[Clinical evaluation of ondansetron suppository].
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Aged↗
Biomedical subjects
T Yamanouchi
Publications and source records attributed to T Yamanouchi.
Common reabsorption system of 1,5-anhydro-D-glucitol, fructose, and mannose in rat renal tubule.
1,5-Anhydro-D-glucitol (AG) is a major polyol, 99.9% of which is reabsorbed by the kidney. However, such reabsorption is inhibited by competition with glucose excreted in excess, i.e., glucosuria. Under such conditions, AG is excreted into the urine. We administered various types of sugars to rats by continuous intravenous infusion for two hours to evaluate the competition between AG and these sugars for renal reabsorption in vivo. The reabsorption of AG was significantly inhibited by competition with fructose and mannose. The excretion of AG in the 120 min after a load of 3.64 mmol of fructose was 1.99 +/- 0.33 mumol, that after 3.64 mmol of mannose loading was 2.34 +/- 0.43 mumol. These levels were comparable to the AG excretion observed after the administration of the same amount of glucose (3.87 +/- 0.61 mumol). No competition was observed with sucrose, xylose, myoinositol or galactose. The reabsorption of fructose and mannose was significantly inhibited by the presence of AG (P < 0.001) after a mixed load. Results suggest that AG is reabsorbed in the renal tubule by an AG/fructose/mannose-common transport system that is distinct from the major glucose reabsorption system. These findings may help to clarify the specific transport systems for various sugars in the renal tubule, as well as their physiological importance.
Absorption↗
Clinical usefulness of serum 1,5-anhydroglucitol in monitoring glycaemic control.
BACKGROUND: To evaluate prospectively the clinical value of measuring serum concentrations of 1,5-anhydroglucitol (1,5AG) in monitoring glycaemia in patients with newly diagnosed non-insulin-dependent diabetes mellitus (NIDDM), we measured serum 1,5AG in 56 such patients. METHODS: 28 patients (group A) were started on, and continuously received, an oral hypoglycaemic agent for at least 6 weeks. The other 28 patients (group B) were given such agents for 4 weeks, and then stopped taking them for at least 2 weeks. All patients were then followed for an additional 10 weeks. Serum 1,5AG, fructosamine, glycated haemoglobin (HbA1c), and self-monitoring of blood glucose were monitored every 14 days for 16 weeks. FINDINGS: When sudden worsening of glycaemia occurred within 2 weeks, entailing withdrawal of oral treatment, 1,5AG accurately detected the slight change in glycaemia whereas HbA1c and fructosamine both failed to detect it. Although the change was detected by measurement of fasting plasma glucose (FPG) concentrations, FPG was less sensitive than 1,5AG. In patients with "near-normoglycaemia" (HbA1c about 6.5%) in the preceding 8 weeks, those who showed a lower concentration of 1,5AG (<10.0 micrograms/mL) manifested a higher mean daily plasma glucose concentration even though HbA1c measurement suggested good control of glycaemia. Results of 1,5AG were correlated more strongly with the FPG (r=0.790) and mean daily plasma glucose (r=-0.835) estimated on the same day than those estimaoffted in the preceding 2, 4 and 8 weeks, and with a fall in the Spearman correlation coefficient at any preceding time interval. INTERPRETATION: Because 1,5AG accurately detected a slight change in glycaemia without delay, it is suitable for use in monitoring for strict control of glycaemia, an important clinical goal.
Biomarkers↗
Effect of percutaneous transluminal coronary angioplasty on exercise ventilation in patients with coronary artery disease and normal left ventricular function.
We evaluated the ventilatory response to exercise before and after percutaneous transluminal coronary angioplasty (PTCA) in 22 patients with coronary artery disease (CAD) and normal left ventricular systolic function to determine the effect of exercise-induced myocardial ischemia on the ventilatory response. Subjects performed a symptom-limited maximal ergometer exercise test in the sitting position. The ventilatory response was evaluated in terms of the slopes of minute ventilation (VE) and carbon dioxide production (VCO2) during exercise (slope 1 and slope 2, defined as below and above the respiratory compensation threshold, respectively). Slope 1 of the correlation between (VE) and (VCO2) was significantly greater in patients with CAD (27.3 +/- 2.6) than in the age-matched control group (23.7 +/- 2.6; p < 0.01). Slope 2 was also significantly greater in patients (41.0 +/- 4.8) than in the control group (29.7 +/- 2.9; p < 0.01). Slope 1 of the correlation between (VE) and (VCO2) decreased significantly in the 14 patients in whom PTCA was successful but did not decrease in the 8 patients in whom PTCA failed. Our results suggest that myocardial ischemia increases exercise ventilation in patients with CAD and normal left ventricular systolic function and that its effect is reversible.
Adult↗
Effect of warming of exercising legs on exercise capacity in patients with impaired exercise tolerance.
OBJECTIVE: The purpose of this study was to determine whether warming of exercising legs improves exercise capacity in patients with cardiac disease and low exercise tolerance. BACKGROUND: Exercising muscle temperature reflects both muscle metabolic rate and muscle blood flow. Increase in muscle temperature in exercising legs is impaired in patients with chronic heart failure. We hypothesized that the mechanisms responsible for impairment of temperature increase in exercising muscle might be related to those responsible for low exercise tolerance. METHODS: We studied 17 patients with cardiac disease whose anaerobic threshold (AT) ranged from 6.6 to 14.8 ml/kg/min (mean 11.2 +/- 1.9 SD). Subjects performed symptom-limited sitting cycle ergometer exercise with or without warming of the thighs. Both thighs were warmed by use of hot packs fixed by supporters. To determine the effect of the supporters themselves on AT and peak VO2, the same ergometer exercise was performed by 7 patients with or without supporters. Peak VO2 and AT were determined by concomitant respiratory gas monitoring. RESULTS: 1) Warming of the thighs increased deep temperature in the thighs (1.0 approximately 2.8 degrees C). 2) AT and peak VO2 were significantly improved in the warming exercise compared with the non-warming exercise (p < 0.01, p < 0.01). 3) There was no significant difference in AT or peak VO2 between the exercise with and without supporters. CONCLUSION: The findings of this study indicate that warming of exercising legs improves exercise capacity in patients with cardiac disease and low exercise tolerance.
Aged↗
Dose-dependent effect of niceritrol on plasma lipoprotein-a.
Lipoprotein-a, Lp(a), is a variant form of low density lipoprotein (LDL) that contains apolipoprotein-a, whose structure has 75-85% homology with plasminogen. Elevated plasma levels of Lp(a) are considered to be one of the independent risk factors for cardiovascular disease. We studied the effects of niceritrol, a nicotinic acid derivative, on plasma Lp(a) levels in 72 patients with hypercholesterolaemia. The dose of niceritrol was increased every 4 weeks, from 750 to 1500 and then to 2250 mg day-1. The final dose was adjusted to obtain a plasma cholesterol level less than 5.69 mmol l-1. Niceritrol led to significant decreases in plasma levels of median Lp(a), from 16.1 mg dl-1 (interquartile intervals, 8.7 to 32.8) to 11.1 mg dl-1 (interquartile intervals, 6.6 to 21), the mean reduction rate being 17.6%. In the group with pretreatment Lp(a) levels of over 20 mg dl-1, Lp(a) decreased by 10.0, 22.0 and 31.8% at the doses of 750, 1500, and 2250 mg day-1, respectively. In the group with levels less than 20 mg dl-1, only the dose of 2250 mg day-1 was effective in the reduction of Lp(a). The results suggest that the reduction of Lp(a) was dependent on the dose of niceritrol and on the pretreatment level of Lp(a). In conclusion, niceritrol is effective, in a dose-dependent manner, for reducing Lp(a) levels.
Aged↗
[Obesity and the related diseases: gout].
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Alcohol Drinking↗
Prolonged hyperalimentation as a possible cause of renal tubular dysfunction: evaluation of 1,5-anhydro-D-glucitol resorption and N-acetylglucosaminidase excretion in humans.
1. A major polyol found in the sera and other tissues of humans, 1,5-anhydro-D-glucitol, is mainly ingested in the diet and is excreted in urine. We compared the influence of the long-term administration of total parenteral nutrition free of 1,5-anhydro-D-glucitol with that of total enteral nutrition on the serum level of 1,5-anhydro-D-glucitol in 46 patients who could not take food by mouth. 2. The serum concentration of 1,5-anhydro-D-glucitol and its kinetics remained unchanged in the group receiving total enteral nutrition (n = 21) over a period of 12 months. However, after 1 month on total parenteral nutrition (n = 25), the serum level of 1,5-anhydro-D-glucitol decreased, falling to about one-sixth the pretreatment level in the 12th month. Because the serum level of 1,5-anhydro-D-glucitol continued to decline, falling below the limit at which its renal reabsorption is normally activated, this decrease did not seem to be caused directly by a nutritional deficiency of this substance. 3. The urinary excretion of 1,5-anhydro-D-glucitol was closely correlated (r = 0.792) with that of N-acetyl-beta-glucosaminidase; but not with the serum creatinine level or of the urinary excretion of microalbumin or of urinary beta 2-microglobulin. We observed no glucosuria, hyperuricuria or changes in serum electrolytes during total parenteral nutrition. 4. The reduction in the serum level of 1,5-anhydro-D-glucitol and the urinary excretion of N-acetyl-beta-glucosaminidase were correlated with the duration of total parenteral nutrition administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Absorption↗
Effects of L- and DL-carnitine on patients with impaired exercise tolerance.
We designed this study to determine whether orally administered L- and DL-carnitine can improve exercise tolerance in a group of patients with exercise intolerance. Nineteen patients with cardiac disease were randomly divided into 2 groups, an L-carnitine treatment group (n = 9) and a DL-carnitine treatment group (n = 10). Eight additional age-matched patients served as an untreated control group. Subjects in both carnitine treatment groups underwent cardiopulmonary exercise testing on a cycle ergometer in order to determine peak exercise time, peak oxygen uptake (VO2), lactate threshold (LT) and ventilatory threshold (VT) before and after the oral administration of 900 mg/day of L- or DL-carnitine for 2 weeks. Basal values of peak exercise time, peak VO2, LT and VT did not differ significantly among the 3 groups. Peak exercise time and peak VO2 tended to be increased in the L-carnitine treatment group, and tended to be decreased in the DL-carnitine treatment group. Both LT and VT (ml/kg/min) were significantly improved (LT: from 9.7 +/- 0.6 to 10.8 +/- 1.0, p < 0.05; VT: from 9.8 +/- 0.8 to 11.8 +/- 1.9, p < 0.02) by the administration of L-carnitine, while LT was significantly decreased (from 11.0 +/- 2.0 to 9.6 +/- 1.2, p < 0.05) and VT tended to be decreased by the administration of DL-carnitine (from 11.6 +/- 2.0 to 10.8 +/- 2.4). In the untreated control group, no significant changes were observed in the values of exercise tolerance between the 2 series of exercise testings. In neither group did carnitine modify hemodynamic parameters at rest or during exercise. In conclusion, this study demonstrated that L-carnitine increases and DL-carnitine decreases exercise tolerance in patients with impaired exercise tolerance.
Administration, Oral↗
Exercise-induced rise in arterial potassium is enhanced in patients with impaired exercise tolerance.
We assessed the changes in arterial potassium concentration during exercise and recovery in relation to exercise tolerance in patients with impaired exercise tolerance. Sixteen patients with cardiac disease were subjected to a cardiopulmonary exercise test on a cycle ergometer. Arterial potassium and lactate concentrations were measured every minute during and after exercise, and ventilatory threshold (VT) and lactate threshold (LT) were identified. Before exercise, arterial potassium concentration was 3.8 +/- 0.3 mEq/l. It increased to 4.1 +/- 0.3 mEq/l at LT (p < 0.002 versus at rest), to 4.2 +/- 0.3 mEq/l at VT, and to 4.8 +/- 0.5 mEq/l at peak exercise (p < 0.001 versus at LT, p < 0.001 versus at VT). At an exercise intensity equivalent to 30, 40, 50 or 60% of predicted maximum oxygen uptake, the increase in arterial potassium showed a negative and significant correlation with %LT (r = -0.62 approximately -0.72, p < 0.01 approximately 0.05) and %VT (r = -0.62 approximately -0.75, p < 0.001 approximately 0.05), where %LT and %VT represent the ratios of LT and VT to the predicted maximum oxygen uptake, respectively. There was a good correlation between the rate of fall in potassium concentration during recovery and its increase during exercise. It was concluded that in patients with impaired exercise tolerance, the greater the degree of exercise intolerance, the greater the increase in arterial potassium concentration during exercise, and the steeper the fall in potassium concentration during recovery. Because the rise in potassium concentration during exercise and its fall during recovery were greater when the exercise level exceeded the anaerobic threshold, exercise levels below the anaerobic threshold are recommended for patients with cardiac diseases.
Aged↗
Usefulness of hyperventilation thallium-201 single photon emission computed tomography for the diagnosis of vasospastic angina.
To establish a safe and sensitive diagnostic procedure for detecting coronary vasospasm, we utilized 201-thallium myocardial SPECT combined with hyperventilation (HV-SPECT) in 29 patients with vasospastic angina (VAP) and 11 controls. Twenty-five of 29 patients with VAP and 5 of 11 controls developed transient perfusion defects on HV-SPECT, resulting in a sensitivity and specificity calculated at 86% and 55%, respectively. Overall accuracy in identifying corresponding vessels with coronary vasospasm, respectively. Coronary vasospasm tended to be identified more accurately in the left anterior descending branch and the right coronary artery than in the circumflex branch (75%, 71% and 50%, respectively). The hyperventilation test induced ischemic ECG changes in 11 of 29 patients with VAP, yielding a sensitivity of 38%. Analyzing the washout rate of HV-SPECT in patients with VAP, both the extent and severity scores of patients with ischemic ECG changes were larger than those of patients without. No serious complications occurred during HV-SPECT. In conclusion, HV-SPECT was a safe and sensitive procedure as a primary diagnostic approach for VAP. From the results of washout analysis, HV-SPECT could detect more mild myocardial ischemia than could the ECG, and seemed quite useful especially for detecting coronary vasospasm accompanied by minimal ischemic ECG changes.
Adult↗
[Hyperuric acidemia and obesity].
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Age Factors↗
[Seven cases of ulcerative colitis associated with pyoderma gangrenosum].
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Adult↗
Prevention of diabetes by thymic hormone in alloxan-treated rats.
We investigated the effects of facteur thymique sérique (FTS), a thymic peptide hormone, on alloxan- and streptozotocin-induced diabetes in rats. Pretreatment with intravenous injection of FTS significantly suppressed both alloxan- and streptozotocin-induced hyperglycemia. The effects of FTS were time dependent. FTS suppressed hyperglycemia in a dose range of 1-6600 micrograms/kg. Alloxan-induced hyperglycemia was completely prevented when FTS was injected in doses of 40-50 micrograms/kg 1 min before injection of alloxan. Histological examination of islet areas showed that alloxan-induced destruction of beta-cells was inhibited by FTS. FTS had no significant effects on lymphocyte subsets and immunity-related cells or on plasma superoxide dismutase activity and total glutathione level. The blood half-life time of exogenously injected FTS was short (2-3 min), indicating acute internalization of FTS into pancreatic beta-cells. Our results suggested that FTS acutely and directly blocks some initial effect of alloxan, preventing the destruction of beta-cells.
Amino Acid Sequence↗
Transport and accumulation of 1,5-anhydro-D-glucitol in the human erythroleukemia cell line K-562.
The transport and intracellular accumulation of 1,5-anhydro-D-glucitol (AG) was studied in the human erythroleukemia cell line K-562 by gas chromatography-mass spectrometry in conjunction with liquid scintillation spectrometry. K-562 cells contained 106 +/- 6 nM/10(6) cells of free AG, primarily in the cytosol. Addition of physiologic amounts of AG to the extracellular medium resulted in rapid intracellular incorporation of AG, with a half-saturation time of 5 s. Intracellular accumulation was linear for 2 h and subsequently reached saturation. AG uptake was temperature and concentration dependent with an apparent Km of 127 mM. AG uptake and accumulation was not inhibited by fructose, fucose, galactose, mannose, glucose, or 3-O-methyl-D-glucose and was less affected by cytochalasin B or phloretin than that of 2-deoxyglucose. Phloridzin did not affect AG uptake but did inhibit 2-deoxyglucose uptake. Efflux of AG from K-562 cells depended on external AG concentration alone and was not affected by extracellular glucose concentration. Intracellular AG concentration decreased rapidly and reached zero within 10 min following removal of AG from the external medium. We therefore propose that both transport and countertransport of AG in K-562 cells are mediated by a specific carrier system.
Biological Transport↗
Significance of distributed representation in the output layer of a neural network in a pattern recognition task.
In the cerebral cortex, it is assumed that information is represented by the activity pattern of an assembly of neurons and the synaptic efficacies among them. A distributed representation of pattern is incorporated in the output layer of a neural network with an error back-propagation algorithm, in order to study its technological merits. The network has three layers, which consist of a 32 x 32 array of units (1024) for the input layer, 6-25 units for the hidden layer and 12 units for the output layer. 12 triangular patterns with a variety of parameters are presented to the input layer. Three output-layer units are assigned to each input figure. After initial learning, the network responds to the learned pattern with high accuracy. In addition, it responds with high accuracy to similar but unpresented patterns, showing a generalisation for patterns. The network shows resistance to unit de-activation procedures. When the input layer is exposed to the learned pattern, the hidden-layer units show associative activation pattern. These results indicate that the organisation of information representation in the output layer in a neural network strongly influences both the performance of the whole network and information representation in the hidden layer.
Association↗
Mitochondrial diabetes mellitus: prevalence and clinical characterization of diabetes due to mitochondrial tRNA(Leu(UUR)) gene mutation in Japanese patients.
Mutations in the mitochondrial gene were recently identified in a large pedigree of diabetes mellitus and deafness. As the mitochondrial gene is materially inherited, Japanese diabetic patients whose mothers were also diabetic were screened, using peripheral leucocytes, for an A to G transition at nucleotide pair 3243 of the mitochondrial gene, a tRNA(Leu(UUR)) mutation. This mutation was identified in four pedigrees from among 300 unrelated patients who were screened. Diabetes co-segregated with the mutation, except in one young subject, and was maternally inherited. The apparent onset of disease occurred between 11 and 68 years of age. Some of the affected members developed hearing impairment and congestive heart failure due to cardiomyopathy, though generally long after the onset of diabetes, and these patients had therefore not been diagnosed as having a specific form of diabetes. The duration of sulphonyl-urea treatment was not more than 8 years in these pedigrees and affected members were prone to progression to insulin-requiring diabetes. Thus, these patients were secondary sulphonylurea failures. Long-term follow-up revealed that the underlying disorder in affected members is a progressive impairment of insulin secretion. Some were initially diagnosed as having IDDM based on an apparent acute onset in youth and the clinical severity of their diabetes. Others were regarded as having MODY with an aggressive course. The mitochondrial gene mutation or diabetes is not transmitted to all offspring of the affected mothers.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗