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Biomedical subjects

B Szende

Publications and source records attributed to B Szende.

At least 91 records · Page 5Linked to original sources
PubMed1995

Tyrphostin induces non-apoptotic programmed cell death in colon tumor cells.

The programmed cell death inducing effect of the EGF receptor tyrosine kinase inhibitor alpha-cyano-3,4-dihydroxycinnamthioamide (AG213) was investigated in vitro on HT-29 human colon tumor. AG213 at concentrations between 45 to 450 microM blocks the proliferation of HT-29 cells. Morphological findings suggest that the selective tyrosine kinase inhibitor AG213 induces Clarke III type (non-lysosomal vesiculate cytoplasmic) programmed cell death; unlike ATP analog non-selective tyrosine kinase inhibitors like Genistein which were found to induce apoptosis. Cycloheximide and Actinomycin-D reduced the effect of AG213 pointing to the fact that protein and RNA synthesis are also needed for this form of cell death. Acid phosphatase activity was found in the Golgi and in the newly formed intracytoplasmic vacuoles 3 hours after AG213 treatment which disappeared by 6 hours. The induction of Clarke III cell death by tyrosine kinase inhibitors may open a new modality to selective killing of tumor cells.

Acid Phosphatase↗
PubMed1994

Olive oil decreases liver damage in rats caused by carbon tetrachloride (CCl4).

Oral carbon tetrachloride (CCl4) poisoning of the liver of male F-344 rats was modified by dissolving CCl4 in various oils (sunflower, corn, fish and olive). After 8 weeks of CCl4 treatment (3 x 0.2 ml/kg body weight every other day, dissolved in aliquots of 0.5 ml of each types of oil) the rats were sacrificed and the ratio of connective tissue in the liver was determined by morphometry after picrosirius staining. The percentage of collagen fibres increased in all CCl4-treated groups compared to the controls. This increase was almost the same (6-8%) in the case of CCl4 dissolved in sunflower, corn or fish oil, but when olive oil was applied as a solvent, the collagen ratio was only 2-4 percent. On the bases of this finding olive oil is considered as less harmful to the liver in acute CCl4 poisoning than other oils.

Animals↗
PubMed1994

Accuracy of admission and pre-autopsy clinical diagnoses in the light of autopsy findings: a study conducted in Budapest.

Pre- and post-autopsy diagnoses of underlying cause of death were compared in consecutive autopsies on persons aged 30 to 80 years; 1000 from each of two pathology departments in Budapest. Data on admission diagnoses and on contributory causes of death were also analysed. At autopsy, the percentages of deaths by underlying cause were neoplasms (any site) 34.9%, diseases of the circulatory system 40.2%, digestive system 13.8%, endocrine, nutritional, metabolic or immune systems 2.7%, and respiratory system 2.2%. For these five disease groupings, the percentages of cases diagnosed clinically as the underlying cause of death which were confirmed at autopsy were, respectively, 90.9%, 84.0%, 82.9%, 55.2% and 32.5%. Although, out of 697 cases with an autopsy diagnosis of neoplasia as the underlying cause, there were only 61 (8.8%) where neoplasms were not diagnosed clinically as the underlying cause, this conceals the fact that in 130 (18.7%) the two diagnoses differed as to the site of the primary neoplasm (ICD 3 digit code). The fact that 43% of post-mortem diagnoses (ICD major category) of underlying cause are missed on admission, and that 19% are missed clinically, indicates that improved clinical diagnostic procedures have not diminished the need for high autopsy rates. Morbid anatomy needs to be better resourced.

Adult↗
PubMed1994

[Hungarian university lecturers and professors of pathology from Arányi to the present days].

Lajos Arányi (Lostainer), who introduced pathological anatomy into Hungary, was born in Komárom in 1812. He lost his father at the age of three, and then was adopted by one of his wealthy uncles. Arányi first studied at the faculty of arts and later law at university, but after a cholera epidemic in 1831, in which he helped the infected in Pest, he changed his mind and went over to the faculty of medicine. After he had received his degree he worked as an assistant to Ferenc Bene from 1837. Two years later he spent six months at Italian clinics, and four years in Vienna. In Vienna, where he worked with Professor Rokitansky at the Allgemeines Krankenhaus, he learned the techniques of pathology, and studied the humouralpathological theory of his principal, and above all the clinicopathologic views of the Vienna medical school. Returning home he decided to introduce patholoogy into the medical curriculum. In his objectives he was helped by Ignác Stáhly, Agost Schöpf-Merei and János Balassa. His introductory lecture took place in 10 April 1844, and his regular lectures and demonstrations started from the autumn. His autopsy records were rather modern, he used clear and logical categories. ...

Education, Medical↗
PubMed1994

The concentration of LH-RH receptors in the nuclei of pancreatic cancer cells. Effect of (D-Trp6)LH-RH on tumor-bearing Syrian golden hamsters.

LH-RH analogs cause some inhibition of growth of pancreatic cancers. Syrian golden hamsters bearing chemically induced pancreatic cancers were treated with [D-Trp6]LH-RH for 3 d before sacrifice. LH-RH receptors were localized by electron-microscopic immunohistochemistry in the tumor cells of both treated and untreated hamsters. [D-Trp6]LH-RH treatment resulted in a marked increase in the concentration of LH-RH receptors in the nuclei. The dissociation constants (Kd) and the maximal binding capacity of the LH-RH receptors (Bmax), measured by radioreceptor assay, were higher in the nuclei of the pancreatic tumor cells of hamsters treated with [D-Trp6]LH-RH than in the untreated controls. Pancreatic cells of tumor-free hamsters did not show immunostaining for LH-RH receptors. A possible correlation between the increase in the concentration of the LH-RH receptors in the nuclei and the tumor growth-inhibiting activity of [D-Trp6]LH-RH is suggested.

Animals↗
PubMed1993

Expression of steroidogenic enzyme messenger ribonucleic acids and corticosteroid production in aldosterone-producing and "nonfunctioning" adrenal adenomas.

"Nonfunctioning" adrenal adenomas are often diagnosed in patients without recognizable clinical symptoms of adrenocortical hyperfunction. The objective of this study was to determine directly the steroidogenic activity of such adenomas (n = 12) and compare them histologically and functionally to normal human adrenals (n = 6) and aldosterone-producing adenomas (n = 15). The histological appearances of nonfunctioning and aldosterone-producing adenomas were surprisingly similar. Nonfunctioning adrenal adenomas expressed all mRNAs of P450scc, P450c17, P450c21, adrenodoxin, and adrenodoxin reductase with relative levels comparable to those found in normal adrenals. Consistent with their hormone-producing nature, these adenomas had cortisol and aldosterone contents as high as those in normal adrenal tissues, a significantly (P < 0.05) increased 17-hydroxyprogesterone content, and a disproportionally low expression of P450c21 mRNA compared to aldosterone-producing adenomas. Cells isolated from both aldosterone-producing and nonfunctioning adrenal adenomas exhibited highly ACTH-sensitive cortisol and aldosterone production, suggesting again the presence of both zona glomerulosa-like and zona fasciculata-like steroidogenesis in these adenoma tissues. These results indicate that so-called nonfunctioning adrenal adenomas are not without steroidogenic activity. Therefore, the assumption that adrenal adenomas are entirely nonfunctioning in the absence of recognizable hormonal hyperfunction may not be correct.

Adenoma↗
PubMed1993

The effect of amino acids and amino acid derivatives on cell proliferation.

The effect of certain amino acids and amino acid derivatives on cell proliferation have been studied in the author's Institute for more than 25 years. The optically active forms of arginine, lysine, aspartic acid and glutamic acid influence the growth of transplantable rat tumors. L-arginine, D-lysine, L-aspartic acid and D-glutamic acid promoted; D-aspartic acid, L-glutamic acid, D-arginine and L-lysine inhibited tumour growth. E-amino trimethyl-lysine (TML) stimulated cell proliferation in various cell systems (bone marrow, small intestine, cultured lymphocytes). When administered simultaneously with high doses of Cyclophosphamide, Vincristin or Doxorubicin to tumour-bearing mice, TML decreased the toxicity of the antitumour drugs, resulting in a higher rate of survivors. L-leucine methyl ester caused cell death of mouse peritoneal macrophages by inducing disruption of macrophages.

Amino Acids↗
PubMed1992

Inhibition of two-step urinary bladder carcinogenesis by the somatostatin analogue RC-160.

Fisher 344 female rats were exposed for 4 weeks to the initiator carcinogen N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) 0.05% in the drinking water and thereafter to the promoter carcinogen mitomycin C (0.08 mg per animal per week) intravesically for 12 weeks. High incidence of urinary bladder transitional cell cancers was observed (17 in situ and 17 invasive carcinomas among 40 rats). When the somatostatin analogue RC-160 (D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2) was administered s.c. at the dose of 50 micrograms per animal per day during 6-week period of promotion with mitomycin C, the incidence of urinary bladder cancer was dramatically reduced. Only 1 in situ carcinoma was observed among 20 rats and only preblastomatous lesions (dysplasias and papillomas) occurred. This effect could indicate that RC-160 interferes with the process of promotion by induction of enhanced apoptosis (programmed cell death) of the dysplastic urothelial cells. RC-160 could be tried therapeutically for the hormonal prevention of malignant transformation of preneoplastic lesions in the urinary bladder.

Amino Acid Sequence↗
PubMed1992

The diverse modification of N-butyl-N-(4-hydroxybutyl) nitrosamine induced carcinogenesis in urinary bladder by dibromodulcitol and dianhydrodulcitol.

The effects of intravesical therapy with adriamycin, 1.6-dibromo-1.6-dideoxydulcitol (DBD) or with 1.6-dianhydrodulcitol (DAD) on bladder carcinogenesis were investigated in rats. To induce premalignant lesions in the urinary bladder female Sprague-Dawley rats received 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in their drinking water for 4 weeks and then post-treated intravesically with one of the antitumor drugs and examined once a week for 3 months. These antitumor drugs in healthy rats (i.e. without the pre-administration of BBN) did not cause any significant morphological changes in the urinary bladder after intravesical application once a week for 3 months. In the applied dose BBN alone induced only premalignant lesions in the urinary bladder. However, neoplastic lesions occurred in the groups treated with BBN and adriamycin (9 papillomas and 3 carcinomas in 14 animals). Similarly intravesical application of DBD after BBN administration resulted 5 carcinomas among the 11 animals. On the contrary no urinary bladder tumor was found in the animals treated with BBN and DAD. As DAD is one of the conversion products of DBD it is conceivable that the difference between DBD and DAD action may be due to the formation of other solvolytic product from DBD than DAD.

Administration, Intravesical↗
PubMed1992

Congenital osteogenesis imperfecta associated with arteriopathia calcificans infantum.

A 25-year-old mother during pregnancy was treated by accident with clomifen (Clostilbegyt). Ultrasound scan, performed in the 32nd gestational week, showed polyhydramnion and abnormally short, deformed fetal limbs. The newborn male infant died 20 minutes after caesarean section. Autopsy revealed osteogenesis imperfecta accompanied by a rare vascular alteration i.e. arteriopathia calcificans infantum. The possible relationship between the two diseases and estrogen therapy is discussed.

Arteries↗
PubMed1991

Localization of receptors for luteinizing hormone-releasing hormone in pancreatic and mammary cancer cells.

Previous work showed that hamster and human pancreatic tumors but not normal pancreata exhibit low-affinity cell-membrane receptors for luteinizing hormone-releasing hormone (LHRH). Although the regression of experimental pancreatic cancers induced by treatment with LHRH agonists or antagonists could be explained in part by the creation of sex-steroid deficiency, direct effects mediated by LHRH receptors might also play a role. Here, we demonstrate that pancreatic tumor cells do exhibit high-affinity binding sites for LHRH, but only in their nuclei; low-affinity sites are associated with the cell membranes. These binding sites appear to be LHRH receptors since electron microscopic immunohistochemical studies show that an antibody to the LHRH receptor reacted with sites in the nucleus of pancreatic tumor cells. Immunoreactive sites in the nucleus also were found in a restricted set of normal hamster pituitary cells thought to be luteinizing hormone-secreting cells and in MXT mouse mammary tumor cells. Such nuclear receptors may be involved in the transmission of the direct action of LHRH analogues on the tumor cells, resulting in the enhancement of programmed cell death.

Animals↗
PubMed1991

Histological changes in Dunning prostate tumors and testes of rats treated with LH-RH antagonist SB-75.

Rats bearing Dunning R-3327 hormone-dependent prostate tumors were treated with LH-RH antagonist SB-75 in the form of microcapsules for sustained delivery administered every 3 weeks and which released 24, 48, 72 micrograms/day respectively. The effects were compared with those of microcapsules of the agonist D-Trp-6-LH-RH releasing 25 micrograms/day. Both types of LH-RH analogs significantly inhibited tumor growth over a period of treatment lasting 8 weeks. The effect of SB-75 was dose-dependent. The total inhibition of spermatogenesis, as well as atrophic signs in the prostate and seminal vesicles, demonstrated a marked suppression of the pituitary-gonadal system by these analogs. The histological signs of tumor regression were analyzed. The vascular content of tumors did not change after the treatments, but an increased amount of connective tissue was found in the treated tumors, especially after administration of SB-75. Both the agonist and the antagonist caused a moderate decrease of the number of mitotic cells and a marked increase of apoptosis in the tumors. The apoptotic index, i.e. the percentage of tumorous glands showing signs of apoptosis, reached 40-50% in treated groups, compared to only 15% in controls. An apoptotic index of 60% was noted in a separate group of rats treated with 200 micrograms SB-75/animal/day for 3 days. The signs of enhanced apoptosis disappeared 1 week after the short-term treatment. The induction of apoptosis by LH-RH analogs seemed to be of greater importance in tumor growth inhibition than their antimitotic effect. These results extend our previous observations on the efficacy of LH-RH antagonists in inhibition of various cancers. This histopathologic evaluation clearly supports our contention that modern antagonists of LH-RH, free of edematogenic effects, inhibit the growth of Dunning prostate tumors. Because of the immediate inhibitory effects, the use of LH-RH antagonists might lead to an improvement in the clinical response in patients with prostate cancer.

Animals↗
PubMed1991

Morphological studies on the effect of L-leucine methyl ester on mouse peritoneal macrophages in vitro.

Mouse peritoneal macrophages (MO) were treated in culture with 5 mM L-leucine methyl ester (L-Leu-OMe), for 5, 10, 20, 40, and 60 min. The treatment resulted in rapid vacuolisation of the cytoplasm due to the dilatation and disruption of lysosomes. Autophagy caused by lysosomal enzymes destroyed most of the cytoplasmic organelles by 40 minutes after L-Leu-OMe treatment, but the cell membrane and nucleus were in many MOs resistant to the damage. 60 min after L-Leu-OMe treatment most of the MOs were killed. It is supposed that the disruption of the lysosomes is caused by formaldehyde produced by the hydrolysis of L-Leu-OMe.

Animals↗
PubMed1991

The effect of D-penicillamine on CCl4-induced experimental liver cirrhosis.

The effect of D-penicillamine (Pe) on liver fibrosis-cirrhosis induced by chronic CCl4 and phenobarbital (Pb) administration in Fischer 344 male rats was studied. Morphometric analysis did not reveal a decrease in the amount of connective tissue fibers after Pe-treatment. Compared to the CCl4 and Pb-treated control groups, Pe had no significant effect on the concentrations of hydroxyproline, a parameter of collagen degradation, either; however, it increased the glycosaminoglycan concentrations. Lymphocyte stimulation by Con-A in the Pe-treated groups did not differ from that of the CCl4 and Pb-treated ones. According to our studies, Pe-treatment was ineffective in rats with liver fibrosis-cirrhosis induced by CCl4 and Pb administration. It seems that Pe can be effective only in the cirrhosis types accompanied by a considerable copper accumulation due to suppression of the toxic effects of copper.

Animals↗
PubMed1991

Liver damaging effect of suramin in normal and carbon-tetrachloride treated rats.

Male Fischer 344 (F344) rats were treated with phenobarbital + carbon tetrachloride (CCl4) for 16 weeks to induce liver cirrhosis. Another group of rats received 50 mg/kg iv suramin once a week for 16 weeks. The third group of rats was treated with both phenobarbital + CCl4 and suramin. After 16 weeks of suramin treatment, a massive periportal infiltration composed of macrophages, many of them containing glycosaminoglycans in their cytoplasm, mast cells, and other inflammatory cells were observed. This lesion was added to the liver cirrhosis caused by CCl4 in the group treated with suramin and CCl4. The changes in glycosaminoglycan metabolism caused by suramin did not influence the CCl4 cirrhosis. Since suramin has been reported to be a prototype of a new generation of antitumor compounds, we suggest caution in the use of chronic suramin treatment, especially in patients with livers which are already damaged.

Animals↗
PubMed1991

Immunocytochemical demonstration of tissue transglutaminase indicative of programmed cell death (apoptosis) in hormone sensitive mammary tumours.

Tissue transglutaminase (TG) positive tumour cells in MXT mouse mammary cancer were localized by immunohistochemistry. The number of TG-positive tumour cells increased after treatment with analogs of luteinizing hormone-releasing hormone (LH-RH) and somatostatin, which inhibit tumour growth by the enhancement of apoptosis (programmed cell death). TG positivity has been previously reported to be closely linked with apoptosis. In this study, the increase in the number of TG positive tumour cells after hormonal treatment was well correlated with the augmented apoptotic index, i.e. the ratio of tumourous glandular structures which contained tumour cells showing the signs of programmed cell death. TG-positive tumour cells are, therefore, believed to be undergoing programmed cell death.

Amino Acid Sequence↗