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Biomedical subjects

K Koide

Publications and source records attributed to K Koide.

At least 19 recordsLinked to original sources

Takayasu arteritis in Japan.

Takayasu arteritis is a disease on which many investigations have been conducted to determine its causes, clinical features and treatment, since 1908 when it was reported by Dr. Takayasu. The first nationwide epidemiological survey on Takayasu arteritis was conducted over 3 years from 1973 through 1975 by a research group on "aortitis syndrome", a disease specified by the Ministry of Health and Welfare. Another nationwide survey on this disease over a period of 3 years was carried out from 1982 through 1984 by a research group focusing on "systemic vascular lesion", another disease specified by the Ministry of Health and Welfare. The present study reports on the combined results of these two nationwide epidemiological surveys.

Adolescent

Metabolism of L-amino acids in a marine bacterium isolated from mackerel intestines in relation to eicosapentaenoic acid biosynthesis.

Metabolism of glucose and L-amino acids in an obligately aerobic marine bacterium isolated from Pacific mackerel intestines was investigated for the mechanism and pathway of eicosapentaenoic acid (EPA) biosynthesis. This bacterium could not uptake glucose but the cell-free extract of this bacterium had the enzymatic activities of L-alanine oxidase (EC 1.4.3.2), L-alanine dehydrogenase (EC 1.4.1.1). L-serine dehydratase (EC 4.2.1.13), and malate dehydrogenase (EC 1.1.1.40), and of seven enzymes involved in the TCA cycle of the usual aerobes. On the other hand, the carbon-13 concentration in cellular fatty acids of the bacterium, especially that in their methyl carbon atoms in contrast to their carbonyl carbons, increased drastically when the bacterium was grown in the presence of 13CH3COONa. These results indicate that: (i) the TCA cycle works in this bacterium, (ii) glucose is not utilized and pyruvic acid is in vivo synthesized from L-alanine, L-serine, and malic acid, and (iii) EPA and other cellular fatty acids are in vivo synthesized from acetyl coenzyme A by the usual de novo synthesis route.

Amino Acids

[Impairment of acid-base balance in renal failure].

It is very critical for the living organism to maintain homeostasis of body fluid volume and its electrolyte composition by renal regulation, including acid-base balance. In renal failure, impaired acid-base balance is inescapable because of disturbed urinary acidification, one of the major renal functions. Among all types of acid-base imbalance, metabolic acidosis is a major one in renal failure. For better understanding of this issue, several fundamental items for the renal mechanisms of urinary acidification must be discussed first, and the pathophysiological features and their relevant treatment for acid-base imbalances in renal failure, next. Moreover, some comments on the practical aspects, in long-term dialyze uremic patients, is also provided.

Acid-Base Imbalance

[The molecular basis for the steroid hormone actions in the kidney].

Steroid hormones such as mineralo- and glucocorticoids act as important regulators for the kidney to maintain the body fluid homeostasis. During the past 40 years, numerous investigations have been dedicated to the elucidation of precise mechanisms of steroid hormone actions in their target tissues including the kidney. Now it is well recognized that cellular actions of steroid hormones can be accomplished by two step processes, namely a specific receptor binding in the cytosol and/or the nucleus and a new protein synthesis through a gene transcription. The efforts for the isolation and purification of steroid hormone receptors have been also made and followed by the great successes of molecular techniques in the cDNA cloning and determination of amino acid sequences for them in recent years. The revealed high homology of the functional domains of receptors has renewed the issues of how tissue specificities of steroid hormone actions are determined. The identification of steroid-induced proteins and cellular steroid hormone metabolites would be also important issues to be studied.

11-beta-Hydroxysteroid Dehydrogenases

A study of oral adsorbent in chronic renal failure.

In order to examine the effect on the progression of chronic renal failure (CRF), we have applied an oral adsorbent (AST-120) composed of spherical porous carbon particles to patients with chronic renal failure undergoing conservative therapy. Its effect was observed in improvement of uremic symptoms, improvement of slope in linear regression of reciprocal of serum creatinine vs. time plots and delayed initiation of hemodialysis, compared to control patients, together with reduced uremic peak 2a in HPLC analysis of serum and lower levels of beta 2 microglobulin in AST-120 group than in control. The improvements of uremic symptoms, creatinine and 2a levels were confirmed in double blind study where background of patients were evenly randomized between AST-120 and placebo groups and no improvement was observed in placebo group. The result leads us to conclude that the oral adsorbent therapy is expected as an useful therapy for retardation of progression of CRF.

Administration, Oral

[Clinical significance of thrombocytopenia associated with hemorrhagic cerebrovascular diseases].

We investigated the clinical significance of thrombocytopenia (platelet counts less than 10 x 10(4)/mm3) associated with hemorrhagic cerebrovascular disease. This study was conducted in 96 patients suffering from hemorrhagic cerebrovascular diseases. We divided the clinical course into 3 stages: acute (from the 1st to 7th day), subacute (8th-21st day) and chronic (after the 22nd day). The average age of the patients with thrombocytopenia (TCP) was 60.6 years old. TCP was more frequent in men (81.3%) than in women (18.7%). TCP developed in 18.6% (8/43) of patients with subarachnoid hemorrhage (SAH) and in 15.1% (8/53) of those with intracerebral hemorrhage (ICH). Among the patients with SAH, four were in the acute stage, three in the subacute stage and two in the chronic stage. TCP due to SAH was more likely to develop in the acute and/or subacute stage. TCP due to SAH showed two peak appearances: the first was within 24 hours (n = 3), and the second was around 10 days after onset (n = 3). The cause of TCP in its late peak appearance was presumed to be the consumption of platelets due to microembolism induced by vasospasm and/or hemodilution therapy. Among patients with ICH, five cases were in the acute stage, three in the subacute stage and two in the chronic stage. TCP due to ICH was more likely to develop in the acute stage. Fifty percent (4/8) of the patients with ICH had TCP on admission. This data suggested that TCP was possibly a cause or an inducer for ICH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult