Effect of Highvolume Platelet Reduction Therapy on White Blood Cell Count and Hemoglobin Level in Patients with Thrombocytosis / 中国实验血液学杂志

OBJECTIVE@#To explore the effect of high volume platelet reduction therapy on the white blood cell (WBC) count and hemoglobin (Hb) level in patients with thrombocytosis.@*METHODS@#Thirty-two plateletphoreses were performed for patients with thromocytosis by using ELP or MNC program of blood component isolator of COBE spectra continuous flow concentrifugation and the ACD-A preservation solution for blood as blood anticoagulant. In each treatment of patients, 2.5-3.0 tines total blood volume (TBV) were circulated, then the platelet suspension of 1/5-1/4 time TBV was prepared and collected.@*RESULTS@#A single plateletpheresis took (212.53±41.54) minutes in which (8 812.63±2087.15) ml blood were treated, and (798.84±190.77) ml platelet suspension was collected. In the suspension, the platelet count was 4 486.50 (3 058.50-5 279.50)×10/L, containing 3 455.50 (2 288.68-4 226.71)×10. WBC count was 13.79 (10.21-20.72)×10/L, containing 11.90(7.81-14.40)×10. Hemoglobin concentration was (3.28±1.25) g/L，containing (2.62 ± 1.17) g. Before and after plateletpheresis, the patients' platelet count was 1 263.00 (1 052.50-1 807.50)×10/L and (778.83±247.25)×10/L（Z=4.94, P＜0.01), WBC count was 9.96(6.44-14.01)×10/L and 8.59(5.37, 13.12)×10/L (Z=13.31, P＜0.05), Hemoglobin concentration was (112.63 ± 24.56)g/L and (109.55 ± 24.46)g/L (t=1.68，P＞0.05).@*CONCLUSION@#Using continuous flow centrifugation and blood component separating in plateletpheresis for the patients with thrombocytosis can obviously decrease the high ratio of platelets, and improve the effect of plateletpheresis. The high volume platelet reduction therapy can lead to decrease of WBC count to some alent, degree but WBC count still in the normal range, moreover not affect the hemoglobin level significantly.

Effect of Licofelone on Expression of Fractalkine Induced by Interleukin-18 in Mesangial Cells / 实用儿科临床杂志

Objective To study the effect of Licofelone,a novel non-steroid anti-inflammatory drug,on the expression of Fractalkine induced by interleukin-18(IL-18) in mesangial cells.Methods Rat mesangial cells were cultured and divided into IL-18 stimulated group,Licofelone-treated group and normal control group.The cells in IL-18 stimulated group were stimulated by 10 ?g/L IL-18 for 24 h.In Licofelone-treated group,ahead of exposure of IL-18 for 24 h,cells were treated with Licofelone in the doses of 10,50 and 100 ?mol/L for 30 min.Additionally,the mesangial cells without treatment of IL-18 and Licofelone were used as normal control group.Reverse transcription-polymerase chain reaction(RT-PCR) was used to measure the level of Fractalkine mRNA.The expressions of Fractalkine protein in every group were detected with enzyme linked immunosorbent assay (ELISA).Results In normal control group,the expression level of Fractalkine mRNA was 179.0?21.0.After exposure of IL-18 for 24 h,the level of Fractalkine mRNA was 1 220.1?185.7,which was higher than that in normal control group (t=9.646 P

Transfection of Lipoxin A4 receptor-like protein gene enhanced the inhibitory effect of Lipoxin A4 on human lung fibroblasts proliferation induced by connective tissue growth factor / 中华儿科杂志

<p><b>OBJECTIVE</b>Lipoxin A(4) is formed by the metabolism of arachidonic acid. Anti-inflammatory and anti-proliferative effect of lipoxin A(4) has been shown in many human diseases. Recently, as a novel high affinity receptor for ligand lipoxin A(4), Lipoxin A(4) receptor-like protein (LRLP) has been identified. Currently close attention is paid to the important contribution of connective tissue growth factor (CTGF) in lung fibrosis. The purpose of the study was to transfect LRLP gene into human lung fibroblasts and investigate the mechanism of its enhancing antagonistic effect of Lipoxin A(4) on human lung fibroblasts proliferation induced by connective tissue growth factor.</p><p><b>METHODS</b>Eukaryocytic expression vector pEGFP/LRLP which contained LRLP and green fluorescence protein fusion gene (GFP) was constructed and transfected into human lung fibroblasts (HLF). After selecting with G418, HLF/LRLP cell clone which stably expressed LRLP/GFP fusion protein was isolated and characterized by the laser scanning confocal microscope. Cultured HLF and HLF/LRLP were stimulated for 24 h with CTGF (1 microg/ml) in the presence and absence of pretreatment of Lipoxin A(4) (10.0 nmol/L) for 30 min. Inhibition of cell proliferation was determined by MTT assay. Cell cycle analysis was performed by flow cytometry. Western blot was used to detect the expression of cyclin D(1) protein. Electrophoretic mobility shift assay (EMSA) was employed to detect the DNA binding activity of STAT(3).</p><p><b>RESULTS</b>(1) HLF/LRLP cell clone which stably expressed LRLP and GFP fusion protein was successfully obtained. (2) Proliferation of HLF and HLF/LRLP was induced by 1 microg/ml CTGF. Pretreatment with 10 nm Lipoxin A(4) inhibited the proliferation of HLF and HLF/LRLP. And the inhibitory rate of HLF/LRLP was significantly higher than that of HLF [(54.1 +/- 4.2)%, (21.2 +/- 3.7)%, P < 0.05]. (3) The flow cytometry analysis showed that compared with HLF, more HLF/LRLP were arrested at G(0)/G(1) phase in the presence of pretreatment of Lipoxin A(4). [(76.3 +/- 3.5)%, (60.8 +/- 2.0)%, P < 0.05]. (4) Ten nmol/L Lipoxin A(4) antagonized CTGF induced increase of cyclin D(1) protein expression in HLF and HLF/LRLP. And its antagonistic effect on HLR/LRLP was stronger than that on HLF (P < 0.05). (5) Ten nmol/L Lipoxin A(4) antagonized CTGF induced increase of STAT(3) DNA binding activity, and its antagonistic effect on HLF/LRLP was more powerful than that on HLF (P < 0.05).</p><p><b>CONCLUSIONS</b>Transfection of Lipoxin A(4) receptor-like protein gene enhanced the inhibitory effect of Lipoxin A(4) on human lung fibroblasts proliferation induced by CTGF. Its mechanism might be related to regulation of cyclin D(1) protein expression and STAT(3) DNA binding activity.</p>

Induction of monocyte chemoattractant protein-1 expression in human mesangial cells by angiotensin II: role of c-Jun N-terminal kinase-c-Jun/activator protein-1 signal pathway / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the role of c-Jun N-terminal kinase (JNK)-c-Jun/activator protein-1 (AP-1) signal pathway in expression of monocyte chemoattractant protein-1 (MCP-1) in experimental rat glomerulonephritis.</p><p><b>METHODS</b>Nephrotoxic sera nephritis (NTN) was induced by injection of anti-GBM antibody into the tail veins of rats. Electrophoretic mobility shift assay (EMSA) and non-radioactive kinase assay were used to detect the activity of AP-1 and JNK in kidneys and angiotensin II-stimulated human mesangial cells. Ribonuclear protection assay was used to detect MCP-1 expression in cultured human mesangial cells.</p><p><b>RESULTS</b>Significant up-regulation of JNK and AP-1 was observed in NTN rats (3.82 +/- 0.58) folds and (5.36 +/- 0.61) folds, as compared with the controls. Supershift assay demonstrated that c-Jun and c-Fos were the predominant subunits involved. Activation of JNK and AP-1 significantly correlated with MCP-1 expression in NTN rats. Angiotensin II enhanced the expression of MCP-1 and activation of JNK and AP-1 in cultured human mesangial cells in a dose-dependent manner, with maximal stimulation seen at 100 nmol/L (20.99 +/- 4.71) folds, (6.91 +/- 1.65) folds and (7.82 +/- 1.32) folds respectively. Significant down-regulation of AP-1 activation and MCP-1 expression were observed in angiotensin II-induced human mesangial cells pretreated with JNK specific inhibitor SP600125.</p><p><b>CONCLUSIONS</b>Angiotensin II and MCP-1 may play an important role in glomerulosclerosis via the JNK-c-Jun/AP-1 signal pathway.</p>

Expression of monocyte chemoattractant protein-1 in experimental rat glomerulonephritis is mediated by NF-kappaB/IkappaB signal pathway / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the role of NF-kappaB/IkappaB signal pathway in mediating the expression of monocyte chemoattractant protein-1 (MCP-1) in experimental rat glomerulonephritis.</p><p><b>METHODS</b>Nephrotoxic serum nephritis (NTN) was induced by injection of anti-GBM antibody into the tail veins of rats. Electrophoretic mobility shift assay (EMSA) and Western Blot were used to detect the activation of NF-kappaB, nuclear translocation of p65 subunit and degradation of IkappaBalpha and IkappaBbeta in rat renal tissue. MCP-1 expression in glomeruli and renal tubules was also assessed by immunohistochemistry and ribonuclease protection assay. This was further correlated with the activation of NF-kappaB.</p><p><b>RESULTS</b>There was an obvious expression of MCP-1 in glomeruli and renal tubules. Significant up-regulation of NF-kappaB activation, nuclear translocation of p65 subunit, and degradation of IkappaBalpha and IkappaBbeta were also observed in NTN rat renal tissue, as compared to the control group. A positive correlation was noted between NF-kappaB activation and MCP-1 expression.</p><p><b>CONCLUSIONS</b>NF-kappaB/IkappaB signal pathway may play an important pathogenetic role in glomerulonephritis, with mediating the expression of MCP-1.</p>