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Biomedical subjects

T Kishi

Publications and source records attributed to T Kishi.

At least 145 records · Page 8Linked to original sources
PubMed1986

The inhibitory effect of lysozyme on the glomerular basement membrane thickening in spontaneous diabetic mice (NSY mice).

Currently, there is no effective treatment for diabetic microangiopathy. We have been examining, therefore, the effects of lysozyme on the renal conditions of spontaneous diabetic mice (NSY mice). We assessed the changes in glomerulus following the administration of lysozyme, using the thickness of the glomerular capillary basement membrane as an indicator. Littermate, male F19 NSY mice were divided into two groups. One of the groups (Group L) was treated with lysozyme; the other control group (Group C) with physiological saline. Group L received a daily intramuscular injection of lysozyme solution for 4 or 8 weeks. The thickness of the glomerular capillary basement membrane was measured in order to assess the effect of lysozyme administration. In the 4-week series, the thickness was 4783 +/- 1760 A in Group C and 3266 +/- 777 A in Group L, while in the 8-week series it was 6011 +/- 2043 A in Group C and 3540 +/- 431 A in Group L. In both series of Group L, a distinct inhibitory effect on the basement membrane thickening was found. The present findings suggest that lysozyme may be effective in human diabetic nephropathy. However its clinical usefulness must be confirmed in future studies.

Animals↗
PubMed1986

Alveolar lymphocyte proliferation induced by Propionibacterium acnes in sarcoidosis patients.

The proliferation of lymphocytes induced by Propionibacterium acnes (P. acnes) was measured by the in vitro incorporation of 3H-thymidine. The mean response rate of alveolar lymphocytes obtained by bronchoalveolar lavage was 2.23 +/- 0.89 in nine untreated sarcoidosis patients, 0.85 +/- 0.17 in five sarcoidosis patients given corticosteroids and 0.78 +/- 0.29 in 11 controls. The proliferation was significantly enhanced in the untreated patients compared to both the treated patients (p less than 0.01) and controls (p less than 0.001), but there was no significant difference in response rates between the treated patients and controls. The response rate of alveolar lymphocytes was significantly higher in four active patients (3.05 +/- 0.61) than in four inactive patients (1.77 +/- 0.44) (p less than 0.05) and in the controls (p less than 0.001). In sarcoidosis patients, the response rates showed a good correlation with activities of serum lysozyme (r = 0.695, p less than 0.01), and with percentages of lymphocytes in bronchoalveolar lavage fluid (r = 0.591, p less than 0.05). There was a low correlation between angiotensin-converting enzyme activities and the response rates (r = 0.508, p less than 0.1). Neither peripheral blood lymphocytes in sarcoidosis patients nor in controls showed any response to P. acnes, but alveolar lymphocytes of the untreated active sarcoidosis patients were sensitive to P. acnes. The lymphocytes activated by P. acnes may play a central role in the induction of alveolitis in sarcoidosis patients.

Adult↗
PubMed1986

The metabolism of 1-phenyl-2-(N-methyl-N-furfurylamino)propane (furfenorex) in the rat in vivo and in vitro.

The metabolism of 1-phenyl-2-(N-methyl-N-furfurylamino)propane (furfenorex) was studied in the rat in vivo and in vitro. Nine metabolites with only traces of the unchanged drug were obtained from urine after oral administration of furfenorex to rats. The major metabolite was an acidic compound, isolated and identified as 1-phenyl-2-(N-methyl-N-gamma-valerolactonylamino)propane. Amphetamine, methamphetamine and their hydroxylated metabolites were excreted as minor metabolites. Metabolites excreted in two days after administration of the drug amounted to about 20% of dose. The acidic metabolite, a major metabolite in vivo, was not detected after incubation of furfenorex with rat-liver microsomes. The major metabolic routes of furfenorex in vitro were N-demethylation and N-defurfurylation which produced 1-phenyl-2-(N-furfurylamino)propane (furfurylamphetamine) and methamphetamine, respectively. The formation of furfurylamphetamine and methamphetamine were catalysed by rat-liver microsomes supplemented with NADPH and O2, and were inhibited by either SKF 525-A or CO. The formation of both metabolites were inhibited by 2-methyl-1,2-bis-(3-pyridyl)-1-propanone (metyrapone), but not by 7,8-benzoflavone. They were enhanced by pretreatment of rats with phenobarbitone, but not with 3-methylcholanthrene. These data suggested that N-demethylation and N-defurfurylation of furfenorex were mainly mediated by cytochrome P-450 but not cytochrome P-448.

Animals↗
PubMed1986

Serum levels of coenzyme Q10 and lipids in patients during total parenteral nutrition.

Serum levels of coenzyme Q10 (CoQ10) as well as lipids were determined in patients during total parenteral nutrition (TPN). The mean CoQ10 levels (M +/- SD) were 0.77 +/- 0.30 microgram/ml for 108 normal subjects and 0.59 +/- 0.35 microgram/ml for 95 patients before TPN. The mean CoQ10 level of the patients decreased significantly to 0.35 +/- 0.23 microgram/ml one week after the start of TPN, and then remained almost unchanged during TPN for up to 6 weeks. When the patients receiving TPN (TPN patients) were grouped according to their clinical diagnoses, the mean CoQ10 level of patients with cancer was significantly lower than that of the other patients without cancer in 4 week therapy, but there was no difference in the levels between the patients with and without diseases of the gastrointestinal tract. Serum levels of total cholesterol (T-Chol) and esterified cholesterol in TPN patients also declined below their respective normal ranges, but not to the same extent in comparison to CoQ10. The levels of triglycerides (TG), phospholipids (PL), non-esterified fatty acids, low density lipoproteins, very low density lipoproteins, chylomicrons, and cholesterol in the high density lipoprotein fraction in serum of TPN patients were within their normal ranges. The levels of CoQ10 in TPN patients were correlative to those of T-Chol, TG, and PL, and decreased rapidly prior to the latter levels.

Adolescent↗
PubMed1985

High-performance liquid chromatography of coenzyme Q-related compounds and its application to biological materials.

A convenient and precise method for the separation and determination of coenzyme Q (CoQ)-related compounds (CoQ homologues, plastoquinone-9, ubichromenol-9, etc.) was developed using high-performance liquid chromatography (HPLC). All compounds tested were separated using a reverse-phase column with a suitable mobile phase and detected at a wavelength of 275 nm. CoQ extracts in plasma and erythrocytes were purified by thin-layer chromatography prior to HPLC analysis, but such purification was not necessary when determining CoQ in urine and tissues. Hydroquinone forms of CoQ existing in animal tissues were oxidized to the corresponding quinone forms with potassium hexacyanoferrate(III). This HPLC method was applied satisfactorily to the determination of the contents of CoQ homologues in human and animal samples. CoQ10 was the only homologue detected in human samples, and CoQ8, CoQ9 and CoQ10 were native homologues of CoQ in rat tissues. Ubichromenol-9 and plastoquinone-9 were not detected in these samples.

Adult↗
PubMed1985

Decreased monocyte-mediated cytostasis of human cancer cell in patients with lung cancer.

In vivo animal studies support the concept that monocytes and macrophages are important in the immune surveillance of oncogenesis and that in vitro activated murine macrophages are cytocidal for tumour cells. In this study, the tumour cell cytotoxic activity of human peripheral blood monocytes was examined by measuring the inhibition of 3H-thymidine uptake in the human cancer cell line, established in our laboratory from human squamous cell lung cancer. The monocytes from 8 of the 31 lung cancer patients (26%) showed a percentage growth inhibition of less than 69.8%, which exceeded the 95% confidence limits of the percentage growth inhibition observed with healthy control monocytes. On the other hand, among the 16 sarcoidosis and the 8 tuberculosis cases no value was below 69.8%. However, there was no significant difference between the growth inhibition and the clinical stages or histological type. When OK-432, a Streptococcal agent, was administered in vivo to patients with lung cancer, an elevation of the growth inhibition was observed in 7 out of 8 patients. It was confirmed that the tumour cell cytostatic activity of the monocyte is suppressed in patients with lung cancer, and these monocyte deficits hinder the inhibition of tumour growth and metastasis.

Cell Division↗
PubMed1985

Inhibition by adenine of in vitro immunological functions of normal and adenine phosphoribosyltransferase-deficient human lymphocytes.

Exogenous adenine strongly inhibited mitogen-stimulated transformation, cytoplasmic immunoglobulin production, and natural killer activity of human mononuclear leukocytes at the high concentration of 1.0 mM. These inhibitions by adenine were not due to cytotoxicity, because the viability of cultured cells was not affected by adenine up to 1.0 mM. As the magnitude of inhibition by adenine of these in vitro immunological functions was similar in normal and adenine phosphoribosyltransferase-deficient cells, its inhibition was not mediated by corresponding nucleotides. Adenine at the concentration of 0.1 mM caused 50% inhibition of cytoplasmic immunoglobulin production without alternating cell proliferation or viability. This suggests that an appropriate concentration of adenine may inhibit the differentiation of B cells to plasma cells rather than affecting cell proliferation. Understanding the mechanisms of adenine inhibition may lead to new approaches for the regulation of immune responses.

Adenine↗
PubMed1985

Natural killer activity in two cases of ataxia telangiectasia.

We report two cases of ataxia telangiectasia in which a small number of T cells and a slightly diminished response to phytohaemagglutinin or concanavalin A were observed. In one case, serum IgA was undetectable. In spite of T and/or B cell involvement, natural killer activity and the percentage of natural killer cells determined by monoclonal antibodies Leu 7 were normal in both cases.

Adolescent↗
PubMed1985

LPF-induced T cell colony formation: effect of PMA and interleukin-2, and surface marker analysis.

We demonstrated that a primary exposure to the lymphocytosis promoting factor (LPF) of Bordetella pertussis-induced T cell colony formation. Colony formation was observed when mononuclear cells (MNC) were cultured at concentrations of more than 1 X 10(6)/ml, and reached a peak on day 8. However, the number of colonies generated with LPF was about one-third induced with phytohaemagglutinin (PHA). Removal of monocytes from MNC or T cells resulted in the failure of colony formation, but colony growth could be restored by the addition of monocytes or B enriched cells, indicating that they were required for the optimal colony growth induced by LPF. In the absence of accessory cells, optimal colony growth from monocyte depleted T cells could be obtained when an appropriate concentration of phorbol myristate acetate (PMA) or interleukin-2 (IL-2) was added in the cultures with LPF. PMA did not enhance LPF-induced colony formation in the cultures containing a sufficient amount of exogeneous IL-2. These findings suggest that IL-2 is essential to LPF-induced colony formation. Surface marker analysis showed that most of LPF-induced colony cells were T cells. The percentages of T4+ and T gamma cells of LPF-induced colony cells were more, and T8+ cells less, than those of PHA-induced colony cells. Ia1, T9 and Tac antigens were detected on many colony cells induced by LPF or PHA. These results indicate that the phenotype of LPF-induced colony cells differs from those of PHA, but the sequential antigen expression on lymphocytes triggered by IL-2 might be similar in both LPF- and PHA-induced colony formation.

Antigens, Surface↗
PubMed1984

Quantitative determination of coenzyme Q10 in human blood for clinical studies.

A quantitative method for the determination of coenzyme Q10 (CoQ10) in human blood has been devised which allows recovery of essentially 100% of the CoQ10. The use of whole blood rather than plasma includes the CoQ10 in white cells. The method utilizes TLC instead of saponification to fractionate lipid impurities, because CoQ10 is sensitive to saponification, and utilizes CoQ11 as an internal standard which is advantageous over CoQ9 and a synthetic quinone. The final step of HPLC frequently reveals a peak with a retention time like that of CoQ9 which, being less than that of CoQ10, can be near other peaks of impurities.

Chromatography, High Pressure Liquid↗
PubMed1984

Myocardial sarcoidosis with a tumor-like left atrial thrombus.

We report here an elderly woman who started vague complaints around the age of 50, was proved to be a sarcoidosis by negative skin reaction with purified protein derivative, bilateral hilar lymphadenopathy, and sarcoid lesions in biopsied liver and lymph nodes, and died of cardiac insufficiency after 15 years of the illness. Necropsy revealed a huge tumor-like left atrial thrombus with nonspecific fibrous lesions throughout the myocardium, a pulmonary hamartoma, pneumonia, liver cell necrosis, and cholecystopathy. To our knowledge, this may be the first case of myocardial sarcoidosis associated with this kind of atrial thrombus, although the sarcoidosis and thrombus may have occurred independently.

Aged↗