Li-Ping Ma

Sun Yat-Sen University, Guangzhou, Guangdong Sheng, China

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Publications (19)3.45 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The quantitative identification and enrichment of viable regulatory T cells (Treg) requires reliable surface markers that are selectively expressed on Treg. Foxp3 is the accepted marker of natural Treg, but it cannot be used to isolate cells for functional studies. CD127 is a new surface marker expressed in Treg cells. In this study, two populations of Treg, including CD4(+)CD25(+)CD127(low/-) and CD4(+)CD25(+)Foxp3(+)T cells, and profiles of the Foxp3 expression in CD4(+)CD25(+)CD127(low/-) cells were compared to evaluate which population is better. The peripheral blood cells were collected and spleen suspension of BALB/C mice were prepared, and using triple staining CD4, CD25, CD127 and CD4, CD25, Foxp3. The profiles of Treg, including CD4(+)CD25(+)CD127(low/-) and CD4(+)CD25(+)Foxp3(+) were detected by flow cytometry. The quadruple staining CD4, CD25, Foxp3 and CD127 were used to determine the CD127 expression in CD4(+)CD25(+)Foxp3(+) cells. The results showed that on T cell subset the median expression levels of CD4(+), CD4(+)CD25(+) were 39.02%, 5.35% in peripheral blood and 23.49%, 3.86% in spleen. On CD4(+) T cell subset, the median expression level of CD4(+)CD25(+)CD127(low/-) and CD4(+)CD25(+)Foxp3(+)T cells were 7.13%, 3.97% in peripheral blood and 12.8%, 8.23% in spleen. The ratio of CD4(+)CD25(+)CD127(low/-) T cells was higher than that of CD4(+)CD25(+)Foxp3(+) cells in both peripheral blood and spleen cells (P < 0.01). The CD4(+)CD25(+)CD127(low/-) cells highly expressed Foxp3, while the CD4(+)CD25(+)Foxp3(+)T cells lowly expressed CD127. It is concluded that compared with the CD4(+)CD25(+)Foxp3(+) populations, CD4(+)CD25(+)CD127(low/-) T cells better fit the definition of naturally occurring regulatory T cells in peripheral blood cells and spleen of BALB/C mice. CD127(low/-) is a charicteristic marker on surface of CD4(+)CD25(+) Treg cells, and has been confirmed to be more specific marker for quantitatively sorting Treg cells.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 11/2012; 20(6):1469-73.
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    ABSTRACT: To investigate the effect of a microsomal prostaglandin E synthase-1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60 cells. HL-60 cells were treated with different concentration of MK886 (10, 25, 50 µmol/L) for 24 h. Flow cytometry, Western blot and ELISA were used to measure cell cycle, cyclin D1, mPGES-1, PGE(2), Akt, P-Akt and C-MYC. The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phospholation and C-MYC expression, down-regulation of cyclin D1 expression.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 10/2012; 20(5):1072-6.
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    ABSTRACT: This study was aimed to investigate the effect of MK886, a mPGES-1 inhibitor, on apoptosis and drug resistance of leukemia HL-60/A cell line. Expression of mPGES-1 was assayed by QT-PCR and Western blot. The effect of MK886 on HL-60/A cell proliferation was assayed by CCK-8 method, and flow cytometry was used to detect cell apoptosis. The expression of Akt and P-Akt was detected by Western blot. PGE2 was measured by ELISA. Effect of MK886 (10 µmol/L) on the chemotherapeutic sensitivity of HL-60/A cells and expression of mdr-1 mRNA and P170 protein were investigated too. The results indicated the expression of mPGES-1 was higher in HL-60/A cells. MK886 inhibited HL-60/A cell proliferation and induced apoptosis in a time- and concentration-dependent manner. Expression of mPGES-1 and P-Akt and synthesis of PGE2 decreased significantly. MK886 reduced expression of mdr-1 and P170 protein and enhanced the sensitivity of HL-60/A cells to chemotherapeutic drugs. It is concluded that MK886 can inhibit HL-60/A cell proliferation, induce apoptosis and enhance sensitivity to chemotherapeutic drugs, the mechanism of which possibly associates to down-regulation of mPGES-1/PGE2 synthesis, reduction P-Akt expression and decreasing mdr-1 and P170 protein expression.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 07/2012; 20(4):829-34.
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    ABSTRACT: This study was purposed to investigate the inhibitory effect of bactericidal permeability-increasing protein (BPI) on lipopolysaccharide (LPS)-mediated activation of platelets. Venous blood samples were obtained from 10 healthy volunteers and were prepared into platelet-rich plasma (PRP, 1 × 10(8)/ml). Experiments were divided into four groups: normal platelet group (untreated group); LPS group, BPI group and BPI+LPS group. PRP were stimulated by LPS (10 µg/ml) in the presence and absence of BPI (100 µg/ml) or BPI alone. Then platelets were harvested and determined for Toll-like receptor-4 (TLR-4) with flow cytometry (FCM), the supernatant was used for detection of cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) with enzyme-linked immunosorbent assay (ELISA). The results showed that as compared with normal platelet group, TLR-4 expression on platelets was significantly increased under LPS stimulation (P < 0.001); the levels of TNF-α and IL-6 in the supernatant were also remarkably elevated (P < 0.001). However, either TLR-4 expression or the cytokine levels significantly decreased in the presence of BPI when platelets underwent LPS-challenge (P < 0.05), but still were higher than that in normal platelet group. Stimulating the platelets with BPI alone could not enhance the TLR-4 expression and cytokine levels. It is concluded that BPI has the ability to inhibit the LPS-induced platelet activation.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 01/2012; 20(1):129-32.
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    ABSTRACT: To observe the expression of cyclin D1, hTERT, and telomerase activity in MNC, HL-60, HL-60A and to explore their effects on leukemogenesis and drug-resistance, normal human peripheral blood mononuclear cells, HL-60 cells sensitive to adriamycin and HL-60A cells resistant to adriamycin were investigated. The cell cycle was analyzed by flow cytometry, and the apoptosis was analyzed by Annexin V-FITC(+) PI staining. Expressions of cyclin D1 and hTERT were determined by real-time PCR and Western blot. Telomerase activity was detected by TRAP-ELISA. The results indicated that the percentage of MNC, HL-60 and HL-60A in S phase was (10.21 + 2.11)%, (44.93 + 3.00)%, and (51.38 + 1.10)% respectively; the percentage of apoptosis cells was (16.14 + 2.13)%, (7.53 + 0.92)%, (4.15 + 0.96)% respectively; the expression of mRNA and protein for cyclin D1 and hTERT increased; the telomerase activities of HL-60 and HL-60A were higher (p = 0.000), whereas the difference between HL-60 and HL-60A was no statistically significant (p = 0.232); positive correlation between cyclin D1, hTERT and telomerae activity had been found (p < 0.01). It is concluded that the cells of S phase increased while the apoptotic cells decreased in HL-60 and HL-60A, especially in HL-60A, which may be due to the up-regulation of cyclin D1, hTERT and telomerase activity.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 07/2011; 19(4):911-5.
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    ABSTRACT: This study was aimed to clarify whether valproic acid (VPA) induces apoptosis of leukemia HL-60 cell line and its possible mechanism. The effect of different concentrations and treatment time of VPA on HL-60 cell proliferation was assayed by cytotoxicity test (CCK-8 method) and fluorescence microscopy, and flow cytometry was used to detect cell apoptosis. The expressions of telomerase subunit h-tert mRNA and apoptosis-related protein as well as caspase-3 activity were detected by real time-quantitative PCR, Western blot and ELISA respectively. The results indicated that VPA inhibited proliferation of HL-60 cells and induced cell apoptosis in a dose dependent manner (r = -0.87). The expressions of anti-apoptotic protein BCL-2 and h-tert mRNA were significantly decreased while the pro-apoptotic protein BAX and caspase-3 activity increased after treatment with VPA. The apoptosis rate of HL-60 cell was negatively correlated with expression of h-tert mRNA. It is concluded that VPA can inhibit leukemia HL-60 cell proliferation and induce apoptosis. The VPA displays anti-leukemia activity possibly through reducing h-tert mRNA and BCL-2 protein expression, increasing BAX expression and activity of caspase-3.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 11/2010; 18(6):1445-50.
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    ABSTRACT: To investigate the effect of 3'-meisoindigo on the proliferation and the biological function of the splenocyte and thymocyte of mouse, which were 8 weeks old masculinity BALB/c, C57BL/6 and F1 hybridization mouse. Cells of thymus and spleen were harvested and prepared as the unicell suspension, then treated with 5, 10, 15, 20, 25 micromol/L 3'-meisoindigo. The cell proliferation was by MTT method, concentration of IL-12 was dectected by ELISA method, the mRNA levels of Bcl-2 and CDK2 were decected by RT-PCR. The cell cycle, apoptosis ratio, death ratio and intracellular ROS concentration were detected by FCM method. The protein level of Bcl-2, CDK2 and Bax were detected by immumofluorescence method. 15, 20, 25 micromol/L 3'-meisoindigo can inhibit the proliferation of thymocyte and splenocyte (P < 0.05). It had dose-dependent and time-dependent manner. 3'-meisoindigo inhibit the secretion of IL-12, even at 5 micromol/L concentration. 15 micromol/L 3'-meisoindigo decrease the mRNA level of Bcl-2 and CDK2, induced apoptosis and G2 arrestting of the thymocyte and splenocyte. (P < 0.05). The intracellular ROS level increased after treated by 3'-meisoindigo at 15 micromol/L for 24 h (P < 0.05). There were no difference among three germ line mouse. Above 15 micromol/L, 3'-meisoindigo can inhibit the proliferation and externalization function of thymocyte and splenocyte from different germ line mouse, meanwhile the mRNA and protein level of Bcl-2 and CDK2 decrease, the Bax protein expressed increased, the intracellular ROS level increase too.
    Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials 07/2010; 33(7):1124-9.
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    ABSTRACT: The study was aimed to investigate the expression of Toll-like receptor 4 (TLR4) on platelets and to determine whether platelet TLR4 involves in its activation induced by lipopolysaccharide (LPS). Human platelet-rich plasma (PRP) and platelet suspension obtained from 15 healthy individuals pretreated with a concentration of 0.2 microg/ml of LPS in the presence or absence of thrombin (1 U/ml) for 1 hour. The expressions of TLR4, CD62P (P-select) and CD40L on platelets were detected by flow cytometry, and platelet TLR4 expression was further determined by Western blot analysis. The results indicated that the percentage of TLR4-positive platelets induced by thrombin was increased by 32.34% compared with the resting platelets (25.44%, p < 0.05). TLR4 expression on platelets treated with LPS was remarkably elevated in the presence or absence of thrombin. However, the expression level of the former was much higher than that of the latter and thrombin stimulation alone (p < 0.05). Moreover, the similar results were found in Western blot analysis. Synchronously, expressions of CD62P and CD40L on resting platelets were 6.39% and 2.45%, they were also markedly increased when treated with thrombin (42.68% and 14.8%) and LPS respectively, and the increases of expression of CD62P and CD40L were more significant when stimulated with both LPS and thrombin (63.03% and 13.94%). Although anti-TLR4 antibody inhibited significantly the increase of TLR4, CD62P and CD40L on platelets induced by LPS, which did not affect their increase induced by thrombin. In conclusion, the evidence has been shown that functional TLR4 can be expressed on human platelets. It may involve in platelet activation as an important mediator of LPS-induced CD62P and CD40L expressions on platelets.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 12/2009; 17(6):1564-8.
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    ABSTRACT: To investigate the effect of valproic acid on the expression of P27(Kip1) and P170 and drug resistance of leukemia HL60/HT cell line and explore its possible mechanisms. HL-60/HT cells were derived from HL-60 cells induced by harringtonine (HT) in gradient concentrations. The inhibitory effect of valproic acid on the proliferation of HL-60 and HL-60/HT cells was evaluated by MTT assay, and the P27(Kip1) expression, P170 expression and cell cycle of the cells were analyzed with flow cytometry. The multidrug-resistant HL-60/HT was acquired, which showed a stable drug-resistant index with increased IC(50) of HT, VCR, DNR and Ara-c by 9.30, 5.20, 4.91 and 3.65 folds, respectively, as compared with those of HL60 cells. The expression of P27(Kip1) in HL-60/HT cells was significantly lower but P170 expression significantly higher than that of HL-60 cells and normal mononuclear cells (P<0.05). The expressions of P27(Kip1) and P170 showed no significant difference between normal mononuclear cells and HL-60 cells. The growth inhibition rate of VPA combined with Ara-C was significantly higher than that of valproic acid or Ara-C alone in HL-60/HT cells and HL-60 cells (q=1.37 and 1.51, respectively). HL-60/HT and HL-60 cells cultured in the presence of VPA resulted in a significant increase in the expression of P27(Kip1) and the G(1)-phase cells (P<0.05), but the expression of P170 underwent no significant changes (P>0.05). HL-60/HT cells have lower P27(Kip1) expression compared with HL-60 cells. Valproic acid can inhibit the growth of HL-60/HT cells and enhance their Ara-C sensitivity possibly by increasing P27(Kip1) expression and causing cell cycle arrest in G(1) phase.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 04/2009; 29(3):423-7.
  • Chinese medical journal 01/2006; 118(23):2020-4. · 0.90 Impact Factor
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    ABSTRACT: To investigate the changes of the goblet cells in the intestine during the restitution process of the gut barrier after hemorrhagic shock. Forty-nine Sprague-Dawley rats with body weight of 250-300 g were divided into control group (n=7) and experimental group (n=42). Rats in the experimental group was further divided into 6 groups (n=7 each) according to different time point at 1, 3, 6, 12, 24, and 36 hours after hemorrhagic shock resuscitation. The specimens from ileum tissue were taken to observe the morphological chan ges of the intestinal mucosa. The number of goblet cells was determined by light microscope and/or electron microscope. The contents of trefoil factor family 3 (TFF3) of goblet cells were examined using GC-9A gas chromatographic instrument. After hemorrhagic shock, mucosal epithelial injury was obvious in the small intestine. Tissue restitution was found after 3 hours, and mostly established after 12 hours. Following tissue restitution,the denuded mucosal surface was covered intensively by goblet cells. The number of goblet cells on the intestinal mucosa was reduced significantly from 243+/- 13 at 1 h to 157+/- 9 at 24 h (r=- 0.910, P< 0.01), and returned to normal level at 36 h. In the experimental group, the content of TFF3 in the intestinal mucosa increased significantly at 12 hours, decreased, but was still higher at 24 hours (t=3.24, P< 0.05). The goblet cells play a key role in the restitution of intestinal mucosa. High expression of TFF3 may facilitate the intestinal mucosal restitution in the early phase.
    Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery 11/2005; 8(6):510-2.
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    ABSTRACT: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response to ischemia/reperfusion injury. Forty-seven Sprague-Dawley rats with body weight of 250-300 g were divided into two groups: control group (sham shock n = 5) and experimental group (n = 42). Experimental group was further divided into six groups (n = 7 each) according to different time points after the hemorrhagic shock, including 0(th) h group, 1st h group, 3rd h group, 6th h group, 12th h group and 24th h group. All the rats were gavaged with 2 mL of suspension of lactulose (L) (100 mg/2 mL) and mannitol (M) (50 mg/each) at the beginning and then an experimental rat model of hemorrhagic shock was set up. The specimens from jejunum, ileum and colon tissues and the blood samples from the portal vein were taken at 0, 1, 3, 6, 12 and 24 h after shock resuscitation, respectively. The morphological changes of the intestinal mucosa, including the histology of intestinal mucosa, the thickness of mucosa, the height of villi, the index of mucosal damage and the numbers of goblet cells, were determined by light microscope and/or electron microscope. The concentrations of the bacterial endotoxin lipopolysaccharides (LPS) from the portal vein blood, which reflected the gut barrier function, were examined by using Limulus test. At the same time point, to evaluate intestinal permeability, all urine was collected and the concentrations of the metabolically inactive markers such as L and M in urine were measured by using GC-9A gas chromatographic instrument. After the hemorrhagic shock, the mucosal epithelial injury was obvious in small intestine even at the 0(th) h, and it became more serious at the 1st and the 3rd h. The tissue restitution was also found after 3 h, though the injury was still serious. Most of the injured mucosal restitution was established after 6 h and completed in 24 h. Two distinct models of cell death-apoptosis and necrosis-were involved in the destruction of rat intestinal epithelial cells. The number of goblet cells on intestinal mucosa was reduced significantly from 0 to 24 h (the number from 243+/-13 to 157+/-9 for ileum, 310+/-19 to 248+/-18 for colon; r = -0.910 and -0.437 respectively, all P<0.001), which was the same with the large intestine, but the grade of injury was lighter with the values of mucosal damage index in 3 h for jejunum, ileum, and colon being 2.8, 2.6, 1.2, respectively. The mucosal thickness and the height of villi in jejunum and ileum diminished in 1 h (the average height decreased from 309+/-24 to 204+/-23 microm and 271+/-31 to 231+/-28 microm, r = -0.758 and -0.659, all P<0.001; the thickness from 547+/-23 to 418+/-28 microm and 483+/-45 to 364+/-35 microm, r = -0.898 and -0.829, all P<0.001), but there was no statistical difference in the colon (F = 0.296, P = 0.934). Compared with control group, the urine L/M ratio and the blood LPS concentration in the experimental groups raised significantly, reaching the peak in 3-6 h (L/M: control vs 3 h vs 6 h was 0.029+/-0.09 vs 0.063+/-0.012 vs 0.078+/-0.021, r = -0.786, P<0.001; LPS: control vs 3 h vs 6 h was 0.09+/-0.021 vs 0.063+/-0.012 vs 0.25+/-0.023, r = -0.623, P<0.001), and it kept increasing in 24 h. The gut barrier of the rats was seriously damaged at the early phase of ischemic reperfusion injury after hemorrhagic shock, which included the injury and atrophy in intestinal mucosa and the increasing of intestinal permeability. Simultaneously, the intestinal mucosa also showed its great repairing potentiality, such as the improvement of the intestinal permeability and the recovery of the morphology at different phases after ischemic reperfusion injury. The restitution of gut barrier function was obviously slower than that of the morphology and there was no direct correlation between them. Compared with the small intestine, the large intestine had stronger potentiality against injury. The reduction of the amount of intestinal goblet cells by injury did not influence the ability of intestinal mucosal restitution at a certain extent and it appeared to be intimately involved in the restitution of the epithelium.
    World Journal of Gastroenterology 10/2005; 11(35):5485-91. · 2.55 Impact Factor
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    ABSTRACT: To observe the effects of pravastatin on platelet-derived nitric oxide system in hypercholesterolemia (HC) and atherosclerosis (AS) in rabbits, and the relationship between these changes and atherosclerosis courses. Thirty male New Zealand white rabbits were randomly divided into three groups, 12 in group A, 12 in group B, and 6 in group C. All of them were fed daily with cholesterol-rich food during the first 12 weeks. In addition, in group A, pravastatin (10 mg) was orally administered daily. At the end of the 12th week, 6 in group A and B were killed randomly and their aortas were removed and the pathologic changes were observed. In the following 12 weeks, food enriched with cholesterol was substituted with normal food in all three groups. Pravastatin treatment was continued or started in the remaining members of group A and group B, but not in group C. At the end 24th week, all rabbits were killed and their aortas were examined for the fatty-streaks or atherosclerotic plaques. The expressions of endothelial NOS (eNOS) mRNA and inducible NOS (iNOS ) mRNA, NOS activity, NO production and the level of the serum lipids were measured at 0, 6th, 12th, 18th and 24th week. The expression levels of platelet-derived NOS mRNA, eNOS mRNA ratio in group A had no difference at above time points, while in group B were reduced significantly at 6th week and 12th week compared with at 0 week (P <0.01), and increased at 18th week and 24th week compared with 12th week (P <0.05). The expression levels of eNOS mRNA in group C were reduced at 6th, 12th and 18th, 24th week compared with 0 week (P <0.05 and P <0.01, respectively), and were reduced in groups B and C compared with group A at 6th ,12th week (P < 0.05) and increased in group A and B compared with group C at 18th, 24th week (P <0.01). The expression levels of iNOS/mRNA among the three groups had no difference. Pathologic finding of the arteries: AS was not found in group A from the 12th to 24th week. While in group B, there were a lot of fatty-streaks on the entire intima of all large arteries at the 12th week. There were also fatty-streaks in the ascending aorta, but were improved at the 24th week. In group C, there were marked plaques in the entire aorta at the 24th week. The expressions of platelet-derived eNOS mRNA, NOS activity, NO production are decreased in HC or AS rabbits. Pravastatin can up-regulate expressions of platelet-derived eNOS mRNA, NOS activity, leading to preventing or improving the pathological courses of AS.
    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 09/2005; 26(9):539-42.
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    ABSTRACT: To explore the effects of chloride channels on the regulation of platelet cytoplasmic free calcium concentration ([Ca2+]i) and platelet aggregation (PAG). Freshly separated platelets were activated by thrombin. Chloride channel blockers DIDS or NFA and calcium channel blockers SK&F96365 or nifedipine were added to study the effects on platelet [Ca2+]i and PAG by a single reagent or the combination of reagents and find out the interactions among DIDS, NFA, SK&F96365 and nifedipine. Both DIDS and NFA could inhibit the thrombin (1 U/ml) induced PAG in a dose-dependent manner, whereas had little effect on resting [Ca2+]i. As compared with the control group, DIDS, SK&F96365 and Nifedipine could significantly reduce the PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05). The combination of DIDS and SK&F96365 had greater effects in reducing the PAG, Ca2+ release and Ca2+ influx than either reagent alone (P < 0.05). The combination of DIDS and nifedipine also had greater effect than each alone in reducing Ca2+ release (P < 0.05). The combination of NFA and SK&F96365 weakened each other's effect on Ca2+ release (P < 0.05), while NFA and nifedipine weakened each other's effects on PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05). DIDS and NFA have no effect on the resting [Ca2+]i and the leak calcium influx of platelet. DIDS can inhibit the Ca2+ release, Ca2+ influx and PAG of platelet induced by thrombin, while NFA can only inhibit the Ca2+ release. The chloride channel and calcium channel blockers have interactions in affecting resting [Ca2+]i and PAG of platelet. The opening of chloride channel can influence the cellular calcium movement of platelet.
    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 03/2005; 26(3):170-4.
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    ABSTRACT: To investigate the platelet activity and function in pregnancy induced hypertension (PIH) and gestational diabetes mellitus (GDM). Twenty-one patients with GDM and 23 patients with PIH in third-trimester were included. Twenty normal pregnant women in third-trimester served as controls. Platelet count (PC), mean platelet volume (MPV) were determined on Cell-DYN 1600 and the expression of CD62P was analyzed on FACSC alibur. (1) PC was (181 +/- 56) x 10(9)/L in PIH, (206 +/- 60) x 10(9)/L in GDM and (229 +/- 56) x 10(9)/L in controls, respectively. PC in PIH was lower than that of controls (P < 0.01), but there was no significant difference between GDM and controls. (2) MPV was (11.2 +/- 2.0) fl in PIH, significantly higher than that of controls (8.7 +/- 1.6) fl (P < 0.001). In GDM, MPV was (9.5 +/- 1.6) fl, without significant difference compared with that of controls. (3) The expression of CD62P increased significantly in PIH compared with controls [CD62P: (42 +/- 13)% vs (26 +/- 7)%, P < 0.001; CD62P(I): 109 +/- 39 vs 75 +/- 13, P < 0.01]. In GDM, the expression of CD62P also increased significantly compared with the normal pregnancy [CD62P(%): (42 +/- 14)% vs (26 +/- 7), P < 0.001; CD62P(I): 100 +/- 42 vs 75 +/- 13, P < 0.05]. (4) All parameters had no significant difference between PIH and GDM. Platelet activity is enhanced in PIH and GDM. It may play an important role in the pathogenesis and development of the two diseases.
    Zhonghua fu chan ke za zhi 02/2005; 40(1):25-8.
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    ABSTRACT: To explore the effects of 2A-1-1 (purified component from Panax notoginsengs saponins) on the aggregation of and Ca2+ influx into human platelets. The aggregation of platelets was tested by nephelometry, Fura-2 fluorescent technique was used for detecting cell [Ca2+]i. The effects of 2A-1-1, nifedipine and SK&F96365 on Ca(2+) influx into human platelets induced by ADP or CPA were observed separately. Nifedipine (< 20 micromol/L) could not inhibit platelet aggregation induced by ADP or the Ca(2+) influx induced by ADP or CPA. SK&F96365 at 20 micromol/L could inhibit the maximal aggregation of platelets induced by ADP with a inhibitory rate of 59.83%, at 15 micromol/L could inhibit the Ca2+ influx induced by CPA or ADP. 2A-1-1 (5, 10 and 20 micromol/L) could inhibit the maximal aggregation of platelets induced by ADP with the inhibitory rates of 47.06%, 53.47% and 71.52%, respectively. 2A-1-1 at 10 and 20 micromol/L could inhibit the Ca2+ influx induced by CPA or ADP. 2A-1-1 can inhibit platelets aggregation, block the ROC (Receptor-dependent Ca2+ channels) and inhibit Ca2+ influx of human platelets.
    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 09/2004; 25(9):544-7.
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    ABSTRACT: To investigate measures to prevent the outbreak of severe acute respiratory syndrome (SARS) in healthcare workers in isolation units. The architectural factors and the infection of healthcare workers in different wards in our hospital between 30 January 2003 and 30 March 2003 were analyzed. Four kinds of isolation wards were evaluated, including the ward where the thirty-first bed lied in on the twelfth floor, the laminar flow ward in the intensive care unit (ICU) where the tenth bed lied in on the fifteenth floor, the ward where the twenty-seventh bed lied in on the thirteenth floor of Building A, and thirty wards on the fourteenth to eighteenth floors of Building B. The ratios (m2/m3) of the area of the ventilation windows to the volume of the room were 0, 0, 1:95 and 1:40, respectively. Numbers of SARS cases in the wards mentioned above were 1, 1, 1 and 96, respectively. The total lengths (hour) of hospitalization were 43, 168, 110 and 1,272, respectively. The infection rates of the healthcare workers in the areas mentioned above were 73%, 32%, 28% and 2%, respectively. The difference of the infection rates was of statistical significance. In addition to strict personal protective measures, isolation of SARS cases in wards with high ratio of the area of ventilation windows to the volume of the room and good ventilation may be the key to preventing the outbreak of SARS in healthcare workers in isolation units.
    Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 11/2003; 26(10):594-7.
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    ABSTRACT: To describe a hospital outbreak of severe acute respiratory syndrome (SARS) and summarize the clinical features and therapeutic approaches. Clinical data in this cohort were collected prospectively as they were identified. The outbreak started with a SARS patient from the community on 30 January 2003, followed by a total of 96 people [76 women and 20 men; mean age (29.5 +/- 10.3) years; 93.8% of whom were health care workers] infected in a short period of time after their exposure to this source patient. The incubation period ranged from 1 to 20 days, with a mean of (5.9 +/- 3.5) days. The initial temperature was (38.3 +/- 0.6) degrees C, while the highest was (39.2 +/- 0.6) degrees C (P < 0.001), with a mean fever duration of (9.0 +/- 4.2) days. Other common symptoms included fatigue, cough, mild sputum production, chills, headache, general malaise and myalgia. The radiographic changes were predominantly bilateral and in the middle or lower lung zones. Leukopenia was observed in 67.7% of this cohort. The mean lowest oxygen saturation was (94.8 +/- 3.1)% with supplementary oxygen through a nasal cannula. 68.8% of the patients were treated with methylprednisolone for a mean period l of (4.9 +/- 2.4) days. The initial dose was (67.3 +/- 28.2) mg/d and the maximal dose was (82.4 +/- 30.5) mg/d. Ninety-five patients (99.0%) had a complete clinical recovery, and 1 patient died of progressive acute respiratory distress syndrome. The mean hospitalized duration was (17.2 +/- 8.0) days. SARS appears to be highly contagious and potentially lethal among health care workers, characterized by acute onset and rapid progression. Corticosteroids, antibiotics, human gamma-globulin, interferon-alpha, and antiviral drugs, although used empirically, might be of some benefits in shortening the clinical course.
    Zhonghua nei ke za zhi [Chinese journal of internal medicine] 07/2003; 42(7):453-7.
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    ABSTRACT: The drugs in the group of the "statins" lower blood lipids, especially cholesterol, thereby reducing a risk factor for, and diminishing the incidence of, clinically important cerebrocardiovascular events. Cardiovascular events and stroke are significant causes of morbidity and mortality in China and the United States. Statins reduce platelet-mediated thrombus formation and atherosclerotic progression through mechanisms not completely elucidated. While important, the lipid-lowering action of statins does not completely explain their multifaceted benefits. Nonlipid related mechanisms are essential to such effects. The authors explore these nonlipid related mechanisms of action of pravastatin that may translate into clinically relevant benefits. This study was conducted in Guangzhou, China. Twenty-one hypercholesterolemic patients were treated with pravastatin--10-20 mg/day for 12 weeks. Blood for tests was obtained at baseline and after 8 and 12 weeks of pravastatin therapy. After 8- and 12-weeks of therapy, significant decreases were observed in the following: (1) total blood cholesterol and low density lipoprotein-C (P < 0.01), (2) ADP-induced maximum platelet aggregation (P < 0.01), (3) TXB2 or thromboxane B2 in platelets (P < 0.01), and (4) expression of GMP-140 or granule membrane protein-140 (P < 0.01). The therapeutic effects of the drug did not vary significantly with length of therapy. Pravastatin induces inhibition of platelet aggregation and expression of TXB2 and GMP-140, the likely causes of thrombus formation, atherosclerotic progression, and subsequently cardiovascular events. These potential beneficial events occur within 8 weeks of pravastatin therapy.
    Journal of the Association for Academic Minority Physicians: the official publication of the Association for Academic Minority Physicians 01/2002; 13(1):23-6.