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G Bertrand

Publications and source records attributed to G Bertrand.

At least 91 records · Page 5Linked to original sources
PubMed1990

The influence of sodium omission on alpha 2-adrenergic inhibition of insulin release by mouse islets.

The mechanisms by which activation of alpha 2-adrenoceptors inhibits insulin release are still incompletely understood. This study, performed with isolated mouse islets, identifies a possible role of Na+ in this inhibition. Regardless of the stimulus used to induce insulin release, the inhibitory effect of low concentrations of clonidine (0.01-0.1 microM) was markedly smaller in the absence of Na+ (with choline or lithium as substitute) than in its presence. The effectiveness of a high concentration of clonidine (1 microM) was, however, not affected by Na+ omission. The results indicate either that Na+ omission indirectly counteracts an effect of clonidine (e.g. on a membrane permeability or on Ca2+ handling), or that Na+ is directly involved in a cellular process (e.g. a Na+ current or the Na+/H+ exchange) controlled by alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1990

Spinal synovial cyst: case report using magnetic resonance imaging.

The case of a 65-year-old woman who developed a spinal synovial cyst at the L4-5 disk space is reported. Her clinical signs and symptoms are presented. A comparison among her preoperative myelogram, computed tomography scan, and magnetic resonance imaging showed magnetic resonance imaging to be more accurate in detailing both the intraoperative and pathological findings.

Aged↗
PubMed1989

Comparison of the inhibition of insulin release by activation of adenosine and alpha 2-adrenergic receptors in rat beta-cells.

Rat islets were used to compare the mechanisms whereby adenosine and adrenaline inhibit insulin release. Adenosine (1 microM-2.5 mM) and its analogue N6(-)-phenylisopropyladenosine (L-PIA) (1 nM-10 microM) caused a concentration-dependent but incomplete (45-60%) inhibition of glucose-stimulated release. L-PIA was more potent than D-PIA [the N6(+) analogue], but much less than adrenaline, which caused nearly complete inhibition (85% at 0.1 microM). 8-Phenyltheophylline prevented the inhibitory effect of L-PIA and 50 microM-adenosine, but not that of 500 microM-adenosine or of adrenaline. In contrast, yohimbine selectively prevented the inhibition by adrenaline. Adenosine and L-PIA thus appear to exert their effects by activating membrane A1 receptors, whereas adrenaline acts on alpha 2-adrenergic receptors. Adenosine, L-PIA and adrenaline slightly inhibited 45Ca2+ efflux, 86Rb+ efflux and 45Ca2+ influx in glucose-stimulated islets. The inhibition of insulin release by adenosine or L-PIA was totally prevented by dibutyryl cyclic AMP, but was only attenuated when adenylate cyclase was activated by forskolin or when protein kinase C was stimulated by a phorbol ester. Adrenaline, on the other hand, inhibited release under these conditions. It is concluded that inhibition of adenylate cyclase, rather than direct changes in membrane K+ and Ca2+ permeabilities, underlies the inhibition of insulin release induced by activation of A1-receptors. The more complete inhibition mediated by alpha 2-adrenergic receptors appears to result from a second mechanism not triggered by adenosine.

Adenosine↗
PubMed1989

An A2-purinoceptor agonist, NECA, potentiates acetylcholine-induced glucagon secretion.

The effect of a stable structural analogue of adenosine, 5'-N-ethylcarboxamidoadenosine (NECA), was studied on glucagon secretion induced by acetylcholine (ACh) in the isolated perfused pancreas of the newborn dog. The perfusion solution contained a physiological concentration of glucose (4.2 mM). In the first set of experiments, ACh (0.5 microM) infused alone for 10 min induced a significant rise of glucagon secretion (370 +/- 98%, 4 min after the beginning of infusion). In the second set, NECA (2.2 nM) infused 10 min before ACh administration, had no effect per se, but considerably increased the response to ACh (929 +/- 262% of basal value within 3 min). So, the more specific A2 purinoceptor agonist, NECA, potentiated glucagon secretion induced by the cholinoceptor agonist, ACh.

Acetylcholine↗
PubMed1989

Effects of extracellular adenine nucleotides on the electrical, ionic and secretory events in mouse pancreatic beta-cells.

1. The mechanisms whereby extracellular adenine nucleotides modulate pancreatic beta-cell function were studied with mouse islets stimulated by 15 mM glucose. 2. Adenosine 5'-triphosphate (ATP) and adenosine 5'-diphosphate (ADP) (100 microM) inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. These changes were rapid but small and transient. 3. alpha,beta-Methylene ADP caused a rapid and sustained inhibition of insulin release, 45Ca efflux and 86Rb efflux from islet cells. It also produced a slight hyperpolarization of the beta-cell membrane, with sustained modification of the pattern but only transient decrease of the intensity of the electrical activity. In the absence of extracellular Ca2+, alpha,beta-methylene ADP increased 45Ca and 86Rb efflux without changing insulin release. Most effects of alpha,beta-methylene ATP were qualitatively similar but quantitatively smaller than those of the ADP-analogue. 4. Adenylylimido-diphosphate (AMP-PNP) slightly increased 45Ca and 86Rb efflux and potentiated insulin release in the presence of extracellular Ca2+. However, its effects on electrical activity in beta-cells were qualitatively similar to those of the alpha,beta-methylene analogues. 5. The small effects of ATP and ADP could result from their degradation into adenosine. alpha,beta-Methylene ADP appears to increase K+ permeability of the beta-cell membrane and to produce a second, intracellular, effect which largely contributes to the inhibition of insulin release. Another recognition site, with higher affinity for triphosphate derivatives, could mediate the small stimulatory effects of AMP-PNP.

Adenine Nucleotides↗
PubMed1989

Difference in the potentiating effect of adenosine triphosphate and alpha, beta-methylene ATP on the biphasic insulin response to glucose.

1. The effects of exogenous adenine nucleotides and structural analogues on the biphasic insulin response to an increase of glucose concentration in the physiological range (from 4.2 to 8.3 mM) were studied in the isolated perfused rat pancreas. Purinoceptor agonists were added either simultaneously or 15 min before increasing glucose. 2. ATP and ADP at 16.5 microM were ineffective per se in the presence of the non stimulatory glucose concentration (4.2 mM) but markedly potentiated the biphasic insulin response to glucose rise in both experimental protocols. 3. Two more stable analogues of ATP and ADP (adenylylimidodiphosphate and alpha, beta-methylene ADP (alpha, beta-MeADP)) at 16.5 microM behaved like the natural compounds: they were ineffective at a glucose concentration of 4.2 mM and potentiated both phases of insulin response to glucose rise. 4. alpha, beta-MeATP added simultaneously with the high glucose concentration, markedly potentiated the first phase of insulin response to glucose rise but did not potentiate the second one. When alpha, beta-MeATP infusion began 15 min before glucose rise, the biphasic response to glucose was not potentiated, in contrast to what occurred with ATP. 5. In the presence of alpha, beta-MeATP, the ATP potentiating effect was unaffected. 6. It is concluded that ATP and ADP, via activation of beta cell P2 gamma purinoceptors, potentiates the biphasic insulin response to an increase of glucose concentration. On the other hand, alpha, beta-MeATP did not behave like natural and other structural analogues of ATP and ADP: this difference appears not to be the consequence of desensitization of beta cell P2 gamma purinoceptors by alpha, beta-MeATP.

Adenosine Diphosphate↗
PubMed1989

Membrane and intracellular effects of adenosine in mouse pancreatic beta-cells.

Mouse islets were used to study the effects of adenosine and its stable analogue L-N6-phenylisopropyladenosine (L-PIA) on pancreatic beta-cell function. At a high concentration (500 microM), adenosine augmented glucose-induced electrical activity in beta-cells and potentiated insulin release. These effects were prevented by the inhibitor of nucleoside transport nitrobenzylthioguanosine. They probably result from the metabolism of adenosine by beta-cells. At a lower concentration (50 microM), adenosine caused a small and transient inhibition of glucose-induced electrical activity and insulin release. L-PIA (10 microM) slightly and transiently inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. When adenylate cyclase was stimulated by forskolin in the presence of 15 mM glucose, insulin release was strongly augmented. Under these conditions, L-PIA and adenosine (with nitrobenzylthioguanosine) caused a sustained inhibition. No such inhibition was observed when insulin release was potentiated by dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). These data are consistent with the existence of A1 purinergic receptors on mouse beta-cells. They could mainly serve to attenuate the amplification of insulin release brought about by agents acting via cAMP.

Adenosine↗
PubMed1989

Diabetes and impaired response of glucagon cells and vascular bed to adenosine in rat pancreas.

Previous studies have shown that adenosine, by activation of purinergic A2-receptors, stimulates glucagon secretion and increases vascular flow rate in isolated perfused pancreases from nondiabetic rats. Because alpha-cell function and blood flow control are known to be disturbed in diabetes, we investigated whether adenosine was still effective in streptozocin-induced diabetic (STZ-D) rats. Our experiments were performed on isolated perfused rat pancreases. Whereas, in normal rats, adenosine (1.65 microM) induced a 200% increase in glucagon output and a 25% rise in the pancreatic vascular flow rate, in rats diabetic for 5-6 wk, this nucleoside was ineffective on glucagon secretion, and its vasodilatory effect was strongly reduced. Long-term in vivo insulin treatment that reversed high glycemia levels was able to restore in large part both adenosine effects. In contrast, a short-term in vitro pretreatment with insulin was unable to restore the nucleoside effects. We conclude that STZ-D suppresses the stimulatory effect of adenosine on alpha-cells and strongly reduces its vasodilator properties; these abnormalities may be corrected in large part by long-term insulin treatment with normalization of glycemia.

Adenosine↗
PubMed1989

[Experimental study of Vicryl used as a filling material. Preliminary note].

The combination VICRYL and bone wax is studied as filling material in periodontal locations in dogs. Histological studies were carried out at one, two, six and nine months. Bone formation is already quite marked at two months, and total at six months. A desmodont and a secondary cement are formed. At six and nine month, reattachment is excellent.

Animals↗
PubMed1989

Flow cytometric analysis of DNA abnormalities in colorectal carcinomas.

We report a flow cytometric study on ploidy in 117 colorectal cancers. An aneuploid cell population was found in more than 70% of adenocarcinomas. Ploidy was found to be stage-related; aneuploid tumors with DNA index greater than or equal to 1.4 were found mainly in Dukes' C and Dukes' D stages (P less than 0.02). Tumors of the caecum and of the ascending colon were more often found to be diploid than those of the other sites. There was a progressive increase in the proportion of cells in S-phase depending on whether they were from normal tissue, inflammatory mucosa or adenocarcinomas. The proportion of cells in S-phase was significantly larger in aneuploid tumors (P less than 0.001). The data presented above suggest that aneuploidy and the proportion of non-resting cells could be important prognostic factors for colorectal cancers. The latter are independent of the stage of the disease and histological differentiation.

Adenocarcinoma↗
PubMed1988

Effects of 2-methylthio ATP on insulin secretion in the dog in vivo.

The effects of 2-methylthio ATP, an ATP analogue that is more specific for the P2Y receptor, were investigated on insulin secretion in the anesthetized dog in vivo. 2-Methylthio ATP was infused directly into the pancreaticoduodenal artery for 15 min. The infusion was performed so as to obtain a pancreaticoduodenal artery blood level of about 15 microM. 2-Methylthio ATP induced an immediate and significant stimulation of insulin secretion measured from the pancreaticoduodenal vein by means of a T-shaped catheter. After the infusion was stopped, the secretion of insulin progressively decreased and at 30 min was close to basal values. The stimulation of insulin secretion induced a transient but significant reduction of peripheral venous blood glucose levels.

Adenosine Triphosphate↗
PubMed1988

Cavernous hemangiomas of the spinal cord: MR imaging.

In three patients with histologically proved cavernous hemangiomas of the spinal cord, magnetic resonance (MR) imaging was superior to myelography, delayed computed tomography (CT) myelography, and contrast-enhanced CT in depicting the lesion. The presence of mixed subacute and chronic hemorrhage, suggested by mixed high- and low-signal-intensity components of these lesions on MR images, may be characteristic of this rare, intramedullary vascular malformation.

Adult↗
PubMed1988

Cavernous angiomas of the spinal cord.

Five cases of histologically verified cavernous angiomas of the spinal cord are reported. Acute lower-extremity sensory disturbance was the initial symptom in four patients, and one presented with weakness of the hand. Progressive neurological deficit occurred in all patients, but the clinical course and outcome were extremely variable. Myelography revealed an intramedullary lesion in two cases but was completely normal in three; magnetic resonance imaging was diagnostic in these patients. Subtotal removal was accomplished in two cases, and myelotomy and biopsy were carried out in three. Four of the cavernous angiomas were located in the cervicothoracic region, whereas one was found in the thoracolumbar cord. All of the patients exhibited characteristic gross and microscopic features as well as hemosiderin-laden macrophages indicating remote hemorrhage. The diagnostic, therapeutic, and prognostic implications of this rare condition are discussed.

Adult↗
PubMed1988

[Melanotic adenocarcinoma of the uterus. Neuroendocrine tumor of the uterus].

The case reported concerns a 76-year-old woman under treatment for a previously diagnosed "poorly differentiated endocervical adenocarcinoma". New biopsies revealed an adenocarcinomatous tumor with unexpected melanotic pigmentation. The patient underwent cesium therapy followed by colpohysterectomy with lymphadenectomy. As there were no metastases, external complementary radiotherapy was not used. Four months after surgery, a large recurrence was detected; surgical excision proved impossible but revealed a grossly pigmented tumor from which several samples were taken. The patient died 11 months after the first consultation. No autopsy was performed. Morphological study was done on the initial biopsy, on the uterine tumor and on the recurrent tumor, using histological, cytological, ultrastructural and immunohistochemical techniques. Flow cytometry and biochemical study were also carried out on the recurrent tumor. All the samples studied histologically revealed uniform tumor morphology showing a poorly differentiated adenocarcinoma with an irregular distribution of melanin pigmentation (Fontana +). Electron microscopy confirmed the epithelial nature of the tumor, showing differentiated apical poles with villosities, linked by desmosomes. Basement membranes were irregularly present. Electron microscopy also demonstrated the melanotic nature of the pigmentation with melanosomes and premelanosomes. A few membrane-bound neurosecretory granules were seen. Immunohistochemistry showed that the tumor contains no S 100 protein and that no staining was obtained with monoclonal antibodies against malignant melanoma. Hormonal secretion and chromogranin were not detected. Tumor cells contained neither GFAP nor neurofilaments. Positive staining was obtained for neuron specific enolase and synaptophysin. Tumor cells contained three types of intermediate filament proteins = Vimentin, cytokeratins and peripherin (peripherin is an intermediate filament protein identified in 1984 by Portier, of the college of France, who very kindly supplied the antiserum and was good enough to do most of the biochemical study. Peripherin is considered to be characteristic of the peripheral nervous system. This case is the first example of demonstration of peripherin in a tumor). The biochemical study gave the following results: Cytosol assays for estrogen and progesterone receptors were negative. Vimentin, cytokeratins and peripherin were demonstrated by a study carried out in the Collège de France. No GFAP was found. A study of the metabolism of melanin derivatives showed high levels of urinary dopamine, serum and cytosol L. dopa.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗