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Biomedical subjects

K Goto

Publications and source records attributed to K Goto.

At least 379 records · Page 21Linked to original sources
PubMed1996

Diet-induced hypercholesterolemia increases endothelin-1 release by aortic endothelial cells.

Our previous studies demonstrated the morphological heterogeneity of endothelial cells (ECs) and the emergence of large multinucleated ECs in human and animal atherosclerotic lesions. To investigate the functional alteration of ECs in diet-induced atherosclerosis, immunoreactive endothelin-1 (irET-1) release by ECs of the rabbit aorta was correlated with scanning electron microscopy. Rabbits were fed a cholesterol diet for 12 weeks: by scanning electron microscopy, the area of ECs in the aorta increased in the hypercholesterolemic (HC) group as atherosclerosis progressed. Cultured ECs of the HC group released significantly more irET-1 than ECs of the control. The plasma irET-1 level was also elevated in the HC group. The results obtained suggest that accelerated secretion of ET-1 by ECs contributes to the development of atherosclerotic vascular lesions.

Animals↗
PubMed1996

Possible effects of placental leucine aminopeptidase on the regulation of brain-gut hormones in the fetoplacental unit.

The hydrolysis of somatostatin by human placental subcellular fractions and pregnancy sera was studied in the presence of selective inhibitors and the antibody against pregnancy serum oxytocinase (placental leucine aminopeptidase; EC3.4.11.3) by measuring the released amino acids by high-performance liquid chromatography. We also studied the degradation of other brain-gut hormones, such as glucagon, growth hormone, growth hormone releasing factor, and insulin, in the human placenta and found that the human placenta degrades somatostatin, glucagon, and growth hormone releasing factor, but not insulin and growth hormone. The degradation velocity of somatostatin was ten times greater than that of growth hormone releasing factor in placental microsomal fractions. Our data suggest that the stimulatory control by growth hormone releasing factor is dominant in the fetal growth hormone secretion. Our data also identified the somatostatin-degrading protease in human placenta using placental leucine aminopeptidase. It is known that the mean somatostatin levels in the umbilical artery are about 2.5-fold higher than those in the umbilical vein. Our data on somatostatin levels in umbilical artery and vein of intrauterine growth retardation human fetuses showed that the ratio umbilical artery/vein is around 1. Since insulin is known to be the primary hormone regulating the ratio of fetal growth, our data suggest that the degradation of somatostatin in the placenta is decreased and that elongation of somatostatin effects may result in the inhibition of insulin secretion in the intrauterine growth retardation fetus.

Amino Acid Sequence↗
PubMed1996

Carotid-cavernous sinus fistula and aneurysmal rupture associated with fibromuscular dysplasia. A case report.

A patient with carotid-cavernous sinus fistula associated with fibromuscular dysplasia, who died from rupture of an associated splenic aneurysm despite successful treatment of the CCF, is reported. When multivessel involvement with aneurysmal dilatation is observed in patients with fibromuscular dysplasia, the possibility of aneurysm ruptures in any of the arteries should be considered.

Adult↗
PubMed1996

Synthesis and structure-activity relationships of novel phenylcyanoguanidine derivatives as potassium channel openers.

3,5-Di-substituted phenylcyanoguanidine derivatives with halogen, cyano and/or nitro groups at the 3- and 5-positions of the benzene ring exhibited very strong smooth muscle relaxation activity in vitro, as compared to pinacidil. Among them, N-(3-chloro-5-cyanophenyl)-N'-cyano-N" -tert-pentylguanidine (5s) showed 27-fold more potent activity than pinacidil, and exhibited a stronger and more lasting antihypertensive effect than pinacidil by oral administration to spontaneously hypertensive rats. We propose a new pharmacophore model in which the essential factors for binding to the potassium channel are an NH and a bulky alkyl group.

Animals↗
PubMed1996

Synthesis and biological activity of the metabolites of diethyl 4-[(4-bromo-2-cyanophenyl)carbamoyl]benzylphosphonate (NO-1886).

Five metabolites of diethyl 4-[(4-bromo-2-cyanophenyl)carbamoyl]benzylphosphonate (NO-1886) (1) were synthesized to confirm their proposed structures. The metabolites (2-6) were found to be identical with the synthesized compounds. These metabolites were orally administered to Triton WR-1339-induced hypertriglyceridemic rats, and the plasma levels of triglycerides were measured to estimate lipoprotein lipase activity. All the metabolites showed lower potency than NO-1886.

Animals↗
PubMed1996

Endothelin ETA and ETB receptors mediate endothelin-1-induced apamin-sensitive relaxation in the guinea pig ileum.

Endothelin (ET) receptors involved in ET-1-induced responses of the longitudinal muscle of the isolated guinea pig ileum were studied. ET-1 caused concentration-dependent contractions, while ET-3 and selective ETB-receptor agonists, IRL1620 and sarafotoxin 6c (S6c), showed little or no effect. The ET-1-induced contractions were antagonized by BQ-123, an ETA-receptor antagonist, or PD142893, an ETA/ETB-receptor antagonist, indicating that the contraction is mediated by the ETA receptor. In preparations precontracted with carbachol, ET-1 elicited relaxations at lower concentrations and contractions at higher concentrations. ET-3, IRL1620 and S6c caused relaxations. These relaxations were little affected by BQ-123, but greatly antagonized by PD142893. The ET-1-induced relaxations were slightly affected by BQ-788, an ETB-receptor antagonist, but were markedly inhibited by the combination of BQ-788 and BQ-123. In ETB receptor-desensitized preparations, ET-1-induced relaxations were antagonized by BQ-123, whereas ET-3, S6c and IRL1620 showed no response. All these relaxations were abolished by apamin. These results indicate that ETA and ETB receptors mediate relaxation of the ileal smooth muscle through activation of apamin-sensitive K+ channels.

Animals↗
PubMed1996

Molecular pharmacology and pathophysiological significance of endothelin.

Since the discovery of the most potent vasoconstrictor peptide, endothelin, in 1988, explosive investigations have rapidly clarified much of the basic pharmacological, biochemical and molecular biological features of endothelin, including the presence and structure of isopeptides and their genes (endothelin-1, -2 and -3), regulation of gene expression, intracellular processing, specific endothelin converting enzyme (ECE), receptor subtypes (ETA and ETB), intracellular signal transduction following receptor activation, etc. ECE was recently cloned, and its structure was shown to be a single transmembrane protein with a short intracellular N-terminal and a long extracellular C-terminal that contains the catalytic domain and numerous N-glycosylation sites. In addition to acute contractile or secretory actions, endothelin has been shown to exert long-term proliferative actions on many cell types. In this case, intracellular signal transduction appears to converge to activation of mitogen-activated protein kinase. As a recent dramatic advance, a number of non-peptide and orally active receptor antagonists have been developed. They, as well as current peptide antagonists, markedly accelerated the pace of investigations into the true pathophysiological roles of endogenous endothelin-1 in mature animals; e.g., hypertension, pulmonary hypertension, acute renal failure, cerebral vasospasm, vascular thickening, cardiac hypertrophy, chronic heart failure, etc. Thus, the interference with the endothelin pathway by either ECE-inhibition or receptor blockade may provide an exciting prospect for the development of novel therapeutic drugs.

Animals↗
PubMed1996

Cephalometric comparison of craniofacial morphology between primary bone grafted and nongrafted complete unilateral cleft lip and palate adults.

The effect of primary bone grafts on craniofacial growth was evaluated in adult patients with complete unilateral cleft lip and palate (UCLP). The subjects were 18 UCLP patients with primary bone grafts and a control group of 36 UCLP patients without bone grafts. The former received primary transplantation of autogenous rib bone simultaneously with primary cheiloplasty by the same surgeon between 1963 and 1969. Frontal and lateral cephalograms taken after 16 years of age were traced. Skeletal landmarks were identified on them, and their x,y-coordinates were digitized. The effects of gender and/or primary bone graft on the craniofacial morphology were tested by ANOVA using 21 angles, 8 breadths, 13 distances, and 2 ratios. Nasal cavity breadth was wider in the primary bone grafted group. However, the anterior maxilla in that group was more upward and retruded than that in the nongrafted group. The primary bone grafted group was divided into two subgroups based on the overjet of the incisors: group N = normal overjet; group C = anterior cross-bite. There was no difference in the maxilla between groups N and C. However, the mandible in group C was more anterior and superior than in group N. In conclusion, primary bone graft may impede maxillary horizontal and vertical growth to a certain degree, and severe anterior cross-bite in primary bone grafted subjects may be brought about by mandibular closure.

Adult↗
PubMed1996

Metabolism of diethyl 4-[(4-bromo-2-cyanophenyl)-carbamoyl]benzylphosphonate in the rat.

1. The metabolism of diethyl 4-[(4-bromo-2-cyanophenyl)carbamoyl]benzylphosphonate (NO-1886), an antilipidaemic agent, was evaluated in the rat. 2. 14C-NO-1886 was dosed orally to rats (3 mg/kg) and within 24 h after dosing, 27.9 +/- 2.1 and 63.5 +/- 4.2% of the administered radioactivity was recovered from urine and faeces respectively. 3. The metabolite M-2 was isolated from the urine and faeces, and two other metabolites, M-3 and M-5, were isolated from the urine. Two of them were identified as ethyl 4-[(4-bromo-2-cyanophenyl)carbamoyl]benzylphosphonate (M-2) and 4-[(diethoxy-phosphoryl)methyl)]benzoic acid (M-3), and the other one was considered to be 2-amino-5-bromo-3-cyanobenzene sulphate (M-5) by ms and nmr spectrometry. 4. The major metabolic pathway of NO-1886 was found to be mono-hydrolysis of the diethyl phosphonate. It was also considered that M-5 may have been formed in vivo via 2-amino-5-bromo-benzonitrile (M-1) and 2-amino-5-bromo-3-hydroxybenzonitrile (M-4).

Animals↗
PubMed1996

Treatment of scalp arteriovenous malformation.

We report seven patients with scalp arteriovenous malformations, including two patients with lesions > 10 cm in diameter, who were successfully treated. The principal complaint of each patient was a deforming mass. Each of four patients had a history of blunt traumatic injury. The lesions, each consisting of the nidus, feeders, and draining veins, evolved in all patients. The nidus consisted of fistulae, which exhibited various angioarchitectures as revealed by angiography. A hemangiomatous component was histologically recognized in one patient. In five patients, in whom the lesions were relatively small and whose nidi included only large fistulae, the malformations were remedied by surgical intervention alone or were cured with embolization alone using liquid adhesives. In the two patients with lesions > 10 cm, the nidi consisted of numerous large fistulae and plexiform fistulae in one patient and plexiform fistulae and a hemangiomatous component in the other patient. These patients were treated with a combination of transarterial embolization and surgical intervention. Preoperative embolization greatly reduced blood loss during resection. Total excision and scalp reconstruction using a soft tissue expander were performed in both patients. The cosmetic results were excellent in all of the patients, and no recurrence has been recognized during the follow-up period, which ranges from 31 to 99 months. The treatment of scalp arteriovenous malformations should strive to improve deforming features and to attain a permanent cure. Because each nidus includes a variety of anomalous angioarchitectural features, there should be different means and a combination of treatments for each patient. Embolization alone could be adequate treatment in relatively small lesions, the nidi of which consist only of several large fistulae. For malformations with more extensive, large fistulae or with anomalous components other than large fistulae, a combined endovascular and surgical approach and scalp reconstruction seems to be the best treatment.

Adult↗
PubMed1996

Detection of Clostridium piliforme by enzymatic assay of amplified cDNA segment in microtitration plates.

We developed a simple enzymatic assay system using reverse transcription-polymerase chain reaction products in a microtitration plate to detect Clostridium piliforme in tissue specimens. The reverse transcription-polymerase chain reaction was performed with a biotin-labeled primer directed in a highly conserved area of the C. piliforme 16S rRNA gene. The amplified cDNA was hybridized to an alkaline phosphatase-labeled DNA probe in a microtube, and the mixture was applied to a microtitration well precoated with streptavidin. Then hybridization signals in the microtitration plate were visualized by reaction with substrate for the alkaline phosphatase. When an optical density > 0.200 at 405 nm was considered a positive result, we found that the system could detect the RNA from as few as 10 organisms. The system was also capable of detecting organisms from the liver, mesenteric lymph nodes, and ileum of experimentally infected mice. In the ileum the C. piliforme gene was detected from 1 to 21 days after infection. This result suggests that the intestinal epithelium is one of the sites of persistent infection. We conclude that this enzymatic assay system of reverse transcription-polymerase chain reaction products is simple, rapid, and convenient for the detection of C. piliforme.

Animals↗
PubMed1996

[Pathogenesis and treatments of glucose intolerance with liver cirrhosis in men--lessons from the clinical cases of Fukuoka City Hospital, Department of Internal Medicine, Fukuoka, Japan].

More than 30% of the end stage liver cirrhosis was complicated by the impared glucose tolerance, in some of which insulin supplements may be required to control the blood glucose level. However, there are many unsolved issues on the cause and cares of hyperglycemia in cirrhotic men. Here, we presented a case of liver cirrhosis and hepatocellular caricnoma complicated by the severe glucose intolerance, and summarized our recent insulin therapy on the glucose intolerance of the decompensated liver cirrhosis in Fukuoka City Hospital, Department of Internal Medicine.

Carcinoma, Hepatocellular↗
PubMed1996

[A 46-year-old man with right-side dominant parkinsonism, who suffered a sudden death].

We report a 46-year-old man with right side dominant parkinsonism who died suddenly two years after the onset. The patient was well until the age of 42 years in January of 1993, when he noted an onset of difficulty in using his right hand and then the right leg. Soon after he noted nocturnal urinary incontinence. In January of 1994, a local doctor prescribed 200 mg of levodopa with benserazide and 5 mg of bromocriptine. The patient noted some improvement. Cystometry revealed 300 ml of residual urine. He visited our clinic on 24th of December, 1996. He was alert and oriented. BP was 106/60. He showed masked face and small voice. He walked in stopped posture dragging his feet; retropulsion was noted. He showed moderate bradykinesia and rigidity more on the right side. No resting tremor or cerebellar ataxia was noted. Ankle jerks were somewhat exaggerated but no Babinski sign was noted. He continued to show residual urine, but orthostatic hypotension was absent. Routine laboratory examination was unremarkable, however, his cranial MRI showed atrophy of the left putamen and a T2-linear high signal intensity lesion along the lateral border of the left putamen. On January 15, 1997, he ate certain amount of rice cake and drank alcohol. After coming back home and while changing his clothes, he suddenly complained of chest discomfort and lost consciousness. He was pronounced dead in the afternoon. The patient was discussed in a neurological CPC. Opinions were divided between Parkinson's disease and striatonigral degeneration. The chief discussed arrived at a conclusion that the patient had Parkinson's disease, because he responded to levodopa to some extent and except for nocturnal incontinence he did not have wide spread autonomic failure. Postmortem examination revealed marked loss of neurons and extensive gliosis in the left putamen. The right putamen did not show such changes. The substantia nigra showed gliosis in the lateral part on both side, however, neuronal loss was not apparent. The locus coeruleus was well retained. No Lewy bodies were found. The pontine nucleus and the cerebellum were intact. However, glial cytoplasmic inclusions were seen in oligodendrocytes of the cerebral white matter and the pontine base. The heart and lungs were intact and the cause of the sudden death could not be determined. The pathologic diagnosis is striatonigral degeneration. Such a marked asymmetry of the pathologic change is quite unusual. Probably, the death in the early stage of the disease is the reason for this asymmetry.

Brain↗
PubMed1996

[Early recovery from locked-in syndrome due to brain infarction in a young patient with hypoplasia of bilateral vertebral arteries and a persistence of primitive trigeminal artery].

A 36-year-old man was admitted to Kanto Chuo Hospital because of hearing loss and dysphagia. On admission physical and neurological findings revealed obesity, hypertension, nystagmus, right hearing loss, dysarthria, and dysphagia. Routine laboratory findings disclosed leukocytosis, liver dysfunction, hypercholesterolemia, proteinuria, and glucosuria. Immunological, coagulopathic, and endocrinological findings, electrocardiogram, echocardiogram, and brain CT scan were unremarkable. He was diagnosed as brainstem infarction, and then conservative therapies were begun. Seven hours after admission, he suddenly fell into coma and apneutic state, requiring artificial ventilation. The next day he was fully conscious, but could'nt make any voluntary movements except for vertical eye movements, suggesting locked-in syndrome (LIS). Brain MRI showed infarction of pons, medulla oblongata, and right cerebellum. Cerebral angiography revealed hypoplasia of bilateral vertebral arteries, a persistence of right primitive trigeminal artery (PTA), and retrograde blood flow of basilar artery from the PTA. Then he made a rapid recovery, and on 80th day he was discharged only with right hearing disturbance and mild left cerebellar sign. We speculated that hypoplasia of the bilateral vertebral arteries caused the brain infarction, and that back flow of the basilar artery from the PTA, in part, contributed to the early recovery from the LIS.

Adult↗