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Biomedical subjects

W Zhou

Publications and source records attributed to W Zhou.

At least 289 records · Page 16Linked to original sources
PubMed1997

Intraglomerular C3 synthesis in rats with passive Heymann nephritis.

Passive Heymann nephritis (PHN), a model of human membranous nephropathy, is an immune-complex-mediated glomerulonephritis characterized by the presence of complement-dependent tissue injury. Recent studies have confirmed the synthesis of C3, involved in both the classical and alternative pathways of complement, in injured human and animal renal tissues. However, there is little clear information on the role of local C3 synthesis in the pathogenesis of nephritides such as PHN. In the present study, using nonradioactive in situ hybridization and semiquantitative reverse transcriptase polymerase chain reaction, we examined C3 synthesis in the kidney and its contribution to tissue injury in a rat model of PHN induced by the injection of polyclonal anti-gp330 antibody. C3 mRNA was localized in mesangial cells, glomerular epithelial cells, and cells of Bowman's capsule. During the early stages of PHN, C3 mRNA expression was detected in mesangial cells and glomerular epithelial cells, whereas such expression was limited to mesangial cells during the late stages of the disease. Focal, weak C3 mRNA expression was detected in tubular epithelial cells and occasionally in the interstitium. Semiquantitative polymerase chain reaction demonstrated that the level of C3 mRNA expression correlated with that of proteinuria. Our results suggest that renal cells synthesize C3 mRNA in PHN in a site-specific manner and that locally produced C3 is associated with the development of proteinuria in this model.

Animals↗
PubMed1997

[Experimental study of selective muscarinic receptor antagonists on attenuation of morphine tolerance and dependence in rats].

OBJECTIVE: To characterize the role of muscarinic receptor subtype in the process of the morphine tolerance and dependence. METHODS: The morphine (Antinociception) tolerance was assessed by using hot-plate latency, and morphine dependence was characterized by naloxone-precipitated withdrawal. Intraperitoneal (i.p.) or intrathecal (i.t.) injection of muscarinic M1 selective antagonist pirenzepine or M2 selective antagonist methoctramine was carried out. RESULTS: Methoctramine (i.p.) for 6 days restored the sensitivity to morphine in male Sprague Dawley rats that are tolerant as a result of 6 days of b.i.d. morphine injection, in contrast, saline and pirenzepine (i.p.) did not increase the mean HP latency of morphine tolerant rats. Both methoctramine and pirenzepine in doses did not alter the baseline HP latency. Concurrent treatment with pirenzepine (i.t.) significantly attenuated the development of morphine tolerance produced by twice daily injection of morphine in a dose-dependent manner, however, methoctramine (i.t.) also decreased without dose-relation. In addition, the withdrawal symptoms precipitated by naloxone in morphine dependent rats were blocked by methoctramine (i.p.) or pirenzepine (i.t.) at single dose injection in a dose-dependent manner. Methoctramine (i.t.) at 200 micrograms/kg could partially inhibit the withdrawal symptoms. CONCLUSIONS: The data suggested that the muscarinic receptor subtype predominating M2 receptor at the peripheral and M11 in the spinal cord mediate the process of morphine tolerance and dependence in rat.

Animals↗
PubMed1997

Correlation between retinal fluorescein angiography and blood viscosity and other factors in patients with primary open angle glaucoma.

OBJECTIVE: To investigate the correlation among retinal fluorescein angiography, blood viscosity, and other factors in patients with open angle glaucoma (POAG). METHODS: Multiple step regression analysis was made to investigate the correlation between each of the following blood vessel filling times: the arm-choroid (A-CT), arm-retinal artery (A-AT), and retinal artery-venous (A-VT) of the fundus fluorescein angiography (FFA) in 122 eyes with POAG and each of the following related factors in hemorrheology: whole blood apparent viscosity at low, medium and high shear rates, plasma viscosity and hematocrit. Also, the same analysis was applied to investigate the correlation between each of the A-AT, A-VT of the FFA in 70 eyes with POAG and the following factors: systolic blood pressure, diastolic blood pressure, age and whole blood apparent viscosity at low shear rate. RESULTS: The whole blood apparent viscosity at low shear rate was closely related to A-CT and A-AT, while hematocrit was closely related to A-VT of the FFA. The whole blood apparent viscosity at low shear rate and age, especially the whole blood apparent viscosity, was closely related to A-AT, A-VT of the FFA. CONCLUSION: Blood viscosity can affect the filling times of the FFA in POAG.

Blood Viscosity↗
PubMed1997

[Usage of double immuno-enzyme labeled staining method in forensic pathology].

In this paper we report a kind of double immunoenzyme labelled staining method (single enzyme method). The principle of the method is that HPR will show blue-black color when it meet DAB-CoCL2/H2O2, while it will show brown color as it meet DAB/H2O2, two colors constract very remarkably. This method was used to detect the antigens of hearts and brains which obtained from forensic autopsy. The results showed that the method was sensitive, simple and economical. One of the advantages is that the stained sections can keep for a long time. Thus, is very practical for forensic pathology.

Brain↗
PubMed1997

[The effect of repair of paratendon in tendon healing].

In order to investigate the effect of repair of paratendon in tendon healing, two different ways were performed to repair the transected extensor tendons of chick's toe. End to end suture of the extensor tenon was performed in group 1 while the paratendon was also repaired simultaneously in addition to suture of the tendon in group 2. Gross observation and histological examination were undertaken in the 3rd and 6th week after operation. The result showed, in group 1, extensive adhesion and irregular proliferation of fibroblasts was found in the 3rd week, severe adhesion and irregular arrangement of fibroblasts with less collagen fiber was found in the 6th week; while in group 2, smooth and regular "fusiform structure" was formed, slight adhesion and regular proliferation of fibroblasts were found in the 3rd week, adhesion disappeared and the structure of paratendon and tondon recovered in the 6th week. It was concluded that repair of extensor tendon and paratendon simultaneously could promote the intrinsic tendon healing and prevent tendon adhesion.

Animals↗
PubMed1996

Genetic progression, histological grade, and allelic loss in ductal carcinoma in situ of the breast.

To investigate the relationships of specific allelic losses to progression and histological grade of ductal carcinoma in situ (DCIS) of the breast, we studied PCR-amplified microsatellite markers on ten chromosomal arms in 41 cases of DCIS without synchronous invasive cancer. For all chromosomal arms combined, the number of allelic losses was significantly greater in lesions of intermediate or high nuclear grade (5.6 chromosomal arms/case) than in lesions of low nuclear grade (1.2 chromosomal arms/case). Allelic losses of 16q and 17p were commonly found in low nuclear grade DCIS (38 and 34%, respectively) as well as in intermediate and high nuclear grade DCIS (58 and 95%, respectively). Allelic losses of other chromosomal arms examined (1p, 1q, 6q, 9p, 11p, 11q, 13q, and 17q) were uncommonly seen in low-grade DCIS, but were seen at frequencies of greater than 40% in intermediate- and high-grade DCIS. In 10 of the cases (24%), we identified patterns of allelic loss heterogeneity suggestive of intralesional progression, findings that were possible because multiple tumor foci from each lesion were individually microdissected and studied. For these tumors with allelic loss heterogeneity, we reasoned that chromosomal losses common to all tumor foci most likely preceded the chromosomal losses observed only in tumor foci of a more advanced genetic stage. In 9 of these 10 cases, all tumor foci lost 16q, and in 8 of the 10 cases, all tumor foci lost 17p. Together, these observations indicate that chromosomal losses of 16q and 17p occur early in DCIS progression and are common even in low-grade DCIS. Tumors of intermediate and high nuclear grade usually have allelic losses of significantly more chromosomal arms, often including 1p, 1q, 6q, 9p, 11p, 11q, 13q, and 17q. Allelic loss of these chromosomal arms may occur later in DCIS progression.

Alleles↗
PubMed1996

An activation function in Pit-1 required selectively for synergistic transcription.

Synergistic transcription activation is a key component in the generation of the spectrum of eukaryotic promoter activities by a limited number of transcription factors. Various mechanisms could account for synergy, but a central question remains of whether synergism requires transcription factor functions that differ from those that direct independent activation. The rat growth hormone promoter is synergistically activated by the pituitary-specific transcription factor, Pit-1, and the thyroid hormone receptor (TR). Mutations that disrupted the previously described DNA binding and transcriptional activation domains of both Pit-1 and TR reduced Pit-1/TR synergy in parallel with their effects on the much weaker, independent Pit-1 and TR activations of the rat growth hormone promoter. Thus, Pit-1 and TR amplify each other's intrinsic activities. Mutations of Pit-1 that selectively inhibited synergism with the TR without affecting independent Pit-1 activity were also identified. Pit-1/TR synergy is therefore a consequence of a novel synergism-selective activity and synergism-independent Pit-1 and TR functions.

Animals↗
PubMed1996

Protein kinase C inhibits the CAK-CDK2 cyclin-dependent kinase cascade and G1/S cell cycle progression in human diploid fibroblasts.

Serum stimulation of human diploid fibroblast IMR-90 cells leads to phosphorylation of p33CDK2 at Thr160 and activation of CDK2 kinase, a necessary event for G1/S transition. We report that serum stimulation causes a gradual, sustained increase in the activity of CDK-activating kinase (CAK) that phosphorylates CDK2 at Thr160, which starts by 5 h after serum stimulation and reaches the maximal plateau level at around the G1/S boundary. In this cell type addition of phorbol-12, 13-dibutyrate 5 h but not 16 h after serum stimulation completely inhibits CDK2 kinase activation and DNA synthesis. Phorbol ester treatment does not reduce the protein level of p33CDK2, but does inhibit serum-stimulated increases in the CAK activity and CDK2 phosphorylation at Thr160. The suppression of the CAK activity by the phorbol ester is accompanied by decreases in the message levels of both CDK7 and cyclin H, the catalytic and the positive regulatory subunit of CAK, respectively. These results indicate that in IMR-90 cells activation of protein kinase C in the late G1 phase causes cell cycle arrest before the G1/S boundary at least in part through downregulation of CAK and CAK-mediated CDK2 phosphorylation and activation.

Antibodies↗
PubMed1996

Detection of frequent allelic loss of 6q23-q25.2 in microdissected human breast cancer tissues.

Detection of allelic loss in human breast cancer is hindered by the fact that breast cancer tissues are frequently infiltrated by stromal and inflammatory cells. For this study, we carefully microdissected infiltrating breast cancer tumor cells from contaminating normal cells and analyzed the DNA from these samples for allelic loss on the long arm of chromosome 6 by using a panel of 15 dinucleotide repeat markers. We found 53 of the 66 cases studied (80%) to have allelic loss of either the entire chromosomal arm (37 cases) or a portion of the chromosomal arm (16 cases). One common region that was identified for all tumors with deletions of 6q was the area between markers D6S310/314 and D6S473/255, consistent with a tumor suppressor gene locus at 6q23-6q25.2. The use of tissue microdissection allowed the detection of allelic loss in this chromosomal region in human breast cancer at a much higher frequency than was previously recognized.

Adult↗
PubMed1996

Capillary electrophoresis and electrochemical detection of underivatized oligo- and polysaccharides with surfactant-controlled electroosmotic flow.

Complex polysaccharide mixtures were analyzed directly without derivatization by capillary zone electrophoresis in strongly alkaline solutions and electrochemical detection at a Cu electrode. The positively charged surfactant cetyltrimethylammonium bromide was included in the electrophoresis medium in order to reverse the electroosmotic flow and permit elution to be in order of increasing polysaccharide size. Carbohydrate samples analyzed by this approach included linear maltoses, enzymatically hydrolyzed starch, and commercially available dextrans of up to an average molecular weight of 18,300. Detection by constant-potential oxidation at a Cu electrode was very sensitive, with detection limits for individual carbohydrates generally below the femtomole level.

Cetrimonium↗
PubMed1996

Evidence for altered cellular calcium in the pathogenetic mechanism of acute pancreatitis in rats.

Although several pathophysiological sequences, such as protease activation, free radical generation, and inflammatory mediator release, have been described in acute pancreatitis, the precise mechanism by which acute pancreatitis is initiated is unknown. Cellular calcium, a key physiological signaling element in cell function and also a crucial pathological intracellular messenger in cell injury, appears to be involved in the initiation and development of acute pancreatitis. The present study provides several lines of evidence supporting this suggestion. First, verapamil (a calcium channel blocker) administration was associated with a significant protection of rats from acute pancreatitis induced by high doses of cerulein (50 micrograms/kg/hr, subcutaneously), as evidenced both histologically and biochemically. Second, verapamil was found to minimize the increased tissue levels of calcium, platelet-activating factor, and thromboxane B2 detected during acute pancreatitis. Third, acute pancreatitis could be observed in rats with elevated serum calcium levels at low doses of cerulein (5 micrograms/kg/hr, subcutaneously), but could not be observed in rats with normal serum calcium levels treated with low doses of cerulein. It is proposed that cellular calcium, which is a critical signaling component in the synthesis and release of inflammatory mediators and several other events, may be an important factor in the pathogenesis of cerulein-induced acute pancreatitis.

Acute Disease↗
PubMed1996

Hormonal stimulation of calcium mobilization in the isolated perfused rat pancreas.

Hormone-stimulated cellular Ca2+ mobilization in the isolated perfused rat pancreas was investigated by analyzing the efflux profiles of 45Ca2+ from 45Ca(2+)-loaded pancreata following agonist stimulation. The increased 45Ca2+ efflux reflects the enhanced exchange of Ca2+ across the plasma membrane as a result of increased [Ca2+]i. Both high and low concentrations of the cholecystokinin analog, cerulein, applied to the isolated perfused pancreas gave rise to an increased release of 45Ca3+. The patterns of the increase in 45Ca2+ release were consistently different for high and low concentrations of the agonist. Cerulein infused at a concentration of 10(-11) M induced a release of a small but significant amount of 45Ca2+ which could be abolished by 8-(N,N-diethylamine)octyl-3,4,5-trimethoxy-benzoate (TMB-8), but was not affected by ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Cerulein stimulation at 10(-9) M elicited a marked increase in 45Ca2+ release which was minimized by EGTA, but not by TMB-8. Also, infusion of cerulein stimulated a concentration-dependent amylase secretion response which displayed the same TMB-8- and EGTA-sensitivity pattern as the 45Ca2+ release response. The present study suggests (i) that cellular Ca2+ influx is a prominent feature of the increased 45Ca2+ efflux (i.e., increased [Ca2+]i) induced by pharmacological concentrations of cerulein while physiological concentrations of cerulein cause an increase in [Ca2+]i which is due predominantly to a release of internal Ca2+; and (ii) [Ca2+]i changes are essential for pancreatic enzyme secretion. Although isolated pancreatic acini or cells may lose their sensitivity and physiological responses to various agonists during isolation and preparation, the isolated perfused pancreas is a suitable and very sensitive model in which to study the physiology of Ca2+ mobilization and enzyme secretion.

Amylases↗
PubMed1996

Gastrin receptor expression during azaserine-induced rat pancreatic carcinogenesis.

The hormone gastrin is thought to stimulate the growth of certain pancreatic carcinoma cell lines. We have previously detected the presence of the gastrin receptor in rat pancreatic carcinoma cell lines but not in normal rat pancreas. We had not, however, previously demonstrated that gastrin receptor is expressed in pancreatic carcinomas developing in the rat in vivo. Therefore, in the present study, we examined rat pancreatic tissue at various stages in azaserine-induced pancreatic carcinogenesis for gastrin binding and for the presence of gastrin receptor mRNA to determine the temporal expression pattern of the gastrin receptor during the in vivo development of pancreatic cancer. Autoradiography of pancreatic tissue using (125)I-gastrin-17-I from all azaserine-treated and control animals at 2, 4, 8, and 12 months of age demonstrated no specific gastrin binding. At 18 months of age, normal pancreas, azaserine-induced premalignant pancreatic nodules, and internodular pancreas demonstrated no specific gastrin binding. One of three azaserine-treated animals developed an area of pancreatic acinar cell carcinoma at 18 months of age which exhibited significant specific gastrin binding of 141.8 - 32.8 fmole/gm of tissue. Southern blot analysis of pancreatic RNA isolated from animals at 12 months of age revealed no gastrin receptor mRNA; however, by 18 months of age, gastrin receptor mRNA was present in all azaserine-treated animals but absent in control animals. In summary, specific gastrin binding is present in in vivo azaserine-induced pancreatic acinar cell carcinoma but absent in normal pancreas and azaserine-induced premalignant pancreatic nodules. Gastrin receptor mRNA is first expressed in azaserine-treated rat pancreas at some point between 12 and 18 months of age. These results demonstrate that expression of gastrin receptor is altered in azaserine-treated rat pancreas and may play a role in the development of pancreatic cancer.

Animals↗
PubMed1996

Simultaneous formation of peptides and nucleotides from N-phosphothreonine.

An intramolecular mutual activation between a phosphoryl group and carboxyl group results in the simultaneous formation of nucleotides and peptides by the reaction of nucleosides with N-(O,O-diisopropyl)phosphothreonine in anhydrous pyridine. These results suggest pathways for the simultaneous prebiotic synthesis of peptides and oligonucleotides.

Chromatography, High Pressure Liquid↗
PubMed1996

The effects of external pH on calcium channel currents in bullfrog sympathetic neurons.

We have investigated the effects of external pH (pHo) on whole-cell calcium channel currents in bullfrog sympathetic neurons. The peak inward current increased at alkaline pHo and decreased at acidic pHo. We used tail currents to distinguish effects of pHo on channel gating and permeation. There were large shifts in the voltage dependence of channel activation (approximately 40 mV between pHo and 9.0 and pHo 5.6), which could be explained by binding of H+ to surface charge according to Gouy-Chapman theory. To examine the effects of pHo on permeation, we measured tail currents at 0 mV, following steps to + 120 mV to maximally activate the channels. Unlike most previous studies, we found only a approximately 10% reduction in channel conductance from pHo 9.0 to pHo 6.4, despite a approximately 25 mV shift of channel activation. At lower pHo the channel conductance did decrease, which could be described by binding of H+ to a site with pKa = 5.1. In some cells, there was a separate slow decrease in conductance at low pHo, possibly because of changes in internal pH. These results suggest that changes in current at pHo > 6.4 result primarily from a shift in the voltage dependence of channel activation. A H(+)-binding site can explain a rapid decrease in channel conductance at lower pHo. The surface charge affecting gating has little effect on the local ion concentration near the pore, or on the channel conductance.

Animals↗
PubMed1996

Immortalization of differentiated human keratinocytes by human papillomavirus (HPV) 16 DNA.

Human papillomavirus (HPV) 16 is strongly implicated as having an etiologic role in cervical carcinoma. Human basal keratinocytes have been used in most HPV transformation studies, and transformed cells have exhibited undifferentiated characteristics. However, tumor cells in cervical squamous cell carcinoma are differentiated to certain degrees. Therefore, we hypothesize that HPV may transform not only basal cells but also differentiated keratinocytes. Human keratinocytes isolated from neonatal foreskin were induced to differentiate by treatment with 2 mM Ca2+ for various times (24, 48, 72 and 96 h) and were transfected with HPV 16 DNA. After G418 selection and repeated subculture, HPV 16-transformed cells were derived from each group of the Ca(2+)-treated and untreated cells. HPV DNA was detected in the transformed cells by polymerase chain reaction (PCR). Southern analysis and two-dimensional gel results indicated that HPV 16 DNA had been integrated into the chromosomes. The HPV 16-transformed cells exhibited an indefinite lifespan and were not tumorigenic in nude mice. They also showed the morphology and expressed the markers of differentiated keratinocytes. This study showed that differentiated human keratinocytes could be immortalized by HPV 16, and this may be a better model for cervical carcinomas in humans.

Animals↗