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Biomedical subjects

Q Li

Publications and source records attributed to Q Li.

At least 649 records · Page 36Linked to original sources
PubMed1997

Fusion of phospholipid vesicles induced by the ribosome inactivating protein saporin.

The single chain ribosome-inactivating protein Saporin-S6 (SO-6) induces the fusion of acid phospholipid vesicles. The extent of fusion was measured by resonance energy transfer assay between the N-(7-nitro-2-1,3-benzoxadiazol-4-yl)-dimyristoylphosphatidyl lithanolamine (NBD-PE)(donor) and N-(lissamine rhodamine B sulphonyl)-diacylphoshaidylethanolamine (Rh-PE) (acceptor) incorporated in the vesicle. The saturated lipid/protein molar ratio is approx. 100:1. The time course of fusion of vesicles induced by the protein showed that the process was completed within 10 minutes, and the size of the particles in the medium was enlarged which conforms the occurrence of the fusion occurring. The fusion is temperature dependent and the liquid-crystalline state lipid is more apt to fuse than the gel phase lipid. The effect of SO-6 is also dependent on ionic strength and pH, high salt concentration and basic pH may abolish fusion, which suggests that both electrostatic and hydrophobic components may be involved in the process.

Hydrogen-Ion Concentration↗
PubMed1997

Effects of hydrostatic pressure on the activity of rat ribosome and cell-free translation system.

The effects of high hydrostatic pressure on the protein synthesis activity of rat liver ribosome and the reconstructed cell-free translation system were studied. The results indicated that the activity of the ribosome decreased with the increase in applied pressure and the activity was totally lost as pressure went up to 2,400 bar, but there was a plateau approximately from 300 to 1,200 bar where the activity only had a minor change. The activity of the cell-free translation system seems to be more sensitive to pressure. Its activity was entirely lost when the pressure was up to 900 bar. The activity of rat ribosome and the cell-free translation system treated by pressure below 900 bar could be almost completely restored by incubation after releasing the pressure, but could be partially restored at higher pressure.

Animals↗
PubMed1997

Fpg protein releases a ring-opened N-7 guanine adduct from DNA that has been modified by sulfur mustard.

Transfection of the Escherichia coli fpg gene into Chinese hamster ovary cells has been reported to enhance survival after exposure to aziridine (C. Cussac and F.Laval, 1996, Nucleic Acids Res., 24, 1742-1746). This result suggests that Fpg protein protects cells from toxicity by removing ring-opened N-7 guanine adducts from DNA, and raises the possibility that Fpg protein would offer protection from other agents that alkylate the N-7 position of guanine. Since the major adduct formed by sulfur mustard in DNA is 7-hydroxyethyl-thioethylguanine (HETEG), we have investigated the action of Fpg protein on the ring-opened form of this adduct (ro-HETEG). A substrate containing ro-HETEG was prepared by alkaline treatment of DNA modified by [14C]sulfur mustard. Fpg protein purified from an over-producing strain of E. coli released ro-HETEG from this substrate in an enzyme- and time-dependent manner, and at a rate that is similar to that at which it releases ring-opened 7-methylguanine. Thus, Fpg protein acts efficiently on ro-HETEG, and may offer some protection against the toxic action of sulfur mustard.

Adenine↗
PubMed1997

Comparative vasoconstrictor effects of angiotensin II, III, and IV in human isolated saphenous vein.

Elevated levels of angiotensin (Ang II) and its degradation products angiotensin III (Ang III) and angiotensin IV (Ang IV) may contribute to the regulation of vascular tone under various clinical circumstances. We investigated the contractile effects of Ang III and Ang IV in endothelium-denuded human saphenous vein (SV) preparations and compared them with those of Ang II. The veins were suspended in organ chambers, and changes in isometric force were recorded. Ang II (0.1-100 nM), Ang III (1 nM-3 microM), and Ang IV (0.3 microM-0.1 mM) caused concentration-dependent contractions with comparable maximal responses (Emax). Ang III was 16 times less active than Ang II, whereas Ang IV was approximately 2,700-fold less potent than Ang II. In the presence of the aminopeptidase-A and -M inhibitor amastatin (10 microM), the potencies of Ang III and Ang IV were increased by approximately 16 and 12 times, respectively, although no changes of Ang II potency were observed. The AT1-selective Ang II receptor antagonist losartan (10 and 100 nM) but not the AT2-selective antagonist PD123177 (1 microM), shifted the concentration-response curves (CRC) for the angiotensin peptides to the right in a parallel manner. Preincubation with indomethacin (10 microM), a cyclooxygenase inhibitor, did not influence the CRCs for any of the angiotensin peptides studied. Tachyphylaxis was investigated by constructing a second series of CRCs for the angiotensin peptides after an interval of 60 min. Ang II showed strong tachyphylaxis (the Emax value of the second Ang II CRC was approximately 50% of the first), whereas Ang III and Ang IV did not. Our results indicate that in endothelium-denuded human SV, both Ang III and Ang IV are less potent but similarly efficacious vasoconstrictor agents compared with Ang II. Endogenous aminopeptidase activity may counteract the effects of the angiotensin peptides. The contractile responses to all three peptides are mediated via AT1-receptors but not AT2-receptors.

Aged↗
PubMed1997

Chaperone functions common to nonhomologous Epstein-Barr virus gL and Varicella-Zoster virus gL proteins.

Herpesviruses encode the complex-forming, essential glycoproteins gH and gL. Maturation and transport of gH are dependent on coexpression of its chaperone, gL. The gL proteins of alpha herpesviruses and gamma herpesviruses do not have a significant percentage of amino acid sequence homology. Yet, as we report herein, the diverse gL glycoproteins of Epstein-Barr virus (EBV) and varicella-zoster virus (VZV) were functionally interchangeable, although membrane expression and maturation of gH were separate functions for these viruses. In VZV both functions were performed by a single protein. EBV required two separate glycoproteins, one of which can be replaced by its homologous protein from VZV, a distant relative of EBV. Collectively, these results suggested that VZV gL is a simpler form of the gL chaperone protein than EBV gL.

Herpesvirus 3, Human↗
PubMed1997

Epstein-Barr virus uses HLA class II as a cofactor for infection of B lymphocytes.

Infection of B lymphocytes by Epstein-Barr virus (EBV) requires attachment of virus via binding of viral glycoprotein gp350 to CD21 on the cell surface. Penetration of the cell membrane additionally involves a complex of three glycoproteins, gH, gL, and gp42. Glycoprotein gp42 binds to HLA-DR. Interference with this interaction with a soluble form of gp42, with a monoclonal antibody (MAb) to gp42, or with a MAb to HLA-DR inhibited virus infection. It was not possible to superinfect cells that failed to express HLA-DR unless expression was restored by transfection or creation of hybrid cell lines with complementing deficiencies in expression of HLA class II. HLA class II molecules thus serve as cofactors for infection of human B cells.

Antibodies, Monoclonal↗
PubMed1997

The relationship between tumor necrosis factor and human immunodeficiency virus gene expression in lymphoid tissue.

In tissue culture models of chronic human immunodeficiency virus type 1 (HIV-1) infection, cytokines such as tumor necrosis factor alpha (TNF-alpha) activate viral gene expression. We sought evidence that TNF-alpha might similarly regulate viral gene expression in vivo in the major lymphoid tissue (LT) reservoir. We used in situ hybridization, quantitative image analysis, and double-label techniques to compare cytokine and HIV-1 RNA levels in sections of tonsil and lymph node tissues obtained from individuals in early and later stages of HIV-1 infection. The levels of TNF-alpha gene expression in LT from HIV-1-infected an uninfected individuals were indistinguishable, and we found no correlation between TNF-alpha gene expression in LT and the level of HIV-1 gene expression in LT. There is thus little evidence that in vivo TNF-alpha significantly influences HIV production in LT.

Gene Expression↗
PubMed1997

Sheltering of gamma-globin expression from position effects requires both an upstream locus control region and a regulatory element 3' to the A gamma-globin gene.

Integration position-independent expression of human globin transgenes in transgenic mice requires the presence of regulatory elements from the beta-globin locus control region (LCR) in the transgene construct. However, several recent studies have suggested that, while clearly necessary, such elements are not by themselves sufficient to realize this effect. In the case of the human fetal gamma-globin genes, previous results have indicated that additional regulatory information required for sheltering of gamma-globin transgene expression from position effects may reside downstream from the A gamma gene. To investigate this possibility, we established 17 lines of transgenic mice carrying constructs comprising a micro-LCR (microLCR) element, an A gamma-globin gene fragment, and a variable length of 3' sequence information beyond the A gamma 3' HindIII site. gamma-Globin expression during development was studied in 170 individual F2 progeny from these lines. We find that gamma-globin expression becomes sheltered from position effects when the normally position-sensitive microLCR-A gamma construct is extended by 600 bp beyond the 3' HindIII site to include a previously identified regulatory sequence (the A gamma-globin enhancer), the functional significance of which in vivo had heretofore been unclear. The results suggest that the mechanism whereby an upstream LCR achieves sheltering of globin gene expression from position effects involves cooperation with a gene-proximal regulatory element distinct from the promoter region.

Animals↗
PubMed1997

Identification of putative c-Myc-responsive genes: characterization of rcl, a novel growth-related gene.

The c-Myc protein is a helix-loop-helix leucine zipper oncogenic transcription factor that participates in the regulation of cell proliferation, differentiation, and apoptosis. The biochemical function of c-Myc has been well described, yet the identities of downstream effectors are just beginning to emerge. We describe the identification of a set of c-Myc-responsive genes in the Rat1a fibroblast through the application of cDNA representational difference analysis (RDA) to cDNAs isolated from nonadherent Rat1a and Rat1a-myc cells. In this system, c-Myc overexpression is sufficient to induce the transformed phenotype of anchorage-independent growth. We identified 20 differentially expressed cDNAs, several of which represent novel cDNA sequences. We further characterized one of the novel cDNAs identified in this screen, termed rcl. rcl expression is (i) directly stimulated by c-Myc; (ii) stimulated in the in vivo growth system of regenerating rat liver, as is c-myc; and (iii) elevated in human lymphoid cells that overexpress c-myc. By using an anti-Rcl antibody, immunoblot analysis, and immunofluorescence microscopy, the Rcl protein was found to be a 23-kDa nuclear protein. Ectopic expression of the protein encoded by the rcl cDNA induces anchorage-independent growth in Rat1a fibroblasts, albeit to a diminished extent compared to ectopic c-Myc expression. These data suggest a role for rcl during cellular proliferation and c-Myc-mediated transformation.

Amino Acid Sequence↗
PubMed1997

Gastric epithelial morphogenesis in normal and transgenic mice.

The epithelium located in the corpus of the adult mouse stomach forms mucosal invaginations known as gastric units. Gastric units are populated by members of the pit, parietal, and neck-zymogenic cell lineages all of which are derived from multipotent stem cells. Gastric unit morphogenesis was examined in normal embryonic day 18 (E18) to postnatal day 28 (P28) FVB/N mice with electron microscopy and multilabel immunohistochemistry. E18 units appear as short, solid infoldings (primordial buds), 92% of whose cells represent pit, parietal, and neck cell precursors. Although the total number of cells per bud does not change from P1 to P7, immature cells decrease to 22% as differentiated pit, neck, and parietal cells appear. From P7 to P15, lineage precursors and their differentiated progeny increase and buds elongate. Between P15 and P21 the multipotent stem cell and its descendants are assembled into a distinct proliferative zone (isthmus) located in the midportion of each unit, and cellular migration-differentiation programs become compartmentalized. To examine the role of parietal cells in regulating gastric unit morphogenesis, nucleotides -1035 to +24 of the mouse H(+)-K(+)-adenosinetriphosphatase beta-subunit gene were used to express simian virus 40 large T antigen (SV40 TAg) exclusively in this lineage. SV40 TAg amplified the normally rare pre-parietal cell and disclosed a pre-parietal cell precursor. Pre-parietal cells and their precursors were the predominant cells in E18-P1 transgenic buds. At later stages of development (P1-P28) there was a block in differentiation of pre-parietal to mature parietal cells, a decrease in neck cells, and a marked depletion of zymogenic cells. These findings suggest that members of the parietal cell lineage are the source of instructions that affect the neck-zymogenic cell lineage, even before the gastric unit is compartmentalized into its anatomically distinct pit, isthmus, neck, and base regions.

Animals↗
PubMed1997

Coronary constriction impairs cardiac function and induces myocardial damage and ventricular remodeling in mice.

To establish whether coronary artery narrowing (CAN) in mice was accompanied by depressed ventricular function, tissue injury, and modifications in cardiac anatomy, the left coronary artery was constricted in FVB/N mice and the animals were killed 7 days later. CAN consisted of a 53% reduction in luminal diameter, which resulted in a twofold increase in left ventricular end-diastolic pressure. Left ventricular systolic pressure and left ventricular + and -dP/dt decreased 15, 21, and 11%, respectively. Left ventricular weight-to-body weight ratio increased 33%. This hypertrophic adaptation was characterized by a 9 and 20% increase in the longitudinal and transverse cavitary diameters, which provoked a 1.5-fold expansion in chamber volume. In contrast, wall thickness decreased 15%. These anatomic and functional changes induced a threefold elevation in diastolic stress. Foci of reparative fibrosis were found in the endomyocardium and epimyocardium, involving 2-3% of the tissue. Finally, myocyte loss in the ventricle was 15%, and myocyte hypertrophy was 38%. Impaired ventricular function, diastolic Laplace overloading, myocyte loss, and decompensated eccentric hypertrophy in mice after CAN mimic the ischemic cardiomyopathic heart in humans.

Animals↗
PubMed1997

Effects of Plasmodium berghei infection on arteether metabolism and disposition.

Arteether (AE) is primarily deethylated to dihydroqinghaosu (DQHS) in rats and humans. Conversion of AE to DQHS was impaired in microsomes from rats infected with Plasmodium berghei. The Km for AE was 175.1 +/- 49.1 and 124.4 +/- 115.1 mumol/l, and Vmax was 2.24 +/- 0.45 and 1.22 +/- 0.67 nmol AE formed/mg protein/min in control and infected microsomes (p < 0.05), respectively. Calculated intrinsic clearance (CLint = initial Vmax/Km) for AE was only 4% lower in infected microsomes. Apparent pharmacokinetic parameter estimates for AE using the isolated perfused rat liver demonstrated no differences (p > 0.05) in volume of distribution, clearance, and half-life between normal and infected animals. Malaria infection resulted in decreased biliary excretion of free AE and DQHS. The majority of AE is eliminated via biliary excretion of conjugated DQHS, which is approximately 500-fold higher than free DQHS and 75-fold higher than free AE on a molar basis.

Animals↗
PubMed1997

Longitudinal change in basal ganglia volume in patients with Huntington's disease.

Cross-sectional MRI studies demonstrating an association between caudate atrophy and symptom severity and duration of symptoms in patients with Huntington's disease (HD) have been assumed to reflect longitudinal changes in basal ganglia, but such neuropathologic progression has never been directly demonstrated. Subjects in the current study were 23 HD patients at various stages of the disorder who had two MRI images at least 10 months apart (mean interimage interval = 20.8 months). We measured volumes of caudate, putamen, and globus pallidus blind to the order of the images. For each structure, we calculated a change score by subtracting the volume obtained on the follow-up imaging from that obtained on the initial imaging. Results indicated significant decreases over time in caudate, putamen, and total basal ganglia volume. Age at onset and length of trinucleotide repeat correlated significantly with amount of volume change in caudate and total basal ganglia, even after controlling for length of interimage interval, duration of disease, and measures of symptom severity. Amount of change in basal ganglia structures was not significantly correlated with neurologic symptom severity at the time of the initial imaging or duration of symptoms. This is the first longitudinal MRI study to document progressive basal ganglia atrophy in HD, and suggests that quantitative neuroimaging with serial MRI may be useful in monitoring effectiveness of potential treatments. In addition, demonstration of greater rate of basal ganglia atrophy in patients with earlier symptom onset suggests that treatment effects may be more quickly observed in this subgroup of patients than in the general HD population.

Adult↗
PubMed1997

Stretch-induced proliferation of cultured vascular smooth muscle cells and a possible involvement of local renin-angiotensin system and platelet-derived growth factor (PDGF).

This experiment was designed to investigate the possible involvement of angiotensin II (Ang II) and platelet-derived growth factor (PDGF) in the mechanism underlying stretch-induced proliferation of vascular smooth muscle cells (SMCs). SMCs from the rabbit aortic media were grown on polystyrene rubber-bottomed dishes coated with type I collagen. Cells were stretched cyclically by a vacuum-operated downward flexion of the culture dish bottom. A 1.4- to 1.6-fold increase in proliferation of SMCs was induced by cyclic stretching, as determined by [3H]-thymidine incorporation, in a stretch force-dependent manner in the range of 5% to 15% elongation, 30 cycles/min for 24 h. Expression of PDGF-B chain mRNA was up-regulated in a time-dependent manner in the range of 2 to 24 h, 10% elongation, and 30 cycles/min. Saralasin, a selective antagonist of Ang II, and captopril, an angiotensin I converting enzyme inhibitor, significantly suppressed the stretch-induced proliferation of SMCs. Blockade of angiotensinogen mRNA translation by antisense oligonucleotide inhibited proliferation under the mechanical strain. Stretch-induced proliferation was inhibited by 78% in the presence of anti-PDGF-AB neutralizing antibody. Increased expression of PDGF-B chain mRNA under the mechanical strain was inhibited by treatment with saralasin. Our results indicate that the stretch-induced proliferation of cultured SMCs is mediated at least in part via increased production of Ang II by the local renin-angiotensin system and a subsequent up-regulation of PDGF-B chain mRNA in an autocrine-paracrine manner.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Dynamic structure of the sarcin/ricin domain in rat 28S ribosomal RNA investigated by hybridization with oligodeoxynucleotide.

In the static state of the ribosome, its S/R domain is not accessible to a probe of 1 4-mer oligodeoxyribonucleotide complementary to the region. However, during the in vitro translation process, the probe can specifically hybridize with the region in ribosome and inhibit translation. It appears that the S/R domain is well-protected when the ribosome is in the static state. This site is partially exposed at some stage(s) of translation. These results indicate that the S/R domain is not a simple single-strand, but a reversibly dynamic structure.

Animals↗
PubMed1997

Endotoxin induces increased intracellular cathepsin B activity in THP-1 cells.

Macrophage cathepsin B (CB) is implicated in tissue injury in inflammatory diseases. Lipopolysaccharide (LPS) is an activator of macrophages whose effect on CB is unknown. This study was undertaken to investigate the potential of macrophages as a source of increased CB and to determine if exposure to LPS might stimulate CB levels. As a model we chose the macrophage-like tumor line, THP-1. Incubation with LPS led to a time and dose-dependent increase in CB activity. LPS potentiated interferon-gamma (IFN-gamma)-induced elevations of CB and led to an additive increase in CB activity. Pretreatment of the cells with LPS not only caused a marked stimulation of CB activity over that seen with IFN-gamma alone, but also decreased the concentration and exposure time to the cytokine necessary to achieve maximum induction of the enzyme. The LPS and IFN-gamma induced CB increases were abolished by cycloheximide or actinomycin D in the cultures, indicating that the increases in CB required increased RNA transcription and de novo protein synthesis. Direct measurement of CB mRNA showed increases. These data indicate that although LPS alone appears to induce the production of CB in THP-1 cells, it augments IFN-gamma induced increases, suggesting that two signals are necessary for maximum CB induction in this system.

Cathepsin B↗
PubMed1997

[The long-term effect of nifedipine (control release tablets) in patients with chronic obstructive pulmonary disease and cor pulmonale].

OBJECTIVE: To observe the long-term effect of nifedipine (control release tablets) in patients with chronic obstructive pulmonary disease and cor pulmonale. METHODS: A randomized, double blind, placebo-controlled design was made, two hundred and two patients (FEV1/FVC was 47.35% +/- 8.10%) were divided into two groups: nifedipine group (20 mg Bid) 102 cases, placebo group (one tablet Bid) 100 cases. RESULTS: The equilibrium test between both groups was comparable. Two-year follow-up rates of both groups were 94% and 89%, respectively. The comparision of the nifedipine to placebo group was as follows: in nifedipine group, the improvement of dyspnea, fatigue and exercise capacity showed significantly better results (P < 0.05); FEV1 and PaCO2 deterioration was unremarkable (P > 0.05); the pulmonary impedance plethysmogram B-Y1 that reflects pulmonary vascular compliance appeared significant improvement (P < 0.05) and the mortality of the disease that was the most important observation endpoint was declined (P = 0.051), but some electrocardiographic index reflected right ventricular load became worse (P < 0.05). CONCLUSIONS: Long-term taking controlled release-nifedipine is a safe, effective measure which might improve life quality and decrease mortality in patients with chronic obstructive pulmonary disease and chronic cor pulmonale, however the drug can not slow down or reverse the progress of this illness.

Adult↗