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Biomedical subjects

Z Y Yan

Publications and source records attributed to Z Y Yan.

At least 19 recordsLinked to original sources
PubMed2000

Effects of morphine on rheological properties of rat red blood cells.

To evaluate the effect of morphine on red blood cells, in vivo and in vitro rat models of morphine dependence were established. Rheological properties of rat red cells were measured by ektacytometry; the biophysical changes in the membrane of rat red cells were measured by the Fourier-Transformed Infrared technique (FT-IR) and the fluorescence depolarization method. The results show that the membrane fluidity of red cells was greatly reduced by morphine and the secondary structure of membrane proteins was changed. This suggests that morphine affects the rat red cell membrane directly, rather than through opioids-receptors.

Animals↗
PubMed2000

A study of hemorheological behaviour for patients with Alzheimer's disease at the early stages.

To evaluate the change of hemorheological indexes for patients with Alzheimer's disease (AD) at the early stages and to discuss effects of these changes on AD, high shear value of whole blood viscosity (etabh), reduced high shear value of whole blood viscosity (retabh), low shear value of whole blood viscosity (etabl), reduced low shear, value of whole blood viscosity (retabl), KT value of whole blood viscosity, hematocrit (HCT) and blood plasma viscosity (etaP) were measured in 31 patients with probable AD at the early stages and 33 age-matched healthy subjects. There were significant differences of all hemorheological indexes between AD group and control group except HCT. Step discriminant analysis revealed 81.25% of overall group-classified accuracy in a hemorheological discriminant function consisting of etabl, retabl, retabh and HCT. Significant difference of hemorheological indexes existed between AD and age-matched healthy control subjects. The results showed that measurement of hemorheological indexes could be used as one of reference standards of diagnosis in AD.

Aged↗
PubMed2000

Influence of neuraminidase on the characteristics of microrheology of red blood cells.

Surface charge was removed from RBC (erythrocyte) membrane to different degrees with biochemical methods, i.e., treatment of RBCs with neuraminidase, either using different doses for the same incubation time (1 hour) or using the same dose (75 milli-unit) for different incubation time. Several rheological properties of the RBCs with surface charge removal were observed, including the deformation index DI (using traditional ektacytometry) orientation index (DI)or and small deformation index (Dl)d (using new ektacytometry), the viscosity at low and high shear rates (using a cone-plate rotating viscosimeter). In addition, photographs of RBCs aggregation under a microscope and the histograms of RBC aggregate size after treatment with neuraminidase were obtained. It is found from these experiments that the decrease of the surface charge of RBCs leads to the decrease in the deformation and orientation indices as well as the increase in blood viscosity.

Animals↗
PubMed1999

Allelic imbalance at the LKB1 (STK11) locus in tumours from patients with Peutz-Jeghers' syndrome provides evidence for a hamartoma-(adenoma)-carcinoma sequence.

Patients with Peutz-Jeghers' syndrome (PJS) develop hamartomatous gastrointestinal polyps and characteristic pigmentation, as a result of germline mutations in the LKB1 gene. The hamartomas in PJS were long considered to be without malignant potential. There is, however, accumulating epidemiological evidence to suggest that PJS predisposes to cancers at several different sites (colon, pancreas, breast, ovary, testis, and cervix), although large enough patient samples are rarely available to prove this. Allelic imbalance [allele loss, loss of heterozygosity (LOH)] has previously been reported in a small number of PJS polyps, suggesting that LKB1 acts as a tumour suppressor in these tumours. This study confirms allelic loss at LKB1 in PJS polyps and shows that LOH also occurs in cancers of the colon, breast, and cervix in PJS patients. Allele loss was additionally found in a colonic adenoma from a PJS patient, strongly suggesting the existence of a hamartoma-(adenoma)-carcinoma sequence in tumourigenesis. These results provide molecular evidence that PJS patients are predisposed to cancers at several sites, as a direct result of selection for loss of the 'wild-type' LKB1 allele in tumours. Given the rare involvement of LKB1 in sporadic cancers, these data also suggest that the indirect effect on cancer risk (or 'bystander effect') proposed for hamartomas in juvenile polyposis does not apply to carcinomas in PJS.

AMP-Activated Protein Kinase Kinases↗
PubMed1999

Allele loss and mutation screen at the Peutz-Jeghers (LKB1) locus (19p13.3) in sporadic ovarian tumours.

Germline mutations in the LKB1 (STK11) gene (chromosome sub-band 19p13.3) cause characteristic hamartomas and pigmentation to develop in patients with Peutz-Jeghers syndrome. Peutz-Jeghers syndrome carries an overall risk of cancer that may be up to 20 times that of the general population and Peutz-Jeghers patients are at increased risk of benign and malignant ovarian tumours, particularly granulosa cell tumours. Loss of heterozygosity (allele loss, LOH) has been reported in about 50% of ovarian cancers on 19p13.3. LKB1 is therefore a candidate tumour suppressor gene for sporadic ovarian tumours. We found allele loss at the marker D19S886 (19p13.3) in 12 of 49 (24%) sporadic ovarian adenocarcinomas. Using SSCP analysis, we screened ten ovarian cancers with LOH, 35 other ovarian cancers and 12 granulosa cell tumours of the ovary for somatic mutations in LKB1. No variants were detected in any of the adenocarcinomas. Two mutations were detected in one of the granulosa cell tumours: a mis-sense mutation affecting the putative 'start' codon (ATG --> ACG, M1T); and a silent change in exon 7 (CTT --> CTA, leucine). Like BRCA1 and BRCA2, therefore, it appears that LKB1 mutations can cause ovarian tumours when present in the germline, but occur rarely in the soma. The allele loss on 19p13.3 in ovarian cancers almost certainly targets a different gene from LKB1.

AMP-Activated Protein Kinase Kinases↗
PubMed1999

Germline mutations of the LKB1 (STK11) gene in Peutz-Jeghers patients.

Germline mutations of the LKB1 (STK11) serine/threonine kinase gene (chromosome 19p13.3) cause Peutz-Jeghers syndrome, which is characterised by hamartomas of the gastrointestinal tract and typical pigmentation. Peutz-Jeghers syndrome carries an overall risk of cancer that may be up to 20 times that of the general population. Here, we report the results of a screen for germline LKB1 mutations by DNA sequencing in 12 Peutz-Jeghers patients (three sporadic and nine familial cases). Mutations were found in seven (58%) cases, in exons 1, 2, 4, 6, and 9. Five of these mutations, two of which are identical, are predicted to lead to a truncated protein (three frameshifts, two nonsense changes). A further mutation is an in frame deletion of 6 bp, resulting in a deletion of lysine and asparagine; the second of these amino acids is conserved between species. The seventh mutation is a missense change in exon 2, converting lysine to arginine, affecting non-conserved amino acids and of uncertain functional significance. Despite the fact that Peutz-Jeghers syndrome is usually an early onset disease with characteristic clinical features, predictive and diagnostic testing for LKB1 mutations will be useful for selected patients in both familial and non-familial contexts.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

An animal model to study erythrocyte senescence with a narrow time window of erythrocyte production.

Using the method of inducing spherocytic anemia in the rabbit with antibody serum, we have developed an animal model in which red blood cells (RBCs) can nearly grow synchronously. With this model, we determined that the surface charge density on the RBC membrane decreased with cell aging. The change was not linear, being much more profound in the latter half of RBC life span. There was a positive correlation between the mean RBC density and its "age" (r = 0.847, p < 0.01). However, the density distribution of the RBCs at the same "age" showed a broad range, and the density values for RBC groups with different ages showed considerable overlap. This indicates that the density gradient technique can be used to separate RBC population into fractions with different mean ages, but has a low resolving power for obtaining individual RBCs of a given "age".

Anemia↗
PubMed1998

An animal model to study erythrocyte senescence with a narrow time window of erythrocyte production: alterations in osmotic fragility and deformability of erythrocytes during their life span.

Using the model in which the entire RBC population was nearly synchronously produced following the induction of spherocytic anemia in the rabbit with antibody serum, we determined the changes of RBC osmotic fragility and deformability with aging. The results showed that the osmotic fragility increased with the RBC aging process in a nonlinear manner, being much more profound in the later part of the RBC life span. The RBC deformation index (DI) was measured by an ektacytometry. It is found that the DI decreased with RBC aging in a nonlinear fashion, with increasingly greater changes in the later part of the RBC life span. The alterations of RBC mechanical properties with aging may be attributable to a number of factors, including changes of RBC size and shape, and the viscoelasticity of the cytoplasm and membrane.

Anemia, Hemolytic↗
PubMed1997

Bacterial scavengase p20 is structurally and functionally related to peroxiredoxins.

Scavengase p20 was recently identified as a novel family of bacterial antioxidant enzymes possessing thioredoxin-linked thiol peroxidase activity. In this study, the Escherichia coli gene coding for scavengase p20 was isolated from three different strains and the nucleotide sequence was determined. Multiple alignment of amino acid sequence revealed that a previously unidentified Cys-61 is most conserved among all bacterial p20 scavengases and corresponds to the active site in the well-characterized peroxiredoxins. Phylogenetic analysis further supported that scavengase p20 is a novel subfamily of peroxiredoxins. Site-directed mutagenesis studies demonstrated that Cys-61 is indispensable for the antioxidant activities of scavengase p20. Taken together, our findings strongly suggest that the p20 scavengases are structurally and functionally related to peroxiredoxins.

Amino Acid Sequence↗
PubMed1997

Scavengase p20: a novel family of bacterial antioxidant enzymes.

A novel antioxidant enzyme designated scavengase p20 was identified in various pathogenic bacteria through database searching for sequences strikingly homologous to a recently discovered Escherichia coli thiol peroxidase p20. The direct biochemical evidence for the existence of scavengase p20 in Haemophilus influenzae, Streptococcus pneumoniae and Helicobacter pylori was provided by protein microsequencing and by in vitro assays for antioxidant activities. Overlapping genes encoding scavengase p20 and superoxide dismutase were recognized in H. pylori and their functional implications are discussed.

Amino Acid Sequence↗
PubMed1996

Ischemia/reperfusion alters uric acid and ascorbic acid levels in liver.

Tissue damage in ischemia/reperfusion injury may be mediated by oxidative stress caused by reactive oxidant species. Since such reactive species are difficult to measure directly, changes in antioxidant concentrations are often used as an indication of oxidative stress. In this study, microdialysis membranes were inserted into the livers of anesthetized rats to determine the effects of ischemia/reperfusion on the extra-cellular concentrations of two antioxidants, uric acid and ascorbic acid. Total hepatic ischemia was induced for 30 min by clamping the portal triad and was followed by 60 min of reperfusion. Uric acid and ascorbic acid concentrations were measured in microdialysis perfusates by high-performance liquid chromatography with electrochemical detection. Initial uric acid and ascorbic acid concentrations were high after insertion of membranes into the liver and decreased rapidly within 90 min (P < 0.001; ANOVA with repeated measures). Uric acid concentrations increased over 300% after ischemia and by 600% during the first 30 min of reperfusion (n = 8; P < 0.05). Ascorbic acid concentrations were 60% higher than controls after ischemia and 90% higher during the first 30 min of reperfusion (n = 8; P < 0.05). Alterations in concentrations of these redox-active molecules may be associated with oxidative stress in liver extracellular fluid during ischemia/reperfusion.

Animals↗
PubMed1996

Magnetic resonance imaging (MRI) of a cookie in comparison with time-lapse photographic analysis (TLPA) during baking process.

Magnetic Resonance Imaging (MRI) has been used to study the baking of a cookie. The structural and dynamic changes occurring during baking have been monitored, including changes in the internal moisture saturations and distribution. The images reveal the moisture distribution is initially uniform, and during baking a gradient in moisture develops from the interior to the edge. Changes in physical dimensions calculated from the data are consistent with those obtained from time-lapsed photography.

Cooking↗
PubMed1996

NMR applications in complex food systems.

The rheological and functional properties of food components are related to their molecular structure, morphology, and atomic mobilities. NMR provides a powerful tool for elucidating chemical structures, molecular conformations, and interactions of components in food systems. Quantitative analysis of sugars, fats, and other principal compounds in complex food systems was achieved by high-resolution liquid NMR. In addition to information available from liquid experiments, solids NMR experiments can reveal differences and changes in crystal packing of structures in food model systems. Interpretation of experimental results is enhanced by molecular modeling of key food compounds. Models for fat crystallization are carried out to enhance understanding of the molecular structures involved in the fat crystallization process. Recently, MRI has also shown significant impact on food science and technology. Some examples of NMR applications are given in this presentation.

Crystallization↗
PubMed1996

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach.

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate {1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor} attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

Animals↗
PubMed1995

Ischemia-reperfusion increases gastric motility and endothelin-1-induced vasoconstriction.

The purpose of our study was to 1) examine the effect of ischemia-reperfusion on gastric vascular resistance and motility, 2) determine whether endothelin-1 (ET-1)-induced vasoconstriction is enhanced after ischemia-reperfusion, and 3) assess the effect of superoxide dismutase (SOD) on these ischemia-reperfusion-induced alterations. These experiments used a mechanically perfused ex vivo gastric segment of chloralose-anesthetized dogs. We first evaluated the effect of varying the duration of total ischemia on reperfusion-induced changes in gastric vascular resistance and motility. In other experiments, responses to ET-1 (10(-10) M) were compared before and after 30-min ischemia and 30-min reperfusion, with saline or SOD (10 U/ml) infused intra-arterially to the stomach during reperfusion. Our results show that 1) after ischemia, vasodilation is seen initially on reperfusion followed by a slowly developing, progressive increase in vascular resistance, 2) the force of gastric contractions was reduced during ischemia but elevated immediately on reperfusion, 3) vasoconstrictor responses to ET-1 are enhanced after ischemia-reperfusion, and 4) SOD reduced the enhanced response to ET-1 and force of contractions. Our findings support the hypothesis that reactive oxygen metabolites contribute to augmented vascular reactivity and hypercontractility after ischemia-reperfusion.

Animals↗
PubMed1994

Phosphoramidon attenuates big endothelin-1-induced vasoconstriction in canine stomach.

We compared the effects of endothelin-1 and its precursor, big endothelin-1, on vascular resistance of a blood-perfused ex vivo stomach segment of chloralose-anesthetized dogs. In separate groups of dogs, endothelin-1 or big endothelin-1 was infused intra-arterially directly to the gastric segment. Endothelin-1 caused statistically significant dose-related increases in gastric vascular resistance at final blood concentrations of 0.15-10 nM. Although each dose was given for only 5 min, endothelin-1 at concentrations > 0.6 nM caused sustained responses with vascular resistance remaining above control values for approximately 45-90 min. In contrast, however, big endothelin-1 caused a small but statistically significant vasoconstriction only at the highest concentration (10 nM). In other experiments, using 15-min peptide infusions, we found that pretreatment with phosphoramidon, an inhibitor of endothelin-converting enzyme, markedly reduced response to big endothelin-1 but not to endothelin-1. Our results demonstrate that endothelin-1, but not big endothelin-1, is a potent vasoconstrictor of the canine gastric microcirculation. In addition, it appears that big endothelin-1 is degraded to endothelin-1 in the stomach by a phosphoramidon-sensitive metalloproteinase.

Animals↗
PubMed1994

Role of prostaglandins in angiotensin II-induced gastric vasoconstriction.

The purpose of our study was to examine the role of prostaglandins in angiotensin II (ANG II)-induced gastric vasoconstriction. ANG II produced statistically significant, dose-related increases in vascular resistance of a mechanically perfused ex vivo stomach segment of chloralose-anesthetized dogs. We next examined the effect of cyclooxygenase inhibitors on responses to ANG II. Indomethacin (10 mg/kg), which blocked the vasodilator response to intra-arterial arachidonic acid, augmented the maximal increase in perfusion pressure during ANG II infusion. Similar results were found using a different cyclooxygenase inhibitor, meclofenamic acid. In the final experiments we used an enzyme immunoassay to measure 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) plasma concentrations. ANG II produced dose-related increases in gastric venous but not arterial levels of 6-keto-PGF1 alpha, the major metabolite of prostacyclin. Our results are consistent with the hypothesis that release of vasodilatory prostaglandins attenuates the vasoconstrictor response to ANG II in the gastric microcirculation.

6-Ketoprostaglandin F1 alpha↗