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Biomedical subjects

M Walser

Publications and source records attributed to M Walser.

At least 163 records · Page 9Linked to original sources
PubMed1969

Reversible stimulation of sodium transport in the toad bladder by stretch.

Short-circuit current and transepithelial potential difference were measured in toad hemibladders mounted as sacs on glass cannulae. When sac volume was changed by adding or removing fluid, short circuit current responded by increasing or decreasing during the ensuing half-hour. The time course of the response and its magnitude indicated that it was not artefactual. Furthermore, net sodium flux responded similarly. Sac volume, and thus bladder surface area, could be varied from 0.03 to 0.4 cm(2)/mg wet weight. The mean response to either decreases or increases was 10 muA/cm(2). Everted hemibladders, however, responded less. Neither hydrostatic pressure, nor increased chloride conductance, nor increased access of oxygen or glucose to the mucosa was responsible for the response. Tissue conductance did vary markedly with volume, and may have played a role, but sodium conductance did not vary with volume in a consistent manner. The results indicate the existence of an intrinsic mechanism in this tissue which alters sodium transport in response to stretch.

Animals↗
PubMed1968

ATP splitting and calcium binding by brain microsomes measured with a rapid perfusion method.

Rat brain microsomes, immobilized on a filter, were perfused with ATP-containing solutions in a device which made possible rapid change of perfusion media and frequent sampling of effluent. Inorganic phosphate production could be measured 10 times per sec. When ATP, sodium, or potassium was absent from the first perfusion medium and present in a second, and introduced without interrupting flow, phosphate output rose within a few tenths of a second. Inhibition by ouabain began within 0.3 sec but did not become maximal for at least 10 sec. Rapid binding of ouabain was minimal or absent, as was rapid release of ouabain on introducing potassium abruptly. Although the preparation bound some calcium reversibly, no measurable uptake of calcium occurred coincident with activation by ATP or by potassium, and no measurable release of calcium occurred coincident with the onset of ouabain inhibition. However, activation by sodium was consistently associated with simultaneous release (within < 1 sec) of calcium, averaging 46 pmole per mg of protein. Calcium release in response to sodium also occurred in the absence of ATP or in the presence of ouabain. At 0 degrees C sodium produced neither activation nor calcium release. The results are consistent with the possibility that sodium and calcium are competitively bound, even in the absence of ATP, to an active site on the enzyme distinct from the sites of potassium activation or glycoside inhibition.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of experimental liver disease on the utilization for protein synthesis of orally administered alpha-ketoisocaproate.

The incorporation of orally administered 1-14C-alpha-ketoisocaproate into the leucine of proteins in rats was compared with the incorporation of [3H]leucine itself administered simultaneously and expressed as a ratio, R. This ratio in whole body protein has been shown to be approximately equal to the nutritional efficiency of alpha-ketoisocaproate as a dietary substitute for leucine. In normal rats on a 14% protein diet, R in whole body protein (0.30 +/- 0.01) and in the protein of various organs was the same whether the isotopes were given by single injection or 6-hr constant infusion. Thus, both techniques yield the same time-independent parameter, R, which measures the relative efficiency of alpha-ketoisocaproate as a substitute for leucine. R varied between organs as follows: liver (0.22 +/- 0.01) less than kidney less than heart less than salivary gland less than brain less than muscle (0.42 +/- 0.01). In rats with galactosamine-induced acute liver failure (Group I), carbon tetrachloride-induced cirrhosis (Group II), or portal-systemic shunts (Group III), whole body protein R and R in the protein of organs other than the liver was generally increased compared with controls, as was R in circulating IgG in Group III; R in liver protein was unchanged (Groups II and III) or slightly lower than controls (Group I). Thus, severe liver disease and portal-systemic shunting both increase the utilization of alpha-ketoisocaproate for synthesis of protein in the body as a whole and in most organs. In the liver, however, alpha-ketoisocaproate utilization for protein synthesis is unaffected or slightly reduced.

Animals↗
PubMedDate not supplied

Creatinine excretion as a measure of protein nutrition in adults of varying age.

The use of the creatinine height index (CHI) as a measure of protein nutrition is reviewed. Any such cross-sectional measurement is inherently limited. Using published values for urinary creatinine excretion per kilogram body weight in adult subjects of varying age and values for "ideal" weight as a function of height, we have derived normal values for expected creatinine excretion in men and women of varying height. These permit the derivation of an age-corrected CHI. Possible explanations for the normal decrease in creatinine excretion with age include (1) decreasing lean body mass with age, (2) decreasing proportion of muscle in lean body, and (3) lower meat intake in older persons. Diet has an important influence if meat intake is substantial or if consumption of a creatine-free diet is prolonged. Creatinine metabolism and extrarenal excretion are minor, except in subjects with reduced renal function. Application of a correction for constant extrarenal clearance of creatinine in patients with chronic renal failure probably is not valid. Further observations of creatinine excretion in normal subjects of varying age and height are needed.

Adolescent↗
PubMedDate not supplied

Evidence for an anabolic action of essential amino acid analogues in uremia and starvation.

Nitrogen-free analogues of essential amino acids, when administered with those essential amino acids for which analogues are ineffective or unavailable, exert three actions that may be beneficial in protein-deficient or protein-intolerant subjects. First, they bring about an increase in the concentrations of essential amino acids in the blood at the expense of the concentrations of certain non-essential amino acids, notably alanine and glutamine. This effect is most readily demonstrated in children with congenital defects of the urea cycle enzymes, but can also be seen during daily therapy of adults with portal-systemic encephalopathy. Second, these compounds promote nitrogen balance through their suppressive effect on urea synthesis (an effect not attributable to re-utilization of ammonia derived from urease action in the gut). This action is demonstrable in obese subjects who are already conserving nitrogen maximally at the end of a prolonged fast and can also be shown in the first week of fasting when the branched-chain keto acids alone are administered. In both situations, improved nitrogen conservation persists long after the analogues are metabolized, suggesting enzyme adaptations. In chronic uremics, nitrogen balance can be maintained in some (but not all) patients on very low nitrogen intakes. Third, these mixtures may delay or reverse the progressive decline in glomerular filtration rate characteristic of chronic renal failure in some cases: thus, for example, 5 of 6 patients taken off chronic dialysis have maintained lower serum urea concentrations without evidence of protein malnutrition for periods of 2-24 months.

Amino Acids↗