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Biomedical subjects

S Katayama

Publications and source records attributed to S Katayama.

At least 199 records · Page 11Linked to original sources
PubMed1996

Genetic analysis of the sam mutations, which induce sexual development with no requirement for nutritional starvation in fission yeast.

The cAMP pathway and the Ras pathway are the two major pathways to sexual development in the fission yeast Schizosaccharomyces pombe. To understand the cAMP pathway or the related pathway, we analyzed mutants that display a phenotype similar to cyr1-, that is, hyper-sporulation. Nine mutants termed sam (sporulation abnormal mutant), which are highly inclined to sexual development despite the presence of nitrogen sources, were partially characterized. Cyclic AMP was detected in all nine sam mutant cells, and over-expression of the adenylyl cyclase gene (cyr1) failed to suppress the hyper-sporulation phenotype of these sam mutants, suggesting that none of the sam mutants were likely to be allelic to cyr1. Epistatic tests of sam mutants showed that they were divided into two dominant and seven recessive mutants. Dominants were able to make spores in sam/sam+ heterodiploid cells upon abundant nutrients. Both two dominant mutants bypassed the inability to make spores in ras1 deficient diploid cells, suppressed the deficiency to execute sporulation in byr2 deficient diploid cells, but failed to suppress the byr1 deficiency. Two dominant mutations seem not to occur within the byr2 gene.

Base Sequence↗
PubMed1996

Metformin decreases blood pressure and obesity in OLETF rats via improvement of insulin resistance.

To determine whether improvement of insulin resistance decreases blood pressure as well as obesity, metformin (100 mg/kg/d) or vehicle was administered for 20 weeks to 12-week-old male Otsuka Long-Evans Tokushima Fatty (OLETF) rats (n = 10 each), a newly developed animal model of non-insulin-dependent diabetes mellitus (NIDDM) with mild obesity, hyperinsulinemia, and hypertriglyceridemia. Oral administration of metformin ameliorated glucose intolerance and attenuated the insulin response to glucose loading (2 g/kg, i.p.), as evidenced by a decrease in the area under the curve for glucose and insulin at 24 weeks by 19% and 37%, respectively. At 21 weeks, systolic blood pressure was significantly lower in the metformin group than in controls (130 +/- 1.9 vs. 143 +/- 2.7 mmHg, p < 0.01), despite no difference in body weight. Subsequently, blood pressure tended to be slightly but insignificantly lower in the metformin group, and body weight was significantly lower in the metformin group (532 +/- 9.8 vs. 587 +/- 10.3 g at 31 weeks, p < 0.01). Metformin treatment also lowered the level of serum triglycerides (9.4 +/- 0.6 vs. 13.2 +/- 0.5 mmol/l, p < 0.01) and the plasma norepinephrine concentration (4,222 +/- 373 vs. 7,548 +/- 1,058 pg/ml, p < 0.01). These results suggest that metformin-induced improvement of insulin resistance in obese rats with NIDDM may lower blood pressure, as well as decrease sympathetic activity and reduce body weight.

Aging↗
PubMed1996

Decrease in serum levels of thyroid hormone in patients with coronary heart disease.

The aim of this study was to evaluate the relationship between subclinical hypothyroidism and/or autoimmune thyroid disease and coronary heart disease (CHD). Ninety seven patients diagnosed as having CHD by a coronary angiography (CHD group) and 103 healthy subjects matched for age, sex and body mass index (control group) were included in the study. Thyroid function, thyroid autoantibodies and serum lipid concentrations were measured in the CHD and control groups. The CHD group exhibited significantly decreased serum free T3 (FT3) and free T4 (FT4) levels, and significantly increased serum TSH levels as compared with the control group, indicating a significant decrease in thyroid function in the CHD patients. Serum high density lipoprotein cholesterol (HDL-C) levels were significantly decreased in the CHD group. The incidence of subclinical hypothyroidism and thyroid autoantibodies was similar in both two groups. These observations were also true of women even after those who had diabetes mellitus (DM), hypertension (HT) and a smoking habit were excluded. This was not the case, however, in men without DM, HT, or a smoking habit. Patients with CHD had significantly lower serum levels of HDL-C than the control subjects, regardless of gender (P < 0.01). In the group with CHD, there was no difference between the serum lipid levels in patients with subclinical hypothyroidism and those with normal thyroid function. Female patients with CHD had significantly lower serum levels of thyroid hormone and HDL-C, but their subclinical hypothyroidism or thyroid autoimmunity did not seem to be related to the development of CHD.

Aged↗
PubMed1996

LDL apheresis reduces the susceptibility of LDL to in vitro oxidation in a diabetic patient with hemodialysis treatment.

OBJECTIVE: We studied whether LDL apheresis would alter the susceptibility of LDL to in vitro oxidative modification induced by copper ion in a diabetic patient undergoing hemodialysis treatment. RESEARCH DESIGN AND METHODS: Isolated LDL was dialyzed against phosphate-buffered saline and resuspended at a concentration of 0.3 mg cholesterol mass/ml buffer LDL oxidation was then initiated by addition of 1.66 mumol/l CuSO4, and the formation of conjugated dienes was continuously monitored spectrophotometrically at 234 nm. RESULTS: The duration of the lag phase of LDL obtained after LDL apheresis was markedly longer than that of LDL obtained before LDL apheresis. The propagation rate and the maximum conjugated diene formation of LDL oxidation were not changed after LDL apheresis. CONCLUSIONS: A LDL subfraction that was susceptible to oxidation was removed by LDL apheresis, resulting in reduction of susceptibility of LDL to in vitro oxidation remaining in plasma. LDL apheresis may be of clinical importance for preventing atherosclerotic disease in diabetic patients undergoing hemodialysis.

Aged↗
PubMed1996

Bradykinin may not be involved in improvement of insulin resistance by angiotensin converting enzyme inhibitor.

We have previously demonstrated that captopril ameliorates glucose intolerance by partially preventing the reduction in postprandial skeletal muscle blood flow. The present study was designed to clarify the mechanism by which ACE inhibitors affect glucose metabolism in fructose (FRU)-fed Wistar rats with hypertension, glucose intolerance and hyperinsulinemia. Eight-week-old male rats (n = 51) were divided into six groups. Controls were given a normal chow, while fructose-rich (55%) chow was administered to the remainder for eight weeks. The different groups were administered alacepril (ALA, 30 mg/kg/day) with or without a continuous infusion of Hoe 140, a kinin B2 receptor antagonist (150 micrograms/kg/day), Hoe 140 alone or TCV-116 (1 mg/kg/day), an angiotensin II receptor antagonist, alone. After measuring the body weight and systolic blood pressure (BP), steady-state plasma glucose (SSPG) levels were determined. FRU significantly increased BP from 141 mmHg in controls to 156 mmHg. ALA with or without Hoe 140 decreased BP to 124 mmHg or 117 mmHg, respectively, but Hoe 140 alone did not affect BP. TCV-116 also decreased BP to 116 mmHg. The SSPG levels increased from 7.58 mM in controls to 8.98 mM in FRU-fed rats. This was lowered with both ALA and TCV-116. Hoe 140 alone, however, did not affect SSPG levels. Hoe 140 did not show any effects on ALA-induced improvement of SSPG. These results suggest that the improvement in glucose tolerance observed with ACE inhibitors is not due to the kinins, and angiotensin II receptor antagonists also improve insulin sensitivity.

Angiotensin Receptor Antagonists↗
PubMed1996

[Tactile extinction following the cerebral sinus thrombosis. A study using event-related potentials].

We reported a 46-year-old woman in whom cerebral sinus thrombosis manifested itself in headache and weakness while she was on an oral estrogen preparation. The neurological examinations revealed monoparesis of the right upper extremity, hyperactive right deep tendon reflex and disturbance of the joint sense, stereognostic sense, two-point discrimination and skin writing sense in the right upper extremity, in addition to tactile extinction. Brain CT showed empty triangle sign. MRI revealed infarction near the left postcentral gyrus and thrombosis of right sigmoid sinus. In the MRA study, there was low signal intensity in the posterior portion of the superior sagittal sinus and right transverse sinus. Short latency SEP in upper extremity showed that the central conduction time was normal, while the amplitude of wave components after N20 was reduced on the right side. Both palms were given bilateral or unilateral pressure stimuli. When event-related potentials (ERP) were evoked, using bilateral stimuli as a rare target, and left unilateral stimuli as a non-target, the P 300 latency was prolonged to 450 msec but was restored to normal with the improvement of tactile extinction. These results seem to suggest that the tactile extinction is ascribable to a disturbance of recognition at the higher brain function level and that ERP can be a useful objective yardstick in the evaluation of extinction phenomenon.

Event-Related Potentials, P300↗
PubMed1996

[The impaired glucose tolerance in the pathogenesis of dyslipidemia].

It is well known that hyperlipidemia is often present in patient with impaired glucose tolerance, obesity and/or hypertension. All of these are risk factors for coronary artery disease (CAD). The coexistence of these risk factors markedly increase the likelihood of CAD. Recently, it has been reported that the impaired glucose tolerance and insulin resistence are associated with the increased proinsulin, which is linked to the risk of CAD. We review that the impaired glucose tolerance is an important factor causing dyslipidemia. The characteristic of dyslipidemia associated with the impaired glucose tolerance include hypertriglyceridemia, high level of VLDL and low level of HDL cholesterol. They also associate with accumulation of remnant lipoproteins and appearance of small dense LDL. In addition, we pointed out that the increased number of risk factors is associated with elevated insulin and proinsulin level.

Coronary Disease↗
PubMed1996

Scleroderma-polymyositis overlap syndrome associated with anti-Ku antibody and rimmed vacuole formation.

Scleroderma-polymyositis overlap syndrome is strongly associated with certain autoantibodies, such as anti-PM-Scl antibody and anti-Ku antibody. We describe a case of scleroderma-polymyositis overlap syndrome associated with anti-Ku antibody, which revealed rimmed vacuole formation in addition to intranuclear and intracytoplasmic filamentous inclusions in muscle biopsy specimens.

Adult↗
PubMed1996

[The mechanism of controlling regional cerebral blood flow in patients with localization-related epilepsy].

INTRODUCTION: Hypoperfusion around the seizure foci has been reported in interictal CBF studies of partial epilepsy. Hypoperfusion may reflect some interictal pathophysiology characteristic of epilepsy, but the mechanism remains to be elucidated. In order to elucidate the controlling system of rCBF in patients with CPS (complex partial seizure), we measured by positron emission tomography rCBF and CO2 vasoreactivity performing a hyperventilatory task, and made comparisons between the affected and contralateral sides of the temporal lobes in CPS patients and the temporal lobe of normal volunteers. We also measured PaCO2, pH, PaO2 and respiratory rate at rest to elucidate the CBF maintaining system. SUBJECTS: 15 volunteers and 12 medically controlled patients with CPS were examined. The affected side of the brain of the patients was determined by dominance of EEG paroxysm. METHOD: For measuring rCBF, the Shimadzu HEADTOME-IV system (8mm FWHM) and H2(15)O (740-1480 [MBq]/scan) bolus injection method were employed. First a rest scan, then a hyperventilatory task scan was performed, at 20 min. intervals between each scan. During the rest scans, the subjects were required to close their eyes, which were covered through the transmission scan and all the other scans. They were monitered with EEG to insure that they were not asleep. Room lights were dimmed, room sounds were kept to a minimum and noises were damped with earplugs. During the hyperventilatory tasks, the subjects were asked to inspire deeply at a rate of 15/min. for 4.5 min. from 3 min. before the scan up to the end of the 1.5 min. scan, and monitored with a respiratory band around the abdomen. Arterial blood gas pressures (PaCO2, pH and PaO2) were also measured with a blood gas analyzer (Radio Meter ABL 330) at the beginning and at the end of the scans. [HCO3-] was calculated on the formula of Henderson-Hasselbalch. Vascular response to PaCO2 change: VrCO2 was defined as follows: VrCO2 = 100 x (CBFh-CBFr)/CBFr/(PaCO2h-PaCO2r) the subscripts h: hyperventilatory r: resting conditions. RESULTS: Blood gasses, rCBF and corrected-rCBF at rest: In the patients, PaCO2 (mmHg) = 46.11 +/- 2.32, pH = 7.374 +/- 0.020, [HCO3-] (mEq/ml) = 25.98 +/- 1.15, CBF (ml/100g/min) = 45.51 +/- 9.33, corrected-CBF (ml/100g/min) = 40.06 +/- 7.27. In the volunteers, PaCO2 = 40. 67 +/- 2.37, pH = 7.400 +/- 0.021, [HCO3-] = 24.36 +/- 1.66, CBF = 48.76 +/- 8.54, corrected-CBF = 48.02 +/- 9.04. PaCO2 and [HCO3-] in the patients were significantly higher than those in the volunteers. pH and corrected-CBF were significantly lower than those in the volunteers. CBF showed no difference. VrCO2 in the temporal lobe: In the affected side of the patients, VrCO2 = 1.976 +/- 0.54. In the contralateral side of the patients, VrCO2 = 2.145 +/- 0.667. In the temporal lobe of the volunteers, VrCO2 = 2.557 +/- 0.898. In both sides of the temporal lobe of the patients, VrCO2 was significantly lower than those in the volunteers. COMMENTS: The effect of anticonvulsant drugs and the suppressive mechanism around the foci are supposed to reduce CBF of CPS patients. We suppose another mechanism, which is vasoconstriction. A significant difference was noted in CO2-vasoreactivity in the temporal lobe between patients and volunteers. Also no difference was noted in rCBF in the temporal lobe between the volunteers and the patients, when the arteries were maximally constricted with the HIV-task. These two results suggest that vasoconstrictive mechanism may be among the factors for the hypoperfusion seen in the temporal lobe of the patients. In patients, PaCO2, [H+], [HCO3-] were significantly higher compared with the volunteers, which suggests the mechanism of respiratory acidosis. Owing to this hypercapnia, global CBF in the patients is maintained in compensation for the hyperfusion and vasoconstriction seen around the foci. CO2 acts as an anticonvulsant and also reduces glucose metabolites which accumulate around the foci.

Adult↗
PubMed1996

[A case of Dyke-Davidoff-Masson syndrome with total hemiatrophy].

We reported a 39-year-old man with Dyke-Davidoff-Masson syndrome presenting with total hemiatrophy. The patient had a muscle defect in the left occipital lesion at birth and left hemiatrophy including the face in his infancy. The present illness consists of atrophy of the left face, trunk and extremities, a muscle defect accompanied with scleroderma of the left dorsal cervical lesion, bilateral pes cavus, cleft palate, left hemiparesis, including facial palsy and diminished superficial sensation of the left side of the body. Decrease in right cranial volume and slight elevation of the right temporal pyramid and the superior border of the orbit were seen on the X-ray study of the head. Atrophy of the right cerebrum and cerebral peduncle was seen on magnetic resonance imaging. These findings suggest that hemiatrophy of the brain was responsible for total hemiatrophy of the body in this patient. The etiology of cerebral hemiatrophy is not known. There is only a report of Dyke-Davidoff-Masson syndrome accompanied with total hemiatrophy.

Adult↗
PubMed1996

[The role of nicotinic receptor in memory impairment: a study using event-related potentials and midlatency responses].

To evaluate the efficacy of chronic nicotine administration in dementia, electrical field distributions of event-related potentials (ERPs) and midlatency response (MLR) were recorded and were analyzed in terms of time and space. The study was carried out on 22 normal individuals and 17 patients with dementia (vascular dementia, Alzheimer disease and Parkinson disease). Nicotine was delivered transdermally from a nicotine patch (22.5 to 52 mg/day) for 2 or 4 weeks. Dementing patients showed abnormal ERPs in latency, amplitude and electrical field on the scalp. Decreased amplitude and electrical field abnormality of P1 in MLR was also seen in some patients with dementia. These abnormal ERPs and MLR of the patients improved after administration of nicotine especially in P300 latency of ERPs and P1 amplitude of MLR. These data suggest that nicotine administration might be useful as a cognitive enhancer in memory impairment.

Dementia↗
PubMed1995

Characterization of a specific monoclonal antibody 9F5-3a and the development of assay system for oxidized HDL.

We obtained a monoclonal antibody 9F5-3a against oxidative low-density lipoprotein (LDL) modified with CuSO4 and established a sandwich ELISA for detection of oxidized high-density lipoprotein (oxHDL). The 9F5-3a was reacted strongly with oxHDL and to a lesser degree with oxLDL and LDL. In contrast, little or no reactivity was found with HDL. When the generation of oxHDL was limited by the addition of alpha-tocopherol and catalase, reactivity to 9F5-3a was reduced. Incubation of oxHDL with excess lyso-phosphatidylcholine (lyso-PC) also reduced immunoreactivity, but not by only lyso-PC. These results suggested that the epitope is possibly associated with oxHDL-linked lyso-PC induced mainly by the hydroxyl radical.

Animals↗
PubMed1995

[A case report of aldosterone-producing adrenocortical adenoma complicated with chronic renal failure associated with nephrocalcinosis: review of APAs complicated with chronic renal failure].

A 57-year-old man was admitted to our hospital because of dyspnea due to congestive heart failure caused by hypertensive heart disease in September, 1992. Twenty years ago, he was diagnosed to be hypertensive, and in 1980, he was diagnosed to at our hospital to have primary aldosteronism (PA) due to a right aldosterone-producing adrenocortical adenoma (APA). There were no hypertensive vascular complications at that time. He refused surgical removal, and anti-hypertensive drugs including spironolactone were administered. However, his drug compliance was very inaccurate. On this recent admission, left ventricular hypertrophy associated with impaired contractivity, hypertensive retinal change and mild protein uria were noted, but no hematuria was detected. His renal function was impaired (Ccr: 15.2ml/min). An abdominal CT scan showed a typical right APA, bilateral renal atrophy and fine granular calcification at renal medulla, even though he had no hypercalcemia and hypercalciuria. In addition, multiple cerebral infarction was demonstrated by a brain CT scan, along with coronary artery stenoses at the right coronary artery and left circumflex branch by coronary angiography and bilateral multiple renal artery stenoses by renal angiography. Right adrenalectomy and renal biopsy were performed. Histological examinations revealed a yellow tan-colored APA, many sclerotic glomerulus, and severely hyarinized renal arterioles. After adrenalectomy, blood pressure was not normalized but was controlled easily by hypotensive agents. Impaired renal function was not improved and deteriorated slightly but did not get worse there after. Since 1959, including ours, 22 cases of APAs complicated with chronic renal failure were reported in Japan. In conclusion, surgical removal should be recommended for APA, even if the patient's condition is complicated with chronic renal failure.

Adrenal Gland Neoplasms↗
PubMed1995

Molecular cloning and sequencing of the hcs gene, which encodes 3-hydroxy-3-methylglutaryl coenzyme A synthase of Schizosaccharomyces pombe.

We have cloned and sequenced the hcs gene, which is thought to encode a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase consisting of 447 amino acids, from the fission yeast Schizosaccharomyces pombe. The predicted amino acid sequence of the hcs product of S. pombe has homology with the HMG-CoA synthase of rat (47.8%), chicken (49.2%), hamster (47.1%) and human cells (46.9%). One of the hcs genes was replaced with a marker gene in the diploid cell. No viable hcs-disrupted haploid was isolated after tetrad dissection, suggesting that the hcs gene is essential for growth. However the hcs-defective mutant could be grown on a medium containing 5 mg/ml mevalonate. These results strongly support that the hcs gene encodes HMG-CoA synthase and S. pombe contains a single copy of the hcs gene.

Amino Acid Sequence↗
PubMed1995

Effect of troglitazone (CS-045) and bezafibrate on glucose tolerance, liver glycogen synthase activity, and beta-oxidation in fructose-fed rats.

To clarify the relationship between lipid and glucose metabolism abnormalities in fructose-fed rats, we examined whether an improvement of insulin sensitivity by troglitazone (CS-045) or a decrease in plasma lipids by bezafibrate affects the relationship between serum levels of lipid and glucose. In addition, we also examined changes in liver glycogen metabolism and beta-oxidation in fructose-fed rats. Troglitazone ameliorated fasting hyperlipidemia, hyperglycemia, and hyperinsulinemia. In addition, it augmented glycogen synthase activity by 53%, and decreased the mitochondrial palmitic acid beta-oxidation rate and ketone body production rate by 27% and 55%, respectively. However, hyperglycemia and liver glycogen synthase activity were not improved by bezafibrate treatment despite a marked reduction of serum triglyceride (TG) levels resulting from a 1.76-fold increase in mitochondrial oxidation and a 2.04-fold increase in hepatic ketone body production. These results suggest that abnormalities in glucose and lipid metabolism in fructose-fed rats, which are ameliorated by troglitazone, may be closely linked to reduced glycogen synthase activity in the liver.

Animals↗
PubMed1995

Projection of cardiovascular afferents to the lateral nodulus-uvula of the cerebellum in rabbits.

Vagal and aortic afferent projections to the nodulus and uvula of the cerebellar vermis were examined in anesthetized and paralysed rabbits. Electrical stimulations of vagal and aortic nerves at a frequency of 1/s produced field potentials in the lateral cortical region of the contralateral nodulus-uvula with a latency of 6.5-19 ms. These potentials were negative in the molecular layer and positive in the granular layer. At a higher stimulation rate (30/s), these potentials were reduced by 60-65% of the control value. These results indicate that the lateral cortical region of the nodulus-uvula receives contralateral vagal and aortic afferent signals via climbing fibers. Electrical stimulation of vagal nerves also produced field potentials in the lateral region of the ipsilateral nodulus-uvula with a latency of 6-10.5 ms. Their laminal profile was characteristic of mossy fiber responses. At a higher stimulation rate (30/s), the reduction of these potentials was only 35%. Thus the lateral nodulus-uvula also receives the ipsilateral vagal afferent signals via mossy fibers. Following injection of horseradish peroxidase into the small areas of the lateral nodulus, labeled cells were found in bilateral intercalatus nucleus, prepositus hypogrossal nucleus, Roller nucleus, medial fascicullus longitudinalis, and medial and lateral vestibular nuclei. These nuclei may contain precerebellar neurons in the pathway from the vagal nerve to the lateral nodulus-uvula via mossy fibers.

Animals↗