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Biomedical subjects

K Goto

Publications and source records attributed to K Goto.

At least 433 records · Page 24Linked to original sources
PubMed1995

[Multivariate autoregressive analysis of carotid artery blood flow waveform in a newborn with multicystic encephalomalacia].

We analyzed the carotid artery blood flow waveform (CABFW) through multivariate autoregressive analysis in a case with multicystic encephalomalacia (MCE) after neonatal asphyxia and compared the result with those of 35 healthy newborns. The total power of CABFW was at the -2 SD level of the value for 35 healthy newborns, and the power, % power, bio-informing amounts and damping time of component 3 (damping frequency 11.15 Hz) were less than -2 SD of the values in 35 healthy newborns. The Pulsatility Index (PI) of anterior cerebral artery (ACA) was high (0.76). These results suggest that cerebral blood flow decreases because of cerebral vasoconstriction in MCE after neonatal asphyxia.

Brain Diseases↗
PubMed1995

[Seroprevalence of HTLV-I in various ocular diseases in central Japan].

Recently human T-cell lymphotropic virus type I (HTLV-I) has been shown to be responsible for a kind of uveitis in southwestern Japan, where HTLV-I infection is highly endemic. To investigate further the association of HTLV-I with various ocular diseases, we studied HTLV-I seroprevalence in 1,350 patients in central Japan, where HTLV-I infection is not endemic. Of 1,350 patients with various ocular diseases, 40 (2.96%) were seropositive for the retrovirus. There was no statistically significant difference in HTLV-I seroprevalence among various ocular diseases. Four of 9 (44.4%) seropositive cases from southwestern Japan developed HTLV-I associated uveitis (HAU), whereas only 2 of 26 (7.7%) seropositive cases from central Japan developed HAU. The difference was statistically significant (p < 0.05). This suggests that the incidence of HAU could be influenced by environmental or hereditary factors. On the other hand, 3 of 7 (42.9%) patients with episcleritis showed HTLV-I infection.

Adolescent↗
PubMed1995

Prolongation of kidney graft survival by cyclophosphamide-induced tolerance in rats.

In this study, we have extended a cyclophosphamide (CP)-induced tolerance system to kidney transplantation in rats to examine whether or not we can overcome fully allogeneic (major histocompatibility complex plus minor histocompatibility) antigen barriers in organ transplantation. In the recipient Lewis (LEW, RT1(1)) rats that were primed intravenously with 4 x 10(8) spleen cells plus 2 x 10(8) bone marrow cells from Brown-Norway (BN, RT1n) rats and treated intraperitoneally with 100 mg./kg. of cyclophosphamide (CP) 2 days later, the survival of kidney allografts, but not skin allografts, from BN was prolonged as compared with that in the untreated LEW rats. Some of the kidney allografts survived for more than 100 days without further immunosuppressants. The tolerant state induced was tolerogen specific, and the suppression of tissue damage of the grafted kidney in such tolerant rats was also confirmed by the histopathological findings of the grafted kidney. These results indicate that considerable levels of tolerance can be induced, at least in organ transplantation, across fully allogeneic antigen barriers in rats by a CP-induced tolerance system. We believe that the present study is the first step in applying our CP-induced tolerance system using skin grafting in the murine model to clinical organ transplantation.

Animals↗
PubMed1995

Cloning and mapping of a very short (10-kb) EcoRI fragment associated with facioscapulohumeral muscular dystrophy (FSHD).

Facioscapulohumeral muscular dystrophy (FSHD) is a dominantly inherited muscular disorder and the gene for FSHD has been mapped to chromosome 4q35. Recently, the DNA rearrangements associated with the disease were found in the EcoRI fragment detected by the probes p13E-11 and pFR-1, and deletions of the 3.3-kb KpnI repeat units within the EcoRI fragment are thought to cause the disease. In this study, we cloned the FSHD-associated EcoRI fragments (the shortest fragments identified to date: 10 kb) from 2 severely affected patients (unrelated). Restriction enzyme maps of the genomic fragments in the 2 patients revealed that the 10 kb fragments were identical and contained only one 3.3-kb KpnI repeat unit. These results suggest that deletions of the 3.3-kb KpnI repeat units are likely to associate with FSHD, and that the 10 kb fragments may provide a means of understanding the molecular details involved at the site of the chromosomal rearrangements in FSHD.

Adolescent↗
PubMed1995

Inflammatory response in facioscapulohumeral muscular dystrophy (FSHD): immunocytochemical and genetic analyses.

To investigate the nature of the inflammatory response in facioscapulohumeral muscular dystrophy (FSHD), we analyzed mononuclear cells in muscle sections obtained from 18 FSHD patients and 8 controls. Monoclonal antibodies reactive for T cells, T cell subsets, B cells, and NK cells were used for cell typing. Macrophages were identified by acid phosphatase reaction. The localization of perforin, granzyme A, MHC-I and -II, dystrophin, and alpha-actinin antigens was also examined. We found that all FSHD patients, both familiar and sporadic cases, had greater amounts of mononuclear cellular infiltrates in muscle than controls, in whose specimens only few extra vascular mononuclear cells were counted. Seventy-two percent (13 of 18) of the patients had more than 50 inflammatory mononuclear cells per 1000 muscle fibers, and 33% (6 of 18) patients had numerous inflammatory cells exceeding 600 per 1000 muscle fibers (1835 +/- 482 SE). Nonnecrotic fibers invaded by mononuclear cells with either T8+, perforin+, or granzyme A+ were not observed in FSHD, while a few degenerating fibers were superficially invaded by T cells and macrophages. Occasional T cells were observed moving through the blood vessel wall. The increased number of necrotic fibers was paralleled by an increased number of inflammatory cells (r = 0.783, P = 0.0001). Genetic analysis, using the probes p13E-11, pFR-1, D4S139, and D4S163, was done in 6 patients (3 familiar, 3 sporadic) who had numerous inflammatory infiltrates. These 6 patients had small (< 28 kb) EcoRI fragments associated with the disease, and the disease was linked to 4q35. These results suggest that, in chromosome 4-linked FSHD: (1) inflammatory changes in muscle are a common histological feature; (2) mononuclear cellular infiltrates may enhance muscle fiber damage; but (3) T-cell-mediated cytotoxicity directed against muscle fibers is unlikely. We speculate that the immune effector mechanism in FSHD is different from that in previously reported inflammatory myopathies and Duchenne muscular dystrophy.

Adolescent↗
PubMed1995

Characterization of a tandemly repeated 3.3-kb KpnI unit in the facioscapulohumeral muscular dystrophy (FSHD) gene region on chromosome 4q35.

A 3.3-kb KpnI repeat unit within the tandem repeat locus (D4Z4) and its upstream 2.5-kb HincII/KpnI fragment of the facioscapulohumeral muscular dystrophy (FSHD) gene region at 4q35-qter were sequenced and characterized. The 3.3-kb KpnI unit was 3303 bp in length and contained two homeodomain sequences, one LSau-like sequence, and several microsatellites. The GC content in the 3.3-kb unit was very high (73%), while it was only 35% in the nonrepeated region of the 2.5-kb fragment. We identified 99% homologous sequences (918 bp) in the 3' end of the 3.3- and 2.5-kb fragments. These findings suggested that the repeated sequences at the D4Z4 start from 918 bp upstream to the first KpnI site.

Base Sequence↗
PubMed1995

[Relative size of the ventricle to the hemisphere in the neonatal MRI].

Using a software program for measuring surface area, we quantified the relative size of four parts of the lateral ventricles, including the body, the trigone, the anterior horn and the occipital horn, compared to the hemispheres in the axial plane of magnetic resonance imaging (MRI) in neonates. In 44 neonates without any neurological disorders from 26 to 41 weeks of gestational age (GA), MRI was performed between 12 and 124 postnatal days. The mean of the relative size of the ventricle compared to the hemisphere (RSVH) among the subjects showed a significant left-right asymmetry that was observed only in the occipital horn. However, in the body, the anterior horn and the occipital horn, the percentage of neonates with a larger left RSVH compared to the right RSVH was significantly higher than the percentage of neonates with a larger right RSVH compared to the left RSVH. The RSVH of the body and the occipital horn increased according to the number of postnatal days and decreased according to GA. Measuring RSVH was useful in assessing the size of the ventricle in the axial plane of neonatal MRI. It clarified the fact that normative asymmetry, GA of subject, and the number of postnatal days should be considered in assessing the size of ventricle.

Cerebral Ventricles↗
PubMed1995

[Status epilepticus in two patients with Sotos syndrome].

Two patients with Sotos syndrome showed very intractable and prolonged status epilepticus, resulting in poor outcomes. Clinical seizures and EEG abnormalities in patients with Sotos syndrome are sometimes noted, but they are usually mild. These two patients showed hypoplasia of corpus callosum on MRI. We considered the mechanism of intractable seizures, and emphasized the importance of careful management for their seizures and EEG abnormalities.

Brain Diseases↗
PubMed1995

[The effect of subconjunctival injection of endothelin-1 on intraocular pressure in the rabbit].

Endothelin-1 (ET-1) is a potent vasoconstrictive peptide produced in part by vascular endothelial cells. In order to investigate its effects on the episcleral vascular system and intraocular pressure (IOP), we injected ET-1 (3, 10, 30, 100, 300, 1,000 pmol) into the subconjunctival space of rabbits and measured IOP with a manometer. Injection of a dose higher than 10 pmol caused a transient increase of IOP. Mean maximum elevation rate of IOP for each dose of ET-1 was 14.9 +/- 0.9%, (mean +/- standard error) 43.5% +/- 9.5%, 40.8 +/- 7.5%, 46.9 +/- 9.8%, and 84.1 +/- 22.6. Next, we injected 1,000 pmol into the subconjunctival space, and continuously measured IOP and ocular pulse pressure with a manometer. IOP increased rapidly after ET-1 injection. Maximal increase of IOP was observed at 22.7 +/- 9.2 min after ET-1 injection, and IOP decreased after the peak. The ocular pulse pressure increased with IOP elevation and decreased with the IOP reduction. We speculated that the transient elevation of IOP was caused by increase of aqueous outflow resistance, and the decrease of IOP was caused by decrease of aqueous outflow resistance and decrease of blood flow in the ciliary body and the choroid. This strongly suggests that subconjunctival injection of ET-1 could have a large effect on the episcleral vascular system, aqueous outflow, and blood flow in the ciliary body and the choroid.

Animals↗
PubMed1995

[Removal of infected pacemaker leads in the elderly under extracorporeal circulation: two case reports and review of Japanese literature].

Two elder cases in whom infected pacemaker leads were removed under extracorporeal circulation (ECC) are reported. The leads could not be with drawn without direct sharp dissection under ECC because they had become firmly encased with fibrous tissue within the right ventricle. Postoperative courses were uneventful and neither of these patients has experienced recurrent infection to date. Removal with ECC seems to be a safe and effective procedure even in the elderly, provided that cardiac function is good.

Age Factors↗
PubMed1995

Endothelin-1-induced downregulation of ETB receptor mRNA: participation of cAMP.

In this study we examined the participation of cAMP formation in endothelin-1 (ET-1)-induced downregulation of ETB receptor mRNA in ROS 17/2 rat osteosarcoma cells. Dibutyryl cAMP induced downregulation of ETB receptor mRNA in a time-dependent manner. ET-1 induced production of inositol phosphates and an increase of cAMP level in ROS 17/2 cells. A stimulatory effect on cAMP level was also observed when A23187 plus PMA was added to the cells. The increase in cAMP level induced either by ET-1 or by A23187 plus PMA was inhibited by indomethacin. The downregulation of ETB receptor mRNA induced by ET-1 was significantly inhibited by indomethacin. These results suggest that the ET-1-induced downregulation of ETB receptor mRNA in ROS 17/2 cells may be partly mediated through the increase in cAMP level secondary to the activation of the phosphoinositide hydrolysis/Ca2+ transduction cascade.

Animals↗
PubMed1995

Increased endothelin-1 binding sites in the cardiac membranes in rats with chronic heart failure.

The effects of experimental chronic heart failure (CHF) on the density and affinity for endothelin-1 (ET-1) binding was studied in the rat heart. Because it has been reported that ET-1 binding sites on cultured cardiocytes are downregulated by pretreatment with ET-1, we also studied the plasma concentrations of ET-1 in rats with CHF. Three weeks after ligation of the left coronary artery, rats developed chronic heart failure (CHF rats). The plasma concentrations of ET-1, as measured by a sandwich-enzyme immunoassay, were significantly higher in CHF rats than in sham-operated rats [4.80 +/- 0.33 vs. 0.91 +/- 0.11 (mean +/- SEM) pg/ml; p < 0.01]. [125I]ET-1 binding experiments on rat cardiac membranes revealed that the binding site density (Bmax) was significantly higher in the CHF rats than in the sham-operated rats (243.0 +/- 20.0 vs. 154.8 +/- 17.4 fmol/mg protein; p < 0.05), whereas the values for the dissociation constant (Kd) were not different between the two groups (28.7 +/- 7.0 vs. 29.8 +/- 1.9 pM). Therefore, in the CHF rats, although plasma concentrations of ET-1 were elevated, the density of myocardial ET receptors was increased. Because ET-1 has potent inotropic and hypertrophic effects on cardiac myocytes, it is suggested that the effects of endogenous ET-1 in the heart are different between the CHF rats and the sham-operated rats.

Animals↗
PubMed1995

Altered production of endothelin-1 in the hypertrophied rat heart.

Although endothelin-1 (ET-1) has been shown to have potent hypertrophic effects in cultured cardiac myocytes, there is no evidence that the production of ET-1 is altered in the hypertrophied heart in vivo. We investigated mRNA and peptide levels of ET-1 in the rat heart hypertrophied due to pressure or volume overload. One week after surgery of abdominal aortic banding (AB) or aortic valve regurgitation (AR; the aortic valve was destroyed by a polyethylene catheter), the rats were sacrificed. Control sham-operated rats were also studied (AB-sham and AR-sham). The left ventricular (LV) weight to body weight ratio was significantly higher in AB rats than in AB-sham rats. It was also significantly higher in AR rats than in AR-sham rats. Therefore, AB rats and AR rats developed LV hypertrophy due to pressure and volume overload, respectively. The expression of ET-1 mRNA in the LV was markedly higher in AB rats than in AB-sham rats. The peptide level of ET-1 was also significantly higher in the LV of AB rats than in that of AB-sham rats. However, the expression of ET-1 mRNA in the LV of AR rats was similar to that of AR-sham rats. The present findings suggest that the production of ET-1 in the heart differs between pressure and volume overload-induced hypertrophy in rats.

Animals↗
PubMed1995

Possible sources of endothelin-1 in damaged rat brain.

We investigated the sources of endothelin-1 (ET-1) detected in the damaged brain tissue of rats after cold injury. ET-1 in the injured sites was increased 1-5 days after the injury. Physiologic observations revealed that breakdown of the blood-brain barrier occurred and that plasma-derived albumin exuded into the brain parenchyma after cold injury. Radiolabeled ET-1, which was injected into the left cardiac ventricle, was detected in the tissue at the injury site, and ET-1-like immunoreactivity was observed in the brain capillaries in the damaged tissues. TGF-beta 1, which is a tissue regeneration factor, potently induced the expression of ET-1 mRNA in cultured astrocytes. These results suggest that ET-1 is produced through a variety of ways in the damaged brain.

Animals↗
PubMed1995

Plasma endothelin-1 levels after exercise in patients with congenital heart disease.

We have previously reported that plasma endothelin-1 (ET-1) levels were significantly increased after exercise in healthy athletes. In the present study, venous plasma ET-1 levels were measured to investigate whether the role of ET-1 during exercise differs between healthy athletes and patients with congenital heart disease. Seven patients (mean age 13 years) performed symptom-limited treadmill exercise (Bruce protocol). All patients were in class I of the NYHA functional classification. The mean end-exercise O2 utilization was 32 ml/min/kg (166% of ventilatory threshold). Blood sampling was carried out in the seated position. The plasma ET-1 level was 1.21 pg/ml before exercise and did not alter immediately after or 30 min after exercise. The plasma level of norepinephrine was markedly elevated immediately after exercise and returned to the basal level 30 min after exercise. The present study demonstrated that exercise failed to alter plasma ET-1 levels in patients with congenital heart disease.

Adolescent↗
PubMed1995

[Genetic analysis of facioscapulohumeral muscular dystrophy (FSHD)].

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant muscular disorder which is characterized by progressive weakness and atrophy of the facial, shoulder-girdle and upper arm muscles, and occasional subsequent pelvic-girdle and lower limb involvement. The gene responsible for FSHD has been localized to chromosome 4q35-qter, although a few 4q-unlinked families are known. To examine FSHD-associated DNA rearrangements in the Japanese population, we performed Southern blot analysis of the genomic DNA, using the p13E-11 and pFR-1 probes. Most of the Japanese FSHD patients (> 95%) had specific smaller (< 28 kb) EcoRI fragments which cosegregated with the disease. Restriction enzyme maps of the polymorphic EcoRI fragment detected by the probes have revealed that the disease occurs due to a deletion of the integral numbers of the 3.3kb KpnI tandemly repeated fragments (D4Z4) which contain homeobox-like sequences. Indeed, we cloned and characterized the FSHD-associated EcoRI fragments (the shortest fragment identified to date: 10kb) from two severely affected patients (unrelated). The 10kb fragment were identical and contained only one 3.3kb KpnI repeat unit. Although we still do not know whether truncation deletion of the D4Z4 region could produce FSHD directly or indirectly (position effect), we now beginning to understand FSHD. In the next step, FSHD gene products (mRNA and protein) responsible for the disease should be investigated.

Chromosomes, Human, Pair 4↗
PubMed1995

Hepatic cytokeratin changes in obstructive jaundice: before and after biliary drainage.

We investigated the changes in hepatic cytokeratins in obstructive jaundice by immunohistochemistry. The results can be summarized as follows: 1) In accordance with the progression of the jaundice, the lobular and cellular distribution of cytokeratin reactivity in hepatocytes expanded. 2) Cytokeratin reactivity in obstructive jaundice was improved by removal of the bile duct obstruction (decompression), but this decompressive effect deteriorated in the case of prolonged jaundice. 3) It is suggested that the specific lobular and cellular distribution and/or the changes in cytokeratin aggregation might be of value in determining the stage and in predicting the prognosis of obstructive jaundice.

Animals↗