Postnatal Development of Circadian Rhythm in Serum Cortisol Levels in Children

PEDIATRICS ◽  
1983 ◽  
Vol 72 (3) ◽  
pp. 399-404 ◽  
Author(s):  
Shoju Onishi ◽  
Genji Miyazawa ◽  
Yutaka Nishimura ◽  
Satoru Sugiyama ◽  
Takeshi Yamakawa ◽  
...  

High-pressure liquid chromatography was used to study the development of blood adrenocortical circadian rhythm in a total of 64 children, ranging in age from 1 month to 15 years. Patients with endocrine diseases, congenital anomalies, and diseases of the central nervous system were excluded from this study. Determination of corticosteroid concentration was possible with 20 to 100 µL of serum. Twenty-four hour patterns were determined at six-hour intervals. A distinct circadian rhythm with an amplitude comparable to that of an adult emerged at approximately 6 months of age.

1981 ◽  
Vol 96 (3) ◽  
pp. 394-397 ◽  
Author(s):  
Jau-Nan Lee ◽  
Markku Seppälä ◽  
Tim Chard

Abstract. High pressure liquid chromatography (HPLC) and radioimmunoassay were employed to characterize luteinizing hormone-releasing factor (LRF)-like material in the human placenta. Methanol extracts of the placenta were washed with acetic acid and chloroform, further purified on coarse octadecylsilane columns, fractionated on HPLC, and tested by radioimmunoassay. In HPLC, placental LRF had the same retention time as synthetic LRF, and such fractions gave an inhibition curve which was parallel to that of synthetic LRF in radioimmunoassav. It is concluded that human placental I.RF is similar or identical to LRF in the central nervous system.


1973 ◽  
Vol 72 (2) ◽  
pp. 308-318 ◽  
Author(s):  
J. Köbberling ◽  
A. v. zur Mühlen

ABSTRACT In eight normal volunteers the circadian rhythm of cortisol was established by the determination of free urinary corticoids in 2 h urine samples by the competitive protein binding method. After two control days dexamethasone was infused between 10 p. m. and 4 a. m. in doses between 50 and 400 μg/h. These experiments were repeated after pre-treatment with 400 mg diphenylhydantion/day for one week and again after pre-treatment with 800 mg carbamazepine/day. Under the influence of these anti-convulsant drugs the circadian rhythm of free urinary corticoids was still present but showed more irregularities and sometimes additional peaks in the course of the day. The 24 h excretion values, the peak and the nadir values and the time of the morning peaks were not significantly different from the control days. The degree of suppression by dexamethasone was dose related both with and without the application of the anti-convulsants but under the influence of both these drugs comparable effects could only be achieved by 2 to 4 fold higher doses of dexamethasone. The suppression of basal and impulsive cortisol activities was inhibited in a similar way. According to these results it can be assumed that the anti-convulsants interfere with the feedback mechanism by decreasing the sensitivity of the central nervous system to changes in plasma glucocorticoid concentrations. An intact feedback mechanism does not seem to be an essential condition for the circadian rhythm.


PEDIATRICS ◽  
1960 ◽  
Vol 25 (2) ◽  
pp. 309-315
Author(s):  
Harry H. White ◽  
Fred D. Fowler

Chronic lead encephalopathy must be considered in the differential diagnosis of pediatric patients who present with manifestations of schizophrenia, behavior disorders or degenerative diseases of the central nervous system. Determination of urinary coproporphyrin is a simple, fast screening procedure applicable to office practice. The prognosis for normal mental development following encephalopathy is poor. It is hoped that early recognition of the more subtle signs of central nervous system involvement will allow treatment to be instituted soon enough to prevent the crippling mental deterioration which is so often a sequela of lead poisoning.


1998 ◽  
Vol 13 (supplement) ◽  
pp. 120-121
Author(s):  
Masaharu NAKAJIMA ◽  
Tomoko OHTA ◽  
Nozomi KAWAKAMI ◽  
Susumu YAMATO ◽  
Kenji SHIMADA ◽  
...  

1998 ◽  
Vol 9 (2) ◽  
pp. 224-244 ◽  
Author(s):  
I. Kjær

Neuro-osteology stresses the biological connection during development between nerve and hard tissues. It is a perspective that has developed since associations were first described between pre-natal peripheral nerve tissue and initial osseous bone formation in the craniofacial skeleton (Kjær, 1990a). In this review, the normal connection between the central nervous system and the axial skeleton and between the peripheral nervous system and jaw formation are first discussed. The early central nervous system (the neural tube) and the axial skeleton from the lumbosacral region to the sella turcica forms a unit, since both types of tissue are developmentally dependent upon the notochord. In different neurological disorders, the axial skeleton, including the pituitary gland, is malformed in different ways along the original course of the notochord. Anterior to the pituitary gland/sella turcica region, the craniofacial skeleton develops from prechordal cartilage, invading mesoderm and neural crest cells. Also, abnormal development in the craniofacial region, such as tooth agenesis, is analyzed neuro-osteologically. Results from pre-natal investigations provide information on the post-natal diagnosis of children with congenital developmental disorders in the central nervous system. Examples of these are myelomeningocele and holoprosencephaly. Three steps are important in clinical neuro-osteology: (1) clinical definition of the region of an osseous or dental malformation, (2) embryological determination of the origin of that region and recollection of which neurological structure has developed from the same region, and (3) clinical diagnosis of this neurological structure. If neurological malformation is the first symptom, step 2 results in the determination of the osseous region involved, which in step 3 is analyzed clinically. The relevance of future neuro-osteological diagnostics is emphasized.


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