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Biomedical subjects

K Tada

Publications and source records attributed to K Tada.

At least 307 records · Page 17Linked to original sources

[Correlation of serum gamma-seminoprotein and serum prostate-specific antigen in patients with prostate cancer].

Enzyme immunoassays (EIAs) using rabbit anti-gamma-seminoprotein (gamma-Sm) antibody and rabbit anti-prostate-specific antigen antibody (PA) for measurements of gamma-Sm and PA were developed in order to determine the correlation between serum gamma-Sm levels and serum PA levels in patients with prostate cancer. Each EIA for measurement of gamma-Sm or PA was revealed to be sensitive and reproducible by fundamental analysis of the quality of EIAs. A significant correlation was established between serum gamma-Sm levels and serum PA levels which were measured by these assays and expressed as protein concentration of seminal plasma (r = 0.99). This result coincided with our previous observation that gamma-Sm and PA are immunologically identical materials. We conclude, therefore, that gamma-Sm and PA should be regarded as tumor markers identical to each other for serodiagnosis of prostate cancer.

Antigens, Neoplasm↗

Defective gene in lactic acidosis: abnormal pyruvate dehydrogenase E1 alpha-subunit caused by a frame shift.

A patient with lactic acidosis showed a lowered pyruvate dehydrogenase E1 activity and fatigued on slight exercise. The cDNA encoding the pyruvate dehydrogenase E1 alpha-subunit from his lymphocytes, transformed by infection of Epstein-Barr virus, was cloned and sequenced. The nucleotide sequence determination revealed that the gene had a deletion of four nucleotides at the second codon upstream from the termination codon. This deletion would lead to a reading-frame shift and make a new termination codon at the 33d codon downstream from the "normal" termination codon. An S1 nuclease-protection experiment confirmed the presence of mRNA with its deletion in the patient. Amplification, by the polymerase chain reaction method, of the genomic-DNA region from his peripheral blood cells showed that the deletion was localized in an exon and that it was not caused by an abnormal splicing at the intron/exon junction. This is the first report on cloning a defective gene of the pyruvate dehydrogenase complex.

Acidosis, Lactic↗

[A case of nonpenetrating ureteral avulsion].

A 7-year-old boy who had been in a traffic accident was hospitalized in Hamamatsu Red Cross Hospital with diagnosis of head abrasion, contusion of abdomen and multiple fractures. On the 17th day of hospitalization, he complained of left flank pain and high fever. Examinations by IVP and enhanced computed tomographic scan revealed a left ureter avulsed at the level of uretero-pelvic junction. Operative reconstruction by end-to-end anastomosis of the ureter was performed immediately. The function of left ureter was recovered 4 months after operation. This rare case of ureteral avulsion is briefly discussed along with a review of the recent literature.

Accidents, Traffic↗

[EEG analysis of high-dose fentanyl anesthesia--a comparison of rapid sequence anesthesia and the conventional method].

Twenty-one patients who underwent cardiac surgery were assigned to receive high-dose fentanyl rapid sequence anesthesia or conventional high-dose fentanyl anesthesia. In conventional method group, power of delta wave decreased with respect to time. But in rapid sequence group, no decrease was seen until the end of operation. Good maintenance of delta wave in rapid sequence group may be achieved by higher plasma fentanyl concentration and the absence of acute tolerance. In conclusion, high-dose fentanyl rapid sequence anesthesia is a useful method for cardiac surgery.

Adolescent↗

Brain histamine in Alzheimer's disease.

The concentration of histamine (HA) has been determined by high-performance liquid chromatography (HPLC) with fluorometric detection in 21 different regions of brains from patients with senile dementia of the Alzheimer type (SDAT) and subjects (CB) whose causes of death were not related to neuropsychiatric, neurological and/or neurodegenerative diseases. The highest levels of HA in the central nervous system (CNS) of both control (CB) and SDAT samples were found in the posterior hypothalamus (CB = 3.13 +/- 0.63 pmol/mg; SDAT = 7.75 +/- 1.43 pmol/mg, p less than 0.005), where the HA neurons are located, and in the anterior hypothalamus (CB = 1.77 +/- 0.33 pmol/mg; SDAT = 2.82 +/- 0.45 pmol/mg, p less than 0.005). The lowest HA levels were detected in the cerebellum (CB = 0.12 +/- 0.04 pmol/mg; SDAT = 0.24 +/- 0.09 pmol/mg, p less than 0.01) and medulla oblongata. HA levels were significantly higher in SDAT than in CB in the following areas: motor cortex (Brodmann's area 4) (A4), premotor cortex (A6), postcentral gyrus (A1,2), posterior parietal cortex (A5,7), superior temporal gyrus (A41,42), temporal pole (A38), primary and secondary visual cortices (A17,18), anterior and posterior regions of the hypothalamus, putamen, caudate nucleus, nucleus accumbens, thalamus, hippocampus, pons, medulla oblongata and cerebellum. No changes were seen in globus pallidus and corpus callosum. Since the origin of HA in the brain is dependent upon three main compartments (neuronal, mast cell, vascular smooth muscle), with approximately 60-80% of the total HA belonging to the neuronal pool, on the basis of neurochemical data we postulate that the increase in the levels of HA in SDAT might account for or be associated with alterations in neuroendocrine, cognitive, neurovascular and sleep-wakefulness functions.

Aged↗

[Two siblings of Leber's congenital amaurosis with an increase in very long chain fatty acid in blood: relationship between peroxisomal disorders and Leber's congenital amaurosis].

We reported two siblings of Leber's congenital amaurosis associated with increased level of very long chain fatty acid (VLCFA) in blood. Case 1, a 3 1/2-year-old boy had congenital blindness, severe psychomotor retardation, hepatomegaly, profound hypotonia, loss of deep tendon reflexes, muscular atrophy and weakness, and non-convulsive status epilepticus characterized by a sudden respiratory failure, and also showed a flat electroretinogram, non-pigmentary retinal degeneration, severe atrophy of the brain stem and cerebellum, hepatic fibrosis, decreased motor and sensory conduction velocities and atlanto-axial instability. Sural nerve biopsy revealed severely decreased number of total myelinated fibers without remarkable demyelination or remyelination. Case 2, an elder sister of case 1, with pigmentary retinal degeneration, hepatomegaly and pericarditis had died at 3 months. Autopsy revealed hypomyelination and heterotopy of the cerebral white matter, hepatic fibrosis, renal microcysts and normal adrenal cytoarchitecture. In case 1, the level of VLCFA was increased twofold and sevenfold of controls in serum and in red cell membrane, respectively. Phytanic or trihydroxycholestanoic acid was not detected in the serum and bile. Normal shaped peroxisomes were definitely recognized in biopsied liver by means of electronmicroscopic histochemistry. From the above findings, these patients was thought to be a new variant of peroxisomal disorders relating to degradation of VLCFA, other than Zellweger syndrome, infantile Refsum disease and infantile adrenoleukodystrophy. It was concluded that peroxisomal functions should be studied in cases of Leber's congenital amaurosis.

3-Hydroxyacyl CoA Dehydrogenases↗

The impaired expression of glycine decarboxylase in patients with hyperglycinemias.

Glycine decarboxylase, a constituent of the glycine cleavage system, in patients with either nonketotic or ketotic hyperglycinemia (NKH and KH) was examined using an anti-chicken glycine decarboxylase antibody. Patients with NKH who have lesion in glycine decarboxylase are differentiated by its expressed level in the liver. One group is cases of the neonatal onset type who have neither activity of the enzyme nor protein reactive to the antibody. The other is a case of the late onset type who shows low but detectable activity of the enzyme and the desirable amount of the immunoreactive material. In the liver of a patient with KH not showing the appreciable activity of H-protein, ubiquitous amount of protein reactive to anti-H-protein IgG is detected and amount of glycine decarboxylase has also been lowered. It is suggested that several mechanisms may be involved in determining the expressed level of glycine decarboxylase in patients with hyperglycinemias.

Adult↗

Activities of lysosomal enzymes in rabbit brain with experimental neurofibrillary changes.

Rabbits were injected intracerebrally with aluminum salt leading to experimental neurofibrillary change formation as a model of Alzheimer neurofibrillary change. Eleven days after the injection, the brain tissues were excised from the cortex, hippocampus, and cervical region of spinal cord. Five lysosomal enzymes (cathepsin D, beta-glucuronidase, acid phosphatase, acid DNase, alkaline DNase) were assayed and compared with the control. Cathepsin D, acid DNase and beta-glucuronidase activities increased significantly in all 3 areas of aluminum-injected brain. On the other hand, acid phosphatase and alkaline DNase activities remained at the same level. The results showed the lysosomal enzymes did not change in parallel after aluminum administration, suggesting a role of the increased enzymes in the brain with neurofibrillary changes.

Acid Phosphatase↗

Neurofilament degradation by bovine brain cathepsin D.

The effect of cathepsin D on bovine neurofilament protein was studied biochemically, immunologically, and morphologically. Degradation products of each neurofilament triplet by bovine brain cathepsin D at neutral pH were identified by electrophoresis and immunoblotting with anti-neurofilament antibodies. The 68-kDa subunit was the most susceptive to cathepsin D proteolysis among the triplet proteins. All of the triplet gave rise to partial degradates of the 50-kDa size. The reconstituted fiber from neurofilament triplet proteins and the 68-kDa subunit protein were attacked by cathepsin D and the mode of disruption of the fiber structure was studied by electronmicroscopy.

Animals↗

Hyperamino-acidaemia and hyperammonaemia in epileptic children treated with valproic acid.

Serum amino acid pattern, blood ammonia, and serum valproic acid (VPA) levels were estimated in 75 epileptic children with and without VPA therapy. The incidence of patients with hyperammonaemia (greater than 60 mumol/l) in patients treated with only VPA or with a combination of VPA and other antiepileptic drugs was 19% and 20% respectively. Hyperammonaemia was not observed in patients receiving other drugs. Elevated levels of serum glycine, alanine and serine were more common in epileptic patients treated with VPA alone and with VPA in combination with other drugs than in patients receiving other drugs. A significant positive correlation was found between the serum levels of glycine and alanine, of glycine and serine, and of serine and alanine. These findings may indicate a mitochondrial dysfunction caused by VPA.

Adolescent↗

Congenital contracture of the infraspinous muscle. A case report.

Posterior subluxation of the glenohumeral joint and a posterior, winged scapular deformity have been reported in a patient with congenital contracture of the infraspinous muscle. The present case was successfully treated by resection of the contracted band within the infraspinous muscle, glenoid osteotomy, reverse Putti-Platt, and resection of the protruding part of the scapula. To our knowledge, this is the first case reported of congenital contracture of the infraspinous muscle. The pathogenesis of the deformity in this case is discussed.

Adolescent↗

Human renin gene assigned to chromosome band 1q42 by in situ hybridization.

A gene coding for renin was assigned to human chromosome region 1q42 by in situ hybridization. Many genes in this region belong to multigene families whose members may be located on the same or different chromosomes. Genes located on the long arm of chromosome 1 appear to have been involved in several instances of gene duplication.

Chromosome Mapping↗

Extensive defects of mitochondrial electron-transfer chain in muscular cytochrome c oxidase deficiency.

This study was undertaken to estimate the extent of molecular defects in the mitochondrial electron-transfer chain of a patient with mitochondrial myopathy. Biochemical and immunochemical studies were performed on the skeletal muscle mitochondria. Spectrophotometry and enzyme activity measurements localized a definite defect at the segment of cytochrome c oxidase (complex IV) of the electron-transfer chain. Immunoblotting and immunoprecipitation studies using the anti-complex IV antibody revealed that the contents of subunits 1, 4, 5, 6, and 7 of complex IV were markedly diminished and that subunit 2 was almost absent. Immunohistochemistry of the muscle tissue revealed a considerable accumulation of immunoreactive materials of complex IV in the ragged-red fibers. The immunoblots using the anti-NADH-ubiquinone oxidoreductase antibody demonstrated that the contents of NADH-ubiquinone oxidoreductase subunits were 47% of control and that the contents of three subunits were considerably decreased. The contents of ubiquinol-cytochrome c oxidoreductase subunits were also somewhat low (77% of control) and one of the minor contaminants detected in the control was completely absent. High-resolution one-dimensional sodium dodecyl sulfate-urea-gel electrophoresis disclosed that six additional unidentified polypeptides in the control were markedly diminished or completely missing. These results demonstrate that the molecular defects in the mitochondrial electron-transfer chain are more extensive than would be expected from either spectral analysis or enzyme activity measurements alone, and involve not only complex IV but also NADH-ubiquinone oxidoreductase and ubiquinol-cytochrome c oxidoreductase and several unidentified mitochondrial proteins.

Adult↗

Excision of the lunate in Kienböck's disease. Results after long-term follow-up.

Excision of the lunate was performed for 18 patients with Kienböck's disease; 14 were followed up for an average of almost 12 years. Carpal collapse progressed with time, but rearrangement of the remaining carpal bones preserved a satisfactory range of movement and grip strength. Degenerative changes were not severe. All the patients had relief of pain, were able to carry out their normal activities, and all but two could perform strenuous activities.

Adult↗

Neuroarthropathy of the foot in leprosy.

Among 449 patients with leprosy, 40 had clinical and radiographic evidence of neuroarthropathy in 50 feet. These changes were classified into four types according to the joints first involved by major lesions: ankle (25 feet), midtarsal (15 feet), tarsometatarsal (7 feet) and subtalar (3 feet). The progression of joint destruction was different in each type, but despite the severe destructive changes seen in radiographs, the patients had relatively few complaints. The muscles innervated by the peroneal nerve were severely paralysed in ankle and midtarsal types and it seems that, over a long term, repeated trauma and/or abnormal stress may lead to these types of neuroarthropathy. Neuropathy was less severe in the tarsometatarsal type of joint degeneration; the pathogenesis in this type seemed to be mainly direct trauma to the forefoot.

Adult↗