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Biomedical subjects

Y Matsubara

Publications and source records attributed to Y Matsubara.

At least 271 records · Page 15Linked to original sources
PubMed1988

[Nutritional support for preoperative patients with esophageal cancer].

Nutritional support for patients undergoing major operations seems to be very important for improving the operative results, especially in preoperative patients with conditions such as esophageal carcinoma. In our department, patients who have lost more than 10% of their normal weight have been given intravenous hyperalimentation for at least two weeks preoperatively to prevent postoperative pulmonary complications. However good responses to nutritional support were not always obtained in these patients. One of the reasons was thought to be possible inadequacy of the nutritional support, for example, in the amount of energy intake. The purpose of this study was to clarify the energy requirements of anorexic patients by examining the relationship between energy expenditure and nutritional status. Fifty-three male patients with thoracic esophageal carcinoma given radical surgery were studied retrospectively. These patients were divided into two groups: group 1 consisted of 39 patients who had lost little or no weight (greater than or equal to 90% UsWt), and group 2 consisted of 14 patients who had lost more than 10% of their pre-illness weight (less than 90% UsWt). In order to estimate the energy requirement, resting energy expenditure (REE) was measured using indirect calorimetry and the formula of Weir, and compared with the basal energy expenditure (BEE) as predicted using the formula of Harris-Benedict which was calculated from the height, weight, age and sex. Nutritional status was also assessed by measuring various nutritional parameters in each patient on admission. The mean values of body weight, %IBW (ideal body weight), %AMC (arm muscle circumference as percentage of standard), %TSF (triceps skinfold as percentage of standard) and %GS (grip strength as standard) were significantly lower and REE higher in group 1 than in group 2. However those of TP, alb and BEE showed no significant difference. Negative correlations between REE and body weight, %AMC, and %GS were seen respectively, and a positive correlation between REE and BEE was also seen in group 1, although no significant correlation was seen in group 2. These results suggested that the energy requirement of anorexic patients should be estimated by measuring the REE in each individual to obtain an effective response.

Energy Metabolism↗
PubMed1987

Molecular cloning and nucleotide sequence of cDNA encoding the entire precursor of rat liver medium chain acyl coenzyme A dehydrogenase.

cDNA encoding the precursor of rat liver medium chain acyl-CoA dehydrogenase (EC 1.3.99.3) was cloned and sequenced. The longest cDNA insert isolated was 1866 bases in length. This cDNA encodes the entire protein of 421-amino acids including a 25-amino acid leader peptide and a 396-amino acid mature polypeptide. The identity of the medium chain acyl-CoA dehydrogenase clone was confirmed by matching the amino acid sequence predicted from the cDNA to the NH2-terminal and nine internal tryptic peptide sequences derived from pure rat liver medium chain acyl-CoA dehydrogenase. The calculated molecular masses of the precursor medium chain acyl-CoA dehydrogenase, the mature medium chain acyl-CoA dehydrogenase, and the leader peptide are 46,600, 43,700, and 2,900 daltons, respectively. The leader peptide contains five basic amino acids and only one acidic amino acid; thus, it is positively charged, overall. Cysteine residues are unevenly distributed in the mature portion of the protein; five of six are found within the NH2-terminal half of the polypeptide. Comparison of medium chain acyl-CoA dehydrogenase sequence to other flavoproteins and enzymes which act on coenzyme A ester substrates did not lead to unambiguous identification of a possible FAD-binding site nor a coenzyme A-binding domain. The sequencing of other homologous acyl-CoA dehydrogenases will be informative in this regard.

Acyl-CoA Dehydrogenase↗
PubMed1987

Isolation of cDNA clones coding for rat isovaleryl-CoA dehydrogenase and assignment of the gene to human chromosome 15.

Rat liver mRNA encoding the cytoplasmic precursor of mitochondrial isovaleryl-CoA dehydrogenase was highly enriched by polysome immunopurification using a polyclonal monospecific antibody. The purified mRNA was used to prepare a plasmid cDNA library which was screened with two oligonucleotide mixtures encoding two peptides in the amino-terminal portion of mature rat isovaleryl-CoA dehydrogenase. Thirty-one overlapping cDNA clones, spanning a region of 2.1 kbp, were isolated and characterized. The cDNA sequence of a 5'-end clone, rIVD-13 (155 bp), predicts a mitochondrial leader peptide of 30 amino acid residues and the first 18 amino acids of the mature protein. These consecutive 18 residues completely matched the amino-terminal peptide determined by automated Edman degradation of the rat enzyme. The leader peptide contains six arginines, has no acidic residues, and is particularly rich in leucine, alanine, and proline residues. Southern blot analysis of DNAs from human-rodent somatic cell hybrids with an isolated rat cDNA (2 kbp) assigned the isovaleryl-CoA dehydrogenase gene to the long arm of chromosome 15, region q14----qter. The chromosomal assignment was confirmed and further refined to bands q14----q15 by in situ hybridization of the probe to human metaphase cells. This location differs from that of the gene for medium-chain acyl-CoA dehydrogenase, a closely related enzyme, which has been previously assigned to chromosome 1.

Animals↗
PubMed1987

Molecular basis of isovaleric acidemia and medium-chain acyl-CoA dehydrogenase deficiency.

Our early study of isovaleric acidemia (IVA) indicated that isovaleryl-CoA is dehydrogenated by an enzyme that is specific for isovaleryl-CoA. We subsequently identified and purified isovaleryl-CoA dehydrogenase (IVD) and 2-methyl-branched chain acyl-CoA dehydrogenase, which were previously unknown. We also purified and characterized three previously known acyl-CoA dehydrogenases. Five acyl-CoA dehydrogenases share similar molecular features and reaction mechanisms, indicating a close evolutionary relationship. Using the tritium release assay and [35S]methionine labeling/immunoprecipitation, we showed that IVA is due to a mutation of IVD. We also demonstrated that there are at least 5 distinct forms of mutant IVD, indicating an extensive molecular heterogeneity. Furthermore, we cloned cDNAs encoding IVD and medium-chain acyl-CoA dehydrogenases. The comparison of their complete primary sequences revealed a high degree of homology, indicating that these enzymes belong to a gene family, the acyl-CoA dehydrogenase family.

Acyl-CoA Dehydrogenases↗
PubMed1987

Postinflammatory remyelination in the spinal cord of mice infected with mouse hepatitis virus, JHM strain.

The spinal cords in mice surviving acute infection for 30 days following lumbar inoculation with mouse hepatitis virus, JHM strain, were examined for virus growth and pathologic changes by light and electron microscopy. Virus titer reached a maximum level on day 6 postinoculation (p.i.) and became negative on day 10 p.i. On days 5 to 10 p.i. there were severe disruption of myelin sheath and marked phagocytosis of myelin by macrophages. Viral particles were seen in degenerating glial cells. On days 15 to 20 p.i. proliferation of oligodendrocytes was noticed in association with thinly myelinated axons with decreased number of macrophages. On days 25 to 30 p.i. affected axons were mostly remyelinated by oligodendrocytes and the interaxonal space was packed with the processes of fibrous astrocytes containing myelin debris and lipid droplets. In the subpial areas of more widespread lesions some axons were remyelinated by Schwann cells.

Animals↗
PubMed1987

[Prosthetic reconstruction of the trachea and carina].

We have performed prosthetic reconstruction of the trachea and carina in 12 patients since 1979. We used Neville's prosthesis in 7 patients and Katsura's prosthesis in 5 patients. Seven patients were operated on for lung cancer, 2 patients for adenoid cystic carcinoma of the trachea and the others for large cell carcinoma of the trachea, thyroid cancer and tuberculous granuloma, respectively. Prosthetic reconstruction of the trachea was performed in 4 patients. Carinal resection was performed in 8 patients: With right sleeve pneumonectomy in 4 patients, with right upper lobectomy in 2 patients and only carinal resection in 2 patients. Prosthetic reconstruction after the carinal resection was performed using 3 straight types, 1 curved type and 4 bifurcated types. With regard to the complications of the prosthetic reconstruction, dehiscence at the anastomotic site was seen in 5 patients, granulation in 4 patients, empyema in 3 patients, massive hemorrhage in 2 patients and migration of the prosthesis in 1 patient. Five patients survived more than 1 year. The longest survival time was 43 months. To prevent complications of the prosthetic reconstruction, we improved the anastomotic method, reinforced the anastomotic site with Marlex mesh and protected the surrounding vessels with Lyodura.

Adult↗
PubMed1986

A possibility to recognize chirality by an excitable artificial liquid membrane.

Studies were made on oscillations across a liquid membrane consisting of an oil layer, nitrobenzene containing picric acid, between two aqueous layers: a solution of 1.5 M ethanol and 5 mM optically-active cationic detergent, the D- or L-form of N-alpha-methylbenzyl-N,N-dimethylmyristylammonium bromide, on the left and 0.1 M D- or L-form of various ligands, such as glucose, arabinose, alanine, glutamic acid, threonine, leucine, proline, or phenylalanine on the right. This system showed sustained rhythmic oscillations of electrical potential of 200-300 mV with intervals of the order of 1 min. The frequency of oscillations depended on the combination of chiralities of the detergent and ligand. This means that the two forms (D and L) of chiral ligands can be distinguished by differences in the electrical response of the liquid membrane.

Amino Acids↗
PubMed1986

Chemoreception of sugars by an excitable liquid membrane.

Studies were made on electrical oscillations across a liquid membrane consisting of an oil layer, nitrobenzene containing picric acid, between two aqueous layers. This system showed sustained rhythmic oscillations of electrical potential of 200-300 mV with intervals in the order of 1 min. It was found that the histogram of frequency of oscillations was characteristic depending on the structures of the sugars. The histograms of glucose, fructose, galactose and sorbose showed a single maximum whereas those of sorbitol and mannitol showed double maxima.

Carbohydrates↗
PubMed1986

Molecular cloning of cDNAs encoding rat and human medium-chain acyl-CoA dehydrogenase and assignment of the gene to human chromosome 1.

Rat liver mRNA encoding the precursor of medium-chain acyl-CoA dehydrogenase was purified to near homogeneity by polysome immunoadsorption using a polyclonal, monospecific antibody. A single-stranded, 32P-labeled cDNA probe was synthesized using the enriched mRNA as template and was used to screen directly 15,000 colonies from a total rat liver cDNA library constructed in pBR322. One clone [600 base pairs (bp)] was positively identified by hybrid-selected translation combined with mitochondrial processing of translated products. Using the isolated rat cDNA as probe, 43,000 colonies from a human liver cDNA library were screened. Three overlapping clones (1100 bp, 500 bp, and 400 bp) were isolated and positively identified by hybrid-selected translation. The largest human cDNA clone was subcloned into the transcription vector pGEM-2, which contains a bacteriophage T7 RNA polymerase promoter. In vitro transcription of this recombinant, followed by in vitro translation, showed that the cDNA clone coded for approximately 80% of the medium-chain acyl-CoA dehydrogenase protein. The sizes of rat and human mRNAs encoding the precursor of medium-chain acyl-CoA dehydrogenase were 2.2 and 2.4 kilobases long, respectively, as determined by blot hybridization analysis of electrophoretically fractionated poly(A)+ RNA. Southern blot analysis of DNAs from human-rodent somatic cell hybrids with an isolated human cDNA assigned the gene coding for this enzyme to the short arm of chromosome 1, band p31. The chromosomal assignment was confirmed by in situ hybridization of the probe to human metaphase cells. Direct screening of cDNA libraries using a highly enriched mRNA to generate a probe, as demonstrated in this study, may provide the most rapid and convenient approach to cDNA cloning of low-abundance mRNAs.

Acyl-CoA Dehydrogenase↗
PubMed1986

Neurovirulence in mice of neural cell-adapted canine distemper virus.

Neurovirulence of the Onderstepoort strain of canine distemper virus (CDV) adapted to human neural cell lines was determined by the intracerebral inoculation of DDD mice at 3 and 5 weeks of age. Intensity of neurovirulence was estimated by histopathological changes in the central nervous system and clinical symptoms. The original virus propagated in Vero cells induced leptomeningoencephalitis, whereas neuroblastoma-adapted virus induced nerve cell degeneration and mild encephalitis with relatively low morbidity and fatality. In contrast, the viruses adapted to glioblastoma and oligodendroglioma caused high morbidity and fatality. The latter two viruses induced necrotizing encephalopathy including edema and hyperemia. In addition, the glioblastoma-adapted virus induced formation of giant cells. The oligodendroglioma-adapted virus caused demyelination and spongy state associated with degeneration of glial cells and axons. These observations are discussed in regard to a possible correlation between the neurovirulence of CDV in mice and its tropism for neural cells in vitro.

Aging↗