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D Schönberg

Publications and source records attributed to D Schönberg.

At least 19 recordsLinked to original sources
PubMed1998

Ligand blot analysis of insulin-like growth factor-binding proteins using biotinylated insulin-like growth factor-I.

A nonradioactive method for the detection of insulin-like growth factor-binding proteins (IGFBPs) was developed utilizing human recombinant insulin-like growth factor-I (IGF-I) biotinylated with N-hydroxysuccinimido-biotin. Human plasma samples were separated by 15% SDS polyacrylamide gel electrophoresis, and proteins were transferred to nitrocellulose by Western blotting. The nitrocellulose sheets were incubated overnight with IGF-I-biotin at 4 degrees C. The next day streptavidin-peroxidase was added for 1 h, and IGFBPs were visualized by an enhanced chemiluminescence system. Five characteristic bands with molecular weights of 41 and 39 (IGFBP-3), 34 (IGFBP-2), 30 (IGFBP-1) and 24 kD (IGFBP-4) were detected. Binding was specific for IGFs, since unlabeled IGF-I inhibited IGF-I-biotin binding. IGFBP ligand blots with biotinylated IGF-I and (125)I-IGF-I yielded comparable results. The suitability of the new assay for clinical purposes was demonstrated by several clinical examples. In summary, a rapid, reliable, nonradioactive assay for qualitative analysis of IGFBPs has been developed.

Adult↗
PubMed1992

Influence of antibodies against IGF-I, insulin or their receptors on proliferation of human acute lymphoblastic leukemia cell lines.

To evaluate the potential role of IGF-I and insulin as growth-promoting factors in malignant lymphocyte development, we examined established T-acute lymphoblastic leukemic (ALL) cell lines with increasing stage of differentiation, HSB2, HUT78, CEM, MOLT3, Jurkat, JM-P, JM-886, and four established preB- and B-ALL cell lines REH, SKW6 CESS, BJAB for production of IGF-I and growth in the presence of antibodies, directed against IGF-I or insulin or their receptors. Basal DNA synthesis of the early differentiated T-cell lines HSB2 and HUT78, as well as the B-cell line REH, could be inhibited in a dose-dependent manner by both monoclonal antibodies against IGF-I (ASC41) and antibodies against the IGF-I receptor (alpha-IR3), suggesting that IGF-I acts as an auto- or paracrine growth factor for these cells via the IGF-I receptor. From these cells HUT78 and REH secreted IGF-I into cell culture medium. DNA synthesis of the further differentiated T-cell lines CEM and MOLT3 was inhibited by alpha-IR3 and antibodies directed against the insulin receptor (RPN.538) and against insulin (RPN.1661). These results suggest that insulin via the IGF-I receptor or insulin receptor can function as an autocrine or paracrine growth factor in these T-ALLs. Proliferation of the most differentiated T-ALL Jurkat and JMP was inhibited only by alpha-IR3 and 2C2, an antibody directed against the IGF-II receptor, suggesting that IGF-I or IGF-II acting via the IGF-I receptor or IGF-II receptor may be involved in proliferation of these cell lines. Inhibition of the DNA synthesis by RPN.538 and RPN.1661 indicate a more important role for insulin in growth of leukemias of the B-ALL cell lines SKW6 and CESS.

Antibodies, Monoclonal↗
PubMed1992

Characterisation of insulin-like growth factor I receptors of human acute lymphoblastic leukaemia (ALL) cell lines and primary ALL cells.

The expression of insulin-like growth factor I (IGF-I) receptors (IGR-IR) on human B-lineage and T-lineage acute lymphoblastic leukaemias (ALL) representing different maturational stages has been studied. Immature (stage I) and mature (stage II) T ALL as well as pre-B ALL cell lines expressed high numbers of IGF-IR with high affinity for IGF-I. In contrast, on T ALL, stage II and B ALL only low specific binding of 125I-IGF-I was detected. No binding of 125I-IGF-I to Burkitt lymphoma cells was found. Primary human T, pre-B and cALL cells also expressed IGF-IR with Kd for IGF-I and IGF-IR number per cell in the same range as the investigated cell lines. Crosslinking of 125I-IGF-I to T and pre-B ALL cells revealed IGF-IR alpha-subunits of 135 and 116 kD for HSB2. Gene expression of IGF-IR could be detected in all T ALL cell lines but was undetectable in SKW6, a B ALL cell line.

Antibodies, Monoclonal↗
PubMed1992

Diagnosis of growth hormone deficiency.

Many ways of evaluating the physiological state of hGH secretion exist, some of which have been touched upon and none of which has as yet proven infallible. Apart from important clinical features like history, physical data and growth rate, the diagnosis of altered pituitary function is based on tests and their interpretation. The physician responsible has to be informed on their effectiveness and pitfalls. Results should be interpreted in relation to developmental age (bone age) rather than chronological age. Research is under way to try to facilitate the diagnosis of varying degrees of alterations of hGH secretion. Reliability in predicting the effect of therapy with hGH is the ultimate aim in order to prevent unnecessary cost and disappointment for the patients. With the help of doctors involved in child care, such as physicians at kindergarten or school, it should be possible to start the slow process of investigating growth disorders at an early age.

Deficiency Diseases↗
PubMed1990

Improved preparative separation of human B and T lymphocytes and determination of relative mobilities of B and T lymphoblast cell lines by free flow electrophoresis.

The improved quantitative separation of human B and T lymphocytes by free flow electrophoresis is presented. Buffer systems with different compositions are tested analytically and partly preparatively for their effect on the separation profile. The best result is achieved with a modified phosphate-buffered saline and allows the enrichment of unstimulated, functionally intact B and T lymphocytes as well as monocytes in three distinct fractions. Furthermore, the electrophoretic mobilities of six established acute lymphoblastic leukemia cell lines are determined with regard to the mobilities of the healthy cells.

B-Lymphocytes↗
PubMed1989

Pulsatile gonadotropin secretion in pubertal children with chronic renal failure.

We have examined physiological nocturnal secretion of gonadotropins in 6 boys and 2 girls with end-stage renal disease, who had either delayed or disturbed puberty. The 5 patients treated by dialysis had reduced gonadotropin pulsatility for their stage of pubertal maturation, whereas the 3 patients with successful kidney grafts demonstrated a higher nocturnal rise and increased amplitude of gonadotropin pulsatility. It is suggested that the improved gonadotropin pulsatility of transplanted patients is due to their restored renal function.

Adolescent↗
PubMed1989

Demonstration of type I insulin-like growth factor receptors on human platelets.

Human platelets, freshly isolated from healthy human adults, express receptors for insulin-like growth factor I. The IC50 for displacement of 125I-IGF-I binding by unlabeled IGF-I was 0.2 nM, by IGF-II 32 nM by insulin 160 nM. Scatchard analysis of IGF-I binding demonstrates dissociation constants of 0.14 +/- 0.08 nM for high affinity binding site and 54 +/- 18 nM for low affinity binding site. The presence of the alpha-subunit of type I IGF receptor, as high affinity binding site, was verified by affinity crosslinking of 125I-IGF-I to platelet surface membranes. Under reducing con-conditions a Mr = 135,000 band was preferentially labeled. The complete type I IGF receptor complex, which revealed under nonreducing conditions, has an approximately molecular mass of Mr greater than 400,000. The immunoprecipitation of the 125I-IGF-I cross-linked type I receptor with alpha IR-3 confirmed the results achieved by affinity crosslinking.

Adult↗
PubMed1988

Preparative separation of human B and T lymphocytes by free flow electrophoresis.

An electrophoretic method for the quantitative separation of human B and T lymphocytes in a carrier-free system is presented. The method is based on the fact that B and T lymphocytes show marked overlap in their size and density characteristics, but differ sufficiently in surface charge to be separable by electrophoresis. The technique is performed in phosphate-buffered saline and appears to be especially suitable for the enrichment of nonstimulated, functionally intact lymphocytes which can be directly used for further immunological or biochemical studies.

B-Lymphocytes↗
PubMed1983

Hypothalamo-pituitary-gonadal axis in children with chronic renal failure.

Delayed puberty in children with chronic renal failure (CRF) may be due to gonadal dysfunction, increased plasma binding of gonadal hormones, or changes of the hypothalamo-pituitary axis. Plasma androgens were studied in 17 prepubertal boys with preterminal CRF. In addition, the response of luteinizing and follicle-stimulating hormones (LH, FSH) to luteinizing-releasing hormone (LHRH) was followed in the plasma of these boys and of 12 prepubertal girls with CRF. Plasma testosterone (T) was significantly lower in the CRF boys than it was in the controls (mean, 9 vs. 22 ng/ml) and concerned also the free T fraction (2.5% in both groups). Dihydro-T was similarly reduced in CRF, resulting in a normal T/DHT ratio. Basal plasma LH levels were significantly elevated in boys (1.0 vs. 0.5 ng/ml) and in girls with CRF (1.4 vs. 0.4 ng/ml), whereas mean basal FSH values were similar to controls. After LHRH administration, peak levels of LH and FSH were not different in CRF and control children; however, the absolute differences from basal to peak values were lower in CRF. These findings may indicate that Leydig cell dysfunction in CRF already occurs before the onset of puberty. The blunted LH and FSH responses to LHRH suggest an additional disturbance at the hypothalamo-pituitary level.

Adolescent↗
PubMed1983

[Normal puberty].

Explore the source record for details and available documents.

Adolescent↗
PubMed1981

[Neonatal screening for hypothyroidism in the Federal Republic of Germany (author's transl)].

Screening for neonatal hypothyroidism was introduced in 1979 in nearly all West German provinces on a regional basis as an additional preventive investigation. In February 1980 provincial control was replaced by uniform financing of screening for the whole country by public sick funds. Eleven out of 14 regionally organised screening laboratories took part in an enquiry into the incidence, clinical symptoms and causes of inborn hypothyroidism. Among 427 430 newborn infants tested 137 children with inborn hypothyroidism were detected in 1979/80. The incidence of 1:3100 corresponds to European figures. On average treatment could be instigated by the 12th day of life. Clinical symptoms of hypothyroid newborns differed in part markedly from classical signs of hypothyroidism. About 30% of the mothers had goitre. The cost-benefit relationship of newborn hypothyroidism screening is 1:10.

Germany, West↗
PubMed1978

[Neonatal screening for hypothyroidism. Preliminary results from different methods (author's transl)].

In a regional study 2062 newborns were screened for congenital hypothyroidism by determination of TSH in plasma or dried blood spots on the fifth day of life. Three newborns with congenital hypothyroidism were detected. All of them showed high TSH-levels between 462 and 2192 micromicron/ml. One newborn with a congenital goiter had a TSH-level of 143 micromicron/ml. Additionally, in a follow-up study of 50 newborns with jaundice TSH, T4, T3 and reverse T3 during the first 120 h of life were measured. Efficiency of the different methods concerning their applicability to mass screening is discussed.

Congenital Hypothyroidism↗
PubMed1977

[Oestrogen treatment of girls with increased growth (author's transl)].

Forty-one pubescent girls of constitutionally tall stature were given conjugated oestrogens for a continuous period averaging twenty-two months. Oral progestin was also given, daily for five days during the second half of each menstrual cycle. Average predicted height of the girls was 186.5 cm, average final height was only 179.2 cm. In half of the girls in whom treatment had been started before menarche the height reduction was 2 cm greater than in those started after menarche. There were no severe side effects. Extreme care should be taken to limit strictly the indications for this treatment. Only girls with a growth prognosis above 183 cm should be considered. Therapeutic overstimulation of the endometrium must be avoided. Earlier views that the cessation of growth under oestrogen is due to early epiphyseal closure have been shown to be wrong. Growth frequently ceases long before epiphyseal closure. Reduction of somatomedin production was found to be the cause. The average serum somatomedin level fell to 56.9% of basal concentration after six months' treatment. At the same time, the circadian profile of growth hormone indicated a threefold increase above basal level. This phenomenon probably reflects a negative feedback mechanism between growth hormone and somatomedin.

Adolescent↗
PubMed1976

Repeated circadian growth hormone, luteinizing hormone, and follicle-stimulating hormone in children: influence of 9-alpha-fluorohydrocortisone.

Growth hormone (GH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in plasma of 5 children at different pubertal stages and suffering from moderate orthostatic complaints, were measured by radioimmunoassay (RIA). Parameters for secretory capacity were arginine loading and circadian hormonal patterns in hourly intervals from 8 a.m. to 8 p.m. and in half-hourly intervals from 8 p.m. to 8 a.m. before and after 6 weeks treatment with 9-alpha-fluorohydrocortisone (9-alpha-F, Astonin-H, Fa. Merck, Darmstadt, 0.1--0.2 mg/day. Plasma GH during arginine tests and in circadian levels remained unchanged, but circadian LH showed a consistent slight rise in all children. With pubertal development, magnitude and timing of GH peaks increased in boys, and rather decreased in the two girls toward late puberty. Episodic fluctuation of LH and FSH were more marked during sleep, and increased in the three bosy as puberty advanced. Similar intraindividual patterns for GH and LH, but not for FSH were noted in 4 children. Timing of GH and LH peaks appeared to be correlated. An intrinsic hereditary long-term regulatory principle is discussed.

Adolescent↗