Use of the gracilis muscles for sphincteric construction after abdominoperineal resection. Technique and preliminary results.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
A Mariotti
Publications and source records attributed to A Mariotti.
Protein-metabolism kinetics and energy-substrate utilization in infants fed parenteral solutions with different glucose-fat ratios.
The relative effect of glucose and lipids on whole-body protein-metabolism kinetics was assessed in seven infants undergoing parenteral feeding. Protein intake was kept constant and nonprotein energy was either provided as glucose alone or as an isoenergetic glucose-lipid mixture according to a randomized crossover trial. Protein metabolism and energy-substrate utilization were assessed by a primed, constant L-[13C]leucine infusion, combined with indirect calorimetry. There was a significant difference in the pattern of energy-substrate utilization according to regime. Protein turnover (11.3 +/- 0.7 vs 9.8 +/- 0.4 g.kg-1.d-1; P less than 0.05), protein breakdown (8.4 +/- 0.6 vs 7.1 +/- 0.4 g.kg-1.d-1; P less than 0.05), and amino acid oxidation rates (2.7 +/- 0.4 vs 1.4 +/- 0.5 g.kg-1.d-1; P less than 0.05) were higher for the glucose than the glucose-lipid treatment, whereas protein-synthesis rates did not significantly differ. These results suggest that the nature of energy substrates delivered to parenterally fed infants may affect protein metabolism.
Calorimetry, Indirect↗
Desquamative gingivitis: revisited.
Desquamative gingivitis is a clinical condition which can encompass a variety of histopathologies. It has not yet been established whether desquamative gingivitis is a distinct hormone-mediated disease entity or a variety of dermatologic diseases (i.e. pemphigus vulgaris, benign mucous membrane pemphigoid, etc.). In this manuscript the epidemiologic, clinical, histopathologic, immunologic and etiologic aspects as well as possible therapeutic modalities for the management of hormone-mediated desquamative gingivitis are examined.
Estrogens↗
Estimation of Carbon and Nitrogen Allocation during Stalk Elongation by C and N Tracing in Zea mays L.
Zea mays L. (cv Dea) plants grown to the stage of stalk elongation, were allowed to assimilate (13)CO(2) and (15)N-nitrates from 45 to 53 days after sowing. Isotopic abundances in labeled nutrients were slightly enriched compared to natural abundances. The new C in plant was acropetally distributed and the new N was preferentially accumulated in the sheath and stalk in the medium region. C input was 25-fold higher than N input. The new C in total plant C was 20%, whereas it was 10% for N. The stalk acted as a major sink because it accumulated, respectively, 27.5 and 47.5% of the C and N inputs. The new C in soluble carbohydrates was 76% in growing organs (upper stalk) and only 39% in source leaves, whereas it was 43% and 13% in starch, respectively. New N in nitrates+amino-acids spanned in the range from 20% (leaf) to 50% (stalk). New C and N in soluble proteins were, respectively, 13.4 and 3.8% in leaves, 8.8 and 9.6% in stalk, and 8.7 and 14.3% in roots. In the middle stalk and leaves, the proteins and carbohydrates represent an equivalent C and N source for remobilization.
Journal Article↗
C and N Mobilization from Stalk and Leaves during Kernel Filling by C and N Tracing in Zea mays L.
The sink capacity of the stalk in Zea mays L. (cv DEA) during the elongation period was previously investigated with (13)C and (15)N tracing. The chase experiment described here demonstrates the different behavior of intermediary reserves for C and N remobilization until full maturity of the kernels. Carbon incorporated during stalk elongation participated mainly in cellulose formation in vegetative organs appearing after the labeling period; the remobilization to kernels was low (0.5%). Soluble carbohydrates and proteins were the main intermediary sink compounds, starch being little remobilized. N first incorporated in roots, sheaths, stalk, blades was translocated to the kernel; 42% of the labeled N were recovered in kernels where they represented 8% of the total N. Cob, husk, and shank acted first as N sinks and then as N sources during ear development. It appeared that aminoacids used for synthesis of kernel proteins have a common origin, except for glutelin G(3).
Journal Article↗
Characterization of fibroblasts derived from human periodontal ligament and gingiva.
Growth characteristics and macromolecular synthesis of fibroblasts derived from human periodontal ligament (PDLF) and gingiva (GF) have been compared in cell culture. Cells were isolated from explants and plated at 500,000 cells/100 mm culture dish (day 0) with daily changes of culture medium. DNA histograms were obtained by flow microfluorimetric analysis to confirm the growth state of the cell cultures. Human PDLF cultures became confluent at day 6 as determined by cell number and cell cycle analysis while GF were confluent by day 4. Initially, DNA content of logarithmically growing cells was significantly greater in GF cultures; however, when confluent, DNA content and cell number was greater in PDLF cultures. Total protein content in GF was slightly greater than PDLF until day 7 but this difference was not significant. Analysis of collagen and noncollagen protein synthesis revealed a greater trend in noncollagen protein synthesis in the GF cultures compared to PDLF cultures. Analysis of glycosaminoglycans in the culture medium of GF and PDLF revealed similar distributions of components. In the cellular fraction, GF had greater amounts of hyaluronic acid and heparin and lesser amounts of chondroitin sulfates A and C than PDLF cultures. The results indicate that the growth characteristics of PDLF and GF, although similar in many respects, do exhibit specific differences in proliferative rates and macromolecular synthesis. The differences observed in these parameters may be important during in vivo events, such as guided tissue regeneration, where significant functional differences are observed between gingival connective tissue and periodontal ligament connective tissue.
Adult↗
Recovery of [13C]-bicarbonate as respiratory 13CO2 in parenterally fed infants.
Ten infants on continuous total parenteral nutrition (TPN) were infused with NaH13CO3 for 6 h in order to assess the amount of 13C recovered as breath 13CO2. Protein intake was 2.8 +/- 0.3 g/kg/d and non-protein energy intake 107 +/- 4 kcal/kg/d (447 +/- 18 kJ/kg/d), provided either as glucose alone or as an isoenergetic glucose-lipid mixture. In the five infants receiving glucose as the sole non-protein energy source, total CO2 production (559 +/- 50 mumol/kg/min), natural 13C abundance of breath CO2 (-11.8 +/- 0.6 delta % versus PDB) and basal 13CO2 production (6.1 +/- 0.6 mumol/kg/min) were higher than in the five infants infused the glucose-lipid mixture (465 +/- 30 mumol/kg/min, P less than 0.02; -16.1 +/- 0.5 delta %, P less than 0.01 and 5.0 +/- 0.3 mumol/kg min, P less than 0.02, respectively). There was a good agreement, in the glucose-infused infants, between the net glucose oxidation rate measured by indirect calorimetry (25.6 +/- 2 g/kg/d) and the glucose oxidation rate estimated from the 13C natural abundances of breath CO2 and infused substrates (23.5 +/- 3 g/kg/d). Steady state 13C enrichment of breath CO2 was reached in all infants after 120 min infusion and ranged from 11.0 to 21.5 delta % over baseline. Steady state 13C enrichment was negatively related to total CO2 production (r = -0.72; P less than 0.02). In contrast, steady state 13CO2 production in excess of baseline was only correlated to bicarbonate infusion rate (r = 0.95; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Bicarbonates↗
Antagonism of androgen and estrogen effects in guinea pig seminal vesicle epithelium and fibromuscular stroma by keoxifene (LY156758).
Using separated epithelium (SVE) and fibromuscular stroma (SVM) of guinea pig seminal vesicle, the antihormonal effects of daily subcutaneous administration (14 and 28 days) of the benzothiophene keoxifene (LY156758; [6-hydroxy-2-(4-hydroxyphenyl)benzo(b) thien-3-yl] [4-(2-1-piperidinyl) ethoxyl] phenyl) methanone hydrochloride) in intact, castrate, and androgen/estrogen-maintained castrate animals was evaluated. The compound was devoid of agonist activity in castrated males, in that the compound had no stimulatory effect on SVM wet weight or DNA content. In vitro cytosolic binding of [3H]estradiol (E2) in the SVM was decreased in a concentration-dependent manner by keoxifene, but the compound did not perturb the binding of [3H]dihydrotestosterone (DHT) in the SVM or SVE. Likewise, keoxifene administration to castrated males treated with exogenous steroids antagonized the estrogen-induced hyperplastic response of the SVM, whereas no interference with androgen-induced growth of the SVM or SVE was observed. Keoxifene treatment of intact male guinea pigs produced regression of the androgen-sensitive SVE as well as the androgen/estrogen-sensitive SVM. Keoxifene-induced decreases in guinea pig serum testosterone levels were associated with this activity. Histological analysis of the seminal vesicle under these conditions suggests androgen deprivation. These findings indicate that keoxifene is a physiological antagonist of androgen action in the intact male guinea pig. The pure estrogen antagonist properties of keoxifene and its ability to decrease accessory sex organ epithelium and fibromuscular stroma in vivo suggest potential applications of the benzothiophenes in the medical management of prostatic neoplasia.
Androgen Antagonists↗
Actions and interactions of estradiol and retinoic acid in mouse anterior prostate gland.
Experiments were designed to define the ability of retinoic acid to block the estrogen-induced metaplasia in the mouse anterior prostate gland (coagulating gland), and to elucidate some of the biochemical correlates of the actions and interactions of these two compounds. In castrated mice, the estrogen-induced metaplasia of epithelial cells consisted of multi-layered, nonpolarized cells, which accumulated to fill the lumen of the acini. Retinoic acid had no discernable effect on epithelial morphology of castrates, but significantly reduced the estrogen-induced metaplasia. Likewise, the estrogen-induced increases in the prostatic wet weight, ratio of ribonucleic to deoxy ribonucleic acids (RNA/DNA) and glycosyltransferases, as well as the decreases in 21,000 and 28,000 Mr soluble proteins were prevented by retinoic acid; the retinoid had no effect on these various parameters when administered alone to castrates. In contrast, the cyclic 3',5'-adenosine monophosphate (cAMP)-dependent phosphorylations at 16,000, 18,000, and 25,000 Mr and the activities of the type II cAMP-dependent kinase were uniformly reduced by both estradiol and retinoic acid. Tests of the action of the anti-estrogen LY-156758 on estrogen and retinoid effects showed that for those parameters on which retinoic acid was anti-estrogenic, LY-156758 was also anti-estrogenic. However, the qualitatively similar effects of retinoic acid and estradiol, which were confined to selected aspects of protein phosphorylation, were not antagonized by LY-156758. It is concluded that in the mouse anterior prostate, retinoic acid has both anti-estrogenic and estrogenic actions, and the latter may occur independently of the estrogen receptor.
Animals↗
Androgen and estrogen effect on guinea pig seminal vesicle muscle: a combined stereological and biochemical study.
A combined electron microscopic stereological and biochemical study of the smooth muscle cells of guinea pig seminal vesicles was performed in intact, castrated, castrated and dihydrotestosterone- or estradiol-treated adult animals. Castration led to cell atrophy as determined stereologically by a decreased single cell volume and biochemically by no change in DNA content coupled with an increase in the DNA concentration. Treatment of castrates with dihydrotestosterone restored both the stereological and biochemical parameters of the cell size to slightly supranormal levels. The estrogen-induced increase in muscle weight and DNA content appeared to be due only to hyperplasia of muscle cells and not to a proliferation of fibroblasts or to infiltration by inflammatory cells. In all treatment groups, including the estrogen-treated castrates, more than 95% of the cells in the tissue were smooth muscle cells, and there was no evidence that polyploidy contributed to changes in DNA levels. In addition, in the estrogen-treated muscles, DNA concentration remained high, and the stereologically determined cell size remained low. Therefore, both morphological and biochemical evidence indicate that androgen induces hypertrophy, whereas estrogen induces hyperplasia of muscle cells. The correction of stereological and biochemical data validates the application of stereological cell size determination for smooth muscle cells in organs that hardly can be separated into stromal and epithelial components; eg, the prostate.
Animals↗
Irreversible androgen induced growth in seminal vesicle smooth muscle.
The dihydrotestosterone (DHT)-sustained normal pubertal development of the guinea pig seminal vesicle epithelium proved to be highly reversible in that 4 weeks after cessation of hormone treatment there were significant reductions in epithelial wet weight, DNA content, and collagen content. In contrast, the DHT-induced prepubertal development of smooth muscle DNA and collagen contents were not significantly reduced following hormone withdrawal. In adult animals treated daily with DHT for 4 weeks, there was an increase in collagen content of approx 80% above either castrate or normal controls, which also proved to be irreversible. These findings indicate that the autophagic mechanisms, which are activated upon withdrawal of the androgenic stimulus and serve to degrade epithelial cells and the associated collagenous matrices, are not operant in the smooth muscle of the organ.
Aging↗
Growth responses of the guinea pig seminal vesicle epithelium and muscle to long-term treatment with dihydrotestosterone and/or estradiol benzoate.
The three-month treatment regimen with dihydrotestosterone (DHT) and estradiol (E2B) which was capable of producing a supranormal growth of the canine prostate gland equal to that occurring in spontaneous canine benign prostatic hypertrophy, failed to produce similar changes in either the epithelium or smooth muscle of the guinea pig seminal vesicle. The factor limiting the growth response in the seminal vesicle epithelium and muscle of the castrate guinea pig proved to be the lack of a DHT-estradiol benzoate (E2B) synergism, since the growth responses in seminal vesicle tissues to the three-month treatment with DHT alone were similar to that previously recorded for the canine prostate. The lack of a DHT-E2B synergism in the guinea pig seminal vesicle may be responsible for the absence of spontaneous hypertrophy of this organ and other organs such as the human seminal vesicle with advancing age.
Animals↗
Androgenic regulation of estrogenic action on accessory sex organ smooth muscle.
Our previous research has shown that 4 weeks of daily estrogen treatment, started on the day of castration, resulted in significant growth of the guinea pig seminal vesicle smooth muscle, yet little or no estrogenic effect on muscle tissue weight or DNA content was observed when the treatment was initiated after a 1-month period of castration induced regression. With the hypothesis that castration induced reductions in estrogenic sensitivity were due to alterations in the intracellular fate of estradiol in the muscle, we determined, following the intravenous injection of 3H-estradiol to normal, 24-hour castrates and 1-month castrates, the whole muscle tissue accumulation and subcellular distribution of 3H-estradiol. In the same 3 experimental groups, we also determined, using in vitro exchange assays with 3H-estradiol, the number of estrogen binding sites in both the cytosol and salt (1.2 M KCl) soluble fraction of the crude nuclear-myofibrillar pellet. It was found that the loss of estrogenic sensitivity in the 1-month castrate was not due to a reduction in either whole tissue accumulation, subcellular distribution, cytosol binding or salt-soluble nuclear binding of 3H-estradiol. Restoration of estrogenic responses in muscle DNA content and wet weight was achieved by priming 1-month castrates with 5 daily injections of dihydrotestosterone immediately prior to the onset of estrogen treatment. Shorter periods of androgen priming (e.g., 1, 2 or 3 days) slightly enhanced, but did not completely restore, estrogenic responses in muscle wet weight and DNA content. For estrogen sensitive parameters of muscle growth, such as collagen and RNA content, which were not altered in their response to the estrogen treatment by a 1-month period of castration-induced regression, androgen priming prior to estrogen treatment had no effect. Therefore, testicular androgens regulate selected facets of estrogenic sensitivity in guinea pig seminal vesicle smooth muscle; changes in the muscle cytosol or salt-soluble nuclear myofibrillar estrophiles do not appear to be responsible for the changes in estrogenic sensitivity.
Androgens↗
The hormonal maintenance and restoration of guinea pig seminal vesicle fibromuscular stroma.
Using the separated epithelium and muscle preparation of the guinea pig seminal vesicle, we designed studies to investigate the hormonal control of epithelial collagen, muscle collagen and muscle cells. All hormone treatment regimens involved a comparison of the effects of hormone maintenance (homrone treatments initiated on the day of castration) versus hormone restoration (hormone treatments initiated after a castration-induced regression) on these 3 components of the fibromuscular stroma. In the epithelium, castration induced a 35 per cent decline in collagen content, which was either returned to normal by androgen restoration of prevented by androgen maintenance. In all androgen treatment regimens, changes in epithelial collagen correlated with changes in epithelial wet weight, cell number, RNA content and cell size. In contrast, growth of the epithelium was not stimulated by estrogen maintenance or restoration. Castration reduced muscle wet and dry weight, as well as cell size and RNA content, but there was no effect on cell number and collagen content. Androgen maintenance or restoration reversed the castration-induced regression in all parameters and also caused collagen content to increase 35 percent above normal. Estrogen maintenance of castrates sustained wet weight, dry weight and RNA content at normal and stimulated supranormal increases in both collagen content and cell number. Similarly, estrogen restoration induced supranormal increases in collagen content and returned RNA content to normal. However, estrogen's ability to stimulate supranormal increases in cell number and restore wet and dry weight to normal was lost after a castration-induced muscle regression. In summary, components of the guinea pig seminal vesicle fibromuscular stroma have been shown to be sensitive to androgens and/or estrogens. The action of androgen on these tissue components was independent of the state of tissue regression, whereas with the exception of RNA and collagen content all the effects of estrogen were significantly reduced with castration-induced regression of the tissue.
Animals↗
Collagen and cellular proliferation in spontaneous canine benign prostatic hypertrophy.
Towards defining an animal model for study of cellular as well as extracellular matrix accumulation in human benign hypertrophy (BPH), cell number and levels of collagen and zinc were measured in normal and spontaneously hypertrophied canine prostate glands. The increased gland weight in canine BPH was accompanied by increased contents of DNA, collagen and zinc. Concentrations of collagen and zinc in BPH did not differ from normal. These findings indicate that canine BPH involves true hyperplasia and may represent an overgrowth of normal cellular and extracellular components. Canine BPH may prove to be a useful animal model for study not only of cellular proliferation, but also of the connective tissue and zinc accumulation in the human disease.
Animals↗
Nitrogen Isotope Fractionation Associated with Nitrate Reductase Activity and Uptake of NO(3) by Pearl Millet.
Nitrogen isotope fractionation by Pearl Millet (Pennisetum americanum L. and P. mollissimum L.) grown on nitrate was associated with nitrate reductase activity. Fractionation was evidenced at the step of nitrate reduction when the substrate-to-enzyme ratio was high (possibly saturating for the active sites of the nitrate reductase enzyme), for instance in young seedlings having a low nitrate reductase activity or in seedlings grown on high nitrate concentration.When the substrate concentration was low (and, hence, the active sites of the enzyme were possibly not saturated), the isotopic discrimination could only be associated with the uptake of nitrate into the cell. In that case, isotopic fractionation was null. It is concluded that the uptake of nitrate does not discriminate among nitrogen isotopes.
Journal Article↗
N abundance of nodules as an indicator of N metabolism in n(2)-fixing plants.
This paper expands upon previous reports of (15)N elevation in nodules (compared to other tissues) of N(2)-fixing plants. N(2)-Fixing nodules of Glycine max (soybeans), Vigna unguiculata (cowpea), Phaseolus vulgaris (common bean), Phaseolus coccineus (scarlet runner bean), Prosopis glandulosa (mesquite), and Olneya tesota (desert ironwood) were enriched in (15)N. Nodules of Vicia faba (fava beans), Arachis hypogaea (peanut), Trifolium pratense (red clover), Pisum sativum (pea), Lathyrus sativus (grass pea), Medicago sativa (alfalfa), and Lupinus mutabilis (South American lupine) were not; nor were the nodules of nine species of N(2)-fixing nonlegumes. The nitrogen of ineffective nodules of soybeans and cowpeas was not enriched in (15)N. Thus, (15)N elevation in nodules of these plants depends on active N(2)-fixation. Results obtained so far on the generality of (15)N enrichment in N(2)-fixing nodules suggest that only the nodules of plants which actively fix N(2) and which transport allantoin or allantoic acid exhibit (15)N enrichment.
Journal Article↗
Hormonal control of accessory sex organ fibromuscular stroma.
Using the surgically separated epithelium and muscle preparation of the guinea pig seminal vesicle, quantitative determinations were made of the hormonal sensitivities of three components of male accessory sex organ fibromuscular stroma. The parameters measured were epithelial collagen, muscle tissue cell number, and muscle tissue collagen. Epithelial collagen increased approximately tenfold between one week of age and adulthood. This growth was completely prevented by castration and was sustained at normal levels of maintenance of prepubertal castrates with dihydrotestosterone (DHT). Castration of adult animals reduced epithelial collagen 40%; such reductions were prevented by DHT treatment. Estrogen treatment of adult castrates, either alone or in combination with DHT, had no anabolic effect on the epithelium. In all of these studies, changes in epithelial collagen correlated with changes in epithelial wet weight, DNA content, and RNA/DNA. From 1 week of age to adulthood, growth of seminal vesicle muscle involved marked increases in wet weight, DNA content, RNA/DNA, and collagen content. Increments in all parameters were prevented by prepubertal castration and were sustained at normal levels in castrates by DHT treatment. However, in adult animals, muscle DNA content and collagen levels were insensitive to castration and androgen replacement; only tissue weight and cell size (RNA/DNA) were androgen sensitive. Estrogen treatment of adult castrates caused supranormal increases in muscle DNA and collagen; changes in collagen were irreversible. The effects of simultaneous treatment of DHT and estrogen did not differ from those of DHT alone. Therefore, normal postnatal development of the stromal components, epithelial collagen, muscle cells, and muscle collagen was androgen dependent, but in adult animals, only epithelial collagen retained androgenic sensitivity. Estrogen induced supranormal and irreversible growths in the muscle.
Androgens↗