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65 巻, 3 号
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SFD児とそのcatch up growthにおける考察山崎 敦子, 森川 肇, 上田 康夫, 望月 眞人1989 年 65 巻 3 号 p. 137-151
発行日: 1989/03/20
公開日: 2012/09/24
ジャーナル フリーIGF-I/SMC shows mitogenic activities in a wide variety of cell types and stimulates cell growth in vitro and in vivo. Unlike most other peptide hormones, IGF-I/SMC circulates in the plasma as macromolecular complexes with specific plasma binding proteins, approximate molecular weight of 150K and 40K daltons.
In order to elucidate the roles of IGF-I/SMC for fetal and postnatal development, the levels of plasma IGF-I/SMC, distribution of circulating IGF-I/SMC on its binding proteins, and profiles of unsaturated somatomedin binding proteins (USBP) were estimated in newborns and a growth-retarded infant (leprechaunism).
The concentrations of IGF-I/SMC in cord plasma increased gradually after the 28th week of gestation and reached 37.3 ± 14.6ng/ml (Mean ± S.D.) in full term infants. Although the levels of IGF-I/SMC in cord plasma were significantly lower than those in non-pregnant women (188 ± 58), they showed a positive correlation with birth weight and relative birth weight (R.B.W. : percentage comparison to the average birth weight of normal infants in the same gestational week).
In adult plasma, immunoreactive IGF-I/SMC was eluted predominantly in 150K dalton region (73.5%) and to a lesser extent (26.5%) in 40K dalton, and two apparent peaks of USBP could also be determined in both 150K and 40K dalton regions.
On the other hand, in fetal plasma 84.4% of immunoreactive IGF-I/SMC was eluted in 40K region on the 20th week, but on the 26th week, 71.6% of IGF-I/SMC was eluted in 150K region and after the 35th week, more than 70% of IGF-I/SMC was determined in 150K region as observed in adult plasma. However, 150K·USBP could not be detected in cord plasma obtained from appropriate-for-date (AFD) infants until after the 35th week of gestation.
Additionally, a positive correlation was demonstrated between 150K·USBP/40K·USBP ratio and birth weight. Some cases of small-for-date (SFD) infants whose IGF-I/SMC circulated mainly as 150Kcomplex could catch up on their growth early in postnatal life. However, in the SFD newborns, if either 150K·USBP or 150Kcomplex of IGF-I/SMC could not be detected, their growth spurt was remarkably delayed until a year after birth. Furthermore, the similar disorders of IGF-I/SMC distribution and its USBP profile were also observed in the case of leprechaunism, who showed severe intrauterine and postnatal growth retardation.
These results suggest that IGF-I/SMC might play important roles in fetal growth as well as postnatal development and that the analysis of circulating forms of IGF-I/SMC and USBP in the cord plasma might be useful in elucidating intrauterine growth retardation and in predicting postnatal growth catch up.抄録全体を表示PDF形式でダウンロード (1460K) -
モノクローナル抗体を用いたラジオイムノアッセイ法による検討直海 晶二郎, 梅田 照久, 岩岡 大輔, 三浦 史博, 佐々木 雅人, 中山 真人, 北本 康則, 佐藤 辰男1989 年 65 巻 3 号 p. 152-160
発行日: 1989/03/20
公開日: 2012/09/24
ジャーナル フリーTo clarify the molecular nature and dynamics of circulating a human atrial natriuretic polypeptide (αhANP) in chronic renal disease, the plasma concentrations of αhANP were determined by radioimmunoassays using two distinct monoclonal antibodies (MoAbs). One MoAb (10B1) recognized N-terminus of αhANP, while the other (C351) recognized the ring structure. The preliminary studies revealed a close correlation (r=0.97, p<0.0001) between plasma αhANP measured with 10B1 and C351 MoAbs, supporting the theory that the main circulating form is αhANP (1-28). Therefore, the more sensitive radioimmunoassay using MoAb (C351) was used in the present studies. The plasma αhANP was 3.8 ± 1.7 (mean ± SD) in healthy subjects, 2.7 ± 1.4 fmol/ml in patients with chronic glomerulonephritis without renal failure, 16.2 ± 16.8 fmol/ml in patients with chronic renal failure, and 24.3 ± 10.5 fmol/ml in patients under maintenance hemodialysis. Thus, the elevation of plasma αhANP was related to the stages of renal damage. Although the plasma αhANP in 18 patients under maintenance hemodialysis declined significantly (p<0.01) after hemodialysis, their levels (17.9 ± 9.0 fmol/ml) after hemodialysis were still higher than those in healthy subjects. On the other hand, a positive correlation (r=0.65, p<0.05) between αhANP and creatinine in blood was found only in the group of chronic renal failure before maintenance hemodialysis. These results suggest that an impaired metabolism of αhANP in the kidney might play an important role in the elevation of plasma αhANP as well as the stimulation of αhANP secretion caused by the expansion of extracellular fluid.抄録全体を表示PDF形式でダウンロード (782K) -
篠原 充1989 年 65 巻 3 号 p. 161-173
発行日: 1989/03/20
公開日: 2012/09/24
ジャーナル フリーThe STS (steroid sulfatase) gene which has been assigned to the short arm of human X chromosome (band p22) is thought to have escaped from Lyon's inactivation. For that reason, the STS enzyme activities differ between male and female according to the number of X chromosomes in cells. In this report, the STS enzyme activities were studied in different human tissues such as placentas, lymphocytes, and cultured fibroblasts of normal individuals and sex anomaly patients. Tritium labelled dehydroepiandrosterone sulfate (DHA-S) was used as the reaction substrate.
The placental STS activities between normal male and female subjects showed a significant difference in spite of wide variences that were ascertained not to be the effects of methodological alterations involving enzyme purification, substrate concentration, and activity calculation (units per mg of protein or DNA). Further, in lymphocytes and fibroblasts which had low levels of enzyme concentration compared with placentas, the STS enzyme activities were also significantly different between both sexes. These results confirmed that the STS gene in cells of tissues tested here seemed to be inactive at the gene level and followed the gene dosage effect to some extent.
The enzyme activity was also studied in 17 patients with sex anomalies using lymphocytes and cultured fibroblasts. The cells of 45, X Turner syndrome and of Klinefelter syndrome with 47, XXY or other karyotypes, showed slightly lower levels of enzyme activity when compared with control values of normal males or females. The enzyme activity in intersexual disturbances, especially XX male and XX true hermaphrodites, showed intermediate levels between normal male and female values. This result may give support to the concept that at least one X chromosome in these diseases is genetically abnormal due to X-Y interchanges, something that has been partly proved recently by analysis of H-Y antigen and Y-specific DNA probes.
The present study on the STS enzyme activity revealed the presence of a gene dosage effect of STS gene between males and females not precise but rather rough in quantity, and it pointed out problems, some of which were related to genetic and environmental factors modifying the STS gene expression in normal individuals as well as sex anomaly patients.抄録全体を表示PDF形式でダウンロード (1344K) -
森 昌朋, 入内島 徳二, 村上 正己, 小林 節雄1989 年 65 巻 3 号 p. 174-181
発行日: 1989/03/20
公開日: 2012/09/24
ジャーナル フリーThe possible existence of binding protein for TRH was studied in rat serum. Synthetic TRH was incubated in rat serum and extracted in 90% methanol for measurement of tripeptide by RIA. The amount of TRH in serum at 37 C decreased progressively with incubation time, while that of tripeptide, which was incubated in serum at 60 C, significantly decreased 5 min after incubation, but TRH concentration afterward remained unchanged until 60 min. The concentration of TRH, which was incubated in serum at 37 C for 30 min, did not differ from that which was successively incubated at 60 C for 60 min. An elution pattern of TRH incubated in serum on a Sephadex G-25 was similar to that of authentic tripeptide, and this elution profile was not changed by heating at 60 C. An isoelectric focusing analysis of TRH incubated in serum showed a single peak of pI 8.2 which was not distinguished from the authentic peptide and was not changed by heating. These data indicate that TRH-degradation in rat serum is not dependent on its binding protein.抄録全体を表示PDF形式でダウンロード (648K) -
竹田 省, 桑原 慶紀, 水野 正彦1989 年 65 巻 3 号 p. 182-189
発行日: 1989/03/20
公開日: 2012/09/24
ジャーナル フリーOxytocin metabolism seems to occur mainly in the kidney and the liver. Placental cystine amino peptidase (CAP), which inactivates oxytocin by cleavage of the bond between the N-terminal cystine residue and adjacent tyrosine, rises progressively with advancing gestation. The role of CAP in oxytocin metabolism is not clear. To clarify this issue, the authors measured oxytocin metabolic clearance rate (MCR) by the constant infusion of 3 mU/min and 6 mU/min synthetic oxytocin in 14 adult subjects : 5 pregnant women (38 - 41 weeks gestation), 4 puerperal women and 5 nonpregnant women.
Oxytocin MCR (mean ± SE) during infusion of 3 mU/min was 20.9 ± 2.6 ml/kg/min in pregnant women; 16.9 ± 2.4 ml/kg/min in puerperal women; 19.7 ± 3.3 ml/kg/min in nonpregnant women. Oxytocin MCR during infusion of 6 mU/min was 22.1 ± 3.3 ml/kg/min in pregnant women and 22.7 ± 3.1 ml/kg/min in nonpregnant women. These values were statis-tically similar. Mean (± SE) CAP values were 143.5 ± 7.8 mU/ml in pregnant women, 60.8 ± 3.0 mU/ml in puerperal women, and 13.8 ± 2.7 mU/ml in nonpregnant women. CAP levels in pregnant women were significantly higher than others.
3 H-oxytocin degradation was studied in vitro in pooled plasma of pregnant and nonpregnant women. 85% of original 3 H-oxytocin was destroyed in pregnant plasma during 1 hour but only below 10% was destroyed in nonpregnant plasma in 2 hours.
These results suggest that CAP in pregnant women may not play a role in the inactivation of oxytocin in vivo, thus differing from its role in vitro.抄録全体を表示PDF形式でダウンロード (665K)
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