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C Zhu

Publications and source records attributed to C Zhu.

At least 199 records · Page 11Linked to original sources
PubMed1994

Virulence properties and attaching-effacing activity of Escherichia coli O45 from swine postweaning diarrhea.

Escherichia coli O45 isolates associated with swine postweaning diarrhea in Québec were characterized with respect to virulence determinants genetically and investigated for their attaching and effacing (A/E) activities by experimental inoculation of gnotobiotic piglets and by the HEp-2 cell adherence assay. All of 32 isolates tested were negative for enterotoxigenic and verotoxigenic E. coli virulence determinants, heat-labile enterotoxin (LT), heat-stable enterotoxins (STap, STb), verotoxins (VT1, VT2), and F4 (K88), F5 (K99), F6 (987P), and F41, except one STb-positive and two F4-positive isolates. A total of 25 isolates hybridized with an EaeA probe, and 11 hybridized with an enteropathogenic E. coli adherence factor (EAF) probe. None of 32 isolates hybridized with a bundle-forming pilus (BFP) probe. The EAF, EaeA, and BFP factors have been associated with human enteropathogenic E. coli strains. A total of 10 of 12 eaeA-positive porcine O45 isolates induced A/E lesions characterized by intimate adherence of bacteria to the intestinal epithelial cell membrane with effacement of the microvilli, similar to those of human attaching-effacing E. coli. However, A/E lesions were not observed in the piglets inoculated with any one of three eaeA-negative O45 isolates. All E. coli O45 isolates were non-adherent to HEp-2 cells. Thus, we have demonstrated the production of typical A/E lesions by nonenterotoxigenic E. coli O45 isolates from swine postweaning diarrhea. The results indicate the significance of the eaeA gene in A/E activities of these isolates and suggest that EAF and BFP are not involved in O45 E. coli infection of weaning piglets.

Adhesins, Bacterial↗
PubMed1993

Characterization of broken DNA molecules associated with V(D)J recombination.

We previously demonstrated that DNA molecules with double-strand breaks at variable-(diversity)-joining [V(D)J] recombination signal sequences are relatively abundant in mouse thymocytes. This abundance strongly suggests that the mechanism of V(D)J recombination involves double-strand cleavage at recombination signals. As a first step toward understanding the mechanism of cleavage, we used a sensitive PCR assay to characterize the structure of one class of cleavage products, the signal ends, in detail. Here we demonstrate that most of these ends are blunt and terminate in 5' phosphoryl groups. Virtually all of the flush signal ends are full length. A minor subpopulation of broken ends terminates in short single-strand extensions. We have found no evidence for covalent DNA-protein linkages involving the signal ends. These data allow further refinement of the double-strand cleavage model for V(D)J recombination.

Animals↗
PubMed1993

Determination of adhesion force between single cell pairs generated by activated GpIIb-IIIa receptors.

A biophysical approach was used to directly determine the avidity of the junction between two Chinese hamster ovary (CHO) cells bearing recombinant GpIIb-IIIa in the presence and absence of fibrinogen. Micromanipulation was used to induce conjugation of the cell pairs with or without activating the GpIIb-IIIa molecules with monoclonal antibody (MoAb) 62. Activation of GpIIb-IIIa caused an increase in the force required to separate the conjugates. The molecular bonding force between cells bearing activated GpIIb-IIIa and fibrinogen molecules was found to be 2.1 x 10(-7) dyne, which is 3.7 times higher than that between nonactivated GpIIb-IIIa and fibrinogen (5.7 x 10(-8) dyne). The results provide a quantitative assessment of the molecular bonding force between fibrinogen and the GpIIb-IIIa expressed on cell surface. The findings indicate that the activation of GpIIb-IIIa leads to an increase in the adhesive force in CHO cell aggregation by increasing the strength of the GpIIb-IIIa-fibrinogen bonds rather than the number of these bonds.

Animals↗
PubMed1993

Angiotensin-converting enzyme inhibitors have no effect on ovulation and ovarian steroidogenesis in the perfused rat ovary.

The null hypothesis of this study was that the angiotensin-converting enzyme inhibitors, captopril and teprotide, would not reduce the number of ovulations in vivo and in vitro in the rat. Captopril (in three regimens) was administered continuously beginning prior to pregnant mare's serum gonadotropin and hCG to trigger ovulation. The number of in vivo ovulations were counted. Ovaries similarly primed with pregnant mare's serum gonadotropin were dissected and perfused in media with hCG and captopril (two regimens) or teprotide (one regimen). The number of in vitro ovulations and steroid production in the perfusions were evaluated. The results were evaluated by the Student's t test. Power calculations gave only a 20% chance of missing a 16% difference in ovulations or steroidogenesis. There was no inhibition of ovulation or change in steroid production in angiotensin-converting enzyme treated rats in vivo or in vitro. While angiotensin II has been shown to be an important mediator in the mechanism of ovulation, angiotensin-converting enzyme inhibition via captopril or teprotide does not result in angiotensin II antagonistic effects. Hypothetical mechanisms to explain this paradox are presented.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

The angiotensin II antagonist saralasin inhibits ovulation in the perfused rat ovary.

OBJECTIVE: Our null hypothesis was that the angiotensin II antagonist saralasin does not reduce the number of ovulations in the rat ovarian perfusion model. STUDY DESIGN: Ovaries from pregnant mare's serum gonadotropin-stimulated immature rats were perfused with nutrient media to which luteinizing hormone and 3-isobutyl-1-methylxanthine had been added to induce ovulation. Test perfusions were treated with saralasin 1 mumol/L (n = 0.5) and compared with controls (n = 5) with the Student t test. Perfusions with both saralasin and angiotensin II and dose-response evaluations were performed. RESULTS: Saralasin-treated ovulations were 6.6 +/- 1.3 (mean + SEM) compared with 18.6 +/- 3.9, p < 0.02. The effects of saralasin could be reversed with the addition of an equimolar amount of angiotensin II. Dose-response evaluations showed a progressive inhibition of ovulation at 10(-8) to 10(-6) mol/L. CONCLUSION: The angiotensin II antagonist saralasin inhibits ovulation in a dose-dependent fashion; this effect is canceled by the addition of equimolar concentrations of angiotensin II.

Angiotensin II↗
PubMed1992

A region of antisense RNA from human p120 cDNA with high homology to mouse p120 cDNA inhibits NIH 3T3 proliferation.

The human nucleolar p120 protein is a proliferation-associated antigen which is expressed in G1 and peaks during the early S phase of the cell cycle. Overexpression of the human p120 protein caused the transformation of NIH 3T3 cells and expression of an antisense p120 construct inhibited the growth of NIH 3T3 cells (Perlaky et al., Cancer Res., 52:428-436, 1992). The middle region of the antisense p120 RNA was found to be almost as inhibitory as the full length antisense construct but the 5' and 3' antisense portions did not affect NIH 3T3 cell proliferation. After the mouse p120 complementary DNA was cloned and sequenced, comparison with the human p120 complementary DNA showed a striking conservation of 85% of the nucleotide sequence and 96% of the amino acid sequence. The two ends of the p120 molecule had less homology in their nucleotide and amino acid sequences. Based on this homology, the observed inhibitory effects of the middle portion of antisense human p120 RNA may be related to suppression of mouse p120 expression by RNA:RNA duplex formation. The high evolutionary conservation of the middle region suggests it has a critical role for the function of this protein.

3T3 Cells↗
PubMed1992

[Studies on the technological process for preparing medicated leaven].

This paper takes as index the content of free acids and total acids, the action of pepsin in the stomachs of hungry mice, impelling functions and intestines of hungry mice and makes a comparison of the raw products with the processed products of medicated leaven. It is suggested that bran-perched or burnt perched leaven is better for invigorating the function of the spleen and promoting digestion.

Animals↗
PubMed1991

A thermodynamic and biomechanical theory of cell adhesion. Part I: General formulism.

The equilibrium thermodynamics calculus of cell adhesion developed by Bell et al. (1984, Biophys. J. 45, 1051-1064) has been extended to the general non-equilibrium case. In contrast to previous models which could only compute the end results of equilibrium states, the present theory is able to calculate the kinetic process of evolution of adhesion, which may or may not approach towards equilibrium. Starting from a basic constitutive hypothesis for Helmholtz free energy, equations of balance of normal forces, energy balance at the edge of the contact area and rate of entropy production are derived using an irreversible thermodynamics approach, in which the restriction imposed by the Second Law of Thermodynamics takes the place of free energy minimization used by Bell et al. (1984). An explicit expression for adhesion energy density is derived for the general transient case as the difference of the usable work transduced from chemical energy liberation from bond formation of specific crosslinking molecules and the repulsive potential of non-specific interactions. This allows the energy balance to be used as an independent boundary equation rather than a practical way of computing the adhesion energy. Jump conditions are obtained from the conservation of crosslinking molecules across the edge of adhesion region which is treated as a singular curve. The bond formation and lateral motion of the crosslinking molecules are assumed to obey a set of reaction-diffusion equations. These equations and the force balance equation within the contact area, plus the jump conditions and the energy balance equation at the edge form a well-posed moving boundary problem which determines the propagation of the adhesion boundary, the separation distance between the two cell membranes over the contact area as well as the distributions of the crosslinking molecules on the cell surfaces. The behavior of the system depends on the relative importance of virtual convection, lateral diffusion and bond formation of the crosslinking molecules at the edge of the adhesion region, according to which two types of rate limiting cases are discussed, viz, reaction-limited and diffusion-limited processes.

Animals↗
PubMed1991

Inhibition of ovulation in the perfused rat ovary by the synthetic collagenase inhibitor SC 44463.

A new, powerful, synthetic inhibitor of mammalian tissue collagenases and related metalloproteinases is inhibitory to ovulation in perfused rat ovaries. Ovaries of immature rats, primed with 20 IU of eCG, were dissected and perfused with 0.1 micrograms/ml LH and 0.2 mM 3-isobutyl-1-methylxanthine (IBMX) for 20 h. Addition of SC 44463 (N4-hydroxy-N1-[1S [(4-methoxphenyl)methyl]-2-(methylamino)-2-oxoethyl]- 2R-(2-methylpropyl)butane-diamide) at a concentration of 25 nM inhibited ovulation by 55% (9.6 +/- 1.7 ovulations per ovary, mean +/- SEM, compared to a control value of 21.7 +/- 1.7); and 250 nM inhibited ovulation by 75% (5.3 +/- 1.1 ovulations per ovary). We previously showed that the related compound SC 40827 inhibited ovulation by 70% when used at a concentration of 25 microM (Brännström et al., Endocrinology 1988; 122:1715-1721). We now show that SC 44463 is 100, 500, and 75 times more powerful than SC 40827 in blocking ovulation, inhibiting action of ovarian interstitial collagenase, and inhibiting action of the small metalloproteinase of the rat uterus, respectively. SC 44463 also inhibits ovarian type IV collagen-digesting activity 50% at a concentration of 18 nM. Ovulation occurs after 9-12 h of perfusion with LH. Compound SC 44463 (25 nM) showed its full inhibitory capacity when added to the medium as late as 7 h after LH, but there was no significant inhibition when it was added at 9 h. This suggests that the major collagenolytic events occur beyond 7 h after stimulation by LH.

1-Methyl-3-isobutylxanthine↗
PubMed1991

A tissue inhibitor of metalloproteinases and alpha-macroglobulins in the ovulating rat ovary: possible regulators of collagen matrix breakdown.

Immature female Sprague-Dawley rats were primed with 20 IU eCG at 28 days of age and treated with 10 IU hCG 48 h later. Ovulation followed at 12-14 h. Ovaries were extracted at various times after hCG by use of Triton X-100 and 10 mM CaCl2 (Triton extract) followed by heating to 60 degrees C for 6 min with 0.1 M CaCl2 in 50 mM Tris/0.15 M NaCl, pH 7.5 (heat extract). These extracts were tested for their ability to inhibit tissue metalloproteinases by use of the small uterine metalloproteinase (UMP) of the rat. The ovary contains three plasma-derived inhibitors (alpha 1-macroglobulin [alpha 1 M], alpha 2-macroglobulin [alpha 2 M], and alpha 1 inhibitor3 [alpha 1I3]) and one tissue-derived inhibitor of the tissue inhibitor of metalloproteinases (TIMP) family. alpha 1 I3 was shown to inhibit UMP and rat collagenase. The concentration of the tissue inhibitor rose 5-fold from 0.6 micrograms UMP blocked per gram wet tissue in ovaries not primed with eCG to 3.2 micrograms UMP blocked at 8 h after hCG. Over this same time interval, the sum of alpha 1M + alpha 2M per gram of ovary rose 7-fold from 3.2 to 22.4 micrograms UMP inhibited and alpha 1I3 rose 2-fold from 4.4 to 10.7 micrograms UMP inhibited. The increases in the tissue inhibitor are interpreted to be due to increased synthesis by the tissue, whereas the changes in alpha-macroglobulins are postulated to be due to increased vascularity and increased permeability of the vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗