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Biomedical subjects

B Zhang

Publications and source records attributed to B Zhang.

At least 217 records · Page 12Linked to original sources
PubMed2000

Immunochemical fecal occult blood test is inadequate for screening test of stomach cancer.

The present study was carried out to investigate the diagnostic accuracy of the immunochemical fecal occult blood test in the screening for stomach cancer. In the hospital-based case-control study, the test was positive in 6 (14.3%) subjects with stomach cancer, in 32 (76.2%) subjects with colorectal cancer, and in 10 (7.9%) healthy subjects, respectively, showing a significant difference in detection rate between the subjects with stomach cancer and colorectal cancer (p < 0.01). In the population-based cross-sectional study, detection rate for stomach cancer was 0.13% and 0.15% for negative and positive groups decided by immunochemical fecal occult blood test, indicating no significant difference. These results reveal that the immunochemical fecal occult blood test is inadequate as the screening test for stomach cancer and suggest that examination of the upper digestive tract is unnecessary in cases where the result of fecal occult blood test is positive with no sign of colorectal diseases.

Case-Control Studies↗
PubMed2000

Localization of inducible nitric oxide synthase to mast cells during ischemia/reperfusion injury of skeletal muscle.

Nitric oxide contributes to tissue necrosis after ischemia-reperfusion (IR). A biochemical and immunohistochemical study was made of the amounts and localization of both Ca++-independent nitric oxide synthase (NOS) II and Ca++-dependent (NOS I and NOS III) in rat skeletal muscle after ischemia and 0.5, 2, 8, 16, and 24 hours reperfusion. NOS II was not detectable in control muscle or during ischemia, was first detected after 2 hours reperfusion, increased further by 8 hours, and remained elevated at 24 hours. Both NOS II and nitrotyrosine, a marker of peroxynitrite formation, were localized exclusively to mast cells except after 24 hours reperfusion when some macrophages and neutrophils also showed positive immunoreactivity. Mast cells underwent extensive degranulation during reperfusion. NOS I was not detected in injured or control muscle. The level of NOS III, which was localized to the endothelium of blood vessels of all sizes in control muscle, decreased progressively during ischemia and reperfusion to reach undetectable levels after 16 hours reperfusion. These findings indicate that most of the nitric oxide formed during IR injury is generated by NOS II located almost exclusively in mast cells.

Animals↗
PubMed2000

Reversal of the vasoconstrictor step of hyperacute xenogeneic rejection of the liver by endothelin antagonists.

The role of endothelin in the initial vasoconstrictor step of hyperacute xenogeneic rejection was investigated. Isolated rat livers were perfused in recirculation. Perfusion with human sera provided an ex vivo model of hyperacute rejection in a discordant combination. Perfusion of 10% xenogeneic serum induced a marked (70%) and sustained reduction of the liver flow and induced the release of endothelin into the perfusion medium. In contrast, perfusion of 10% allogeneic serum or of 10% decomplemented human serum induced a weak (25%) and transient reduction of the liver flow and induced the release of minimal amounts of endothelin. The simultaneous administration of BQ 123 and BQ 788, the respective antagonists of ET(A) and ET(B) endothelin receptors, or that of bosentan, a mixed ET(A)/ET(B) antagonist, antagonized the vasoconstrictor effect of 10% xenogeneic human serum, as well as that of 10(-9) M endothelin-1. The vasoconstrictor effects of xenogeneic serum on liver circulation are, at least partly, mediated through the release of endothelin by the graft.

Animals↗
PubMed2000

Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells.

Multiple tau gene mutations are pathogenic for hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), with filamentous tau aggregates as the major lesions in the CNS of these patients. Recent studies have shown that bacterially expressed recombinant tau proteins with FTDP-17 missense mutations cause functional impairments, i.e., a reduced ability of mutant tau to bind to or promote the assembly of microtubules. To investigate the biological consequences of FTDP-17 tau mutants and assess their ability to form filamentous aggregates, we engineered Chinese hamster ovary cell lines to stably express tau harboring one or several different FTDP-17 mutations and showed that different tau mutants produced distinct pathological phenotypes. For example, delta K, but not several other single tau mutants (e.g., V337 M, P301L, R406W), developed insoluble amorphous and fibrillar aggregates, whereas a triple tau mutant (VPR) containing V337M, P301L, and R406W substitutions also formed similar aggregates. Furthermore, the aggregates increased in size over time in culture. Significantly, the formation of aggregated delta K and VPR tau protein correlated with reduced affinity of these mutants to bind microtubules. Reduced phosphorylation and altered proteolysis was also observed in R406W and delta K tau mutants. Thus, distinct pathological phenotypes, including the formation of insoluble filamentous tau aggregates, result from the expression of different FTDP-17 tau mutants in transfected Chinese hamster ovary cells and implies that these missense mutations cause diverse neurodegenerative FTDP-17 syndromes by multiple mechanisms.

Animals↗
PubMed2000

Analysis of the mechanism by which glucose inhibits maltose induction of MAL gene expression in Saccharomyces.

Expression of the MAL genes required for maltose fermentation in Saccharomyces cerevisiae is induced by maltose and repressed by glucose. Maltose-inducible regulation requires maltose permease and the MAL-activator protein, a DNA-binding transcription factor encoded by MAL63 and its homologues at the other MAL loci. Previously, we showed that the Mig1 repressor mediates glucose repression of MAL gene expression. Glucose also blocks MAL-activator-mediated maltose induction through a Mig1p-independent mechanism that we refer to as glucose inhibition. Here we report the characterization of this process. Our results indicate that glucose inhibition is also Mig2p independent. Moreover, we show that neither overexpression of the MAL-activator nor elimination of inducer exclusion is sufficient to relieve glucose inhibition, suggesting that glucose acts to inhibit induction by affecting maltose sensing and/or signaling. The glucose inhibition pathway requires HXK2, REG1, and GSF1 and appears to overlap upstream with the glucose repression pathway. The likely target of glucose inhibition is Snf1 protein kinase. Evidence is presented indicating that, in addition to its role in the inactivation of Mig1p, Snf1p is required post-transcriptionally for the synthesis of maltose permease whose function is essential for maltose induction.

Base Sequence↗
PubMed2000

Use of oral corticosteroids in the United Kingdom.

Administration of oral corticosteroids is associated with the development of osteoporosis and an increased risk of fractures. However, the size of the treated sub-population who would benefit from preventive therapy remains uncertain. The objective of this study was to investigate the usage pattern of oral corticosteroids in a large sample representative of the general population in England and Wales. Information was obtained from the General Practice Research Database (GPRD) which contains medical records of general practitioners. Oral corticosteroid users were patients aged 18 years or older who received one or more prescriptions for oral corticosteroids. Over 1.6 million oral corticosteroid prescriptions were issued to the cohort of 244 235 oral corticosteroid users. At any point in time, oral corticosteroids were being used by 0.9% of the total adult GPRD population. The highest use (2.5%) was by people between 70 and 79 years of age. Respiratory disease was the most frequently recorded indication for oral corticosteroid treatment (40%). Patients with arthropathies were most likely to use long-term, continuous treatment, and patients with chronic obstructive pulmonary disease least likely (19.3% and 6.1%, respectively, used oral corticosteroids for more than 2 years). The overall use of bone-active medication (oestrogens, bisphosphonates, vitamin D, and calcitonin) during oral corticosteroid treatment was low (between 4.0% and 5.5%). The current population in the UK at risk of developing corticosteroid-induced fractures might be as large as 350 000. Identification of these patients will be important for implementing preventive strategies in a cost-effective manner.

Administration, Oral↗
PubMed2000

Oral corticosteroids and fracture risk: relationship to daily and cumulative doses.

OBJECTIVE: This study examined the effects of daily and cumulative oral corticosteroid doses on the risk of fractures. METHODS: Information was obtained from the General Practice Research Database, which contains medical records of general practitioners in England and Wales. The study included 244 235 oral corticosteroid users and 244 235 controls. RESULTS: Patients taking higher doses (at least 7. 5 mg daily of prednisolone or equivalent) had significantly increased risks of non-vertebral fracture [relative rate (RR)=1.44, 95% confidence interval (CI) 1.34-1.54], hip fracture (RR=2.21, 95% CI 1.85-2.64) and vertebral fracture (RR=2.83, 95% CI 2.35-2.40) relative to patients using oral corticosteroids at lower doses (less than 2.5 mg per day). Fracture risk was also elevated among people with higher cumulative exposure to oral corticosteroids over the study period, but this effect was almost wholly removed by adjustment for daily dose, age, gender and other confounding variables. CONCLUSIONS: These findings suggest that the adverse skeletal effects of oral corticosteroids manifest rapidly and are related to daily dose. The level of previous exposure to oral corticosteroids was not a strong determinant of the risk of fracture. Preventive measures against corticosteroid-induced osteoporosis should therefore be instituted as soon after the commencement of glucocorticoid therapy as possible.

Administration, Oral↗
PubMed2000

Relationships between a sign of rectal bleeding and the results of an immunochemical occult blood test, and colorectal cancer.

A cross-sectional study based on medical check-up was carried out to investigate the association between signs of rectal bleeding and colorectal cancer, and the results of an immunochemical faecal occult blood test. The 9625 patients received both an immunochemical faecal occult blood test using a two-consecutive-day method and colonoscopy. They were then divided into two groups, according to the results of a self-completed questionnaire on the signs of rectal bleeding. The positivity rate of the immunochemical faecal occult blood test as well as the positive predictive value for colorectal cancer were determined in these two groups. The faecal occult blood test was positive in 9.3% of patients with rectal bleeding and in 4.4% of patients without rectal bleeding, and the positive predictive value for colorectal cancer was 0.79 and 0.27 in patients with and without rectal bleeding, respectively. This indicates a significant difference in the positivity rate (P < 0.001) as well as the positive predictive value (P < 0.05) between these two groups. The results suggest that there are positive associations between the signs of rectal bleeding and the results of immunochemical faecal occult blood test, and between the patients presenting with rectal bleeding and colorectal cancer.

Adult↗
PubMed2000

Digital rectal examination sampling of stool is less predictive of significant colorectal pathology than stool passed spontaneously.

OBJECTIVES: To compare the positivity rate and the positive predictive value of an immunochemical faecal occult blood test (FOBT) carried out by using stool samples obtained during a routine screening method and those obtained during digital rectal examination. DESIGN: Screening programme-based, cross-sectional study. METHODS: In a screening programme-based, cross-sectional study, 1,044 subjects who received both an immunochemical FOBT and colonoscopy were divided into two groups according to stool collection techniques--the routine screening method and the digital rectal examination method. The positivity rate of the immunochemical FOBT, as well as the positive predictive value for colorectal cancer and large adenomatous polyp, were determined in the two groups. RESULTS: The positivity rate and positive predictive value were 3.8% and 60.0% (10.0% for cancer and 50.0% for adenomatous polyp) in the routine screening group, and 9.4% and 26.5% (4.1% for cancer and 22.4% for adenomatous polyp) in the digital rectal examination group, respectively, indicating a significant difference in the positivity rate (P < 0.01) as well as the positive predictive value (P< 0.05) between the two groups. CONCLUSIONS: These results show that digital rectal examination sampling of stool is less predictive of significant colorectal pathology than stool passed spontaneously, and therefore the latter is the preferred method for stool sampling.

Chi-Square Distribution↗
PubMed2000

Genetic diversity in the matrix metalloproteinase family. Effects on function and disease progression.

Atherosclerosis is an example of a complex trait, where the course of the disease is influenced by a combination of common variation in a constellation of genes and the effect of a wide range of environmental variables. Thus, the underlying disease mechanisms will be modulated by genetic diversity and the effect this diversity has on an individual's response to environmental challenges such as smoking, diet, and exercise. Unlike the consequences of mutations in severe single-gene disorders on protein function, the impact of individual common, functionally important sequence changes in genes contributing to multifactorial diseases is likely to be very small. The challenge is to dissect the contribution that each of these genes makes to the disease process. We have tackled this by identifying common genetic variants, studying their effects on function, and applying them to the analysis of association in appropriately structured and suitably powered studies. Even with our incomplete understanding of the disease, the list of potential candidate genes we could study is vast; but, we do know from pathological studies that a wide spectrum of structural architecture exists in atherosclerotic plaques, suggesting that remodeling of vascular connective tissue is fundamentally important. Matrix remodeling is controlled by a complex network of cell and matrix interactions, the net outcome of which is the product of a balance between synthetic and degradative processes. Our work has focused on the family of enzymes and inhibitors most directly associated with matrix turnover--the matrix metalloproteinases (MMPs) and their natural inhibitors (TIMPs, tissue inhibitors of MPs). We specifically searched for functionally relevant genetic variants that might modulate the delicate control of matrix turnover. Using these molecular genetic strategies to investigate the impact of natural genetic variation on vascular matrix remodeling has begun to shed new light on the importance of these genes in atherogenesis.

Arteriosclerosis↗
PubMed2000

Metabolic signals trigger glucose-induced inactivation of maltose permease in Saccharomyces.

Organisms such as Saccharomyces capable of utilizing several different sugars selectively ferment glucose when less desirable carbon sources are also available. This is achieved by several mechanisms. Glucose down-regulates the transcription of genes involved in utilization of these alternate carbon sources. Additionally, it causes posttranslational modifications of enzymes and transporters, leading to their inactivation and/or degradation. Two glucose sensing and signaling pathways stimulate glucose-induced inactivation of maltose permease. Pathway 1 uses Rgt2p as a sensor of extracellular glucose and causes degradation of maltose permease protein. Pathway 2 is dependent on glucose transport and stimulates degradation of permease protein and very rapid inactivation of maltose transport activity, more rapid than can be explained by loss of protein alone. In this report, we characterize signal generation through pathway 2 using the rapid inactivation of maltose transport activity as an assay of signaling activity. We find that pathway 2 is dependent on HXK2 and to a lesser extent HXK1. The correlation between pathway 2 signaling and glucose repression suggests that these pathways share common upstream components. We demonstrate that glucose transport via galactose permease is able to stimulate pathway 2. Moreover, rapid transport and fermentation of a number of fermentable sugars (including galactose and maltose, not just glucose) are sufficient to generate a pathway 2 signal. These results indicate that pathway 2 responds to a high rate of sugar fermentation and monitors an intracellular metabolic signal. Production of this signal is not specific to glucose, glucose catabolism, glucose transport by the Hxt transporters, or glucose phosphorylation by hexokinase 1 or 2. Similarities between this yeast glucose sensing pathway and glucose sensing mechanisms in mammalian cells are discussed.

Fermentation↗
PubMed2000

Gene expression in the rat supraoptic nucleus induced by chronic hyperosmolality versus hyposmolality.

Magnocellular neurons of the hypothalamo-neurohypophysial system play a fundamental role in the maintenance of body homeostasis by secreting vasopressin and oxytocin in response to systemic osmotic perturbations. During chronic hyperosmolality, vasopressin and oxytocin mRNA levels increase twofold, whereas, during chronic hyposmolality, these mRNA levels decrease to 10-20% of that of normoosmolar control animals. To determine what other genes respond to these osmotic perturbations, we have analyzed gene expression during chronic hyper- versus hyponatremia. Thirty-seven cDNA clones were isolated by differentially screening cDNA libraries that were generated from supraoptic nucleus tissue punches from hyper- or hyponatremic rats. Further analysis of 12 of these cDNAs by in situ hybridization histochemistry confirmed that they are osmotically regulated. These cDNAs represent a variety of functional classes and include cytochrome oxidase, tubulin, Na(+)-K(+)-ATPase, spectrin, PEP-19, calmodulin, GTPase, DnaJ-like, clathrin-associated, synaptic glycoprotein, regulator of GTPase stimulation, and gene for oligodendrocyte lineage-myelin basic proteins. This analysis therefore suggests that adaptation to chronic osmotic stress results in global changes in gene expression in the magnocellular neurons of the supraoptic nucleus.

Animals↗
PubMed2000

Use of oral corticosteroids and risk of fractures.

Treatment with oral corticosteroids is known to decrease bone density but there are few data on the attendant risk of fracture and on the reversibility of this risk after cessation of therapy. A retrospective cohort study was conducted in a general medical practice setting in the United Kingdom (using data from the General Practice Research Database [GPRD]). For each oral corticosteroid user aged 18 years or older, a control patient was selected randomly, who was matched by age, sex, and medical practice. The study comprised 244,235 oral corticosteroid users and 244,235 controls. The average age was 57.1 years in the oral corticosteroid cohort and 56.9 years in the control cohort. In both cohorts 58.6% were female. The most frequent indication for treatment was respiratory disease (40%). The relative rate of nonvertebral fracture during oral corticosteroid treatment was 1.33 (95% confidence interval [CI], 1.29-1.38), that of hip fracture 1.61 (1.47-1.76), that of forearm fracture 1.09 (1.01-1.17), and that of vertebral fracture 2.60 (2.31-2.92). A dose dependence of fracture risk was observed. With a standardized daily dose of less than 2.5 mg prednisolone, hip fracture risk was 0.99 (0.82-1.20) relative to control, rising to 1.77 (1.55-2.02) at daily doses of 2.5-7.5 mg, and 2.27 (1.94-2.66) at doses of 7.5 mg or greater. For vertebral fracture, the relative rates were 1.55 (1.20-2.01), 2.59 (2.16-3.10), and 5.18 (4.25-6.31), respectively. All fracture risks declined toward baseline rapidly after cessation of oral corticosteroid treatment. These results quantify the increased fracture risk during oral corticosteroid therapy, with greater effects on the hip and spine than forearm. They also suggest a rapid offset of this increased fracture risk on cessation of therapy, which has implications for the use of preventative agents against bone loss in patients at highest risk.

Administration, Oral↗
PubMed2000

Structural organization and fine distribution of lymphatic vessels in periodontal tissues of the rat and monkey: a histochemical study.

The structural organization and fine distribution of lymphatic vessels in the periodontal tissues (gingiva, periodontium and alveolar process) were examined by light and electron microscopy using an enzyme-histochemical method. Whole mount preparations of periodontal membranes peeled from the teeth and cryostat sections of normal or decalcified tissues treated with EDTA were double-stained using 5'-nucleotidase (5'-Nase)-alkaline phosphatase (ALPase) and examined by light microscopy. This staining procedure allowed the lymphatic vessels in the periodontal tissue to be differentiated from blood vessels. Well-developed 5'-Nase-positive lymphatics were observed in the gingiva and periodontium. The histochemical aspects of 5'-Nase activity in lymphatic vessels are discussed in detail, with special reference to the supply of Mg++ ions. A network of 5'-Nase-positive lymphatics was observed in whole mount preparations of the periodontal membrane for the first time. This network was also observed in the tissue sections. More 5'-Nase-positive lymphatics were seen in the root area of the periodontium than in the cervical area. 5'-Nase-positive lymphatics in residual tissue blocks remaining after cryostat sectioning and in whole mount preparations were highlighted with good contrast and resolution on backscattered electron images produced by scanning electron microscopy. Dense granular precipitations resulting from the 5'-Nase reaction were observed on the luminal surface of the lymphatic endothelial cells as well as on the basal side but were absent in the blood vessels.

5'-Nucleotidase↗
PubMed2000

In vivo metabolism of HDL, apo A-I, and lp A-I, and function of HDL--a clinical perspective.

Serum levels of high density lipoprotein cholesterol (HDL-C) are inversely correlated with coronary heart disease (CHD). Kinetic studies indicate that the mechanism for the variation in HDL levels associated with various pathophysiologic states includes changes in the fractional catabolic rate (FCR) and/or the synthesis rate of HDL and its major proteins apolipoprotein (apo) A-I and apo A-II. The antiatherogenic effects of HDL are thought to be mainly due to its role in reverse cholesterol transport. HDL is an assembly of heterogeneous particles. HDL enlarges when it takes up cellular cholesterol, and shrinks when HDL cholesterol ester (CE) is transfered to low density lipoprotein (LDL) and very low density lipoprotein (VLDL) particles. The functional ability of HDL (to remove cellular cholesterol) has drawn considerable attention. The fractional esterification rate of cholesterol in HDL (FER(HDL)) has been established as a functional assay of HDL, and reflects the size of HDL particles. We investigated the clinical significance of FER(HDL) and its relationship to the quantity of HDL. FER(HDL) values were inversely correlated with levels of HDL-C and large lipoprotein containing apo A-I (LpA-I). The association between FER(HDL) and CHD changed with serum HDL-C levels: increased FER(HDL) values significantly increased the risk of CHD when serum HDL-C levels were low, while there was no such relationship when HDL-C levels were high. We concluded that the combination of HDL-C levels and FER(HDL) is a stronger indicator of CHD than either the HDL-C level (quantitative measure of HDL) or FER(HDL) (functional measure of HDL) alone.

Animals↗
PubMed2000

Effect of onset age of strabismus on the binocular responses of neurons in the monkey visual cortex.

PURPOSE: By 6 weeks of age, neurons in the monkey's primary visual cortex acquire qualitatively adult-like binocular response properties and behaviorally stereopsis emerges. In this study, it was determined whether the onset of strabismus has a more severe impact on cortical binocularity before or after this critical developmental age. METHODS: Infant monkeys were fit with a light-weight helmet which held a total of 27 diopters of base-in prisms in front of their two eyes for a fixed period of two weeks. For one group of infant monkeys, prism-rearing began at 2 weeks of age and for a second group, the onset was at 6 weeks of age. Immediately after the rearing period, i.e., at 4 weeks and 8 weeks of age, respectively, extracellular single-unit recording methods were used to determine the nature and severity of alterations in the binocular response properties of V1 neurons. Dichoptic sinewave gratings were used as visual stimuli. RESULTS: In comparison to normal age-matched infants, V1 neurons in both strabismic groups exhibited reductions in sensitivity to interocular spatial phase disparities (disparity sensitivity) and a higher prevalence of binocular inhibitory interactions (binocular suppression). However, the reduction in disparity sensitivity and the magnitude of binocular suppression were much greater in the late (6-8 weeks) than the early (2- 4 weeks) onset group. CONCLUSIONS: Discordant binocular signals due to brief periods of early strabismus have more serious effects on the development of binocular properties of V1 neurons if they occur shortly after rather than before the emergence of stereopsis (i.e., when the binocular connections are relatively more mature but the visual cortex still shows a high degree of plasticity).

Age of Onset↗
PubMed2000

[Resistance of Bcl-2 adenovirus vector to HepG(2) cell apoptosis induced by ethanol].

OBJECTIVE: To evaluate the role of Bcl-2 family proteins in hepatocytic apoptosis caused by ethanol. METHODS: We induced hepatocytic apoptosis in HepG(2) cells with ethanol and detected the apoptosis with TUNEL assay. Bcl-2, Bax, and Bak protein expression in the hepatocytes was determined by immunohistochemistry method. We also observed the expression of Bcl-2 protein in HepG(2) cells infected with Bcl-2 adenovirus vector and its protection against hepatocytic apoptosis caused by ethanol. RESULTS: No obvious cytotoxicity was noted in 0.2% and 1% ethanol treatment group, while it developed in 3% ethanol treatment group and accompanied by a marked expression of Bax, Bak proteins. CONCLUSION: The overexpression of Bax, Bak proteins may play a role in HepG(2) cell apoptosis induced by ethanol and can be blocked effectively by Bcl-2 adenovirus vector.

Adenoviridae↗