Biomedical subjects

B Zhou

Publications and source records attributed to B Zhou.

At least 91 records · Page 5Linked to original sources

PubMed2000

[Some geographical features of the location and gene mutation of cancers occurring in Nantong City, China].

OBJECTIVE: To detect the location and geographical features of gene mutation of the cancer based on 30,709 clinical tumor biopsies. METHODS: Thirty thousand seven hundred and nine cases of tumor biopsy materials were collected from the Department of Pathology of Nantong Cancer Hospital between June 1974 and December 1987. The address of the village and county of patients was collected and statistical analysis was performed on data from lab examination. DNA sequencing of 31 cases of hepatocellular carcinoma (HCC) was performed at the Department of Pathology of the Medical College of Tokyo University, Japan. RESULTS: The data suggested that different carcinomas occurred predominantly in some districts and the frequency and type of mutation of the P53 gene in the HCC were different in different districts. CONCLUSION: It seems that based on the clinical biopsy materials, carcinomas of the uterus cervix (CC) and nasopharynx tend to occur in some districts of Nantong City and the frequency and type of mutation of the gene P53 of the HCC were different in different districts. The reason for this is not understood and further study will be done.

China↗

PubMed2000

[Analysis on maternal deaths of cesarean section in Shanghai].

OBJECTIVE: To analyze the causes of maternal deaths of cesarean section and the potential risks of it. METHODS: A retrospective study on maternal deaths of cesarean section from 1978 to 1997 was carried out. RESULTS: (1) The rate of cesarean section in 1978-1987 was 15.55% (258,158/1,659,892), which was significantly lower than that of 29.39% (365,376/1,243,337) in 1988-1997 (P < 0.01). (2) During the 20 years there were 430 cases of maternal deaths in Shanghai. Among them, 150 cases were maternal death after cesarean section which accounted for 34.88%. (3) Maternal mortality rate of cesarean section cases was 24.05/10(5)(150/623,534) which significantly higher (P < 0.01) than that of vaginal delivery, 12.28/10(5)(280/2,279,695). The relative risk of maternal deaths in cesarean section group increased when the cesarean section rate was over 30.00%. (4) The rank order of maternal deaths of cesarean section was as follows: PIH (pregnancy induced hypertension), Cardiac diseases, embolisms, haemorrhage, hepatic diseases, and infections. (5) The relative risk of PIH death either for cesarean section or for vaginal delivery was significantly decreased in 1988-1997, compared to the former 10 years. (6) Of 150 cases of maternal deaths of cesarean section, 43 cases (28.67%) were related to the cesarean section with embolism ranking the first, haemorrage the second and infection the third. CONCLUSIONS: In order to reduce maternal mortality of cesarean section, it is important to pay attention to (1) the prevention and treatment of PIH, heart diseases and embolisms, (2) the indications of cesarean section, (3) improvement of the quality of cesarean section, and (4) pre- and post-operational management.

Cause of Death↗

PubMed2000

[Study on the relation between hypertensive left ventricular hypertrophy in very old people with neurohormonal factors and ventricular arrhythmias].

OBJECTIVE: To study the relation between hypertensive left ventricular hypertrophy (LVH) in very old people (> 80 year) with neuro-hormone factors and ventricular arrhythmias. METHODS: Measurements were made on the heart rate variation, renin (Ren), angiotensin-II (AT-II), aldosterone (Ald), insulin (Ins), Holter and ambulatory blood pressure monitor in 60 cases of 2 groups: 30 with primary hypertension in very old people and LVH (group A); 30 with simple primary hypertension in very old people (group B). RESULTS: (1) There was no significant difference of AT-II and Ren among group A and B (P > 0.05); (2) Ins and Ald value in group A was much higher than group B (P all < 0.01); (3) Very lower frequency (VLF) and low frequency (LF) and LF/HF (high frequency) in group A were significantly higher than group B (P < 0.01, 0.05, 0.05, respectively); (4) incidence of premature ventricular beats and myocardial ischemia in group A were higher than those in group B. CONCLUSIONS: (1) Sympathetic nerve excitability in group A was greatly increased; (2) Hypertensive LVH were closely associated with Ald and Ins level, but not with AT-II and Ren; (3) There was obvious correction between group A and premature ventricular beats and ischemia.

Aged↗

PubMed2000

[Distribution of IL-1 beta in periodontium of experimental osteoporosis rats during orthodontic tooth movement].

OBJECTIVE: The purpose of this research is to study the expression change of IL-1 beta induced by forces in the periodontium of osteoporosis rats. METHODS: Eighteen SD rats were randomly divided into three groups: the normal controlled, the normal orthodontically controlled and the experimental group of osteoporosis. Six weeks after ovariectomy, the first molars were moved mesially by 50 g force created from elastic-thread for one week in the force loading groups. Then the rats were killed, and the 5 microns-thick mesiodistal sections of maxillary teeth, including the roots and periodontium were made. IL-1 beta were localized immunohistochemically in periodontium, and semiquantitative analysis of cellular-staining intensity was done by microphotometry. RESULTS: The IL-1 beta of periodontal ligament cells without loading force were mildly stained in the controlled group, but the staining intensity increased significantly in the periodontium of orthodontically moved teeth, and it showed more strengthened staining in the periodontium of force-loading teeth in osteoporosis rats. CONCLUSION: The results demonstrate that periodontal ligament cells respond to mechanical force by increased production of IL-1 beta, and this can be enhanced by osteoporosis. IL-1 beta is an important cytokine in the process of orthodontically periodontal remodeling.

Animals↗

PubMed2000

[Effects of intranasal budesonide on the infiltration and activation of eosinophils in nasal polyps].

OBJECTIVE: To assess the effects of topical nasal steroid application on the infiltration and activation of eosinophils in nasal polyps. METHODS: Nasal polyps from intranasal budesonide treated patients (n = 16) and untreated patients (n = 16) were investigated. The samples were stained with histochemical and ABC immunohistochemical methods. RESULTS: The majority of eosinophils in nasal polyps were activated eosinophils. Compared with untreated polyps, the proportion of activated eosinophils (EG2+/eosinophil ratio) was significantly less in steroid-treated polyps. Although the numbers of total eosinophils and actived eosinophils were lower in steroid-treated polyps, both of the differences were not statistically significant. CONCLUSIONS: It emphasized that the actived eosinophils play a key role in the pathogenesis of nasal polyps. The effects of intranasal steroid treatment on the number of eosinophils (total and activated) was more profound then on the proportion of activated eosinophils.

Administration, Topical↗

PubMed2000

[Determination of the immune function of the erythrocyte and leucocyte and the activity of IL-4 and IFN-gamma in patients with allergic rhinitis].

OBJECTIVE: To investigate the immune function of erythrocyte (RBC) and leucocyte (WBC), and variety of the interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) among patients with allergic rhinitis. METHODS: IL-4 and IFN-gamma secreted by peripheral blood mononuclear cells (PBMC) were measured and compared with immune adhesive and BA-ELISA method. RESULTS: Results showed the RBC and WBC immune adhesive function and IFN-gamma were significantly decreased than of the control, and IL-4 activity were significantly higher than the controls (P < 0.01) in patients with perennial allergic rhinitis. CONCLUSION: These results suggest that RBC and WBC the immune function and IL-4 and IFN-gamma may play an important role in allergic rhinitis.

Adolescent↗

PubMed2000

The value of 99mTc-MIBI myocardial perfusion spect imaging in detecting coronary artery disease in patients with valvular disease before operation.

OBJECTIVE: The aim of this study was to detect coronary artery disease using 99mTc-MIBI myocardial perfusion imaging in patients with valvular disease. METHODS: Thirty patients with valvular disease confirmed by echocardiography underwent 99mTc-MIBI myocardial perfusion imaging using multiSPECT 1h after stress test (exercise, dipyridamole or dobutamine test) and were performed coronary angiography within 1 month before valvular operation. RESULTS: For 29 out of the 30 patients, the results of 99mTc-MIBI myocardial perfusion imaging were similar with those of coronary angiography, the concordance rate was 96.7% and the negative predictability was 100%. CONCLUSION: 99Tc-MIBI myocardial perfusion imaging is a reliable non-invasive method for detecting coronary artery disease in patients with valvular disease and so as to draw up suitable operation programs for them.

Coronary Angiography↗

PubMed1999

Mechanism of mitogen-activated protein kinase phosphatase-3 activation by ERK2.

The mitogen-activated protein kinase phosphatase 3 (MKP3)-catalyzed hydrolysis of aryl phosphates in the absence and presence of extracellular signal-regulated kinase 2 (ERK2) was investigated in order to provide insights into the molecular basis of the ERK2-induced MKP3 activation. In the absence of ERK2, the MKP3-catalyzed hydrolysis of simple aryl phosphates does not display any dependence on pH, viscosity, and the nature of the leaving group. Increased catalytic activity and enhanced affinity for oxyanions are observed for MKP3 in the presence of ERK2. In addition, normal bell-shaped pH dependence on the reaction catalyzed by MKP3 is restored in the presence of ERK2. Collectively, these results suggest that the rate-limiting step in the absence of ERK2 for the MKP3 reaction corresponds to a substrate-induced conformational change in MKP3 involving active site rearrangement and general acid loop closure. The binding of ERK2 to the N-terminal domain of MKP3 facilitates the repositioning of active site residues and speeds up the loop closure in MKP3 such that chemistry becomes rate-limiting in the presence of ERK2. Remarkably, it is found that the extent of ERK2-induced MKP3 activation is substrate dependent, with smaller activation observed for bulkier substrates. Unlike simple aryl phosphates, the MKP3-catalyzed hydrolysis of bulky polycyclic substrates exhibits bell-shaped pH rate profiles in the absence of ERK2. Furthermore, it is found that glycerol can also activate the MKP3-catalyzed reaction, increase the affinity of MKP3 for oxyanion, and restore the bell-shaped pH rate profile for the MKP3-catalyzed reaction. Thus, the rate of repositioning of catalytic groups and the reorienting of the electrostatic environment in the MKP3 active site can be enhanced not only by ERK2 but also by high affinity substrates or by glycerol.

Binding Sites↗

PubMed1999

Purification and subunit characterization of the rat liver endocytic hyaluronan receptor.

The endocytic hyaluronan (HA) receptor of liver sinusoidal endothelial cells (LECs) is responsible for the clearance of HA and other glycosaminoglycans from the circulation in mammals. We report here for the first time the purification of this liver HA receptor. Using lectin and immuno-affinity chromatography, two HA receptor species were purified from detergent-solubilized membranes prepared from purified rat LECs. In nonreducing SDS-polyacrylamide gel electrophoresis (PAGE), these two proteins migrated at 175- and approximately 300 kDa corresponding to the two species previously identified by photoaffinity labeling of live cells as the HA receptor (Yannariello-Brown, J., Frost, S. J., and Weigel, P. H. (1992) J. Biol. Chem. 267, 20451-20456). These two proteins co-purify in a molar ratio of 2:1 (175:300), and both proteins are active, able to bind HA after SDS-PAGE, electrotransfer, and renaturation. After reduction, the 175-kDa protein migrates as a approximately 185-kDa protein and is not able to bind HA. The 300-kDa HA receptor is a complex of three disulfide-bonded subunits that migrate in reducing SDS-PAGE at approximately 260, 230, and 97 kDa. These proteins designated, respectively, the alpha, beta, and gamma subunits are present in a molar ratio of 1:1:1 and are also unable to bind HA when reduced. The 175-kDa protein and all three subunits of the 300-kDa species contain N-linked oligosaccharides, as indicated by increased migration in SDS-PAGE after treatment with N-glycosidase F. Both of the deglycosylated, nonreduced HA receptor proteins still bind HA.

Animals↗

PubMed1999

Overexpression of ribonucleotide reductase as a mechanism of resistance to 2,2-difluorodeoxycytidine in the human KB cancer cell line.

In this study, human oropharyngeal epidermoid carcinoma KB cells that were resistant to 2,2-difluorodeoxycytidine (dFdCyd) were selected and designated the KB-Gem clone. The KB parental cell line IC50 was 0.3 microM dFdCyd, as compared with the KB-Gem clone IC50 of 32 microM dFdCyd. The KB-Gem clone demonstrated overexpression of ribonucleotide reductase (RR) M2 subunit mRNA (9-fold) and overexpression of M2 protein (2-fold); RR activity was 2.3-fold higher than the KB parental cell line. Both the dATP and dCTP pools of the KB-Gem clone increased 2-fold over the parental cell line, with no change in the dGTP and dTTP pools. Reverse transcriptase-PCR was used to clone the cDNA of deoxycytidine kinase (DCK). Resulting sequences revealed two silent mutations in the KB-Gem clone. The amino acid sequence of the DCK protein and mRNA expression remained unchanged. The KB-Gem clone's DCK enzyme activity was 56% of that of the parental cell line. After the endogenous dNTPs were removed with a G-25 column, no difference was evident between the enzyme activities of the KB-Gem clone and parental cells. Thus, contrary to previous hypotheses, DCK deficiency does not play the primary role in the resistance mechanism of dFdCyd, accepting a secondary role to the overexpression of the target gene, RR, and pool expansion.

Antimetabolites, Antineoplastic↗

PubMed1999

Structural basis for antibody catalysis of a disfavored ring closure reaction.

The catalysis of disfavored chemical reactions, especially those with no known natural enzyme counterparts, is one of the most promising achievements of catalytic antibody research. Antibodies 5C8, 14B9, 17F6, and 26D9, elicited by two different transition-state analogues, catalyze disfavored endo-tet cyclization reactions of trans-epoxy alcohols, in formal violation of Baldwin's rules for ring closure. Thus far, neither chemical nor enzyme catalysis has been capable of emulating the extraordinary activity and specificity of these antibodies. X-ray structures of two complexes of Fab 5C8 with the original hapten and with an inhibitor have been determined to 2.0 A resolution. The Fab structure has an active site that contains a putative catalytic diad, consisting of AspH95 and HisL89, capable of general acid/base catalysis. The stabilization of a positive charge that develops along the reaction coordinate appears to be an important factor for rate enhancement and for directing the reaction along the otherwise disfavored pathway. Sequence analysis of the four catalytic antibodies, as well as four inactive antibodies that strongly bind the transition-state analogues, suggests a conserved catalytic mechanism. The occurrence of the putative base HisL89 in all active antibodies, its absence in three out of the four analyzed inactive antibodies, and the rarity of a histidine at this position in immunoglobulins support an important catalytic role for this residue.

Amino Acid Sequence↗

PubMed1999

Apoptosis in tracheoesophageal embryogenesis in rat embryos with or without adriamycin treatment.

PURPOSE: The aim of this study was to determine whether apoptosis participates in separation of the foregut into trachea and esophagus and to evaluate the potential role of apoptosis in the development of esophageal atresia and tracheoesophageal fistula (EA + TEF) induced by Adriamycin. METHODS: Timed-pregnant rats were injected daily with either saline or Adriamycin (2 mg/kg) intraperitoneally on days 6 to 9 of gestation. Paraffin sections were prepared from 31 experimental and 31 control embryos at days 12 and 13 of gestation. Condensed nuclei were identified on the paraffin sections using the TUNEL method. Apoptosis was quantified by counting the positively stained cell nuclei in transverse sections of embryos. RESULTS: In day 12 control embryos the number of apoptotic nuclei in both lateral ridges of the foregut was high (15.67 +/- 1.38) but relatively low (4.17 +/- 0.80) in Adriamycin-treated embryos (P< .0001). In day 13 Adriamycin-treated embryos, the number of apoptotic nuclei in the region of the upper esophageal pouch was extremely high (23.78.5 +/- 2.20) compared with no detectable apoptotic nuclei in the control embryos. CONCLUSIONS: Apoptosis is required for normal tracheoesophageal embryogenesis and may be an important mechanism to be involved in the embryological development of esophageal atresia and tracheoesophageal fistula.

Animals↗

PubMed1999

Critical timing of bladder embryogenesis in an adriamycin-exposed rat fetal model: a clue to the origin of the bladder.

BACKGROUND/PURPOSE: Administration of Adriamycin (ADR) in utero to pregnant rats (vaginal plug, day 0) on gestational days (GD) 6 to 9 resulted in the offspring having a cluster of malformations, including absence of bladder in 100% of cases. This study aimed to determine the critical timing of the embryological window in bladder development in this animal model. METHODS: Timed-pregnant rats were divided randomly and injected intraperitoneally with ADR at 2 mg/kg on GD 6 to 9; GD 7 to 10; GD 8 to 11; GD 9 to 12; GD 6,8, and 9 (missing GD 7); and GD 6, 7, and 9 (missing GD 8). The control group received saline. Fetuses were harvested near term on GD 21 and dissected under a dissecting microscope and examined for gross anorectal and urogenital anomalies. RESULTS: Administration of ADR on GD 6 to 9 (n = 63); GD 7 to 10 (n = 42); and GD 6, 7, and 9 (n = 35) resulted in 100%, 83%, and 77% bladder agenesis respectively, in contrast with 53% and 26% on GD 8 to 11 (n = 36) and GD 6, 8, and 9 (n = 49), respectively. The control (n = 52) and the GD 9 to 12 (n = 27) groups all had normal bladder development. The proportion of other urogenital and anorectal anomalies mirror that of bladder agenesis. CONCLUSION: The results showed GD 7 to be the critical embryological timing in which bladder development can be affected by ADR, possibly by targeting the gene that is expressed in the embryonic bladder during this narrow time interval.

Animals↗

PubMed1999

Epidemiological study of hip fracture in Shenyang, People's Republic of China.

The aim of this study was to investigate the incidence and epidemiology in 1994 of hip fracture in Shenyang, a large city in the northeast of The People's Republic of China, using register information and medical records collected from the 36 hospitals in Shenyang. The hip fracture data were restricted to cervical or trochanteric types. A subset (59% of total) of medical records of hip fracture was used to investigate the causes of hip fracture. The causes were classified as simple fall, fall from a bicycle during cycling, bicycle accident, car accident, and fall from a height. There was a total of 453 hip fractures (206 in women and 247 in men) in the population over 50 years of age. The age-adjusted 1 year cumulative incidence rate was 67/100,000 (95% confidence interval [CI] = 58-76/100,000) for women and 81/100,000 (95% CI = 71-91/100,000) for men. The standardized incidence rate against the 1985 U.S. population was 87/100,000 (95% CI = 77-97/100,000) for women and 100/100,000 (95% CI = 89-111/100,000) for men. The mean (+/-standard deviation) age of patients with a hip fracture was 67.5+/-9.8 years for men and 66.9+/-9.0 years for women. The overall male-to-female ratio of hip fracture was 1.21:1 for age-adjusted hip fracture incidence and 1.15:1 for standardized incidence. Simple fall accounted for 70% hip fractures in women but caused only 49% in men (chi2 = 11.2, degrees of freedom [df] = 1,p = 0.0008). The frequency of hip fractures caused by a fall from a bicycle was higher in men (28%) than women (10%) (chi2 = 13.0, df = 1,p = 0.0003). The results of this study indicate (1) a low incidence of hip fracture in a Chinese population compared with more affluent countries, and (b) a higher incidence in men than women that is related in part to a higher incidence of accidents, especially bicycle-related ones.

Accidental Falls↗

PubMed1999

Gene transfer in utero biologically engineers a patent ductus arteriosus in lambs by arresting fibronectin-dependent neointimal formation.

Closure of the ductus arteriosus requires prenatal formation of intimal cushions, which occlude the vessel lumen at birth. Survival of newborns with severe congenital heart defects, however, depends on ductal patency. We used a gene transfer approach to create a patent ductus arteriosus by targeting the fibronectin-dependent smooth muscle cell migration required for intimal cushion formation. Fetal lamb ductus arteriosus was transfected in utero with hemagglutinating virus of Japan liposomes containing plasmid encoding 'decoy' RNA to sequester the fibronectin mRNA binding protein. Fibronectin translation was inhibited and intimal cushion formation was prevented. We thus established the essential role of fibronectin-dependent smooth muscle cell migration in intimal cushion formation in the intact animal and the feasibility of incorporating biological engineering in the management of congenital heart disease.

Animals↗

PubMed1999

Comparative stability of ethanol production by Escherichia coli KO11 in batch and chemostat culture.

Differing claims regarding the stability of the recombinant ethanologen E. coli KO11 are addressed here in batch and chemostat culture. In repeat batch culture, the organism was stable on glucose, mannose, xylose and galactose for at least three serial transfers, even in the absence of a selective antibiotic. Chemostat cultures on glucose were remarkably stable, but on mannose, xylose and a xylose/glucose mixture, they progressively lost their hyperethanologenicity. On xylose, the loss was irreversible, indicating genetic instability. The loss of hyperethanologenicity was accompanied by the production of high concentrations of acetic acid and by increasing biomass yields, suggesting that the higher ATP yield associated with acetate production may foster the growth of acetate-producing revertant strains. Plate counts on high chloramphenicol-containing medium, whether directly, or following preliminary growth on non-selective medium, were not a reliable indicator of high ethanologenicity during chemostat culture. In batch culture, the organism appeared to retain its promise for ethanol production from lignocellulosics and concerns that antibiotics may need to be included in all media appear unfounded.

Bioreactors↗

PubMed1999

Induction of vascular smooth muscle cell tenascin-C gene expression by denatured type I collagen is dependent upon a beta3 integrin-mediated mitogen-activated protein kinase pathway and a 122-base pair promoter element.

Tenascin-C is an extracellular matrix glycoprotein, the expression of which is upregulated in remodeling arteries. In previous studies we showed that the presence of tenascin-C alters vascular smooth muscle cell shape and amplifies their proliferative response by promoting growth factor receptor clustering and phosphorylation. Moreover, we demonstrated that denatured type I collagen induces smooth muscle cell tenascin-C protein production via beta3 integrins. In the present study, we examine the pathway by which beta3 integrins stimulate expression of tenascin-C, and define a promoter sequence that is critical for its induction. On native collagen, A10 smooth muscle cells adopt a stellate morphology and produce low levels of tenascin-C mRNA and protein, whereas on denatured collagen they spread extensively and produce high levels of tenascin-C mRNA and protein, which is incorporated into an elaborate extracellular matrix. Increased tenascin-C synthesis on denatured collagen is associated with elevated protein tyrosine phosphorylation, including activation of extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2). beta3 integrin function-blocking antibodies attenuate ERK1/2 activation and tenascin-C protein synthesis. Consistent with these findings, treatment with the specific MEK inhibitor, PD 98059, results in suppression of tenascin-C protein synthesis. To investigate whether beta3 integrin-dependent activation of ERK1/2 regulates the tenascin-C promoter, we transfected A10 cells with a full-length (approx. 4 kb) mouse tenascin-C gene promoter-chloramphenicol acetyltransferse reporter construct and showed that, relative to native collagen, its activity is increased on denatured collagen. Next, to identify regions of the promoter involved, we examined a series of tenascin-C promoter constructs with 5' deletions and showed that denatured collagen-dependent promoter activity was retained by a 122-base pair element, located -43 to -165 bp upstream of the RNA start site. Activation of this element was suppressed either by blocking beta3 integrins, or by preventing ERK1/2 activation. These observations demonstrate that smooth muscle cell binding to beta3 integrins activates the mitogen activated protein kinase pathway, which is required for the induction of tenascin-C gene expression via a potential extracellular matrix response element in the tenascin-C gene promoter. Our data suggest a mechanism by which remodeling of type I collagen modulates tenascin-C gene expression via a beta3 integrin-mediated signaling pathway, and as such represents a paradigm for vascular development and disease whereby smooth muscle cells respond to perturbations in extracellular matrix composition by altering their phenotype and patterns of gene expression.

Animals↗

PubMed1999

Ro 31-8220 inhibits release of interleukin-1 and interleukin-6 from mouse peritoneal macrophages induced by fibrin fibrinogen degradation products.

AIM: To study the effect of fibrin fibrinogen degradation products (FFDP) on release of interleukin-1 (IL-1) and interleukin-6 (IL-6) from mouse peritoneal macrophages, and the effect of a new selectively potent protein kinase C inhibitor Ro 31-8220 (Ro). METHODS: IL-1 and IL-6 activities were measured by thymocyte proliferation assay and B9 cell proliferation methyl thiazolyl tetrazolium (MTT) colorimetric method, respectively. RESULTS: Ro 0.01-1 mumol.L-1 obviously inhibited FFDP-induced release of IL-1 and IL-6 from mouse peritoneal macrophages. CONCLUSION: Ro exerted inhibitory effects on FFDP-induced release of IL-1 and IL-6 in vitro.

Animals↗