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Biomedical subjects

F Meng

Publications and source records attributed to F Meng.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Different serum lipid adjustment drugs for the treatment of hyperlipidemic fatty liver].

OBJECTIVE: To research the effect of different serum lipid adjustment drugs, Simvastatin and Fenofibrate, on hyperlipidemic fatty liver. METHODS: The rat models of hyperlipidemic fatty liver induced by high fat diet were treated with Fenofibrate and Simvastatin respectively to investigate the change of the liver index, liver function, the serum and liver lipid, MDA, and pathologic histology. RESULTS: The liver index and the content of triglyceride (TC1.80 +/-0.20/2.10+/-0.33), total cholesterol (TG 0.76+/-0.18/1.09+/-0.31), MDA both in the serum and the liver in the model group were significantly higher than those in control group. Slight or moderate hepatic steatosis was observed in model group. Fenofibrate decreased serum triglyceride, total cholesterol, and MDA both in serum and liver significantly, but increased the ALT, ALP, liver index, liver lipids, and finally leading to severe hepatic steatosis. Simvastatin lowered the level of lipid and MDA both in serum and liver, and liver histology was improved nearly to normal. Moreover, little side effect on the liver was observed. CONCLUSIONS: Simvastatin can be applied for prevention and treatment of hyperlipidemic fatty liver safely and effectively, while Fenofibrate can not.

Animals↗
PubMed2001

[Gene typing of merozoite surface protein 1 of Plasmodium falciparum isolates from Hainan Province].

OBJECTIVE: To identify the genotype of merozoite surface protein 1 (MSP1) of Plasmodium falciparum isolates from Hainan Province. METHODS: Nested PCR was applied to amplify the MSP1 of Blocks 2 and 3 Plasmodium falciparum isolates from Hainan Province. Two allelic family representative gene fragments were sequenced. RESULTS: From 36 out of 39 blood samples from Plasmodium falciparum patients, 44 gene fragments of blocks 2 and 3 of the MSP1 were amplified, of which the MAD20-type allele was dominant(75%). followed by K1-type allele. No RO33-type allele was found. The mixed infection rate of the two different allelic type was 19.4%. Sequence analysis showed that the sequences of MAD20- and K1-type isolates from Hainan Province were highly homologous to that of the MAD20 and K1 allelic prototypes. CONCLUSION: Two principal allelic types of MSP1 gene, MAD20- and K1-type, exist in malaria endemic areas in Hainan Province, the MAD20-type being the dominant.

Alleles↗
PubMed2001

[Monte Carlo simulation of FCS in a laser gradient field].

Fluorescence correlation spectroscopy (FCS) is a powerful tool for probing biological process inside living cells. It measures fluorescence fluctuations of small number of molecules and derive information on molecular kinetics and reactions. We have developed a Monte Carlo model to simulate Browning motion of Rayleigh particles in a laser gradient field. The simulation reveals relations between laser field strength and measured parameters from FCS, such as diffusion coefficient and number density of the particles. The simulated results agree qualitatively to the experimental results obtained using fluorescent spheres. Empirical relations from the simulation are also discussed.

Computer Simulation↗
PubMed2000

The "chip" as a specific genetic tool.

DNA microarrays are powerful tools for the analysis of the organization and regulation of the brain, in both illness and health. Such messenger RNA expression methods are outgrowths of a marriage between the several genome sequencing projects and a wide variety of physical, chemical, optical, and electronic systems. The advantages of microarray analyses include the ability to study the regulation of several genes or even the entire genome in a single experiment. However, there are substantive issues associated with the use of these tools that need to be considered before drawing conclusions about the genomic regulation of the brain. These issues include the loss of most anatomic (i.e., cellular and circuit) specificity, only fair sensitivity, lack of absolute quantitative data, poor comparability between studies, and high variability in sample values, to mention the most obvious. In this review we point to some of the solutions proposed for these problems and novel techniques and approaches for newer methods. Among these are methods for making arrays more sensitive, including nonarray messenger RNA expression systems. The future of this field and its links to deeper protein and cell biology are both emphasized.

Clinical Laboratory Techniques↗
PubMed2000

Selectivity of mu-opioid receptor determined by interfacial residues near third extracellular loop.

We hypothesized that the selectivity profile of the rat mu-opioid receptor for opioid receptor-selective ligands is determined by the nature of the amino acid residues at highly divergent sites in the ligand-binding pocket. To determine which characteristics of these residues contribute to opioid receptor ligand selectivity, we made various mutant receptors that replaced the Lys(303) and Trp(318) residues near the extracellular interface of transmembrane domains VI and VII, respectively. Ligand binding determinations using transiently transfected monkey kidney epithelial (COS-1) cells show that Lys(303) mutations cause little change in the receptor binding profile, whereas the Trp(318) mutant receptors have considerably lower affinity for micro-opioid receptor-selective ligands and greatly increased affinity for delta-opioid receptor-selective ligands. The nature of these mutations show that this effect is not due to sterics or charge alone. [35S]guanosine-5'-O-(3-thio)-triphosphate ([35S]GTPgammaS) activity assays show that these residues may influence functional, as well as binding selection. We conclude that a primary role for Trp(318) is to form a basis for ligand selectivity.

Amino Acid Substitution↗
PubMed2000

Switching agonist/antagonist properties of opiate alkaloids at the delta opioid receptor using mutations based on the structure of the orphanin FQ receptor.

In an earlier study, we have demonstrated that by mutating five amino acid residues to those conserved in the opioid receptors, the OFQ receptor could be converted to a functional receptor that bound many opioid alkaloids with nanomolar affinities. Surprisingly, when the reciprocal mutations, Lys-214 --> Ala (TM5), Ile-277 --> Val/His-278 --> Gln/Ile-279 --> Val (TM6), and Ile-304 --> Thr (TM7), are introduced in the delta receptor, neither the individual mutations nor their various combinations significantly reduce the binding affinities of opioid alkaloids tested. However, these mutations cause profound alterations in the functional characteristics of the mutant receptors as measured in guanosine 5'-3-O-(thio)triphosphate binding assays. Some agonists become antagonists at some constructs as they lose their ability to activate them. Some alkaloid antagonists are transformed into agonists at other constructs, but their agonistic effects can still be blocked by the peptide antagonist TIPP. Even the delta inverse agonist 7-benzylidenenaltrexone becomes an agonist at the mutant containing both the Ile-277 --> Val/His-278 --> Gln/Ile-279 --> Val and Ile-304 --> Thr mutations. Thus, although the mutated residues are thought to be part of the binding pocket, they are critically involved in the control of the delta receptor activation process. These findings shed light on some of the structural bases of ligand efficacy. They are also compatible with the hypothesis that a ligand may achieve high affinity binding in several different ways, each having different effects on receptor activation.

Animals↗
PubMed2000

Fullerene-sensitized

[reaction: see text] Fullerene catalyzes the cycloaddition of dimethyliminodiacetate to maleimides under photolysis to form 2,5-dimethoxycarbonylpyrrolidine derivatives.

Journal Article↗
PubMed2000

Fcgamma receptor-mediated phagocytosis in macrophages lacking the Src family tyrosine kinases Hck, Fgr, and Lyn.

Macrophage Fcgamma receptors (FcgammaRs) mediate the uptake and destruction of antibody-coated viruses, bacteria, and parasites. We examined FcgammaR signaling and phagocytic function in bone marrow-derived macrophages from mutant mice lacking the major Src family kinases expressed in these cells, Hck, Fgr, and Lyn. Many FcgammaR-induced functional responses and signaling events were diminished or delayed in these macrophages, including immunoglobulin (Ig)G-coated erythrocyte phagocytosis, respiratory burst, actin cup formation, and activation of Syk, phosphatidylinositol 3-kinase, and extracellular signal-regulated kinases 1 and 2. Significant reduction of IgG-dependent phagocytosis was not seen in hck(-)(/)-fgr(-)(/)- or lyn(-)(/)- cells, although the single mutant lyn(-)(/)- macrophages did manifest signaling defects. Thus, Src family kinases clearly have roles in two events leading to FcgammaR-mediated phagocytosis, one involving initiation of actin polymerization and the second involving activation of Syk and subsequent internalization. Since FcgammaR-mediated phagocytosis did occur at modest levels in a delayed fashion in triple mutant macrophages, these Src family kinases are not absolutely required for uptake of IgG-opsonized particles.

Actins↗
PubMed2000

Phosphatidylinositol 3-kinase and mTOR mediate lipopolysaccharide-stimulated nitric oxide production in macrophages via interferon-beta.

Bacterial lipopolysaccharide (LPS) elicits responses by macrophages that help the body repel infections. Recent evidence indicates that phosphatidylinositol 3-kinase (PI 3-kinase) may mediate some of these responses. Here, we show that exposing macrophages to LPS rapidly increased membrane-associated PI 3-kinase activity and also elevated p70 S6 kinase activity. Inhibitors of PI 3-kinase or the mammalian target of rapamycin (mTOR) fully blocked p70 S6 kinase activation, implying that this kinase is controlled by PI 3-kinase and mTOR. These inhibitors also substantially reduced LPS-induced nitric oxide (NO) production. This inhibition was, in part, attributable to impaired LPS-stimulated secretion of interferon-beta, an autocrine co-factor for NO production. However, the addition of exogenous interferon-beta did not fully restore NO production, indicating that the NO response was being inhibited by another mechanism as well. Together, these data suggest that PI 3-kinase, mTOR, and possibly p70 S6 kinase mediate LPS-induced NO production by regulating the secretion of interferon-beta and by a second undefined mechanism.

Androstadienes↗
PubMed2000

Interleukin-1 beta, tumor necrosis factor-alpha and lipopolysaccharide induce expression of monocyte chemoattractant protein-1 in calf aortic smooth muscle cells.

To investigate whether interleukin-1 beta(IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS) induce expression of monocyte chemoattractant protein-1 (MCP-1) mRNA and protein in calf aortic smooth muscle cells(SMCs), calf aortic SMCs were cultured by a substrate-attached explant method. The cultured SMCs were used between the third to the fifth passage. After the cells became confluent, the SMCs were exposed to 2 ng/ml IL-1 beta, 20 ng/ml TNF-1 alpha and 100 ng/ml LPS respectively, and the total RNA of SMCs which were incubated for 4 h at 37 degrees C were extracted from the cells by using guanidinium isothiocyanate method. The expression of MCP-1 mRNA in SMCs was detected by using dot blotting analysis using a probe of gamma-32P-end-labelled 35-mer oligonucleotide. After a 24-h incubation, the media conditioned by the cultured SMCs were collected. The MCP-1 protein content in the conditioned media was determined by using sandwich ELISA. The results were as follows: Dot blotting analysis showed that the cultured SMCs could express MCP-1 mRNA. After a 4-h exposure to IL-1 beta, TNF-alpha and LPS, the MCP-1 mRNA expression in SMCs was increased (3.6-fold, 2.3-fold and 1.6-fold, respectively). ELISA showed that the levels of MCP-1 protein in the conditioned media were also increased (2.9-fold, 1.7-fold and 1.1-fold, respectively). The results suggest that calf aortic SMCs could express MCP-1 mRNA and protein. IL-1 beta and TNF-alpha can induce strong expression of MCP-1 mRNA and protein, and the former is more effective than the latter.

Animals↗
PubMed2000

[A comparison between latanoprost and timolol in treatment of patients with primary open-angle glaucoma and ocular hypertension].

OBJECTIVE: To evaluate the therapeutic value of latanoprost on glaucoma. METHODS: In an open-label fashion, multicenter, randomized control clinical trial, the efficacy and adverse drug reactions of topical application of 0.005% latanoprost once daily were compared with that of 0.5% timolol twice daily for 12 weeks in patients with open-angle glaucoma or ocular hypertension. RESULTS: The study included 128 patients (63 patients in latanoprost group and 65 patients in timolol group) and 117 patients remained at the end of the study (60 cases in latanoprost group and 57 cases in timolol group). Comparing 12 weeks with baseline diurnal intraocular pressure (IOP), the IOP reduction (mean +/- standard deviation) in latanoprost group was (7.5 +/- 0.3) mm Hg (1 mm Hg = 0.133 kPa) (32%, t = 22.73, P < 0.0001) greater than the reduction in timolol group (6.1 +/- 0.3) mm Hg (26%, t = 17.94, P < 0.0001), the difference between the two groups being significant (F = 9.54, P = 0.0026). Two patients treated with timolol and none treated with latanoprost were withdrawn from the study because of inadequate IOP control; 3 patients with latanoprost had foreign body sensation. In latanoprost group, there was one patient whose eyelashes became darker and longer at the last visit (the 12th week). No ocular and systemic adverse events related to the two drugs were found. CONCLUSION: It is demonstrated that 0.005% latanoprost topically applied once daily is well tolerated and more effective in reducing IOP than 0.5% timolol topically applied twice daily. Thus, latanoprost has the potential to be a new first-line antiglaucoma drug.

Adrenergic beta-Antagonists↗
PubMed2000

[Effects of IL-1beta, TNF-alpha and lipopolysaccharide on the expression of MCP-1 in human umbilical vein endothelial cells].

OBJECTIVE: To investigate whether the proinflammatory cytokines IL-1beta, TNF-alpha and lipopolysaccharide (LPS) enable to induce the expression of MCP-1 mRNA and protein in human umbilical vein endothelial cells (HUVECs). METHODS: After a four-hour exposure to 2 ng/ml IL-1beta, 20 ng/ml TNF-alpha or 100 ng/ml LPS, total RNA of HUVECs was extracted by single-step method. The expression of MCP-1 mRNA in HUVECs was examined by dot blot analysis using a probe of gamma-(32)P-end-labelled 35 mer oligonucleotide. Meanwhile, MCP-1 protein in the cytoplasm was detected by SABC immunostaining. RESULTS: Dot blot analysis showed that cultured HUVECs were able to express MCP-1 mRNA at a low level. Exposure to IL-1beta, TNF-alpha and LPS resulted in a 7.8-fold, 2.6-fold and 1.2-fold induction of MCP-1 mRNA expression in HUVECs, respectively. The cells on the coverglass in all groups revealed MCP-1 immunoreactivity. Densitometry scans showed that the mean absorbance (A) values of the cells in LPS, TNF-alpha and IL-1beta groups were 0.078 +/- 0.113, 0.102 +/- 0.005 and 0.117 +/- 0.010, respectively; whereas the absorbance values of the control group was 0.051 +/- 0.004. There were significant differences between all the experimental groups and the control group (F = 193.25, P < 0.01). CONCLUSIONS: IL-1beta and TNF-alpha induce a strong expression of MCP-1 mRNA and protein in HUVECs. Both cytokines may be involved in the atherogenesis by inducing the liberation of MCP-1 by endothelial cells and increasing the recruitment of monocytes into the subendothelial space.

Cells, Cultured↗
PubMed2000

[Autologous bone marrow transplantation for patients with chronic myelogenous leukemia after in vitro purging of the graft with bcr/abl antisense oligodeoxynucleotides].

OBJECTIVE: To investigate the efficacy of autologous bone marrow transplantation (ABMT) for patients with chronic myelogenous leukemia (CML) after in vitro purging of the graft with bcr/abl antisense oligodeoxynucleotides (AS-ODN). METHODS: Five CML patients, 2 in chronic phase (CP), 1 in accelerated phase (AP) and 2 in blast crisis (BC), all confirmed the presence of b3a2 bcr/abl mRNA by RT-PCR (reverse transcriptase-polymerase chain reaction). Patients had received 2 courses of intensive chemotherapy for "in vivo purging" before bone marrow harvesting. The autologous bone marrow cells were concentrated by CS3000plus and then incubated with 18-mer phosphorothioate bcr/abl AS-ODN (40 - 60 microg/ml, for 48 - 60 h). Conditioning regimens were TBI + Cy (total body irradiation + cyclophosphamide) or MAC + CCNU. RESULTS: After intensive chemotherapy, ph(+) cells in bone marrow reduced to 34% (24% - 46%) and the numbers of bcr/abl mRNA (+) CFU-GM to 45.6% (33% - 58%). After bcr/abl AS-ODN in vitro purging, two patients were bcr/abl mRNA negative and three positive with the number of bcr/abl mRNA (+) CFU-GM markedly reduced. Delayed hematopoietic reconstitutions were observed in all patients after ABMT. During a more than 2 years follow-up period, three patients obtained major cytogenetic remission (MCR) and lasted for 9 - 12 months and the durations of CP after ABMT were longer than that before ABMT. One of this three in BC before ABMT being survived disease-freely for 37 months with bcr/abl mRNA (-) after ABMT. Another patient in BC had a short duration of MCR and relapsed at +7 months. One patient died from severe infection and bleeding at day +74 because of delayed reconstitution. CONCLUSION: ABMT with bcr/abl AS-ODN purged graft can result in quite long duration of MCR and prolonged CP in some patients with CML.

Adolescent↗
PubMed1999

[Allogeneic peripheral stem cell transplantation (PBSCT) for hematological malignancies].

OBJECTIVE: To evaluate the efficacy of allo-PBSCT in hematological malignancies. METHODS: Sixteen patients with hematological malignancies were treated by allo-PBSCT, started from march 1997. Five of them were ALL (CR1 4, CR2 1), 2 ANLL (CR1), 8 CML(CP 5, AP 3), and one NHL(PR). The median age was 33(18-49) years. Conditioning regimen was TBI 9-10 Gy + CTX 120 mg/kg, or TBI 10 Gy + CTX 120 mg/kg + Vp16 500 mg. A combination of cyclosporine and methotrexate was administered to prevent acute GVHD. All donors received G-CSF 5 micrograms.kg-1.d-1 for 5 to 6 days. One or three leukapheresis procedures were performed by CS 3000 plus blood cell separator to collect a median mononuclear cells of 9 x 10(8)/kg recipient weight [range(5.79-13.7) x 10(8)/kg], including a median CD34+ cells 13.9 x 10(6)/kg [range(5.69-49.00) x 10(6)/kg]. RESULTS: All patients were engrafted and hematopoietic reconstitution was rapid: neutrophils achieving 0.5 x 10(9)/L on day 12 (range, 10-15), platelets > 30 x 10(9)/L on day 13 (range, 8-24). More than grade II aGVHD occurred in 3(18.7%), and localized cGVHD in 3 patients. Leukemia relapse occurred in one patients. The median follow-up duration was 13 months. Eleven patients were alive in disease-free situation. CONCLUSION: Allo-PBSCT can rapidly reconstitute hematopoiesis with incidences of aGVHD and cGVHD not more than that in BMT.

Adolescent↗
PubMed1999

[The detection of T-cell receptor gene rearrangement in myelodysplastic syndromes].

OBJECTIVE: To analyse the T cell receptor (TCR) gene rearrangement in myelodysplastic syndromes (MDS). METHODS: Polymerase chain reaction (PCR) was used to detect the TCRVgammaI-Jgamma gene rearrangement in 36 cases of MDS. RESULTS: 8 cases (22.2%) were found to have TCRVgammaI-Jgamma gene rearrangement. The TCR gene rearrangement positive rate was higher in RAEB, CMML and RAEBT subtypes than that in RA and RAS subtypes (P < 0.05). The average time MDS evolving to acute leukemia was shorter in the MDS patients with TCRVgammaI-Jgamma for gene rearrangement than that in patients without (P < 0.01). CONCLUSION: TCR gamma gene rearrangement can also be found in some MDS patients and the detection of TCRgamma gene rearrangement might be helpful to identify the prognosis and the development of MDS.

Adolescent↗