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Biomedical subjects

M Woo

Publications and source records attributed to M Woo.

At least 73 records · Page 4Linked to original sources
PubMed1990

Acute reduction of atrial overload during vasodilator and diuretic therapy in advanced congestive heart failure.

Although acute afterload reduction is known to improve cardiac output in patients with congestive heart failure (CHF), the effect of therapy on the atrial overload directly causing congestive symptoms has not been systematically studied. Atrial volumes and mitral and tricuspid regurgitation, in addition to left ventricular ejection fraction and indexes of left ventricular contractility (mean acceleration, ejection time and peak systolic pressure/end-systolic volume index), were measured using 2-dimensional and Doppler echocardiography and color flow imaging in 30 patients with advanced CHF, before and after acute vasodilator and diuretic therapy tailored to hemodynamic goals. Therapy increased stroke volume by 64% (36 +/- 10 to 55 +/- 14 cc), decreased right atrial pressure by 45% (15 +/- 5 to 8 +/- 4 mm Hg), systemic vascular resistance by 36% (1,700 +/- 400 to 1,030 +/- 300 dynes s cm-5) and pulmonary capillary wedge pressure by 37% (31 +/- 6 to 19 +/- 6 mm Hg) (all p less than 0.001). Echocardiography showed simultaneous reductions in left and right atrial volumes: 24 +/- 19 and 18 +/- 12%, respectively (p less than 0.001). Mitral and tricuspid regurgitation measured by color flow fraction both decreased by a mean of 44% (p less than 0.001). While ejection fraction increased from 15 +/- 5 to 19 +/- 7% (p less than 0.001), there were no changes in relatively load-independent indexes of contractility. Therefore, acute therapy with vasodilators and diuretics in advanced CHF causes reductions in atrial volumes and atrioventricular valve regurgitation that are evident from serial noninvasive studies and may play a major role in the improvement of congestive symptoms.

Adolescent↗
PubMed1990

The effect of L-carnitine supplementation in 4 pentenoic acid treated rats.

The effects of prolonged administration (7 days) of 4 pentenoic acid (4PA, 20 mg/kg/day) or 4PA (20 mg/kg/day) with L-carnitine (200 mg/kg/day) on carnitine metabolism and morphological changes of liver mitochondria were assessed in rats. 4PA-treated rats showed hyperammonemia, decreased levels of blood glucose, free fatty acids and beta-OH-butyrate, and of free carnitine in serum, muscle and liver, increased excretion of acylcarnitine in urine, and enlarged mitochondria with microvesicular steatosis, when compared to saline-injected control rats, respectively. 4PA plus L-carnitine rats showed decreased levels of blood ammonia and increased levels of beta-OH-butyrate, compared to the 4PA group. On the other hand, the levels of free carnitine in serum and liver in rats treated with both 4PA and L-carnitine were increased, when compared to controls. The ratio of acylcarnitine to free carnitine excreted in urine in 4PA-treated rats was higher than that in either the control or 4PA plus L-carnitine group. The liver mitochondria in the 4PA plus L-carnitine group were the same as in the controls. The results suggested that the abnormal biochemical and morphological findings due to only 4PA may be relieved with L-carnitine supplementation.

Ammonia↗
PubMed1990

Carnitine metabolism and morphometric change of liver mitochondria in valproate-treated rats.

The effect of the administration for 7 or 28 days of 50 mg/kg/day valproate (VPA) on carnitine metabolism and morphological changes of liver mitochondria in immature rats was evaluated. The dose of VPA was almost the same as that we clinically used. Carnitine concentrations in serum, red blood cells (RBC), muscle, liver and urine were measured. The rats treated with VPA for 7 days showed no significant change in carnitine concentration in each tissue examined or by morphology. In the serum, RBC and muscle of rats treated with VPA for 28 days, free carnitine levels decreased, while acylcarnitine levels and the ratio of acylcarnitine to free carnitine (acyl/free ratio) increased. Mitochondrial enlargement was also induced and urinary acyl/free ratio of VPA treated rats was higher than that of control rats after the 14th day of the treatment. These results suggest that carnitine deficiency and morphometric changes in mitochondria occur time dependent even if the dose of VPA is clinically appropriate.

Animals↗
PubMed1990

Lesch-Nyhan syndrome with delayed onset of self-mutilation: hyperactivity of interneurons at the brainstem and blink reflex.

We studied a case of Lesch-Nyhan syndrome with delayed onset of self-mutilation. Athetotic cerebral palsy and mental retardation were diagnosed at 1 year old, but the disease was not suspected until age 8 years when he began biting his lips and fingers. There was no obvious alteration of catecholamine in urine and CSF. We attempted to induce a series of blink reflexes by electric, mechanical and photic procedures. The R1 amplitude increased and the latency of the R2 shortened compared with controls. This shows that not only orbicularis motoneuron itself, but also uncrossed interneurons, are in a state of hyperexcitability. The contralateral R2 was poor which was in favour of hypoexcitability of the crossed interneurons at the brainstem. The significant large response was obtained by photic procedure which was in favour of hyperexcitability of the motoneurons. Therefore, it is demonstrated that a thorough examination of blink reflexes provides a useful method for examination of a state of the underlying neural activity.

Blinking↗
PubMed1990

Patients with endocrine ophthalmopathy not associated with overt thyroid disease have multiple thyroid immunological abnormalities.

Twenty-two apparently euthyroid patients with endocrine ophthalmopathy not associated with goiter, antithyroid microsomal or antithyroglobulin antibodies, or overt thyroid disease (so-called ophthalmic Graves' disease) were tested for subclinical hyperthyroidism or hypothyroidism. We measured 131I uptake and scan, serum T3 (by RIA), and serum TSH using a sensitive (by immunoradiometric assay) assay. Three patients were found to be hyperthyroid, and 1 was hypothyroid. The remaining 18 patients, who remained euthyroid throughout the study period, were investigated for evidence for antibody-mediated immunity against thyroid antigens. We measured antibody-dependent cell-mediated cytotoxicity against fresh thyroid cells using a 51chromium release assay, thyroid membrane-reactive antibodies in an enzyme-linked immunosorbent assay incorporating solubilized thyroid membranes, and TSH receptor-binding antibodies using a RRA and carried out sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blotting with patient sera for antibodies reactive with 64 and 110 kDa (thyroid peroxidase) membrane proteins. Bands were demonstrated, on SDS-PAGE, at 64 or 110 kDa in 13 patients, antibody-dependent cell-mediated cytotoxicity tests were positive in 7 patients, and enzyme-linked immunosorbent assay was positive in 4 of the 17 patients tested. In addition, TSH receptor antibody tests were positive in 5 patients, none of whom had other evidence for hyperthyroidism. Finally, significant lymphocyte infiltration was demonstrated on aspiration biopsy in 3 patients. All 18 patients had positive tests in at least 1 of the immunological assays. We believe that these data support the hypothesis that endocrine ophthalmopathy always occurs in patients with overt or subclinical Graves' hyperthyroidism, Hashimoto's thyroiditis, or thyroid immunological abnormalities. Those patients previously described as having euthyroid Graves' disease should, thus, be considered to have associated thyroid immunological abnormalities even though histological confirmation (from aspiration needle biopsy) may be obtained in only a minority of the patients. The possibility that the mechanism for this close association is cross-reactivity of cytotoxic antibodies against a thyroid/eye muscle cell surface shared antigen is discussed in the context of recent evidence from the authors' laboratory.

Adult↗
PubMed1990

The role of protamine dose assay in reversal of heparin following extracorporeal circulation for open heart surgery.

The amount of protamine required for the neutralisation of heparin following cardiopulmonary bypass was determined by a Protamine Titration Assay using the principle of the dose--response curve and the patient's estimated blood volume. In 300 open heart surgery patients, infusion of the determined dose of protamine normalised the Activated Clotting Time (ACT) to baseline levels in 97% of these patients and produced adequate hemostasis. Our present study showed that the dose of protamine dropped to 75% of the dose calculated by conventional method of heparin to protamine ratio of 1:1. This had minimised the adverse effects of excessive protamine administration and optimised coagulation control after extracorporeal circulation.

Adolescent↗
PubMed1989

Single-dose pharmacokinetics of intravenous ampicillin plus sulbactam in healthy elderly and young adult subjects.

The pharmacokinetics of intravenous ampicillin and sulbactam, a beta-lactamase inhibitor, were evaluated in two different age groups. Twelve healthy elderly subjects (age 65-93 years) and 12 healthy young adult subjects (age 20-35 years) received both a dose of ampicillin 1 g plus sulbactam 0.5 g and a higher dose of ampicillin 2 g plus sulbactam 1 g after a one-week period between doses. A reverse-phase high-pressure liquid chromatography method was used for the quantitation of ampicillin and sulbactam in serum and urine. The pharmacokinetic parameters for both ampicillin and sulbactam were calculated by computer-based two-compartment nonlinear model. After a 30-min infusion, serum concentrations of both drugs declined in a biexponential manner for both doses. Elderly subjects demonstrated significantly lower total clearances (Clt) than young adult subjects of ampicillin 1 g (220.0 +/- 104.2 vs 360.0 +/- 95.8 ml/min/1.73 m2), ampicillin 2 g (72.6 +/- 36.6 vs 306.8 +/- 109.77 ml/min/1.73 m2), sulbactam 0.5 g (122.3 +/- 47.8 vs 263.9 +/- 93.7 ml/min/1.73 m2), and sulbactam 1 g (171.2 +/- 85.8 vs 391.7 +/- 70.8 ml/min/1.73 m2), respectively. Significance was defined as P less than 0.05. Renal clearance was also significantly reduced in the elderly subjects. Area under the curve was found to be significantly increased in the elderly subjects compared to the young subjects for both ampicillin and sulbactam as were the beta elimination half-lives. No significant difference in the apparent volume of distribution, when adjusted for body weight, was found for either sulbactam (P greater than 0.95) or ampicillin (P greater than 0.95) between the two groups. Linear regression analysis revealed that age was significantly correlated with the Clt of ampicillin 1 g (r = 0.85, P less than 0.001), ampicillin 2 g (r = 0.90, P less than 0.001), sulbactam 0.5 g (r = 0.80, P less than 0.001), and sulbactam 1 g (r = 0.93, P less than 0.001). A multivariate analysis showed a slight improvement in correlation when creatinine clearance was added to age and compared with Clt. Urinary recovery of both ampicillin and sulbactam was approximately 60% after 14 h.

Adult↗
PubMed1988

Shaking rat Kawasaki (SRK): a new neurological mutant rat in the Wistar strain.

Shaking rat Kawasaki (SRK), a newly discovered neurological mutant rat in the Wistar strain, is described. The abnormalities of SRK rats are transmitted as an autosomal recessive trait. The neurological signs are shaking of the body and an ataxic-paretic gait from day 10 postnatal. The affected rats survive for about 1 month. Macroscopically, the cerebellum is small and frequently the vermis and paraflocculus lacking. The most conspicuous histological finding in the central nervous system is malposition of the neurons in the cerebral cortex, hippocampus and cerebellum. Myelination and synapse formation are intact. Abnormal myelinated fibers are present in the molecular layer of the cerebral cortex and in the central gray matter of the spinal cord. These morphological abnormalities resemble those reported in the reeler mutant mouse. SRK rats are another good animal model of human congenital malformations with neuronal migration disorders.

Animals↗
PubMed1988

Perifascicular atrophic fibers in childhood dermatomyositis with particular reference to mitochondrial changes.

Ten of 17 muscle biopsy specimens from 15 patients with childhood dermatomyositis (DM) showed distinct perifascicular atrophy. The atrophic fibers showed the following characteristics: (1) decreased cytochrome c oxidase (CCO) activity, (2) rare positive reaction with acridine orange (AO) staining, (3) type 2C reaction in 7.9% (0.4-17.5%) of the fibers, (4) an increased number of activated satellite cells, (5) mitochondria which were increased in number but decreased in size, (6) a significantly decreased CCO activity in isolated mitochondria (51.6 +/- 30.3 nmol/min per mg mitochondrial protein) as compared with that in the controls (103.6 +/- 41.5). The major pathogenetic mechanism in muscles in childhood DM is thought to be ischemia due to involvement of the microvasculature. The presence of type 2C fibers and increased numbers of activated satellite cells reflect a focal repair process taking place concomitantly in the damaged myofibers. Mitochondrial enzyme defect, especially CCO deficiency is present not only in genetic disorders with mitochondrial involvement but in other neuromuscular disorders including inflammatory myopathies.

Age Factors↗
PubMed1987

Muscle fiber growth and necrosis in dystrophic muscles: a comparative study between dy and mdx mice.

Histopathological and morphometric studies of murine dystrophic muscles in the early postnatal period were performed. In dy mice, obtained by in vitro fertilization, scattered necrotic fibers were noted at 10 days of age followed by poorly compensated regeneration leading to muscle fiber loss, marked variation in fiber size, and fibrous and adipose tissue proliferation. In mdx mice, clusters of necrotic muscle fibers seen at 10-15 days were followed by well compensated regeneration with little fibrosis. There appeared to be no delay in muscle fiber growth and fiber type differentiation in both dy and mdx mice up to 10 days of age since there was no distinct difference in muscle fiber size, fiber type differentiation and the incidence of myosatellite cells between dystrophic muscles and those from age-matched control mice. Muscle fibers appeared to undergo necrosis only when they had reached a certain stage of maturation since at early stages of development or regeneration they rarely became necrotic. The difference in clinical symptoms between dy and mdx mice may result from differences in their regenerative response to necrosis.

Animals↗
PubMed1987

Muscle involvement in pyruvate dehydrogenase complex (PDHC) deficiency.

Muscle biopsies from a 13-month-old female infant with a delay in developmental milestones, lactic acidosis and visual disturbance, and a 6 year-old female with frequent epileptic fits are described. Biochemical studies of biopsied muscles and skin fibroblasts demonstrated markedly decreased pyruvate dehydrogenase complex (PDHC) activity to about 16% of normal value. Muscle histochemistry in both patients showed disorganized intermyofibrillar networks containing large diformazan granules on NADH-TR, small angulated fibers with high nonspecific esterase (NSE) activity and basophilic fibers. Ragged-red fibers and increased lipid droplet accumulation were absent. Patient 1 had increased numbers of type 2C fibers (11.3%) and mild fiber type grouping. On electron microscopy, most mitochondria were nearly normal. There were focal aggregates of mildly enlarged mitochondria in the subsarcolemmal areas in both patients. Morphometric study showed that the mean mitochondrial size and the mitochondrial percentage of fiber volume were not significantly different amongst patients and normal controls.

Child↗
PubMed1987

Carnitine metabolism in valproate-treated rats: the effect of L-carnitine supplementation.

The effect of the administration for 7 days of valproate (500 mg/kg/day) or valproate (500 mg/kg/day) plus L-carnitine (200 mg/kg/day) on carnitine concentrations in serum, red blood cells, muscle, liver, and urine was evaluated. In the serum and muscle of the valproic acid (VPA) group, free carnitine levels decreased, while acyl-carnitine levels and acyl/free ratio increased, when compared to those of the control. When L-carnitine was given to the VPA group, the free carnitine levels increased in the serum, muscle, and liver, and the acyl/free ratio decreased in all tissues when compared to those of the VPA group. The mean of free carnitine level in urine of the VPA group was not different but acylcarnitine increased when compared to values of controls, and after the supplementation with L-carnitine the acylcarnitine (from day 4 to 7) levels were decreased compared to the VPA group. The serum beta-OH-butyrate level in the VPA group was decreased when compared to those of controls and VPA plus L-carnitine groups. These results indicate that L-carnitine supplementation protects against the alteration in carnitine metabolism induced by the administration of VPA.

Animals↗
PubMed1986

In situ radiation-inactivation size of fibroblast membrane-bound acid beta-glucosidase in Gaucher type 1, type 2 and type 3 disease.

The radiation-inactivation size of membrane-bound acid beta-glucosidase in cultured skin fibroblasts of four normal individuals, five Gaucher type 1 (non-neuropathic), four Gaucher type 2 (acute neuropathic) and three Gaucher type 3 (sub-acute neuropathic) patients was determined using the radiation-inactivation method. The radiation-inactivation size of the enzyme in the control, Gaucher type 2 and Gaucher type 3 fibroblasts ranged from 94 000 to 128 800, and no statistical significant difference was found in the enzyme size between the normal and Gaucher cells nor among the Gaucher type 2 and type 3 cells. Contrary to the normal, Gaucher type 2 and Gaucher type 3 enzyme, the radiation-inactivation size of membrane-bound acid beta-glucosidase in all of the Gaucher type 1 fibroblasts tested is significantly higher, ranging from 158 400 to 235 300. The size of the control lysosomal enzyme, sphingomyelinase, also determined by the radiation-inactivation method in fibroblasts of normal individuals and patients with the three Gaucher subtypes, was between 70 000 and 74 500 and indistinguishable from each other. Since the molecular weight of acid beta-glucosidase subunit determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis was about 60 000 (Pentchev, P.G., Brady, R.O., Hibbert, S.P., Gal, A.E. and Shapiro, C. (1973) J. Biol. Chem. 248, 5256-5261), the above data suggest that: (i) the normal fibroblast enzyme, as well as the Gaucher type 2 and type 3 mutant enzyme, in the membrane-bound form, exists as a dimer; (ii) the underlying biochemical and genetic defect in non-neuropathic (type 1) and neuropathic (type 2 and type 3) Gaucher disease is very different from each other; and (iii) subunit interaction of the mutant enzyme may be present in Gaucher type 1 fibroblasts, resulting in the formation of a higher-molecular-weight aggregate.

Adult↗
PubMed1986

Serum and urinary carnitine and organic acids in Reye syndrome and Reye-like syndrome.

Free and acyl-carnitine in serum and urine, and urinary organic acids were measured in 6 patients with Reye syndrome and Reye-like syndrome. The free and total carnitine concentrations were significantly reduced in serum during the acute phases of the diseases. Thus, the ratio of acylcarnitine to free carnitine was significantly increased. Urinary excretion of acylcarnitine was greatly increased, and the acylcarnitine to total carnitine ratio was therefore greater than in controls. The urinary organic acids comprised large amounts of lactic acid, dicarboxylic acids and ketone bodies. It is suggested that carnitine deficiency is induced as more carnitine is consumed to buffer the increased amount of toxic acyl-CoA compounds metabolized from free fatty acids and the many organic acids. These results indicate that administration of L-carnitine should generally be considered in patients with Reye syndrome and Reye-like syndrome.

Acids↗