucleus in PBS group at each given interval after ROSC was significantly higher than that in UTI group.The number of viable neurons in cerebral cortex in UTI group was higher than that in PBS group,while the number apoptosis neurons was fewer in UTI group.Conclusions UTI attenuated the general inflammatory response after ROSC in rat,decreased the activation of NF-κB pathway,and subsequently attenuated the expression of TNF-α and IL-6,and finally decreased the neurons apoptosis.

Objective To explore whether the peritoneal cooling was better than other cooling methods on protection neuron damage of the hippocampus CA1 after cardiopulmonary resuscitation (CPR) in New Zealand rabbits.Methods Forty eight adult New Zealand rabbits were induced ventricular fibrillation by AC current and were resuscitated after cardiac arrest for 5 minutes.The rabbits were randomly divided into four groups according to the way of cooling methods,nomothermia group ( NT),peritoneal cooling group (PC),surface cooling group (SC) and local cooling group (LC).The changes of tympanic membrane temperature were recorded in each animal and blood plasma concentrations of electrolyte were tested in each group at different time points after restore of spontaneous circulation (ROSC).Brain tissue were removed,the numbers of vigorous and apoptotic neurons in the hippocampus CA1 area were counted after ROSC at 72h.One-way ANOVA or Mann-Whitney rank was used to determine the statistical significance between two groups.LSD-t test for multiple comparisons,R × C test for ROSC comparisons,a two-tailed value of P ＜0.05 was considered statistically significant. Results Hypothermia was rapidly induced in PC after ROSC,and the time of arriving at target temperature was (26 ±7) min in PC,(60 ±9) min in SC,(69 ± 12) min in LC respectively; in the maintain hypothermia period,the tympanic membrane temperature was maintained at 33～ 35 ℃ in each group exception nomothermia group (NT).There were no differences with main electrolyte,acid-abase liquid balance and renal function between each group at each time point after ROSC.The numbers of vigorous neurons in hippocampus CA1 area were ( 37.07 ± 6.43 ) /40 × in NT group,(35.13 ± 6.97) /40 × in LC group,(55.76 ± 10.13 ) /40 × in PC group,and (50.70 ± 7.38 ) /40 × in SC group (PC:NT,P＜0.01,SC:NT,P＜0.01,PC:SC,P=0.043,PC:LC,P＜0.01,LC:NT,P=0.52).The numbers of apoptotic neurons were (44.07 ±6.09) /40 × in NT group,(29.88 ±4.81 ) /40× in PC group,( 33.55 ± 5.67 ) /40 × in SC group and ( 42.27 ± 5.20 ) /40 × in LC group respectively (PC:NT,P ＜0.01,SC:NT,P ＜0.01,PC:LC,P ＜0.01,SC:LC,P ＜0.01,PC:SC,P=0.026,LC:NT,P =0.364 ).Conclusions The new peritoneal cooling method could rapidly induce and maintain hypothermia,and it had better protections on neurons in hippocampus CA1 than surface cooling and local cooling method after ROSC in New Zealand rabbits.

Objective To investigate the clinic effect of Linezolid for community acquired methicillin resistant staphylococcus aureus (MRS A) pneumonia. Methods The clinic data of the patient- were collected from the First Affiliated Hospital of Sun Yat-Sen University, in addition, the body temperature and white blood cell counts were obtained as the index of treatment. Results It was proved that Linezolid was effective in treating community acquired MRSA pneumonia and showed well tolerance with few adverse events. Conclusion Linezolid demonstrated good clinical and antibacterial activity but very few adverse reactions in elderly patients with community acquired MRSA pneumonia.

Objective To investigate whether Ulinastatin (UTI) would minimize the systemic inflammatory response,lessen cardiac dysfunction and protect neurons against injury in hippocampus CA1area after restoration of spontaneous circulation (ROSC). Methods Animal models of cardiac arrest were established in 24 New Zealand rabbits,and those animals were randomly (random number) divided into control group and UTI treated group after ROSC.Changes in the levels of plasma inflammatory cytokines TNF-α and IL-6 were assayed before cardiac arrest and 4,8,12 and 16 hours after ROSC.Cardiac function including FS,EF and E/A were observed with ultrasonography before cardiac arrest and 4,8,12 and 16hours after ROSC,and viable and apoptotic neurons in hippocampus CA1 area and infiltrations of MPO positive cells in myocardium,cerebrum,liver,kidney and intestine were counted 72 hours after ROSC.The t-test or Mann-Whitney rank sum test was used to verify the specified theoretical distribution functions of the biomarkers tested by Kolmogorov-Smirnov test,POST HOC test was used for the multiple comparisons,and Pearson correlation analysis was used to investigate the correlation between inflammatory cytokines and cardiac function. Results The levels of TNF-α and IL-6 in UTI group were lower than those in control group as those data got 4,8,12 and 16 hours after ROSC (P ＜0.05).EF and E/A in UTI treated group were higher than those in the control group as those data got 4,8,12 hours after ROSC.FS values obtained 4 h and 8 hours after ROSC were higher in UTI group than those in control group ( P ＜ 0.05 ).The Pearson correlation analysis showed that the levels of TNF-α and IL-6 significantly correlated with EF after ROSC.The number of viable neurons in CA1 area of control group was ( 13.22 ± 0.97) which was lower than that in UTI group ( 16.89 ± 1.45 ) ( P =0.003 ),while the number of apoptotic neurons in hippocampus CA1 area was higher in control group than that in UTI group (15.67 ± 1.37) vs.(13.67 ± 1.03 ) (P =0.019).The numbers of MPO positive cells were significantly lower in liver,kidney and intestine in group UTI than those in control group. Conclusions UTI could inhibit the infiltration of MPO positive cells in liver,kidney and intestine,decreasing the levels of TNF-α and IL-6 in plasma,in turn lessening cardiac dysfunction and protecting neurons from injury in hippocampus CA1 area after ROSC of New Zealand rabbits.

Objective To evaluate the effect of percutaneous coronary intervention (PCI) or thrombolysis,in patients with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA),in the presence of ST-elevation myocardial infarction (STEMI).We demonstrated the benefits of the two therapies on ROSC patients in hospital discharge and neurological recovery,and clarified the importance of ROSC,so as to guide the treatments for OHCA in the presence of STEMI.Methods It was performed a meta-analysis of clinical studies located in PUBMED and MEDLINE databases from January 1995 to October 2011.OHCA patients with ROSC were as our study objects,the hospital discharge and neurological recovery rates,of patients with and without PCI or thrombolysis,were assessed in patients with ROSC after OHCA in the presence of STEMI.In the same Cohort Study,between received and rejected PCI,or between received and rejected thrombolysis in OHCA patients with ROSC as treated group and control group,using Review Manager 5.1 software to analyze,respectively.Furthermore,we also compared the differences in hospital discharge and neurological recovery rates between patient groups who received PCI or thrombolysis by Pearson x2 analysis.Results The meta-analysis showed that the rate of hospital discharge improved with both PCI (odds ratio [OR],1.65 ; 95％ confidence interval [CI],1.05-2.59,P ＜ 0.01)and thrombolysis (OR,2.03 ; 95％ CI,1.24-3.34,P ＜ 0.01) in patients with ROSC after OHCA,in the presence of STEMI.We also found that there were not significant differences between with PCI and with thrombolysis in the rate of hospital discharge (63.00％ vs.65.19％,P =0.548) and neurological recovery (88.62％ vs.91.25％,P =0.351) for the patients with ROSC after OHCA (P ＞0.05).Conclusions In patients with ROSC after OHCA in the presence of STEMI,both PCI and thrombolysis improved hospital discharge rates.Furthermore,there were similar efficacy in hospital discharge and neurological recovery rates between with PCI and with thrombolysis.

Objective To investigate the variation of biomarker of coagulation, anti-coagulation, fibrinolysis in elderly critical patients and find out whether they are related to the disease severity. Methods Sixty-seven patients were no less than 60 years old. Eligible criteria: coincidence with the diagnostic criteria of systemic inflammatory response syndrome (SIRS) and APACHE Ⅱ score was no less than 10 scores. Blood sample was drawn from the venous for the test of biomarker (APTT, PT, TT, D-D, Fib, AT-Ⅲ , PC, PAI-1). According to the existent status,all the patients were divided into two groups:survival group (43 cases) and death group(24 cases) ,meanwhile,according to the diagnostic criteria of MODSE,all the patients were divided into MODSE group (30 cases) and non-MODSE group (37 cases). Results There were significant differences in APACHE Ⅱ score between MODSE group and non-MODSE group, survival group and death group [(25.83 ± 1.19) scores vs(18.1±20.73) scores and(18.81±0.72) scores vs(26.50 ± 1.42) scores](P <0.01). The PT and D-D in MODSE group anti death group were higher than those in non-MODSE group and survival group, the differences were significant (P <0.05),while the activity of AT-Ⅲand PC in MODSE group and death group were lower than those in non-MODSE group and survival group, the differences were significant (P <0.05). The PT,D-D and PAI-1 were positively correlated to APACHE Ⅱ score (related coefficients were 0.328, 0.308, 0.335,P <0.05). The AT-Ⅲ and PC were negatively correlated to APACHE Ⅱ score (related coefficients were -0.469, -0.559,P <0.01). Conclusions The abnormality of eoagnlation-fibfinolysis system exists in elderly critical patients. The extended PT, elevated D-D and PAI-1 ,descended PC and AT-Ⅲ are the hints of disease severity and poor prognosis.

Objective To establish a new model of cardiac arrest (CA) in rats by transcutaneous electrical epicardium stimulation. Method Two acupuncture needles connected to the anode and cathode of a stimulator were transcutaneously inserted into the epicardium as electrodes. The stimulating current was steered to the epicardium and the stimulation was maintained for 3 minutes to induce CA. Cardiopulmonary resuscitation (CPR) was performed at 6 minutes after a period of nonintervention. Results The success rate of induction was 12/20 at the current intensity of 1 mA; and reached 20/20 when the current intensity was increased to 2 mA. The average time from the electrical stimulation to CA induction was (5. 10 ± 2. 81) seconds. When the electrical stimulation stopped, 18/20 rats had ventricular fibrillation and 2/20 rats had pulseless electrical activity. CPR was performed for averagely 207.4 ( ± 148.8) seconds. The restoration of spontaneous circulation was 20/20. The death rate within 4 hours after CA was 5/20, and the 72-hour survival rate was 10/20. There were only two cases of complications, a minor muscle contraction and a minor lung lobe injury. Conclusions The model of CA in rats induced by transcutaneous electrical epicardium stimulation is a stable model that requires low-intensity current and has fewer complications.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.