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Biomedical subjects

Y Horikawa

Publications and source records attributed to Y Horikawa.

At least 73 records · Page 4Linked to original sources
PubMed1998

Submicrometre-area high-energy-resolution photoelectron spectroscopy system.

A submicrometre-area photoelectron spectroscopy system that uses a multi-layer-coated Schwarzschild objective as the soft X-ray microbeam optics has been developed. The system is located at an undulator beamline (BL-16U) at the Photon Factory in the High Energy Accelerator Research Organization. By knife-edge measurement, the microbeam size was estimated to be 160 nm at the sample position using a 25-75% criterion. Photoelectron spectral measurements revealed that the Fermi edge width was 0.12 eV, which means that the instrumental resolution was 0.05 eV, after removing the natural broadening of the Fermi edge at room temperature. This system offers both high energy resolution and high spatial resolution.

Journal Article↗
PubMed1998

Suprachiasmatic nucleus in a patient with multiple system atrophy with abnormal circadian rhythm of arginine-vasopressin secretion into plasma.

We performed a quantitative investigation of arginine-vasopressin (AVP) immunopositive neurons in the suprachiasmatic nucleus (SCN), which is the endogenous clock of the brain of a patient with multiple system atrophy (MSA) who exhibited nocturnal polyuria associated with decreased urinary specific gravity and depression of nocturnal AVP secretion. Eleven age- and sex-matched subjects were used as controls. Although, the number of AVP-positive neurons was decreased in neither the supraoptic nucleus nor the paraventricular nucleus, the number of AVP-positive neurons in the SCN was decreased and gliosis was present in the SCN. The cytoplasmic area of AVP-immunopositive neurons in the SCN was smaller in the patient than in the control subjects. These findings raise the possibility that SCN is involved in MSA and the neurodegeneration in the SCN results in altered circadian rhythm of AVP secretion and nocturnal polyuria.

Adult↗
PubMed1998

[A case of traumatic aneurysm of the brachiocephalic artery].

Traumatic aneurysm of the brachiocephalic artery is rate. We presented a case of traumatic aneurysm of the brachiocephalic artery caused by traffic accident. A 28-year-old woman suffered a blunt chest trauma. A chest X-ray revealed a widening of the superior mediastinum and multiple rib fractures. CT scanning demonstrated left hemothorax with lung contusion and upper mediastinal hematoma. An aortography was performed which showed aneurysmal dilatation at the origin of the brachiocephalic artery. The patient underwent an operation 24 hours after chest injury. An aorto-right common carotid artery and right subclavian artery bypass with bifurcated Dacron graft was performed while monitoring temporary artery pressure. After resection of aneurysm, We found that about 3 cm longitudinal laceration of intima on the posterior wall of brachiocephalic artery. Her post operative condition was good and no neurological defect was noted.

Accidents, Traffic↗
PubMed1998

Sporadic motor neuron disease with severe sensory neuronopathy.

We report a 62-year-old man with sporadic motor neuron disease (MND) of 52 months' duration with progressive sensory disturbance and high cerebrospinal fluid protein content. Neuropathologically, both the upper and lower motor neuron systems were severely affected, and light and electron microscopy revealed Bunina bodies and skein-like inclusions, which are characteristic of amyotrophic lateral sclerosis, in the remaining anterior horn cells. Moreover, there was severe degeneration without inflammatory infiltrates in the spinal posterior columns, spinal ganglia, and peripheral sensory nerves. These findings suggest that this case may be an unusual variant of sporadic MND with severe somatic sensory system involvement.

Brain↗
PubMed1998

Bifurcations in the decremental propagation of a spike train in the Hodgkin-Huxley model of low excitability.

Response of a nerve fiber of low excitability to periodic stimulus pulses is studied with computer simulation of the Hodgkin-Huxley model. The excitability of the Hodgkin-Huxley model is reduced by decreasing the equilibrium potential for the sodium ion and by increasing the temperature, so that the decremental propagation of spikes occurs in the refractory period. It is shown that, as the period of stimulus pulses is decreased, the propagation length of the spikes is continuously changed, and period-doubling bifurcations occur. The response of a nerve fiber of low excitability is then qualitatively different from that of a normal fiber.

Animals↗
PubMed1998

Mitochondrial calcium in relaxed and tetanized myocardium.

The elemental composition of rat cardiac muscle was determined with electron probe x-ray microanalysis (EPMA) of rapidly frozen papillary muscles and trabeculae incubated with ryanodine (1 microM) in either 1.2 or 10 mM [Ca2+]o-containing solutions, paced at 0.6 Hz or tetanized at 10 Hz. Total mitochondrial calcium increased significantly, by 4.2 mmol/kg dry weight during a 7 s tetanus, only in muscles tetanized in the presence of 10 mM [Ca2+]o when cytoplasmic Ca2+ is 1-4 microM (Backx, P. H., W.-D. Gao, M. D. Azan-Backx, and E. Marban. 1995. The relationship between contractile force and intracellular [Ca2+] in intact rat trabeculae. J. Gen. Physiol. 105:1-19). Comparison of total mitochondrial with free mitochondrial Ca2+ reported in the literature indicates that the total/free ratio is approximately 6000 at physiological or near-physiological levels of total mitochondrial calcium. Increases in free mitochondrial [Ca2+] consistent with regulation of mitochondrial enzymes should be associated with increases in total mitochondrial calcium detectable with EPMA. However, such increases in mitochondrial calcium occur only as the result of prolonged, unphysiological elevations of cytosolic [Ca2+].

Animals↗
PubMed1998

Decreased nitric oxide-mediated natural killer cell activation in chronic fatigue syndrome.

BACKGROUND: L-Arginine (L-Arg), one of the essential amino acids, has been reported to have an immunomodulatory effect. The precise mechanism of the L-Arg-induced natural killer (NK) cell activation remains unresolved,and the effect of L-Arg on NK cells in chronic fatigue syndrome (CFS) patients has not been estimated. METHODS: NK cell function was evaluated in 20 subjects with CFS and compared with that in 21 healthy individuals. RESULTS: In healthy control subjects, NK activity was significantly increased after treatment with L-Arg, an NK function enhancer, for 24 h, whereas the same treatment failed to enhance NK activity in the CFS patients. We thus focused on L-Arg metabolism, which involves nitric oxide (NO) production through NO synthase (NOS). The expression of inducible NO synthase (iNOS) transcripts in peripheral blood mononuclear cells was not significantly different between healthy control subjects and CFS patients. The L-Arg-mediated NK cell activation was abolished by addition of NG-monomethyl-L-arginine, an inhibitor for iNOS. Furthermore, incubation with S-nitroso-N-acetyl-penicillamine, an NO donor, stimulated NK activity in healthy control subjects but not in CFS patients. CONCLUSION: These results demonstrate that the L-Arg-induced activation of NK activity is mediated by NO and that a possible dysfunction exists in the NO-mediated NK cell activation in CFS patients.

Adjuvants, Immunologic↗
PubMed1998

Mutation/polymorphism scanning of glucose-6-phosphatase gene promoter in noninsulin-dependent diabetes mellitus patients.

Glucose-6-phosphatase (G6Pase) catalyzes the rate-limiting step of gluconeogenesis, and hepatic G6Pase activity is increased in diabetes. We have cloned and analyzed the human G6Pase gene promoter region and identified putative regulatory sequences for insulin, cAMP, glucocorticoid, and hepatocyte nuclear factors. The promoter region of the G6Pase gene was analyzed in 154 noninsulin-dependent diabetes mellitus patients and 90 control subjects by PCR-single strand conformation polymorphism and direct sequencing methods. Polymorphisms were not found in any subjects. The results suggested that in noninsulin-dependent diabetic patients, the major cause of the hepatic glucose overproduction was not attributed to dysregulation of the G6Pase gene due to mutation/polymorphism of its promoter region.

Adolescent↗
PubMed1998

Gastric emptying of three different size of indigestible radiopaque markers in healthy subjects.

The gastric emptying of indigestible solids is affected by the size, specific gravity, shape, consistency and the compressibility of the indigestible solids and depends largely on the composition of the meal. The threshold size is about 3.0 mm in canine. But it is reported that the estimates made for dogs may not apply to humans. I evaluated whether the size of indigestible solids affects gastric emptying in healthy subjects with food which had the same specific gravity as the indigestible solids. We used three sets of 20 ring shaped radiopaque markers, which had the same specific gravity (1.2), shape, consistency, and compressibility, but different diameters (2.0 mm, 4.5 mm and 7.0 mm). After the subjects ingested the three sets of 20 markers with food, the number of markers evacuated from the stomach was counted every 15 min until all the markers were evacuated. The median numbers of discharged markers of 2.0 mm, 4.5 mm and 7.0 mm were 5 (0-5), 1 (0-3) and 3 (0-4) at 60 min, 15 (3-18), 10 (6-9) and 13 (11-16) at 120 min (median, 25th-75th percentile), respectively. There was no statistically significant difference between the numbers of the three types of discharged markers during observation. The lag time (the period from the time of ingestion of the markers to the time when the first marker left the stomach) of the 2.0 mm, 4.5 mm and 7.0 mm markers was 52.5 (45-105), 67.5 (60-105), and 52.5 (45-105) min, respectively, and there was no statistically significant difference. In conclusion, the radiopaque markers of different diameters (below 7.0 mm) left the stomach in the same pattern.

Adult↗
PubMed1998

Preventive effect of ACE inhibitor on interstitial myofibroblast formation and matrix deposition in a nephrotic model.

The nephrotic mouse (ICGN strain) is a useful model for progressive nephrotic syndrome (NS). In the present study, we demonstrated the preventive effects of enalapril, an angiotensin converting enzyme (ACE) inhibitor, on the progression of renal dysfunction and tubulo-interstitial fibrosis in the NS mice. Administration of enalapril (5 mg/dL in drinking water) to the 4-week-old NS mice for a 4-week-period did not improve their nephrotic symptoms such as albuminuria and hypoalbuminemia, but significantly suppressed the increases in blood urea nitrogen and serum creatinine levels. Renal histopathology demonstrated that the administration of the ACE inhibitor significantly attenuated the progression of the tubular and interstitial lesions (tubular dilatation, luminal cast accumulation and interstitial expansion) rather than the glomerular sclerotic changes. The suppression of the increase in blood urea nitrogen level by enalapril depended on the attenuated tubular injury rather than on the unchanged glomerular matrix deposition. Immunohistochemical examination revealed that the administration of the ACE inhibitor suppressed the formation of myofibroblasts, identified by the alpha-smooth muscle actin-positive cells, in the interstitial spaces. Consequently, interstitial matrix deposition was significantly reduced in the NS mice treated with enalapril. From the results obtained with the spontaneous nephrotic model, we emphasize a possibility that ACE inhibitor may be effective for attenuating progression of renal dysfunction and fibrosis in human NS, even if the ACE inhibitor fails to improve nephrotic symptoms such as albuminuria and hypoalbuminemia.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Markedly reduced expression of platelet c-mpl receptor in essential thrombocythemia.

Thrombopoietin (TPO) is implicated as a primary regulator of megakaryopoiesis and thrombopoiesis through binding to the cytokine receptor c-Mpl (the product of the c-mpl proto-oncogene). In an effort to determine the pathophysiological role of TPO-c-Mpl system in essential thrombocythemia (ET), we have examined the levels of serum TPO and the expression and function of platelet c-Mpl in 17 patients with ET. In spite of extreme thrombocytosis, serum TPO levels were slightly elevated or within normal range in most, if not all, patients with ET (mean +/- SD, 1.31 +/- 1.64 fmol/mL), as compared with normal subjects (0.76 +/- 0.21 fmol/mL). Flow cytometric and Western blot analyses revealed that the expression of platelet c-Mpl was strikingly reduced in all patients with ET. Furthermore, the expression of platelet c-mpl mRNA was found to be significantly decreased in the ET patients tested. In contrast, almost identical levels of GPIIb/IIIa protein and mRNA were expressed in platelets from ET patients and normal controls. In addition to expression level, activation state of platelet c-Mpl was investigated in ET patients. Immunoblotting with anti-phosphotyrosine antibody showed that no aberrant protein-tyrosine phosphorylation was observed in platelets of ET patients before treatment with TPO, and the levels of TPO-induced protein-tyrosine phosphorylation, including c-Mpl-tyrosyl phosphorylation, roughly paralleled those of c-Mpl expression, suggesting that c-Mpl-mediated signaling pathway was not constitutively activated in platelets of ET patients. These results suggested that the TPO-c-Mpl system may not be directly linked to pathogenesis of ET, and that gene(s) mutated in ET may be important in regulating the levels of c-mpl gene expression in addition to the growth and differentiation of multipotential hematopoietic stem cells.

Adolescent↗
PubMed1997

Presence and comparison of Ca2+ transport activity of annexins I, II, V, and VI in large unilamellar vesicles.

This study evaluated whether annexins I, II and VI possess Ca2+ transport activity in phospholipid membranes by the burst method, and the activity of each was compared with that of annexin V. Briefly, in the presence of 400 microM Ca2+, each annexin at 50 nM was added to large unilamellar vesicles (LUV) which were then burst in fura-2 solution with 0.2% Triton X-100, followed by examination of Ca2+ signals. Annexins I, II, V and VI were all shown to express, each to a different degree, Ca2+ activity toward phosphatidylserine/phosphatidyl- ethanolamine-LUV. Ca2+ signal intensity increased dependent on annexin concentration, and the Ca2+ transport activity of annexin V and VI was higher than that of annexin I and II. However, none of annexin I, II, V and VI expressed Ca2+ transport activity in LUV produced using phosphatidylcholine. Ca(2+)-incorporated LUV with no annexin showed signals whose intensity was proportional to Ca2+ concentration. The Ca2+ transport activity of the annexins could be effectively measured by the burst method. Ca2+ signal intensity would thus appear to be unique for each of the annexins and to be determined by the particular function and specificity of each of those considered in this study.

Animals↗
PubMed1997

Neuropathology of sporadic amyotrophic lateral sclerosis of long duration.

We performed post-mortem examinations of three patients with progressive neurogenic amyotrophy of long duration. One patient had been clinically diagnosed as having sporadic amyotrophic lateral sclerosis (ALS) and two had been diagnosed with progressive spinal muscular atrophy (PSMA). The disease durations were 10, 17 and 20 years, respectively, and all of the patients died of respiratory failure with no artificial respiratory support. In all of the patients, both the upper and lower motor neuron systems were affected; degeneration of the former was definite, but was milder than that usually encountered in sporadic ALS patients, and the histopathology of the latter was identical to that of sporadic ALS. Light microscopy revealed Bunina bodies, which are characteristic of sporadic ALS, in the remaining anterior horn cells of each patient. In addition, ubiquitin-positive skein-like inclusions were also identified, immunohistochemically, in the remaining anterior horn cells of each patient. Neuron counts indicated that the number of neurons was preserved in Clarke's column in these patients, but was significantly reduced in the intermediolateral nucleus, compared with control subjects. Based on these findings, we think that these three patients, with long disease durations, were affected by essentially the same underlying disease process as that of sporadic, classical ALS. Moreover, we question the neuropathological occurrence of sporadic ALS without involvement of the upper motor neuron system, namely, pure PSMA or lower motor neuron disease.

Aged↗
PubMed1997

Spinocerebellar ataxia type 6: CAG repeat expansion in alpha1A voltage-dependent calcium channel gene and clinical variations in Japanese population.

Autosomal dominant spinocerebellar ataxias (SCAs) are clinically and genetically a heterogeneous group of neurodegenerative disorders. Recently, mild CAG repeat expansion in the alpha1A voltage-dependent calcium channel gene has been found to be associated with a type of autosomal dominant SCA (SCA6). We analyzed 98 Japanese families with autosomal dominant SCAs, for whom CAG repeat expansions of the SCA1, SCA2, Machado-Joseph disease/SCA3, and dentatorubral-pallidoluysian atrophy genes were excluded, and 5 apparently sporadic cases of cortical cerebellar atrophy. The diagnosis of SCA6 was confirmed in 30 families (31%) comprising 47 affected individuals and 1 sporadic case. The size of expanded CAG repeats ranged from 21 to 26 repeat units and was found to be correlated inversely with age at onset. We identified 2 SCA6 patients homozygous for expanded CAG repeats, whose ages at onset were earlier than the 95% lower confidence level, suggesting the presence of a gene dosage effect of expanded CAG repeat. Ataxia is the most common initial symptom found in 45 of the 48 patients. Patients with a prolonged disease course showed other accompanying clinical features including dystonic postures, involuntary movements, and abnormalities in tendon reflexes.

Adult↗