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F Bronner

Publications and source records attributed to F Bronner.

At least 37 records · Page 2Linked to original sources
PubMed1987

[A statistical model for interpreting the antibiogram].

Up to now, to interpret antibiotic susceptibility tests, the common practice has been to use: first, breakpoints without any quantitative justification, secondly, concordance curves between the different measurement techniques; these are not well adapted to the heterogeneous character of bacterial populations. We hereby propose another method: it is based on a global data analysis for each bacterial species, each antibiotic family and each measurement technique. So, we have drawn up a new model for the interpretation, both global and data-processed; it is based on qualifying classes, which are obtained and interpreted by hierarchical ascendent classification, principal components analysis, and comparison with pharmacological data. It can be used by any biologist. What is more, justified breakpoints with a numerical risk and quality control are defined. There are also some additional uses: evaluation of the effect of new antibiotics, standardization of new measurement techniques, detection of the emergence of new bacterial resistance in patients, guidance for research into unknown resistance mechanisms and characters.

Computers↗
PubMed1986

An analysis of intestinal calcium transport across the rat intestine.

Kinetic analysis of transmural calcium transport, as evaluated by in situ intestinal loops, has confirmed the existence of two transport processes, a saturable, transcellular one that is regulated by vitamin D and predominates in the proximal intestine and a nonsaturable process similar in intensity throughout the intestine. Transport data obtained from everted sac experiments are kinetically consistent with events in the in situ loop. Analysis of the three component steps making up the saturable process, i.e., entry across the brush-border membrane, intracellular diffusion, and extrusion across the basolateral membrane, indicates that intracellular diffusion is likely to be the limiting step. Active calcium transport varies directly and proportionately with the content of calcium-binding protein (CaBP), a specific molecular expression of the action of vitamin D. Since CaBP is a cytosolic protein, it may act to facilitate calcium diffusion, a proposition advanced by Kretsinger, Mann, and Simmons and supported here quantitatively. We calculate that the rate of intracellular calcium diffusion in the absence of CaBP is only approximately 1/70 of what is found in the vitamin D-replete cell. Similar considerations have led to the proposal that calcium moved by the nonsaturable process travels largely via the paracellular route. The kinetic parameters derived here, i.e., Vm = 22 mumol X h-1 X g (wt wt-1, Km = 3.9 mM, and a nonsaturable rate of 0.16/h, can be used to predict calcium absorption data as determined in previously published balance experiments.

Aging↗
PubMed1986

Localization of vitamin D-dependent active Ca2+ transport in rat duodenum and relation to CaBP.

Vitamin D-replete (+D) and vitamin D-deficient (-D) rats received by intraperitoneal injection varying amounts of 1,25-dihydroxyvitamin D3, and 4 h (+D) or 9 h (-D) later everted duodenal sacs were prepared to evaluate active calcium transport, i.e., the amount of calcium found in the serosal fluid. At the same time, duodenal calcium-binding protein (CaBP) content was measured. Calcium transport was a close positive function of CaBP content. It was not detectable when CaBP content was zero and increased linearly without plateauing as CaBP content increased to 100 nmol calcium bound/g mucosa. Trifluoperazine (TFP) inhibited active calcium transport in a concentration-dependent manner. Experiments using vesicles prepared from brush-border or basolateral membranes indicated that TFP inhibited the calcium-extrusion process, with virtually no effect on calcium entry. It is concluded that vitamin D exerts its major regulation of active calcium transport in the rat duodenum via CaBP on transport steps beyond brush-border entry.

Animals↗
PubMed1985

Saturable and nonsaturable copper and calcium transport in mouse duodenum.

Duodenal copper and calcium absorption was evaluated in 30-day-old normal male Swiss mice by an in situ loop procedure. For both ions, the 90-min absorption values yielded a curve that was resolvable into a hyperbolic (saturable) and a linear (nonsaturable) function. The two ions differed, however, in total absorption and the relative importance of the two functions. For copper, the maximum saturable component of transepithelial movement (Jmax) was 127 +/- 2.4 (SE) pmol in 90 min, the apparent half-saturation constant of the saturable process (Kt) was 4.3 +/- 0.7 microM, and the slope of the nonsaturable function was 0.011 +/- 0.006. Thus, when luminal copper equaled plasma copper (approximately equal to 15 microM), only 8% was absorbed, nearly all of which was by the saturable component. For calcium, on the other hand, Jmax was 4.8 +/- 0.1 mumol, the Kt was 27 +/- 2 mM, and the slope was 0.10 +/- 0.01. At luminal calcium concentrations equal to the inorganic plasma calcium (1 mM), calcium absorption was 75%, but only 80% of that was moved by the saturable process. The findings suggest the existence of separate transport mechanisms for copper and calcium.

Animals↗
PubMed1979

Regulation of intestinal calcium-binding protein in rats: role of parathyroid hormone.

Intestinal calcium-binding protein (CaBP) levels of rats fed a high (1.5%) Ca diet were the same whether the animals were parathyroidectomized (PTX), sham-operated controls pair-fed with the PTX animals, or sham-operated controls fed ad libitum. Consequently, a given base level of CaBP seems to be parathyroid hormone independent and not closely related to feed intake. On the other hand, whereas the ad libitum fed controls more than doubled their intestinal CaBP in response to a 2-day low-calcium (0.02%) regimen, neither the parathyroidectomized animals nor the pair-fed sham-operated controls were able to do so. Since the latter two groups consumed less feed and therefore less vitamin D than the ad libitum fed animals, the inability to increase CaBP in response to a low-calcium diet may have been caused by a restricted vitamin D intake rather than by the absence of parathyroid hormone.

Animals↗
PubMed1979

Effect of lactose on duodenal calcium-binding protein and calcium absorption.

Rats were fed a purified diet containing 30% lactose and calcium absorption was measured in duodenal loops in situ following instillation of 1.25 or 10 mM CaCl2 solutions. Lactose feeding caused absorption to be depressed from 88 to 69% (1.25 mM Ca solution) and from 71 to 43% (10 mM Ca solution). The effect of lactose feeding was more pronounced in 5-month old rats than in 2-month old rats. In the lactose-fed rats, calcium-binding protein (CaBP), measured by a competitive binding assay following partial purification, was depressed on the average from 24 to 10 nmoles Ca bound per mg protein. The effect of the lactose ingestion can be likened to the effect expected from continued high calcium intake, i.e., a decrease in the efficiency of calcium absorption and a decrease in CaBP.

Aging↗
PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗