Biomedical subjects

S J Shi

Publications and source records attributed to S J Shi.

18 recordsLinked to original sources

PubMed2001

DNA exhibits multi-stranded binding recognition on glass microarrays.

In the course of exploring the hybridization properties of glass DNA microarrays, multi-stranded DNA structures were observed that could not be accounted for by classical Watson-Crick base pairing. Non-denatured double-stranded DNA array elements were shown to hybridize to single-stranded (ss)DNA probes. Similarly, ssDNA array elements were shown to bind duplex DNA probes. This led to a series of experiments demonstrating the formation of multi-stranded DNA structures on the surface of microarrays. These structures were observed with a number of heterogeneous sequences, including both purine and pyrimidine bases, with shared sequence identity between the ssDNA and one of the duplex strands. Furthermore, we observed a strong binding preference near the ends of duplexes containing a 3'-homologous strand. We suggest that such binding interactions on cationic solid surfaces could serve as a model for a number of biological processes mediated through multi-stranded DNA.

DNA↗

PubMed2001

Genetic disruption of atrial natriuretic peptide receptor-A alters renin and angiotensin II levels.

We have studied cardiovascular and renal phenotypes in Npr1 (genetic determinant of natriuretic peptide receptor-A; NPRA) gene-disrupted mutant mouse model. The baseline systolic arterial pressure (SAP) in 0-copy mutant (-/-) mice (143 +/- 2 mmHg) was significantly higher than in 2-copy wild-type (+/+) animals (104 +/- 2 mmHg); however, the SAP in 1-copy heterozygotes (+/-) was at an intermediate value (120 +/- 4 mmHg). To determine whether Npr1 gene function affects the renin-angiotensin-aldosterone system (RAAS), we measured the components of RAAS in plasma, kidney, and adrenal gland of 0-copy, 1-copy, and 2-copy male mice. Newborn (2 days after the birth) 0-copy pups showed 2.5-fold higher intrarenal renin contents compared with 2-copy wild-type counterparts (0-copy 72 +/- 12 vs. 2-copy 30 +/- 7 microg ANG I. mg protein(-1). h(-1), respectively). The intrarenal ANG II level in 0-copy pups was also higher than in 2-copy controls (0-copy 33 +/- 5 vs. 2-copy 20 +/- 2 pg/mg protein, respectively). However, both young (3 wk) and adult (16 wk) 0-copy mutant mice showed a dramatic 50-80% reduction in plasma renin concentrations (PRCs) and in expression of renal renin message compared with 2-copy control animals. In contrast, the adrenal renin content and mRNA expression levels were 1.5- to 2-fold higher in 0-copy adult mice than in 2-copy animals. The results suggest that inhibition of renal and systemic RAAS is a compensatory response that prevents greater increases in elevated arterial pressures in adult NPRA null mutant mice. However, the greater renin and ANG II levels seen in 0-copy newborn pups provide evidence that the direct effect of NPRA activation on renin is an inhibitory response.

Aldosterone↗

PubMed1999

Increased activity and expression of Ca(2+)-dependent NOS in renal cortex of ANG II-infused hypertensive rats.

We have previously demonstrated that nitric oxide (NO) exerts a greater modulatory influence on renal cortical blood flow in ANG II-infused hypertensive rats compared with normotensive rats. In the present study, we determined nitric oxide synthase (NOS) activities and protein levels in the renal cortex and medulla of normotensive and ANG II-infused hypertensive rats. Enzyme activity was determined by measuring the rate of formation of L-[(14)C]citrulline from L-[(14)C]arginine. Western blot analysis was performed to determine the regional expression of endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) isoforms in the renal cortex and medulla of control and ANG II-infused rats. Male Sprague-Dawley rats were prepared by the infusion of ANG II at a rate of 65 ng/min via osmotic minipumps implanted subcutaneously for 13 days and compared with sham-operated rats. Systolic arterial pressures were 127 +/- 2 and 182 +/- 3 mmHg in control (n = 13) and ANG II-infused rats (n = 13), respectively. The Ca(2+)-dependent NOS activity, expressed as picomoles of citrulline formed per minute per gram wet weight, was higher in the renal cortex of ANG II-infused rats (91 +/- 11) than in control rats (42 +/- 12). Likewise, both eNOS and nNOS were markedly elevated in the renal cortex of the ANG II-treated rats. In both groups of rats, Ca(2+)-dependent NOS activity was higher in the renal medulla than in the cortex; however, no differences in medullary NOS activity were observed between the groups. Also, no differences in medullary eNOS levels were observed between the groups; however, medullary nNOS was decreased by 45% in the ANG II-infused rats. For the Ca(2+)-independent NOS activities, the renal cortex exhibited a greater activity in the control rats (174 +/- 23) than in ANG II-infused rats (101 +/- 10). Similarly, cortical iNOS was greater by 47% in the control rats than in ANG II-treated rats. No differences in the activity were found for the renal medulla between the groups. There was no detectable signal for iNOS in the renal medulla for both groups. These data indicate that there is a differential distribution of NOS activity, with the Ca(2+)-dependent activity and protein expression higher in the renal cortex of ANG II-infused rats compared with control rats, and support the hypothesis that increased constitutive NOS activity exerts a protective effect in ANG II-induced hypertension to maintain adequate renal cortical blood flow.

Angiotensin II↗

PubMed1997

Elevated blood pressure in spontaneously hypertensive rats consuming a high sucrose diet is associated with elevated angiotensin II and is reversed by vanadium.

OBJECTIVE: To determine the changes in serum angiotensin II (Ang II) and endothelin-1 levels induced by vanadium treatment of sugar-fed rats in order to investigate the relationship between changes in blood pressure and Ang II and endothelin-1 levels. METHODS: Male spontaneously hypertensive rats (SHR) were fed starch (control), sucrose, and sucrose plus vanadium compounds at various concentrations. The systolic blood pressure of the rats was estimated by tail-cuff plethysmography. Serum Ang II and endothelin-1 levels were measured by radioimmunoassay. RESULTS: There were increases in systolic blood pressure (by 8%) and in serum Ang II (by 20%) in sucrose-fed SHR compared with control. In sucrose plus vanadium-fed SHR, the lowering of the systolic blood pressure (by 11-16% of the sucrose-fed value) was accompanied by a significant decrease in Ang II levels (by 25-60% of the sucrose-fed value) and an increase in endothelin-1 level (by 61-76% of the sucrose-fed value). CONCLUSION: That Ang II levels are elevated in sucrose-induced hypertension and decreased after vanadium therapy suggests that the renin-angiotensin system plays a role in the induction of hypertension in this model. On the other hand, the elevation of endothelin-1 levels associated with a decreased systolic blood pressure might be secondary to vanadium stimulation of endothelial cells. The data suggest that endothelin-1 is not involved in sugar-induced elevations of the blood pressure.

Angiotensin II↗

PubMed1997

Study on plasma-spraying coating bioactive ceramics onto silicon nitride surface as composite endosteal implants.

The successful key of endosteal implants depends on the properties of implant materials which are very important for oral implantology at the present. Because silicon nitride has high strength and hydroxylapatite (HA) and flourapatite (FA) have good biocompatibility. In this paper, we apply silicon nitride as base material. Plasma spray HA, FA onto its surface as composite endosteal implants. Physical and chemical properties test, includes X-ray diffraction (XRD), scanning electronic microscope (SEM), EDAX and bonding strength test (push-out test). The results indicate: after plasma-spraying coating, crystalline phase of HA and FA unchanged and form a lot of pores among the crystal particles. Those pores benefit bone growing into them. It is very important for implants to be fixed in bone for long time, Ca/P ratio has no significant change. Bonding strength test results indicate: Si3N4-HA 23.6MPa, Si3N4-FA 27.12 MPa are higher than that of Ti-HA 15.07 MPa. On the basis of these studies, they are kinds of ideal implant materials.

Apatites↗

PubMed1995

Enhanced predictability of myocardial infarction in Japanese by combined genotype analysis.

To explore the genes responsible for myocardial infarction and restenosis after percutaneous transluminal coronary angioplasty, we performed association studies of the polymorphisms of the angiotensinogen and angiotensin-converting enzyme (ACE) genes. In the first study, normotensive myocardial infarction patients (n = 103) and control subjects (n = 103), who were matched for established risk factors with the myocardial infarction patients, were randomly selected. The angiotensinogen-TT genotype (T indicates threonine instead of methionine at position 235) was more frequent in the myocardial infarction group than in the control group (P < .05). The ACE-DD genotype (D indicates a deletion polymorphism in intron 16) was also more frequent in the myocardial infarction group (P < .0001). The odds ratio estimated by the combined analysis of the angiotensinogen-TT and ACE-DD genotypes (11.2) was markedly increased compared with that estimated separately from the angiotensinogen-TT (1.75) or ACE-DD (4.43) genotype. In the second study, we investigated 91 consecutive patients with acute myocardial infarction who underwent successful direct angioplasty. Combined analysis showed that the angiotensinogen-TT genotype did not enhance the predictability of myocardial infarction from the ACE-DD genotype. In conclusion, the angiotensinogen-TT genotype is a predictor for myocardial infarction, as well as the ACE-DD genotype, and the combined analysis of the angiotensinogen-TT and ACE-DD genotypes further enhanced the predictability of myocardial infarction in Japanese, suggesting its future clinical usefulness.

Angioplasty, Balloon, Coronary↗

PubMed1994

Augmentation by converting enzyme inhibition of accelerated endothelin release from rat mesenteric arteries following nephrectomy.

We investigated the release of endothelin-1 (ET) from rat mesenteric arteries to clarify its pathophysiological role in the sustained hypertension of spontaneously hypertensive rats (SHR) following nephrectomy and the regulatory mechanism of the ET release which might be modified by vascular angiotensins and bradykinins. Nephrectomy increased the plasma level of ET and enhanced the ET release in both SHR and Wistar-Kyoto rats (WKY). CV-11974, an angiotensin II receptor antagonist, did not affect the ET release from arteries of nephrectomized rats. On the contrary, infusion of captopril, a converting enzyme inhibitor, further enhanced the ET release in both intact and nephrectomized rats. These findings suggest that the release of ET from mesenteric arteries may be regulated by bradykinins, but not by angiotensins. This pressor substance does not contribute to the sustained hypertension because the enhanced production of ET observed in both SHR and WKY. However, there is a possibility that the exaggerated responsiveness of vascular ET may in part account for local vascular tone and vascular remodeling in renal dysfunction.

Analysis of Variance↗

PubMed1994

Augmentation of angiotensin II release from isolated mesenteric arteries of Wistar-Kyoto and spontaneously hypertensive rats following nephrectomy.

1. We previously reported that angiotensin II release from the mesenteric arteries of Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) increased in a time-dependent manner as a result of the isolation of the arteries and perfusion. This phenomenon appeared to be due to the withdrawal of circulating angiotensin II (AII). 2. The purpose of the present study was to test the hypothesis that vascular AII generation may be negatively regulated by circulating AII in WKY and SHR, and to clarify the role of this vascular angiotensin II in the sustained hypertension of SHR following nephrectomy. 3. The mesenteric arteries from kidney-intact and nephrectomized WKY and SHR were perfused and the amount of AII released into the perfusate was measured. The effects of the angiotensin converting enzyme inhibitor, captopril, and the effects of supplementation of renal renin and circulating angiotensins to nephrectomized rats, by blood exchange between kidney-intact and nephrectomized rats, on AII release were examined to clarify the pathway of vascular AII generation after nephrectomy. 4. Nephrectomy caused augmentation of vascular AII release both in WKY and SHR in spite of the abolishment of circulating renin. Captopril reduced this enhanced release of AII, but blood exchange did not affect it. There was no significant difference in these responses between WKY and SHR. 5. These results suggest that WKY and SHR have in common a potent pathway for production of vascular AII in response to the withdrawal of circulating AII, although this pathway is not responsible for the sustained hypertension of SHR after nephrectomy. The precise pathophysiological role of this pathway remains to be elucidated.

Angiotensin II↗

PubMed1994

Activated angiotensin II generation and regulation in rat mesenteric arteries following nephrectomy.

The objectives of the present study were to test the hypothesis that vascular angiotensin II (AII) generation may be negatively regulated by circulating AII in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), and to clarify the role of this vascular AII in the sustained hypertension seen in SHR following nephrectomy. The mesenteric arteries from kidney-intact and nephrectomised WKY and SHR were perfused, and the level of AII released into the perfusate were measured. The effects of CV-11974, a newly developed nonpeptide AII receptor antagonist, on AII release were examined to investigate the existence of a local feedback system in the blood vessels. Nephrectomy augmented vascular AII release both in WKY and SHR despite the reduction in circulating AII. CV-11974 significantly increased AII release from the mesenteric arteries of kidney-intact rats. There were no significant differences in these responses between WKY and SHR. These results suggest that WKY and SHR share a potent pathway for producing vascular AII in response to the withdrawal of circulating AII, although this pathway is not responsible for the sustained hypertension seen in SHR after nephrectomy.

Angiotensin II↗

PubMed1992

[Stress distribution in the periodontal tissue around roots of an inclined abutment by 3-D photoelasticity].

The stress distribution in the periodontal tissue around roots of a mesially inclined mandibular second molar as the the abutment of a fixed bridge was analysed by the three dimensional photoelasticity. It was shown by 3-D photoelasticity that the stress distribution in the alveolar bone around the roots of the abutment was modified by the placement of the fixed bridge. The maximum stress points in alveolar bone around the roots of abutment were also located.

Biomechanical Phenomena↗

PubMed1991

Endothelin modulates L-NG-nitroarginine-induced enhancement of vasoconstriction evoked by norepinephrine.

The interaction of endothelin-1 (ET-1), a novel vasoconstrictor peptide synthesized according to the encoded amino acid sequence, with L-NG-nitroarginine (NOARG), an L-arginine-reversible inhibitor of endothelium-derived relaxing factor (EDRF) on adrenergic receptors, was investigated. Male Sprague-Dawley rats were used in this study. Mesenteric arteries were isolated and perfused with Krebs-Ringer solution at a constant flow rate. The vasoconstrictor responses to exogenous norepinephrine were determined. Low concentrations of ET-1 (10(-11) and 10(-10) M) potentiated the pressor responses to norepinephrine without affecting the baseline perfusion pressure. Simultaneous NOARG (10(-5) M) infusion with ET-1 (10(-11) M) into the mesenteric arteries caused further enhancement of the pressor responses to exogenous norepinephrine (200 ng) without affecting the baseline perfusion pressure: 126 +/- 15% to 262 +/- 45% (p less than 0.05, vehicle control: 100%). This facilitatory effect of NOARG on the pressor response to norepinephrine was attenuated with L-arginine (10(-4) M) infusion, but not D-arginine. These results suggest that ET, one of the endothelium-derived vasoconstricting factors, interacts with EDRF to modulate the tone of resistance vessels.

Animals↗

PubMed1991

[Castable glass-ceramic-synthesizing and testing].

This paper introduces the composition of Castabe Glass-Ceramic (CGC), synthetic technique and physical and chemical properties. By means of TEM, SEM, XRD and EPMA techniques, the structure of CGC on K2O-MgO-Al2O-SiO2-F glass, type and size of crystallization are investigated. The results are as follows: the main crystal phase is tetrasilicic flourmica (K2Mg2.5Si4-O10F2), refractive index = 1.53, transparency = 48%, Density = 2.7 g/cm3, elastic modulus = 68.22 GPa, breaking strength = 141.1 MPa, breaking durability = 1.83 and V. H. = 505 kg/mm2. Base the above properties described, the function of CGC is similar to the Dicor (Dentsply. Int. U. S. A.) which is one of the well known material in western countries in now days.

Biocompatible Materials↗

PubMed1985