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Biomedical subjects

M Nagae

Publications and source records attributed to M Nagae.

22 records · Page 2Linked to original sources

Selective urinary excretion of phosphatidyl ethanolamine in patients with chronic glomerular diseases.

Urinary phospholipids and lipoproteins in chronic glomerular diseases were analyzed. The subjects used were 26 patients consisting of 14 with chronic glomerulonephritis and 12 with nephrotic syndrome. Nine healthy normals served as controls. Phospholipids were isolated by one-dimensional thin-layer chromatography (TLC) using an internal standard for quantification and partially by two-dimensional TLC and, furthermore, quantified by two different methods to ascertain the kinds of phospholipids. Urinary lipoproteins were isolated by density gradient ultracentrifugation and analyzed by electrophoresis. The urinary excretion of phosphatidyl ethanolamine (PE) was recognized exclusively in the patient group and that of phosphatidyl serine (PS) in most cases with nephrotic syndrome. The daily urinary PE excretion rate was closely correlated to the urinary albumin excretion rate. However, phosphatidyl choline (PC) and sphingomyelin (SPH), which are main phospholipids in serum and red blood cell membranes, in most cases were hardly detected in urine. These observations were confirmed by two-dimensional TLC using valuable spot tests for identification of phospholipids and also by the two different quantification methods. In density gradient ultracentrifugation, urinary lipoproteins did not form such peaks as seen in the profiles of serum lipoproteins. The presence of urinary lipoproteins in two nephrotic patients has been shown, but although the method used was not very sensitive, it was suggested that lipoproteins were hardly excreted into urine as the lipoprotein deficient fraction (LPDF) (d greater than 1.21 g/ml), in which albumin is predominant. PE was found mainly in LPDF of urine, although the amount of PE in urinary lipoproteins was very limited.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The prolactin-releasing mechanism of the hypothalamo-pituitary axis in pregnancy.

The purpose of this study was to investigate the prolactin (PRL)-releasing mechanism of the hypothalamo-pituitary axis in pregnancy. Forty-six gravidas in the first and second trimesters received bromocriptine (BRC), 2.5 mg orally, metoclopramide (MCP), 10 mg intravenously, or thyrotropin-releasing hormone (TRH), 500 micrograms intravenously. Additionally, BRC was given orally to another 42 gravidas 60 minutes prior to the intravenous injection of MCP or TRH. The plasma PRL levels decreased significantly after BRC and remained significantly elevated after MCP or TRH administration. However, there were no significant differences of PRL response to these agents between the first- and second-trimester groups. The PRL release from the pituitary by MCP or TRH was suppressed significantly by pretreatment of BRC in the gravidas. We concluded that the control mechanism of PRL secretion remained unchanged in the first and second trimesters.

Adult↗

[The effects of metoclopramide on maternal, umbilical and amniotic fluid prolactin at delivery].

Sixteen normal pregnant woman at delivery were administered 10 mg of Metoclopramide (MCP) intravenously, and the Prolactin (PRL) levels in the maternal plasma and in the amniotic fluid were measured by RIA before and after the administration, and in the umbilical plasma after the administration. Eight other pregnant women at term were studied similarly without the administration of MCP and served as the control. In this experiment, there was a significant increase only in the maternal plasma PRL but not in the amniotic fluid PRL nor in the umbilical plasma PRL. Furthermore, by using an intrauterine pressure catheter and a maternal intravenous cannula we measured the amniotic fluid PRL and the maternal plasma PRL about every 20 minutes during 3 hours before and after the intravenous administration of MCP 10mg. The maternal plasma PRL increased promptly and remained high for 150 minutes, while there was no significant change in the amniotic fluid PRL. This obvious discrepancy supports the hypothesis that decidua is the source of amniotic fluid PRL and suggests an independent regulation of amniotic fluid PRL.

Amniotic Fluid↗