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Biomedical subjects

J Y Cheung

Publications and source records attributed to J Y Cheung.

87 records · Page 5Linked to original sources
PubMed1985

Effects of metabolic acidosis on viability of cells exposed to anoxia.

The effects of metabolic acidosis were examined in isolated rat hepatocytes under substrate-free oxygenated or anoxic conditions. Lowering extracellular pH to 6.6 under aerobic conditions had no deleterious effects on the cells as determined by trypan blue exclusion, lactate dehydrogenase (LDH) release, cellular K+ and Ca2+ content, and ability to increase ATP levels after nutrients and adenosine were added to media. Cytosolic pH was measured in aerobic cells at varying extracellular pH using 6-carboxyfluorescein. By using values for cytosolic pH obtained in this manner together with 5,5-dimethyl[2-14C]oxazolidine-2,4-dione (DMO) distribution data, a method was derived for determining intramitochondrial pH. The pH gradient across the mitochondrial membrane was found not to change with a decrease in extracellular pH from 7.4 to 6.9. At pH 6.9 hepatocytes were protected against anoxic injury as compared with cells incubated at pH 7.5 or 6.6. This protection was manifested by a decrease in vital dye uptake and LDH release, maintenance of higher cellular K+ content, less stimulation of respiration with succinate, improved recovery of ATP levels after return to an oxygenated nutrient environment, and maintenance of normal cellular Ca2+ content after reoxygenation. Recovery of cellular ATP content was independent of ATP levels, total adenine nucleotide pool, and energy charge ratio at the end of the anoxic period. Measurement of cytoplasmic pH in anaerobic cells by [14C]DMO distribution showed progressive cellular acidification with lowering of extracellular pH. The protective effects observed at pH 6.9 are not unique to hepatocytes since isolated renal cortical tubules exposed to anoxia have improved ATP levels on reoxygenation at this pH when compared with tubules incubated at pH 7.5.

Acidosis↗
PubMed1984

Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics.

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.

Aged↗
PubMed1984

Mechanism of protection by verapamil and nifedipine from anoxic injury in isolated cardiac myocytes.

This study was designed to determine whether slow Ca2+ channel blocking agents exert a direct protective effect on the anoxic myocardial cell and, if so, what the mechanism of protection is. Isolated Ca2+-tolerant rat cardiac myocytes were incubated under aerobic or anaerobic conditions, with or without verapamil or nifedipine, in the resting and contractile state. Protection against cell injury was assessed by preservation of rod-shaped morphology, cellular ATP levels, intracellular ionic composition, and lactate dehydrogenase release. Resting myocytes incubated anaerobically lost their rod-shaped appearance, accumulated Na+ and lost K+, and suffered a significant loss of cellular ATP. The release of lactate dehydrogenase into the medium was increased twofold, indicating significant membrane injury. Verapamil (1 microM) or nifedipine (1 microM) did not afford any protection against anoxic injury as measured by these parameters. Furthermore, on reoxygenation, anoxic verapamil- and nifedipine-treated myocytes had significantly higher cellular Ca2+ levels than control aerobic cells. When anoxic myocytes were paced at a rate of 300/min for 10 min, there were marked decreases in the number of rod-shaped cells and cellular ATP levels, whereas identically paced aerobic cells sustained no significant injury. Verapamil (1 microM) or nifedipine (1 microM) protected cells paced at 300/min from anoxic injury, but the cells were unable to sustain contraction rates at the frequency of the imposed pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Hormonal regulation of protein phosphorylation in isolated rat heart cells.

We used a recently developed preparation of calcium-tolerant isolated rat cardiac ventricular cells to investigate certain aspects of hormone-mediated protein phosphorylation in heart tissue. Isoproterenol or dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) promoted the phosphorylation of at least 13 proteins and promoted the dephosphorylation of a single protein of relative molecular weight (Mr) 21,000, whose phosphorylation appeared to be stimulated by insulin. The isoproterenol-induced protein phosphorylations reached maximum levels for most proteins within 5 min at slightly different rates. However, when excess propranolol was added to the cells after exposure to isoproterenol, there appeared to be two major patterns of dephosphorylation: proteins that remained fully phosphorylated after propranolol addition, exemplified by proteins tentatively identified as troponin I and C-protein, and proteins that were rapidly dephosphorylated after propranolol, exemplified by phospholamban, the modulator of the sarcoplasmic reticulum calcium-dependent ATPase. The Mr 21,000 protein was rapidly dephosphorylated in response to isoproterenol and was rephosphorylated after addition of propranolol. This protein remains unidentified; it is not the Mr 19,000 myosin light chain whose phosphorylation state was unaffected by isoproterenol. This preparation of isolated heart cells provides a convenient way to investigate the biochemical effects resulting from exposure of the heart to hormones and can separate direct hormonal effects from those resulting from changes in contractility or heart rate.

Animals↗
PubMed1984

CT measurements of cranial growth: normal subjects.

Growth patterns of the cranium measured directly as head circumference have been well documented. With the availability of computed tomography (CT), cranial dimensions can be obtained easily. The objective of this project was to establish the mean values and their normal variance of CT cranial area of subjects at different ages. Cranial areas and its long and short axes were measured on CT scans for 215 neurologic patients of a wide age range who presented no evidence of abnormal growth of head size. Growth patterns of the cranial area as well as the numeric product of its linear dimensions were determined via a curve fitting process. The patterns resemble that of the head circumference growth chart, with the most rapid growth observed in the first 12 months of age and reaching full size during adolescence. It is believed that the availability of such reference, in addition to the head circumference measurement, will be valuable to the CT reviewer in determining the growth status of head size.

Child, Preschool↗
PubMed1983

Effects of verapamil in models of ischemic acute renal failure in the rat.

This study was designed to determine whether verapamil protects renal function in experimental ischemia in the rat and, if so, whether the protection is mediated by verapamil's vasodilatory action or by an effect on renal cells independent of vascular perfusion. Inulin clearance (CIn) was examined for 3 h subsequent to 40 min of unilateral intrarenal infusion of norepinephrine (0.75 microgram X kg-1 X min-1) and 3 and 48 h subsequent to 40 min of unilateral renal pedicle clamp. In norepinephrine-induced ischemia CIn fell to 0.8 +/- 0.4% of preischemic values in saline-treated kidneys and 0.5 +/- 0.3% in verapamil post-treated kidneys. By contrast, CIn fell only to 52.3 +/- 6.5% of preischemic values in verapamil-pretreated kidneys. Verapamil pretreatment significantly counteracted the intrarenal vasoconstriction produced by norepinephrine, sustaining renal blood flow during the norepinephrine infusion. In pedicle clamp-induced ischemia verapamil pre- and posttreatment had no beneficial effect on preservation of glomerular filtration rate, whereas mannitol pretreatment was beneficial. Parallel studies in the isolated perfused rat kidney confirmed the in vivo observations. In conclusion, verapamil exerts no protective effect on renal function at 3 or 48 h when ischemia is induced by renal pedicle clamp. Likewise, verapamil administration subsequent to norepinephrine-induced ischemia is ineffective in preserving renal function. Verapamil pretreatment in norepinephrine-induced ischemia preserves renal function probably by attenuating the vasoconstrictive ischemic insult due to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1982

Effects of extracellular calcium removal and anoxia on isolated rat myocytes.

Calcium-tolerant myocytes were isolated from adult rat ventricles by successive perfusion and incubation with buffer containing collagenase and hyaluronidase. Greater than 70% of the cells excluded trypan blue, maintained normal morphology, and contracted in response to an externally applied electric field. We have characterized metabolic defects present in isolated calcium-tolerance myocytes when exposed to low concentrations of extracellular calcium under aerobic and anaerobic conditions. In control cells exposed to 1.25 mM Ca2+, the following metabolic parameters were measured (in mumol/g protein): adenosine triphosphate (ATP) 28.8 +/- 3.3, creatine phosphate (CrP) 49.1 +/- 7.5, intracellular Na+ 37.7 +/- 8.1, intracellular K+ 352.9 +/- 49.3, cellular Ca2+ 12.3 +/- 1.8, as well as rate of protein synthesis 0.34 +/- 0.03 mumol . g protein-1 . h-1. In aerobic cells incubated in medium without added Ca2+, the corresponding values (in mumol/g protein) were ATP 27.9 +/- 4.4, CrP 25.3 +/- 4.3, intracellular Na+ 130.9 +/- 23.1, intracellular K+ 217.2 +/- 32.0, cellular Ca2+ 3.9 +/- 1.0, and rate of protein synthesis 0.09 +/- 0.02 mumol . g protein-1 . h-1. These data indicated major metabolic aberrations in myocytes exposed to medium low in Ca2+ (less than 10 microM). Metabolic depression was most severe in cells incubated in the absence of both Ca2+ and O2. It is postulated that Ca2+ removal resulted in an increase in Na+ and K+ permeability, causing a net gain of intracellular Na+ and loss of intracellular K+. These ionic shifts might stimulate the activity of membrane-associated Na+-K+-ATPase, accounting for lower levels of CrP.

Adenosine Triphosphate↗
PubMed1978

Effect of insulin on kinetics of sugar transport in heart muscle.

Insulin increased the maximal rate of sugar transport in the perfused rat heart, but had essentially no effect on the Michaelis constant of sugar entry or half-maximal constant for equilibrium exchange. In control hearts, the following kinetic parameters of 3-O-methylglucose transport were measured: Michaelis constant for entry, 7-10 mM; equilibrium exchange constant, 7 mM; and activity constant (Vmax/Km) from 0.02 to 0.1 ml/g.min. In insulin-treated hearts, these values were 6 mM, 3 MM, and 2.2 ml/g.min, respectively. These changes in transport constants were consistent with a model in which 1) sequestered carrier was released by the hormone or 2) carrier movement, in all forms and directions, was accelerated. Measurements of glucose transport in control hearts indicated that the Michaelis constant for entry was 4 mM and the activity constant, 0.5 ml/g.min. In insulin-treated hearts, quantitation of transport parameters was prevented by accumulation of intracellular glucose.

Animals↗
PubMedDate not supplied

Detection and deletion of motion artifacts in electrogastrogram using feature analysis and neural networks.

Electrogastrogram is a surface measurement of gastric myoelectrical activity, and electrogastrography has been an attractive method for physiological and pathophysiological studies of the stomach due to its noninvasive nature. Motion artifacts, however, ruin the electrogastrogram (EGG), and make the analysis very difficult and sometimes even impossible. They must be eliminated from EGG signals before analysis. Up to now, this can only be done by visual inspection, which is not only time-consuming but also subjective. In this study, a method using feature analysis and neural networks has been developed to realize automatic detection and elimination of the motion artifacts in EGG recordings by computer. Experiments were conducted to investigate the characteristics of different motion artifacts. Useful features were extracted, and different combinations of the features used as the input of the neural network were compared to obtain the optimal performance for the detection of motion artifacts using the artificial neural network.

Biomedical Engineering↗
PubMedDate not supplied

Stress induced in heart and other tissues by rat dermal exposure to JP-8 fuel.

Limited information is available regarding the development of systemic organ stress by dermal exposure to JP-8 fuel. In this study, the systemic stress potential of this fuel is evaluated in a rat model subjected to dermal applications of JP-8 for 7 days at 300 microl per day. Tissue histology indicated that JP-8 induces morphological alterations that suggest that tissue stress in the heart is more substantial than stress in the kidney and liver. Immunoblot analysis of tissues revealed increased levels of the inducible heat shock protein 70 (HSP70) in the heart, kidney, and liver after this dermal JP-8 exposure. This exposure also leads to increased levels of heme oxygenase-1 (HO-1/HSP3) in the liver. Additionally during this exposure, a negative regulator of inflammation, IkappaBalpha (inhibitor of NF-kappaB), was increased in the liver, slightly increased in the kidney, and not increased in the heart. Two regions of the rat brain were also examined and HSP70 and IkappaBalpha were increased in the cerebellum but not significantly increased in the cortex. This study indicates dermal JP-8 exposure causes systemic alterations that are associated with cytoprotective activities (e.g., in the liver) as well as potentially toxic mechanisms (heart and kidney).

Administration, Cutaneous↗
PubMedDate not supplied

A two-dimensional Doppler ultrasonic probe for flow measurement.

The use of a single-transducer pulsed-Doppler ultrasound system in clinical practice has been severely limited, not only by the effects of acoustics and physiologic parameters, but also by inaccuracy because the Doppler angle between the transducer axis and the flow velocity is unknown. In this study, a dual-transducer pulsed-Doppler ultrasound system was used because the Doppler angle could be directly calculated for more accurate determination of the fluid flow velocity vector. From the velocity estimate and velocity profiles, other flow characteristics such as volume flow rates and shear stress can also be estimated. Experimental results indicated that the new transducer model could increase the accuracy of fluid flow velocity measurement and thereby improve the ability to estimate the characteristics of turbulent fluid flow for research and diagnostic purposes.

Blood Flow Velocity↗