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Biomedical subjects

G Brabant

Publications and source records attributed to G Brabant.

At least 19 recordsLinked to original sources
PubMed1995

Extracellular ATP and UTP increase cytosolic free calcium by activating a common P2u-receptor in single human thyrocytes.

In single human thyrocytes extracellular ATP, ATP-gamma-S, ADP and UTP caused a concentration-dependent biphasic increase in [Ca2+]i. Consistent with a P2u-receptor the rank-order of potency was ATP = UTP > ATP-gamma-S > ADP, and cross-desensitization of the Ca2+ responses occurred between ATP and UTP. The initial transient peak in [Ca2+]i was resistant to extracellular Ca2+ depletion which demonstrates mobilisation of internal Ca2+ by IP3 whose formation was rapidly enhanced by ATP and UTP. By contrast, the sustained plateau phase required influx of external Ca2+. Ca2+ influx occurs most likely through a capacitative Ca2+ entry mechanism, which was shown to exist in these cells by experiments performed with thapsigargin. Thus, low micromolar concentrations of extracellular ATP and UTP activate a common P2u-receptor coupled to the C(a2+)-phosphatidylinositol signalling cascade in human thyrocytes. This indicates that extracellular nucleotides from various sources might play an important role in human thyroid physiology.

Adenosine Triphosphate↗
PubMed1995

Cognitive functioning in experimental hypoglycaemia assessed with event-related potentials.

Cognitive effects of experimentally induced hypoglycaemia were investigated by event-related brain potentials (ERPs) in auditory and visual classification tasks. In a cross-over design eight healthy male subjects (age 22-27 years) were studied under control conditions or following administration of 0.15 IU insulin kg-1. The ERPs showed preserved early cortical components, while the N2 component was greatly reduced in both modalities. P3 components did not show an influence of hypoglycemia. These results suggest that the cognitive deficits are due to an impairment of automatic feature extraction from the stimuli.

Adult↗
PubMed1995

Vasopressin induces frequency-modulated repetitive calcium transients in single insulin-secreting hit cells.

Ca2+ is central to the stimulation of insulin secretion from pancreatic beta-cells. Arginine-vasopressin (AVP) may participate in the modulation of insulin release. In the present study, the AVP-induced changes in cytosolic free Ca2+ ([Ca2+]i) were investigated in single fura-2 loaded insulin-secreting HIT cells. Stimulation with AVP (0.1-5 nM) caused repetitive Ca2+ transients. The frequency but not the amplitude of the Ca2+ transients was modulated by the concentration of AVP. High concentrations of AVP (10-100 nM) triggered a biphasic rise in [Ca2+]i. In Ca(2+)-free medium AVP caused only one or two Ca2+ transients. Withdrawal of extracellular Ca2+ rapidly abolished the AVP-induced Ca2+ transients in all cells tested. The Ca2+ channel blocker, verapamil (50 microM), reduced amplitude and frequency of the Ca2+ transients by about 25% and 60%, respectively, and terminated the Ca2+ transients in 2 of 6 cells. When HIT cells were incubated in Ca(2+)-free medium, and extracellular Ca2+ was restored, there was a small increase in [Ca2+]i. If, however, the agonist-sensitive Ca2+ pool was functionally depleted by repetitive stimulation with high concentrations of AVP or thapsigargin in Ca(2+)-free medium before extracellular Ca2+ was restored, an agonist-independent increase in [Ca2+]i was observed, which was transiently larger than in the control cells, and was mainly preserved in the presence of verapamil. Thus, depletion of the agonist-sensitive Ca2+ pool enhances the influx of extracellular Ca2+ through a Ca2+ entry mechanism independent from verapamil-sensitive voltage-dependent Ca2+ channels (VDCC).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Pulsatile growth hormone secretion in normal-weight and obese men: differential metabolic regulation during energy restriction.

Metabolic changes such as obesity and fasting modulate pulsatile growth hormone (GH) release in man, but the underlying mechanisms are still elusive. We studied the temporal pattern of pulsatile GH release in five normal-weight men (mean +/- SD: age, 29.8 +/- 4.9 years; body mass index [BMI], 24.3 +/- 1.8 kg/m2) and five obese men (age, 27.8 +/- 4.8 years; BMI, 38.9 +/- 4.8 kg/m2) during their regular energy consumption and the last 24 hours of a 96-hour fasting period. GH plasma levels were determined at 10-minute intervals and glucose level was measured every 20 minutes. GH pulse analysis was performed with three different algorithms. Insulin-like growth factor-I (IGF-I), IGF-II, IGF-binding proteins (IGFBP-1, -2, and -3), and IGF-binding capacity (IGF-BC) were evaluated in samples collected at 7:00 AM, 3:00 PM, and 11:00 PM. Twenty-four-hour mean GH was basally higher in normal subjects (1.1 +/- 0.6 mU/L) than in overweight subjects (0.4 +/- 0.2, P < .01 v normal). The significant fasting-induced GH increase in normal-weight men (to 5.6 +/- 2.2 mU/L, P < .05 v basal) was inversely related to BMI (r = -.86, P = .0006). GH pulse amplitudes but not frequencies were different for both groups and were increased by fasting in normal subjects but not in obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of continuous and pulsatile administration of pituitary rat thyrotropin and recombinant human thyrotropin in a chronically cannulated rat.

Pulsatile secretion of thyrotropin (TSH) is a well characterized phenomenon in the human, yet only limited data are available from animal studies. We propose a combined model of chronic catheterization and suppression of endogenous TSH release in the rat allowing us to apply quantified pulses of different preparations of thyrotropin intravenously with minimal interference with endogenously produced hormone. Sprague-Dawley rats treated with drinking water containing 3,5,3'-triiodothyronine (T3) showed a significant 6-fold decrease of the rat TSH (rTSH) level after four days. Free thyroxine (FT4) levels were 9-fold below unsuppressed levels; FT4 response to exogenous TSH application above this suppressed baseline level was selected as an endpoint. Infusion studies compared pulsatile with continuous TSH administration. A low and a high dose of rTSH and recombinant human TSH (rec-hTSH) were administered. Levels of FT4 were compared after two and four days and responsiveness to a standard high bolus of rTSH 6 h after end of infusion was assessed. With regard to its potency for FT4 release, differences indicating a general trend as to superior efficiency of pulsatile TSH stimulation of the thyroid gland in comparison to continuous stimulation could be observed in all four experiments. More pronounced effects were seen after 2 and 4 days of high rTSH infusion and after 4 days of low rec-hTSH infusion. Comparison of FT4 responses to rTSH boli showed a 2- and 6-fold higher response in the pulsatile group compared to the continuous group after low and high rTSH infusion, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Time series prediction of plasma hormone concentration. Evidence for differences in predictability of parathyroid hormone secretion between osteoporotic patients and normal controls.

Recent evidence links osteoporosis, a disease of bone remodeling, to changes in the dynamics of parathyroid hormone secretion. We use nonlinear and linear time series prediction to characterize the secretory dynamics of parathyroid hormone in both healthy human subjects and patients with osteoporosis. Osteoporotic patients appear to lack the periods of high predictability found in normal humans. Our results may provide an explanation for why an intermittent administration of parathyroid hormone is effective in restoring bone mass in osteoporotic patients.

Adult↗
PubMed1995

Regulation of the cell-cell adhesion protein, E-cadherin, in dog and human thyrocytes in vitro.

E-cadherin, a cell-cell adhesion protein specifically expressed at the basolateral membrane of thyrocytes, is variably dysregulated in thyroid carcinomas in parallel to the dedifferentiation of the tumors. No data are currently available on the regulation of E-cadherin in messenger RNA (mRNA) expression by physiological stimulators of thyroid proliferation and differentiation. The present study investigated the control of E-cadherin steady state mRNA levels and protein expression in primary cultures of dog and human thyrocytes under the influence of physiological regulators of thyroid differentiation and dedifferentiation using Northern blot analysis and immunohistochemistry. Following dedifferentiation by epidermal growth factor and fetal calf serum in primary cultures of dog and human thyrocytes, E-cadherin steady state mRNA expression was low but easily detectable. Stimulation of the cells by TSH (1 mU/ml) or forskolin (10 microM) induced an increase in E-cadherin mRNA levels with a maximal effect after 20 h. An up-regulation of E-cadherin protein levels are also observed by immunostaining with anti-E-cadherin antibodies. A concentration-response relation determined for TSH stimulation (10 microU/ml to 10 mU/ml) led to a concentration-dependent stimulation of E-cadherin mRNA levels and a parallel increase in protein expression with a minimal effective concentration of 10-30 microU/ml. These effects depend on protein synthesis as they are completely blocked by the presence of 10 micrograms/ml cycloheximide. Treatment with EGF did not markedly alter E-cadherin mRNA expression, whereas removal of insulin from the medium slightly decreased E-cadherin mRNA and protein levels. There is, therefore, a qualitative parallelism between the effect of the various factors on E-cadherin protein and mRNA levels. These results suggest that the cell-cell adhesion protein E-cadherin is under the control of the TSH-cAMP-dependent pathway and may play an important physiological role on the action of this pathway in proliferation and differentiation.

Animals↗
PubMed1995

Functional and morphological changes of the thyroid gland following 5 days of pulsatile TRH stimulation in male rats.

The aim of the present study was to evaluate in vivo the selective effects of a small increase in plasma TSH levels on thyroid function, proliferation and morphology. Chronically catheterized male Sprague-Dawley rats were stimulated i.v. over 5 days either with TRH (2 micrograms TRH in 100 microliters 0.9% (w/v) NaCl (TRH-P) or the NaCl carrier alone (P), both given as pulses every 2 h. Control groups were cotreated i.v. with 10 micrograms thyroxine (T4)/100 g body weight per day (TRH-P + T4) starting 2 days before pulsatile stimulation. TSH plasma levels were approximately doubled by TRH-P (P < or = 0.001), T4 plasma levels significantly increased (P < or = 0.001) but tri-iodothyronine plasma levels did not change compared with treatment with P. No significant changes between groups were found in thyroid weight and in intrathyroidal iodine content, but the percentage of 5-bromo-2'-desoxyuridine-labelled thyrocytes as a marker of proliferation in TRH-P-treated animals was significantly increased over P or TRH-P + T4 (P < or = 0.001). Ultrastructural analysis of the thyroid evaluated by electron microscopy revealed a significant increase in the number of lysosomes (P < or = 0.001). The size of the endoplasmic reticulum (ER) in relation to the cytoplasm was significantly increased when treated with TRH-P compared with P or TRH-P + T4 (P < or = 0.001). Post-embedding immunogold staining revealed Tg as a major product within ER cisternae. Immunogold labelling was moderate in controls and higher densities of gold particles were obtained in TRH-P-treated animals (P < or = 0.001). In conclusion, short-term pulsatile TRH stimulation increasing the plasma levels of immunoreactive TSH only twofold is capable of inducing hypertrophy of the thyrocytes by gross ultrastructural changes which are paralleled by an increase in circulating T4. These data underscore the dominant role of TSH on thyroid ultrastructure within the narrow boundaries of normal physiological regulation.

Animals↗
PubMed1995

Implications of host pancreatic hormones in the restart of grafted liver.

Regulatory roles of insulin and glucagon in hepatic metabolism and function are well described. However, little is known about implications of host pancreatic hormones in primary function of grafted liver. This study aimed to investigate it in relation to hepatic mitochondrial function. Insulin, c-peptide, and glucagon in peripheral blood were monitored for 2 days in clinical liver transplantation by a continuous sampling technique to avoid influences of hormonal oscillation. In grafts with immediate function (n = 10), smooth increase of arterial ketone body ratio reflecting hepatic intramitochondrial redox state was accompanied by increased c-peptide and decreased glucagon, resulting in the increase of c-peptide/glucagon ratio. In other functioning grafts (n = 20), where ketone body ratio was rather lower, increased glucagon level, observed also during anhepatic phase, resulted in the slower increase of c-peptide/glucagon ratio. There were accompanied by increased free fatty acid and ketone body levels. In primary nonfunction (n = 4), rapid increase of c-peptide accompanied by hyperglycemia resulted in the accelerated increase of c-peptide/glucagon ratio, but ketone body ratio did not show any increase. Insulin/c-peptide ratio also showed a rapid increase. These findings suggest that the increase of insulin/glucagon ratio in portal blood, potentially influenced by recipient condition, is associated with the recovery of mitochondrial energy metabolism in survived hepatic grafts. However, this relationship does not work in failed grafts, where irreversible impairment of energy metabolism is attributed to graft itself.

Adolescent↗
PubMed1992

In vitro and in vivo regulation of thyrotropin receptor mRNA levels in dog and human thyroid cells.

Regulation of thyrotropin (TSH) receptor (TSHr) mRNA accumulation as compared with two other thyroid differentiation markers (thyroglobulin and thyroperoxidase (TPO] has been investigated by Northern blot. In dogs in vivo, chronic stimulation of the thyroid TSHr mRNA although it increased the levels of thyroglobulin and TPO mRNA. In dogs treated with thyroxin, the quiescent thyroids expressed normal levels of TSHr and TPO mRNA but depressed levels of thyroglobulin mRNA. In primary cultures of dog thyrocytes, dedifferentiation of the cells by treatment with epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate led to decreased TSHr mRNA levels and nearly abolished thyroglobulin and TPO gene expression. However, TSHr mRNA was always present, compatible with the fact that these cells, when treated by TSH, reexpress differentiation. Treatment of the cells with TSH or forskolin transiently increased the TSHr mRNA level after 20 h, an effect inhibited by cycloheximide. This up-regulation was confirmed at the protein level: forskolin-treated cells showed an enhanced cAMP response to TSH and an increased binding of labeled TSH to their membranes. Long term TSH treatment led to a slight down-regulation of TSHr mRNA in dog thyrocytes, but in human thyroid cells no marked down-regulation was observed.

Animals↗
PubMed1992

Early adaptation of thyrotropin and thyroglobulin secretion to experimentally decreased iodine supply in man.

Five healthy male volunteers (aged 25 to 28 years) were studied both after 4 weeks of treatment with 200 micrograms iodine/d orally (PO) and following experimental iodine depletion by treatment with 3 x 300 mg perchlorate/d PO over a 4-week period, in an attempt to better define the early adaptive responses to an alteration in iodine supply in thyroid function. Intrathyroidal iodine, serum triiodothyronine (T3), free T3 (FT3), thyroxine (T4), free T4 (FT4), reverse T3 (rT3), thyroxine-binding globulin (TBG), thyroglobulin (Tg), and thyrotropin (TSH) levels (10-minute sampling over 24 hours) were measured at the end of iodine administration and at the end of perchlorate treatment. Thyroid volume was determined by sonography, and iodine content was determined by fluorescence scintigraphy. TSH pulses were analyzed by computer-assisted programs. Comparing both experimental situations, perchlorate treatment significantly reduced intrathyroidal iodine concentration (4.0 +/- 1.3 to 3.0 +/- 1.2 nmol/mL, P less than .05), but thyroid volume and total serum T4, T3, FT3, and TBG levels were not altered. Mean 24-hour serum TSH levels (1.8 +/- 0.3 to 1.0 +/- 0.3 mU/L, P less than .001), amount of TSH secreted/pulse (0.5 +/- 0.1 to 0.3 +/- 0.1 mU/L, P less than .001), and FT4 levels (15.7 +/- 1.7 to 14.3 +/- 1.4 pmol/L, P less than .005) were significantly diminished, whereas Tg levels (18.6 +/- 10.0 to 35.1 +/- 14.0 ng/mL, P less than .01) were significantly increased. Thyroid-specific antibodies were normal and were not altered by treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Gene expression of differentiation- and dedifferentiation markers in normal and malignant human thyroid tissues.

Steady state mRNA transcript levels of thyroid differentiation markers such as TSH receptor (TSHR), thyroglobulin (Tg) and thyroid peroxidase (TPO) as well as a potential marker of dedifferentiation, c-myc, marker were investigated in patients with thyroid tumors and in normal controls using Northern blot analysis. Blots were normalized by acridine orange staining whereas analysis of beta-actin mRNA levels revealed highly variable levels already in normal tissue suggesting regulation of this "constitutively" expressed gene. Determination of c-myc mRNA revealed increased steady state mRNA levels in anaplastic carcinomas (ATC) as compared to normal tissues. However, in some patients c-myc transcript levels were lower in the tumor than in the adjacent normal tissue reducing the significance of c-myc as a marker of dedifferentiation. High levels of TSH mRNA were found in control thyroids, whereas in ATC no normal TSHR mRNA was detected. In PTC and follicular thyroid carcinomas (FTC) the transcripts varied from increased to markedly reduced levels. In one patient with FTC 2 independent preparations of the tumor revealed different results, undetectable and clearly detectable TSHR mRNA levels. Xenotransplantation of this tissue on nude rats showed a variable expression pattern in the individual xenotransplantations suggesting heterogeneity of the tumor tissue. Tg and TPO mRNA were strongly expressed in normal tissues and completely lost in all ATC. In differentiated thyroid tumors the transcript levels of Tg and TPO varied from normal to complete loss of expression of either Tg or TPO, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Acridine Orange↗
PubMed1992

Circadian changes in pulsatile TSH release in primary hypothyroidism.

OBJECTIVE: We evaluated pulsatile and circadian TSH secretion in primary hypothyroidism. DESIGN: In a prospective study, blood was sampled every 10 minutes during 24 hours for assay of TSH (IRMA). Thyroid hormones and TSH responsiveness to TRH were then measured. SUBJECTS: Nine patients with overt primary hypothyroidism, seven patients with subclinical hypothyroidism and 16 healthy controls. MEASUREMENTS: Computer-assisted analysis by the Desade and Cluster programs. RESULTS: Both computer-assisted programs revealed an increased TSH pulse amplitude in both overt and subclinical hypothyroidism versus controls (Desade: 36.9 +/- 31.4 (mean +/- SD) (P < 0.001) and 2.8 +/- 1.9 (P < 0.001) vs 0.4 +/- 0.2 mU/l; Cluster: 25.6 +/- 25.1 (P < 0.001) and 2.4 +/- 1.4 (P < 0.001) vs 0.4 +/- 0.2 mU/l). TSH pulse frequency remained unchanged with approximately 10 pulses/24 hours. A highly significant correlation was found between the mean 24-hour TSH concentration and the TSH pulse amplitude in all controls and patients but not to TSH pulse frequency. The nocturnal TSH surge was absent in six out of nine patients with overt primary hypothyroidism. The deficient nocturnal rise of TSH in primary hypothyroidism vs controls (22 +/- 51 vs 82 +/- 41%, P < 0.001), was associated with a loss of the usual nocturnal increase in TSH pulse amplitude and frequency. CONCLUSIONS: Mean 24-hour TSH pulse amplitude is increased in primary hypothyroidism, but TSH pulse frequency remains unchanged. The decrease of the nocturnal TSH increase in primary hypothyroidism is associated with a loss of the usual nocturnal increase in TSH pulse amplitude and frequency.

Adult↗
PubMed1992

The pulsatile GH secretion in acromegaly: hypothalamic or pituitary origin?

OBJECTIVE: We studied the effects of different modes of octreotide therapy on the pulsatile pattern of GH release in an attempt to define better its regulation by growth hormone-releasing hormone (GHRH) and somatostatin and its effects on IGF-I plasma levels in acromegaly. DESIGN: In six acromegalic patients not cured by previous treatment we compared the 24-hour GH secretion profiles under basal conditions with subcutaneous (s.c.) bolus injections of 100 micrograms octreotide every 8 hours and with continuous s.c. infusions of the same daily dose. Blood samples were taken every 10 minutes over 24 hours followed by a GHRH test (100 micrograms GHRH i.v.) with blood sampling every 15 minutes for another 2 hours. After a 4-week interval all patients were treated either by the bolus or continuous mode of octreotide application in a randomized cross-over design. On day 4 of treatment blood sampling and GHRH test were repeated. Octreotide treatment was withdrawn for another 4 weeks; all patients then received the alternate application mode and were measured under similar conditions. MEASUREMENTS: Serum GH and plasma IGF-I concentrations were analysed by serial array averaging. IGF-I levels were measured in two different assays with and without previous protein extraction. For GH pulse detection three different algorithms (Cluster, Pulsar, Desade) were applied. RESULTS: With both treatments, the initially elevated basal 24-hour mean serum GH concentrations (58.0 +/- 9.7 mU/l mean +/- SEM) decreased significantly (bolus: 11.5 +/- 4.9 mU/l, P < 0.001 vs basal; continuous infusion: 7.6 +/- 1.9 mU/l, P < 0.001 vs basal) after 4 days. GH suppression was significantly more pronounced following continuous infusion than bolus (P < 0.05). IGF-I plasma concentrations were lowered significantly (P < 0.05) with both forms of treatment which did not differ between themselves. Bolus and continuous infusion treatment significantly inhibited (P < 0.05) the amplitudes of pulsatile GH release, but did not change the pulse frequency. In two of the patients, GHRH stimulation did not increase GH serum levels suggesting a constitutive activation of adenylyl cyclase. CONCLUSION: Continuous subcutaneous octreotide treatment in acromegaly suppresses mean GH levels better than bolus injection. The number of GH pulses remains unaffected by both modes of treatment providing evidence against a somatostatinergic mechanism of pulsatile GH secretion in these patients. The unchanged frequency of pulsatile GH release in the patients unresponsive to exogenous GHRH indicates that this pattern might be independent of hypothalamic GHRH and somatostatin and suggests a pituitary-derived mechanism for GH pulse generation in acromegaly.

Acromegaly↗
PubMed1992

Classification of dynamical diseases by new mathematical tools: application of multi-dimensional phase space analyses to the pulsatile secretion of parathyroid hormone.

The biological importance of dynamic hormonal secretion has been demonstrated. There is good evidence from recent studies that parathyroid hormone (PTH) which plays an important role in bone physiology is secreted in a pulsatile manner. In this study we performed a classification of two 'dynamical diseases' namely osteoporosis and hyperparathyroidism by the visualization of dynamic PTH-secretion in multidimensional phase spaces.

Adult↗
PubMed1992

Temporal pattern of pancreatic insulin and C-peptide secretion and of plasma glucose levels after nutritional stimulation.

The dependency of the secretory pattern of insulin and C-peptide on either oral ingestion of the energy substrates glucose and protein or gastric distension was determined in nine healthy male subjects. To analyze secretion dynamics, high frequency blood sampling, computed estimation of individual hormone half-lives, deconvolution of data, and pulse analysis of the deconvoluted data by the Cluster program were used. After stimulation with oral glucose and protein, baseline insulin, C-peptide, and glucose levels increased in parallel, forming two or three large increases (macropulses), with a mean duration of 63.8 min. The frequency of high frequency insulin and C-peptide pulses was unchanged, whereas a significantly increased amplitude formed the basis of insulin/C-peptide macropulses after both oral stimulations. No changes in baseline insulin/C-peptide concentrations or in amplitude or frequency were observed after a challenge with 400 mL H2O (n = 3). Gastric distension with an equal volume of H2O (400 mL) did not influence pancreatic hormone secretion. Insulin and C-peptide secretions were pulsatile, with a frequency of approximately one pulse per 12 min correlated to C-peptide pulses. When calculated by multiple regression analysis glucose, insulin and C-peptide plasma levels increased simultaneously after the challenge with either glucose or protein, suggesting a neuronal or humoral intestinal-pancreatic regulation of pancreatic hormone secretion. These findings suggest that high frequency insulin and C-peptide pulses form the basis of insulin and C-peptide plasma levels after meal stimulation.

Administration, Oral↗
PubMed1992

The nude rat is established as a model for endocrine studies: regulation of thyroid function and xenotransplantation of a thyroid tumor cell line.

The thyroid physiology of athymic nude rats, rnu/rnu, is characterized and established here as an animal model to study transplanted thyroid tumors. Male rats were catheterized 5 days before experiments were started. The mean thyroid-stimulating-hormone (TSH) plasma concentrations were 2.9 +/- 0.6 ng/ml during infusion of 0.25 ml/h of 0.9% NaCl (n = 12). T3 plasma concentrations were 2.6 +/- 0.4 ng/ml. T4 plasma levels were 22.0 +/- 5.6 micrograms/dl. A bolus of 0.1 mg thyrotropin-releasing hormone (TRH) significantly increased TSH plasma concentrations (P less than or equal to 0.001; from 2.9 +/- 0.6 to 7.8 +/- 1.1 ng/ml, n = 12). No pulsatile TSH secretion was observed in a 2-hour period with blood samples taken every 10 minutes (n = 12) and hourly sampling disclosed no circadian variation of TSH during a 24-hour period (n = 4). Successful xenografting was possible in 12 of 15 cases using a follicular thyroid carcinoma cell line (FTC 133). Measurement of human thyroglobulin (hTg) by a hTg IRMA revealed high levels in rats with functional FTC tumors, whereas no hTg was detected in untransplanted rats or animals with nonfunctional transplants.

Animals↗