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Biomedical subjects

P Weber

Publications and source records attributed to P Weber.

At least 325 records · Page 18Linked to original sources

[Computerized scanning analyses of FITC-labelled microscopic slides (author's transl)].

FITC-labelled virus antigen was analysed in infected cells by means of scanning-fluorometry. According to the predetermined classification the values were computerized and printed out by a mosaic printer or by a coordinate-recorder as a profile graph or a perspective image. The total impression of the 3 dimensional print-out of the quantificated topographic distribution of antigen accumulations within the cells can be optimated by variation of the angle of view.

Animals↗

Urinary cyclic AMP and renal concentrating capacity in infants.

In 15 infants between 1 and 31 weeks the effect of antidiuretic hormone (ADH) on the renal concentrating capacity and urinary cyclic AMP (cAMP) was tested. A significant decrease of urine flow and a significant increase of osmolality, urea and cAMP was observed indicating that the distal nephron of the infant kidney is responsive to exogenous ADH and that its effect is mediated by cAMP. The results of a second series with 52 normally hydrated infants demonstrate that the nonlinear age-related increase of osmolality and urea in urine is accompanied by a similar pattern of cAMP excretion, pointing out that the maturation of the concentrating capacity seems to be related to an increasing responsiveness of the cAMP system to ADH. Furthermore the results raise the possibility that increasing concentrations of urea and solutes in the medulla and papilla of the infant kidney may have--in the presence of very low ADH secretion--an additional stimulating effect on cAMP formation.

Age Factors↗

Electroimmunoassay of alpha-2-opsonic protein during reticuloendothelial blockade.

Physiological regulation of reticuloendothelial (RE) phagocytic activity by a plasma opsonic factor has been documented. In the recent study, serum levels of this alpha-2-opsonic protein in rats during colloid-induced RE blockade were measured utilizing an electroimmunoassay (Rocket immunoelectrophoresis) with monospecific antiserum to the purified alpha-2-glycoprotein. RE blockade was produced by the intravenous injection of the gelatinized "RE-test-lipid emulsion" at a dose of 50 mg/100 g body wt. The opsonic activity of serum at various intervals during colloid-induced RE blockade as measured by tissue slice bioassay manifested a high correlation (r = 0.98) with the serum opsonic protein concentration as measured by the electroimmunoassay. During RE blockade (30 min), there was a rapid depletion of the opsonic alpha-2-glycoprotein to 20% of the initial preinjection levels. Serum concentration of this glycoprotein remained low for at least 2-3 h after which time its concentration progressively increased with approximation of normal values by 6 h postblockade. Opsonic protein concentration at 24 h postinjection were significantly (P less than 0.05) elevated above controls. Thus, colloid-induced RE blockade is associated with the removal of this glycoprotein from the serum and recovery from RE blockade is accompanied by a restoration of opsonin levels. The electroimmunoassay can provide a sensitive technique to monitor this humoral factor known to exert a physiological control on the RE system.

Alpha-Globulins↗

The chemical nature of a pancreatic cardiodepressant factor.

The presence of a cardiodepressant factor of pancreatic origin has been reported in the plasma of experimental animals and man in a variety of shock states. It has been suggested that the depression of developed tension of the isolated cat papillary muscle may be caused by excess NaCl in the bathing medium rather than a specific cardiodepressant peptide. Incubated pancreatic homogenate was used as a source of this factor, and after protein precipitation, ultrafiltration (10,00 and 1,000 MW), dialysis and lyophilization, the residue was applied to a Sephadex G-10 column in order to ensure the removal of all salts. The protein effluent of the Sephadex column contained all the cardiodepressant activity of the filtered, dialyzed pancreatic homogenate and none of the salt content. To further isolate this cardiodepressant factor, the active residue was applied to a cellulose column and eluted with butanol: glacial acetic acid: water (25:26 v/v/v). This elution gave 8 distinct peptide peaks, one of which, peak 4, contained significant depressant activity. Thus, a cardiodepressant peptide of approximately 250-1,000 MW exists in pancreatic homogenates and this compound is not excess NaCl in the assay system.

Animals↗

The fluorescent demonstration of tissue aldehydes with dansylhydrazine.

Dansylhydrazine, previously introduced in a selective fluorescent cytochemical method for the demonstration of sialic acid residues of cellular glycoconjungates, may be broadly applied as a specific, covalently bonded fluorochrome of aldehyde residues, both those naturally occurring as in elastin or those generated through PAS or Feulgen-type procedures.

Aldehydes↗

Effects of ADH on the activity and function of the renin-angiotensin-aldosterone system in infants and in children.

In babies ranging in age from 1 to 25 weeks and in children between 1 and 14 years, plasma renin activity and urinary aldosterone activity were determined in relation to urinary sodium excretion. A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. A second stimulus was observed in the influence of the hypothalamo-neurohypophyseal system, when the plasma renin activity was suppressed by administration of antidiuretic hormone and sodium excretion increased due to a decreased aldosterone activity. Our study suggests that there exists a feedback between the renin-angiotensin-aldosterone system and ADH release and that this feedback plays an important role in the regulation of water and electrolyte balance in the young infant.

Adolescent↗

Stimulation and inhibition of renal PG biosynthesis: effects on renal blood flow and on plasma renin activity.

In the present investigation prostaglandins (PGs) were determined in the renal cortex and the functional effects of the renal PGs on renal hemodynamics and on the renin-angiotensin system were evaluated. The levels of PGs, determined by mass fragmentography, were in the medulla: PGE2 4.36 +/- 1.04 mug/g and PGF2 alpha 1.6 +/- 0.50 mug/g and in the cortex: PGE2 0.19 +/- 0.04 mug/g and PGF2 alpha 0.21 +/- 0.07 mug/g. The unequivocal demonstration of PGs in the renal cortex forms a biochemical basis for a role of PGs in the regulation of renal hemodynamics and of the renin-angiotensin system.

Angiotensin II↗

Interactions between the renal prostaglandins and the renin--angiotensin system.

Although the PGs operate mainly in the renal medulla the demonstration of PG biosynthesis in the renal cortex has provided a biochemical basis for a direct relationship between the PGs and the renin-angiotensin system. The formation of PGs is influenced by circulating levels of A I probably by indirect mechanisms. That the release of renin at least under certain experimental conditions is dependent on the PG system is suggested by the following findings: 1. C20:4 increases PRA in the rabbit and rat. 2. Indomethacin decreases PRA in the rabbit. 3. C20:4 stimulates renin release from slices of rabbit kidney cortex. 4. Reduced renal perfusion pressure and ischemia are accompanied by release of both PGs and renin. 5. The release of PG and renin following renal ischemia is blocked by treatment with indomethacin. The actions of the renin-angiotensin system and the renal PGs are, as far as we know them, antagonistic to each other. PGEs are vasodilator, increase renal blood flow, inhibit adrenergic neurotransmission, and cause excretion of electrolytes and water. Conversely, A II is vasoconstrictor, decreases renal blood flow, stimulates adrenergic neurotransmission, and conserves water and electrolytes. Thus, the interaction between the renal PGs and renin seems to be one in which the two hormonal systems stimulate each other's formation or release, but opposes each other's actions. Further studies are necessary to reconcile this apparent contradiction.

Angiotensin II↗