Objective To explore the impact of enteral nutrition (EN)support on patients with advanced cancer.Methods 83 cases with advanced cancer were selected,the patients were randomly divided into two groups, 42 cases in the observation group,41 cases in the control group.The observation group was given EN support com-bined with parenteral nutrition (PN)support,while the control group was only given the PN support.Immune function CD +4 ,CD +4 /CD +8 ,IgA,IgG,nutrition indicators [serum albumin (ALB),transferrin (TF)and 24h urea nitrogen (24hUP)]before and 10d after surgery as well as complications were compared.Results The differences of CD +4 , CD +4 /CD +8 ,IgA,IgG,ALB,TF and 24h UP between the two groups before surgery were not statistically significant (P >0.05);10d after surgery,CD +4 ,CD +4 /CD +8 ,IgA,IgG levels in the control group were (52.4 ±4.4)%,(1.8 ± 0.3)%,(2.7 ±0.3)g/L and (11.4 ±2.1)g/L,which in the observation group were (55.9 ±5.6)%,(2.1 ± 0.5)%,(2.9 ±0.5)g/L and (12.9 ±2.3)g/L,CD +4 /CD +8 ,IgA,IgG were significantly higher in the observation group(t =2.408,2.521,2.332,2.359,all P <0.05);10d after surgery,ALB,TF and 24h UP in observation group were (36.6 ±2.3)g/L,(2.9 ±0.2)g/L,and (0.7 ±0.3)g/L,which were (32.4 ±1.5)g/L,(2.2 ±0.1)g/L,and (0.4 ±0.1)g/L in the control group,the differences were statistically significant (t =7.493,15.34,4.648,P <0.05).The incidence rate of complications in the observation group was 9.5% (4 /42),which in the control group was 26.8%(11 /41),the difference was statistically significant (χ2 =4.196,P <0.05).Conclusion EN support for patients with advanced cancer is benefit for immune function improvment and nutrition improvement,and can reduce the risk of complications.

Objective To evaluate the effect of palliative care in the treatment of pain and life quality in later period tumor patients.Methods 103 patients with advanced tumors in our hospital were selected and divided into group A(51 patients) and group B(52 patients) based on the methods of treatment.The patients in group A were given conventional treatment,and the patients in group B were given palliative care program on the basis of the treat-ment in group A.The effects of the groups A and B were observed and compared.Results The pain levels of group A and B before treatment had no statistically significant difference (P>0.05).The pain level score of group B after treatment was (26.41 ±3.55)points,which was lower than (32.56 ±7.12)points in group A,and the difference was statistically significant (t=6.430,P<0.05).The difference in life quality of the two groups before treatment was not significant (P>0.05).After treatment,the life quality score of group B was (66.85 ±6.75)points,which was higher than (53.39 ±6.74)points in group A,and the difference was statistically significant (P<0.05).Conclusion It is effective for palliative care to treat the patients with advanced tumors on their pain management and quality of life, which is worthy of clinical application.

Objective To investigate the changes of hepatocyte growth factor (HGF) and vascular endothelial growth factor(VEGF) after partial hepatectomy in patients with liver cirrhosis and their relationship with liver regeneration. Methods Thirty-five patients with partial hepatectomy between June 2007 and August 2009 were enrolled,according to whether cirrhosis were divided into cirrhosis group (16 cases) and non-cirrhosis group (19 cases). Liver size were measured with angiographic computed tomography at 7,30,90 d after operation. Regeneration rate of remnant liver were calculated. The serum concentrations of HGF and VEGF were meaaured. Postoperative hepatic function and complications incidence rate were comparatively analyzed. Results Compared with non-cirrhosis group, the postoperative hepatic function of cirrhosis group suffered serious damage. In non-cirrhosis group, the remnant liver regeneration rate reached (63.6± 15.9)%, (79.4 ± 17.2)%, (97.2 ± 18.3)% at 7,30,90 d after operation,in cirrhosis group,it reached (41.7 ± 10.7)%, (55.7 ± 13.2)%, (76.6 ± 12.5)%, liver in non-cirrhosis group regenerated rapidly (P <0.05). After hepatectomy,the HGF levels in cirrhosis group increased significantly at 1,3,7 d than those in non-cirrhosis group(P ＜ 0.05), but the VEGF levels were lower. Conclusions Liver in the patients with cirrhosis regenerate slowly and it may be due to in part through a decrease in VEGF. Whether it may,when given therapeutically represent a strategy to optimize liver regeneration in problematic patients needs to be clarified.

Objective To study the immunological pathogenesis of gluteal muscle contracture. Methods In 43 children with gluteal muscle contracture and 22 normal control cases, peripheral blood T-lymphocytes, B-lymphocyte and its subset were analyzed with flow cytometry. Results The percent of CD4+, B-lymphocyte and CD4+/CD8+ in children with gluteal muscle contracture were all significantly higher than those in the control(P0.05). Conclusion There is disorder of immunological regulation in children with gluteal muscle contracture. Immunologic factors may play an important role in the pathogenesis of gluteal muscle contracture.

Objective To observe the effect of allicin on the action potential duration (APD) and L-type calcium current (ICa,L) in the ventricular myocytes of rabbits with heart failure in order to explore the mechanisms of therapeutic effect of allicin on cardiac arrhythmias complicated with heart failure.Methods Forty-five New Zealand White male rabbits were randomly (random number) assigned to 3 groups (n=15 in each group):sham operated group (sham group),heart failure group (HF group),and heart failure treated with allicin group (HF+All group).The rabbit heart failure model was established by abdominal aortic constriction coupled with aortic regurgitation,the ventricular myocytes were obtained by enzyme double digestion,and the whole cell clamp was used to record action potential and calcium current.The action potential duration (APD),Ica,L and gating mechanism were observed during heart failure and allicin administered.Data were processed with pCLAMP version 10.2.Statistical analysis was performed using SPSS 17.0.Comparisons among groups were carried out using ANOVA,and SNK-q was used for multiple comparison as post-hoe.Results (1) Prolonged APD was found during heart failure,APD50 was prolonged from (93.4±4.7) ms in sham group to (115.5±6.2) ms in HF group(P＜0.01).After administration of allicin 30 μmol/L,APD50 was shortened to (105.2±5.5) ms (P＜0.05).(2) The density of ICa.L increased during heart failure,peak current density increased increased from (-8.4±0.6) pA/pF in sham group to (-15.1± 1.1) pA/pF while 0 mV attained at depolarizations (P＜0.01).After administration of allicin 30 μmol/L,the current density reduced to (-10.1+0.8) pA/pF (P＜0.01).The effect of allicin presented in both voltage dependent and consentration dependent manner.(3) According to the gating mechanism study,the main mechanism of lowering the density of ICa,L by allicin after heart failure was the acceleration of the steady inactivation of the channel,and the de-escalation of the recovery kinetic after the inactivation of the channel.Conclusions Allcin can be used to reduce the calcium current of ventricular myocytes in animal heart failure model,it has the potential of clinical use in treating cardiac arrhythmias during heart failure.

Objective To explore the regulation and mechanism of Cav1.2 current by KCNE1. Methods Transient transfection was used to transfer Cav1.2 channel plasmids separately or together with KCNE1 plasmids into HEK293 cells. The experiment was divided into 2 groups (15 cells in each group):Cav1.2 group, Cav1.2+KCNE1 group.The whole-cell patch clamp technique was used to record Cav1.2 current and gating dynamics. Results After co-transfection of KCNE1 with Cav1.2, Cav1.2 current decreased significantly. At 0 mV, peak current density of Cav1.2 was reduced from (-14.8±2.5) pA/pF to (-7.5±1.6) pA/pF (n=15, P<0.01). Based on the gate control mechanism, it is found that the regulation of Cav1.2 current by KCNE1 mainly makes the steady-state inactivation curve of the channel shifted to a more negative direction, thus accelerating the inactivation. Meanwhile, the recovery process of the channel after inactivation is slowed down and the recovery time constant was prolonged. Conclusions The KCNE1 subunit can reduce the current density of Cav1.2 by changing the channel inactivation and recovery process.

Objective To observe the effect of KN93, a CaMK Ⅱ inhibitor, on delayed afterdepolarization (DAD) and calcium ion in ventricular myocytes of rabbits with heart failure, and to investigate the effect of CaMK Ⅱ signaling pathway on trigged arrhythmia after heart failure. Methods Thirty male New Zealand White rabbits were randomized(random number) into the sham operated group (sham group), heart failure group (HF group) and heart failure with KN93 group (HF+KN93 group) (n=10 each group). The rabbit heart failure model was established by abdominal aortic constriction combined with aortic valve regurgitation. The ventricular myocytes were isolated by double enzyme digestion. The action potential and the transient inward current (Iti) were recorded by the whole-cell patch-clamp. The intracellular calcium transient was measured by the ion concentration measurement system. The main calcium transporter protein was detected by Western blotting. Data were analyzed by pCLAMP10.2. Statistical analysis was performed using SPSS 17.0. Comparisons among groups were conducted using ANOVA, and SNK-q multiple comparison procedure was utilized for post-hoc analysis.Results (1) After induction of heart failure, DAD and increment of trigger activity (TA) were observedin rabbit ventricular myocytes. Treatment of KN93 with 1.0 μmol/L reduced the events of DAD and TA.(2) After induction of heart failure, Iti densities were increased from -0.12±0.02 pA/pF to -0.95±0.06pA/pF at the polarization potential of -50 mV (n=10, P<0.01). The current densities were reduced to -0.44±0.04 pA/pF after application of 1.0 μmol/L of KN93 (n=10, P<0.01). (3) KN93 led to decrementof intracellular calcium ion concentration and calcium transient amplitude, and acceleration of the decayprocess of calcium transient. (4) KN93 upregulated the expression of pPLN and SERCA2a, increased the uptake of intracellular calcium ion, downregulated the expression of NCX, decreased the Iti, and reduced the occurrence of DAD and TA. Conclusions KN93 can reduce the intracellular calcium ion concentration of the heart failure animal model, and the occurrence of the DAD and TA. CaMK Ⅱ may be a new therapeutic target for arrhythmias in the heart failure.