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Biomedical subjects

C Tessier

Publications and source records attributed to C Tessier.

At least 37 records · Page 2Linked to original sources
PubMed2000

Involvement of SOCS-1, the suppressor of cytokine signaling, in the prevention of prolactin-responsive gene expression in decidual cells.

The cells forming the rat decidua produce PRL and PRL-related proteins and express both the long and short forms of the PRL receptor. Yet, only a defined subpopulation, the mesometrial cells, express the PRL-dependent alpha2-macroglobulin gene. This gene is silenced in vivo in the antimesometrial cells and in the GG-AD cell line, derived from antimesometrial cells. To examine whether the lack of alpha2-macroglobulin expression is due to defective components in the PRL signaling pathway, we compared the relative expression of Janus kinase 2 (Jak2), signal transducer and activator of transcription 5 a and b (Stat5 a and b), suppressor of cytokine signaling-1 (SOCS-1), and the tyrosine phosphatase SHP-2 mRNA in mesometrial and antimesometrial decidua on days 12 and 13 of pseudopregnancy, the time of maximal alpha2-macroglobulin expression. We found no significant differences in the relative expression of either Jak2, Stat5 (a and b), or SHP-2 in the two cell populations. However, we discovered a profound difference in the expression of SOCS-1, an inhibitor of the Jak/Stat pathway. This gene was highly expressed in the antimesometrial cells and in the GG-AD cells, which do not produce alpha2-macroglobulin. Immunoprecipitation experiments with GG-AD cells revealed that although Jak2 and Stat5 coprecipitate in response to PRL stimulation, no phosphorylation of Jak2 and Stat5 could be observed. To examine whether SOCS-1 plays a role in silencing the alpha2-macroglobulin gene, we cultured GG-AD cells in the presence of either a SOCS-1 antisense oligonucleotide or an irrelevant oligonucleotide for 4, 12, and 28 h. Cells were also treated with PRL. Within 4 h of SOCS-1 antisense treatment, alpha2-macroglobulin mRNA expression was initiated. After 28 h, only cells treated with PRL and SOCS-1 antisense oligonucleotide retained the ability to express the alpha2-macroglobulin gene. In summary, results of this study reveal that constitutive expression of SOCS-1 can prevent PRL signaling and that the lack of PRL-induced expression of alpha2-macroglobulin in a defined decidual cell population is largely due to SOCS-1 expression in these cells.

Animals↗
PubMed2000

[Wasting and postoperative infection in cancer patients].

Denutrition decreases immunological responses of non-cancer patients, the healing is altered whereas infectious complications increase. Now during hospitalization, malnutrition prevails in cancer patients. The suppression of the adaptability to fasting which reduces the expenditure of energy at rest, an a normal metabolic response to nutrients' supply with the impossibility to compensate totally the metabolic deficits with the artificial nutrition alone, raise the fear of postoperative disorders, particularly an increase of the infectious risk. The key point is therefore to identify the cachexia's degree owing to a simple, predictive and consensual index. This check-up allows a postoperative complications' prevention by starting up a perioperative refeeding in high-risk subjects: that is to say all severe wasting patients, the people booked for a severe surgical procedure, especially for oesophageal and gastric neoplasms. Actually, we consider that the quality of the results depend more on the making up of the different nutritional solutions dispensed than to strictly providing for cancer patients' wants, which could be harmful in the postoperative period. Supplementation with antioxidant micronutrients or arginine, glutamine, ribonucleic acids and omega-3 fatty acids would allow an immuno- modulation of the renutrition. But complications strictly due to preoperative denutrition are still to be established.

Cachexia↗
PubMed1999

Rat decidual prolactin. Identification, molecular cloning, and characterization.

Establishment and maintenance of pregnancy require the activity of a highly specialized maternal tissue, the decidua. It is well established that the human decidua synthesizes and releases prolactin. However, in the rat, no study has been able to demonstrate the production of prolactin by the decidua. In this report, we established for the first time using Northern blot analysis and reverse transcription-polymerase chain reaction, Western blot analysis, immunocytochemistry, and enzyme-linked immunosorbent assay, that a defined cell population located in the rat antimesometrial decidua expresses prolactin mRNA, as well as synthesizes and secretes this hormone. By reverse transcription-polymerase chain reaction and rapid amplification of cDNA ends, we cloned a full-length cDNA for rat decidua prolactin, whose sequence was identical to that of pituitary prolactin. Our results also showed that pituitary prolactin appeared to down-regulate decidual prolactin levels. Under these circumstances, inhibition of pituitary prolactin secretion led to a rise in both decidual prolactin mRNA and protein expression. Moreover, addition of exogenous prolactin to primary decidual cells in culture also caused a marked decrease in decidual prolactin mRNA expression. Finally, treatment of primary decidual cells with steroid hormones or 8-bromo-cAMP revealed a differential regulation of decidual prolactin expression from that of pituitary suggesting a tissue-specific regulation of prolactin gene expression, possibly through the use of an alternative promoter in rat decidua.

Amino Acid Sequence↗
PubMed1999

The expression of interleukin-6 (IL-6), IL-6 receptor, and gp130-kilodalton glycoprotein in the rat decidua and a decidual cell line: regulation by 17beta-estradiol and prolactin.

The cytokine interleukin 6 (IL-6), a major mediator of immune and acute phase responses of the liver, has been implicated in the termination of pregnancy once expressed in the uterus. This study was undertaken to investigate the expression and regulation of genes encoding IL-6 and IL-6 receptor (IL-6R) in rat decidual tissue. Total RNA obtained from rat decidual tissue on different days of pseudopregnancy was analyzed by RT-PCR using specific primers for IL-6, IL-6R, and 130-kDa glycoprotein (gp130). Ribosomal L19 primers served as an internal control. IL-6R and gp130 were found to be expressed in the decidua throughout development, while no messenger RNA (mRNA) for IL-6 was detected. Interestingly, within several hours of culture, decidual explants acquired the ability to express IL-6. The apparent ability of decidual cells to express IL-6 and its lack of expression in vivo led us to examine whether the IL-6 gene is actively inhibited. Primary decidual cells were cultured in the presence of estradiol, progesterone, or PRL. Progesterone showed no effect, whereas estradiol and PRL reduced the level of IL-6 mRNA expression. To examine the mechanism by which these hormones inhibit IL-6 expression, we used a simian virus 40-transformed decidual cell line (GG-AD), which expresses only estrogen receptor-beta (ERbeta). Like primary decidual cells in culture, GG-AD cells express IL-6, IL-6R, and gp130 mRNA. When cultured in the presence of estradiol (0-100 ng/ml), mRNA for IL-6 and its receptor components were down-regulated in a dose-dependent manner. Estradiol also caused a dose-dependent decrease in IL-6 protein secretion into the culture medium. The inhibitory effect of estradiol on IL-6 mRNA expression was reversed by the antiestrogen ICI-164,384. Similar inhibition of IL-6 and gp130 mRNA expression was observed with PRL treatment. However, PRL had no effect on IL-6R mRNA levels. PRL inhibition of IL-6 expression was totally reversed by tyrphostin AG490, a JAK2 inhibitor. In summary, the results of this investigation indicate that IL-6 expression, which is detrimental to the maintenance of pregnancy, is inhibited in the rat decidual tissue. This inhibition is induced by PRL and estradiol, which down-regulate not only IL-6 expression, but also the expression of IL-6 receptor and signaling proteins. The results also suggest that PRL signaling to the IL-6 gene is mediated through the long form of PRL receptor and involves JAK2 activation, whereas that of estradiol can be transduced by estrogen receptor-beta.

Animals↗
PubMed1999

Regulation and role of the insulin-like growth factor I system in rat luteal cells.

The relationship between insulin-like growth factor I (IGF-I), a hormone which has potent metabolic effects and stimulates protein synthesis, and prolactin and oestradiol was examined to investigate a possible mechanism for the luteal cell hypertrophy that is responsible for the increase in size of the corpus luteum. A luteal cell line (GG-CL) derived from large luteal cells of the pregnant rat corpus luteum was used. IGF-I, IGF-I receptor and oestrogen receptor beta mRNA contents were determined by semiquantitative RT-PCR. The results revealed that prolactin upregulates the expression of IGF-I mRNA in luteal cells, but not that of its receptor. IGF-I had no effect on the expression of its receptor but caused a dose-related increase in the expression of oestrogen receptor beta. Furthermore, whereas IGF-I upregulated oestrogen receptor beta expression, oestradiol downregulated expression of mRNA for both IGF-I and its receptor. This effect of oestradiol is not mediated through progesterone which is stimulated by oestradiol in the corpus luteum. The developmental studies indicate that mRNA for IGF-I and its receptor are not expressed in tandem throughout pregnancy. Whereas the receptor mRNA is expressed at higher concentrations in early pregnancy, that of its ligand is highly expressed close to parturition. Collectively, the results indicate that prolactin stimulates luteal IGF-I production, which in turn acts on the luteal cell to stimulate expression of oestrogen receptor beta. Luteal cells with increased oestrogen receptor beta can respond fully to oestradiol, leading to cell hypertrophy.

Analysis of Variance↗
PubMed1999

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Competitive Bidding↗
PubMed1998

Nuclear location of PLA2-I in proliferative cells.

We have previously demonstrated that pancreatic PLA2 (PLA2-I) stimulates the proliferation of UIII cells, a stromal cell line derived from normal rat uterus. In order to gain further insight into the mechanism of action of PLA2-I, we have investigated the intracellular processing of PLA2-I. Either highly proliferative or growth arrested UIII cells were analyzed. Growth arrested cells were obtained from a contact inhibited monolayer or from aristolochic acid-treated cultures. Using cellular fractionation, western blotting, immunocytochemistry and confocal microscopy, we demonstrate that endogenous PLA2-I was mainly located in the nucleus in highly proliferative cells whereas its location was cytoplasmic in non proliferative cells. When non confluent UIII cells were incubated with nanomolar amounts of exogenous PLA2-I, the enzyme was internalized and, in the majority of cells, appeared within the nucleus. Both internalization and nuclear location of exogenous PLA2-I were suppressed by the addition of aristolochic acid to the culture medium. Binding experiments performed on purified nuclear preparations showed the presence of specific cooperative binding sites for PLA2-I. Collectively our data suggest that the proliferative effect exerted by pancreatic PLA2 in UIII cells is mediated by a direct interaction of the enzyme at the nuclear level. Putative mechanisms and targets are discussed.

Animals↗
PubMed1997

Long-term follow-up after adjuvant chemotherapy in completely resected early stage ovarian carcinoma.

OBJECTIVE: To evaluate the impact of standardized staging, surgery and adjuvant chemotherapy on survival of patients with completely resected early ovarian carcinoma. STUDY DESIGN: We performed a multicentric retrospective analysis of 283 patients with early stage ovarian carcinoma consecutively treated between 1977 and 1993. Borderline tumours were excluded. A comprehensive staging was performed during initial laparotomy. Patients were treated by standardized surgical resection and all excepted stage IA received a 6-course adjuvant chemotherapy. RESULTS: Eighty patients were excluded because of incorrect substaging, inadequate surgery and adjuvant therapy. The analysis was performed on 203 patients with completely resected early stage ovarian cancer (139, stage I; 64, stage II). Relapse-free survival and overall survival rates for stage I were 66 and 69%, respectively. Relapse-free survival and overall survival rates for stage II were 57 and 61% respectively. Median time of relapse was 18 months (range, 1-107 months). Sites of relapse were peritoneum (45%), retroperitoneal lymph nodes (37%) and distant metastases (18%). Relapses occurring within 18 months had a median survival after relapse of 9 months while later relapses had a median survival of 22 months (P = 0.005). There was no significant difference in relapse-free and overall survival according to the age, performance status and pathology. Cisplatin-based chemotherapy improved the 10-year overall survival of patients with stage IIB and IIC as compared to chemotherapy without cisplatin (oral melphalan. CMF regimen); 91 vs. 33% (P = 0.012) and 75 vs. 42% (P = 0.05), respectively. Cisplatin-based regimens did not improve survival in stage IA, IB and IIA. CONCLUSIONS: Early ovarian cancers have a good prognosis after comprehensive staging, complete surgery and adjuvant chemotherapy. Cisplatin-based regimens compared to melphalan and CMF showed a significant increase of survival in stage IIB and IIC. Prognosis of relapse depends on the relapse-free interval duration.

Adult↗
PubMed1996

The level of pancreatic PLA2 receptor is closely associated with the proliferative state of rat uterine stromal cells.

Rat uterine stromal cells (U(III)) express pancreatic type PLA2 (PLA2-I) receptor and internalize the enzyme bound to receptors. Here, we investigate the proliferating effect and alterations in binding of PLA2-I. There is a dramatic decline in PLA2-I binding in U(III) cells as they progress from a non-confluent proliferating state (40,000 sites/cell) to a confluent state (1300 sites/cell). Intracellular concentration of PLA2-I changed with the alteration in binding, suggesting that regulation in the PLA2 binding capacity may have important implications in growth control mechanisms.

Animals↗
PubMed1996

Binding and internalization of extracellular type-I phospholipase A2 in uterine stromal cells.

The cellular uptake of extracellular type-I phospholipase A2 (PLA2) was investigated in rat uterine stromal cells (UIII) in culture, which were found to express the high-affinity binding site for mammalian type-I PLA2, with a measured KD of 6.4 nM, a Bmax of 0.1-1 pmol/mg of DNA at 4 degrees C, and a molecular mass of about 200 kDa. When UIII cells were treated with type-I PLA2 at 37 degrees C, the ligand specifically associated with the cells increased, reaching a plateau after 90 min of incubation, whose level was about 5-fold higher than that measured if cells were maintained at 4 degrees C. We could determine that the PLA2 was bound to plasma membrane receptors which were responsible for internalization of the ligand, and that the binding sites were still suitable for binding at the level of plasma membrane during UIII cell incubation at 37 degrees C. Proteolysis of internalized PLA2 could be clearly detected only after 90 min of UIII cell incubation with the ligand at 37 degrees C, and most of the intracellular PLA2 consisted of the apparently intact 14 kDa enzyme. By cross-linking studies, we found that most of the internalized PLA2 was not associated with the receptor, supporting the conclusion that in our experimental system a single pool of membrane receptors for mammalian type-I PLA2 undergoes cycles of ligand binding, intracellular transfer and release of PLA2, followed by restoration of binding sites on the plasma membrane. We calculated that the rate of internalization of the ligand by one receptor molecule in UIII cells at 37 degrees C is about three molecules of type-I PLA2 per h.

Animals↗
PubMed1996

Determination of cadmium-metallothioneins in zebra mussels exposed to subchronic concentrations of Cd2+.

Metallothioneins have been detected and investigated in zebra mussels (Dreissena polymorpha) using high-performance liquid chromatography (size exclusion) coupled with microatomization-AAS or inductively coupled plasma mass spectrometry. The mussels were exposed to 0.2, 2, and 20 micrograms/liter Cd2+ (as CdCl2) for 1 month under controlled temperature and dietary conditions. Elevated (relative to control) concentrations of tissue Cd2+ were detected in all specimens exposed to 2 micrograms Cd/liter and more than 50% of the specimens exposed to 0.2 micrograms Cd/liter, demonstrating that Dreissena cannot regulate Cd2+ at trace exposure concentrations. In most specimens, at least 85% of the measured Cd2+ was bound to metallothioneins. After reduction and exposure to excess Cd2+, the metallothionein fraction of all extracts adsorbed similar quantities of Cd2+, indicating that the physiological concentration of metallothionein in the exposed specimens remained similar to the basal concentration in the control specimens. Thus, a short-term exposure to environmentally relevant concentrations of Cd2+ did not produce a genetic induction of metallothionein biosynthesis as generally observed in specimens exposed to higher concentrations of d10 metals.

Animals↗
PubMed1995

Docosahexaenoic acid is a potent inhibitor of rat uterine stromal cell proliferation.

The effect of different families of fatty acids on the proliferation of rat uterine stromal cells (UIII) was studied. Docosahexaenoic acid (DHA) exerted a strong and dose-dependent inhibitory effect (IC50 approximately 2 microM), whereas arachidonic acid (AA) stimulated UIII cell proliferation at the optimal concentration of 10 microM. Oleic, linoleic and linolenic acids were ineffective from 0.1 to 10 microM. The inhibitory effect of DHA was independent of the eicosanoid biosynthesis and lipid peroxidation, since it was not reversed by the addition of the antioxidant BHT and no significant production of oxidized species from DHA occurred in our culture conditions.

Animals↗
PubMed1995

[Subjective evaluation of voice and speech after supra-cricoid partial laryngectomy].

A prospective perceptual evaluation of the voice and speech after supra-cricoid partial laryngectomy over the first post-operative six months was performed. Ten male patients were evaluated at one, three and six months by five listeners. A voice profil was drawn from defined acoustical parameters studied, and a chronology in the voice improvement was observed. Voice therapy aims could be suggested.

Aged↗
PubMed1994

Phospholipase A2 inhibitors regulate the proliferation of normal uterine cells.

The effects of inhibitors of phospholipase A2, cyclooxygenase, lipoxygenase and cytochrome P450 activity on the proliferation of normal rat uterine stromal cells (UIII) were studied. At non-cytotoxic doses, inhibitors of cyclooxygenase, lipoxygenase and cytochrome P450 activity had no effect; UIII cells did not lose their ability to synthesize and secrete arachidonic acid metabolites, mainly prostaglandin I2 and prostaglandin E2, after successive passages. Inhibition of prostaglandin production did not affect their proliferation. In contrast, phospholipase A2 inhibitors significantly reduced UIII cell proliferation in a reversible and dose-dependent manner. Aristolochic acid was the most potent inhibitor with an IC50 of 0.3 mumol/l on day 7 of culture. Moreover, low doses of arachidonic acid stimulated UIII cell proliferation. Thus the proliferation of normal uterine stromal cells appears to be independent of arachidonic acid oxygenated metabolites, contrary to what is observed in tumor cells, but requires an intact phospholipase A2 pathway.

Animals↗
PubMed1993

[Comparative pharmacokinetics of antibiotics in blood, csf and brain].

The Knowledge of the antibiotic's cerebral diffusion is essential to define a of neurosurgical antibioprophylaxis' strategy. Without references in the medical world-literature, we've decided to compare the pharmacological kinetics in the blood, the cerebrospinal fluid and the sound cerebral tissue of common used molecules in neurosurgery that is to say: amoxicillin, cefamandole, metronidazole and pefloxacin. The results show that the cerebral levels of metronidazole and pefloxacine are rapidly high with an extended duration (> 10 times the M.I.C. of the sensitive bacteriae), but the tissue penetration of amoxicillin is hazardous and shot-duration for cefamandole (undosable after 3 hours).

Adult↗
PubMed1992

Alternative staffing services. Contract transcription.

Contract medical transcription services can be of great assistance in meeting the demands for transcription, without jeopardizing patient, physician, or institutional confidentiality. You simply must require the contract service to provide at least the same degree of protection and preservation of confidentiality that you should require inhouse. To achieve this you must make these requirements explicit, comprehensive, comprehensible, believable, and enforceable. Discuss the requirements with prospective contractors. Review them at least annually with existing contractors and when contracts are due for renewal. Be sure to specify the consequence of breaching confidentiality, and if there are breaches, enforce the terms of the contract. Consult your institution's legal counsel both in developing the contract and in enforcing its provisions. Take into consideration your department's and institution's policies, AHIMA's statement on confidentiality, as well as local, state, and federal laws. Above all, never lose sight of the patient. Ultimately, it is not patient information that you are obligated to protect. It is the patient.

Confidentiality↗