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Biomedical subjects

T Kadar

Publications and source records attributed to T Kadar.

At least 55 records · Page 3Linked to original sources
PubMed1988

Lack of relationship between the levels of prolactin receptors and steroid receptors in women with breast cancer.

The levels of prolactin receptors (PRL-R), based on a new micro-method, estrogen receptors (ER) and progesterone receptors (PG-R), were determined in 159 breast cancer specimens. Sixty-seven of 159 tumors (42%) had PRL-R levels of 20 fmol/mg protein or higher, and were regarded as PRL-R positive. In 60 of the 159 samples (38%), no PRL-R could be detected, and the remaining 32 samples (20%) were considered borderline. While a positive correlation was found between the presence of ER and PGR, no correlation was detected between PRL-R and any steroid receptors (r = -0.024 for ER vs PRL-R, 0.052 for PGR vs PRL-R and 0.002 for ER + PGR vs PRL-R). Furthermore, PRL-R in levels of 20 fmol/mg protein or higher were found in 35% of samples in which no steroid receptors were detected as well as in 38% and in 27% of samples which exhibited positive ER or PGR respectively (greater than or equal to 20 fmol/mg protein). On the other hand, in 47% of the samples possessing both ER and PGR, the PRL receptors could not be found. These results clearly demonstrate that in the human breast cancer, the presence of PRL-R is independent of the status of either ER or PGR. It is suggested that the measurement of PRL-R could serve as a chemical marker to guide a possible therapeutic use of PRL-suppressing drugs in women with breast cancer.

Adult↗
PubMed1986

Micromethod for the determination of free and total prolactin receptors: measurement of receptor levels in normal and malignant mammary and prostate tissues.

A sensitive micromethod for the determination of free and total prolactin receptors in normal or malignant tissues has been developed. Positive and negative quality controls are incorporated in the procedure. Either whole tissue or the pellet fraction remaining from tissue that had undergone processing for estrogen receptors can be used. Crude microsomal and plasma membrane fractions obtained by homogenization and differential centrifugation are incubated with labeled prolactin in the presence or absence of increasing amounts of unlabeled hormone. The labeled ligand is prepared by a stoichiometric iodination procedure in which one atom of iodine-125 is incorporated into one molecule of the hormone, resulting in an intact labeled prolactin with a high specific activity of 170-186 muCi/micrograms (1 Ci = 37 GBq). Human prolactin labeled by this procedure has much greater specific binding capacity to various rat tissues than does iodinated rat prolactin. This technique permits an accurate measurement of prolactin receptors in as little as 50 micrograms of membrane protein. Highest levels of free and total prolactin receptors were found in the liver of 60-day-old female rats that served as a positive control. Liver of immature 21-day-old male rats, devoid of prolactin receptors, was used as a negative control. The amount of detectable free receptors was dependent on the level of circulating plasma prolactin. In 3-day postpartum lactating rats with high prolactin levels in plasma, all prolactin receptors in the mammary glands were found to be occupied, and no free receptors could be detected. When these receptors were desaturated from the endogenous prolactin by exposure to 3 M MgCl2, one class of receptors in a high quantity (1.75 nmol/mg of protein) and with a moderate affinity (Kd = 6.41 X 10(-9) M) was detected. A similar type of receptor was found in the mammary glands of rats at midpregnancy and of cycling adult female rats. In malignant rat mammary tissue, however, fewer receptors (27 pmol/mg of protein) but with a very high affinity (Kd = 6.8 X 10(-14) M) were detected. Normal ventral and dorsolateral rat prostate contained two classes of prolactin receptors (Kd = 3.46 X 10(-10) M and 1.93 X 10(-8) M). In the cancerous rat prostate, however, only one of these two classes of receptors was detected, and the number was smaller.

Animals↗
PubMed1985

A quaternary anti-cholinesterase probe for determining the integrity of the blood--brain barrier.

7-(Methylethoxyphosphinyloxy)-1-methyl quinolinium iodide (MEPQ), a new quaternary anti-cholinesterase (anti-ChE) compound was prepared and evaluated as a potential probe for assessing changes in the blood-brain barrier (B-BB) permeability. MEPQ was found to be 170 times more potent in its cholinesterase inhibitory activity than phospholine iodide, a previously reported anti-ChE probe in B-BB research. In rats and mice with impaired B-BB induced by osmotic opening, MEPQ readily penetrated through the damaged site as demonstrated by considerable reduction of ChE activity. In controls, brain ChE activity remained unaffected. It is suggested that MEPQ is a useful probe for both qualitative (histological staining) and quantitative (brain homogenated) assessment of permeability changes in the B-BB.

Animals↗
PubMed1985

Distribution of 3H-soman in mice.

3H-soman (specific activity 10 Ci/mMol), a potent irreversible cholinesterase inhibitor, was administered IV to mice in a dose of one LD-50, which corresponds to 0.25 mCi/mouse. Animals were sacrificed at 5 min, 2 h and 24 h, and whole body autoradiography was performed. High levels of radioactivity in lung and skin were observed at all time intervals after injection. The central nervous system showed very low concentrations of radioactivity, which remained so for 24 h post-injection. Considerable accumulation of 3H-soman in the urine and gall-bladder, and in the intestinal lumen, may indicate these as pathways of soman excretion. Quantitative determinations of radioactivity in various tissue samples were consistent with the above-mentioned findings. It is concluded that the nature of the persistent binding of soman to lung and skin is striking, and may indicate the existence of specific sites for soman depots.

Animals↗
PubMed1984

Synthesis of potent heptapeptide analogues of cholecystokinin.

Nine new analogues of acetyl-CCK-heptapeptide (Ac-Tyr(SO3H)2-Met3-Gly4-Trp5-Met6-Asp7-Phe8-NH2 ) were synthesized by solid-phase methodology. In a first series, the Asp7 residue was replaced by hydroxy amino acid sulfate esters. In another series, Gly4 was substituted by D-Ala, while Trp5 and Met6 were replaced by their D enantiomer. The introduction of the sulfate ester was performed with a new, mild, crystalline, and stable reagent, pyridinium acetyl sulfate. Each analogue that contained Tyr(SO3H)2 and a hydroxy amino acid sulfate ester [Ser(SO3H), Thr(SO3H), or Hyp(SO3H)] in position 7 proved to be more potent (1.9, 1.7, and 3.0 times, respectively) than CCK-8 in vitro (isolated gallbladder strips). While devoid of gastrin-like activity in vivo, these analogues had potent anticonvulsive activity. The analogues containing a D-amino acid residue were less potent than the parent compound in vitro. The D-Ala4 replacement, however, yielded a compound that was 40% as potent as CCK-8 in the in vitro test but showed prolonged duration of action on sphincter Oddi. While the 7-substituted Ac-CCK heptapeptides are among the most potent CCK analogues reported so far, the D-Ala4 replacement resulted, for the first time, in prolonged activity in vivo.

Amino Acid Sequence↗
PubMed1984

[Analysis of the effect of cholecystokinin octapeptide on the monoamine level in rat brain limbic structures in the process of satiation].

The authors studied the changes in monoamine levels in rat brain limbic structures during natural satiation and satiation after intraperitoneal injection of cholecystokinin octapeptide (CCK-8) in doses 5 and 10 micrograms/kg following 24- and 48-hour food deprivation. Injection of CCK-8 was found to reduce food consumption in hungry rats by 2.5 times on an average. Of the test animals, 25% appeared resistant to CCK-8, showing no reduction in food consumption. Satiation after the 24-hour food deprivation caused characteristic changes in the levels of noradrenaline, dopamine and serotonin in the limbic structures of the brain, similar to the changes in monoamine levels in the limbic structures of animals, in which food motivation was suppressed by injection of CCK-8. The responses of the monoaminergic system of the brain limbic structures to satiation induced by CCK-8 injection after the 48-hour food deprivation differed qualitatively from the responses to natural satiation. It is concluded that the inhibitory action of CCK-8 on food motivation in rats determined by the 24-hour fasting is likely to be mediated via the monoamine system of the hypothalamus, tonsils and hippocamp. However, the data obtained suggest a different mechanism of the satiating action of CCK-8 under marked food motivation after long-term periods of food deprivation.

Animals↗
PubMed1983

The pathogenesis of synergistic lung damage in mice by an environmental irritant (H2SO4) and particulate antigen.

Daily inhalation by mice of an environmental irritant (H2SO4) followed by consequent respiratory immunization with a particulate antigen (sheep red blood cells, SRBC) induced severe interstitial pneumonitis. Inhalation of H2SO4 per se resulted in accumulation of i.v. injected globulin in the lungs of mice, without significant change in lung weight. In addition, when marker colloidal carbon particles were injected i.v. following H2SO4 inhalation, the carbon was rapidly trapped in the capillary wall in the lungs. Homologous anti-SRBC serum instilled into the respiratory tract followed by subsequent SRBC inhalation produced inflammation and injury similar to that generated by H2SO4 in combination with particulate antigen. It is postulated that following irritant inhalation, the permeability of alveolocapillary membranes increases, so that immune complexes formed by pre-existing circulating antibodies and inhaled antigen can initiate subsequent lung injury.

Animals↗
PubMed1979

Whole body autoradiography of 3H-phencyclidine in mice.

The present whole-body autoradiographic study demonstrates that the circulatory system is practically free of radioactivity, already 5 min after intravenous administration of 3H-Phencyclidine to mice. At this time, however, high radioactive levels appear in the lachrymal gland, nasal mucosa, bone marrow and spleen, as well as in the urinary, digestive, respiratory and reproductive systems. High accumulation is maintained up to 20 min after administration and, thereafter, radioactivity declines continuously with increasing time. After 6 h, radioactivity disappears in most organs, but remains notable in the kidney, lung and liver, as well as in the salivary and lachrymal glands. After 24 h, detectable amounts still persist in the liver, lung and in the salivary and lachrymal glands. The brain shows very low amounts of radioactivity during the whole period of observation. In pregnant mice, the drug accumulates in the placenta and partly crosses the placental barrier into the foetal tissues.

Animals↗
PubMed1977

Corticosteroid-induced changes in glucose metabolism of chondrocytes.

Immature mice were treated for up to 12 weeks with daily doses of triamcinolone diacetate. Using quantitative histochemical methods, the proximal epiphyseal plate of the humerus was studied at regular intervals. By the tenth injection significant decrease was noted in the acid glycosaminoglycans content (25%) and in the neutral mucopolysaccharides (30%). Concomitantly, a marked increase was noted in the intracellular depots of glycogen (70%). It is suggested that the hormone's antiglycolytic effect in cartilage caused the glucose metabolic pathway to divert in the direction of glycogen synthesis, and thereby interfered with the normal synthetic pathway of the chondrocytes. The hormone's primary effect on the cells' hexose metabolism could be responsible, at least in part, for its inhibitory influence on bone growth.

Animals↗
PubMed1977

Age-related changes in the cellular population of the growth plate of normal mouse.

Age-related changes in the number of cartilage cells within the proximal growth plate of the humerus were determined in normal ICR male mice. The rates of reduction in the number of proliferative and hypertrophic chondrocytes were calculated and compared during the animals' first 6 months of life. It was found that during the period of highest growth activity, between weanling and sexual maturation, the rate of cell production is hardly decreased, thus maintaining the thickness of the cartilaginous growth plate and thereby enabling an extensive bone growth. A close correlation was found between the following skeletal activities: decrease in longitudinal bone growth, narrowing of the epiphyseal growth plate and a decrease in the proliferative activity of young chondrocytes.

Age Factors↗
PubMed1977

Quantitative changes in the cellular population of the growth plate of triamcinolone-treated mice.

Triamcinolone-induced changes in the number of cartilage within the proximal growth plate of the humerus were determined in ICR male mice. It was found that pharmacological doses of corticosteroid hormone possess a direct inhibitory effect upon the proliferative activity of young cartilage cells and thereby adversely affect the growth potential of this growth center. Concomitantly, the activity of chondroclasts also appears to be depressed, thus resulting in a decreased rate of cartilage reorption followed by a slight increase in the number of hypertrophic chondrocytes. It therefore appears that systemic treatment with corticosteroid hormones inhibits the renewal of cartilage cells in the epiphyseal plate, leading to an accelerated 'aging' of this growth center with subsequent impairment of long bone growth.

Animals↗