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Biomedical subjects

Y Tahara

Publications and source records attributed to Y Tahara.

At least 109 records · Page 6Linked to original sources
PubMed1985

[Contribution of amino acid deficiency to primary hypothyroidism associated with protein-calorie malnutrition].

A 68-year-old male patient without any previous thyroidal disease developed three times of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Because of his diabetes mellitus, alcoholic hepatitis, chronic pancreatitis and blind loop syndrome, his nutritional balance was easily disturbed leading to PCM. Although he recurrently developed primary hypothyroidism associated with PCM, this condition was completely restored by protein-calorie repletion. The possibility of dietary iodine deficiency was negated by the observation that his daily urinary iodine secretion was more than 4 mg/day. Plasma amino acid analysis revealed severe depletion of phenylalanine, tyrosine and other essential amino acids and raised the possibility that this hypothyroidism was caused by amino acid deficiency. In order to clarify the mechanisms of this primary hypothyroidism, we have investigated the change of thyroid functions during protein-calorie repletion by total parenteral nutrition (TPN). We then removed iodine from the nutrients for TPN to ascertain that iodine deficiency was not the cause of the primary hypothyroidism in the present case. In spite of the removal of iodine, serum T4 and T3 suddenly increased from 1.1 micrograms/dl and less than 25 ng/dl to 3.5 micrograms/dl and 59 ng/dl, respectively, in a few days after the beginning of TPN. They continued to increase thereafter and reached 6.3 micrograms/dl and 115 ng/dl in 6 weeks. Serum free T4 also showed a sudden increase from 0.56 ng/dl to 1.7 ng/dl after TPN and remained above 1.3 ng/dl thereafter. Serum reverse T3 showed a rapid increase after TPN, but, 4 weeks later, returned to the previous level before TPN. Serum TSH decreased from 120 microU/ml to 17 microU/ml in a few days after TPN and reached a level within normal range in 4 weeks. Serum TBG gradually increased from 10.7 micrograms/ml to 29.2 micrograms/ml in 6 weeks. These results show that the T4 synthesis was extremely impaired by PCM in spite of the strong stimulation by TSH and that this suppression of T4 synthesis by PCM led the patient recurrently to the primary hypothyroidism. We have next investigated the possibility whether the deficiency of phenylalanine and tyrosine could cause a suppression of T4 synthesis because tyrosine is an important substrate of T4. For this purpose we removed phenylalanine and tyrosine from TPN and added iodine to prevent iodine deficiency due to prolonged iodine-depleted nutrition. Reduction of phenylalanine and tyrosine resulted in a marked decrease in serum T4, T3 and TBG in 7 weeks, but gave no change to free T4. Serum TSH remained within normal range.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1985

Stimulation of protein glycosylation in cultured hepatoma cells by polyprenyl phosphates.

The aim of this work was to selectively stimulate N-glycosylation of proteins in cultured AH 70Btc hepatoma cells. Dolichyl phosphate, alpha-dihydrodecaprenyl phosphate and solanesyl phosphate were entrapped in egg lecithin liposomes and supplied to the cells. After treatment with 0.6-15 nmol of the polyprenyl phosphates/3 ml/dish for 48 hr, the incorporations of [14C]glucosamine into N-linked saccharide chains of glycoproteins and into lipid intermediates were increased to various extents. The stimulation by alpha-dihydrodecaprenyl phosphate was most significant and 15 nmol of the lipid/dish increased the incorporation into N-linked saccharide chains of glycoproteins by about 80%. The incorporations of [14C]glucosamine into O-linked saccharide chains and of [14C]leucine into proteins were not changed significantly by alpha-dihydrodecaprenyl phosphate. When the N-linked glycopeptides prepared from the cells and those from the cells treated with the polyprenyl phosphate were compared by Sephadex G-50 column chromatography, no significant difference was observed. Analysis of reduced cellular glycoproteins by sodium dodecyl sulfate/polyacrylamide-gel electrophoresis showed that alpha-dihydrodecaprenyl phosphate increased the incorporation of [14C]glucosamine into N-linked saccharide chains of certain high-molecular-weight glycoproteins. In addition, the polyprenyl phosphate enhanced the adhesiveness of the cells to the substratum, probably as a result of the stimulation of N-glycosylation of proteins.

Animals↗
PubMed1984

Potentiation of anticancer agents by new synthetic isoprenoids. II. Inhibition of the growth of transplantable murine tumors.

The antitumor effects of combinations of synthetic isoprenoids-decaprenylamine.HCl, N-(p-methylbenzyl)decaprenylamine.HCl [N-(PMB)-decaprenylamine.HCl], and decaprenoic acid-with anticancer agents were studied in male ICR mice with ascites sarcoma 180 (S180) and in male BALB/c mice with fibrosarcoma Meth A. Decaprenylamine.HCl, N-(PMB)-decaprenylamine.HCl, and decaprenoic acid were tested in combination with bleomycin A2 (BLM) on S180. Decaprenoic acid was also examined in combination with BLM or 5-fluorouracil (FUra) for effects on fibrosarcoma Meth A. The dosages of synthetic isoprenoids used in the combination therapy were much below the median lethal dose. In the low-dosage schedule, decaprenylamine.HCl, N-(PMB)-decaprenylamine.HCl or decaprenoic acid considerably enhanced the antitumor effect of BLM on S180; e.g., the T/C value (mean survival time of treated mice/mean survival time of controls) for decaprenylamineHCl plus BLM, N-(PMB)-decaprenylamine.HCl plus BLM, or decaprenoic acid plus BLM was 294, 357, and 279% respectively, and the combinations increased life-span 2.4-fold, 2.3-fold, or 1.8-fold, respectively, as compared to the effects of BLM alone. The combination of BLM or FUra with decaprenoic acid, when administered by iv injection to mice with fibrosarcoma Meth A (solid tumor system), did not produce synergism. However, a preventive effect of decaprenoic acid monotherapy was observed: Decaprenoic acid at 3 mg/kg resulted in 38.9% suppression of tumor growth 21 days after inoculation.

Animals↗
PubMed1984

[Quantitation of left-sided valvular regurgitation by gated cardiac blood pool scan: evaluation of a new approach using the Fourier amplitude ratio].

Utilizing the Fourier amplitude ratio (FA ratio), we evaluated a new approach for quantitating valvular regurgitation by the gated cardiac blood pool scan. The subjects consisted of 36 patients with documented left ventricular regurgitation of grade I-IV (group 1), 24 patients with myocardial infarction including severe cardiac dysfunction (group 2), and 15 normal persons (group 3). From each pixel of the gated cardiac blood pool scan, a time-activity curve was obtained and the first-harmonic Fourier analysis was performed. Two functional images; namely, the phase and amplitude images, were generated. To generate the FA ratio, the region of interest was drawn around each ventricle in the amplitude image. The FA ratio was calculated using the following formula; FA ratio = left ventricular amplitude value/right ventricular amplitude value. The FA ratio was 2.66 +/- 1.75 (mean +/- S.D.) in group 1; 1.29 +/- 0.27 in group 2; and 1.11 +/- 0.19 in group 3. The FA ratio for group 1 was significantly higher than those of groups 2 and 3 (p less than 0.001). There was no significant difference between the FA ratios of groups 2 and 3. In patients with regurgitation, the FA ratio was 1.50 +/- 0.37 in patients with grade I, 1.97 +/- 0.34 in grade II, 2.73 +/- 0.95 in grade III; and 6.65 +/- 2.14 in grade IV. There was a good agreement between the FA ratios and quantitative angiographic estimates of regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Potentiation of anticancer agents by new synthetic isoprenoids. I. Inhibition of the growth of cultured mammalian cells.

In this study, 9 new synthetic isoprenoids with 9-10 isoprene chains were tested. One-fifth of the D10 value (concentration of drug that reduced colony-formation ability to 10% that of control) for each isoprenoid was calculated from dose-response curves of Chinese hamster V79 cells or human HeLa cells in culture. That dose was combined with various anticancer agent [1-(4-amino-2-methylpyrimidin-5-yl)methyl-3-(2-chloroethyl)-3-n itrosurea HCl, bleomycin A2 (BLM), cisplatin, doxorubicin (Dx), 5-fluorouracil, mitomycin, and 6-mercaptopurine] to test whether isoprenoids can potentiate the cytotoxic effect of anticancer agents against cultured mammalian cells. Among the 9 isoprenoids tested, decaprenoic acid, dacaprenylamine.HCl, and N-(p-methylbenzyl)decaprenylamine.HCl significantly potentiated BLM and Dx. Some isoprenoids increased intracellular levels of anticancer agents. Both enhanced uptake and reduced efflux of Dx were observed.

Animals↗
PubMed1983

The lipopolysaccharide from Pseudomonas aeruginosa NCTC 8505. Structure of the O-specific polysaccharide.

Structural studies have been carried out on the O-specific fraction from the lipopolysaccharide of Pseudomonas aeruginosa NCTC 8505, Habs serotype 03. The O-specific polysaccharide has a tetrasaccharide repeating-unit containing residues of L-rhamnose (Rha), 2-acetamido-2-deoxy-D-glucose (GlcNAc), 2-acetamido-2-deoxy-L-galacturonic acid (GalNAcA), and 2,4-diacetamido-2,4,6-trideoxy-D-glucose (BacNAc2). The following structure has been assigned to the repeating-unit: leads to 3)Rhap(beta 1 leads to 6)GlcpNAc(alpha 1 leads to 4)GalpNAcA(alpha 1 leads to 3)BacpNAc2(alpha 1 leads to. The parent lipopolysaccharide is a mixture of S, R, and SR species, and its high phosphorus content is partly due to the presence of triphosphate residues, as found for other lipopolysaccharides from P. aeruginosa. In addition to phosphorus, heptose, a 3-deoxyoctulosonic acid, and amide-bound alanine, the core oligosaccharide contains glucose, rhamnose, and galactosamine (molar proportions 3:1:1). The rhamnose and part of the glucose are present as unsubstituted pyranoside residues: other glucose residues are 6-substituted.

Carbohydrate Sequence↗
PubMed1983

Salivary gland glucagon is a fictitious substance due to tracer-degrading activity resistant to protease inhibitors.

A high level of glucagon immunoreactivity was apparently detected in acid-saline extract from rat submandibular glands, but tracer glucagon added to the assay mixture was mostly damaged in spite of the presence of protease inhibitors commonly used in radioimmunoassay. Gel-filtration of the extract on a Bio-Gel P-10 column revealed strong tracer-degrading activity at the void fraction where the apparent immunoreactivity was eluted. Serial changes in apparent immunoreactivity of the extract fit well on the theoretical curve of an exponential tracer degradation. These findings indicate that the salivary gland glucagon is a fictitious substance due to tracer degradation during radioimmunoassay. Further study revealed that the glucagon molecule was hydrolyzed at the arginyl bonds and split into two fragments during incubation with the acid-saline extract from rat submandibular glands.

Animals↗
PubMed1982

[Measurement of left-sided valve regurgitation by gated cardiac blood pool scans using stroke volume imaging].

Radionuclide gated cardiac blood pool scan was used to quantify the left-sided valvular regurgitation by calculating the ratio of left ventricular to right ventricular stroke counts (the stroke count ratio) obtained directly from the "stroke volume image." The subjects consisted of 21 patients and 11 control subjects. In 21 patients, contrast angiography disclosed that 10 had isolated mitral regurgitation, nine had isolated aortic regurgitation and two had combined mitral and aortic regurgitation. The degree of aortic and/or mitral regurgitation was judged using the Sellers' criteria. The stroke count ratio was 1.34 +/- 0.21 (mean +/- SD) in a group without regurgitation, 1.73 +/- 0.13 in a group of patients with grade I, 2.14 +/- 0.19 in grade II, 2.76 +/- 0.58 in grade III and 5.04 +/- 0.27 in grade IV regurgitation. There was a good agreement between the stroke count ratios and quantitative angiographic estimates of regurgitation. Furthermore, the use of the "stroke volume image" (obtained from the subtraction of end-systolic from end-diastolic images) allowed a simplified drawing of the region of interest and avoided the problem in selecting the background. For its simplicity, we found little interobserver and intraobserver variations (r = 0.98 in the former and r = 0.99 in the latter). Therefore, this method permits a noninvasive and reliable assessment of the severity of left-sided valvular regurgitation, and has a great potential clinical utility in the long-term follow-up of asymptomatic patients with regurgitation, and in the evaluation of the results of medical and surgical interventions.

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