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Biomedical subjects

J S Jin

Publications and source records attributed to J S Jin.

At least 19 recordsLinked to original sources
PubMed2001

Impact of triethylamine as a mobile phase additive on the resolution of racemic amino acids on an (+)-18-crown-6-tetracarboxylic acid-derived chiral stationary phase.

Recently, a new HPLC chiral stationary phase (CSP) prepared by covalently bonding (+)-(18-crown-6)-2,3,11,12-tetracarboxylic acid on silica gel was successfully employed in resolving various racemic natural and unnatural amino acids containing a primary amino group. Current work details on-going efforts to improve the effectiveness of this type of material. The analytes used in this study included various substituted phenylalanines, phenylglycine homologues and other primary amino acids. In an attempt to increase enantioselectivity, the effect of methanol and triethylamine modifiers was evaluated in an aqueous mobile phase containing sulfuric acid. In general. retention time increased with increasing methanol and triethylamine concentration. In addition, highest enantioselectivities were obtained with high methanol and high triethylamine; however, these conditions produced excessively long retention. All of the analytes were well resolved on the CSP with a mobile phase of 20% methanol containing 14.3 mM triethylamine and 10.0 mM sulfuric acid.

Amino Acids↗
PubMed2001

Effect of S20787, a novel Cl--HCO3- exchange inhibitor, on intracellular pH regulation in guinea pig ventricular myocytes.

S20787 has recently been proposed to be a selective Cl--HCO3- anion exchange (AE) inhibitor in rat cardiomyocytes. The AE transporter mediates sarcolemmal acid influx but is only one part of the cardiac cell's dual acid loading mechanism, the other part being a sarcolemmal Cl--OH- exchanger (CHE). We have therefore (1) investigated the differential effects of S20787 on the AE and CHE transporters in isolated guinea pig ventricular myocytes and (2) re-examined the influence of the drug on other sarcolemmal acid transporters by monitoring its effect on intracellular pH (pH(i)) recovery from alkali or acid loads. The pH(i) was measured using microspectrofluorimetry (carboxy-SNARF-1). The results indicate that CHE activity was unaffected by the drug (1-20 microM), whereas up to 78% of AE activity was blocked (K(i) = 3.9 microM). Thus, S20787 targets only the AE component of the dual acid influx system. Activities of other acid-transporting carriers, such as Na+-H+ exchange, Na+-HCO3- co-transport and the monocarboxylic acid transporter, were unaffected by the drug. The inhibitory efficacy of S20787 for AE in guinea pig cardiomyocytes appears to be considerably higher (approximately 78%) than proposed previously for rat cardiomyocytes (50%). This is most likely because, in both cells, a significant fraction (20-30%) of acid influx is mediated through the S20787-insensitive CHE transporter. Previous studies made no allowance for the CHE component, which would result in an underestimation. S20787 is thus a highly selective AE inhibitor which may be useful as an experimental tool and a potential cardiac protective agent in the heart.

Animals↗
PubMed2001

[Cardiac arrhythmias in pilots under positive (+Gz) acceleration].

OBJECTIVE: To study the relationship between cardiac arrhythmias and autonomic nervous regulation in pilots under +Gz acceleration. METHOD: Dynamic ECG during +Gz exposures in 36 orthostatic intolerance pilots and 62 healthy pilots were analysed and compared. RESULT: The orthostatic intolerance pilots had obviously lower +Gz tolerance and more cardiac arrhythmias. The cardiac arrhythmias could affect +Gz tolerance. CONCLUSION: The cardiac arrhythmias under +Gz acceleration could be taken as an index of evaluating cardiovascular compensatory function and warning against acceleration (+Gz) induced loss of consciousness (G-LOC).

Acceleration↗
PubMed2000

An adaptive nonlinear diffusion algorithm for filtering medical images.

The nonlinear anisotropic diffusive process has shown the good property of eliminating noise while preserving the accuracy of edges and has been widely used in image processing. However, filtering depends on the threshold of the diffusion process, i.e., the cut-off contrast of edges. The threshold varies from image to image and even from region to region within an image. The problem compounds with intensity distortion and contrast variation. We have developed an adaptive diffusion scheme by applying the Central Limit Theorem to selecting the threshold. Gaussian distribution and Rayleigh distribution are used to estimate the distributions of visual objects in images. Regression under such distributions separates the distribution of the major object from other visual objects in a single-peak histogram. The separation helps to automatically determine the threshold. A fast algorithm is derived for the regression process. The method has been successfully used in filtering various medical images.

Algorithms↗
PubMed1999

Endothelium dependent and independent relaxations induced by ceramide in vascular smooth muscles.

The second messenger of sphingomyelin signaling, ceramide, acts as an intracellular signal via phosphatase activation and protein kinase C (PKC) inhibition. We tested the hypothesis that ceramide may have an regulatory role in determining vascular tone. Natural ceramide was applied to phenylephrine precontracted aortic rings from Sprague-Dawley rats in an organ bath. In endothelium-intact aortic rings, concentrations of ceramide at 10(-6) and 10(-5) mole/L induced 24 +/- 6 and 52 +/- 7% relaxation, respectively. Removal of the endothelium significantly inhibited ceramide-induced relaxation to 13 +/- 5% (10(-6) mole/L) and 29 +/- 5% (10(-5) mole/L). Similar inhibition was observed in endothelium-intact aortic rings pretreated with N omega-nitro-L-arginine (10(-4) mole/L) or methylene blue (10(-5) mole/L), suggesting that endothelium-derived nitric oxide is involved in ceramide-induced relaxation. N-acetylsphingosine (C2-ceramide), N-hexanoylsphingosine (C6-ceramide), N-palmitoylsphingosine (C16-ceramide) and D-sphingosine all demonstrated dose-dependent relaxation responses in endothelium-intact vessels. Sphingomyelin signaling through the nitric oxide-dependent mechanism may have an important role in regulating vascular tone.

Animals↗
PubMed1999

Ceramide-induced vasorelaxation: An inhibitory action on protein kinase C.

Experiments were designed to examine the role of sphingosine, PP2A phosphatases, and protein kinase C (PKC) inhibition in mediating the vasodilatory effects of ceramide in rat thoracic aorta. Sphingosine did not cause vasorelaxation, and oleoylethanol-amine, a ceramidase inhibitor, did not affect sphingomyelinase-induced relaxation. Okadaic acid potentiated the relaxation response to ceramide. These observations rule out involvement of sphingosine and PP2A phosphatases in mediating ceramide-induced relaxation. Sphingomyelinase attenuated contractile and single-cell intracellular calcium responses to phorbol ester. Chelerythrine incubation potentiated the relaxation response to ceramide. These observations support a role for PKC inhibition in mediating the vasodilatory effects of ceramide.

Amidohydrolases↗
PubMed1998

The role of the endothelium in ceramide-induced vasodilation.

Ceramide, a novel sphingomyelin-derived second messenger mediates cellular signals of cytokines such as tumor necrosis factor-alpha (TNF-alpha). In the present study, we hypothesized that the endothelium contributes to ceramide-induced vasodilation. We report that relaxation to ceramide in endothelium-intact rat thoracic aortic rings is greater than in endothelium-denuded or endothelial nitric oxide synthase (endothelial NO synthase)-inactivated rings. We conclude that the endothelium contributes to ceramide-induced relaxation possibly through an interaction between sphingomyelin hydrolysis and endothelial NO synthase within caveolae.

Animals↗
PubMed1997

Electrical and mechanical effects of a novel antihypertensive quinazoline derivative, 3-[[4-(2-methoxyphenyl) piperazin-1-ly]methyl]-5-(methylthio)-2,3-dihydroimidazo [1,2-c]quinazoline, on guinea pig ventricular muscles.

Electrical and mechanical effects of 3-[[4-(2-methoxyphenyl)piperazin-1-ly]methyl]-5-(methylthio)-2,3-+ ++dihydroimidazo[1,2-c]quinazoline (DL-017), a new synthesized antihypertensive agent, were studied in guinea-pig ventricular papillary muscles. In muscle fibers driven at 1 Hz, DL-017 decreased the twitch force in a concentration-dependent manner and significantly increased the action-potential duration and decreased intracellular Na+ activity (ai(Na)) and maximal rate of upstroke of action-potential (Vmax) when concentrations were greater than 1 microM. Phenylephrine in the presence of 1 microM propranolol produced a concentration-dependent positive inotropy. DL-017 (0.01 microM) antagonized the positive inotropic effect of phenylephrine and shifted the concentration-response curve to the right. In K+-depolarized muscle fibers, 0.1 microM DL-017 significantly decreased the contractile force without changing the slow action potential. In low-[K+]o and high-[Ca2+]o solutions, a train of stimuli triggered a spontaneous rhythm that could be abolished by 3 microM DL-017. Our results suggest that DL-017 not only exhibits an alpha1-antagonistic effect but also induces negative inotropy by a decrease in myofibrillar calcium sensitivity and inhibits Na+ channels at higher concentrations, contributing to the drug's negative inotropic and type-I antiarrhythmic effects.

Action Potentials↗
PubMed1997

Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation.

Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 +/- 6.8% of control) than NZ rats (40.9 +/- 6.4% of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60%, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.

Acetylcholine↗
PubMed1996

Central and peripheral effects of asymmetric dimethylarginine, an endogenous nitric oxide synthetase inhibitor.

We tested the hypothesis that the endogenous nitric oxide synthetase (NOS) inhibitor, asymmetric dimethylarginine (ADMA), regulates cardiovascular function by central mechanisms. In in vivo studies, rats received intracerebroventricular (i.c.v.) injection of isotonic saline, ADMA (1 mg), l-arginine (3 mg), and N omega-nitro-l-arginine methylester (l-NAME, 1 mg). Baroreflex function was then assessed by intravenous (i.v.) injection of phenylephrine. Central application of exogenous NOS inhibitor, l-NAME, increased mean arterial blood pressure and decreased heart rate. However, application of the endogenous NOS inhibitor, ADMA, decreased mean arterial blood pressure and heart rate simultaneously (-39 +/- 6 mm Hg and -50 +/- 8 beats/min, respectively). Both l-NAME (i.c.v.) and ADMA (i.c.v.) significantly inhibited the baroreflex function, indicating a regulatory role of central nitric oxide in controlling baroreflex function. In contrast to the central effect, intravenous injection of ADMA caused dose-dependent increases in mean arterial blood pressure that could be blocked by l-NAME pretreatment. In vitro studies using aortic rings demonstrated that ADMA (10(-4)M) significantly increased the concentration of acetylcholine for the threshold response (EC15) and half-maximal response (EC50). This indicates that ADMA inhibits the constitutive isoform of NOS in the endothelium. ADMA may have functional importance in regulating cardiovascular function by mechanisms in addition to the inhibition of nitric oxide synthesis.

Animals↗
PubMed1996

Calcium channel activity increased by plasma from ischemic hindlimbs of rats: role of an endogenous NO synthase inhibitor.

We tested the hypothesis that an endogenous nitric oxide synthase (NOS) inhibitor released from ischemic hindlimbs increases the activity of calcium channels in vascular smooth muscle, thus contributing to the increased contractile response to calcium agonists. Hindlimb ischemia was generated in rats by infrarenal aortic cross clamping for 5 h, after which plasma was obtained from femoral vein blood. Incubating naive aortic rings (endothelium intact) for 2 h in plasma collected from ischemic rats significantly reduced relaxation to acetylcholine in precontracted rings and increased contraction to the calcium channel agonist, BAY K 8644. However, in isolated smooth muscle cells (without endothelium) loaded with fura-2, no difference was noted in BAY K 8644-stimulated intracellular calcium concentration. The contractile responses to sodium fluoride, serotonin, and calcium ionophore A23187 were not different in either ischemic or control plasma-incubated rings. The augmentation of the contractile response to BAY K 8644 was significantly inhibited by nitroglycerin (10-8 M) and by exposure to calcium-free solution. N omega-nitro-L-arginine (without plasma incubation)-pretreated rings also demonstrated hyperresponsiveness to BAY K 8644. The increase in responsiveness to BAY K 8644 exhibited a negative correlation with the maximal relaxation to acetylcholine (r = -0.99), suggesting that the apparent increase in activity of calcium channels is mediated through inhibition of nitric oxide by an endogenous NOS inhibitor on endothelium.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

A stereo model using LoG and Gabor filtering.

This paper presents a computational model for stereopsis. Laplacian of Gaussian filters are used to extract spatial features and a set of one-octave Gabor filters is used to extract orientation information from a scene. A mapping from a 3D space onto two 2D image planes is derived using a Gaussian sphere model. The determinant of the Jacobian of the mapping is derived and matching is performed using zero-crossings associated with their orientation information. Relaxation labelling is used as a co-operative process for solving the correspondence problem.

Computer Simulation↗
PubMed1995

Inhibition of vascular nitric oxide-cGMP pathway by plasma from ischemic hindlimb of rats.

The hypothesis was tested that plasma from ischemic hindlimbs facilitates hypertension. Ischemia-induced hypertension was generated in rats by infrarenal aortic cross clamping for 5 h after which plasma was obtained from femoral vein blood. In vitro contractile activity of naive aortic rings incubated for 2 h in plasma collected from ischemic rats demonstrated reduced relaxation to acetylcholine and nitroglycerin. Methylene blue (10(-5) M) induced greater contraction in rings incubated in control vs. ischemic plasma, suggesting that endogenous guanylate cyclase activity is decreased by ischemic plasma. However, 8-bromo-guanosine 3',5'-cyclic monophosphate (cGMP) relaxed equally strips incubated in ischemic or control plasma. Acetylcholine-induced nitrite release was significantly lower in ischemic vs. control plasma-incubated strips (8.6 +/- 2.7 vs. 28.2 +/- 2.3 ng/10 mg tissue wt, respectively). The impaired relaxation to acetylcholine in ischemic plasma-incubated rings was significantly increased by L-arginine but not by prior treatment of ischemic plasma with heating or superoxide dismutase and catalase. These findings suggest the impaired relaxation is mediated through inhibition of the nitric oxide-cGMP pathway. Prolonged blunting of vasodilation by ischemic plasma may therefore contribute to maintenance of a sustained vasoconstriction and ischemic hypertension.

Acetylcholine↗
PubMed1995

Stimulation of endogenous nitric oxide pathway by L-arginine reduces declamp mortality and attenuates hypertension associated with aortic cross-clamp-induced hindlimb ischemia in rats.

We tested the hypotheses that maintaining the activity of nitric oxide by L-arginine infusion would counteract the release of an endogenous nitric oxide synthase inhibitor, improve survival, and decrease intraoperative hypertension after infrarenal aortic cross-clamp surgery. Hindlimb ischemia was generated by infrarenal aortic cross-clamping and tying of the left femoral artery for 5 hours in rats with bilateral femoral and sciatic nerves cut. Mean blood pressure significantly increased during the 5-hour ischemic period in ischemic rats (no drug treatment). Baroreceptor function was inhibited in ischemic rats assessed by intravenous dose response to phenylephrine and nitroprusside after 5 hours of ischemia, suggesting baroreceptor resetting. In ischemic rats infused with L-arginine the intraoperative hypertension was prevented during the 5-hour period, suggesting that this hypertension may be mediated by nitric oxide inhibition. The rates of survival and arrhythmias 2 hours after declamping were 50% in ischemic rats and 100% in ischemic rats treated with N omega-nitro-L-arginine (a nitric oxide synthase inhibitor) 10 minutes before declamping. In ischemic rats infused with L-arginine the survival rate was significantly increased to 100% and the arrhythmic rate was inhibited. We conclude that L-arginine prevents hypertension during cross-clamping and decreases the mortality rate and arrhythmias after declamping by maintaining nitric oxide synthesis. These results suggest that humoral factors released from the ischemic hindlimb may inhibit endogenous nitric oxide production, thus contributing to intraoperative hypertension, arrhythmias, and high mortality rate after aortic cross-clamp surgery.

Animals↗
PubMed1992

Enhanced renal response to intracerebroventricular angiotensins II and III in spontaneously hypertensive rats.

The acute effects of intracerebroventricular (i.c.v.) administration of angiotensin III (ANG III) on blood pressure (BP) and renal function were investigated in spontaneously hypertensive rats (SHR, n = 31) and Wistar-Kyoto (WKY) normotensive rats (n = 6). ANG II was also administered to the same rats for comparison of its renal effect. BP and renal clearance responses were measured before and during ANG injections. The results showed that i.c.v. injections of 1, 5 and 50 pmol of ANG III did not significantly alter BP in SHR, but a high dose of ANG III (50 pmol) caused a vasopressor effect (7 +/- 4 mmHg) in WKY rats. There were significant increases in renal plasma flow (RPF), glomerular filtration rate (GFR), urine flow, absolute and fractional excretions of sodium and potassium, osmolar clearance and free water reabsorption rate following i.c.v. administration of ANG III in both SHR and WKY rats. However, the enhancement in renal responsiveness to ANG III was greater in SHR than in the WKY group. At 5 pmol of ANG III, the peak increases in GFR (96 +/- 23%), diuresis (316 +/- 102%) and natriuresis (712 +/- 281%) in SHR were significantly greater than those in WKY rats (40 +/- 13%, 152 +/- 89%, 229 +/- 130%, resp.). The renal effect of central ANG III was blocked by i.c.v. ANG III antagonist, [Ile7]-ANG III, but was enhanced by bestatin, an ANG III metabolic enzyme inhibitor. I.c.v. administration of ANG II at 50 pmol increased BP in both SHR and WKY rats (14 +/- 3 and 10 +/- 3 mmHg, resp.). Greater diuretic and natriuretic responses to ANG II were also noted in SHR than in WKY rats. These results indicate that central ANG III is as active as ANG II in modulating renal function. Furthermore, the enhanced renal response to i.c.v. ANGs II and III in SHR suggests a hyperactive central RAS implicated in BP and body fluid regulation in this genetic hypertensive strain.

Angiotensin II↗
PubMed1992

Angiotensin-converting enzyme inhibition causes deterioration in renal function in one-kidney Goldblatt hypertensive rats with and without renal arterial stenosis.

1. The renal and hypotensive effects of a new angiotensin-converting enzyme (ACE) inhibitor, cilazapril, were evaluated in 18 one-kidney, one-clip Goldblatt hypertensive rats (1K1C), 10 one-kidney normotensive rats (1K) and eight 1K1C rats with acute unclipping (1KU). Cilazapril was infused intravenously (25 micrograms/kg per min) into anaesthetized rats, and the arterial blood pressure (BP) and renal clearance of rats were measured. 2. In 1K rats, cilazapril reduced BP from 123 +/- 4 to 117 +/- 4 mmHg (P < 0.05), and produced diuresis, natriuresis and kaliuresis without significantly changing glomerular filtration rate (GFR). 3. In 1K1C rats, cilazapril significantly reduced BP (from 157 +/- 5 to 143 +/- 6 mmHg; P < 0.05), GFR (14.4 +/- 6.7%), urine flow (27.1 +/- 8.5%) and sodium excretion (39.4 +/- 7.4%). Mechanically graded reductions of renal arterial pressure alone also produced parallel decreases in GFR and renal excretory function. 4. In 1KU rats, removal of the renal arterial clip significantly decreased BP and increased renal function. Subsequent infusion of cilazapril further reduced BP and urinary excretions of sodium and water but did not significantly change GFR. 5. These results suggest that the renal function of the 1K1C hypertensive model is pressure-dependent, and that ACE inhibitor exerts a mild antihypertensive effect but causes a pressure associated reduction in renal function. Furthermore, the detrimental effect of ACE inhibitor on the residual kidney persists after acute surgical correction of the stenosis.

Animals↗
PubMed1992

[Blood and urine prostaglandin E2 and prostaglandin F2 alpha in patients with chronic gastritis and peptic ulcer].

The blood and urine prostaglandin E2 (PGE2), Prostaglandin F2 alpha (PGF2 alpha) in 106 cases of chronic gastritis and peptic ulcer were investigated by RIA. Meanwhile, the relationship among PGE2, PGF2 alpha and the Syndromes of TCM were approached. The result showed: In comparing with the normal control, the blood and urine PGE2 of 106 cases were obviously higher (P < 0.01), but PGF2 alpha was not (P > 0.05). The urine PGE2 and PGF2 alpha of moderate gastritis were markedly higher than those of mild gastritis (P < 0.05), but there were no significant difference between blood PGE2, PGF2 alpha of moderate gastritis and those of mild gastritis (P > 0.05). The blood PGE2, PGE2/PGF2 alpha ratio of Dampness-Heat in Spleen-Stomach Syndrome and the blood PGE2/PGF2 alpha ratio of incoordination between Liver and Stomach Syndrome were higher than those of Spleen Stomach Deficiency Syndrome in all the cases (P < 0.05). Compared with the normal control, both the decreased amplitude of blood PGE2/urine PGE2 and increased amplitude of blood PGF2 alpha/urine PGF2 alpha ratio showed as following: Spleen-Stomach Deficiency Syndrome > incoordination between Liver and stomach Syndrome > Dampness-Heat in Spleen-Stomach Syndrome. This study suggested: (1) There was a close relation between PGE2 and chronic gastritis and peptic ulcer; (2) There was no correlation between blood PGE2, PGF2 alpha and urine PGE2, PGF2 alpha; (3) PG was possibly a useful objective parameter to the Syndrome Differentiation in TCM.

Adult↗