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Biomedical subjects

J Hrnciar

Publications and source records attributed to J Hrnciar.

At least 55 records · Page 3Linked to original sources

[Neuroglycopenic syndromes in malignant tumors].

Based on observations of five of own patients the author analyzes the causes of spontaneous hypoglycaemia in malignant tumours and assumes three mechanisms of development: 1. Metastatic affection of the liver reduces the reserves of homeostatically usable glycogen and can reduce also the amount of utilized insulin and glucagon, and this weakens the effectivity of contraregulating hormones. 2. In case of large mesenchymal tumours it is assumed that the cause of hypoglycaemia is the neoplastic formation of IGF II. For these hypoglycaemic states a low concentration of C-peptide, IRI (immunoreactive insulin), absence of response of growth hormone to hypoglycaemia, high IGF II in the tumour and plasma and high mRNA for IGF II in the tumour is typical. 3. In hypoglycaemic states with massive metastases in the liver, high IRI and C-peptide it is assumed the cause of hypoglycaemia is a metastatizing insular tumour or a nes.dioblastoma. In those instances concurrent peptic ulcers (gastrin production) are frequent.

Adult↗

[Is our cardiovascular program effective?].

The author analyzes the causes why the cardiovascular programme of the Ministry of Health of the SSR and the regional programme of the control of arterial hypertension were not as effective as similar programmes abroad. In his opinion the reason is the low and late detection rate of cardiovascular diseases, shortcomings of dispensary care, pharmacotherapy and differential diagnosis, and the low interest taken by society. Acute cardiovascular and cerebrovascular attacks increased in 1960-1980 annually by 8% and 6% resp. This rise was arrested in 1980-1982 which could be the first signs of the effect of the cardiovascular programme in selected model districts and of the control of arterial hypertension in all districts of the Central Slovakian region.

Adult↗

[Paraneoblastic endocrinne syndromes--mechanisms of paraneoblastic hormone production].

The author deals with mechanisms of paraneoblastic hormone production. Paraneoblastic production of protein hormones is closely linked with processes of malignant transformation of cells which takes place as a result of dysregulation of hyperactive c-oncogens. Products of these oncogens either directly code growth factors or form their receptors or the receptors of dijerent hormones. The product of the family of c-ras-oncogens creates by excessive formation of G-proteins an excessively long activation of adenyl cyclase by hormones which act via cAMP. Under the influence of c-oncogens proliferating and differentiating stem cells reach in larger amounts the APUD stage of differentiation, where they express their genes for the formation of the entire range of protein hormones. Their ectopic formation may acquire biological or clinical significance, as relatively many cells remain in the APUD stage of differentiation, if the process of postscriptional adjustment of the formed hormones is not impaired.

Cell Transformation, Neoplastic↗