Biomedical subjects

F Varga

Publications and source records attributed to F Varga.

At least 37 records · Page 2Linked to original sources

PubMed1996

Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in mouse osteoblastic cells.

Thyroid hormone (T3) is a known regulator of the transcription rate of specific genes. By subtractive hybridization of T2-treated osteoblastic cells, differentially expressed messenger RNAs (mRNAs) were enriched in the form of double stranded complementary DNA (cDNA) fragments. Sequencing of a differentially expressed cDNA that detects a 2.6-kilobase mRNA in Northern blots revealed to homology in the EMBL-Genebank data bases. A mouse genomic library was screened, and the isolated genomic DNA was identified as part of the insulin-like growth factor-binding protein-4 (IGFBP-4) gene including the 3'-untranslated region to which the cloned cDNA fragment was mapped by sequencing. We observed an up-regulation of the 2.6-kilobase IGFBP-4 mRNA transcript in the presence of T3 or retinoic acid. The induction of the IGFBP-4 transcript persisted up to 48 h. This response was inhibited by cycloheximide as well as actinomycin D. Long term induction studies revealed that the T3 effect is present during the complete culture period, with a constant rise in IGFBP-4 mRNA levels until 14 days. Under these culture conditions, the DNA content of MC3T3-E1 cells were significantly reduced by T3 and retinoic acid, indicating the repressive effect of both hormones on cell growth. Western immunoblots showed that the transcriptional induction is consequently transduced to increased IGFBP-4 levels in the conditioned medium of T3-treated cells. Our data show that thyroid hormone and retinoic acid stimulate transcription of IGFBP-4 mRNA in osteoblasts, resulting in increased IGFBP-4 secretion into the medium. IGFBP-4, a known inhibitor of cellular proliferation, might contribute to the antiproliferative effect of T3 and retinoic acid on osteoblasts.

Animals↗

PubMed1996

The cellular protooncogenes c-fos and egr-1 are regulated by prostacyclin in rodent osteoblasts and fibroblasts.

PGs are local regulators of various cellular functions. They exert their effects via specific PG receptor subtypes. Induction of c-fos gene expression has been described for arachidonic acid and its metabolite PGE2. We demonstrate that another very short half-lifed prostanoid metabolite, namely prostacyclin (PGI2), is a regulator of immediate-early genes. PGI2 transiently induced the growth-associated immediate-early genes c-fos and egr-1 in osteoblastic as well as fibroblastic cell lines. Furthermore, we showed that PGI2 dose dependently stimulated new DNA synthesis in the osteoblastic cell line MC3T3-E1. Although PGI2 is known to be a potent inducer of cyclooxygenases, we showed that this pathway is not necessary for protooncogene induction by PGI2. Our data indicate a direct effect of PGI2 on immediate-early gene expression, which does not depend on the synthesis of other prostanoids. Intracellular signal transduction mechanisms were studied with the protein kinase inhibitor H-7, a potent inhibitor of PGI2-induced c-fos expression. Experiments with phorbol esters revealed that protein kinase C activity is not obligatory for the effect of PGI2 on c-fos expression. We conclude from these results that PGI2, a rapidly inactivated prostanoid, has a major impact on cellular oncogene expression and growth in mesenchymally derived cells.

3T3 Cells↗

PubMed1995

The regulatory role of thyroid hormones in bone cell growth and differentiation.

The clinical effects of thyroid hormones on bone in hypo- and hyperthyroidism are well known but their fundamental role in the regulation of bone remodeling is still poorly understood. In this review the current literature is summarized and experimental data from our laboratory are presented. The direct stimulation of bone resorption by thyroid hormones in organ culture, which in part is mediated by prostaglandins and TGF-beta, and the effect of different agents thereon are reviewed. More recent data concerning thyroid hormone action in the osteoblastic cell line MC3T3E1, are summarized. From their effect on proliferation and alkaline phosphatase activity, we conclude that thyroid hormones accelerate osteoblastic differentiation. The regulation of the transcriptional expression of certain genes by nuclear T3 receptors and their effect on osteoblastic target genes like IGF-I are reviewed. In addition a novel role of triiodothyronine as inhibitor of growth factor induced transcriptional expression of regulatory genes (c-fos, c-jun) is suggested.

Alkaline Phosphatase↗

PubMed1995

B lymphocytes with latent EBV infection appearing in long-term bone marrow cultures (HLTBMCs) from haematological patients induce lysis of stromal microenvironment.

Human long-term bone marrow cultures (HLTBMCs) are a valuable in vitro model for studying the role of the haemopoietic microenvironment. Here we report the spontaneous appearance of EBV-positive B cells in 6/40 HLTBMCs from patients with various haematological diseases after 3-5 months of culture. After subcultivation of these cells, a novel type of cell line could be characterized, which displayed surface markers and morphological features typical for EBV transformed B-cell lines. As the deproteinized and ultrafiltrated culture supernatants of these cell lines were found to contain an agent with stroma toxic properties, they were termed SSB lines (stroma-toxic-agent-secreting B-cell lines). This agent also exhibited a colony-inhibitory activity on in vitro myelopoiesis and erythropoiesis. These properties are typical for the two polyamines spermine and spermidine which were detected at elevated levels in the culture supernatants of SSB lines. The hypothesis that latent presence of EBV in bone marrow may induce an increased synthesis of spermine and spermidine, which are known to be associated with malignant haematological diseases and bone marrow aplasia, is discussed.

B-Lymphocytes↗

PubMed1994

[Zn-content of erythrocytes in overt and subclinical hyperthyroidism].

Assaying the markers in blood reflecting thyroid hormone effect at peripheral tissue level previous data revealing a significantly decreased red-blood cell Zn-content in overt hyperthyroidism compared to euthyroid controls could be confirmed (p < 0.001). In patients with thyrotoxicosis during Metothyrin treatment the Zn-concentration of red-blood-cells normalised about 8 weeks later than the abnormally elevated serum thyroxine and triiodothyronine levels. On the basis of the present findings it is assumed that the Zn-concentration of red-blood cells reflects to a certain degree the circulating levels of thyroid hormones 2 to 3 months prior to the performed examination. The measurement of red-blood cell Zn-content does not seem to be a reliable method for the detection of a possible "tissue"-thyrotoxicosis in cases of subclinical hyperthyroidism.

Erythrocytes↗

PubMed1994

Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3-E1.

Thyroid hormones are known to affect skeletal growth and maturation by influencing both bone resorption and bone formation. Their exact mechanism of action, however, is still unknown. Local factors such as prostaglandins, TGF-beta or IGF-I were suggested to mediate their effects. Thyroid hormones were reported to stimulate expression of IGF-I mRNA in liver and kidney and to increase IGF-I release from bone organ cultures and osteoblast-like cells. Therefore we studied the effect of thyroid hormones on IGF-I mRNA expression in MC3T3-E1 cells. The cells were grown in culture for 5 to 7 days and treated with triiodothyronine (10(-11)-10(-6) M) and thyroxin (10(-6) M) for 1-24 h. Cellular mRNA was isolated and subjected to Northern hybridization. The amount of IGF-I mRNA, which is already expressed in this cell line under control conditions, was markedly enhanced by T3 and T4. This effect was found to be dose-dependent with a maximum at 10(-7) M and could already be seen after 3 h increasing up to 24 h. Our findings indicate that IGF-I expression in osteoblasts is directly regulated by thyroid hormones. We conclude that IGF-I expression belongs to the phenotypic characteristics of mature osteoblasts, and that thyroid hormones play an important role in differentiation of MC3T3-E1 cells along the osteoblastic lineage.

Base Sequence↗

PubMed1993

Bone mineral density in patients with endogenous subclinical hyperthyroidism: is this thyroid status a risk factor for osteoporosis?

OBJECTIVE: The aim of the present study was to elucidate whether endogenous subclinical hyperthyroidism due to a solitary autonomously functioning thyroid nodule affects bone metabolism and is a risk factor for osteoporosis. DESIGN: In a cross-sectional study measurements of bone mineral density were performed in premenopausal and post-menopausal women. Patients were categorized into non-toxic nodular goitre (n = 32), subclinical hyperthyroid (n = 37) and toxic solitary autonomous thyroid nodule (n = 22) subgroups and the results were compared with those of sex and age-matched control reference population (n = 68). MEASUREMENTS: Lumbar spine and femoral neck bone mineral densities were measured by dual energy X-ray absorptiometry. Single-photon absorptiometry was applied to the measurement of bone mineral content in the midshaft of the radius. RESULTS: In the non-toxic nodular goitre group, bone densities for all the scanned sites did not differ from the sex and age-matched reference population. At the L2-4 scanning site a significant decrease in the bone mineral density could be observed only in the toxic nodular goitre group and this decrease was more marked in the postmenopausal (P < 0.001) than in the premenopausal females (P < 0.05). At the femoral neck and midshaft radius the mean densitometric values were slightly, but significantly, lower only in the post-menopausal subclinical hyperthyroid group compared with the reference population (P < 0.01). The bone mineral density of the femoral neck, as well as the bone mineral content of the midshaft radius, was significantly decreased in both the premenopausal and post-menopausal patients with a toxic solitary nodule. CONCLUSION: This study indicates that the bone mineral density of the lumbar spine, femoral neck and the midshaft of the radius are not significantly decreased in premenopausal patients with endogenous subclinical hyperthyroidism resulting from a solitary autonomously functioning thyroid nodule. Conversely, findings hint at the possibility that long-lasting endogenous subclinical hyperthyroidism may be a contributing factor to the development of osteoporosis in some post-menopausal women, mostly at sites where cortical bone preponderates.

Adult↗

PubMed1993

Dependence of glycine conjugation on availability of glycine: role of the glycine cleavage system.

1. Glycine conjugation of benzoic acid was investigated in anaesthetized rats by measuring the disappearance of benzoate from blood, and the appearance of benzoylglycine in blood and urine. 2. Administration of glycine (1-10 mmol/kg,i.v.) increased the capacity of benzoylglycine formation in a dose-dependent fashion, with a maximal rate (8.1 mumol/kg per min) occurring after administration of 5 mmol/kg glycine. The normal endogenous glycine supply (1.7 mM in liver) permits glycine conjugation only at an approximate half-maximal rate (4.5 mumol/kg/per min). 3. The increase in benzoylglycine formation in response to exogenous glycine supply is also a function of the benzoate dosage. Decreased responsiveness at high benzoate dosage indicates that the availability of coenzyme A is another factor that also limits the capacity of glycine conjugation. 4. Cysteamine (200 mg/kg, i.p.), a potent inhibitor of the mitochondrial glycine cleavage system, rapidly increased hepatic glycine concentration 2-3-fold without affecting the concentration of the other co-substrates (i.e. coenzyme A and ATP) of glycine conjugation. 5. Administration of cysteamine increased the blood clearance of benzoate by 50%, the appearance of benzoylglycine in blood, and the urinary excretion of benzoylglycine. 6. It is concluded that the activity of glycine cleavage system is an important determinant of glycine supply and, thereby, the capacity of glycine conjugation of xenobiotics.

Animals↗

PubMed1993

Effect of valproic acid on glycine conjugation of benzoic acid.

Conjugation with glycine proceeds through ATP-dependent coupling of carboxylic acids with coenzyme A (CoA). Therefore, chemicals that form CoA esters may interfere with glycine conjugation. We tested the hypothesis that valproic acid (VPA), which is esterified with CoA in the first step of its mitochondrial beta-oxidation, may compromise glycine conjugation of aromatic carboxylic acids, by investigating the effect of acute VPA administration on glycine conjugation of benzoic acid in rats. VPA administered 1 hr before injection of benzoate only decreased the blood clearance of benzoate and the urinary excretion of benzoylglycine slightly in normal rats. However, in rats loaded with glycine, 2 and 3 mmol/kg of VPA reduced the blood clearance of benzoate by 34 and 59%, diminished the peak blood level of the glycine conjugate and depressed the maximal urinary excretion rate of benzoylglycine by 28 and 66%, respectively. To elucidate the mechanism of VPA-induced inhibition of benzoylglycine formation, the effects of VPA on hepatic levels of cosubstrates and the activities of enzymes involved in glycine conjugation were also determined. One hour after administration of VPA, hepatic ATP levels remained unchanged, whereas the concentration of CoA was reduced by 67 to 73% and that of glycine was increased by 58 to 67%. Activities of the enzymes of glycine conjugation were not influenced by VPA. However, 2-n-propyl-4-pentenoic acid, a metabolite of VPA, inhibited benzoyl-CoA synthetase. In summary, VPA minimally influenced the capacity of glycine conjugation of benzoic acid in normal rats, but decreased it markedly in glycine-loaded rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Increased biliary excretion of glutathione is generated by the glutathione-dependent hepatobiliary transport of antimony and bismuth.

We have recently demonstrated that the hepatobiliary transport of arsenic is glutathione-dependent and is associated with a profound increase in biliary excretion of glutathione (GSH), hepatic GSH depletion and diminished GSH conjugation (Gyurasics A, Varga F and Gregus Z, Biochem Pharmacol 41: 937-944 and Gyurasics A, Varga F and Gregus Z, Biochem Pharmacol 42: 465-468, 1991). The present studies in rats aimed to determine whether antimony and bismuth, other metalloids in group Va of the periodic table, also possess similar properties. Antimony potassium tartrate (25-100 mumol/kg, i.v.) and bismuth ammonium citrate (50-200 mumol/kg, i.v.) increased up to 50- and 4-fold, respectively, the biliary excretion of non-protein thiols (NPSH). This resulted mainly from increased hepatobiliary transport of GSH as suggested by a close parallelism in the biliary excretion of NPSH and GSH after antimony or bismuth administration. Within 2 hr, rats excreted into bile 55 and 3% of the dose of antimony (50 mumol/kg, i.v.) and bismuth (150 mumol/kg, i.v.), respectively. The time courses of the biliary excretion of these metalloids and NPSH or GSH were strikingly similar suggesting co-ordinate hepatobiliary transport of the metalloids and GSH. However, at the peak of their excretion, each molecule of antimony or bismuth resulted in a co-transport of approximately three molecules of GSH. Diethyl maleate, indocyanine green and sulfobromophthalein (BSP), which decreased biliary excretion of GSH, significantly diminished excretion of antimony and bismuth into bile indicating that hepatobiliary transport of these metalloids is GSH-dependent. Administration of antimony, but not bismuth, decreased hepatic GSH level by 30% and reduced the GSH conjugation and biliary excretion of BSP. These studies demonstrate that the hepatobiliary transport of trivalent antimony and bismuth is GSH-dependent similarly to the hepatobiliary transport of trivalent arsenic. Proportionally to their biliary excretion rates, these metalloids generate increased biliary excretion of GSH probably because they are transported from liver to bile as unstable GSH complexes. The significant loss of hepatic GSH into bile as induced by arsenic or antimony may compromise conjugation of xenobiotics with GSH.

Animals↗

PubMed1992

Characterization of a new repetitive sequence that is enriched on microchromosomes of turkey.

We cloned and characterized a new highly repetitive, species-specific DNA sequence from turkey (Meleagris gallopavo). This repeat family, which accounts for approximately 5% of the turkey genome, consists of a 41 bp repeated element that is present in tandem arrays longer than 23 kb. In situ hybridization to turkey metaphase chromosomes (2n = 80) demonstrated that this sequence was located primarily on certain microchromosomes: approximately one-third of the 66 microchromosomes showed a positive signal. With respect to the macrochromosomes, hybridization was seen only in a pericentric position on nos. 2 and 3. The turkey microchromosome (TM) sequence shares motifs (alternating A3-5 and T3-5 clusters separated by 6-8 bp) that have been found previously in other avian tandemly repeated elements, e.g. a chicken microchromosomes sequence, and W (female) chromosome-specific sequences of chicken and turkey. However, the TM sequence does not cross-hybridize under moderately stringent conditions with these other sequences. The spread and amplification of related repetitive sequence elements on microchromosomes and W chromosomes is discussed.

Animals↗

PubMed1992

Effect of lipoic acid on biliary excretion of glutathione and metals.

Several metals are excreted in bile as glutathione complexes, and their biliary excretion is facilitated by increased hepatobiliary transport of glutathione. The present study analyzed the effect of lipoic acid (LA; thioctic acid; 37.5-300 mumol/kg, iv), an endogenous disulfide which can be reduced in vivo to a dithiol, on the hepatobiliary disposition of glutathione-related thiols and the biliary excretion of metals (10 mumol/kg, iv) in rats. Administration of LA enhanced the biliary excretion of reduced glutathione in a dose-dependent fashion. Despite increasing glutathione output, LA (150 mumol/kg, iv) did not increase, but rather decreased, the biliary excretion of methylmercury, cadmium, zinc, and copper, which are transported into bile in a glutathione-dependent manner, as indicated by a marked reduction in their biliary excretion after diethyl maleate-induced glutathione depletion. In contrast, biliary excretion of inorganic mercury, which is minimally affected by glutathione depletion, was dramatically enhanced (12- to 37-fold) by LA administration. Following injection of LA, the concentrations of endogenous disulfides in arterial blood plasma (e.g., cystine, glutathione disulfide, cysteine-glutathione, protein-cysteine, and protein-glutathione mixed disulfides) were considerably diminished, while the levels of endogenous thiols (e.g., glutathione and cysteine) were increased. This finding indicates that LA, probably after enzymatic conversion to dihydrolipoic acid, can reduce endogenous disulfides to thiols. It appears that LA induces the transport of glutathione into bile by the temporary formation of dihydrolipoic acid-glutathione mixed disulfide, which after being translocated into bile is cleaved to LA and reduced glutathione. Because the glutathione molecule thus transported into bile cannot complex metals at the thiol group, this might be the mechanism for the observed failure of the LA-induced increase in biliary excretion of glutathione to enhance the hepatobiliary transport of metals that are transported into bile as glutathione complexes (i.e., methylmercury, cadmium, zinc, and copper). The observations also raise the possibility that endogenous dihydrolipoic acid, by forming a stable complex with mercuric ion, may play the role of a carrier molecule in the hepatobiliary transport of inorganic mercury.

Animals↗

PubMed1992

Biologic markers in blood reflecting thyroid hormone effect at peripheral tissue level in patients receiving levothyroxine replacement for hypothyroidism.

Plasma fibronectin, serum procollagen-III-peptide and sex-hormone binding globulin as not specific markers of thyroid hormone effect at peripheral tissue level were determined and their values were related with serum levels of TSH, free-thyroxine and triiodothyronine during levothyroxine sodium replacement therapy for hypothyroidism. Low levels of biologic markers characteristic of hypothyroidism were normalized in consequence of hormone replacement and a negative correlation between their serum levels and TSH concentration was demonstrated in most subjects. However, in some patients a discrepancy in the response to levothyroxine between the pituitary and other target organs could be revealed. Additional evidence was disclosed that the pituitary thyrotroph sensitizes a minor decrease in serum thyroxine level, which would not be recognized by other target organs. Furthermore, it was revealed that during L-T4 replacement therapy in a large fraction of patients with subnormal serum TSH concentration blood levels of the measured markers often exceeded the upper limit of the normal range indicating the possibility of "tissue"-thyrotoxicosis beside the pituitary in other target organs, too. According to the present study which takes into consideration markers reflecting end-organ responsiveness to thyroid hormones it is recommended to adjust the dose of levothyroxine to maintain serum TSH in the normal range. For patients with subnormal TSH concentration a close follow-up is obligatory and in case od concomitantly raised free-thyroxine level the reduction of the levothyroxine dosage is proposed.

Adult↗

PubMed1992

[The effect of surface etching on tensile strength].

The aim of this study was to investigate the effect of different partial size of corundum used by sand blasting on the surface roughness and on the tensile strength. The conclusions of the authors were as follows: 1. The maximum values of tensile strength were measured when 200-250 microns corundum was used. 2. The values of the R(a) and Rmax were grown proportionally with the grain of corundum, but it was not resulted in the same increase of the tensile strength. 3. After the tensile test the residue of the bonding agent on one surface of the test-piece pairs, always remained significantly higher, than on the other, but this phenomenon cannot be explained by the differences between R(a) and Rmax within the test-piece pairs.

Acid Etching, Dental↗

PubMed1992

Radioimmunoassay of thyrotropin-releasing hormone in euthyroid subjects and in patients with thyroid diseases.

An episodic pattern of fluctuation in serum TRH level was demonstrated in euthyroid males. It is suggested that these rises in serum TRH-IR are due to its pulsatile hypothalamic release, however, it must be remembered that a high proportion of circulating TRH is derived from extrahypothalamic sources. The conception that the TSH surge during late evening is secondary to an increased TRH release could not be proved in the present study. In the euthyroid and primary hypothyroid groups the mean values of serum TRH-IR did not differ, while its level was slightly, but not significantly lower in hyperthyroid patients. The evaluation of a single TRH determination is impeded by the short half-life, low serum level and its production in extrahypothalamic sites, too.

Circadian Rhythm↗

PubMed1991

Glutathione-dependent biliary excretion of arsenic.

This study aimed to clarify whether glutathione (GSH) plays a role in the hepatobiliary transport of arsenic. For this purpose, the biliary excretion of 74As was measured in urethane-anaesthetized rats for 2 hr after the administration of labelled sodium arsenite (50 mumol/kg, i.v.) or arsenate (150 mumol/kg, i.v.) and under the influence of sulfobromophthalein (BSP), indocyanine green (ICG) or diethyl maleate (DEM) which are known to diminish hepatobiliary transport of GSH. Although the biliary excretion of arsenic was different after arsenite and arsenate administration in terms of quantity (19% vs 6% of dose in 2 hr, respectively) and time course, arsenic excretion responded similarly to BSP (50 mumol/kg, i.v.), ICG (25 mumol/kg, i.v.) or DEM (4 mumol/kg, i.p.) irrespective of the injected arsenical. Initially the biliary excretion of arsenic in rats with either arsenite or arsenate was significantly reduced, but then moderately increased by BSP and, more lastingly, depressed by ICG, whereas it was virtually abolished by DEM. The responses of arsenic excretion to BSP, ICG and DEM were related, both proportionally and temporally, to the effects exerted by these agents on the hepatobiliary transport of GSH, as assessed by the biliary excretion of non-protein thiols. These findings indicate that the biliary excretion of arsenic after the administration of either arsenite or arsenate is dependent on the hepatobiliary transport of GSH. Transport of arsenic as a GSH complex may account for the GSH dependence of biliary arsenic excretion.

Animals↗

PubMed1991

Biologic blood markers reflecting thyroid hormone effect at peripheral tissue level in patients receiving levothyroxine replacement for hypothyroidism.

Plasma fibronectin, serum procollagen-III-peptide and sex-hormone-binding globulin as non-specific markers of thyroid hormone effect at peripheral tissue level were determined and their values were related with serum levels of TSH, free-thyroxine and triiodothyronine during levothyroxine sodium replacement therapy for hypothyroidism. Low levels of biologic markers characteristic of hypothyroidism were normalized in consequence of hormone replacement and a negative correlation between their serum levels, and TSH concentration was demonstrated in most subjects. However, in some patients a discrepancy in the response to levothyroxine between the pituitary and other target organs was revealed. Additional evidence was disclosed that the pituitary thyrotroph sensitizes a minor decrease in serum thyroxine level, which would not be recognized by other target organs. Furthermore, it was revealed that during L-T4 replacement therapy in a large fraction of patients with subnormal serum TSH concentration blood levels of the measured markers often exceeded the upper limit of the normal range indicating a possibility of "tissue" thyrotoxicosis, besides the pituitary, in other target organs, too. According to the present study, which takes into consideration markers reflecting end-organ responsiveness to thyroid hormones, it is recommended to adjust the dose of levothyroxine to maintain serum TSH in the normal range. For patients with subnormal TSH concentration a close follow-up is obligatory and in case of concomitantly raised free-thyroxine level the reduction of the levothyroxine dosage is proposed.

Adult↗

PubMed1990

A 41-42 bp tandemly repeated sequence isolated from nuclear envelopes of chicken erythrocytes is located predominantly on microchromosomes.

To study whether specific DNA sequences are associated with nuclear membranes, residual DNA was extracted from DNase-treated nuclear envelopes prepared from erythrocytes of adult chickens (Gallus domesticus). This DNA was then blunt-end ligated into a bacterial plasmid vector. DNA blot analysis and nucleotide sequence determination revealed that approximately 30% of the cloned fragments consisted of different multiples of a 41-42 bp tandemly repeated, partially symmetrical sequence. In situ hybridization to chicken chromosomes demonstrated that the sequence was located primarily on microchromosomes, although some hybridization was also observed to macrochromosomes 7 and 8. Digestion of chicken DNA with any of a number of restriction enzymes did not completely reduce the intensity of a high molecular weight band to which the repeated sequence hybridized. These results, along with those obtained from in situ hybridization, suggested that many copies of this sequence are organized into large tandem arrays, and are not dispersed in many shorter repetitive blocks throughout the chicken genome. Although the repetitive sequence constituted approximately 10% of the chicken genome, it did not hybridize to quail or turkey DNA.

Animals↗