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K Sohmiya

Publications and source records attributed to K Sohmiya.

At least 19 recordsLinked to original sources
PubMed1999

CD36 mediates long-chain fatty acid transport in human myocardium: complete myocardial accumulation defect of radiolabeled long-chain fatty acid analog in subjects with CD36 deficiency.

Long-chain fatty acids (LCFA) are the major energy substrate for heart and their oxidation is important for achieving maximal cardiac work. However, the mechanism of uptake of LCFA by myocardium has not been clarified. We previously reported that bovine myocardial LCFA transporter has a sequence homology to human CD36. Clinically, total defect of myocardial uptake of radiolabeled long-chain fatty acid analog [123I-BMIPP: Iodine-123 15-(p-iodophenyl)-(R,S)-methylpentadecanoic acid] has been reported in some restricted cases, but the etiology has not been clarified. In the present study, we analyzed CD36 expression and CD36 gene in subjects who showed total lack of myocardial 123I-BMIPP accumulation, and, vice versa, evaluated myocardial 123I-BMIPP uptake in subjects with CD36 deficiency. Four unrelated subjects were evaluated, Two were found to have negative myocardial LCFA accumulation by 123I-BMIPP scintigraphy, after which the expression of CD36 on their platelets and monocytes was analyzed. Remaining two subjects were identified as CD36 deficiency by screening, then 123I-BMIPP scintigraphy was performed. Expression of CD36 on platelets and monocytes was measured by flow cytometric analysis. The molecular defects responsible for CD36 deficiency was detected by allele-specific restriction enzyme analysis. CD36 expression was totally deficient in all 4 subjects on both platelets and monocytes. Two subjects were homozygous for a 478C-->T mutation. One was heterozygous for the dinucleotide deletion of exon V and single nucleotide insertion of exon X, and remaining one was considered to be heterozygous for the dinucleotide deletion of exon V and an unknown gene abnormality. All cases demonstrated a completely negative accumulation of myocardial LCFA despite of normal myocardial perfusion, which was evaluated by thallium scintigraphy. In addition, all cases demonstrated apparently normal hepatic LCFA accumulation Thus, these findings suggested that CD36 acts as a major myocardial specific LCFA transporter in humans.

Aged↗
PubMed1998

CD36 abnormality and impaired myocardial long-chain fatty acid uptake in patients with hypertrophic cardiomyopathy.

Some patients with hypertrophic cardiomyopathy (HCM) demonstrate abnormal myocardial long-chain fatty acid (LCFA) metabolism. However, the exact mechanism involved is unknown. Recently, it was proposed that myocardial cells take up LCFAs via a specific mechanism, in which the CD36 molecule has been implicated as a possible candidate molecule. In addition, a high prevalence of CD36 deficiency was also found in a small number of HCM patients. Accordingly, the investigation of abnormality of the CD36 molecule in a large number of HCM patients may be useful in finding the possible cause of HCM. Moreover, the analysis of myocardial LCFA uptake in patients with molecular abnormalities may be helpful in understanding the possible function of this molecule. In this study, in order to discover the relationship between HCM and the CD36 molecular abnormality, the expression level of platelet CD36 and CD36 cDNA in 55 HCM patients was analyzed. Twelve patients showed negligible (<5%) CD36 expression on their platelets. Among them, one was found to be homozygous for the C-478-->T substitution and 6 were heterozygous for the C-478-->T substitution. In 9 patients, CD36 was expressed by less than 50% of the platelets. One of them was found to be heterozygous for the C-478-->T substitution. Two other patients were also found to be heterozygous for this point mutation, although their platelets expressed CD36. Thus, 23 out of 55 (41.8%) HCM patients had negligible (<5%) or reduced (<50%) levels of CD36 expression on platelets, or had a point mutation of CD36 cDNA. These 55 HCM patients were also evaluated with myocardial scintigraphy both for LCFA uptake and perfusion, which showed a moderate to severe discrepancy between myocardial LCFA accumulation and myocardial perfusion in 95.5% of the patients (21/23). On the other hand, 70% of the patients with normal (>90%) CD36 expression (14/20) did not show any severe discrepancies between myocardial LCFA accumulation and myocardial perfusion. These data could suggest that abnormal myocardial LCFA metabolism seen in HCM patients may be related to abnormality of the CD36 molecule, and that abnormalities of this molecule may be linked to the cause of some types of HCM.

Adult↗
PubMed1998

Synchronization, decrease in strength of pattern, illusory contours, and neon-color effect.

When certain elements in a pattern are replaced by colored lines, a spreading of neon-like color can be seen around the lines. Using a variety of neon displaying patterns, we hypothesize that two conditions are critical to the neon effect. One is the occurrence of illusory contours and another a decrease in strength of pattern of the colored lines. On the basis of the two conditions, various phenomena of the neon effect are discussed. Finally, examining the striking characteristics of the neon effect, the vagueness of the colored lines and the spreading of the color of the colored lines over an illusory area wherein the color stimulus does not exist, we conclude that the neon effect is caused by synchronization of strength of pattern.

Color Perception↗
PubMed1998

Connection between synchronization of oscillatory activities at early stages and a final stage in the visual system.

Singer's group and we found synchronized oscillatory responses at early stages and at a final stage in visual processing, respectively. However, the former occurs on a millisecond time scale and the latter on a second time scale. We have considered that this results from a difference in scale of something which takes part in the oscillations. From this viewpoint, here we first find suppression effects on both figure and ground of a pattern and on only the ground in a binocular-rivalry situation and then examine, using the effects of two steps, what oscillates and synchronizes at the last stage for form. Finally, we conclude that the synchronous neuronal oscillations depend on firing patterns of neurons at early stages in the visual system and the psychophysical ones on configurations of the spread effect of strength of pattern involved closely in whole processing of the visual system and the latter originates in the former.

Field Dependence-Independence↗
PubMed1997

Is CD36 deficiency an etiology of hereditary hypertrophic cardiomyopathy?

Hereditary hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease, but the genetic defects are still unclear in many cases. Reduced myocardial long-chain fatty acid (LCFA) uptake has been demonstrated in patients with some types of HCM. In addition, a possible relationship between a shift ofmyocardial substrate utilization and cardiac hypertrophy has been suggested by experimental studies. Myocardial uptake of LCFAs occurs via a specific transporter, which is homologous with human CD36. CD36 deficiency has also been reported in some individuals, and is transmitted as an autosomal dominant trait like HCM. In this study, we analyzed CD36 in 47 patients with HCM [29 with asymmetric septal hypertrophy (ASH) and 18 without ASH], 11 patients with dilated cardiomyopathy (DCM), and 26 patients with pressure-overload cardiac hypertrophy. Eleven patients (37.9%) who had HCM with ASH, one (9.1%) with DCM, and two (7.7%) with pressure-overload hypertrophy showed CD36 deficiency, while none of the HCM patients without ASH had CD36 deficiency. One patient who had HCM with ASH and CD36 deficiency showed no myocardial LCFA uptake, although myocardial perfusion was normal. Reduced myocardial LCFA uptake despite normal myocardial perfusion was demonstrated in the other HCM patients with ASH and CD36 deficiency. Based on the high prevalence of CD36 deficiency in HCM patients with ASH, we hypothesize that this deficiency might be one etiology of hereditary HCM.

Adult↗
PubMed1995

A novel ATP-dependent inward rectifier potassium channel expressed predominantly in glial cells.

We have isolated a novel inward rectifier K+ channel predominantly expressed in glial cells of the central nervous system. Its amino acid sequence exhibited 53% identity with ROMK1 and approximately 40% identity with other inward rectifier K+ channels. Xenopus oocytes injected with cRNA derived from this clone expressed a K+ current, which showed classical inward rectifier K+ channel characteristics. Intracellular Mg.ATP was required to sustain channel activity in excised membrane patches, which is consistent with a Walker type-A ATP-binding domain on this clone. We designate this new clone as KAB-2 (the second type of inward rectifying K+ channel with an ATP-binding domain). In situ hybridization showed KAB-2 mRNA to be expressed predominantly in glial cells of the cerebellum and forebrain. This is the first description of the cloning of a glial cell inward rectifier potassium channel, which may be responsible for K+ buffering action of glial cells in the brain.

Adenosine Triphosphate↗
PubMed1995

Explanation of illusory contours in terms of strength of pattern and its spread effect.

The generation of illusory contours is closely related to distinct parts of a pattern such as dots, line ends, and corner points. On the other hand, the remarkable property is that gaze at one point of the contours diminishes the illusion and a return of gaze to the whole pattern restores it. Therefore, illusory contours depend on local parts and the whole pattern formed by the parts, and fitting data on the two aspects is necessary to clarify underlying mechanisms. We have obtained such data from the experiments performed to elucidate other visual phenomena. On the basis of the data, the concepts of strength of pattern, strength of its spread effect, ridgelines of the spread effect, and a hollow of the spread effect are introduced and then various phenomena on illusory contours, including the Kanizsa triangle, are explained in terms of these concepts.

Attention↗
PubMed1994

What is a crucial determinant in anorthoscopic perception?

There are two important problems in anorthoscopic perception. The first is how a sequence of parts of a figure viewed through a slit is integrated into a whole. The second is how the distortion of an anorthoscopic image along the direction of its motion occurs. To answer the questions, two experiments and two demonstrations were performed by conceiving compound figures of one horizontal and one curvilinear component and a method which permits seeing anorthoscopic and ordinary images at the same time. From the results, the idea of anorthoscopic motion complementary to apparent motion is introduced as a crucial determinant that permits an integration of the parts into a perception of the whole. As regards the distortion of the percept we agree with Rock, et al.'s 1987 assumption but also consider that the distortion depends on the ratio of speed of anorthoscopic motion to real motion.

Attention↗
PubMed1993

Human heart-type cytoplasmic fatty acid-binding protein in serum and urine during hyperacute myocardial infarction.

We have previously reported that serum and/or urinary human heart-type cytoplasmic fatty acid-binding protein (HH-FABPc) can be used as an early indicator of myocardial injury (Clin Biochem 1991; 24: 195-201). To confirm the usefulness of HH-FABPc as an early diagnostic indicator of acute myocardial infarction (AMI), its serum and urinary levels were measured in samples obtained within 6 h after the onset of acute coronary syndrome related symptoms. Samples were collected from 97 patients, who were composed of 63 with AMI, 24 with unstable angina and 10 with chest pain syndrome. The positivity of serum and urinary HH-FABPc and cardiac creatine kinase isozyme MB (CK-MB) was analyzed in these samples. Serum HH-FABPc levels in AMI were above normal in 91.4% (64/70) of the samples tested within 3 h of the onset of symptoms and in 100% (111/111) of those tested at 3-6 h. Elevated urinary HH-FABPc levels in AMI were obtained in 88.9% (8/9) of samples at 0-3 h and in 75% (6/8) at 3-6 h. CK-MB activity in AMI was positive in 20% (8/40) and 66.3% (53/80) of serum samples at 0-3 h and 3-6 h, respectively. HH-FABPc was always positive when a serum sample was positive for CK-MB. Serum HH-FABPc at 0-6 h in chest pain syndrome and in unstable angina were positive in 17.8% (5/28) and 56.7% (34/60), respectively. The elevated HH-FABPc in serum and urine was noted much earlier than that of CK-MB during the hyperacute phase of AMI. HH-FABPc showed high positive value in unstable angina, but it was low in normal coronary patients having chest pain. However, HH-FABPc level in unstable angina and chest pain syndrome was lower than that of AMI. Thus, HH-FABPc may be a valuable indicator for the diagnosis of hyperacute myocardial infarction.

Adult↗
PubMed1993

Plasma and urinary heart-type cytoplasmic fatty acid-binding protein in coronary occlusion and reperfusion induced myocardial injury model.

The leakage of heart-type cytoplasmic fatty acid-binding protein (H-FABPc) from injured myocardial cells has been reported. We have previously proposed that its plasma and urinary levels could be used as an early indicator of myocardial injury and also reflect the severity of myocardial injury. To confirm this hypothesis, the time course of changes of the plasma and urinary H-FABPc was investigated during myocardial injury induced by coronary artery occlusion and reperfusion in dogs. The plasma elimination kinetics and urinary excretion kinetics of H-FABPc were also analysed in dogs which were given a bolus injection of exogenous H-FABPc. The distribution of circulating H-FABPc was determined in mice by whole-body autoradiography using 125I-labelled H-FABPc. In myocardial injury model, plasma and urinary H-FABPc level showed rapid increase after reperfusion. The elimination kinetic study revealed that H-FABPc was mono-exponentially cleared from the circulation. The elimination rate constant (Ke) was 0.0275 +/- 0.0094/min (mean +/- S.D., n = 7) and the disappearance half-time (t1/2) was 27.5 +/- 8.4 min (mean +/- S.D., n = 7). Exogenous H-FABPc appeared in urine soon after administration, with the peak level being at 6.9 +/- 2.0 min (mean +/- S.D., n = 7). Whole-body autoradiography also demonstrated that 125I-H-FABPc accumulated rapidly in the kidneys. This study demonstrated that H-FABPc leaked rapidly from injured myocardium and rapidly appeared in plasma and urine. Infarct size was closely correlated with the calculated H-FABPc release (r = 0.89, r2 = 0.80, P < 0.01, n = 7) and with the amount of the urinary H-FABPc (r = 0.94, r2 = 0.88, P < 0.01, n = 7). These data suggest that measurement of the H-FABPc levels in plasma and urine might be useful for the early detection of myocardial injury and also for the assessment of infarct size.

Animals↗
PubMed1992

Where does an anorthoscopic image appear?

Two experiments were performed to examine where anorthoscopic images appear. In Exp. 1, in which a narrow slit was used, the images were seen as spatially compressed, but also as spatially displaced along each direction of movement even when two patterns were moved simultaneously and in different directions. These results are incompatible with the retinal painting hypothesis. In Exp. 2, in which a wider slit was used, anorthoscopic images appeared immediately after a pattern entered and left the slit. The two images were considered to depend on temporal changes of parts of a pattern passing across left and right edges of the slit, respectively.

Female↗
PubMed1991

Serum and urinary human heart fatty acid-binding protein in acute myocardial infarction.

A competitive enzyme immunoassay (C-EIA) was developed for the measurement of serum and urinary levels of human heart fatty acid-binding protein (hh-FABP), and the appearance and time-course changes of hh-FABP levels were evaluated in patients with acute myocardial infarction (AMI). Control serum and urinary hh-FABP levels, which were determined in 86 serum and 42 urine samples from 86 patients without AMI, were found to range between 0 and 2.8 ng/mL. Serial determinations performed on 11 patients with AMI demonstrated that hh-FABP levels were significantly elevated in the first serum and urine samples obtained within 14 h of the onset of clinical symptoms. Two serum and 2 urine samples obtained only 1.5 h after the onset of symptoms already showed elevated hh-FABP levels, while in the same serum samples the activity of the myocardial-specific isoenzyme of creatine kinase (CK-MB) was still normal. Maximal serum and urinary hh-FABP levels appeared between 5 and 10 h after symptoms developed, and fell sharply towards normal thereafter. The hh-FABP levels in serum and urine both peaked earlier than the elevation of CK-MB activity in serum. The presence of hh-FABP in serum and/or urine seems to be a marker for myocardial damage and could be used as a useful tool for the early diagnosis of AMI.

Adolescent↗
PubMed1991

How does the visual system distinguish between illuminance and reflectance?

The experiments in which the strengths of pattern and of fusion differing in kind from brightness were used as measures indicated that the visual system could distinguish between illuminance and reflectance. From this result and an observation of gray papers by a microscope, it is assumed that luminance has two aspects, one refers to the macroscopic density of photons and another to the proportion of the reflected microscopic areas to the absorbed microscopic areas so that brightness constancy occurs in relation to each of the patterns of the various sizes from a macroscopic pattern visible to the naked eye to a microscopic pattern not visible. It is also mentioned that the strength of fusion is rare but promising as a measure for analyzing brightness.

Attention↗
PubMed1990

Method for representing quantitatively whole properties of visual patterns.

It was assumed that there is a variable, named "strength of fusion," underlying binocular fusion and rivalry. The strength of fusion is the resistance of the fused left- and right-eye patterns to separation. The first task was to obtain a measure of the strength of fusion and the second to examine the strength of fusion as a function of various differences of the patterns. The experiments showed that the angular separation only in the temporalward direction could be used as an appropriate measure of the strength of fusion and its value was maximum when the patterns were identical and decreased as the difference increased. This result supports the assumption about the strength of fusion.

Adult↗
PubMed1987

Fitting index of predominance based on periodicity of strengths of pattern and suppression in binocular rivalry.

The predominance of the strength of pattern over the strength of suppression during binocular rivalry has generally been defined as the percentage of total time of appearance. Is this fit for an index of the predominance? Theoretically, the strengths of pattern and suppression periodically oscillate throughout the observation period. From this assumption, the best fitting indices of predominance were examined. The simplest model of the visual system was one in which the periodicity of the two originates was expressed by a differential equation. Various indices were examined by the solution of its equation so that a power function of the ratio of the time of appearance to that of disappearance was obtained as the most suitable index of the predominance.

Discrimination Learning↗