[The use of T650 in bony filling: experimental and clinical results].
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Biomedical subjects
Publications and source records attributed to G Bertrand.
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The case of a 17-year-young woman with Calcifying Fibrous Pseudotumor is reported. This observation emphasizes 1) A distinctive histologic appearance and the broad spectrum of this entity, 2) The differential diagnosis to consider, 3) The excellent prognostic and the low risk of local recurrence.
The effect of L-glutamate was studied on glucagon secretion from rat isolated pancreas perfused with 2.8 mM glucose. L-Glutamate (3.10(-5)-10(-4)M) induced an immediate, transient and concentration-dependent glucagon release. The three non-N-methyl-D-aspartate (NMDA) receptor agonists, kainate (3.10(-5)-3.10(-3)M), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) (3.10(-5)-10(-4)M) and quisqualate (3.10(-6)-10(-5)M), all elicited a peak-shaped glucagon response. Compared to glutamate, AMPA and quisqualate exhibited a similar efficacy, whereas kainate caused a 4-fold higher maximal glucagon response. In contrast, NMDA (10(-3)M) was ineffective. The selective antagonist of non-NMDA receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5.10(-5)M), totally prevented the glucagon response to 10(-4) M glutamate (IC50 congruent to 0.8 +/- 0.3 10(-6)M) and 3.10(-4)M kainate. Furthermore, quisqualate at a maximal effective concentration (3.10(-4)M) inhibited the response to kainate (10(-3)M). This study showed that L-glutamate stimulates glucagon release in rat pancreas by activating a receptor of the AMPA subtype.
1. In vivo effect of a P2y-purinoceptor agonist, adenosine-5'-O-(2-thiodiphosphate) (ADP beta S), on insulin secretion and glycaemia were studied both in rats and dogs. 2. In anaesthetized rats, i.v. administered ADP beta S (0.2 mg kg-1) produced an insulin response dependent on the nutritional state of the animals, since we observed only a transient increase in overnight-fasted rats and a sustained insulin secretion followed by a reduction in plasma glucose levels in fed rats. During an i.v. glucose tolerance test, ADP beta S enhanced insulin release and thus increased the glucose disappearance rate. 3. In anaesthetized fasted dogs, i.v. administered ADP beta S (0.1 mg kg-1) increased pancreaticoduodenal insulin output and slightly decreased blood glucose levels. 4. In conscious fasted dogs, orally administered ADP beta S (0.1 mg kg-1) transiently increased insulinemia and punctually reduced glycaemia. Furthermore, during an oral glucose tolerance test, orally administered ADP beta S at the same dose markedly enhanced insulin secretion and consequently reduced the hyperglycaemia. 5. In conclusion, the P2y-agonist, ADP beta S, is a potent insulin secretagogue in vivo, improves glucose tolerance and is effective after oral administration. Thus, the P2y-purinoceptors of the beta cell may be a target for new antidiabetic drugs.
A possible implication of endogenously released ATP and (or) ADP in insulin response to glucose stimulation was investigated in the isolated rat pancreas. The first phase of insulin response to the same glucose concentration (8.3 mM) was much higher in pancreas previously perfused in the absence of glucose than in pancreas previously perfused with 4.2 mM glucose. A P2 purinoceptor antagonist, 2,2'-pyridylisatogen tosylate, strongly reduced the higher first phase resulting from glucose deprivation; similarly, it reduced exogenous ATP-potentiated insulin response to a glucose increase from 4.2 to 8.3 mM. In contrast, 2,2'-pyridylisatogen tosylate did not modify the first phase of insulin response to 8.3 or 12.5 mM glucose in pancreas previously perfused with 4.2 mM glucose. Our results suggest that endogenous ATP and (or) ADP released in pancreatic islets in the absence of glucose could activate P2 purinoceptors and increase the magnitude of the first phase of insulin response to a glucose stimulation.
Neurosurgeons are well known for being productive researchers and innovators. Few, however, have possessed the prolific ingenuity of William Cone. In 1934, he and William Penfield were cofounders of the Montreal Neurological Institute where, until 1959, he filled the twin roles of neurosurgeon-in-chief and neuropathologist. Because he did not find writing easy, many of his technical inventions and refinements remained unpublished. His numerous innovations included the extensive use of twist-drill technique for biopsy, drainage for subdural hematoma and cerebral abscess, and ventriculography. In the mid-1940's, he developed power tools driven by nitrogen that led to the modern, universally used air-driven tool systems. He had a special interest in the treatment of spinal dysfunction, for which he invented the Cone-Barton skull-traction tongs along with the Cone spinal operating table. He also devised operative procedures for vertebral fracture-dislocation and craniospinal anomalies. For the maintenance of muscle tone in the paralyzed bladder, he constructed a tidal drainage system. He introduced and popularized ventriculoperitoneal shunting techniques and carried out some of the earliest experimental trails to treat brain infections with sulphonamide and antibiotic drugs. He designed his own set of surgical suction devices, bone rongeurs, and a personal suction "air-conditioning" system for each surgeon. He had a keen early interest in intracranial tumors, and also demonstrated on monkeys how subdural mass lesions caused pupillary dilation and mesial temporal lobe damage due to cerebral compression. His work for the military during World War II on effects of altitude on brain pressure remained classified for many years. The first clipping and excision of an intracranial aneurysm is attributed to Cone. Although Penfield was known as "the Chief," Cone was referred to as "the Boss." His fervent dedication to provide total care to his patients was expressed in round-the-clock vigils; he did not separate "nursing" from "surgical" care. Ultimately, Cone's driving passion for perfection led in part to his tragic death. His accomplishments, inventions, and his example as teacher and physician have become part of neurosurgery's collective legacy.
A case of deep seated lomboaortic lymph node enlargement, due to a storage hitiocytosis by fragments of polyethylene, draining the site of hip joint prosthesis is reported. These lymph node enlargement, made visible by tomodensitometry, were satellites of an ovarian adenocarcinoma. The artificial hip joint operation had taken place 17 years before and 10 years later the patient underwent a secondary operation to replace the prosthesis of the right hip. To the knowledge of the authors this is the first recorded case of lymph node enlargement due to a storage histiocytosis in response to debris shed from hip prosthesis being made visible by way of a radiological examination.
This article is a transcription of several papers on neuroendocrine cancers of the prostate presented to the Uropathology Club in Angers in 1990. It consists of three parts: Firstly, a study of neuroendocrine cells in various organs of the human body, followed by the demonstration of these cells in the normal and pathological prostate. The second part reports 3 cases of neuroendocrine cancers as they are observed in routine practice. A total of 66 cases of pure neuroendocrine cancers have been reported to date in the English language literature. This type of cancer is characterised by a rapid, hormone-resistant course with the development of multiple metastases, frequently visceral. Periods of remission in response to chemotherapy may be observed in some cases. The third part concerns the systematic demonstration of neuroendocrine cells in prostatic adenocarcinoma. The percentage of neuroendocrine cells demonstrated by various histological techniques is directly correlated to an increasingly severe prognosis of the cancer.
The effect of cibenzoline succinate, a new antiarrhythmic agent, was studied on insulin secretion in rats. Experiments were performed both in vivo and in vitro using two preparations: the isolated perfused pancreas and isolated islets. In anaesthetized rats, cibenzoline was able to increase plasma insulin levels and to reduce glycaemia. These effects were observed at 1 mg/kg i.v. in fed rats and at 3 mg/kg i.v. in fasted rats. In the isolated pancreas perfused in the presence of a slightly stimulating glucose concentration (8.3 mM), cibenzoline (2 and 6 microM) elicited a progressive and sustained insulin response in a concentration-dependent manner. In the presence of a non-stimulating glucose concentration (4.2 mM), cibenzoline was ineffective at 2 microM and slightly increased basal insulin release at 6 microM. In isolated islets incubated with 8.3 mM glucose, cibenzoline (6 and 20 microM) caused a concentration-dependent stimulation of insulin release. It is concluded that cibenzoline stimulates insulin secretion by a direct action on pancreatic B cells in rats.
Peptide YY (PYY) has been shown to inhibit stimulated insulin secretion under in vivo conditions in the mouse, the rat, and the dog. In the present study, we investigated the effects of PYY on insulin secretion from the isolated perfused rat pancreas and isolated rat islets. In isolated pancreas perfused in presence of 8.3 mM glucose, PYY at 10(-10) and 10(-9) M, but not at 10(-8) M, inhibited insulin secretion. In the presence of 5.5 mM glucose, PYY (10(-9) M) did not modify basal insulin release but reduced the biphasic insulin response to arginine (10 mM). PYY also markedly reduced the pancreatic vascular flow rate; this effect was observed at all three concentrations tested in a dose-dependent manner. In isolated islets, glucose (15 mM)-stimulated insulin secretion was inhibited by PYY at 10(-7) M. We conclude that in the perfused rat pancreas, PYY inhibits insulin secretion and induces vasoconstriction without a causal relationship. In addition, our results on isolated islets suggest that the inhibitory action of PYY on insulin secretion is exerted through a direct islet action.
1. The effect of L-glutamate has been studied on insulin secretion by the isolated perfused pancreas of the rat. The glutamate receptor subtype involved has been characterized. 2. In the presence of a slightly stimulating glucose concentration (8.3 mM), L-glutamate (5 x 10(-5)-4 x 10(-3) M) induced an immediate, transient and concentration-dependent insulin response. On the other hand, in the presence of a non stimulating glucose concentration (2.8 mM), L-glutamate (10(-3) M) did not modify the basal insulin secretion. 3. The three non-NMDA receptor agonists, kainate (10(-4)-10(-3) M), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, 5 x 10(-5)-10(-4) M) and quisqualate (5 x 10(-6)-5 x 10(-5) M) all provoked a transient and concentration-dependent insulin response from pancreas perfused with 8.3 mM glucose. Compared with glutamate, kainate exhibited a similar efficacy, whereas AMPA and quisqualate elicited only a 3 fold lower maximal insulin response. In contrast, NMDA (10(-4)-10(-3) M) was ineffective. 4. An antagonist of non-NMDA receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5 x 10(-5) M) totally prevented the stimulatory effect of L-glutamate (4 x 10(-4) M) and kainate (2 x 10(-4) M). In contrast, the NMDA receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine ((+) MK801) was without effect. 5. The insulin secretory effect of glutamate (4 x 10(-4) M) was not affected by atropine (3 x 10(-7) M) or tetrodotoxin (3 x 10(-6) M). 6. Quisqualate at a high maximally effective concentration (4 x 10(-4) M) inhibited glutamate (10(-3) M) or kainate (4 x 10(-4) M)-induced insulin release. 7. This study shows that L-glutamate stimulates insulin secretion in rat pancreas, by acting on an excitatory amino acid receptor of the AMPA subtype.
Spontaneous spinal epidural hematomas are well-recognized but rare entities. The standard treatment for these hematomas has been prompt surgical evacuation. The authors report a case of a 76-year-old man who precipitously became paraplegic secondary to a spontaneous spinal epidural hematoma and then experienced the complete resolution of his neurological deficit and the hematoma. We conclude that conservative (nonoperative) management of spontaneous spinal epidural hematomas may be appropriate in those instances in which there is early and sustained neurological recovery confirmed by radiological resolution of the lesion.
The terminology for abnormalities of the lumbar disk has always been a source of confusion. Recent advances in pathological studies have inspired the authors to propose a simple classification of common disk anomalies suitable not only for diagnostic radiologists but also for referring clinicians. Although the diagnosis of a few pathological entities will only be possible with specific imaging techniques, the proposed classification is appropriate for reporting observations from plain films, conventional tomograms, myelograms, discograms, computed tomography scans and magnetic resonance images. All lumbar disks can thus be classified into one or more of the following categories: normal, aging, scarred, ruptured and herniated. A disk herniation is defined as a localized exit of disk material beyond the limits of the original intervertebral space.
The authors report a case of renal collecting duct carcinoma or Bellini duct carcinoma. This rare variety of renal carcinoma, which usually has a poor prognosis, is situated in the renal medulla and pyramid. It is composed of large cells similar to collecting duct cells and can be seen at a distance from the tumor. These cells are arranged in highly suggestive tubular, microcystic and papillary structures. These morphological data are compared with those reported in the literature.
1. The effects of a P2 purinoceptor agonist, adenosine 5'-O-(2-thiodiphosphate) (ADP-beta-S) have been studied on insulin secretion and flow rate of the isolated perfused pancreas of the rat. 2. In the presence of a moderately stimulating glucose concentration (8.3 mM), ADP-beta-S (4.95-495 nM) evoked a biphasic insulin response in a concentration-dependent manner. A comparison of relative potency between ADP-beta-S and adenosine 5'-triphosphate (ATP) showed that ADP-beta-S was 100 times more potent than ATP. On the other hand, in the presence of a non stimulatory glucose concentration (4.2 mM), ADP-beta-S (165 nM) did not modify the basal insulin secretion. 3. ADP-beta-S, at concentrations effective on insulin secretion and also at higher concentrations (1.65 and 16.5 microM), provoked an increase of the pancreatic flow rate in a concentration-dependent manner. 4. Our results show that ADP-beta-S is a potent insulin secretory P2 purinoceptor agonist. As it is resistant to hydrolysis it might be useful in studying the effect of activation of the P2 purinoceptor of beta cells on insulin secretion in vivo.
The present study was aimed at localizing gamma-aminobutyric acid (GABA) and its enzyme of synthesis, glutamic acid decarboxylase (GAD), in the mouse pancreas by immunocytochemical methods. The influence of GABA on hormone release was also studied with normal mouse and rat islets and the isolated perfused rat pancreas. Particular attention was paid to glucagon release to test a recent hypothesis suggesting that GABA mediates the still unexplained glucose-induced inhibition of glucagon release. GABA and GAD were identified only in islet cells and never in the exocrine tissue. Exogenous GABA, baclofen (agonist of GABAB receptors), muscimol (agonist of GABAA receptors), or bicuculline (antagonist of GABAA receptors) did not affect insulin and somatostatin release by isolated mouse or rat islets. GABA was also without effect on glucose-induced electrical activity in mouse B-cells. Glucagon secretion by mouse islets was only slightly inhibited (approximately 20%) by GABA. Since muscimol had a similar effect, and baclofen was ineffective, the inhibition by GABA probably involves GABAA receptor activation. Bicuculline, however, did not antagonize the inhibitory effects of GABA and muscimol, probably because the antagonist alone also decreased glucagon secretion. In contrast to GABA, low (3 mM) and high (20 mM) concentrations of glucose strongly inhibited (approximately 50-65%) glucagon release; this inhibition was not prevented by bicuculline. Similar results were obtained with the perfused rat pancreas; muscimol slightly inhibited glucagon release under various conditions, and bicuculline did not reverse the strong inhibition produced by 16.7 mM glucose. In conclusion, GABA does not affect insulin and somatostatin secretion, but inhibits A-cells, probably by acting on GABAA receptors. It is unlikely, however, that this small inhibitory effect can account for the inhibition of glucagon release produced by glucose.
The terminology for abnormalities of the lumbar disk has always been a source of confusion. Recent advances in pathological studies have inspired the authors to propose a simple classification of common disk anomalies suitable not only for diagnostic radiologists but also for referring clinicians. Although the diagnosis of a few pathological entities will only be possible with specific imaging techniques, the proposed classification is appropriate for reporting observations from plain films, conventional tomograms, myelograms, diskograms, computed tomography scans and magnetic resonance images. All lumbar disks can thus be classified into one or more of the following categories: normal, aging, scarred, ruptured and herniated. A disk herniation is defined as a localized exit of disk material beyond the limits of the original intervertebral space.
The effects of ATP and ADP structural analogues (2-methylthio ATP; alpha,beta-methylene ADP) on somatostatin secretion were tested in dogs. Insulin and glucagon secretion was also evaluated. Our experiments were performed in vivo and in vitro. In vivo, 2-methylthio ATP was infused directly into the pancreaticoduodenal artery of anesthetized dogs and blood was sampled from the pancreaticoduodenal vein. This ATP analogue (approximately 15 microM) immediately induced stimulation of both somatostatin and insulin secretion, which was accompanied by a slight reduction of glycemia. A delayed increase in glucagon output was observed. In vitro, using the isolated perfused dog pancreas uncinate process, alpha,beta-methylene ADP, a stable ADP analogue (16.5 microM), was infused in the presence of a substimulating glucose concentration (4.2 mM). Under these conditions, alpha,beta-methylene ADP immediately induced the stimulation of somatostatin secretion without affecting basal insulin and glucagon secretion. In conclusion our results suggest the presence of P2 purinoceptors on pancreatic somatostatin secreting cells.