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Biomedical subjects

Y Kikawa

Publications and source records attributed to Y Kikawa.

10 recordsLinked to original sources

Urinary leukotriene E4 after exercise challenge in children with asthma.

To assess the role of sulfidopeptide leukotrienes in the pathogenesis of exercise-induced asthma (EIA), the urinary levels of leukotriene E4 (LTE4), a metabolite of LTC4 and LTD4, were measured by RIA before and after exercise in 13 children with EIA and 10 healthy children. Mass spectrometry was used to confirm the presence of LTE4 in urine and the specificity of the RIA. There was no significant difference in the urinary LTE4 levels before exercise between the children with asthma and healthy children (109 [21 to 265] versus 122 [45 to 156] pg/mg of creatinine; median and range). Urinary LTE4 levels increased significantly after exercise in the children with EIA (from 109 [21 to 265] to 196 [40 to 655] pg/mg of creatinine; median and range; p less than 0.05) but not in the healthy children. The children with asthma demonstrated no significant correlation between the LTE4 level after exercise and the degree of bronchoconstriction, as revealed by the maximal percent fall in the peak expiratory flow rate. Taken together with a recent study that pretreatment with a potent and selective LTD4 antagonist markedly attenuated EIA, our findings suggest that sulfidopeptide leukotrienes may play some role in the pathogenesis of this type of asthma with other factors also being involved in determining the overall airway response.

Asthma, Exercise-Induced

Mucopolysaccharidosis VI (Maroteaux-Lamy syndrome) with hearing impairment and pupillary membrane remnants.

A Japanese boy aged 13 months was referred to us because thickened ribs had been observed on a chest X-ray taken during a respiratory infection. mucopolysaccharidosis type VI (MPS VI) was diagnosed based on urinary glycosaminoglycan analysis and low activity of arylsulfatase B in peripheral leukocytes. He had mild pupillary membrane remnants, but no corneal opacities. The auditory brainstem response revealed moderate hearing impairment, which may have caused his subnormal DQ score of 85 at the age of 19 months. Although MPS VI is characterized by normal intellectual development with normal hearing in early infancy, it is important to examine for hearing loss, especially when an infant with this disease shows developmental delay.

Hearing Disorders

Exercise-induced urinary excretion of leukotriene E4 in children with atopic asthma.

Urinary levels of leukotriene (LT) E4, a stable end-product of LTC4 and LTD4, were measured before and after exercise in 10 children with severe asthma and seven children with moderate asthma using HPLC and RIA to clarify the relationship of LT to the severity of asthma and to the degree of bronchospasm in exercise-induced asthma. The urinary LTE4 level significantly increased after exercise in the severe asthma group, but not in the moderate asthma group (14.3 +/- 14.5 to 24.3 +/- 20.6 versus 19.6 +/- 12.3 to 17.6 +/- 10.8 ng/mmol creatinine, p less than 0.05). The urinary LTE4 level increased in 10 patients (eight with severe asthma), and it decreased in seven patients (five with moderate asthma). A significant difference in the degree of bronchospasm after exercise (as shown by the maximal % fall in the peak expiratory flow rate), was seen when patients with increased urinary LTE4 excretion were compared with those with decreased excretion (60.4 +/- 17.3 versus 24.1 +/- 14.3%, p less than 0.01). Our findings suggest that exercise-induced asthma, or at least a subtype of exercise-induced asthma, may partly develop through the release of LTC4.

Asthma, Exercise-Induced

Pathophysiologic study on methylmalonic aciduria: decrease in liver high-energy phosphate after propionate loading in rats.

Methylmalonate or propionate was i.v. infused into B12-deprived and control rats. In the B12-deprived rats, the plasma and liver concentrations of B12 decreased to 8 and 13%, respectively, of those of the control rats. The propionate loading produced a disproportionate increase in liver propionate levels; the mean ratio of methylmalonate to propionate in the liver was approximately 1.0 after methylmalonate loading, whereas it was 0.1 to 0.2 after propionate loading. The liver propionate and methylmalonate levels in the B12-deprived rats were twice as high as those in the control rats. The mean ratio of beta-ATP to inorganic phosphate in the liver, measured with 31P-magnetic resonance spectroscopy, decreased from 0.60 to 0.48 in the B12-deprived rats and from 0.78 to 0.63 in the control rats after methylmalonate loading; the ratio decreased from 0.57 to 0.37 in the B12-deprived rats and from 0.76 to 0.56 in the controls after propionate loading. Statistical analysis showed that propionate loading caused a more marked decrease in ATP than did methylmalonate loading (F = 26.33, degree of freedom 1 and 15; p less than 0.001), while B12-deprivation caused a more marked decrease in ATP than did the control diet (F = 92.26, df 1 and 15; p less than 0.001). The concentrations of tricarboxylic acid cycle intermediates and related organic acids in the livers of the rats suggested that propionate inhibited NAD(+)-dependent enzymes in the cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate

Leukotriene B4 production in children with steroid-responsive nephrotic syndrome.

Leukotriene B4 (LTB4) production in polymorphonuclear leucocytes (PMN) was examined in ten children with steroid-responsive nephrotic syndrome (SRNS) before, during, and after steroid administration. Comparison of LTB4 production was made in 14 children with non-inflammatory disease who were not receiving steroid therapy. No significant change was noted in PMN LTB4 biosynthesis in children with SRNS throughout any phase of the disease. Furthermore, there was no significant difference in LTB4 biosynthesis in PMN between SRNS patients before steroid therapy and patients with non-inflammatory disease. These findings suggest that inhibition of LTB4 production is not involved in the mechanism underlying steroid action in SRNS.

Adolescent

Acute infantile hemiplegia in a patient with propionic acidaemia.

A 10-month-old girl with mild developmental delay became hemiplegic after seizures. Cranial CT scan and magnetic resonance imaging (MRI) revealed no lesions related to vascular diseases, but brain atrophy on the right side was remarkable. Digital subtraction angiography showed slightly decreased visualization of peripheral branches of the right medial cerebral artery. Propionic acidaemia was diagnosed on the basis of high plasma levels of propionic acid and its metabolites and the elevated urinary excretion of these acids. With therapy, the levels of these acids fell, and her left hemiplegia disappeared 3 months later.

Amino Acid Metabolism, Inborn Errors

Diagnosis of iliopsoas pyomyositis by ultrasonography and CT.

A patient with iliopsoas muscle pyomyositis was successfully treated with intravenous antibiotics alone. The diagnosis was made by ultrasonography and X-ray computed tomography after five days of spiking fevers. Ultrasonography and X-ray computed tomography revealed swelling of the muscle body but no abscess formation. We emphasize the usefulness of early diagnostic imaging to allow conservative treatment of iliopsoas muscle pyomyositis.

Child

Delayed auditory brainstem response in thiamin-deficient rats.

We recorded the auditory brainstem responses of rats fed a thiamin-deficient diet. The interpeak latencies between waves I and III, as well as those between waves I and IV, were significantly prolonged from day 24, while the latency of wave I was prolonged on day 26 of the thiamin-deficient diet. These delayed responses were corrected in 2 to 4 days after the initiation of daily intraperitoneal thiamin injections from day 32. The rats that were fed the thiamin-deficient diet, and then sacrificed on day 32, showed a decrease of total thiamin levels in the brain (26% of the level in control rat brains). Based on these results, we emphasize the value of the auditory brainstem response to detect thiamin deficiency.

Animals