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Biomedical subjects

C Bader

Publications and source records attributed to C Bader.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Radiologic study of the ileum-neobladder after radical cystoprostatectomy].

The study reports on radiographic findings obtained from 70 male patients in whom, following radical cystoprostatectomy for carcinoma, an ileum neobladder was created. Morphological appearance and postoperative complications of this continent type of bladder replacement were documented by means of cystography, excretory urography, retrograde urethrography and CT. Specific complications rarely arose from suture insufficiencies of the neobladder itself (n = 3) or from the ileourethral anastomosis (n = 2). Stenoses occurred at the site of the ileourethral (n = 9) and the ureteroileal anastomosis (n = 2). Transient dilatation of the upper urinary tract was observed in the majority of patients. Non-specific complications included pelvic abscesses (n = 2), haematomas (n = 2), lymphoceles (n = 3), and ileus (n = 2).

Adult↗
PubMed1991

Investigation of urinary crystals by Fourier transform infrared microscopy.

Although crystalluria is generally considered a normal finding, sometimes it gives evidence of renal disturbance. Thus, detection and identification of urinary crystals may provide useful data for understanding the etiology of mechanism of the disorder. Light microscopy may be not sufficient to accurately identify the crystals. We investigated the ability of Fourier transform infrared microscopy (FTIRM) to identify isolated crystals of clinical interest. Twenty-five urine samples presenting crystalluria were tested because of their unusual aspect. We successfully identified 16 compounds and showed that crystals with the same apparent morphology can be composed of different substances. Moreover, an unexpected structure may be an insoluble phase of a drug metabolite. We conclude that FTIRM is a good technique for investigating urinary crystals of clinical interest.

Crystallization↗
PubMed1990

Sex steroid hormone modulation of NADPH pathways in MCF-7 cells.

Hormonal modulation of glucose-6-phosphate dehydrogenase (G6PD) and of utilization pathways of NADPH generated by G6PD was studied in the MCF-7 human breast cancer cell line, using a quantitative cytochemical method. Our results show that G6PD is increased by 17 beta-estradiol (estradiol) and synthetic progestin (promegestone R5020). The synthetic antiestrogen tamoxifen has no effect on G6PD activity. When it is present in the medium with estradiol, tamoxifen can oppose the stimulatory effect of estradiol on G6PD activity. Mifepristone (RU 38486) has no effect on G6PD activity, but it inhibits the R5020 stimulation of G6PD activity. After MCF-7 pretreatment with estradiol, there is a much stronger stimulation of G6PD activity by R5020. When we studied the effect of the steroid on the two utilization pathways of NADPH generated by G6PD activity, we observed that, in the cells treated with estradiol, there is an increase in reducing equivalents generated by G6PD activity which only affects the NADPH2 pathway, and that there is cell growth stimulation. When tamoxifen is present in the medium, we found no effect on the NADPH utilization pathways, nor on cell growth. In the presence of R5020, the NADPH2 pathway activity is increased but, under our experimental conditions, there was no effect on cell growth. On the other hand, even though RU 38486 is without effect on total G6PD activity, it does cause a modification in the distribution of reducing equivalents: the NADPH2 pathway activity is decreased, while the NADPH1 pathway is stimulated.

Breast Neoplasms↗
PubMed1988

Thyroglobulin secretion by cultured human thyroid cells from cold nodules.

An elevated serum thyroglobulin level has been demonstrated in patients with cold nodules, without determination of the exact cause. In this preliminary study, we examined thyroglobulin production in vitro by cells from cold nodules and compared it to that of normal cells taken from the contralateral lobe of the same patient. Cells were cultured in monolayer and in collagen gel. Differences were observed between normal and pathological cells depending upon the culture model. We have attempted to interpret these differences which could result from anomalies in the pathological cells at the level of the apical membrane.

Cells, Cultured↗
PubMed1986

Synergism between cytosolic and mitochondrial oxidation: its possible relevance to the metabolism of vitamin D3 in the kidney.

Using frozen liver sections and quantitative cytochemistry it has been established that when cells are allowed to oxidize a cytoplasmic and a mitochondrial substrate simultaneously the resulting oxidative activity is markedly higher than the sum of the oxidation of each substrate measured separately. In the present study this type of synergistic interaction has been confirmed in the kidney, particularly in cells of the pars recta. Our results support the evidence of the influence of cytoplasmic NADPH on the intramitochondrial oxidative process and it is suggested that, in cells of the pars recta, cytosolic NADPH may be involved in intramitochondrial mixed function oxidases such as 1 alpha-hydroxylase: these results could further elucidate the mechanism responsible for the production of the hormonal form of vitamin D3.

Anaerobiosis↗
PubMed1985

(Na-K)ATPase activity along the nephrons in normal and adrenalectomized rats measured by quantitative cytochemistry.

A cytochemical method was used to measure total, ouabain insensitive and specific (Na-K)ATPase activities along the rat nephron. Enzyme activity was expressed as per cent of mean integrated extinction with reference to a calibrated filter. The lowest mean values of total, ouabain-insensitive, and (Na-K)ATPase activities were found in the proximal convoluted tubule (PCT). In the distal convoluted tubule (DCT), total and ouabain-insensitive activities (77.8 per cent and 45.8 per cent, respectively) were significantly higher than in the medullary thick ascending limb (MAL) (66.0 per cent and 24.6 per cent, respectively). Mean values of (Na-K)ATPase activity were significantly lower in DCT than in MAL (32.0 per cent and 41.3 per cent, respectively). Using Lineweaver-Burk plots, the KM ATP value for total ATPase activity was found to be 2.33, 1.79, and 3.63 mM in DCT, MAL, and PCT respectively. Maximal velocity was lower in PCT than in MAL and DCT. For (Na-K)ATPase, the smallest KM value was found in MAL (0.95 mM) and was 2.73 and 5.71 mM in DCT and PCT respectively. Maximal velocity was the highest in MAL (49.3 per cent), lower in DCT (36.1 per cent) and least in PCT (22.5 per cent). ATPase was measured in the MAL and DCT from rats fed a normal (N-Na+) or a high (Hi-Na+) sodium diet, and from Hi-Na+ rats one week after adrenalectomy (ADX). In the MAL, (Na-K)ATPase tended to be higher in Hi-Na+ than in rats, but was significantly lower in ADX than in Hi-Na+.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1985

Effect of plasma levels of parathyroid hormone on NADPH pathways in kidney and liver.

NADPH available for mixed function oxidations (pathway 1) or biosynthetic processes (pathway 2) has been evaluated in different cells from rat liver and kidney. In addition, changes of the proportion of NADPH utilized in each pathway were demonstrated in the same cells from rats showing different circulating levels of parathyroid hormone (PTH). Quantitative levels of NADPH directed into each of these pathways have been measured and histologically located in sections from rat liver and kidney using quantitative cytochemistry and scanning and integrating microdensitometry. Centrilobular hepatocytes utilize the major amount of NADPH, either via pathway 1 or 2. Kidney cells utilize most NADPH via pathway 2, particularly in the distal part of the nephron. The cells of the pars recta have shown the highest capacity to utilize NADPH via pathway 1, which is about half that of centrilobular hepatocytes. In centrilobular cells, the presence of high plasma levels of PTH results in a significant increment of NADPH utilization either via pathway 1 or 2. In kidneys from rats showing high plasma levels of PTH, a selective increase in NADPH utilized via pathway 2 was observed in the distal convoluted tubule whereas a selective increase in NADPH utilized via pathway 1 was demonstrated in cells of the pars recta. These observations provide further information in the understanding of the physiology of kidney and liver cells.

Animals↗
PubMed1985

Renal magnesium and phosphate wastage in a patient with hypercalciuria and nephrocalcinosis: effect of oral phosphorus and magnesium supplements.

We report a 29-year-old man with a mild decrease in glomerular filtration, nephrocalcinosis, hypercalciuria and a renal magnesium leak. He had other features of 'congenital magnesium-losing kidney', such as arthritis and hyperuricemia, short stature and recurrent urinary tract infections, but had no radiological chondrocalcinosis. In addition, pallidal calcification was found. The patient also had a renal phosphate leak. Phosphorus supplements resulted in a decrease in urinary calcium excretion, indicating that hypercalciuria was at least partially a consequence of phosphorus depletion. Plasma and urine magnesium were not affected by phosphorus supplements. Addition of magnesium supplements resulted in a transient and modest decrease in urinary calcium excretion, with no modification in plasma magnesium.

Administration, Oral↗
PubMed1984

Systematic search for 1 alpha,25-dihydroxy-vitamin D3 receptors in human breast carcinomas.

We looked systematically for the presence of receptor like binding sites for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) in the cytosol from 22 breast cancers. Cytosols were centrifuged on 5-20% sucrose gradients after labeling with tritiated 1,25 (OH)2D3 (3H-1,25(OH)2D3 or 25-hydroxyvitamin D3 (25(OH)D3 alone or in the presence of a large excess of these unlabeled sterols. Binding sites for 1,25 (OH)2D3 migrating in the 3.5-3.7 S region were found in 7 out of 22 cancers, while 5.5-6.5 binding sites for 25 (OH)D3 were found in all cytosols. In a patient in whom cytosol containing a 3.5-3.7 S binding site was in sufficient amount, quantification of 1,25 (OH)2D3 binding indicated a KD of 0.28 nM and a maximal binding capacity of 0.15 pmol/mg prot. No relation was found between the presence or the absence of 1,25 (OH)2D3 binding sites and the histological type, the extension of the cancer, the presence of radiological or histological calcifications, the amount of estrogen or progesterone receptors, the plasma calcium or phosphate concentration and the emergence of metastases after 1 year. The significance of the presence of receptor-like binding sites for 1,25-(OH)2D3 in one third of breast cancers remains therefore unknown at the present time.

Breast Neoplasms↗
PubMed1983

Cellular utilization of cytosolic NADPH in kidney and liver cells from rats fed a normal or a vitamin D-deficient diet.

The amount of reducing equivalents from NADPH generated by glucose 6-phosphate dehydrogenase activity (G6PD) used in mixed function oxidation (pathway I) or in reductive biosynthesis (pathway II) has been determined by cytochemical methods and microdensitometry in cells from the pars recta (PR) and distal convoluted tubule (DCT) of the kidney and from centrilobular (CL) and periportal (PP) hepatocytes from rats fed a normal or a vitamin D-deficient diet. In the kidney, pathway I activity was similar to that of pathway II in PR, whereas in DCT pathway II was markedly predominant. Feeding a vitamin D-deficient diet resulted in an increase in the total amount of reducing equivalents in PR and DCT. This increase was due to a rise in pathway I activity in the PR, whereas in the DCT the increase resulted from a stimulation of pathway II activity. Pathway I activity in PR was inversely correlated with plasma calcium, and was significantly decreased when calcium (1 mM) was added in vitro. In the liver the total amount of reducing equivalents generated by G6PD and both hydrogen pathways, was higher in CL than in PP hepatocytes. In CL cells, a vitamin D-deficient diet induced a significant increase in both NADPH pathways. Furthermore, in these cells pathway I activity was inversely related to plasma calcium and was significantly lowered when 1 mM calcium was added in vitro. It is concluded that vitamin D status and calcium influence the production and utilization of cytosolic reducing equivalents both in kidney and liver.

Animals↗
PubMed1982

Effects of weight and glucose ingestion on urinary calcium and phosphate excretion: implications for calcium urolithiasis.

Renal handling of phosphate and calcium was studied in 17 hypercalciuric stone-formers, 6 normocalciuric stone-formers and 10 normal subjects before (fasting state) and 45 and 75 min after the ingestion of 100 g glucose. The ratio of fasting urinary calcium to creatinine (UCa/creat) was higher in hypercalciuric than in normocalciuric stone-formers or controls. A positive correlation was found between weight index and fasting UCa/creat for all subjects studied (r = 0.36; P less than 0.05). A negative correlation was apparent between the weight index and the fasting renal threshold phosphate concentration (TmP/GFR) (r = 0.40; P less than 0.02), the latter parameter being slightly but insignificantly lower in hypercalciuric stone-formers than in controls. After glucose ingestion. UCa/creat rose significantly in all groups. The maximal rise in UCa/creat was also positively correlated with the weight index for all patients ( r = 0.42; P less than 0.02), and 75 min after glucose ingestion, TmP/GFR decreased in all groups, dropping to a significantly lower level in the hypercalciuric patients than in the controls. No correlation was apparent between the weight index and the magnitude of the reduction in TmP/GFR. Plasma 1, 25-dihydroxyvitamin D3 and immunoreactive parathyroid hormone were measured before glucose ingestion and were not correlated either with each other or with plasma phosphorus, TmP/GFR, or UCa/creat before or after glucose ingestion. These results imply that weight is a determining factor in the renal handling of calcium and phosphorus. Such findings might be of importance to the clinical investigation and management of calcium stone-formers.

Adult↗
PubMed1981

[Vitamin D metabolites in a new case of drug-induced hypercalcemia (author's transl)].

The authors report on a new case of severe hypercalcaemia induced by prolonged oral treatment with high doses of vitamin D2. (6 mg/day for 9 months). Blood calcium level did not return to normal until 6 months after the drug was discontinued. The plasma concentration of 25 (OH) D was more than three times the normal value and remained very high throughout the observation period. The plasma concentration of 24, 25 (OH)2 D was slightly raised during treatment but became normal after 15 days, while that of 1,25 (OH)2 D, the active form of vitamin D, remained normal throughout, suggesting that the pathogenesis of vitamin D-induced hypercalcaemia is probably complex.

25-Hydroxyvitamin D 2↗