1.Changes in serum PAI-1,TF and ATⅢ in severe limb injury and their relationship with complications
Jun LAI ; Xiankai HUANG ; Ning KANG ; Cheng PENG
Medical Journal of Chinese People's Liberation Army 1981;0(04):-
Objective To explore the changes in serum plasminogen activator inhibitor 1(PAI-1),tissue factor(TF) and antithrombin Ⅲ(ATⅢ) in early period of severe limb injury,and their relationship with the occurrence of traumatic pre-DIC and DIC after trauma.Methods Thirty-five patients were divided into severe injury group(AIS score ≥3,20 cases),minor injury group(15 cases),and 10 healthy subjects served as control.The 35 patients with injury were divided again into pre-DIC group(10 cases),DIC group(3 cases),and others(22 cases).Fasting peripheral venous blood was collected on day 1,3,6 from the patients and healthy subjects.The changes in TF,ATⅢ and PAI-1 levels were detected and statistically analyzed.Results The PAI-1 levels were higher in minor injury group and severe injury group than that in control group on day 1(P
2.Apoptotic mechanism of leukemic K562 cells induced by mangiferin
Zhigang PENG ; Jun LUO ; Yongrong LAI ; Shanjun SONG
Chinese Traditional and Herbal Drugs 1994;0(05):-
Objective To study the apoptosis mechanism of K562 cell lines induced by mangiferin. Methods The mRNA expression levels of apoptosis-related genes including bcl-2, bax, survivin of K562 cells treated by mangiferin (25—200 ?mol/L) for 24, 48, 72, and 96 h were determined by RT-PCR; the BCR/ABL protein P210 level was detected by Western blotting. Results Mangiferin up-regulated bax gene of K562 cells significantly and down-regulated bcl-2 gene slightly, resulting in an enhancement of the ratio of bax/bcl-2. Mangiferin down-regulated the expression levels of P210 in K562 cells in a time-and concentration-dependent manner and so is the expression level of survivin mRNA in K562 cells. ConclusionThe mechanism of mangiferin-induced apoptosis in K562 leukemic cells might be involved in up-regulating the gene expression of bax and down-regulating the mRNA expression of BCR/ABL protein P210, bcl-2, and survivin.
3.Clinical diagnosis and treatment and pathological analysis of 52 cases with gastrointestinal stromal tumors
Jun WANG ; Duanyi ZHAO ; Xianwen LUO ; Qijun YUE ; Lai WEI ; Lina PENG ; Hongbin SUN ; Zheng ZHANG
International Journal of Surgery 2009;36(11):736-738
Objective To investigate clinical manifestations and clinical diagnosis and treatment and pathological and immunohistochemical features in gastrointestinal stromal tumors. Methods The clinical data of fifty-two cases with gastrointestinal stromal tumors were collected, whose clinical diagnosis and treat-ment and pathological features were retrospectively analyzed from January 1995 to December 2007. Results All patients received operation therapy, only forty-five cases with complete surgical resection. The immu-nohistochemical staining showed that the cases with CD117 positive accounted for 100% (52/52) and CD34 positive accounted for 88.5% (46/52). Conclusions Surgery was necessary for all patients, especially complete surgical resection. Gastrointestinal stromal tumors were poor in preoperative diagnosis, which diag-nosis was based on the immunohistochemical staining of the tumor tissue. CD117 and CD34 tumor markers may help to diagnose gastrointestinal stromal tumors.
5.Effect of transplantation of umbilical cord blood mesenchymal stem cells on traumatic brain injury in rats
Peng ZHANG ; Lai-Jun SONG ; Bo YANG
Chinese Journal of Neuromedicine 2010;09(7):678-681
Objective To investigate the feasibility of human umbilical cord blood mesenchymal stem cells (CB-MSCs) in differentiating into neural-like cells and the effect of CB-MSC transplantation on traumatic brain injury in rats. Methods Healthy Wistar rats were induced into model with experimental traumatic brain injury by drilling and hitting their brain tissue, and then, they were randomized into 3 groups (n=18): model group, control group (injured models + injecting 1.25 μL saline) and CB-MSC transplantation group (injured model + injecting CB-MSC suspension). CB-MSC were derived from separated umbilical cord blood, cultured, marked with BrdU and injected into injured area of rats in the CB-MSC transplantation group. The motor function scale was performed 3 and 10 d after the transplantation, and Y maze test was employed to observe the rat's learning and memory abilities 2 and 4 w after the transplantation. CB-MSC in the CB-MSC transplantation group was detected by immunohistochemistry 2 and 5 w after the transplantation; BrdU-GFAP and BrdU-NSE positive cells were observed. Results Significant differences between the 3 groups were observed in motor function scores on the 10th day of transplantation and in rat's learning and memory abilities with Y maze test 2 and 4 w after the transplantation. BrdU-GFAP and BrdU-NSE positive cells were found in the area of transplantation in the CB-MSC transplantation group only by the end of 2 and 5 w after transplantation. Conclusion CB-MSC transplantation can help the recovery of brain injury in rats and improve the learning and memory abilities; CB-MSC transplanted into the rats' brain tissue can differentiate into neurons-like cell in vivo.
6.Microsurgical treatment of petroclival tumors
Peng ZHANG ; Bo YANG ; Lai-Jun SONG
Chinese Journal of Neuromedicine 2010;09(9):913-915
Objective To discuss the microsurgical treatment and outcome of tumors in the petroclival region. Methods A total of 48 patients with tumors in the petroclival region, had operation between Jan 2002 and Dec 2009, were chosen in the study; their data (their imaging, operation methods and complications) were retrospectively analyzed. Results Total resection of the tumors was achieved in 30 cases, subtotal resection in 11 and largely partial resection in 7. A 4-6-year follow up was performed on 46 patients; except 1 with permanent facial paralysis, the other patients got improvement to varying degrees. Conclusion Total resection rate of tumor in the petroclival region can be increased and complications and mortality can be decreased through full preparation of the operation, proper operation approaches and skillful manipulation of microneurosurgical technique.
7.Study on mismatch repair genes of chronic myeloid leukemia.
Jun LUO ; Zhi-gang PENG ; Yan CHEN ; Yong-rong LAI ; Yu-ying LU ; Shan-jun SONG
Chinese Journal of Hematology 2006;27(2):103-106
OBJECTIVETo investigate the expression and regulation mechanism of mismatch repair (MMR) genes in chronic myeloid leukemia (CML).
METHODSExpression of MMR genes hMSH2, hMSH3, hMSH6, hMLH1 and hPMS2 mRNAs in 62 CML patients and K562 cell line were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of bcr-abl mRNA and MMR genes mRNA were detected by RT-PCR in 26 CML patients with allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and 4 CML patients on imatinib treatment. Expression of bcr-abl mRNA was detected by RT-PCR and tyrosine phosphorylation of BCR-ABL fusion protein by Western blot.
RESULTSExpression of hMSH2, hMSH3 and hMLH1 mRNA was significantly lower in CML and K562 cells than in normal control (P < 0.05). In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased. In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.
CONCLUSIONExpressions of hMSH2, hMSH3 and hMLH1 mRNA were down-regulated by bcr-abl fusion gene.
Adult ; Aged ; Antineoplastic Agents ; pharmacology ; Benzamides ; DNA Mismatch Repair ; Female ; Fusion Proteins, bcr-abl ; genetics ; metabolism ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Humans ; Imatinib Mesylate ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Male ; Middle Aged ; Piperazines ; pharmacology ; Pyrimidines ; pharmacology ; RNA, Messenger ; genetics ; Reverse Transcriptase Polymerase Chain Reaction
8.Gene of DNA-dependent protein kinase catalylic subunit in chronic myeloid leukemia.
Jun LUO ; Zhi-Gang PENG ; Yan CHEN ; Yong-Rong LAI ; Yu-Ying LU ; Shan-Jun SONG
Journal of Experimental Hematology 2007;15(2):248-252
This study was aimed to investigate the expression and regulation mechanism of DNA-dependent protein kinase catalylic subunit (DNA-PKcs) in chronic myeloid leukemia (CML) and its role in blast crisis of CML. Expression of DNA-PKcs mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and DNA-PKcs protein by Western blot in 62 CML patients and K562, as compared to those of 23 normal individual controls. In 26 CML patients received allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and 4 CML patients treated with imatinib, the expression of bcr-abl mRNA and DNA-PKcs protein was detected by RT-PCR and Western blot, respectively. After treatment with imatinib in mononuclear cell (MNC) of CML patients and K562 in vitro, expression of DNA-PKcs mRNA was detected by RT-PCR and DNA-PKcs protein level, tyrosine phosphorylation of bcr-abl fusion protein were detected by Western blot. The results showed that the expression of DNA-PKcs protein was significantly lower in CML and K562 than those in normal control (P<0.05). In 26 CML patients received allo-PBSCT and 4 CML patients treated with imatinib, the expression of DNA-PKcs protein was enhanced while the expression of bcr-abl mRNA decreased. After treatment of MNC of CML and K562 with imatinib in vitro, the expression of DNA-PKcs protein was enhanced while tyrosine phosphorylation of bcr-abl fusion protein decreased. It is concluded that the expression of DNA-PKcs protein is down-regulate by bcr-abl fusion gene, and the bcr-abl fusion gene down-regulate the expression of DNA-PKcs protein by post-transcriptional mechanism; the decrease of DNA-PKcs protein expression may be one of mechanisms underlying the acute transformation of CML.
Adult
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Aged
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Benzamides
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Bone Marrow Cells
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metabolism
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DNA-Activated Protein Kinase
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biosynthesis
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genetics
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Female
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Fusion Proteins, bcr-abl
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biosynthesis
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genetics
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Humans
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Imatinib Mesylate
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive
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genetics
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therapy
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Male
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Middle Aged
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Peripheral Blood Stem Cell Transplantation
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Piperazines
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therapeutic use
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Pyrimidines
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therapeutic use
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RNA, Messenger
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biosynthesis
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genetics
10.Anti-atherosclerosis role of N-oleoylethanolamine in CB2.
Ya-Ting GAI ; Qiang SHU ; Cai-Xia CHEN ; You-Lin LAI ; Wen-Jun LI ; Lu PENG ; Li-Min LIN ; Xin JIN
Acta Pharmaceutica Sinica 2014;49(3):316-321
To observe a PPAR-alpha agonist effect of N-oleoylethanolamine (OEA) on CB2 (cannabinoid receptor 2), an anti-inflammatory receptor in vascular endothelial cell, healthy HUVECs and TNF-alpha induced HUVECs were used to establish a human vascular endothelial cell inflammatory model. Different doses of OEA (10, 50 and 100 micromol x L(-1)) had been given to HUVECs, cultured at 37 degrees C for 7 h and then collected the total protein and total mRNA. CB2 protein expression was detected by Western blotting and CB2 mRNA expression was assayed by real-time PCR. As the results shown, OEA (10 and 50 micromol x L(-1)) could induce the CB2 protein and mRNA expression, but not 100 micromol x L(-1). To detect if anti-inflammation effect of OEA is partly through CB2, CB2 inhibitor AM630 was used to inhibit HUVEC CB2 expression, then the VCAM-1 expression induced by TNF-alpha was detected, or THP-1 adhere to TNF-alpha induced HUVECs was examined. OEA (50 micromol x L(-1)) could inhibit TNF-alpha induced VCAM-1 expression and THP-1 adhere to HUVECs, these effects could be partly inhibited by a CB2 inhibitor AM630. The anti-inflammation effect of OEA is induced by PPAR-alpha and CB2, suggesting that CB2 signaling could be a target for anti-atherosclerosis, OEA have wide effect in anti-inflammation, it may have better therapeutic potential in anti-inflammation in HUVECs, thus achieving anti-atherosclerosis effect.
Anti-Inflammatory Agents
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pharmacology
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Atherosclerosis
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pathology
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Cell Adhesion
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drug effects
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Cells, Cultured
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Endocannabinoids
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pharmacology
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Endothelial Cells
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cytology
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metabolism
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Ethanolamines
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pharmacology
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Humans
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Indoles
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pharmacology
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Monocytes
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drug effects
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Oleic Acids
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pharmacology
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PPAR alpha
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antagonists & inhibitors
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RNA, Messenger
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metabolism
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Receptor, Cannabinoid, CB2
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antagonists & inhibitors
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genetics
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metabolism
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Tumor Necrosis Factor-alpha
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pharmacology
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Vascular Cell Adhesion Molecule-1
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metabolism