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Biomedical subjects

M Owada

Publications and source records attributed to M Owada.

At least 73 records · Page 4Linked to original sources
PubMed1990

[Three siblings with type 3 GM1-gangliosidosis--pathophysiology of dystonia and MRI findings].

GM1-gangliosidosis is a rare neurovisceral storage disease caused by an inherited deficiency of acid beta-galactosidase. The characteristic neurological feature of type 3 (adult or chronic) GM1-gangliosidosis is usually a slowly progressive dystonia with dysarthria due to predominant involvement of basal ganglia. About 20 adult patients with this disorder have been reported in the literature. However, there are no reports of 3 brothers with type 3 GM1-gangliosidosis, and MRI findings. Case 1 (proband): A 28-year-old man was hospitalized because of facial grimace, dysarthria, and generalized dystonia. He was born after normal pregnancy and delivery. His development was normal until 3 years of age when the difficulties of speaking and walking were noticed by his parents. These neurological abnormalities progressed slowly and facial grimace and dystonic movements occurred 7 years later. He could not walk at 22 years of age. On admission, he was bedridden with marked scoliosis and subluxation of the mandibule. The communication was possible only by pointing the words written on the board. Case 2: A 33-year-old man, elder brother of case 1, showed the similar neurological features and clinical course. Slit-lamp examination revealed corneal opacities which were located in the deep stroma. Case 3: A 33-year-old man, elder brother of case 1 or case 2. At age 10-11, he noted similar symptoms as case 1 or case 2. The severity of dystonia was milder than his brothers. A diagnosis of GM1-gangliosidosis in three patients was made on the basis of the following data.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[An experimental study on the fibrosis of scirrhous gastric carcinoma].

9 surgical specimens of gastric carcinoma were examined for their immunoreactivity with type I procollagen antiserum. For specimens of the four Borrmann type IV carcinomas and one of Borrmann type III carcinomas, all of which exhibited abundant fibrous stroma (histologically scirrhous), the cytoplasm of the tumor cells was strongly positive. In contrast, the tumor cells of the non-scirrhous carcinoma (histologically medullary) were poorly reactive to type I procollagen antiserum. We found the cells, which were established from scirrhous carcinoma (KATO III), express type I procollagen mRNA (4.8 kb, 6.0 kb) as revealed by dot blot analysis and Northern blot hybridization. And we determined the presence of type I procollagen related antigen in the cell culture medium of KATO III using RIA and Western blotting. Administration of glucocorticoid to KATO III caused decrease of procollagen mRNA expression. It was revealed that collagen synthesis of scirrhous gastric carcinoma was regulated by glucocorticoid in the same manner of fibroblast.

Adenocarcinoma, Scirrhous↗
PubMed1990

Hereditary fructose intolerance caused by a nonsense mutation of the aldolase B gene.

The nucleotide sequence of a patient's aldolase B gene was determined and showed a substitution of a single nucleotide (C----A) at position 720 in the coding region, which resulted in the 240th amino acid, a cysteine, being changed to a stop codon (TGC----TGA). By an allele-specific oligonucleotide probe and polymerase chain reaction, the patient was shown to be homozygous for the mutation. To examine whether this mutation causes functional defect of the enzyme, the activity of the aldolase B from the patient, expressed in Escherichia coli by using expression plasmid, was measured. No activity was observed, and the predicted product was recovered from E. coli expression plasmid, indicating that this nonsense mutation was the cause of aldolase B deficiency.

Base Sequence↗
PubMed1989

A female case of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor.

The case of a 17-year-old female with a rare form of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor is reported. Laparoscopy showed a tumor 50 mm in diameter in the lower portion of the right lobe of the liver. The tumor was biopsied under ultrasonic guidance, and tentatively diagnosed as adenomatous hyperplasia. The patient was also diagnosed as having type VIII glycogenosis (phosphorylase kinase deficiency).

Adolescent↗
PubMed1988

Immunohistochemical identification of type I procollagen in tumour cells of scirrhous adenocarcinoma of the stomach.

Human gastric carcinomas were tested for their immunohistochemical reactivity with anti-type I procollagen antiserum. In all specimens of scirrhous carcinomas, staining of the tumour cells was strongly positive, while in medullary carcinomas staining of the tumour cells was generally poor. These results suggest that the tumour cells in scirrhous carcinomas produce collagen in their stroma.

Adenocarcinoma, Scirrhous↗
PubMed1988

[Property of scirrhous carcinoma of the stomach defined by collagen metabolism].

Scirrhous carcinoma of the stomach is characterized by the extensive deposition of collagen in the desmoplastic stroma. In the present study, we examined which cell types are responsible for the synthesis of collagen in tissue of scirrhous carcinoma. Furthermore, a RIA for carboxyterminal peptide of human type I procollagen (type I C-peptide) was developed and its clinical implication for serodiagnosis of scirrhous carcinoma of the stomach was evaluated. 1) The immunohistochemical localization of type I procollagen was investigated employing an antibody to procollagen. Strong staining was observed in the cytoplasma of scirrhous carcinoma cells. Furthermore northern blot technique using c-DNA probe of type I procollagen was performed. Tumor cells established from scirrhous carcinoma (KATO III) were expressing mRNA-procollagen type I as revealed by this technique. Thus in scirrhous carcinoma of the stomach, at least some portion of the increased collagen content is due to production by the tumor cells. 2) In scirrhous carcinoma of the stomach, serum type I C-peptide level appeared to increase, while in non-scirrhous carcinoma, serum type I C-peptide level stayed within normal range. Serum type I C-peptide levels corresponded to clinical course who underwent either operation or chemotherapy. Collectively, the measurement of serum type I C-peptide concentrations will provide a new means for diagnosis and monitoring the scirrhous carcinoma of the stomach.

Adenocarcinoma, Scirrhous↗
PubMed1988

[Galactosemia].

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Carbohydrate Epimerases↗
PubMed1987

Treatment of phenylketonuria with a formula consisting of low-phenylalanine peptide. A collaborative study.

A method of preparation of a more palatable therapeutic formula for phenylketonuria (PKU), consisting of low-phenylalanine peptide (LPP), was reported. There were no adverse effects and, in fact, there was a reduced frequency of diarrhea in patients who received LPP formula for more than 6 months. The LPP formula can be used not only as a more palatable therapeutic milk for PKU, but also as an ingredient to make more palatable foods of low-phenylalanine content.

Adolescent↗
PubMed1987

Dihydrobiopterin synthesis defect: an adult with diurnal fluctuation of symptoms.

A deficiency of dihydrobiopterin synthesis was found in a 27-year-old man with mild mental retardation, rigid spasticity, hyperreflexia, dystonia, myoclonus, and delay in the initiation of action, since age 10. Symptoms improved after sleep. Urine contained large amounts of neopterin and a trace of biopterin. Dihydropteridine reductase activity in red blood cells was normal. CSF levels of HVA and 5-HIAA were low. Tetrahydrobiopterin administration lowered serum phenylalanine and improved the symptoms.

Adult↗