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Biomedical subjects

J Brod

Publications and source records attributed to J Brod.

At least 19 recordsLinked to original sources
PubMed1991

Acylceramides and lanosterol-lipid markers of terminal differentiation in cultured human keratinocytes: modulating effect of retinoic acid.

Epidermal differentiation is accompanied by profound changes in the synthesis of a variety of intracellular proteins and intercellular lipids. In conventional, submerged culture keratinocytes have been shown to lose the ability to synthesize the protein markers of differentiation. They re-express them, however, when they are cultured in medium supplemented with delipidized [retinoic acid (RA)-depleted] serum or in air-exposed cultures using de-epidermized dermis (DED) as a substrate. Recent studies have revealed that acylceramides (AC) and lanosterol (LAN), which are present only in trace amounts in cultures of keratinocytes grown under submerged conditions on DED in medium supplemented with normal serum, become expressed in significant amounts when the culture is lifted to the air-liquid interface. Inasmuch as culture conditions may markedly affect the extent of keratinocyte differentiation, the present study aimed to investigate the effect of normal (RA-containing) or delipidized (RA-depleted) serum and of RA administration on lipid composition (especially of the AC and LAN contents) in cells cultured under submerged and air-exposed conditions. To test a possible effect of dermal substrate (used in the air-exposed model), the lipid composition of keratinocytes grown under submerged conditions on a plastic and on a dermal substrate (de-epidermized dermis, DED) has also been compared. The results revealed that under all culture conditions, RA deprivation of fetal bovine serum resulted in a marked increase of total ceramide content. Even under submerged conditions, the presence of both AC and LAN could be detected. In air-exposed culture, the content of these lipids was markedly increased. Addition of RA at 1 microM concentration to cultures grown in RA-depleted medium induced marked changes in lipid composition under all culture conditions tested. In cells grown under submerged conditions (both on plastic and on DED) AC and LAN were no longer present in detectable amounts. Also in air-exposed culture, a marked decrease in the content of these lipids was observed. These results suggest that liposoluble serum components, like RA, control the synthesis of lipids that are present in later stages of epidermal differentiation.

Biomarkers↗
PubMed1985

Volume homeostasis, renal function and hypertension.

A generalised vasoconstriction, for almost a century believed to be the basis of all types of human hypertension, was disproved by recent haemodynamic studies. In our investigation of hypertension in chronic parenchymatous non-uraemic, non-anaemic renal disease, we have established that the earliest haemodynamic abnormality in subjects, of whom over 90% later develop high blood pressure, has actually started while their blood pressure is still normal. This consists of hypervolaemia and a high cardiac output (hyperkinesis) with tissue hyperperfusion. Hypervolaemia is due to a failure of these still normotensive patients to excrete isotonic saline as readily as subjects with completely normal kidneys.The chronic hypervolaemia in these subjects leads to a release of the natriuretic factor which depresses the Na(+)-K(+)-ATPase in the cell membranes and which is responsible for an increase in sodium (and calcium) content of the vascular smooth muscle cells, diminishing their compliance and thus raising the vascular resistance together with the thickening of the vascular wall of the originally hyperperfused vessels. With the disappearance of the vascular adjustment to the increased cardiac output, the blood pressure rises and the 'pressure diuresis' restores the circulating blood volume (and the renal homeostatic efficiency) to normal. With a further rise of the peripheral vascular resistance the cardiac output falls. At this late stage of renal hypertension renin may play a contributory role.Thus, the primary abnormality in the chain of events leading eventually to hypertension is a renal inability to maintain a proper balance between sodium intake and output. This suggested pathophysiological mechanism is probably valid in every kind of human hypertension where a reason for such a disturbance is present.

Blood Volume↗
PubMed1984

Investigations on the Na+, K+-pump in erythrocytes of patients with renal hypertension.

The ouabain-sensitive 42K+ flux from an artificial medium into erythrocytes was measured in 29 control subjects, 66 patients with chronic parenchymatous renal disease and in 32 subjects with primary hypertension. The ouabain-sensitive 42K+ influx was reduced in subjects with chronic renal disease by about 20%, even when they were normotensive. The reduction in these patients was greater than that in patients with essential hypertension. The changes in 42K+ influx and Na+ content with a decrease in the 42K+ influx/Na+ content ratio suggest an inhibition of the Na+ pump in the patients with chronic renal disease. The inhibition of the Na+ pump may be secondary to the hypervolaemia which we suggest is the initial event leading to renal hypertension.

Adult↗
PubMed1981

Glomerular basement membrane and mesangial matrix: a comparative study in different vertebrates.

Perfusion fixation of the rat kidneys with aldehydes and alcian blue demonstrates within the glomerular mesangium various components displaying anionic binding sites. These are the surface coat of the mesangial cells, numerous mesangial microfibrils (probably glycoproteins), and polygonal particles (Presumably proteoglycans). These particles lie close to the mesangial cells and form assemblies of various extension within the mesangial matrix as well. In addition, a discontinuous basement membrane can be recognized which surrounds the mesangial cells. In the hagfish glomeruli (fixed without cationic dye), a prominent layer of microfibrils is interposed between mesangial and endothelial cells. Both these cells show incomplete basement membranes.

Animals↗