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S Chevalier

Publications and source records attributed to S Chevalier.

142 records · Page 8Linked to original sources

Characterization of canine prostatic cells from normal and hyperplastic glands.

Secretory and non-secretory epithelial cells and fibroblasts obtained from normal and hyperplastic canine prostate glands and from prostates of 6-week castrated dogs are cultured in monolayers. Prostatic fibroblasts are grown in non-selective culture medium and found at densities of 1.040-1.045 g/ml in Percoll gradients. Enriched populations of each epithelial cell type area obtained by varying the duration of the culture combined with the use of selective MEM D-Val mixture. When separated by centrifugation in Percoll density gradients, the secretory cells (high A.P.) are found at densities of 1.02-1.03 g/ml whereas the non-secretory cells (low A.P.) have densities of 1.05-1.06 g/ml. Both epithelial cell types are present in the normal and hyperplastic glands at the time of explantation. There is no correlation between the prostatic weight and the proportion of each cell type present in the tissue. On the basis of cell density in Percoll gradients and A.P. activity, those prostates with a high percentage of non-secretory epithelial cells yield better attachment and overall cultures than glands consisting mainly of secretory cells. Our results strongly suggest that non-secretory cells are precursors of the secretory type. In addition, the cells involved in the aging process of the culture are the secretory epithelial cells.

Acid Phosphatase↗

Effect of ribonucleotides on substrate availability for DNA polymerase assays in cytoplasmic fractions of rat intestinal mucosa.

The deoxyribonucleoside triphosphate substrates for DNA synthesis were hydrolysed during the DNA polymerase (EC 2.7.7.7) assay with cytoplasmic subcellular fractions of rat intestinal mucosa. Presumably because of phosphatase (EC 3.1.3.2) activity in these fractions, inorganic phosphate was liberated from the nucleotides, and radioactive thymidine triphosphate was shown to be degraded to thymidine di-and mono-phosphate, thymidine, and thymine. Addition of ATP to the postmicrosomal supernatant increased its DNA polymerase activity by sparing the deoxyribonucleotide precursors from enzymatic degradation.

Acid Phosphatase↗

The enhancement by pervanadate of tyrosine phosphorylation on prostatic proteins occurs through the inhibition of membrane-associated tyrosine phosphatases.

The relapse of prostate cancer during endocrine therapies is attributed to the proliferation of growth factor (GF)-dependent epithelial cells. Such cells are present but in a quiescent state in the normal adult human and dog (experimental model) prostates. GF-signaling pathways involve the activation of protein tyrosine kinases (PTK) whose action is also modulated by phosphotyrosine protein phosphatases (PTPs). To that effect, we have previously reported that dividing canine prostatic epithelial cells exhibited high levels of phosphotyrosyl-(pY)-proteins which were greatly enhanced when incubated in the presence of vanadate. The aim of this study, performed with pervanadate (pV), was to determine whether pV acts either directly by stimulating prostatic PTKs or indirectly by inhibiting PTPs. Upon fractionation, most of the PTK activity was found in membranes of dividing cells and pV selectively increased its activity. This was due to an inhibition of intrinsic PTPs, as demonstrated by dephosphorylation of endogenous pY-proteins which was abolished by pV. This activity was very sensitive to pV (IC50: 150 nM) and was due to non-secreted forms of prostatic acid phosphatase (PAP), a pV inhibited-enzyme, as well as to PTP-1 B, as demonstrated by gel filtration, isoelectric focusing and probing with antibodies. These enzymes were also detected in membranes from human hyperplastic/neoplastic prostates but only PTP-1 B was present in those of prostatic carcinoma PC3 cells. These PTPs, bound to membranes of dividing cells (normal vs neoplastic) where activated PTKs are also located, may be of importance in the development and progression of prostatic proliferative diseases.

Animals↗

Dihydrotestosterone and 3 alpha-androstanediol dynamics in the normal, involuted, and hyperplastic canine prostate.

Perfusion of canine prostatic tissue with [1, 2-3H] 5 alpha-androstane-3 alpha, 17 beta-diol and [4-14C] dihydrotestosterone and the measurement of the isotopic concentrations at the steady state were used to calculate the metabolic dynamics of these steroids by prostatic tissue obtained from normal, castrated or androgen-treated dogs. From the results it was concluded that: Entry of both steroids into the tissue was similar, and no saturation was observed with increasing concentrations of these androgens in the perfusion medium. In contrast, the entry of both steroids was reduced when the perfusion buffer was replaced with diluted plasma. Dihydrotestosterone in prostatic tissue was present in a diffusible form, whereas 3 alpha,17 beta-androstanediol was not. The conversion of 3 alpha, 17 beta-androstanediol to dihydrotestosterone was always higher than the conversion of dihydrotestosterone to 3 alpha, 17 beta-androstanediol; thus, the oxidative pathway was favored. The entry and uptake of both androgens was greatly reduced in those prostates excised from castrated dogs. The uptake of dihydrotestosterone by normal prostatic tissue was 3- to 6-fold higher than the uptake of 3 alpha, 17 beta-androstanediol. However, higher intratissular concentrations of dihydrotestosterone were obtained by increasing the concentration of 3 alpha, 17 beta-androstanediol perfused over that observed by increasing the concentration of dihydrotestosterone perfused. In the hyperplastic tissue, the entry, uptake and metabolism of the two androgens were similar to those observed in the normal gland, but their intratissular concentrations were found to be higher.

Androstane-3,17-diol↗

Characterization of protein-tyrosine kinase activity in the canine prostate.

Following the measurement of the phosphorylation of the substrate poly(Glu80Na,Tyr20) and the analysis of the alkali-resistant phosphorylation of endogenous proteins, the protein-tyrosine kinase of the canine prostate was partially characterized with regard to its subcellular localization, as well as certain kinetic and molecular properties. This kinase was mainly found in the cytosolic fraction (75%); however, its specific activity was similar to that of the residual enzyme present in the particulate fraction. Conditions for optimal activity of both fractions were determined. Under these conditions, several endogenous phosphoproteins (44-63 kilodaltons upon electrophoresis) were alkali resistant and phosphotyrosine was present in all of the major ones (pp63, pp57, pp52, and pp44). The particulate protein-tyrosine kinase activity was partially solubilized (58%) with 0.5% Triton X-100; this percentage was increased to 85% in the presence of 0.25 M KCl. Upon gel filtration, both cytosolic and particulate kinases showed an apparent molecular mass of 44 kilodaltons; these enzymes also phosphorylated similar major alkali-resistant phosphoproteins. The soluble protein-tyrosine kinase, with a sedimentation coefficient of 4.0S and an isoelectric point of 5.5, could be separated from arginine esterase and prostatic acid phosphatase.

Acid Phosphatase↗

Perturbation of rodent hepatocyte growth control by nongenotoxic hepatocarcinogens: mechanisms and lack of relevance for human health (review).

During the development of new industrial and pharmaceutical chemicals, it is necessary to determine whether they are potential carcinogens. However, there are no short-term tests available for nongenotoxic carcinogens that do not damage DNA yet cause tumours in rodent bioassays. The peroxisome proliferators (PPs) constitute a diverse class of nongenotoxic carcinogens that include chemicals of therapeutic, industrial and environmental importance such as hypolipidaemic fibrate drugs, clingwrap/medical tubing plasticizers and certain pesticides and solvents. PPs induce DNA synthesis and suppress apoptosis in rat and mouse hepatocytes, leading to tumour formation. In addition to altering hepatocyte growth and survival, PPs cause peroxisome proliferation and the induction of enzymes of the beta-oxidation pathway. PPs mediate their biological responses in rodents via activation of the nuclear hormone receptor PPARalpha (peroxisome proliferator activated receptor alpha) which regulates expression of the genes associated with response to PPs. The mechanisms through which normally quiescent hepatocytes are recruited into the cell cycle currently remain obscure. However, it is probable that expression of hepatic cytokines by hepatic macrophages (Kupffer cells) may be involved. In common with other classes of nongenotoxic carcinogen, there are remarkable species differences in response to PPs; humans respond to the fibrate hypolipidaemic PPs via a reduction in serum cholesterol but appear refractory to the adverse effects of PPs such as hepatic peroxisome proliferation, DNA synthesis and tumour formation. The molecular basis of the observed species differences in response to PPs is unclear at present, but recent data support a quantitative hypothesis wherein PPARalpha expression levels are sufficient in humans to mediate hypolipidaemia, but too low for transcriptional regulation of the full battery of genes associated with the adverse effects seen in rodents such as peroxisome proliferation, liver enlargement and tumours. A more detailed understanding of the mechanisms through which these chemicals cause tumours in rodents and how humans may differ will assist in extrapolation of rodent data to human risk assessment.

Animals↗

Bombesin modulates the association of Src with a nuclear 110-kd protein expressed in dividing prostate cells.

Polyclonal antibodies produced against a peptide derived from the Fer tyrosine kinase sequence also specifically recognized a 110-kd protein (p110) up-regulated in dividing versus resting dog prostate epithelial cells in vitro. In vivo in the dog prostate, p110 expression was detected when basal cell metaplasia was induced by estrogens after castration but not when renewing the differentiated epithelium with androgens. It was also detected in extracts from the human prostatic carcinoma cell lines LNCaP, DU145, and PC-3, and from 6 out of 11 human prostate cancer tissues analyzed, but not from normal or hyperplastic glands. The tyrosine kinase Src was shown by coimmunoprecipitation to associate with p110, and this interaction was positively modulated by bombesin stimulation of PC-3 cells. However, p110 was not tyrosine phosphorylated. Moreover, it was mainly distributed in the nuclear fraction. This nuclear p110 protein, expressed in dividing prostate epithelial cells and in human prostate cancer cells and tissues, could thus be a downstream mediator of bombesin-signaling pathways, acting via its association with Src.

Animals↗

Protein turnover and requirements in the healthy and frail elderly.

There are as yet no definitive data that warrant the establishment of evidence-based dietary protein recommendations for the elderly. We reviewed the relevance of the new 2002 recommended protein intake of 0.80 g/kg body weight.d for adults to healthy and frail elderly persons. We found that data from published nitrogen balance studies indicate that, a higher protein intake of 1.0 - 1.3 g/k.d is required to maintain nitrogen balance in the healthy elderly, which may be explained by their lower energy intake and impaired insulin action during feeding compared with young persons. Although it needs to be confirmed, a decrease in efficiency of protein utilization with aging may also dictate a higher protein-intake recommendation. Measures of the dynamic aspects of protein metabolism done in the postabsorptive state have shown no change in whole body protein turnover per unit of active metabolic tissue with aging. However, the contribution of muscle protein to wholebody protein metabolism was significantly reduced in the elderly, and explained by their reduced muscle mass and lower rates of myofibrillar protein turnover. Consequently, the contribution of nonmuscle protein, especially that of visceral tissue whose rates of protein turnover are known to be more rapid was proportionally greater with aging. It is conceivable that higher protein consumption rates could compensate for the decrease in availability of muscle amino acids and spare the muscle mass. Despite a paucity of data on the frail elderly population, we present a rationale to justify a greater protein intake of at least equivalent to that of their healthy counterparts. We propose that higher protein intakes for the elderly, and especially the frail population, than those presently recommended may minimize the sarcopenia of aging and thereby protect against some of the health risks of aging.

Aged↗

Effect of recombinant interferon gamma and interleukin-2 and of a monoclonal antibody against interferon gamma on the rat immune response against heart allografts.

We studied the effect of rat rec-IFN-gamma, human rec-IL-2, and an IgG1 monoclonal antibody (DB1) directed against rat IFN-gamma on allograft survival in the rat in various experimental conditions. The DB1 monoclonal antibody did not prolong heart allograft survival in the (LEW/BN)F1 to LEW combination, even when used at high doses (2 mg/rat x 9 days). Rec-IFN-gamma induced major histocompatibility antigen expression in vivo, but its administration had no effect on the graft survival either of untreated LEW recipients of (LEW x BN)F1 heart allografts or of donor blood-transfused LEW recipients. In addition, rec-IFN-gamma alone had no effect on graft survival in cyclosporine-treated rats. In contrast, rec-IL-2 shortened heart allograft survival both in untreated and in cyclosporine-treated recipients. Rec-IFN-gamma partially reversed the effects of rec-IL-2 in cyclosporine-treated rats. The data suggest that in vivo administration of IFN-gamma in allograft recipients may have a suppressor effect, in addition to the postulated augmenting effect on the immune response by increasing MHC antigen expression.

Animals↗

[Identification of community leaders].

Although many methods of measuring leadership have been developed in sociological studies, there are few articles on the feasibility of these methods. The goal of this study was to verify the feasibility of the "modified positional-reputational approach" developed by Nix. The study was conducted in a small community located north of Montreal. Nix's questionnaire was translated, adapted and administered to 49 key informants. Two hundred and fourteen leaders were selected. Three types of leaders were identified: the legitimizers, the effectors and the activists. Through a sociometric analysis, we established links between the different leaders and we described the power structure of the community. Despite a few shortcomings, Nix's approach was found extremely useful.

Community Participation↗

150-kDa proteins in dog serum bind 1.5-kDa growth-promoting factors for androgen-independent canine prostatic epithelial cells.

Fractions obtained by gel filtration or ultrafiltration of dog serum were tested for their mitogenic activity on canine prostatic epithelial cells: two prostatic growth factor (PGF) entities were found, a major one of 150 kDa (PGF-I) and a minor one of 1.5-2.0 kDa (PGF-II). Treatment and/or extraction with acetic acid, hydrochloric acid, or acidified-ethanol or preparations enriched in PGF-I obtained either by ion-exchange chromatography, acetone precipitation, or retention by ultrafiltration membrane (cut-off 30 kDa) resulted, upon gel filtration, in the detection of a mitogenic activity eluting mainly at the position of PGF-II. Acid hydrolysis and proteolysis of PGF-II led to a loss of activity. It is proposed that, in dog serum, mitogenic peptides for prostatic epithelial cells of 1.5 kDa (PGF-II) are found in their free form and/or in association with proteins of 150 kDa (PGF-I).

Animals↗

[Institutionalization of community programs: review of theoretical models and proposal of a model-].

Community-based health promotion programs to change lifestyle habits must remain in their host organizations for extended periods of time in order to have impact. Their effectiveness can be closely linked to their long term viability or institutionalization. To remain viable, these programs must survive beyond initial investment and support by external organizations. However, some programs disappear when external investment is withdrawn. This can be costly and in addition can generate resistance to the implementation of other health promotion programs in the future. Recently, interest in the processes involved in the institutionalization of these programs has increased. Based on 28 publications, this article reviews selected conceptual models that highlight environmental, organizational, community and marketing-related, variables possibly related to the institutionalization process. A new model is proposed to link these diverse models according to: characteristics of the program, characteristics of the host organization, characteristics related to the adoption, implementation and incorporation of the program, and finally characteristics related to the fit (mutual adjustment) between the host and the program.

Community Health Planning↗

[Evaluation of the implementation of an educational curriculum: optimal interventions for the adoption of an educational program of health in elementary schools].

A multiple case study design is used to explain the level of implementation of a "Heart Health" curriculum by grade four teachers of eight schools in a Montreal multiethnic and underprivileged district. An interview and logbook examine the following variables: 1) personal characteristics of the teachers; 2) organizational characteristics of the schools; 3) characteristics of the program; 4) collaboration between the health and educational sectors; and 5) curriculum level of use and fidelity of implementation. The results show in particular that the personal characteristics of the teachers and the characteristics of the program explain the level of implementation of the Heart Health curriculum.

Cardiovascular Diseases↗