Biomedical subjects
Publications and source records attributed to N Hashimoto.
Two patients presented with vertebral arteriovenous fistulae following unintentional puncture of the vertebral artery. A percutaneous transvenous approach was used in both cases and the fistula was successfully embolised with microcoils. A complete cure was achieved in both patients.
Percutaneous transluminal angioplasty (PTA) of the vertebral artery was performed with an autoperfusion balloon catheter in five patients. There were no complications in the form of embolic episodes or neurological deficits due to brain ischaemia during inflation. In critical cases with insufficient collateral circulation during temporary occlusion, the use of an autoperfusion balloon catheter may expand the indications for PTA in patients with ischaemic cerebrovascular disease.
The incidence and causes of peri-operative haemodynamic complications in adult Moyamoya disease were examined by reviewing 55 surgically treated adult patients. Ninety-nine craniotomies were performed in these patients, and eight peri-operative complications (four infarctions, two haemorrhagic infarctions and two reversible ischaemic neurological deficits without a new lesion) were seen. All of the eight haemodynamic complications arose in the initially affected hemispheres regardless of the side of operation. Some nonsurgical haemodynamic risk factors, i.e., hypercapnia, hypocapnia and hypotension/hypovolaemia, were noted in all of the eight cases, although the statistical analysis could not clarify the relevance of such factors to peri-operative complications. Surgical factors which might be responsible for the complications were noted in three cases. Sparing vital collateral vessels and minimum brain retraction as well as avoidance of non-surgical haemodynamic risk factors are considered to be essential to prevent peri-operative haemodynamic brain damage in adult Moyamoya disease.
To determine whether an antibody against hepatic sinusoidal endothelial cells was present in sera of patients with autoimmune hepatitis (AIH) type 1, we measured the serum IgG bound to the glutaraldehyde-fixed cultured rat sinusoidal endothelial cells by enzyme-linked immunosorbent assay. IgG bound to the cells was detected significantly more in patients with autoimmune hepatitis type 1 (97.1%) than in those with primary biliary cirrhosis (13.0%), chronic hepatitis C (5.9%) or B (7.9%), or healthy controls (0%). IgG-F(ab')2 fragments from autoimmune hepatitis patients also bound to the cells, and this binding was observed after absorption of the fragments with rat hepatoma cells, but not after absorption with bovine carotid endothelial cells. Culture of sinusoidal endothelial cells in the presence of IgG from AIH patients significantly reduced the number of viable attached cells. In conclusion, anti-sinusoidal endothelial cell antibody occurred in the sera from patients with autoimmune hepatitis type 1.
The clinical effect of combination therapy with high doses of intravenous nicardipine and intra-arterial infusion of papaverine on symptomatic vasospasm after subarachnoid haemorrhage (SAH) was analysed retrospectively. In 66 of 122 patients who underwent early aneurysm surgery between 1990 and 1993, the intracranial haemodynamics were documented by transcranial Doppler (TCD) ultrasonography. 33 of these 66 patients received high dose nicardipine intravenously (Group I); the other 33 patients were not treated with calcium antagonists (Group II). Symptomatic vasospasm occurred in 6 Group I patients (18%) and in 13 (39%) in Group II patients. All 19 symptomatic patients received an intra-arterial infusion of papaverine; 15 patients (79%) responded well to this therapy and the symptoms were reversed quickly. Although the mean flow velocity (MFV) was not different between the two groups, it was reduced significantly after papverine infusion. Our retrospective analysis suggests that symptomatic vasospasm can be treated effectively with the combination of intravenous high dose nicardipine and intra-arterial infusion of papaverine, and that the correct timing of the infusions is crucial.
The uptake of octanoate in rat brain and its metabolism were investigated by means of intravenously injecting [1-11C] or [1-14C]octanoate as a tracer. The radioactivity in the cerebrum was increased by an injection of [1-11C]octanoate, and reached its peak level (0.33% ID/g) in about 2 to 5 min, and then decreased slowly. The cerebrum-to-blood ratio of the radioactivity increased with time over a period of 30 min. At 30 sec, [1-11C]octanoate that remained unchanged in the cerebrum accounted for only 8% of the total radioactivity, in spite of there being about 90% in the blood. By means of an injection of [1-14C]octanoate, more than 70% of the total radioactivity in the cerebrum was found to be attributable to radiolabeled glutamate and glutamine at each time point measured between 30 sec and 30 min. The results show that [1-11C]octanoate enters rat brain easily and is trapped in the cerebrum, probably in the form of glutamate and glutamine, and the usefulness of [1-11C]octanoate as a radiopharmaceutical for studying brain fatty acid metabolism by positron emission tomography is therefore suggested.
Sixty-five avian Chlamydia psittaci isolates collected worldwide, including 27 previously characterized reference strains, were analysed by restriction mapping of the major outer membrane protein gene (omp1) obtained after DNA amplification by PCR. They were compared to 2 ruminant isolates, a feline pneumonitis and a guinea pig inclusion conjunctivitis (GPIC) isolate. According to their omp1 restriction patterns, avian strains were heterogeneous in that they exhibited 6 and 4 distinct patterns using AluI and MboII restriction enzymes, respectively, thus defining 7 groups. However, 84% of the studied strains belonged to groups 1 to 4, which share a specific fragment triplet of 411, 282 and 102 base pairs in their AluI digestion patterns. Comparisons with serological classifications showed a strict correlation and allowed further intraserovar differentiation. Furthermore, this classification based upon a single gene (omp1) roughly correlated with the data obtained by RFLP of native DNA and DNA/DNA hybridization studies. There was no host or geographic specificity in the pattern exhibited by these strains. The ruminant, feline pneumonitis and GPIC C. psittaci isolates were clearly distinguished from each other and the avian strains. Moreover, this method was clearly able to identify dubiously designated strains as well as mixtures of isolates within a single sample. In conclusion, this PCR approach based upon omp1 restriction mapping enables the differentiation of avian C. psittaci isolates and can be proposed as a taxonomic and epidemiologic tool.
PURPOSE: Elucidating the transport characteristics of S-1090, a new orally active cephalosporin in rat small intestinal brush-border membranes. METHODS: A rapid filtration technique. RESULTS: The uptake of S-1090 was stimulated by an inwardly directed H(+)-gradient, but did not show overshooting uptake. To investigate the transport system, the inhibitory and countertransport effects of various compounds on S-1090 uptake were examined. Although the dipeptides and tripeptides composed of amino acids with aliphatic side chains did not inhibit the uptake of S-1090, those having histidine, proline or tryptophan as the N-terminal amino acid showed an inhibitory effect. Among the oral cephems tested, ceftibuten showed marked inhibition, while cefaclor and cephalexin had no inhibitory effect. Countertransport effects on S-1090 uptake were observed only when the vesicles were preloaded with histidyl peptides such as His-Gly or His-Ala, while other compounds which exhibited inhibition had no countertransport effect. CONCLUSIONS: Based on the above results, there seems to be heterogeneity (multiplicity) in the oligopeptide transport system which may depend on the structure of the N-terminal amino acid. S-1090 may be dominantly transported via a system that recognizes peptides having histidine as the N-terminal amino acid.
A polymerase chain reaction (PCR) for the detection of hantavirus genome was established and applied to analyze the mode of infection of Hantaan virus in adult ICR mice. The cDNA for the S genome segment of Hantaan virus was reverse-transcribed from the total RNA of organs of the infected mice. The sequence in the S genome segment of Hantaan virus was successfully amplified by reverse transcriptase (RT)-PCR followed by nested PCR. In 5-week-old ICR mice inoculated intraperitoneally with Hantaan virus, strain 76-118 (1.3 x 10(5) FFU/mouse), the virus was detected in clots and lungs from 3 to 10 days post-inoculation (p.i.) by nested PCR and virus-isolation techniques. No virus was detected in any specimens collected on 1 day and after 28 days p.i., and in spleens and brains through the observation period by both methods. The antibody which was measured by indirect immunofluorescence antibody assay (IFA) appeared at 7 days p.i. and the geometric mean titer was elevated to its maximum level of 1:203 at 10 days p.i., maintaining the same level until 35 days p.i. These results suggest that adult mice are transiently infected with Hantaan virus.
The objective of this study was to assess the influence of parental obesity on the physical constitution of preschool children. A total of 3187 children aged between 1-6 years and their parents were studied. A child whose per cent obesity (%OB; per cent overweight for age, height and sex) was greater than 15%, and a parent whose body mass index (BMI; kg/m2) was greater than the 95th percentile were defined to be obese (27.40 and 25.97 for a father and a mother, respectively). We found that the incidence of obesity in children with obese fathers (11.5%) was significantly higher than in those with non-obese fathers (6.2%), and a similar difference was obtained between children with obese mothers (14.5%) and with non-obese mothers (6.2%), respectively. The incidence of obesity in children was 6.0% if both parents were non-obese; this incidence rose to 22.7% if one parent was obese, and to 30.8% if both were obese. The %OB of children was more markedly correlated with the mothers' BMI (r = 0.219) than the fathers' BMI (r = 0.165). The %OB of children correlated significantly with fathers' BMI, but only from the age of 3-6 years, whereas mothers' BMI correlated from the age of 1-6 years. We conclude that parental obesity was of significance in determining the development of juvenile obesity even in the preschool period.
Growth hormone (GH) appears to affect the timing of puberty in children. The effects of GH on puberty may be related to direct GH action on ovarian function or may be mediated by IGF-I. To determine the likelihood that GH has direct effects on ovarian function, we compared the ability of GH and IGF-I to increase luteinized granulosa cell steroidogenesis in the absence and presence of gonadotropins. Cells were obtained from women undergoing in vitro fertilization for tubal disorders or male factor infertility and were placed in static culture. GH alone failed to alter progesterone or estradiol accumulation in the medium of cultured luteinized granulosa cells. IGF-I produced no increase in progesterone accumulation but increased estradiol accumulation 5.6-fold compared with cells treated with vehicle. The combination of GH and FSH produced an 0.83-fold increase in estradiol accumulation, whereas the combination of IGF-I and FSH resulted in a 2.9-fold increase in estradiol accumulation above FSH alone. Thus the direct effects of GH on granulosa cell steroid synthesis are modest compared with those of IGF-I. If GH has an effect on ovarian development at puberty, it is likely to be mediated by a GH-induced increase in circulating IGF-I.
Mutations in the insulin receptor gene may lead to insulin resistance and diabetes mellitus in some patients. We have studied an insulin-resistant patient with leprechaunism. Insulin binding to the patient's fibroblasts was markedly decreased. Determination of the nucleotide sequence of the patient's insulin receptor gene revealed heterozygosity for a 2-basepair deletion in exon 15. If the premessenger ribonucleic acid (pre-mRNA) is spliced normally, it causes a replacement of codon 970 in the beta-subunit with a premature chain termination codon, thereby deleting most of the intracellular domain of the receptor. The mRNA transcribed from the allele with a 2-base-pair deletion is likely to be unstable because mRNA transcripts from this allele could not be detected by complementary DNA sequencing. Northern blot analysis showed that the patient's insulin receptor mRNA was decreased by 90% compared with that of a control subject, thus suggesting that the patient is a compound heterozygote for two mutations that decrease levels of insulin receptor mRNA. This deletion mutation in exon 15 seems to be a de novo mutation, because it was not detected in either parent. Investigation of the inheritance of a silent sequence polymorphism in exon 17 provided that the deletion occurred in the maternal allele. Furthermore, linkage analysis suggests that the second mutation is derived from the patient's father, although we could not directly identify it by sequencing the coding region of the insulin receptor gene. Therefore, it is possible that this mutation is present in a regulatory domain of the insulin receptor gene, acting in cis-dominant fashion to reduce the levels of insulin receptor mRNA. Analyses of the hypervariable region in the myoglobin and pMCT118 loci were consistent with the assumption that the father and mother studied here are indeed the biological parents of the diseased patient. We hereby conclude that the patient is a compound heterozygote for two mutant alleles, both of which are responsible for the reduced levels of insulin receptor mRNA and insulin binding.
The effects of intrathecal infusion of brain-derived neurotrophic factor (BDNF) were examined in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonian model in monkeys. Nine Japanese monkeys were divided randomly into three groups, an untreated control (n = 3), a BDNF group (n = 3), and a non-BDNF group (n = 3). Animals in the BDNF group received continuous intrathecal infusion of 10 ml of cell culture medium containing 10 micrograms of BDNF protein; the non-BDNF group received intrathecal infusion of the same culture medium without BDNF. To induce parkinsonian syndromes, a total of 1 mg/kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine was administered intravenously to each monkey in both the BDNF and non-BDNF groups. The neurological signs in the monkeys were monitored for 2 weeks and were scored according to the monkey parkinsonism rating scale; histological changes in the substantia nigra were evaluated after the 2-week observation period. The BDNF-treated animals remained asymptomatic during the 1st week and showed mild parkinsonism during the 2nd week, whereas the non-BDNF group showed typical parkinsonian syndrome during the 1st week, with deterioration in the 2nd week. Histological damage in the substantia nigra correlated well with the clinical features. Severe neuronal cell loss in the substantia nigra was observed in animals with severe parkinsonism (those in the non-BDNF group), whereas significantly less damage was observed in this region in the BDNF group.(ABSTRACT TRUNCATED AT 250 WORDS)
An autopsy case of dermatomyositis with rapidly progressive interstitial pneumonia is reported. a 48-year-old woman was admitted because of facial edematous erythema and muscular weakness. A diagnosis of dermatomyositis was made because of typical erythema and myogenic pattern of EMG, although serum creatine kinase was within normal range. The chest X-ray film showed that interstitial pneumonia was complicated. She was treated with prednisolone of 60 mg/day. Although erythema and althralgia was improved remarkably, interstitial pneumonia was progressed unfavorably. Therefore pulse therapy with methylprednisolone was administered twice, but failed to respond. After that interstitial pneumonia was progressed rapidly, she was died of respiratory failure. The autopsy findings detected that a degeneration and necrosis of striated muscular fibers in whole body, that a mixed findings of usual interstitial pneumonia and diffuse alveolar damage in the lung. Vasculitis and fiblinous pleuritis was also found in the lung. Malignancy was not detected.
A dural arteriovenous malformation (AVM) of the posterior fossa can produce persistent tinnitus, convulsions, and dementia. Successful therapeutic embolization may result in a complete cure, but in some cases, patients do not respond to the treatment. The authors report a patient with a dural AVM of the posterior fossa that did not respond to repeated intravascular treatments, but resulted in an arteriovenous shunt in the scalp around the ventriculoperitoneal shunt system. Although several hypotheses have been proposed on the pathogenesis of dural AVMs, the underlying mechanisms remain unknown. The rare complication we encountered may shed some light on the pathogenesis of dural AVMs.
We conducted field surveys of indigenous rodent species in Hokkaido, Japan from 1980 to 1993. Serum samples were collected from 663 rodents, including Clethrionomys rufocanus, Apodemus speciosus, A. argenteus, and C. rutilus. Antibody to hantavirus was determined by the protein G antibody assay. Positive C. rufocanus were detected in seven of eight collection sites, but no antibody was detected in the remaining rodent species. To reveal the serotype of the circulating virus in C. rufocanus, antibody titers to Hantaan, Seoul, Puumala, and Prospect Hill viruses were compared by means of the focus reduction neutralization test. The titers in positive sera were extremely high to the Sotkamo strain of Puumala virus. Results were confirmed by the reverse transcriptase-polymerase chain reaction, and suggested that Puumala-related viruses are in circulation among C. rufocanus populations in Hokkaido.
In the present study, repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy was performed in patients with unresectable tumors of the liver. Of 36 patients, 16 had primary liver tumors (13 hepatocellular carcinomas and 3 cholangiocellular carcinomas), while 20 had metastatic tumors (7 gastric carcinomas, 10 colon carcinomas, 2 pancreatic carcinomas, and 1 gastric carcinoid). A significantly better survival outcome was found in those with intra-arterial infusion chemotherapy and those without cirrhosis. In the HCC cases, those with the therapy tended to show a better survival as compared with the natural history. Remarkable tumor regression was found in four (67%) of six patients with metastases of gastric cancer.
Collagen disease is systemic autoimmune disease and consists of a lot of diseases with each clinical entity. for exact diagnosis, it is important to choose essential laboratory tests for the patient suspected of collagen disease in daily primary medical care. A guideline for the use of clinical laboratory tests for patients with collagen disease was proposed by the Japan Society of Clinical Pathology. This guideline was discussed repeatedly by subcommittee members of "the uses of clinical laboratory tests in daily primary medical care" and published on September of 1990. When the clinicians are suspected of the collagen disease from detailed history taking and physical examination, they must precisely interpret results of the essential laboratory tests. Urinalysis, hematology, ESR and CRP and Biochemistry show characteristic findings in the collagen disease, respectively. If further suspicion of the collagen disease is intensive, the clinicians proceed with the primary screening tests for collagen disease; rheumatoid factor, ANF, anti DNA antibody, LE test, STS and CH50. Finally, specific tests for each collagen disease are carried out to define the diagnosis; e.g. LE cell, anti-Sm antibody, IC, Coombs test and biopsy of kidney for SLE. This paper is presented on the intention of the guideline of clinical laboratory tests for the collagen disease and its issues. As it passed 4 years after published, this guideline should be more discussed and revised.