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Biomedical subjects

R Yamada

Publications and source records attributed to R Yamada.

At least 307 records · Page 17Linked to original sources
PubMed1982

[Two dimensional echocardiographic diagnosis of mitral valve prolapse syndrome in presumably healthy young students].

We studied the prevalence of mitral valve prolapse (MVP) in presumably healthy young students using two-dimensional echocardiography and compared their clinical pictures with those of hospital patients with MVP. In 265 students undergoing routine physical examination (228 males and 37 females, aged from 18 to 25 years), 29 (11%) were diagnosed as having MVP. There was no sex difference (11% for males and 8% for females). Anterior leaflet prolapse was seen in 26 cases, and anterior and posterior leaflets prolapse was in 3 cases. Twenty-four of the 29 MVP students revealed neither midsystolic click, late systolic murmur nor holosystolic murmur on phonocardiograms (PCG). These 24 students had no cardiac symptoms and the incidence of electrocardiographic (ECG) abnormalities, such as arrhythmias and ST-T changes, was similar to that of students without MVP (4/24 vs 50/236). In contrast, of 54 patients (32 males and 22 females, aged from 15 to 25 years) who were diagnosed as having MVP in the hospital, 28 patients (52%) had no PCG abnormalities. The anterior leaflet was predominantly involved in 42 patients and both anterior and posterior leaflets in 12 patients. These 28 patients visited the hospital because of cardiac symptoms; dyspnea on exertion (3 patients), palpitation (2 patients) or atypical chest pain (7 patients), or abnormal physical examination (11 patients). ECG abnormalities were noticed in 15 of 28 patients (54%). The prevalence of cardiac symptoms and ECG abnormalities were similar to those in 26 patients with PCG evidence of MVP. It was concluded that the prevalence of MVP in young healthy students is 11% and the anterior leaflet is predominantly involved. Most cases were asymptomatic and had no PCG or ECG abnormalities. In contrast, age-matched MVP patients, diagnosed in the hospital with the same two-dimensional echocardiographic criteria, demonstrated similar predominancy of the anterior leaflet prolapse, but had more cardiac symptoms and ECG abnormalities, irrespective of the presence or absence of PCG findings.

Adolescent↗
PubMed1981

Influence of angiotensins (I, II & III) on prostaglandin production by minced rat renal medulla.

Minced rat renal medulla was incubated for 30 min at 37 degrees C in the presence of angiotensin I, II or III (100 ng/ml) to determine the existence of a direct stimulating effect on prostaglandin (PG) production. PGE2, PGF2 alpha, 6-keto PGF1 alpha and Thromboxane B2 (TXB2) were determined by radioimmunoassay. For analysis of data variance, the results were separated according to whether the net output of PGE2 was above or below 1.5 ng PGE2 equivalent/mg tissue/30 min. Under low-output conditions, angiotensin I, II or III stimulated PGE2 production significantly (p less than 0.02) and tended to augment PGF2 alpha production, while under high-output conditions no effect on PGE2 or PGF2 alpha production was observed. Under either output condition, angiotensin I, II or III had no effect on 6-keto PGF1 alpha and TXB2.

Alprostadil↗
PubMed1981

Role of pyridoxal kinase in vitamin B6 uptake by Escherichia coli.

Escherichia coli KG980, a vitamin B6 auxotroph derived from wild strain K12, concentrated exogenous pyridoxal in an energy-dependent manner, and the effects of energy sources and inhibitors on pyridoxal uptake, compared with those on proline uptake indicated that the energy required was in the form of phosphate bonds and not of membrane potential. The vitamin taken up was primarily present as pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate intracellularly, and energy depletion decreased the accumulation as the phosphorylated derivatives but not as unaltered pyridoxal itself. This finding suggested that the intracellular phosphorylation, which was known to require ATP, was essential for the concentrative uptake of the vitamin. The suggestion was confirmed by the following evidence. 1) Pyridoxal oxime inhibited pyridoxal uptake by decreasing the intracellular phosphorylation without affecting the entry of pyridoxal across the cell membrane. 2) A pyridoxal-kinase deficient mutant (HN1) derived from the strain KG980 showed a low ability to take up pyridoxal because of the failure to accumulate it effectively as phosphorylated derivatives. The carrier-mediated nature of pyridoxal uptake, previously suggested by saturation kinetics, was further supported by the present finding that 4'-deoxypyridoxine inhibited pyridoxal uptake competitively, decreasing the intracellular appearance of unmetabolized pyridoxal. It is therefore most likely that pyridoxal enters the cells by facilitated diffusion and is accumulated by conversion to phosphorylated derivatives. Similar results on the uptake of pyridoxine and pyridoxamine are also presented.

Escherichia coli↗
PubMed1981

Inactivation of microbial pyridoxal kinase by pyridoxal.

Pyridoxal kinase from Escherichia coli and bakers' yeast was inactivated by pyridoxal while the enzyme from rat and pig brain was not. The inactivation of the enzyme purified from E. coli was reversible and was rendered irreversible by the reduction with NaBH4. This finding as well as a similar inactivation by 5'-deoxypyridoxal but not by 4'-deoxypyridoxine suggested that the inactivation was due to Schiff base formation. The suggestion was confirmed by the incorporation of tritium label into the enzyme by the reaction of the enzyme with [3H] pyridoxal followed by the treatment with NaBH4. Correlation between the loss of enzyme activity and the amount of pyridoxal bound to the enzyme showed that binding of pyridoxal to one crucial site completely inactivated the enzyme. Pyridoxine and 4'-deoxypyridoxine did not have a protective effect against inactivation indicates that the binding site was not the substrate site. The results of kinetic and equilibrium analyses were consistent with a one-step inactivation mechanism.

Animals↗