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Biomedical subjects

T Nishimura

Publications and source records attributed to T Nishimura.

At least 163 records · Page 9Linked to original sources
PubMed1991

Cloning and structural analysis of cDNA and the gene for mouse transcription factor UBF.

The gene and protein structure of the mouse UBF (mUBF), a transcription factor for mouse ribosomal RNA gene, have been determined by cDNA and genomic clones. The unique mUBF gene consists of 21 exons spanning over 13 kb. Two mRNAs coding for mUBF1 and mUBF2 having 765 a.a. and 728 a.a., respectively, are produced by an alternative splicing of exon 8. It specifies 37 amino acids constituting a part of the regions homologous to high mobility group proteins (HMG box 2). A human UBF (hUBF) cDNA obtained by polymerase chain reaction also indicates the presence of two kinds of mRNAs, the shorter form lacking the same region as mUBF2. Comparison of the cDNAs from hUBF and mUBF revealed an unusual conservation of nucleotide sequence in the 3'-terminal non-coding region. We examined the relative amounts of expression of mUBF1 and mUBF2. The eight tissues studied contained both molecular species, although mUBF2 was the predominant form of UBF. The mRNA of mUBF1 was expressed one half of the mUBF2 in quiescent mouse fibroblasts but reached the same amount in growing state.

Amino Acid Sequence↗
PubMed1991

Binding of calpain fragments to calpastatin.

Their cDNA-derived amino acid sequences predict that the 80-kDa subunits of the micromolar and millimolar Ca(2+)-requiring forms of the Ca(2+)-dependent proteinase (mu- and m-calpain, respectively) each consist of four domains and that the 28-kDa subunit common to both mu- and m-calpain consists of two domains. The calpains were allowed to autolyze to completion, and the autolysis products were separated and were characterized by using gel permeation chromatography, calpastatin affinity chromatography, and sequence analysis. Three major fragments were obtained after autolysis of either calpain. The largest fragment (34 kDa for mu-calpain, 35 kDa for m-calpain) contains all of domain II, the catalytic domain, plus part of domain I of the 80-kDa subunit of mu- or m-calpain. This fragment does not bind to calpastatin, a competitive inhibitor of the calpains, and has no proteolytic activity in either the absence or presence of Ca2+. The second major fragment (21 kDa for mu-calpain and 22 kDa for m-calpain) contains domain IV, the calmodulin-like domain, plus approximately 50 amino acids from domain III of the 80-kDa subunit of mu- or m-calpain. The third major fragment (18 kDa) contains domain VI, the calmodulin-like domain of the 28-kDa subunit. The second and third major fragments bind to a calpastatin affinity column in the presence of Ca2+ and are eluted with EDTA. The second and third fragments are noncovalently bound, so the 80- and 28-kDa subunits of the intact calpain molecules are noncovalently bound at domains IV and VI. After separation in 1 M NaSCN, the 28-kDa subunit binds completely to calpastatin, approximately 30-40% of the 80-kDa subunit of mu-calpain binds to calpastatin, and the 80-kDa subunit of m-calpain does not bind to calpastatin in the presence of 1 mM Ca2+.

Amino Acid Sequence↗
PubMed1991

Buffy coat from families of Alzheimer's disease patients produces intracytoplasmic neurofilament accumulation in hamster brain.

Buffy coat of three members from a family with Alzheimer's disease was inoculated into hamster brains. Eighteen months after the inoculation, all experimental animals were sacrificed for the neuropathological study. Hematoxylin-eosin staining showed no gross vacuolar degeneration, or neuronal loss in the cortex. The spongiform degeneration was minimum. Immunostaining with antibodies against neurofilament 200 kDa subunit protein revealed massive immuno-positive intracytoplasmic inclusion bodies within neurons of the brainstem nuclei. By electron microscopy, the intracytoplasmic inclusion body was shown to be composed of proliferated 10 nm neurofilaments. The intra-cytoplasmic neurofilament proliferation was observed with the hamsters inoculated with the buffy coat from Alzheimer's disease patients as well as an apparently normal member of the family.

Alzheimer Disease↗
PubMed1991

Low glucose-1, 6-bisphosphate and high fructose-2, 6-bisphosphate concentrations in muscles of patients with glycogenosis types VII and V.

The level of glucose-1, 6-bisphosphate, a potent allosteric activator of phosphofructokinase, was markedly decreased in muscles of patients with glycogenosis type VII (muscle phosphofructokinase deficiency) and type V (muscle phosphorylase deficiency). Glucose-1-phosphate kinase activity in muscle was virtually absent in a patient with glycogenosis type VII, whereas it was normal in a patient with type V glycogenosis. Glucose-1-phosphate level was increased in type VII glycogenosis, whereas it was decreased in type V glycogenosis. Another activator of phosphofructokinase, fructose-2, 6-bisphosphate was increased in muscles of patients with both types of glycogenosis although it was much higher in type VII than in type V. This finding may be partly related to the difference of fructose-6-phosphate concentrations. The results suggest that phosphofructokinase would contribute to the major glucose-1-phosphate kinase activity in normal human muscle and would also form a kind of self-activating system.

Fructosediphosphates↗
PubMed1991

[Hepatic parenchymal changes after intraarterial administration of lipiodol: an animal experiment].

The effect of Lipiodol (LPD) on the hepatic parenchyma bearing VX2 tumor was investigated in 12 rabbits. In these rabbits Adriamycin (ADM) soluble Urografin and LPD were injected through the hepatic artery. As the control another 12 rabbits bearing VX2 tumor which were intraarterially injected with ADM solution in saline were used. Liver function tests revealed significantly higher values of serum transaminases in the LPD group than in the control group. Histologically in the LPD group, hepatocellular degeneration was observed and the severity was at its peak 3 days after injection whereas control animals preserved almost normal structure. The degeneration of the tumor-bearing lobe was more severe than that of the tumor-free lobe. This study showed the histologically and functionally demonstrable adverse effects of LPD.

Animals↗
PubMed1991

Assembly, disassembly, and exchange of glial fibrillary acidic protein.

The kinetics and dynamics of glial fibrillary acidic protein (GFAP) assembly was explored by a fluorescence energy transfer assay method. Purified GFAP was stoichiometrically labeled at a single cysteine residue with fluorescein-maleimide. Soluble labeled GFAP in a low ionic strength buffer was assembled into 10 nm filaments by rapidly increasing the ionic strength, and the kinetics of GFAP assembly was monitored by the reduction in fluorescence due to self-quenching of fluorescein. The extent of fluorescence quench correlated with both the formation of 10 nm filament morphology and the amount of protein pelleted at 12,000g. The assembly of GFAP is critically dependent upon both protein and magnesium ion concentration, and at the critical concentration for GFAP assembly is approximately 40 micrograms/ml. Disassembly of GFAP filaments was also observed as a relief of fluorescence quenching after dilution of labeled GFAP filaments. When labeled GFAP filaments were mixed with an excess of unlabeled filaments, a rapid increase of fluorescence was observed, which is due to an exchange of subunits between labeled and unlabeled GFAP filaments. These results indicate that GFAP filaments are dynamic structures and that a small pool of kinetically active unassembled GFAP subunits are in a dynamic equilibrium with assembled GFAP filaments. The ability of GFAP to assemble, disassemble, and undergo subunit exchange has important implications for the organization and dynamics of astroglia cell cytoskeleton during development and in response to injury.

Animals↗
PubMed1991

Immunohistochemical study of microtubule-associated protein 2 and ubiquitin in chronically aluminum-intoxicated rabbit brain.

Experimental neurofibrillary change was produced in rabbit brain by daily subcutaneous aluminum tartrate injection for 40 days. The production of experimental neurofibrillary changes was confirmed by immunostaining with antibodies against neurofilament triplet proteins and the brain tissue was studied immunohistochemically with antibodies against microtubule-associated protein (MAP) 2 and ubiquitin. The hippocampal neurons of the chronically aluminum-intoxicated rabbit brain showed diminished staining of dendrites by anti-MAP2 antibody. The length of anti-MAP2-positive dendrites in hippocampus was significantly shorter than that of the control brain. In the cortex somata of a subset of pyramidal neurons were intensively stained by anti-MAP2 antibody, while the MAP2 immunoreactivity of distal dendrites was diminished. The immunostaining by anti-ubiquitin antibody revealed the positive staining of the neurons bearing experimental neurofibrillary changes in the lower brain stem nuclei. It is speculated that MAP2 dislocation and ubiquitination are accompanying phenomena of the production of experimental neurofibrillary changes in chronically aluminum-intoxicated rabbit brains.

Aluminum↗
PubMed1991

Brain stem auditory-evoked potentials in meningomyelocele. Natural history of Chiari II malformations.

Brain stem auditory-evoked potentials (BAEPs) were recorded in 30 patients with meningomyelocele and shunted hydrocephalus ranging in age from birth to 33 years. Twenty-two of them had Chiari II malformation, one of which was symptomatic. In 22 cases, including 15 with Chiari II malformation, BAEPs were recorded repeatedly after periods ranging from 18 months to 7 years. The results were as follows: (1) III-V interpeak latency (IPL) decreased progressively from prolonged to the normal range with growth until 25 years of age; (2) I-III IPL tended to prolong gradually from the normal range; (3) these findings may indicate that the natural history of Chiari II malformation is delayed maturation of the brain stem and intensification in the elongation and stretching of the hindbrain and lower cranial nerves.

Adolescent↗
PubMed1991

Change of accumulation and filling pattern in evolution of cerebral infarction with I-123 IMP brain SPECT.

Twenty-eight patients with cerebral infarction were examined by brain SPECT with I-123 IMP a total of 46 times from Day 2 to Day 84 after the onset of stroke. Depending on the pattern of change in the abnormal accumulation of I-123 IMP between the early and delayed images, the patients were classified into one of five types. The number of patients in each type and the number of days after infarction at which each type occurred were as follows: Type (I), n = 5 and 4 +/- 2 days; Type (II), n = 8 and 12 +/- 4 days; Type (III), n = 17 and 21 +/- 11 days; Type (IV), n = 13 and 38 +/- 18 days; and Type (V), n = 3 and 60 +/- 16 days. In 12 patients, 30 brain SPECT were performed that showed the chronological evolution of infarction in sequence from Types (I) to (IV). Hyperactivity in the early image was seen in Type (I) with a subsequent image defect, while in Type (II) there was persistent hyperactivity. Hypoactivity in the early image was seen in Types (III), (IV), and (V), and the activity in the delayed image gradually decreased as the process of infarction terminated. The early image reflected the distribution of lipophilic I-123 IMP, indicating regional cerebral blood flow, while the delayed image showed the distribution of hydrophilic I-123 IMP metabolites superimposed on that of lipophilic I-123 IMP which had accumulated in the brain at the first extraction. Combining the early and delayed images of I-123 IMP brain SPECT may help to understand the evolution of cerebral infarction.

Adult↗
PubMed1991

Dietary restriction reduces the incidence of 3-methylcholanthrene-induced tumors in mice: close correlation with its potentiating effect on host T cell functions.

All mice treated with 3-methylcholanthrene (MC) suffered with tumor 114 days after treatment. However, 40% dietary restriction caused a great inhibition of tumor incidence. In order to understand the mechanisms by which dietary restriction decreased the occurrence of tumor in mice, we investigated the correlation between tumor incidence and host T cell immune responses. At 114 days after MC administration, the mice were sacrificed and their T cell immune responses were assessed. Flow cytometry studies demonstrated that dietary restriction caused a marked increase of the proportion of Thy 1.2+, L3T4+ T cells in MC-treated diet-restricted mice. Consistent with this result, T cell responses against concanavalin A and interleukin-2 were also potentiated in spleen cells obtained from MC-treated diet-restricted mice, while spleen cells obtained from MC-treated unrestricted mice showed decreased T cell responses because of their tumor burden. Such potentiation of T cell functions by dietary restriction was also observed at earlier stages of MC-induced tumorigenesis. During the course of carcinogenesis, spleen cells obtained from diet-restricted mice showed decreased natural killer activity in vivo. However, in vitro induction of cytotoxic T cells was markedly augmented in MC-treated diet-restricted mice compared with unrestricted mice. These results strongly suggest that the increase of host T cell immune responses might be one of the major causes for the reduction of tumor occurrence by dietary restriction.

Animals↗
PubMed1991

Continuous determination of cardiac output using a flow-directed Doppler pulmonary artery catheter.

A newly developed, flow-directed, Doppler pulmonary artery catheter that uses multiple ultrasonic transducers to measure instantaneous and continuous cardiac output was evaluated in 20 patients undergoing cardiac and vascular surgical procedures. Cardiac output was determined using the product of the average velocity and the area of the main pulmonary artery. Pulmonary artery area was obtained from measurements of diameter via ultrasound transit time, and average velocity of blood flow was determined from the Doppler shift frequency. Two hundred thirty-eight simultaneous Doppler catheter and thermodilution cardiac output measurements were obtained preoperatively, intraoperatively, and during postoperative recovery. Catheter indwelling time varied from 18 through 94 hours (mean +/- SD, 40 +/- 19 hours) with 2 to 26 (mean +/- SD, 12 +/- 6) sets of triplicate cardiac output measurements obtained per patient. Doppler catheter cardiac output correlated well with thermodilution (r = 0.76, slope or m = 0.87, and SEE = 0.05 with P = 0.0001) and mean predictive error (bias) appeared clinically insignificant (bias +/- SD, -0.13 +/- 0.79 L/min). Accurate, continuous monitoring of instantaneous and mean cardiac output appears possible with use of this Doppler pulmonary artery catheter system.

Blood Flow Velocity↗
PubMed1991

Clinical application of video image flexible ureteronephroscope for diagnosis of upper urinary tract disorders.

Ureteroscopy has become the diagnostic and therapeutic procedure of choice for many conditions of the upper urinary tract. Technology is progressing rapidly in endourology, facilitating both goals. As reported previously, we developed a 2F video image flexible ureteronephroscope. This instrument is the smallest caliber of all ureteronephroscopes available to date. Because of the small diameter the device can be inserted into the ureter cystoscopically in a manner similar to catheter insertion. The procedure is done with the patient under local anesthesia. We performed ureteronephroscopic procedures on 79 patients using mainly a 6F passively deflecting flexible ureteronephroscope, which consists of the aforementioned 2F video image flexible ureteronephroscope and a 3F working channel. The area to be viewed was accessed successfully in 41 of 43 patients (95%). Over-all, diagnostic maneuvers were successful in 64 of 79 patients (87%). We suggest that the 2F and 6F flexible ureteronephroscopes would be indicated when conclusive diagnosis for upper urinary disease is not obtained by other means.

Endoscopes↗
PubMed1991

Radiation-induced cranial nerve palsy: hypoglossal nerve and vocal cord palsies.

Cranial nerve palsies are an unexpected complication of radiotherapy for head and neck tumours. We present a case of this radiation-induced cranial palsy. An 18-year-old female with nasopharyngeal carcinoma developed a right hypoglossal nerve palsy 42 months after cancericidal doses of radiotherapy. In addition, she developed a bilateral vocal cord palsy 62 months after therapy. Follow-up over four years has demonstrated no evidence of tumour recurrence and no sign of neurological improvement.

Adolescent↗
PubMed1991

Venous haemangioma of the neck and mediastinum.

A case of cervico-mediastinal venous haemangioma with diffuse upper respiratory airway involvement is reported. The lesion was considered to be an ordinary supraglottic haemangioma at first. We recommend that adult cases of laryngeal haemangioma should be carefully examined for extra-laryngeal lesions.

Bronchoscopy↗