Bmi-1 as A Molecular Marker for Prognosis of Pediatric ALL / 中国实验血液学杂志

OBJECTIVE@#To study whether the Bmi-1 gene can be a biomarker for analysis of clinical risk stratification and prognosis of ALL patients.@*METHODS@#The expression level of Bmi-1 gene in bone marrow samples from 127 cases of newly diagnosed ALL was detected by qRT-PCR, at the same time the expression level of Bmi-1 protein in bone marrow samples from above-mentioned cases was detected by Western blot. The collected samples were divided into 3 groups: high, intermediate and low risk according to clinical risk stratfication, the relationship between Bmi-1 expression and risk grade of ALL patients was analyzed; at the same time the collected samples were divided into 2 groups: prednisone good response (PGR) and prednisone poor respouse (PPR) according to the sensitivity of prednison test, and the sensitivily to prednisone in 2 groups was compared; moreover, the collected samples were divided into 2 groups: high level and low level according to median of Bmi-1 level, and the relation of Bmi-1 level with prognosis of patients was analyzed by using the Kaplan-Meier method.@*RESULTS@#The expression level of Bmi-1 in low risk group was lowest, while that in high risk group was highest, however that in intermediat risk group was between the low and high risk groups, statistical analysis showed significant difference (P＜0.05). The expression level of Bmi-1 in PPR group was significantly higher than that in PGR group (P＜0.001). The Kaplan-Meier analysis showed that the RFS rate in Bmi-1 high expression group was significantly lower than that in Bmi-1 low expression group (73.0% vs 90.6%) (P＜0.001).@*CONCLUSION@#The Bmi-1 can be used as a molecular marker for the analysis of chinical risk and prognosis of pediatric ALL.

Down-Regulation of MiR-125b Reverses Drug Resistance of Doxorubicin-Resistant Leukemia Cells / 中国实验血液学杂志

OBJECTIVE@#To investigate whether the down-regulation of miR-125b can reverse the drug-resistence of doxorubicine-resistant leukemia cell lines or not, so as to explore a new method for treatment of drug-resistant leukemia patients.@*METHODS@#The expression levels of miR125b in doxorubicine drug-sensitive and doxorubicine drug-resistant leukemia cell lines.HL-60, K562 and HL-60/Dox, the K562/Dox were detected by using RT-qPCR; the up-regulation or inhibition of miR-1256 expression in HL-60/Dox were performed by electroporation transfection, then the viability of cells treated with doxorubicine of different concentration was detected by CCK-8 method, the proliferation inhibition curve of cells was drawed, and the IC was calculated.@*RESULTS@#The miR-125b expression was obviously up-regulated in drug-resistant cell lines HL-60/DOX and K562/DOX, as compared with HL-60 and K562 cell lines. The miR-125b expression level in HL-60/DOX and K562/DOX cells was 15 times and 5 times higher than that in HL-60 and K562 cells, respectively. The up-regulating or inhibiting expression of miR-125b in HL-60/DOX cells found that the proliferation inhibition rate in cells transfected with miR-125b mimic significantly decreased, compared with control group (P<0.01), while the proliferation inhibition rate in cells transfected with miR-125b inhibitor significantly increased, compared with control group(P<0.01).@*CONCLUSION@#The miR-125b expression in HL-60/Dox and K562/Dox cells has been up-regulated, down-regulation of miR-125b expression can reverse the drug resistance of leukemia cells to doxorubicine.

Research progress in interactions between neuron and satellite glial cells / 中国药理学通报

Recent studies suggest that glial cells play an impor-tant role in nervous system. Like astrocytes in the central nervous system,satellite glial cells( SGCs) also participate in the physio-logical and pathological processes of the peripheral nervous sys-tem. SGCs affect neuronal functions through neuro-glial interac-tions. In this review,we summarize the current understanding of how SGCs affect the function of neurons.

Changes in main causes of death in Macao residents from 1986 - 2006 / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Since Macao's return of sovereignty to China in December 1999, the life style of Macao residents has changed. The aim of this study was to investigate changes of death patterns in Macao residents from 1986 to 2006 in order to identify the trends and patterns of major public health problems, which could provide the guidance for developing public health policies.</p><p><b>METHODS</b>A retrospective study was conducted for this investigation. Research data were collected from official websites and statistical yearbooks and classified by the International Classification of Diseases (ICD)-9.</p><p><b>RESULTS</b>It was observed that mortality from the three major causes of (1) infectious, maternal and childhood diseases, (2) chronic non-communicable diseases, and (3) injury and poisoning were 17.7, 298.2 and 26.0 per 100 000, respectively. The largest decrease in death rate over the 21-year study-period was from infectious, maternal and childhood diseases (62.5%). The highest mortality rate was ischemic heart diseases (37.0%). The largest increase in mortality rate was lung cancer (46.9%).</p><p><b>CONCLUSIONS</b>Mortality rate of Macao residents progressively decreased, but the constituent ratio of death from chronic non-communicable diseases was increasing. The mortality rate of lung cancer was clearly ascending, so emphasis should be put on tertiary prevention in future.</p>

Repressing malic enzyme 1 redirects glucose metabolism, unbalances the redox state, and attenuates migratory and invasive abilities in nasopharyngeal carcinoma cell lines / 癌症

A large amount of nicotinamide adenine dinucleotide phosphate (NADPH) is required for fatty acid synthesis and maintenance of the redox state in cancer cells. Malic enzyme 1(ME1)-dependent NADPH production is one of the three pathways that contribute to the formation of the cytosolic NADPH pool. ME1 is generally considered to be overexpressed in cancer cells to meet the high demand for increased de novo fatty acid synthesis. In the present study, we found that glucose induced higher ME1 activity and that repressing ME1 had a profound impact on glucose metabolism of nasopharyngeal carcinoma(NPC) cells. High incorporation of glucose and an enhancement of the pentose phosphate pathway were observed in ME1-repressed cells. However, there were no obvious changes in the other two pathways for glucose metabolism: glycolysis and oxidative phosphorylation. Interestingly, NADPH was decreased under low-glucose condition in ME1-repressed cells relative to wild-type cells, whereas no significant difference was observed under high-glucose condition. ME1-repressed cells had significantly decreased tolerance to low-glucose condition. Moreover, NADPH produced by ME1 was not only important for fatty acid synthesis but also essential for maintenance of the intracellular redox state and the protection of cells from oxidative stress. Furthermore, diminished migration and invasion were observed in ME1-repressed cells due to a reduced level of Snail protein. Collectively, these results suggest an essential role for ME1 in the production of cytosolic NADPH and maintenance of migratory and invasive abilities of NPC cells.