Biomedical subjects

A Dutour

Publications and source records attributed to A Dutour.

64 records · Page 4Linked to original sources

PubMed1986

[Demonstration of a TRH precursor in the pancreas of the newborn rat].

This study allows the indirect demonstration of a precursor for TRH in pancreatic extracts of 2-days old rats. The sequential treatment of these extracts with trypsin and carboxypeptidase A is followed by a large increase in Pyroglutamyl Histidine Proline (TRH-OH). The molecular weight of the protein that gives rise to TRH-OH after enzymatic treatment ranges between 30,000 and 40,000 daltons. During ontogenesis. TRH levels decrease earlier and more rapidly than that of TRH-precursor levels. These data suggest that changes in the processing of TRH-precursor play a role in the diminution of TRH concentrations that is observed during the first two weeks of life.

Animals↗

PubMed1985

TRH and TRH-OH in the pancreas of adult and newborn rats.

TRH and its metabolite TRH-OH have been measured by specific radioimmunoassays in acid extracts of pancreas in adults and developing rats. TRH and TRH-OH immunoreactivity had the same ontogenic pattern with a maximal concentration on day 4 followed by a progressive return towards adult levels on day 20. A significant linear correlation was found between TRH levels and the TRH/TRH-OH ratio. The range of TRH/TRH-OH ratio varied from 136 +/- 1.6, at the peak of concentrations of both peptides, to 18 +/- 3.9 on day 20. Pancreatic TRH and TRH-OH had the same elution pattern as corresponding synthetic peptides both on Biogel P2 and high-pressure liquid chromatography. The origin of TRH-OH as well as its potential function need further investigations.

Age Factors↗

PubMed1985

Evidence for a precursor for TRH in the neonatal rat pancreas.

Immunoreactive TRH-OH is present at low concentrations in acid extracts from 2- days old rat pancreas. The sequential treatment of these extracts with trypsin and carboxypeptidase A is followed by a three- and ten-fold increase in TRH-OH IR respectively. The molecular weight of the protein that gives rise to TRH-OH after enzymatic treatment ranges between 30000 and 40000 daltons. The appearance of TRH-OH in the tryptic digest suggests that TRH-OH is the COOH-terminal sequence of this protein. These results are the first evidence that TRH biosynthesis occurs through a large molecule precursor. However, this is an indirect demonstration since TRH cannot be generated under these conditions due to the lack of enzymatic amidation activity.

Animals↗

PubMed1984

[Anti-B-lymphocyte antibodies in rheumatoid polyarthritis. I.--1st findings in 22 patients].

Anti B and T lymphocyte antibodies were sought in the serum of 22 rheumatoid arthritis patients from the Marseille area. No immunization against T lymphocytes was found. In contrast anti B lymphocyte activity was demonstrated in every diluted serum tested against a panel of 21 cells. In these sera, the complement dependent cytotoxicity was of medium intensity (lysis - 50 to 90 percent), antibody titers were high (medium 1/512) and a zone phenomenon was observed in 14 out of 22 non-diluted sera. As a rule, serum reactivity was slightly higher at 4 degrees C than at 22 degrees or 37 degrees C but at the latter temperature, it seemed to be more related to the target cells than to the serum tested. These anti B lymphocyte antibodies were predominantly IgMs and were not autoantibodies. Their specificity is still under study but already appears to be wide and not HLA related. These antibodies reacted with 9 to 100 percent of the panel cells and 85 percent of the sera recognized over 50 percent of the cells. Thus the antigenic determinants were probably allotypes or idiotypes of Fab fragments from surface immunoglobulins of a B lymphocyte subpopulation. Thus far, no relationship has been demonstrated between the presence or the titer of these antibodies and clinical, biological or genetic features of rheumatoid arthritis. In the future, this method should simplify the detection of Ig seric groups. It already allows detection of antiglobulin factors which could play an immunoregulatory role in rheumatoid arthritis.

Adult↗

PubMedDate not supplied

Influence of endogenous growth hormone-releasing factor (GRF) on the secretion of GH during the perinatal period in the rat.

Passive immunization of pregnant rats with a specific antiserum to rat GRF (GRF-AS) is followed by a decrease in fetal serum GH on the 19th day of gestation. A significant reduction in serum GH is still observed in older fetuses and newborn rats. Pituitary GH content increases in 19- and 20-day-old fetuses after GRF-AS administration to their mothers. These results suggest that endogenous fetal hypothalamic GRF (or placenta GRF) play a physiological role in the secretion of pituitary GH as early as the 19th day of fetal life and may be responsible for the peak of GH release that occurs in fetuses at the end of gestation.

Aging↗

PubMedDate not supplied

Pro-TRH-connecting peptides in the rat pancreas during ontogenesis.

Rat thyrotropin-releasing hormone prohormone (pro-TRH) is a protein containing five copies of TRH, separated by connecting peptides. We have recently developed radioimmunoassays to synthetic peptides corresponding to prepro-TRH(160-169) and prepro-TRH(178-199). In the present study we have used these assays to investigate the ontogenesis of pro-TRH-derived peptides in the rat pancreas. Reverse-phase HPLC analysis of pancreatic extracts from 2-day-old rats showed the presence of two major immunoreactive peptides exhibiting the same retention time as synthetic prepro-TRH(160-169) and prepro-TRH(178-199), respectively. The concentrations of TRH and pro-TRH cryptic peptides in the rat pancreas rose rapidly after birth, reached a maximum at day 2-4 and decreased gradually afterwards. Streptozotocin treatment of newborn rats induced a marked decrease of TRH (96%), prepro-TRH(160-169) (97%) and prepro-TRH(178-199) content (94%) in pancreatic extracts. These results indicate that the evolution of TRH and pro-TRH-derived peptides follows the same pattern during the postnatal period. Our results also suggest that beta-cells are the only source of pro-TRH-derived peptides in the rat pancreas.

Aging↗

PubMedDate not supplied

Regulation of TRH release by the cultured neonate rat pancreas.

The TRH secretory responsiveness of the pancreatic islet cell clusters from newborn rat in organ culture was studied. Basal TRH secretion was stable over a 9-day period. The response to various secretagogues was tested on day 4. TRH secretion was stimulated by high potassium-induced depolarization and also through both cAMP and protein kinase-C dependent pathways. Like insulin, TRH release was stimulated by glucose and arginine and inhibited by somatostatin. These data suggest the existence of a common mechanism for TRH and insulin secretion by the pancreatic beta-cells.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMedDate not supplied

Is troponin I gene therapy effective for osteosarcoma treatment? Study on a human-like orthotopic rat model.

BACKGROUND: An anti-angiogenesis strategy has been widely recognized as a viable approach to fight cancer and more and more anti-angiogenic factors are continually being identified. Among them, the muscular isoform of Troponin I (TnI) has been described as being a powerful anti-angiogenic agent in vitro as well as in vivo. We investigated the therapeutic efficacy of TnI gene therapy in a human-like orthotopic rat osteosarcoma model. MATERIALS AND METHODS: In this tumor model, we evaluated whether the administration of the secreted TnI coding sequence complexed to cationic liposomes (named TnITag cDNA/lCLP) could induce a delay in tumor growth and reduce tumor vasculature. RESULTS: Although TnI specifically inhibited endothelial cell growth in vitro, we were not able to demonstrate any therapeutic efficacy of TnI in the transplantable osteosarcoma model. CONCLUSION: This lack of efficacy probably resulted from the rapid degradation of recombinant TnI by matrix metalloproteinases, especially MMP2, which are present in large amounts in tumors.

Animals↗

PubMedDate not supplied

Tumor endothelial cells are targets for selective therapies: in vitro and in vivo models to evaluate antiangiogenic strategies.

Angiogenesis is a complicated process, essential for tumor progression and metastasis. Extensive work has been done to understand the mechanisms of tumor angiogenesis and identify angiogenesis inhibitors. It is now recognised that tumor endothelial cells present different functional and phenotypic characteristics than normal resting endothelial cells. These differences and advances in molecular biology have allowed the development of selective agents targeting tumor endothelial cells as therapeutic approaches for cancer. These new targeted strategies need to be evaluated in relevant models before being transferred from the laboratory bench to the clinic. In vivo tumor models remain a good way to evaluate the effect of these agents on tumor growth and metastasis. Nevertheless, in parallel to the development of tumor angiogenesis inhibitors, in vitro models have been designed to mimic angiogenesis steps and enable the evaluation of these new drugs. In this paper, after reviewing the phenotypic characteristics of tumor endothelial cells that make them easy to target for antiangiogenic therapy, some of the most commonly used in vitro and in vivo models, which enable the evaluation of antiangiogenic agents, are presented and discussed.

Angiogenesis Inhibitors↗

PubMedDate not supplied

[Severe hyperlactacidemia in 2 children treated for malignant tumors. Role of vitamin B1].

Two cases of children treated for malignant tumor and who developed a severe lacticacidosis are reported. A 2 year-old girl and a 8 year-old boy were treated with chemotherapy, irradiation and multiple surgical procedures for nephroblastoma and lymphoma respectively. These two malnourished patients, under exclusive parenteral nutrition for two weeks without vitamin intakes, suddenly developed neurological, cardiovascular and digestive symptoms, associated with cytopenia and lacticacidosis. Injection of vitamin B1 only corrected these abnormalities within a few hours, proving the role of thiamine deficiency as the cause of the symptoms.

Acidosis, Lactic↗