Search PubMed⌕ Search

Biomedical subjects

A Sakai

Publications and source records attributed to A Sakai.

At least 433 records · Page 24Linked to original sources
PubMed1982

Mutagenicity of N-nitroso compounds formed by the reaction of sulpyrine with nitrite; effects of cysteine and its derivatives.

Cysteine and its derivatives were tested for their effect on the mutagenic activities of nitrosation products of sulpyrine, 1-diketo-butyryl-1-phenyl-2-methyl-2-nitrosohydrazide hydrate (DPMN) and 4-(N-methyl-N-nitroso)aminoantipyrine (MNAA), using Salmonella typhimurium TA100. The addition of cysteine, cysteamine, cysteine methyl ester, glutathione, 2-mercaptoethanol and homocysteine to the mixture of DPMN and bacteria before pre-incubation markedly increased the mutagenic activity of DPMN in the absence of rat-liver microsomal preparation (S9 mix). An approximately thirty-fold increase in the number of revertants was caused by the addition of cysteine at a concentration of 3 mmol/1. Studies of the structure-activity relationship suggest that a thiol group is necessary in order that the compounds exhibit the enhancing effect and that the thiol compounds having an amino group at the beta-position are more active than the others. Both cysteine and glutathione were rather inhibitory in the development of mutagenesis by MNAA in the presence of S9 mix.

Aminopyrine↗
PubMed1981

A case of the left innominate vein passing behind the ascending aorta.

The authors observed the postaortic left innominate vein, which passed behind the ascending aorta, in the body of a 69-year-old Japanese male during dissection in 1979. In this case, no rudiment of the ordinary left innominate vein could be found in front of the arteries arising from the arch of the aorta. There are few reports of this anomaly and an extensive search of the available literature revealed only ten cases, including three in Japan. Adachi classified the postaortic left innominate vein into two types, types I and II, on the basis of the positional relation between the left innominate vein and the ligamentum arteriosum. Our case was of type I, in which the left innominate vein passed ventral to the ligamentum arteriosum and ran across from left to right behind the ascending aorta to join the right innominate vein. The embryological explanation which generally is accepted for the postaortic left innominate vein lies in the transposition of a transverse connection, which becomes the left innominate vein in a later stage of development, between the left and right anterior cardinal veins from the ventral to dorsal sides of the rudiment of the ascending aorta.

Aged↗
PubMed1981

Analysis of alveolar PCO2 control during the menstrual cycle.

We attempted to analyze how PACO2 is regulated during progesterone-induced hyperventilation in the luteal phase. A model for the CO2 control loop was constructed, in which the function of the CO2 exchange system was described as PACO2 = 0.863 x VCO2/VA (gain H = dPACO2/dVA) and that of the CO2 sensing system as VA = S (PACO2 - B). Using this model, we estimated (1) the primary increase in VA (delta VA (op)) produced by progesterone stimulation and (2) the effectiveness (E) of the loop to regulate PACO2, defined as delta PACO2 (op)/delta PACO2 (cl) in which op signifies open-loop and cl, closed-loop. These respiratory variables were investigated throughout the menstrual cycle in 8 healthy women. During the luteal phase, on average, VA increased by 9.4% and PACO2, B and H decreased by 0.33 kPa (2.5 mm Hg), 0.47 kPa (3.5 mm Hg) and 13.6%, respectively, while S and VCO2 did not change significantly. Delta VA (op) increased progressively on successive days of the luteal phase while E remained unchanged at a value of 7.9, thus there was a progressive decrease in PACO2. The decrease in H was considered to lessen delta PACO2 (op) and so reduce the final deviation of PACO2 (delta PACO2 (cl) during the luteal phase. The decrease in B was found to be dependent on delta VA (op).

Adult↗
PubMed1981

Mutagenicity of reaction products of sulpyrine with nitrite.

The mutagenicity of three N-nitroso compounds produced by the reaction of sulpyrine with nitrite, 1-diketobutyryl-1-phenyl-2-methyl-2-nitrosohydrazide hydrate (DPMN), 4-(N-methyl-N-nitroso) aminoantipyrine (MNAA) and 1-acetyl-1-methyl-2-nitroso-2-phenylhydrazine, was tested on Salmonella typhimurium TA100 and TA98. The mutagenicity of related compounds, 4-methyl-aminoantipyrine, 1-acetyl-1-methyl-2-phenylhydrazine, 4-hydroxyantipyrine, sulpyrine and sodium nitrite was also examined. DPMN and MNAA, which are main reaction products in the nitrosation of sulpyrine, and sodium nitrite were mutagenic to TA100, but not to TA98. The other compounds were not mutagenic to either strain. MNAA required metabolic activation with rat-liver microsomal preparation (S9 mix) for the mutagenic activity, while DPMN did not require S9 mix. The mutagenicity of DPMN was remarkably increased by the addition of L-cysteine or glutathione. The enhancing effect was proportional to the concentrations of cysteine (0.4-2.1 mumoles/plate) or glutathione (0.8-6.5 mumoles/plate) added.

Aminopyrine↗
PubMed1981

Estimation of the compliance of the human pulmonary "venous" system from pulmonary artery wedge pressure tracings.

Compliance (delta V/delta P) of the human pulmonary "venous" system was estimated in a total of 37 human subjects, from the pulmonary artery wedge (PAW) pressure tracings, using two equations, (delta V/delta P) slope = 0.4 . k" . SV/(v-d) given in Appendix, and k" = 0.075 PAW + 0.9 given in Method. The estimated compliance of the pulmonary "venous" system was about 7 approximately 15 ml (mmHg)-1 in the control group, the patients of aortic valvular disease with physical capacity of Class I approximately III of the NYHA, and the patients of mitral stenosis with physical capacity of Class I. These values were in good agreement with that estimated by Guyton, i.e., 10 ml (mmHg)-1. For the entire population of pure mitral stenosis (n = 16), compliance (delta V/delta P) of the pulmonary "venous" system could be related to the PAW pressure by a regression curve of delta V/delta P = 1/(0.0106 PAW -0.0173). We pointed out, in discussion, that the present method and an entirely different method using the pulmonary blood volume measurements and passive leg elevation, performed in one and the same patient simultaneously, gave fairly similar values of the compliance of the pulmonary "venous" system.

Adolescent↗