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W Zhou

Publications and source records attributed to W Zhou.

At least 379 records · Page 21Linked to original sources
PubMed1994

A microplate-based bioassay system for measuring porcine serum mitogenic activity.

A bioassay system was developed to measure porcine serum mitogenic activity, which is an indicator of growth factor activity. A MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide++ +] cell proliferation assay was used to monitor cell growth. In comparison with electronic cell counting, this bioassay system is sensitive, economical, and semi-automatic. A non-fusing myoblast cell line, BC3H1, was used, making it possible to increase seeding density and thus improve precision. The assay was carried out in 96-well microplates with automatic reading and data processing by a computer-controlled ELISA reader. Results were highly correlated with Kotts' method. This assay system is of potential value in studying growth regulation in pigs.

Animals↗
PubMed1994

The role of feed consumption and feed efficiency in copper-stimulated growth.

Two experiments were conducted to study the role of feed intake and feed efficiency in Cu-stimulated growth of weanling pigs. In Exp. 1, 42 pigs were randomly assigned into three treatments: 1) control: ad libitum access to a corn-soybean meal-dried whey basal diet; 2) ad libitum/Cu: ad libitum access to the basal diet supplemented with 215 ppm of Cu; or 3) pair-fed/Cu: pair-fed the Cu-supplemented diet to the level of the control. Over the 14-d experiment, the ad libitum/Cu pigs had greater (P < .05) ADG and ADFI than the control pigs. The pair-fed/Cu group had an intermediate ADG. Gain:feed (GF) was not significantly affected by treatments but tended to be improved in the pair-fed/Cu pigs. Feeding copper increased (P < .05) the concentration of Cu in the serum, liver, and brain. Also, feeding Cu increased (P < .05) serum mitogenic activity and growth hormone mRNA concentrations for both feeding methods. In Exp. 2, a 2 x 2 x 2 factorial arrangement of treatments with two levels of Cu (15 vs 200 ppm), two levels of feeding (ad libitum vs restricted [85% of the ad libitum]), and two sources of Cu (Cu sulfate vs Cu lysine) was used in a 24-d experiment involving 96 pigs. Feeding copper increased (P < .05) ADG and GF. The magnitude of the Cu-stimulated growth was reduced by restricted feeding (Cu level x feeding level interaction; P < .05). The ADFI was greater (P < .05) for the pigs fed high dietary Cu only during d 1 to 6. Pigs fed Cu lysine had greater ADG and ADFI than those fed Cu sulfate (P < .05); the benefit in ADG from Cu lysine was reduced by restricted feeding (Cu source x feeding level interaction, P < .05). High dietary Cu stimulated (P < .05) serum mitogenic activity; the stimulation was greater for Cu lysine than for Cu sulfate. Feeding Cu numerically increased GH mRNA concentration. Restricted feeding reduced overall serum mitogenic activity (P < .05), but the response to high dietary Cu and Cu lysine was still evident. In summary, Cu-stimulated growth was largely dependent on a simultaneous increase in feed intake, but there were some improvements in GF. The influence of Cu on serum mitogenic activity was independent of feed intake or growth in both experiments, which indicates a direct action of Cu on the growth regulatory system.

Animal Feed↗
PubMed1994

Stimulation of growth by intravenous injection of copper in weanling pigs.

This study was conducted to examine whether Cu could exert its growth-promoting effect when injected, rather than being fed, and thus bypass the gastrointestinal tract. In two 18-d experiments, pigs were injected every 2 d with a Cu histidinate or histidine solution. Amounts of Cu injected were calculated to simulate varying absorption rates in pigs fed 250 ppm of dietary Cu. In Exp. 1, 44 pigs were randomly assigned to four groups of 11 pigs each. Pigs were injected with four levels of Cu histidinate (0, 5, 10, and 15% estimated apparent absorption coefficients based on calculated feed intake). Average daily gain responded quadratically (P < .05) to levels of Cu histidinate; maximum growth was seen in the 5% group. At d 6, serum mitogenic activity also exhibited a similar quadratic response (P < .05). In Exp. 2, estimated Cu absorptions of 0, 2, 4, 6, and 8% were tested. Forty-five pigs were randomly assigned to five groups of nine pigs each and injected as in Exp. 1. Both ADG and serum mitogenic activity displayed a quadratic response (P < .05); the maximum response was seen in the 4% group. Liver Cu content, superoxide dismutase activity, and serum Cu concentrations were linearly increased (P < .05) with increasing dosage of Cu in both Exp. 1 and 2. Also, brain Cu content linearly increased (P < .05) with increasing dosage of Cu in both Exp. 1 and 2. Also, brain Cu hormone mRNA concentrations in Exp. 2 were not significantly influenced by treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1994

Cholecystokinin receptor characterization and cholecystokinin-A receptor messenger RNA expression in transgenic mouse pancreatic carcinomas and dysplastic pancreas.

Transgenic mice bearing the rat elastase I promoter - SV40 T-antigen (ELSV) fusion gene develop pancreatic acinar cell carcinomas by 3-6 months of age. In other animal models of pancreatic cancer, cholecystokinin (CCK) has been shown to be a tumor promoter. Therefore, we characterized CCK binding properties and CCK-A receptor mRNA expression in pancreatic carcinomas and dysplastic pancreata from the Tg(Ela-1, SV40E+Ela-1, neo)Bri19 strain of ELSV transgenic mice. To accomplish this, we utilized 125I-Bolton-Hunter-labeled-cholecystokinin octapeptide (125I-BH-CCK-8) binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreata from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and 8-week-old nontransgenic male mice (B6SJLF1/J). Optimal saturable CCK-8 binding was detected at pH 6.5, 22 degrees C. Competitive inhibition 125I-BH-CCK-8 binding assays performed on all four mouse pancreatic tissues showed that CCK-8 bound to two classes of CCK binding sites: a high affinity, lower capacity CCK binding site and a low affinity, higher capacity CCK binding site. RT-PCR and Southern blot analysis confirmed the 125I-BH-CCK-8 binding studies by demonstrating CCK-A receptor mRNA expression in the ELSV transgenic pancreatic carcinomas and dysplastic pancreas, as well as in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas from ELSV transgenic mice and normal nontransgenic mouse pancreas all bind 125I-BH-CCK-8 and express mRNA for the CCK-A receptor. In contrast to chemically-induced pancreatic tumors in the rat, ELSV transgenic mouse pancreatic tumors do not appear to significantly overexpress CCK-A receptors.

Animals↗
PubMed1994

[Association of polymorphism for HLA-DQA1 promotor region (QAP) with IDDM].

We have identified the DNA polymorphism for the HLA-DQA1 promotor region (QAP) in patients with early and late onset insulin-dependent diabetes mellitus (IDDM) by PCR direct sequencing. The result showed that single nucleotide substitution at position-92(C-->T-92) and -146 (T-->C-146) were detected in QAP for early and late onset IDDM respectively. These findings suggests that the mutation seems to alter the conformation of QAP so that these are likely to influence the aberrant expression of MHC-class II loci in beta-pancreatic islet cells.

Base Sequence↗
PubMed1994

The clinical analysis of secondary glaucoma following posterior chamber intraocular lens implantation.

We present 14 patients with secondary glaucoma following the implantation of a posterior chamber intraocular lens (IOLs). All patients were unilateral glaucoma, which developed within 1 month following the IOL implantation in 10 cases, and from 1 to 3 years in 4 cases. The angle of anterior chamber was open in 8 patients, and close in 6 ones. Seven patients required treatment of antiglaucomatous medicine; 4 patients underwent laser iridectomy and 3 patients required antiglaucoma surgery. The results showed that the corrected visual acuity was more than 0.5 in 28% of the patients before antiglaucoma treatment and in 50% of the patients after treatment. The main cause of poor vision is glaucomatous optic nerve atrophy. It suggests that it is important to find glaucoma early.

Adolescent↗
PubMed1994

A reciprocal mutation supports helix 2 and helix 7 proximity in the gonadotropin-releasing hormone receptor.

Activation of the pituitary gonadotropin-releasing hormone receptor, a member of the seven-transmembrane G protein-coupled receptor (GPCR) family, triggers a cascade of events leading to gonadotropin release and stimulation of the reproductive system. An unusual feature of this receptor, observed in mice, rats, and humans, is the presence of Asn87 in the second putative transmembrane helix at the location of a highly conserved aspartate in the GPCR family and of Asp318 in the putative seventh transmembrane helix where nearly all other GPCRs have asparagine. The possibility that these residues interact was suggested by this reciprocal pattern and by a three-dimensional model of the gonadotropin-releasing hormone receptor and was investigated by site-directed mutagenesis. Replacing Asn87 in the second transmembrane domain by aspartate eliminated detectable ligand binding. A second mutation, generating the double-mutant receptor Asp87Asn318, recreated the arrangement found in other GPCRs and re-established high affinity agonist and antagonist binding. The restoration of binding by a reciprocal mutation indicates that these two specific residues in helices 2 and 7 are adjacent in space and provides an empirical basis to refine the model of the transmembrane helix bundle of the receptor.

Amino Acid Sequence↗
PubMed1994

Uniparental disomy occurs infrequently in Wilms tumor patients.

Wilms tumors commonly exhibit loss of heterozygosity for polymorphic DNA markers located on the short arm of chromosome 11 at band p15. In some instances, the deleted region does not include 11p13, the location of the WT1 gene, suggesting the existence of a second Wilms tumor gene on 11p. Both the exclusive loss of the maternally derived allele in Wilms tumors and the recent description of constitutional paternal isodisomy for this region in patients with either the Beckwith-Wiedemann syndrome (BWS) or isolated hemihypertrophy have suggested that this second locus is subject to sex-specific genomic imprinting. Given that one of these isodisomic patients had minimal congenital anomalies (hemihypertrophy), we hypothesized that a proportion of Wilms tumors which had not lost heterozygosity for 11p markers (about 60% of all cases) might have arisen consequent to 11p paternal heterodisomy and that patients constitutionally homozygous at 11p15 might harbor paternal isodisomy. We have analyzed 40 Wilms tumor cases to determine the parental origin of the child's 11p15 alleles. Paternal heterodisomy could be excluded in all 28 unilateral and 8/9 bilateral potential candidates. It is intriguing that somatic mosaicism for 11p paternal isodisomy was detected in one child with bilateral Wilms tumor and macroglossia. Isodisomy could only be excluded in one of the three possible cases. Thus, 11p paternal hetero- and isodisomy appear to be uncommon causes of non-anomaly-associated Wilms tumors but may be more frequent in Wilms tumor patients with BWS-associated anomalies.

Aneuploidy↗
PubMed1993

Endogenous complement C3 synthesis in immune complex nephritis.

Human renal epithelial and mesangial cells have been shown to synthesise complement C3 in culture, but the relevance of this finding to the development of complement-mediated nephritis is uncertain. We investigated C3 gene expression in tissue biopsies that showed three main categories of renal injury. By semiquantitative polymerase chain reaction, biopsies from patients with immune-complex glomerulonephritis and those with cell-mediated interstitial nephritis showed increased C3 expression (p < 0.05), but biopsies from patients with non-immune glomerular injury did not. These findings suggest that local C3 production is enhanced in immune-mediated nephritis and are consistent with the hypothesis that locally synthesised complement components are involved in the pathogenesis of tissue injury.

Complement C3c↗
PubMed1993

Protein kinase C-mediated bidirectional regulation of DNA synthesis, RB protein phosphorylation, and cyclin-dependent kinases in human vascular endothelial cells.

In human umbilical vein endothelial cells, activators of protein kinase C (PKC) exert cell cycle-dependent, bidirectional growth regulatory effects. Thus, phorbol 12,13-dibutyrate or 1,2-dioctanoylglycerol potentiates growth factor-induced DNA synthesis up to 3-fold when they act during the early G1 phase, whereas they completely inhibit the initiation of DNA synthesis when they act in the late G1 phase. In addition, the PKC activators induce a rapid inhibition of the ongoing DNA synthesis when they are applied after entry into the S phase. The effects of the PKC activators in both stimulatory and inhibitory directions are abolished in PKC-downregulated cells. The cell cycle-dependent, PKC-mediated bidirectional growth regulation is closely associated with either potentiation or inhibition of RB protein phosphorylation and the histone H1 kinase activity of cyclin-dependent kinases (cdks) cdc2 and cdk2, which normally accumulate along the G1 to the S phase transition. Northern and Western blot analyses of cdc2 and cdk2 have revealed that PKC regulates the cdks at multiple steps in distinct ways. Thus, for cdc2, the levels of mRNA and protein as well as the extent of post-translational modification are all subject to the PKC-mediated regulation. In contrast, the level of mRNA or protein of cdk2 is not affected by PKC stimulation at any phase of the cell cycle. These results demonstrate the existence of a complex array of PKC-cdk signaling pathways, which mediate temporally organized bimodal growth regulation in endothelial cells.

Amino Acid Sequence↗
PubMed1993

Comparative sequence analysis and functional characterization of the cloned sheep gonadotropin-releasing hormone receptor reveal differences in primary structure and ligand specificity among mammalian receptors.

The cloned sheep gonadotropin-releasing hormone (GnRH) receptor was analysed for sequence homology/differences among mammalian receptors and its pharmacology characterized in COS-1 cells. Transmembrane domains TM2, TM3, TM5, TM6 and TM7, and extracellular loop 1 are most highly conserved (> 90%) in this G-protein coupled receptor. The Kd of the sheep receptor in binding assays (4.9 nM) was similar to the human and rat receptors, but lower than the mouse receptor. The rank order of potency of a series of GnRH analogues for binding and inositol phosphate stimulation in transfected COS-1 cells was identical to that of the receptor characterized in sheep pituitary gonadotropes. Northern blot analysis identified four transcripts sized 5.4 kb, 3.6 kb, 2.3 kb and 1.3 kb in sheep pituitaries which were upregulated by castration.

Amino Acid Sequence↗
PubMed1993

The sepsis syndrome in a Dutch university hospital. Clinical observations.

BACKGROUND: Most studies of the cause of sepsis syndrome focus on patients hospitalized in intensive care units. In this study, we analyzed the incidence, cause, and outcome of the sepsis syndrome in all hospitalized patients. METHODS: Clinical and microbiologic data were obtained for 382 patients (5.6% of all patients admitted) from whom blood was drawn for culture. RESULTS: The incidence of the sepsis syndrome was 13.6 per 1000 patients admitted (1.06 per 1000 hospital days), while the incidence of septic shock was 4.6 per 1000. The respiratory tract was the predominant infection site. Of all patients with sepsis syndrome, 38% (n = 35) had positive blood cultures. More than half of these cultures (13 [57%]) were caused by gram-positive microorganisms (excluding patients receiving selective decontamination of the digestive tract and those with intravascular device-related bacteremias). The mortality for patients with sepsis syndrome without shock was 28% (17/61), while for patients with septic shock, it was 55% (17/31). Patients with cardiovascular diseases had a significantly (P < .005) greater risk of dying during a sepsis syndrome episode than patients with other predisposing factors. Multivariate analysis of factors influencing outcome identified the development of shock and an immunocompromised state as being significantly associated with outcome in patients with sepsis syndrome. CONCLUSIONS: Patients fulfilling the criteria for the sepsis syndrome are at great risk of developing septic shock or multiple-organ failure and subsequently dying. In our hospital, the majority of bacteremic episodes were associated with gram-positive microorganisms.

Adult↗
PubMed1993

Stimulation of growth of azaserine-induced putative preneoplastic lesions in rat pancreas is mediated specifically by way of cholecystokinin-A receptors.

Cholecystokinin (CCK) has been shown to stimulate the growth of both normal pancreas and azaserine-induced putative preneoplastic pancreatic lesions in the rat. The present study was performed to determine whether these effects are mediated by way of CCK-A receptors, CCK-B receptors, or both. Sixteen-day-old male Lewis rats were given i.p. injections of azaserine at 30 mg/kg body weight. Starting on day 21, rats were given s.c. injections, 5 days/week for 16 consecutive weeks, of either (a) CCK octapeptide (nonselective CCK agonist) (2.50 micrograms/kg body weight, n = 17), (b) tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2-methylphenylaminocarbonyl++ +)-Asp- (N-methyl)-Phe-NH2 (highly selective CCK-A agonist) (1.84 micrograms/kg body weight, n = 18), (c) [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 (highly selective CCK-B agonist) (2.40 micrograms/kg body weight, n = 18), or (d) normal saline solution (control, n = 17). Rats were subsequently sacrificed, pancreatic weights were determined, and quantitative morphometric analysis of atypical acinar cell foci and nodules was performed. Both CCK octapeptide and the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 stimulated pancreatic growth and the development of acidophilic atypical acinar cell foci and nodules. Furthermore, the effect produced by the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 was greater than that produced by CCK octapeptide. In contrast, the selective CCK-B agonist [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 had no effect. These findings suggest that the growth of putative preneoplastic lesions (acidophilic atypical acinar cell foci and nodules) in the rat pancreas during the early stages of azaserine-induced pancreatic carcinogenesis is mediated specifically by way of CCK-A receptors.

Animals↗
PubMed1993

Effects of abasic sites and DNA single-strand breaks on prokaryotic RNA polymerases.

Abasic sites are thought to be the most frequently occurring cellular DNA damage and are generated spontaneously or as the result of chemical or radiation damage to DNA. In contrast to the wealth of information that exists on the effects of abasic sites on DNA polymerases, very little is known about how these lesions interact with RNA polymerases. An in vitro transcription system was used to determine the effects of abasic sites and single-strand breaks on transcriptional elongation. DNA templates were constructed containing single abasic sites or nicks placed at unique locations downstream from two different promoters and were transcribed by SP6 and Escherichia coli RNA polymerases. SP6 RNA polymerase is initially stalled at abasic sites with subsequent, efficient bypass of these lesions. E. coli RNA polymerase also bypassed abasic sites. In contrast, single-strand breaks introduced at abasic sites completely blocked the progression of both RNA polymerases. Sequence analysis of full-length transcripts revealed that SP6 and E. coli RNA polymerases insert primarily, if not exclusively, adenine residues opposite to abasic sites. This finding suggests that abasic sites may be highly mutagenic in vivo at the level of transcription.

Base Composition↗
PubMed1993

Glycogenolytic and haemodynamic responses to bovine serum albumin in isolated perfused livers from sensitized rats.

Infusion of BSA into isolated perfused livers of rats sensitized by intraperitoneal injection of BSA led to rapid increases in portal-vein pressure, glucose output and the lactate/pyruvate ratio in the effluent perfusate, with concomitant decreases in oxygen consumption and lactate+pyruvate efflux. The responses were attenuated at low (approximately 7 microM) perfusate Ca2+, but were restored on re-addition of normal Ca2+ concentration. Co-infusion of the cyclo-oxygenase inhibitor ibuprofen (50 microM) or of the platelet-activating factor receptor antagonist WEB 2170 (1.2 microM) inhibited haemodynamic responses to BSA (5 micrograms/ml) by 48% and 59% respectively. Responses to BSA were also attenuated by prior infusion of the beta-adrenergic agonist isoprenaline. Glycogen phosphorylase a activity was increased by 26% in livers freeze-clamped 2 min after onset of BSA infusion; tissue prostaglandin E2 content was increased at 2 min, but returned to control levels at 5 min. Homologous desensitization of hepatic responses to BSA was observed, but heterologous desensitization with heat-aggregated IgG did not take place. It is concluded that livers from rats sensitized to antigen respond directly to subsequent antigen administration by vasoconstriction and glycogenolysis, and that autacoid mediators are involved in these responses.

Animals↗