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Biomedical subjects

K Aoki

Publications and source records attributed to K Aoki.

At least 883 records · Page 49Linked to original sources
PubMed1982

Bracken fern, phenacetin, and cancer of the urinary tract.

Bracken fern, a forage contaminant, is causally related to urinary bladder cancer in animals. In this review of experimental studies on carcinogenesis of bracken fern, little evidence of an association between cancer and bracken fern in humans was observed. Clinicoepidemiological studies have shown a high frequency of phenacetin abusers in certain cases of lower urinary tract cancers that indicate case-control studies of phenacetin and related compounds are needed.

Aged↗
PubMed1982

[Host factors in human carcinogenesis].

In human cancers, the contribution of genetic determinants is often difficult to distinguish from environmental influences. However, some cancers are inherited in Mendelian pattern, and some have closely associated with the diseases with hereditary factors. This paper reviewed characteristics of hereditary cancers, the diseases with high incidence of cancers and familial aggregation of cancers, and discussed the role of host factors in the etiology of cancer clinico-epidemiologically.

Adolescent↗
PubMed1981

Estimating evolutionary distance from restriction maps of mitochondrial DNA with arbitrary G+C content.

We develop a mathematical model for estimating evolutionary distance from restriction enzyme maps, which incorporate non-uniformity of the rate of base substitution into the theory and allows for an arbitrary G+C content at equilibrium. When the G+C content differs significantly from 1/2, the traditional model of base changes can introduce a systematic bias which depends upon the base composition of the restriction site. In addition, the accuracy of estimated evolutionary distance depends heavily upon the choice of restriction enzyme in that the expected number of sites is also affected. Monte Carlo experiments are conducted to check the validity of the present theoretical treatment and from which we draw several cautionary notes on estimation. An application is made to the available data on restriction enzyme maps of human mitochondrial DNA where the G+C content is approximately 1/3.

Base Composition↗
PubMed1981

Quantitative changes in myelin proteins in a peripheral neuropathy caused by Tullidora (Karwinskia humboldtiana).

Peripheral nerve demyelination was induced in cats by oral administration of ether extracts of Tullidora (Karwinskia humboldtiana). Proteins from several hindlimb nerves, spinal roots, and dorsal columns of the spinal cord were subjected to slab gel electrophoresis and quantified by densitometry. In Tullidora-treated cats with severe motor disturbances, specific myelin proteins were reduced by at least 50% in motor nerves and less than 25% in cutaneous axons. There was a greater decrease of these proteins in the distal than in the cephalad segments of the sciatic nerve; no changes were detected either in the spinal roots or in the white matter of the spinal cord. Electron microscopy revealed intense demyelination in the motor nerves only. Both the density of the 100 A-thick neurofilaments and the relative proportion of a polypeptide with a molecular weight of 68,000 were considerably increased in the affected nerves. It is tentatively concluded that the active principles of Tullidora may enter the axons through the motor nerve terminals. The distal segments of the motor nerves would then be preferentially affected and demyelination could result from axonal damage.

Animals↗
PubMed1981

Noradrenaline and calcium induced tension in aortic strips of normotensive and spontaneously hypertensive rats.

Development of tension in aortic helical strips was studied using the male Kyoto Wistar normotensive (KNR) and age-, sex-matched spontaneously hypertensive rats (SHR) (8 to 10 weeks) to clarify the contractile response of vascular smooth muscle in SHR. In Ca2+-containing solution, noradrenaline-induced tension was smaller in SHR than in KNR. After washing the strips with Ca2+-free EGTA solution, the tension that developed by the addition of Ca2+ was greater in SHR than in KNR. Tension induced by the combination of Ca2+ and noradrenaline was the same between the KNR and SHR. It is assumed that these differences between the KNR and SHR aortic strips may be attributed to the abnormal contractility of the vascular smooth muscle in SHR.

Animals↗
PubMed1981

Hypotensive action of nifedipine (Ca2+-antagonist) and propranolol in acute trials and its long-term therapy of hypertensive coronary heart disease patients.

The hypotensive effect of nifedipine (a Ca2+-antagonist) was studied in acute tests and during the long-term administration of the drug together with propranolol. Nifedipine (10 mg, sublingually) decreased blood pressure from 174/102 to 136/82 mmHg with increase in heart rate and plasma renin activity. The combination of nifedipine (10 mg, sublingually) and propranolol (0.2 mg/Kg body weight, intravenously) decreased blood pressure from 168/104 to 131/86 mmHg with decrease in heart rate and plasma renin activity. Twenty-five hypertensive patients were treated with nifedipine and propranolol (10 mg x 3 to 4/day) together with or without diuretic for long-term. With the combination therapy, blood pressure of Group I (11 hypertensive patients with coronary heart disease) fell from 211/129 to 140/85 mmHg, blood pressure of Group II (9 severe hypertensive patients without coronary heart disease) from 230/137 to 139/84 mmHg, and blood pressure of Group III (5 established hypertension) from 182/107 to 134/83 mmHg. With this treatment regimen, heart rate and plasma renin activity decreased, and abnormal electrocardiographic findings, hypertensive retinopathy, and renal dysfunction were improved. Nifedipine, in combination with propranolol and a diuretic, is considered an effective treatment of hypertension either with or without coronary heart disease.

Antihypertensive Agents↗
PubMed1981

Histidinemia: biochemical parameters for diagnosis.

A highly specific and sensitive procedure for determining histidase activity, with labeled histidine as the substrate, that requires only 1 to 2 mg of stratum corneum epidermidis has been developed. Methods for determining ratios of urocanic acid to histidine (U/H) in stratum corneum epidermidis and for measuring excretion of histidine and its metabolites by thin-layer chromatography were developed. Application of this triad--stratum corneum epidermidis histidase determination, measurement of stratum corneum U/H, and analysis of excretion of histidine metabolites--should facilitate evaluation of the condition of infants and young children with suspected histidinemia. Moreover, differentiation between patients with the classic form and genetic variants of the disorder should now be possible.

Adult↗