Biomedical subjects

Hong Liu

Publications and source records attributed to Hong Liu.

At least 163 records · Page 9Linked to original sources

PubMed2005

Inhibitory effects of the androgenic gland on ovarian development in the mud crab Scylla paramamosain.

Isolation and characterization of androgenic hormone in decapod crustaceans depend on an effective bioassay of its action. In the present study, the effect of androgenic gland on ovarian development in the mud crab Scylla paramamosain was investigated with a view to develop a bioassay for androgenic hormone. Ovarian regression with degeneration of oocytes occurred in some female crabs implanted with androgenic gland in vivo. In vitro incubation of ovarian tissues at secondary vitellogenesis in extract of androgenic gland resulted in a significant decrease in amino acid uptake by the tissues. We propose that this inhibitory effect could be established as an effective bioassay for the isolation of androgenic hormone in the mud crab.

Androgens↗

PubMed2005

Heart fatty acid binding protein in the rapid evaluation of myocardial damage following valve replacement surgery.

BACKGROUND: Myocardial damage occurs following valve replacement surgery. We estimated the value of heart fatty acid binding protein (H-FABP) in these patients. METHODS: Sixty elected patients were enrolled and distributed into single (group A) and double (group B) valve replacement groups. The clinical data were outlined and blood samples were collected perioperatively for determination of plasma levels of H-FABP, cardiac troponin-I (cTn-I), and CK-MB in both groups. RESULTS: 56 patients completed the study and no significant difference of clinical data was observed except CPB time and ACC time between groups. H-FABP level elevated quickly after reperfusion and peaked significantly earlier than cTn-I and CK-MB, it also declined rapidly but did not return to baseline at 24 h after reperfusion. Three markers' levels were all higher in group B than in group A after reperfusion with significant differences at their peaks and thereafter. Patients with postoperative complications had significantly higher H-FABP levels than usual. H-FABP peak level associated well with the length of CPB and ACC as well as with other 2 markers' peak levels in both groups. CONCLUSION: Compared with cTn-I and CK-MB, H-FABP is an earlier and potentially useful marker in the rapid evaluation of myocardial damage following valve replacement surgery with CPB.

Adult↗

PubMed2005

A rat model of cardiopulmonary bypass with excellent survival.

BACKGROUND: Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of cardiopulmonary bypass (CPB) have been hampered due to the absence of a satisfactory long-term recovery animal model. The objective of this study was to establish a survival experimental model of CPB in rats to meet the requirement of these studies. MATERIALS AND METHODS: Male SD rats (450-550 g) were randomly divided into CPB (n = 10) group and Sham group (n = 10). All rats were anaesthetized and mechanically ventilated. The femoral artery and vein were cannulated for continuous blood pressure recordings and fluid replacement, respectively. The CPB circuit comprised a venous reservoir, a membrane oxygenator, and a roller pump. Blood was drained from the right atrium via a jugular vein catheter and returned to the right carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. CPB was conducted for 60 min at a flow rate of 100-150 ml/kg/min in the CPB group. Haemodynamic investigations, blood gas analysis, and survival studies were performed subsequently. RESULTS: Our data show that the rat model principally simulated the clinical setting of CPB in terms of its construction, configuration, performance, material surface area, and priming volume to blood volume ratio. All CPB rats survived and the 2-week follow-up period remained uneventful. CONCLUSIONS: The rat model of CPB was easy to establish and was associated with excellent survival. This model should facilitate the investigation of the pathophysiological processes concerning CPB-related multiple organ dysfunction and possible protective interventions.

Animals↗

PubMed2005

Effect of scutellarin on nitric oxide production in early stages of neuron damage induced by hydrogen peroxide.

The aims of the present study were to investigate the regulatory function of scutellarin on production of nitric oxide (NO) as well as activities of constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) in early stages of neuron damage induced by hydrogen peroxide. Direct detection of NO production was performed on primary cultures of living rat neuronal cells with an electrochemical sensor. Hydrogen peroxide significantly increased culture supernatant levels of NO, the total integral value of the defined areas (500-6500 sxpA) reached 3.68 x 10(6). Pre-treatment with scutellarin, caused the total integral value to decrease in a dose-dependent fashion (3.24 x 10(6), 2.15 x 10(6), 1.84 x 10(6) for groups 10, 50, and 100 uM scutellarin, respectively). After exposure to 2.0mM hydrogen peroxide for 2h, malondialdehyde (MDA) level, a marker of lipid peroxidation, was remarkably increased. The elevation can be suppressed by scutellarin. Hydrogen peroxide also caused significant loss of neuron viability. In comparison with the control group, scutellarin significant attenuated the loss. Results also showed that hydrogen peroxide increased activity of cNOS, which was markedly inhibited by scutellarin. However, exposure of neuronal cells to hydrogen peroxide did not lead to an increase in iNOS activity. In conclusion, our results suggest that NO production, which increased in early stages of neuron damage induced by hydrogen peroxide can be effectively inhibited by scutellarin. Moreover, our results indicate that increase in NO production is mediated by cNOS.

Animals↗

PubMed2005

Quantum growth of magnetic nanoplatelets of Co on Si with high blocking temperature.

Self-organized Co nanoplatelets with a singular height, quantized lateral sizes, and unique shape and orientation have been fabricated on a template consisting of ordered Al nanocluster arrays on Si(111)-7 x 7 surfaces. Despite their small volume (a few nm(3)), these nanomagnets exhibit an unusually high blocking temperature (>100 K). The perpendicular direction for easy magnetization, the high blocking temperature, the size tunability, and the epitaxial growth on Si substrates make these nanomagnets important for applications in information technology.

Journal Article↗

PubMed2005

Bioactivation of the selective estrogen receptor modulator acolbifene to quinone methides.

Although approved for the treatment of hormone-dependent breast cancer as well as for the prevention of breast cancer in high-risk women, the selective estrogen receptor modulator (SERM) tamoxifen has been associated with an increased risk of endometrial cancer in women. With an understanding of the potential carcinogenic mechanisms of these compounds, SERMs could in principle be designed or selected for use that avoids these problems. Acolbifene (EM-652) is a fourth-generation SERM and the active form of the ester prodrug EM-800. As a pure antagonist of breast tumor development and growth, acolbifene does not stimulate endometrial tissue. However, acolbifene was found in this investigation to form two kinds of quinone methides, either through chemical or through enzymatic oxidation. One was a classical acolbifene quinone methide, which was formed by oxidation at the C-17 methyl group, and the other was a diquinone methide involving the oxidation of two phenol groups. The half-life of the classical quinone methide was determined to be 32 +/- 0.4 s at physiological pH and temperature. The quinone methides reacted with glutathione (GSH) to form five mono-GSH conjugates and five di-GSH conjugates. The majority of GSH conjugates resulted from reaction of the classical acolbifene quinone methide with GSH. Incubations of acolbifene with GSH and either tyrosinase or human and rat liver microsomes also produced acolbifene quinone methide-GSH conjugates. In addition to reaction with GSH, the classical acolbifene quinone methide was also shown to react with deoxynucleosides. One of the major deoxynucleoside adducts was identified as the deoxyadenosine adduct resulting from reaction of the classical acolbifene quinone methide with the exocyclic amino group of adenine. Acolbifene could also induce DNA damage in the S30 breast cancer cell line. These data imply that the classical electrophilic acolbifene quinone methide might contribute to the potential toxicity of acolbifene.

Animals↗

PubMed2005

Bioactivation of the selective estrogen receptor modulator desmethylated arzoxifene to quinoids: 4'-fluoro substitution prevents quinoid formation.

Although selective estrogen receptor modulators (SERMs) are useful in the treatment and prevention of breast cancer, the SERM tamoxifen has been associated with an increased risk of endometrial cancer possibly due to metabolism to electrophilic quinoids. Another SERM, arzoxifene is currently in clinical trials for the treatment of breast cancer, and since it has similar structural characteristics to tamoxifen, it also has the potential to form quinoids. In the current study, the active form of arzoxifene in vivo, desmethylated arzoxifene (DMA), was synthesized and chemically or enzymatically oxidized to DMA diquinone methide. The half-life of DMA diquinone methide at physiological pH and temperature was approximately 15 s. Reaction of DMA diquinone methide with glutathione (GSH) gave four mono-GSH conjugates, two di-GSH conjugates, and one tri-GSH conjugate. In incubations of DMA with GSH and either rat or human liver microsomes, DMA o-quinone-GSH conjugates were detected in addition to DMA diquinone methide-GSH conjugates. A DMA diquinone methide-deoxyguanosine adduct was detected following the incubation of DMA diquinone methide with deoxynucleosides. In preliminary studies with a human breast cancer cell line, DMA induced dose-dependent DNA damage and was more effective at causing DNA damage than raloxifene. These results suggest that DMA can be metabolized to electrophilic/redox-active quinoids, which have the potential to cause toxicity in vivo. A new fluorinated derivative unable to form a diquinone methide, 4'-F-DMA, was synthesized. 4'-F-DMA showed similar estrogen receptor (ER) binding affinity as compared to DMA. The antiestrogenic activity as measured by inhibition of estradiol-mediated induction of alkaline phosphatase activity in Ishikawa cells showed 10-fold lower activity for 4'-F-DMA compared to DMA; however, the antiestrogenic activity was comparable to raloxifene. In microsomal incubations of 4'-F-DMA in the presence of GSH, no GSH adducts were detected. These data suggest that 4'-F-DMA might be a promising SERM with similar activity to DMA and raloxifene and less toxicity.

Alkaline Phosphatase↗

PubMed2005

Inhibitory effect of PPAR-gamma activator on IL-6 and mPGES protein expression in PBMC induced by homocysteine.

The objective was to investigate the relationship between homocysteine (HCY), peroxisome proliferator-activated receptors (PPAR)-gamma and the expression of interleukin 6 (IL-6) and microsomal prostaglandin E synthase (mPGES) by peripheral blood mononuclear cell (PBMC) culture in vitro, as well as to look at the intervention with HCY and PPAR-gamma activators (troglitazone and rosiglitazone). PBMC were isolated from venous blood of normal volunteers and incubated with HCY and PPAR-gamma activator of varying concentrations for 24 hr. The supernatant of the culture medium was collected in order to determine the IL-6 and mPGES levels by ELISA assay. The results show that the expression of IL-6 and mPGES in the HCY experimental group was significantly higher than that in the control group (p<0.01 and p<0.05, respectively). Additionally, the IL-6 and mPGES levels rose with the increase of HCY in a dose-dependent manner (p<0.01 and p<0.05, respectively). PPAR-gamma activator could significantly inhibit the increase of IL-6 and mPGES induced by 100 micromol/L HCY (p<0.05 and p<0.01, respectively). In conclusion, HCY can increase the expression of IL-6 and mPGES, while PPAR-gamma activator can inhibit the increase of IL-6 and mPGES induced by HCY.

Cells, Cultured↗

PubMed2005

Transcriptional adaptation of Shigella flexneri during infection of macrophages and epithelial cells: insights into the strategies of a cytosolic bacterial pathogen.

Shigella flexneri, the etiologic agent of bacillary dysentery, invades epithelial cells as well as macrophages and dendritic cells and escapes into the cytosol soon after invasion. Dissection of the global gene expression profile of the bacterium in its intracellular niche is essential to fully understand the biology of Shigella infection. We have determined the complete gene expression profiles for S. flexneri infecting human epithelial HeLa cells and human macrophage-like U937 cells. Approximately one quarter of the S. flexneri genes showed significant transcriptional adaptation during infection; 929 and 1,060 genes were up- or down-regulated within HeLa cells and U937 cells, respectively. The key S. flexneri virulence genes, ipa-mxi-spa and icsA, were drastically down-regulated during intracellular growth. This theme seems to be common in bacterial infection, because the Ipa-Mxi-Spa-like type III secretion systems were also down-regulated during mammalian cell infection by Salmonella enterica serovar Typhimurium and Escherichia coli O157. The bacteria experienced restricted levels of iron, magnesium, and phosphate in both host cell types, as shown by up-regulation of the sitABCD system, the mgtA gene, and genes of the phoBR regulon. Interestingly, ydeO and other acid-induced genes were up-regulated only in U937 cells and not in HeLa cells, suggesting that the cytosol of U937 cells is acidic. Comparison with the gene expression of intracellular Salmonella serovar Typhimurium, which resides within the Salmonella-containing vacuole, indicated that S. flexneri is exposed to oxidative stress in U937 cells. This work will facilitate functional studies of hundreds of novel intracellularly regulated genes that may be important for the survival and growth strategies of Shigella in the human host.

Adaptation, Physiological↗

PubMed2005

Outbreak of infection caused by Enterobacter cloacae producing the novel VEB-3 beta-lactamase in China.

Over a 4-month period from November 2002 to February 2003, 27 ceftazidime-resistant or cefotaxime-resistant nonrepetitive Enterobacter cloacae isolates were collected from 27 patients hospitalized at HuaShan Hospital, Shanghai, People's Republic of China. The Etest did not detect extended-spectrum beta-lactamases (ESBLs) in those 27 isolates; however, screening by the NCCLS ESBL disk test and confirmatory tests detected ESBLs in 4 of 27 isolates and PCR detected ESBLs in 23 of 27 isolates. The majority of ESBL producers exhibited the same repetitive extragenic palindromic PCR pattern but harbored different ESBL genes. CTX-M-3 was the most prevalent ESBL in our study. Interestingly, 12 clonally related E. cloacae isolates possessed a novel bla(VEB)-type beta-lactamase, bla(VEB-3). Bla(VEB-3) was encoded by the chromosome and was located in an integron. Nine of the 12 isolates harbored both the bla(VEB-3) and the bla(CTX-M-3)-like ESBLs. This is the first report of a VEB-1-like ESBL in China and the first report of the simultaneous presence of VEB-1 and CTX-M-3-like ESBLs in an isolate.

Amino Acid Sequence↗

PubMed2005

Enhanced potency of plasmid DNA microparticle human immunodeficiency virus vaccines in rhesus macaques by using a priming-boosting regimen with recombinant proteins.

DNA vaccines have been used widely in experimental primate models of human immunodeficiency virus (HIV), but their effectiveness has been limited. In this study, we evaluated three technologies for increasing the potency of DNA vaccines in rhesus macaques. These included DNA encoding Sindbis virus RNA replicons (pSINCP), cationic poly(lactide-co-glycolide) (PLG) microparticles for DNA delivery, and recombinant protein boosting. The DNA-based pSINCP replicon vaccines encoding HIV Gag and Env were approximately equal in potency to human cytomegalovirus (CMV) promoter-driven conventional DNA vaccines (pCMV). The PLG microparticle DNA delivery system was particularly effective at enhancing antibody responses induced by both pCMV and pSINCP vaccines and had less effect on T cells. Recombinant Gag and Env protein boosting elicited rapid and strong recall responses, in some cases to levels exceeding those seen after DNA or DNA/PLG priming. Of note, Env protein boosting induced serum-neutralizing antibodies and increased frequencies of gamma interferon-producing CD4 T cells severalfold. Thus, PLG microparticles are an effective means of delivering DNA vaccines in nonhuman primates, as demonstrated for two different types of DNA vaccines encoding two different antigens, and are compatible for use with DNA prime-protein boost regimens.

AIDS Vaccines↗

PubMed2005

The endoplasmic reticulum lumenal domain of the adenovirus type 2 E3-19K protein binds to peptide-filled and peptide-deficient HLA-A*1101 molecules.

E3-19K is a type I membrane glycoprotein expressed by adenoviruses (Ads) to modulate host antiviral immune responses. We have developed an expression system for the endoplasmic reticulum lumenal domain (residues 1 to 100) of Ad type 2 E3-19K tagged with a C-terminal His6 sequence in baculovirus-infected insect cells. In this system, recombinant E3-19K is secreted into the culture medium. A characterization of soluble E3-19K by analytical ultracentrifugation and circular dichroism showed that the protein is monomeric and adopts a stable and correctly folded tertiary structure. Using a gel mobility shift assay and analytical ultracentrifugation, we showed that soluble E3-19K associates with soluble peptide-filled and peptide-deficient HLA-A*1101 molecules. This is the first example of a viral immunomodulatory protein that interacts with conformationally distinct forms of class I major histocompatibility complex molecules. The E3-19K/HLA-A*1101 complexes formed in a 1:1 stoichiometry with equilibrium dissociation constants (Kd) of 50 +/- 10 nM for peptide-filled molecules and of about 10 microM for peptide-deficient molecules. A temperature-dependent proteolysis study revealed that the association of E3-19K with peptide-deficient HLA-A*1101 molecules stabilizes the binding groove. Importantly, our studies showed that peptide-deficient HLA-A*1101 molecules sequestered by E3-19K are capable of binding antigenic peptides and maturing into peptide-filled molecules. This firmly establishes that E3-19K does not block binding of antigenic peptides. Together, our results suggest that Ads have evolved to exploit the late and early stages of the class I antigen presentation pathway.

Adenoviridae↗

PubMed2005

Interleukin-21 receptor gene induction in human T cells is mediated by T-cell receptor-induced Sp1 activity.

Interleukin-21 (IL-21) plays important roles in regulating the immune response. IL-21 receptor (IL-21R) mRNA is expressed at a low level in human resting T cells but is rapidly induced by mitogenic stimulation. We now investigate the basis for IL21R gene regulation in T cells. We found that the -80 to -20 region critically regulates IL-21R promoter activity and corresponds to a major DNase I-hypersensitive site. Electrophoretic mobility shift assays, DNA affinity chromatography followed by mass spectrometry, and chromatin immunoprecipitation assays revealed that Sp1 binds to this region in vitro and in vivo. Moreover, mutation of the Sp1 motif markedly reduced IL-21R promoter activity, and Sp1 small interfering RNAs effectively diminished IL-21R expression in activated T cells. Interestingly, upon T-cell receptor (TCR) stimulation, T cells increased IL-21R expression and Sp1 protein levels while decreasing Sp1 phosphorylation. Moreover, phosphatase inhibitors that increased phosphorylation of Sp1 diminished IL-21R transcription. These data indicate that TCR-induced IL-21R expression is driven by TCR-mediated augmentation of Sp1 protein levels and may partly depend on the dephosphorylation of Sp1.

Amino Acid Motifs↗

PubMed2005

Sevoflurane preconditioning limits intracellular/mitochondrial Ca2+ in ischemic newborn myocardium.

UNLABELLED: Sevoflurane preconditioning (SPC) in adult hearts reduces myocardial ischemia/reperfusion (I/R) injury, an effect that may be mediated by reductions in intracellular Ca(2+) ([Ca(2+)](i)) and/or mitochondrial Ca(2+) ([Ca(2+)](m)) accumulation during ischemia and reperfusion. Because the physiology, pharmacology, and metabolic responses of the newborn differ from adults, we tested the hypothesis that SPC protects newborn myocardium by limiting [Ca(2+)](i) and [Ca(2+)](m) by a K(ATP) channel-dependent mechanism. Fluorescence spectrofluorometry and nuclear magnetic resonance spectroscopy were used to measure [Ca(2+)](i), [Ca(2+)](m), and adenosine triphosphate (ATP) in 4- to 7-day-old Langendorff-perfused rabbit hearts. Three experimental groups were used to study the effect of SPC on [Ca(2+)](m)/[Ca(2+)](i), ATP, as well as hemodynamics and ischemic injury. The role of mitochondrial K(ATP) channels was assessed by exposing the SPC hearts to the mitochondrial K(ATP) channel blocker 5-hydroxydecanoic acid. Our results show that SPC significantly decreased [Ca(2+)](i) and [Ca(2+)](m) during I/R, as well as decreased creatine kinase release during reperfusion and resulted in higher ATP. 5-Hydroxydecanoic acid abolished the effect of SPC on [Ca(2+)], hemodynamics, ATP, and creatine kinase release. In conclusion, decreased [Ca(2+)](i) and [Ca(2+)](m) observed with SPC is associated with greater ATP recovery as well as diminished cell injury. Mitochondrial K(ATP) channel blockade attenuates the SPC effect during I/R, suggesting that these channels are involved in the protective effects of SPC in the newborn. IMPLICATIONS: The results of this study support the hypothesis that sevoflurane preconditioning protects newborn hearts from calcium overload and ischemic injury via a mechanism dependent on mitochondrial KATP channels.

Anesthetics, Inhalation↗

PubMed2005

[Observation on the biological behavior of human umbilical cord blood adherent cells].

To study the possibility of separation and culture of human umbilical cord blood adherent cell (HUCBAC), the umbilical cord blood CD34(+) cells were cultured in Dexter system in order to evaluate and observe the biological behavior of adherent cells in vitro. The results showed that all cells were cultured with Dexter system. By day 9-14 (at a median of 11.2 days), adherent cell colonies formed and reached their maximum at 15-22 days (mean 19.6 days), by day 28, all adherent cells spread over the bottom of Petri dish. By means of light microscopy, these cells were found to differentiate into three kinds of cells in culture of 28 days: fibroblast-liked cell, macrophage liked cell and small-round cells. The ratio of these three kinds of cells was 56.8%, 38%, 5.5% respectively. Cytochemistry assay revealed that the positive rate reached 100% in NSE stain and PAS stain; the adherent cell by ALP stain were shown 35% positive, but in POX stain the result was negative. Immunohistochemistry stain revealed that the positive rate of cord adherent cells for CD106, CD29, CD44, CD45, CD50, Fn, Ln, collagen IV etc reached 96%, 93%, 98%, 68%, 72%, 92%, 74%, 83% respectively. It is concluded there are hematopoietic adherent precursors in cord blood CD34(+) cells and the HUCBAC shows some biological behavior of hematopoietic stromal cells.

Antigens, CD34↗

PubMed2005

[Study on the changes of T-lymphocyte subsets in the patients with endometriosis].

OBJECTIVE: To investigate the function of T-lymphocyte subsets in patients with endometriosis. METHODS: The levels of interleukin-2 (IL-2) and interleukin-6 (IL-6) in the serum, and peritoneal fluid of 30 cases with endometriosis were detected using enzyme linked immunoabsorbent assay and compared with those of 20 non-endometriosis cases. The expression of IL-2 and IL-6 in ectopic endometrial tissue from the patients with endometriosis and the endometrial tissues of 10 normal women was investigated by immunohistochemistry method. RESULTS: Significantly elevated levels of IL-6 (cytokines of T help cell 2) were found in the serum and peritoneal fluid of patients with endometriosis (Median: 5.3 ng/L, 2.1 ng/L, P < 0.05) compared with that of non-endometriosis patients median: 2.5 ng/L, 0.9 ng/L). The level of IL-6 in the serum and peritoneal fluid of endometriosis patients in early stages (stages I, II) was 3.7 ng/L, 1.6 ng/L, significantly lower than those in advanced stages (stages III, IV) (13.6 ng/L, 4.1 ng/L) (P < 0.05). The ratio of IL-2/IL-6 in the serum and peritoneal fluid in patients with endometriosis (0.7, 1.1) was significantly lower than those in the control non-endometriosis group (0.8, 6.2, P < 0.05). The levels of IL-6 detected in the peritoneal fluid of patients with endometriosis had a positive correlation with those in the serum (r = 0.745, P < 0.01). The levels of IL-6 in serum and peritoneal fluid in the patients with endometriosis had a negative correlation with the IL-2/IL-6 ratios in the serum and peritoneal fluid respectively (r = -0.406, r = -0.480, P < 0.05). IL-2 and IL-6 were expressed in the interstitial cells of ectopic endometrial tissue, with an expression rate of 56.7%, and 60.0% respectively. There was significant difference in the expression of IL-2 and IL-6 between the ectopic endometrial tissue and normal endometrial tissue. CONCLUSIONS: The levels of IL-6 in the serum and peritoneal fluid of patients with endometriosis are increased, implying that IL-6 might play a role in the pathophysiology of endometriosis. The ratio of IL-2/IL-6 in the serum and peritoneal fluid was decreased in patients with endometriosis compared with the control group, suggesting shift of Th1 cell toward Th2 cell in patients with endometriosis. Stronger expression of IL-2 and IL-6 in the ectopic endometrial tissues may contribute to the disturbed immune regulation in patients with endometriosis.

Adult↗

PubMed2005

[Influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside to HL-60 cell].

This study was aimed to explore the influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside (Ara C) to HL-60 cell, and to assess its therapeutic value in marrow residual disease. HL-60 cells were cultured and co-cultured with leukemic stromal cells, and SDF-1 activity was inhibited with 10 microg/ml 12G5, then, killing effects of Ara C on HL-60 cells were investigated by MTT and morphology assay. Curves by MTT assay revealed that in the test group of 20 microg/ml Ara C, A(540) values decreased slowly but straightly, however, in control group A(540) values decreased markedly for the first two days, and increased from day 3 or 4. In the test group of 40 microg/ml Ara C, although increasing at constricted range of 7 - 9 days, A(540) values decreased in whole observing period of 12 days, while in control group A(540) values decreased markedly at day 0-3, and increased from day 4. Furthermore, two curves go across each other at day 5, and continue the increasing tendency. Morphology results showed that in both treated groups, the number of HL-60 cell decreased markedly and increased gradually in control group, but just contrary to test group. It is concluded that 12G5 may weaken the killing effect of Ara C on HL60 cell in earlier period, but reinforce the total killing effect and delay the occurrence of drug resistance simultaneously. Thus 12G5 has the therapeutic potential on marrow residual disease.

Antibodies, Monoclonal↗

PubMed2005

[Expression of stromal cell derived factor-1(SDF-1) and its receptor CXCR4 in hematologic malignancies].

The aim was to analyze the expression level of stromal cell derived factor-1 (SDF-1) and its functional chemokine receptor CXCR4 in the patients with hematologic malignant tumor and their clinic significance. 28 patients with hematologic malignant tumor and 12 normal controls were chosen to be experimental objects. CXCR4 expressed on the cell membrane in bone marrow was enumerated by flow cytometry and serum level of SDF-1 was determined by ELISA assay. The result showed that the expression of SDF-1 and CXCR4 in hematologic malignant tumor were higher than that in normal controls, and the expression levels of two molecules were correlated. What is more, the different hematologic malignant tumor had different CXCR4 expression. In conclusion, the high expression of SDF-1 and CXCR4 in serum and bone marrow cells can be used as detective factors to hematologic malignant tumor. A correlation exists between the high expression of CXCR4 and the infiltration of hematologic malignant cells.

Adolescent↗