First Hospital of Baoding

Baoding, China

First Hospital of Baoding

Baoding, China
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Wang S.-Y.,Hebei General Hospital | Hao H.-L.,Hebei General Hospital | Li Y.,Hebei General Hospital | Cheng Z.-Y.,First Hospital of Baoding | And 5 more authors.
Leukemia and Lymphoma | Year: 2012

We explored the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and focal adhesion kinase (FAK) mRNA and protein, and analyzed the relationship between expression levels and clinical staging and extramedullary infiltration in patients with multiple myeloma (MM). The expression levels of mRNA and protein were measured by fluorescence quantitative polymerase chain reaction (FQ-PCR) and Western blotting. Expressions of PTEN and FAK mRNA were significantly different between patients with MM and controls. Spearman bivariate correlation analysis showed that PTEN mRNA was significantly negatively correlated with FAK mRNA. PTEN and FAK mRNA expressions were significantly different between patients with stage I II MM and stage III MM. No difference was found in PTEN mRNA expression, whereas FAK mRNA expression was significantly different between patients with MM with and without extramedullary infiltration. PTEN protein was higher and total FAK (T-FAK) protein was significantly lower in six controls than in 12 patients with stage III MM. Phosphorylated FAK (p-FAK) protein was measured as 0.082 ± 0.040 in 11 patients with MM, but not detected in six controls. No significant difference of PTEN and T-FAK protein was found, while p-FAK protein was significantly different between patients with MM with and without extramedullary infiltration. These results indicate that abnormal expression of PTEN and FAK in patients with MM may be associated with disease progression and extramedullary infiltration. © 2012 Informa UK, Ltd.


PubMed | Baoding University, First Hospital of Baoding and The Peoples Liberation Army 252 Hospital
Type: Journal Article | Journal: Asian Pacific journal of tropical medicine | Year: 2014

To observe the regulatory impact of immune inhibitors on T cells in rats.Forty SD rats were selected and randomly divided into experimental group and control group, Rapamycin (SRL) 0.4 mg/d to fill the stomach of the former one, saline lavage was used with the latter one for two weeks. Using flow cytometry to detect the two groups of rats with spleen and thymus level of CD4+ CD25+ T cells; and the spleen cells FoxP3 mRNA expression; Using ELISA method to detect TGF-, IL-10 levels.The peripheral blood, spleen and thymus of CD4+ CD25+ T cells accounted for the proportion of mononuclear cells were significantly higher than that of control group (P<0.05); FoxP3 mRNA expression quantity also significantly higher than the control group (P<0.05); Experimental TGF- in rats, IL-10 levels are significantly higher than control group (P<0.05).Immune inhibitors can regulatory CD4+ CD25+ foxp3+ T cells in rats, a single nuclear cell proportion increase, shows that it can induce rat CD4+ CD25+ foxp3+ regulatory T cells proliferation.


Jianzhu F.,Chengde Medical College | Qian X.,Chengde Medical College | Yaling Z.,Chengde Medical College | Guimin L.,Chengde Medical College | And 4 more authors.
National Medical Journal of China | Year: 2015

Objective To research the suppressive effect of interferon α2b (IFN-α2h) on angiog;enesis of JAK2 tyrosine kinase gene point mutation (JAK2V617F) positive myeloproliferative neoplasm (MPN) and its anli-angiogenic mechanisms. Methods (1) A total of 42 cases of JAK2V617F positive MPN patients in the No. 1 Hospital ol Baoding were selected between January 2012 and October 2014, including the newly diagnosed group before treatment (n =25) and the IFN-α2b treatment group (:i = 17). Ten cases of idiopathic immune thrombocytopenic purpura (ITP) patients were enrolled as conlrols. JAK2V6I7F/.|Ak2 ratio was detected by real-time fluorescent quantitative PGR to measure mutation; the expression levels of phospliorvlated JAK2 (p-,JNK2), vascular eudolltelial growth (actor (VEGF), h\poxia-inducible Factor-la (HIF-lα) and CDI05 marked microvascular density (MVI)) in hone marrow were delected by immunohislochemistrv. The correlations were analyzed among.1AK2V61 7F mutation burden and VEGF, HIF-lα. and MVD. (2) Human erythroleukemia cell line HEL cells were treated with dillereiil concentrations of IFiN-α2b. The apoptosis was detected by lloechst staining method. The cell viability was delected bv CCk-8 test. Cell migration ability was leslcd by trauswell chambers. The protein expression levels of p-JAK2, VFCF, and HIF-la were delected by Western blot. Results (1)Tlie ratio of J AK2V6I7F/.JAK2 in the IFN-α2b treatment group (22. 69% ± 12.64%) was significantly lower ihan that in Ihe newly diagnosed group (46. 17% ± 19. 32%) (p<0.01). The expression levels of p-JAK2, VEGF, and HIF-la in the newly diagnosed group (82. 41% ± 11. 65%, 64. 72% ±25. 01%, 45. 12% ±20. 28%) were significantly higher than those in the IFN-α2b treatment group (60.93% ± 20.57%, 36.58% ± 15.95%, 32. 15% ± 14.27%) and the control group (43.05% ± 12.59%, 25.69% ± 13.75%. 25.07% ± 15. 49%) (all p<0. 01). MVI) in the newly diagnosed group (26. 58% ±5. 93%) was significantIv higher than that in the treatment group (15.86% ±4.27%) and the control group (10.76% ±4. 01%) (P < 0.01). Spearman correlation analysis showed positiw correlation ol JAK2V6I7F mutation with VEGF and MVI) (r =0.589, P < 0. 05; r =0.511, P < 0. 05). (2) The apoptosis of HEI. cells were increased aller treated with 30 000 171. of IFN-α2b in HEL cells after 24 h. The proliferation of HEL cell were inhibited by different concentrations of IFN-α2b in time- and dose-dependenl manner. The number ol membrane-permeating HEL cells after treated with 5 000 L/L of IFN-α2b in HEL cells after 24 h was significantly lower Ihan that in the untreated cells (52. 9 ± 7. 5 vs 77. 3 ± 6. 1) (P < 0. 05). The expression levels of p-.l AK2, VEGF, and HIF-la were decreased in a dose-dependent manner. Conclusion IFM-a2b may exert an anti-angiogenic effect by inhibiting the VEGF, HIF-la, and MVI) expression iti MPN via.IAK2 signal pathway.


Fu J.,Chengde Medical College | Xu Q.,Chengde Medical College | Zhao Y.,Chengde Medical College | Liu G.,Chengde Medical College | And 4 more authors.
Zhonghua yi xue za zhi | Year: 2015

OBJECTIVE: To research the suppressive effect of interferon α2b (IFN-α2b) on angiogenesis of JAK2 tyrosine kinase gene point mutation (JAK2V617F) positive myeloproliferative neoplasm (MPN) and its anti-angiogenic mechanisms.METHODS: (1) A total of 42 cases of JAK2V617F positive MPN patients in the No.1 Hospital of Baoding were selected between January 2012 and October 2014, including the newly diagnosed group before treatment (n=25) and the IFN-α2b treatment group (n=17). Ten cases of idiopathic immune thrombocytopenic purpura (ITP) patients were enrolled as controls. JAK2V617F/JAK2 ratio was detected by real-time fluorescent quantitative PCR to measure mutation; the expression levels of phosphorylated JAK2 (p-JAK2), vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1α (HIF-1α) and CD105 marked microvascular density (MVD) in bone marrow were detected by immunohistochemistry. The correlations were analyzed among JAK2V617F mutation burden and VEGF, HIF-1α, and MVD. (2) Human erythroleukemia cell line HEL cells were treated with different concentrations of IFN-α2b. The apoptosis was detected by Hoechst staining method. The cell viability was detected by CCK-8 test. Cell migration ability was tested by transwell chambers. The protein expression levels of p-JAK2, VEGF, and HIF-1α were detected by Western blot.RESULTS: (1)The ratio of JAK2V617F/JAK2 in the IFN-α2b treatment group (22.69% ± 12.64%) was significantly lower than that in the newly diagnosed group (46.17% ± 19.32%) (P<0.01). The expression levels of p-JAK2, VEGF, and HIF-1α in the newly diagnosed group (82.41% ± 11.65%, 64.72% ± 25.01%, 45.12% ± 20.28%) were significantly higher than those in the IFN-α2b treatment group (60.93% ± 20.57%, 36.58% ± 15.95%, 32.15% ± 14.27%) and the control group (43.05% ± 12.59%, 25.69%± 1 3.75%, 25.07% ± 15.49%) (all P<0.01). MVD in the newly diagnosed group (26.58% ± 5.93%) was significantly higher than that in the treatment group (15.86%± 4.27%) and the control group (10.76% ± 4.01%) (P<0.01). Spearman correlation analysis showed positive correlation of JAK2V617F mutation with VEGF and MVD (r=0.589, P<0.05; r=0.577, P<0.05). (2)The apoptosis of HEL cells were increased after treated with 30 000 U/L of IFN-α2b in HEL cells after 24 h. The proliferation of HEL cell were inhibited by different concentrations of IFN-α2b in time- and dose-dependent manner. The number of membrane-permeating HEL cells after treated with 5 000 U/L of IFN-α2b in HEL cells after 24 h was significantly lower than that in the untreated cells (52.9 ± 7.5 vs 77.3 ± 6.1) (P<0.05). The expression levels of p-JAK2, VEGF, and HIF-1α were decreased in a dose-dependent manner.CONCLUSION: IFN-α2b may exert an anti-angiogenic effect by inhibiting the VEGF, HIF-1α, and MVD expression in MPN via JAK2 signal pathway.


PubMed | First Hospital of Baoding and Chengde Medical College
Type: Journal Article | Journal: Zhonghua yi xue za zhi | Year: 2016

To research the suppressive effect of interferon 2b (IFN-2b) on angiogenesis of JAK2 tyrosine kinase gene point mutation (JAK2V617F) positive myeloproliferative neoplasm (MPN) and its anti-angiogenic mechanisms.(1) A total of 42 cases of JAK2V617F positive MPN patients in the No.1 Hospital of Baoding were selected between January 2012 and October 2014, including the newly diagnosed group before treatment (n=25) and the IFN-2b treatment group (n=17). Ten cases of idiopathic immune thrombocytopenic purpura (ITP) patients were enrolled as controls. JAK2V617F/JAK2 ratio was detected by real-time fluorescent quantitative PCR to measure mutation; the expression levels of phosphorylated JAK2 (p-JAK2), vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1 (HIF-1) and CD105 marked microvascular density (MVD) in bone marrow were detected by immunohistochemistry. The correlations were analyzed among JAK2V617F mutation burden and VEGF, HIF-1, and MVD. (2) Human erythroleukemia cell line HEL cells were treated with different concentrations of IFN-2b. The apoptosis was detected by Hoechst staining method. The cell viability was detected by CCK-8 test. Cell migration ability was tested by transwell chambers. The protein expression levels of p-JAK2, VEGF, and HIF-1 were detected by Western blot.(1)The ratio of JAK2V617F/JAK2 in the IFN-2b treatment group (22.69% 12.64%) was significantly lower than that in the newly diagnosed group (46.17% 19.32%) (P<0.01). The expression levels of p-JAK2, VEGF, and HIF-1 in the newly diagnosed group (82.41% 11.65%, 64.72% 25.01%, 45.12% 20.28%) were significantly higher than those in the IFN-2b treatment group (60.93% 20.57%, 36.58% 15.95%, 32.15% 14.27%) and the control group (43.05% 12.59%, 25.69% 1 3.75%, 25.07% 15.49%) (all P<0.01). MVD in the newly diagnosed group (26.58% 5.93%) was significantly higher than that in the treatment group (15.86% 4.27%) and the control group (10.76% 4.01%) (P<0.01). Spearman correlation analysis showed positive correlation of JAK2V617F mutation with VEGF and MVD (r=0.589, P<0.05; r=0.577, P<0.05). (2)The apoptosis of HEL cells were increased after treated with 30 000 U/L of IFN-2b in HEL cells after 24 h. The proliferation of HEL cell were inhibited by different concentrations of IFN-2b in time- and dose-dependent manner. The number of membrane-permeating HEL cells after treated with 5 000 U/L of IFN-2b in HEL cells after 24 h was significantly lower than that in the untreated cells (52.9 7.5 vs 77.3 6.1) (P<0.05). The expression levels of p-JAK2, VEGF, and HIF-1 were decreased in a dose-dependent manner.IFN-2b may exert an anti-angiogenic effect by inhibiting the VEGF, HIF-1, and MVD expression in MPN via JAK2 signal pathway.


Zhang C.-H.,First Hospital of Baoding | Zhang C.-H.,Hebei University | Huang Y.,First Hospital of Baoding | Han G.,Peoples Liberation Army 252 Hospital
Asian Pacific Journal of Tropical Medicine | Year: 2014

Objective: To observe the regulatory impact of immune inhibitors on T cells in rats. Method: Forty SD rats were selected and randomly divided into experimental group and control group, Rapamycin (SRL) 0.4 mg/d to fill the stomach of the former one, saline lavage was used with the latter one for two weeks. Using flow cytometry to detect the two groups of rats with spleen and thymus level of CD4+ CD25+ T cells; and the spleen cells FoxP3 mRNA expression; Using ELISA method to detect TGF-β, IL-10 levels. Results: The peripheral blood, spleen and thymus of CD4+ CD25+ T cells accounted for the proportion of mononuclear cells were significantly higher than that of control group (P<0.05); FoxP3 mRNA expression quantity also significantly higher than the control group (P<0.05); Experimental TGF-β in rats, IL-10 levels are significantly higher than control group (P<0.05). Conclusions: Immune inhibitors can regulatory CD4+ CD25+ foxp3+ T cells in rats, a single nuclear cell proportion increase, shows that it can induce rat CD4+ CD25+ foxp3+ regulatory T cells proliferation. © 2014 Hainan Medical College.


Zhiyong C.,First Hospital of Baoding | Wentong L.,First Hospital of Baoding | Xiaoyang Y.,Affiliated Haikou Hospital | Ling P.,University of Sichuan
Medical Oncology | Year: 2012

Phosphatase and tensin homolog (PTEN) acts as a novel tumor suppressor gene. PTEN protein plays an important role in regulating proliferation, apoptosis, invasion, and migration of many cancer cells. PTEN also modulates angiogenesis mediated by vascular endothelial growth factor (VEGF) via down-regulating PI3K/Akt pathway in many solid tumors. However, the effects of PTEN on VEGF and VEGFR1 (FLT1)-mediated angiogenesis, migration, invasion of leukemia cells, and its clinical significance are still unknown in myeloid leukemia. Therefore, we investigated the effect of PTEN on PI3K/Akt and VEGF/FLT1 pathways by transfecting wildtype PTEN gene to induce high expression of wild-type PTEN gene and protein in chronic myelogenous leukemia cell line K562 cells. We also observed the correlation between the expression levels of PTEN and VEGF/FLT1 and its clinical significance in myeloid leukemia patients. We found that the expression reconstitution of wild-type PTEN had significant effect on inhibiting proliferation, migration, and invasion abilities of K562 cells via downregulation of Akt phosphorylation and inhibition of VEGF/FLT1 expression. In myeloid leukemia patients, a negative correlation was found between the expression level of PTEN mRNA and that of VEGF and FLT1 mRNA. Downregulation of PTEN expression accompanied by up-regulation of VEGF and FLT1 mRNA indicated a higher tendency of extramedullary disease in acute myeloid leukemia patients. In conclusion, PTEN could modulate the function of VEGF/VEGFR signaling pathway down-regulation of Akt phosphorylation and that PTEN would be a candidate target to be addressed for inhibiting angiogenesis along with the treatment of myeloid leukemia. © Springer Science+Business Media, LLC 2011.


Liang W.T.,First Hospital of Baoding
Sheng li ke xue jin zhan [Progress in physiology] | Year: 2011

Invasion and metastasis are both the main biological characteristics in malignant tumor which are influence tumor therapeutic effect and prognosis. The tumor cells interact with vascular endothelial cells and cell matrix, penetrate vascular endothelial and degrade the extracellular matrix, and metastasis to the local and distant by the interactions of a variety of signaling molecules. PTEN protein has protein phosphatase and lipid phosphatase dual activity which is produced by PTEN gene. As a tumor suppressor gene, regulates the cell signal pathways to sustain the normal physiological functions, negatively regulates of tumor cell growth and cell cycle, induces apoptosis, and inhibits invasion, infiltrating and metastasis of tumor cells. This article is reviewed about how PTEN participates in inhibiting tumor cell invasion and metastasis.


Cheng Z.Y.,First Hospital of Baoding
Zhonghua yi xue za zhi | Year: 2011

To explore the effects of tumor-suppressing gene wild type PTEN on the cell proliferation, apoptosis and the possible regulations of apoptosis-related molecules Survivin, Xiap and Smac gene in human chronic myeloid leukemia (CML) and cell line K562 cells. (1) The recombinant adenovirus containing green fluorescent protein (GFP) and PTEN (Ad-PTEN-GFP) or empty vector (Ad-GFP) was transfected into K562 cells. The growth of K562 cells was observed by MTT assay while cell cycle and apoptotic rate were assessed by flow cytometry (FCM). PTEN, Survivin, Xiap and Smac mRNA levels were detected by real-time fluorescent relative-quantification reverse transcriptional PCR (FQ-PCR) while PTEN protein levels analyzed by Western blot. (2) The expression levels of PTEN, Survivin, Xiap and Smac mRNA were detected in 10 chronic myelogenous leukemia (CML) patients in chronic phase (CML-CP), 10 CML patients in blast crises (CML-BC) and 10 normal control marrow mononuclear cells (MMNC). The growth of K562 cells was suppressed markedly. And the maximal growth inhibition rate was 38.6% after the transfection of PTEN. Survivin, Xiap, Smac mRNA expression levels were down-regulated by around 6.14, 7.44 and 2.95 folds respectively (0.0700 ± 0.0059, 0.0089 ± 0.0006, 0.0600 ± 0.0039 vs 0.4370 ± 0.0790, 0.0661 ± 0.0072, 0.1580 ± 0.0078 vs 0.4530 ± 0.0810, 0.0700 ± 0.0079, 0.1770 ± 0.0085, all P < 0.01). The mRNA expression level of PTEN in CML-BC patients was lower than that in CML-CP patients and normal control. But Survivin, Xiap, Smac mRNA expression levels were higher in CML-BC patients than those in CML-CP and normal control. The over-expression of PTEN gene may inhibit the proliferation of K562 cells and promote cell apoptosis via the regulation of Survivin, Xiap and Smac genes.


PubMed | First Hospital of Baoding
Type: Journal Article | Journal: Sheng li ke xue jin zhan [Progress in physiology] | Year: 2011

Invasion and metastasis are both the main biological characteristics in malignant tumor which are influence tumor therapeutic effect and prognosis. The tumor cells interact with vascular endothelial cells and cell matrix, penetrate vascular endothelial and degrade the extracellular matrix, and metastasis to the local and distant by the interactions of a variety of signaling molecules. PTEN protein has protein phosphatase and lipid phosphatase dual activity which is produced by PTEN gene. As a tumor suppressor gene, regulates the cell signal pathways to sustain the normal physiological functions, negatively regulates of tumor cell growth and cell cycle, induces apoptosis, and inhibits invasion, infiltrating and metastasis of tumor cells. This article is reviewed about how PTEN participates in inhibiting tumor cell invasion and metastasis.

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