E-cadherin Expression in Children with Acute Leukemia and Its Clinical Significance / 中国实验血液学杂志

OBJECTIVE@#To investigate the correlation of E-cadherin expression level with the clinical characterastics in children with acute leukemia (AL), and to explore the possible regulatory mechanism.@*METHODS@#Real-time quantitative RT-PCR was applied to detect the expression level of E-cadherin in bone marrow samples from 135 child patients diagnosed as AL, and its relevance with clinical indicators was statistically analyzed. The expression levels of E-cadherin, β-catenin, and Akt/p-Akt were detected by using Western blot. The bone marrow samples from 22 children with non-malignant hematological diseases were used as controls.@*RESULTS@#The expression level of E-cadherin significantly decreased in newly diagnosed patients with all 3 types of AL as compared with bone marrow samples from control group (P0.05). The expression level of E-cadherin in the patients from Common-B-ALL group was higher than B-ALL patients with other immunophenotypes (P<0.01), while no significant difference was found among patients grouped by FAB classification. By the correlation analysis of measured data, lower E-cadherin expression level was found to be related with high WBC count and serum lactic dehydrogenase level (LDH) (r=-0.419, r=-0.269), but with low blood platelet count in B-ALL (r=0.335). In T-ALL, expression of E-cadherin was found to be negatively correlated with LDH and percentage of immature cells in the bone marrow (r=-0.567, r=-0.557). In addition, the lower expression of E-cadherin was also found to be related with WBC count and percentage of immature cells in the bone marrow in newly diagnosed AML patients (r=-0.368, r=-0.391). Compared with control group, the expression of E-cadherin was down-regulated significantly (P<0.01), while β-catenin, Akt significantly was up-regulated in 3 types of AL patients (P<0.01). The expression of p-Akt and p-Akt/Akt was up-regulated significantly in T-ALL (P<0.01).@*CONCLUSION@#Lower expression of E-cadherin is related factor of unfavourable prognosis in children with acute leukemia. The expression deficiency or down-regulation of E-cadherin may activate Wnt/β-catenin and PI3K/ Akt signaling pathways to promote the genesis and progress of haematological malignancies, thus resulting in a series of malignant biological behaviors in cells. E-cadherin may be a new prognostic indicator for pediatric acute leukemia, thus to guide individualized hemotherapy.

Current Situation, Insufficiency and Countermeasures of Performance Allocation Model for Clinicians in China / 中国医院管理

The scientific construction and optimization of performance assessment of physicians,focusing on technical services reflecting the value of the medical staff,and paying attention to the connotation of medical services have important significance for effectively mobilizing the enthusiasm for work,and improving public hospital operation efficiency and management level.Through extensive literature research,the paper systematically analyzes the current situation and existing problems of the performance allocation model of public hospitals in China,and puts forward some corresponding suggestions and countermeasures according to the main existing problems.

Expression of β-integrin family members in children with T-cell acute lymphoblastic leukemia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the expression of β-integrin family members in children with T-cell acute lymphoblastic leukemia (T-ALL) and their significance.</p><p><b>METHODS</b>Quantitative real-time PCR analyses were performed to assess the expression levels of β-integrin family members in bone marrow samples from 22 children with newly-diagnosed T-ALL and 21 controls (16 children with non-malignant hematologic disease and 5 healthy donors with bone marrow transplantation). Jurkat cells were treated with integrin inhibitor arginine-glycine-aspartate (Arg-Gly-Asp, RGD) peptide. The cell viability and apoptosis rate were determined by CCK8 assay and flow cytometry respectively.</p><p><b>RESULTS</b>The mRNA levels of integrins β, β, and βwere significantly lower in children with T-ALL than in controls (P<0.05). In T-ALL patients, high integrin βexpression was associated with lower white blood cell counts (<100×10/L), minimal residual disease (MRD) positivity, and day 33 bone marrow negative remission (P<0.05). In T-ALL patients, higher integrin βexpression was associated with relapse of T-ALL (P<0.05). Based on survival curve analysis, higher integrin βexpression was related to lower event-free survival and overall survival rates. RGD peptide treatment inhibited the proliferation of Jurkat cells and increased their apoptosis rate (P<0.05).</p><p><b>CONCLUSIONS</b>β-Integrin may play a role in the occurrence and development of T-ALL by affecting cell proliferation and apoptosis. The expression of integrin β5 is closely related to the risk of relapse of T-ALL. The expression of integrin β3 is closely related the treatment response and prognosis of T-ALL.</p>

Effects of long-term swimming exercise on iron status of rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the effects of different periods of exercise on the iron status.</p><p><b>METHODS</b>Female rats were randomly divided into 3-, 6-, 12-month swimming exercise groups and their corresponding sedentary groups. The hematological indices of iron status and the non-heme iron (NHI) and total NHI (TNHI) of the organs were determined at the end of the desired period.</p><p><b>RESULTS</b>As compared with the corresponding sedentary groups, plasma iron and transferrin-iron saturation of three exercise groups were decreased without significant changes of blood hemoglobin and hematocrit. The NHI contents and TNHI of the liver, spleen and kidney were decreased. Although the NHI contents of the heart decreased, TNHI was not significantly changed. TNHI of the organs in both the exercised and sedentary rats were found to increase with age.</p><p><b>CONCLUSION</b>The exercise-induced low iron status with depleted iron storage is similar to the iron-deficiency status, but it could not be explained using the hypothesis of iron deficiency. Both the NHI redistribution and the maintained iron storage suggests the adaptation of low iron status to exercise. Therefore, the so-called exercise-induced iron deficiency could not exist.</p>