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R Gomis

Publications and source records attributed to R Gomis.

At least 127 records · Page 7Linked to original sources
PubMed1994

[Kienboeck disease: treatment by shortening osteotomy of the radius].

INTRODUCTION: A series of twenty eight cases of Kienbock's disease treated by a shortening osteotomy of the radius are reported. MATERIAL AND METHODS: The series consisted of sixteen male and twelve female patients with an average age of twenty-five and followed for an average of five years. Seventeen patients were manual workers. The dominant side was affected in twenty cases; there were no bilateral cases. The clinical grades before surgery were one case in stage I, ten stage II, thirteen stage III, and four stage IV, using the Decoulx classification. The preoperative distal radio ulnar index was greater than 0 in only one case. Average radial shortening was three millimeters. The osteotomy was stabilized by using dynamic compression plates in fourteen cases, pinning in twelve cases, and staples in two cases. RESULTS: In all the cases, the results on pain relief and muscular strength were satisfactory. During preoperative review, pain was a major complaint in seventeen cases, moderate in nine cases, and slight in two cases. Joint range of motion (ROM) was, in seven cases, greater than seventy-five percent when compared to the opposite hand; in fourteen cases greater than fifty percent; less than fifty percent in five cases and less than twenty-five percent in two cases. Muscular strength, measured by J.A.M.A.R. test, was decreased in six cases by seventy-five percent when compared with the healthy side; in nineteen cases decreased by fifty percent and in three cases decreased by twenty-five percent. On the post-operative review, pain was decreased in all cases: twenty patients were pain free, seven felt slight pain during forced movements. Only one patient showed no improvement: he had a work related injury, with reflex dystrophy. A twelve percent increase in postoperative ROM was noted. Muscular strength improved by an average of forty one percent: 8 cases recovered normal strength, fifteen cases improved strength to seventy-five percent, and five cases improved to fifty percent. The overall clinical result did not seem to depend on the age of the patient or the preoperative radiological stage. They were evaluated using the criteria described by Michon. We obtained fourteen excellent results, ten good, four average. Twenty-five patients have been able to their previous job, three changed jobs. For the preoperative radiological assessment, we followed the Decoulx and the Lichtman scales and considered the distal radio ulnar index, the radial slope, the Linscheid lunate bone dimple incline and the Young and Mac Murtry measurement of the carpal collapse. Radiological assessment showed lunate bone remodeling in the ten cases rated stade II. Nine out of the thirteen patients rated stade III improved: two of them were rated stade II and seven cases presented an improvement of the radiological aspect. Four cases worsened. DISCUSSION: There was no parallel between the radiological evolution of the lunate bone and clinical results. Furthermore, radiological assessment did not show any true relationship between changes in the distal radio ulnar index and radiological evolution. The post-operative distal radio ulnar index was zero in eight cases, greater than one in fourteen cases and greater than two in six cases. Only the obliquity of the radial dimple opposite to the lunate bone is related with the radiological evolution. In the nine cases of stage III that have improved, the radial dimple slope was increased. The four cases of stage III that worsened, it was decreased. CONCLUSION: A shortening osteotomy of the radius is a satisfactory procedure independently of whatever the disease's age, the lunate bone radiological stage and the distal radio ulnar index. The only factor we think capable of modifying the radiological result of necrotic evolution is the lunate bone slope. It appears necessary, during the osteotomy, to increase this slope in order to reduce local pressure.

Adolescent↗
PubMed1994

Impaired function of pancreatic islets from rats with portal hypertension resulting from cirrhosis and partial portal vein ligation.

Increased circulating insulin and glucagon levels are a common observation in patients with cirrhosis, as well as in portal hypertensive models. Hyperinsulinemia and hyperglucagonemia may be caused either by increased beta- and alpha-cell secretion or by defective hepatic clearance of these hormones. To elucidate whether an abnormal endocrine pancreatic function might contribute to the hyperinsulinism or to the hyperglucagonism observed in chronic portal hypertension, insulin and glucagon secretion were measured in vitro in isolated pancreatic islets from rats with partial portal vein ligated and rats with cirrhosis caused by carbon tetrachloride poisoning. Both rats with partial portal vein ligation and rats with cirrhosis caused by carbon tetrachloride poisoning exhibited hyperinsulinism and hyperglucagonism as compared with control rats. Isolated pancreatic islets from both experimental portal hypertensive models showed an impaired insulin secretion after glucose stimulation. On the contrary, glucagon secretion was significantly increased, and there was a markedly enhanced response to arginine. This increased in vitro glucagon production could not be corrected, even in the presence of high glucose concentrations in the incubation medium. Therefore our data show that although hyperglucagonism in rats with partial portal vein ligation and in rats with cirrhosis caused by carbon tetrachloride poisoning is promoted by an enhanced alpha-cell secretion, hyperinsulinism is associated with impaired beta-cell secretion.

Animals↗
PubMed1993

Human pancreatic islet function at the onset of type 1 (insulin-dependent) diabetes mellitus.

Viable human pancreatic islets isolated from a recent-onset Type 1 (insulin-dependent) diabetic patient were used to perform in vitro studies. Pre-proinsulin mRNA and insulin content, as well as insulin response were analysed. Insulin response to glucose and forskolin was completely absent in diabetic islets, as compared to control islets. Insulin content was reduced to only one-third of control values (395.0 +/- 3.5 vs 989.0 +/- 46.3 microU/islet) and 20.7 +/- 3.9% of islets from the diabetic pancreas contained insulin-positive cells in immunofluorescence studies. Northern blot analysis revealed a severe reduction in the content of pre-proinsulin mRNA in diabetic pancreatic tissue. Our results indicate that although markedly decreased, beta cells in human pancreatic islets at the onset of Type 1 diabetes are still present. Nevertheless, pancreatic islet function is disproportionately impaired with a complete absence of an insulin response.

Adolescent↗
PubMed1993

Effects of a short prednisone regime at clinical onset of type 1 diabetes.

The effect of corticosteroids on beta cell function and humoral immune response in type 1 diabetes was tested in a 2-month trial conducted on 32 newly diagnosed patients (age 22.8 +/- 1.4 years, mean +/- S.E.M.). Prednisone was administered at immunosuppressive dosage (1 mg.kg-1.day-1) during the initial 10 days and at a maintenance dosage (0.3 mg.kg-1.day-1) for 50 days. Patients (n = 32) were enrolled within 6 weeks after diagnosis and matched in pairs for age, sex, presence of islet cell antibodies (ICA) and glucagon stimulated C-peptide levels. Insulin discontinuation was not contemplated. All the patients who received prednisone became ICA during treatment but in some (4 out of 10) this effect was only transient. Insulin antibodies (IA) were significantly lower in the prednisone group at second and third month (P < 0.05). No patient experienced complete remission but in 10 prednisone and 4 control patients the insulin requirements were below 0.3 IU/kg (P < 0.05). With similar glycemia the fasting C-peptide levels were higher in the treated patients. The profile of the insulin requirements during the follow-up was different in the two groups and at 9 months the prednisone group needed less insulin than the control (P < 0.05). Interestingly, within the prednisone-treated group and after 6 months, the levels of stimulated C-peptide improved significantly among the ICA+ patients while they were steady or declined in ICA- (P < 0.01). The analysis of variance covariance confirmed a positive interaction between ICA and the administration of prednisone on the outcome of beta cell function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Effects of isradipine and nifedipine retard in hypertensive patients with type II diabetes mellitus.

Twenty patients were randomized to receive either 2.5 mg isradipine twice daily or 20 mg nifedipine retard once daily for 6 months. After 2 weeks of placebo wash-out, evaluations were carried out every 4 weeks. These evaluations included assessment of blood pressure, lipid profile, hemoglobin A1 sigma glucagon, C peptide, and insulin requirements. Both isradipine and nifedipine retard lowered systolic and diastolic blood pressures to normal values (P < .001). However, isradipine was accompanied by a decrease in heart rate (P < .005). Neither drug modified hemoglobin A1c or the glycemic profile. The endogenous insulin-secretion response decreased in both treatment groups (P < .05). In conclusion, isradipine and nifedipine retard are efficacious in the treatment of hypertension in patients with type II diabetes mellitus, and neither treatment produces modification of metabolic control.

Blood Glucose↗
PubMed1993

Regulation of islet amyloid polypeptide in human pancreatic islets.

This study investigated the effect of glucose on islet amyloid polypeptide secretion, content, and mRNA synthesis of human pancreatic islets. The release of islet amyloid polypeptide from fresh isolated islets in response to glucose was parallel to that of insulin. The islet amyloid polypeptide-to-insulin molar ratios in response to 5.5 and 16.7 mM glucose were 1:16 and 1:15 respectively. Islets were cultured for 1 and 7 days at two different glucose concentrations (5.5 and 16.7 mM). The islet amyloid polypeptide response to the 1-day culture was similar to that of the fresh islets; however, after the 7-day culture the islet amyloid polypeptide and insulin secretory responses to glucose were dissociated. The insulin response of islets to a high-glucose stimulus was significantly (P < 0.001) increased, whereas the islet amyloid polypeptide response of islets to the same stimulus was blunted. The IAPP content was greater than insulin content in a molar ratio (1:50 to 1:30) after long exposure of islets to concentrations of high glucose even though the increase was significant for both peptides (P < 0.005). Northern blot analysis of each cultured condition showed an increase of both mRNA IAPP and insulin signals after exposure of islets at 16.7 mM glucose, the maximum mRNA expression being after long exposure to high-glucose concentrations. Quantification of both signals by densitometry showed a greater increase for islet amyloid polypeptide than for insulin. These findings suggest that IAPP can be accumulated in beta-cells after long exposure of human islets to high-glucose concentrations, because glucose increases IAPP synthesis but not secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1993

Signals derived from glucose metabolism are required for glucose regulation of pancreatic islet GLUT2 mRNA and protein.

Pancreatic islet GLUT2 mRNA is known to be regulated in vitro and in vivo by glucose. We have investigated several potential mechanisms mediating the response of islet GLUT2 to glucose. GLUT2 mRNA and protein were measured from isolated rat islets cultured for up to 24 h under selected conditions. Glucose at 11 mM stimulated GLUT2 mRNA 10-fold compared with 2 mM glucose, with no additional increase at 16.7 mM glucose, whereas maximal 4-fold induction of the protein was attained with 16 mM glucose. Time course studies showed a 2.5-fold induction of GLUT2 mRNA apparent after only 8 h of culture at 16.7 mM glucose. Glycolysis inhibitor mannoheptulose suppressed the stimulatory effect of 16.7 mM glucose on GLUT2 mRNA and protein. Metabolizable sugars mannose and glyceraldehyde enhanced transporter mRNA levels, in contrast with the lack of stimulation by nonmetabolizable 2-deoxy-D-glucose. Stimulation by different sugars and glycolysis inhibition led to analogous changes of proinsulin mRNA, suggesting that common signaling mechanisms are shared in glucose regulation of proinsulin and GLUT2 gene expression. Preexposure to mannoheptulose, however, failed to suppress glucose-stimulated insulin release. Tunicamycin, a glycoprotein synthesis inhibitor, did not block the effect of 16 mM glucose on GLUT2 mRNA levels. RNA and protein synthesis inhibitors actinomycin and cycloheximide abolished the enhancing effects of high glucose on GLUT2 mRNA. These findings indicate that glucose metabolism, but not glycoprotein synthesis or substrate interaction with the transporter protein, is instrumental in the stimulatory effects of glucose on beta-cell GLUT2 mRNA accumulation. In addition, ongoing RNA and protein synthesis are required for this effect.

Animals↗
PubMed1993

Effect of hyperlipacidemia on plasma C-peptide concentration during euglycemic hyperinsulinemic clamp.

During constant infusion of exogenous human insulin and glucose to healthy volunteers, a rise in glycemia was still able to stimulate the B-cell as judged from the increase in C-peptide plasma concentration. Nevertheless, under euglycemic conditions, the C-peptide concentration fell well below its initial level. This coincided, however, with severe hypolipacidemia. When the latter phenomenon was corrected through the simultaneous administration of exogenous triglycerides and heparin, a reascension in C-peptide plasma concentration was observed despite persistent hyperinsulinemia. It is proposed, therefore, that the hyperinsulinemic-euglycemic clamp procedure does not represent a reliable approach to explore the possible feedback action of insulin upon its own secretion rate, because of the interference upon B-cell secretory activity of factors such as changes in lipacidemia.

Adult↗
PubMed1992

Analysis of islet cell antibodies reactivity to a human islet cell line.

A human pancreatic beta cell line (HP62) was tested for reactivity with islet cell antibodies (ICA) as compared with previously-established methods. Using indirect immunofluorescence test, we found that HP62 cell line failed to react in a specific way with ICA from type 1 (insulin-dependent) diabetic patients since sera from normal controls showed a reactivity similar to that found in the patients. So, the usefulness of this human beta cell line as a tool of immunological purpose is questioned when indirect immunofluorescence procedures are used.

Autoantibodies↗
PubMed1992

Symptomatic and hormonal hypoglycaemic responses to human and porcine insulin in patients with type I diabetes mellitus.

In recent years there has been great concern that human insulin (HI) may induce fewer hypoglycaemic warning symptoms than porcine insulin (PI). We addressed this issue in eight patients aged 25.6 +/- 3.3 (SEM) years with Type I (insulin-dependent) diabetes mellitus of 15.1 +/- 3.7 years duration who complained that hypoglycaemia unawareness had appeared after transferring from PI to HI. Acute induction of hypoglycaemia was induced on two occasions with semisynthetic HI and purified PI under double-blind conditions. Blood glucose was first clamped for 2 h at 4.4-6.7 mmol l-1 with an intravenous infusion of HI or PI at 50 mU kg-1 h-1 and 20% glucose at a variable rate. Thereafter, insulin infusion alone was maintained for 100 minutes. Heart rate, arterial pressure, reflex times, autonomic and neuroglycopenic signs and symptoms were assessed every 10 min. Arterialized venous blood samples were taken to measure blood glucose every 10 min and catecholamines, insulin, glucagon, growth hormone, and cortisol every 20 min. Autonomic symptoms first appeared at a plasma glucose level of 2.92 +/- 0.21 mmol l-1 with HI vs 2.92 +/- 0.48 mmol l-1 with PI (NS). There were no significant differences between the two studies concerning any of the above mentioned clinical parameters or the counterregulatory hormone responses. A differential effect of insulin species on the ability to perceive hypoglycaemia in patients who ascribed diminished perception of hypoglycaemia to the use of HI was thus not observed.

Adult↗
PubMed1992

Reevaluation of autoantibodies to islet cell membrane in IDDM. Failure to detect islet cell surface antibodies using human islet cells as substrate.

Since their demonstration in 1975, ICSAs have been proposed as serological markers and pathogenic elements in IDDM. ICSAs are detected in the sera of most newly diagnosed IDDM patients by indirect IFL that uses viable preparations of rat islet or insulinoma cells as substrate, but they also can be detected by using human insulinoma or fetal islet cells. We have tried to demonstrate ICSAs in the sera of 31 newly diagnosed diabetic patients, including 6 positive samples on human fetal islet cells, which used their natural target for the first time: normal human islet cells. In spite of using different types of preparations of these cells (i.e., freshly dispersed cell suspensions, monolayer cultures, or dispersed islets after culture), ICSAs could not be detected by IFL under the UV microscope, nor by flow cytometry. In contrast, 9 of 29 of the sera gave a positive staining on the RIN rat insulinoma cells. In an attempt to establish whether the putative ICSA autoantigen is present in the surface of human islet cells in the diabetic pancreas, the insulitis microenvironment was emulated by exposing the islets to three types of stress: 1) cytokines (IFN-gamma and TNF-alpha); 2) heat shock; and 3) hyperglycemia. However, diabetic sera failed again to recognize membrane antigens on the islet cells after either of these treatments. Neither were islet cells from a newly diagnosed diabetic patient stained by its autologous serum (ICA titer > 80 JDF U). These results suggest that ICSA autoantigen is not expressed in the membrane of human islet cells and therefore raises doubts about their proposed pathogenic role.

Adolescent↗
PubMed1991

Metabolic and secretory response of parotid cells to cationic amino acids. Uptake and catabolism of L-arginine and L-ornithine.

L-Arginine and L-ornithine, which stimulate amylase release, are taken up by rat parotid cells. L-Arginine is converted, in an NADPH-dependent manner and to a limited extent to L-citrulline in parotid cell homogenates, despite the absence of ornithine transcarbamylase activity. L-Arginine is largely converted to urea and L-ornithine. The generation of putrescine and polyamines from L-ornithine occurs at a very low rate, relative to the cell content in performed amines. The major fate of exogenous or arginine-derived ornithine consists in its conversion to L-glutamate, which is then further metabolized. These findings raise several hypotheses for the secretory response of the parotid cells to cationic amino acids, including their accumulation as positively charged molecules inside the cell and the generation of either NO, amines, substrates for a transglutaminase-catalyzed reaction, or ATP through oxidative catabolism. However, each of these hypotheses meets with objections, the modality for the stimulation of amylase release by cationic amino acids being eventually considered as an unsettled matter.

Amylases↗
PubMed1991

Effects of single dose irradiation on pancreatic beta-cell function.

We have irradiated abdominal cavity of 23 rats with 10 Gy irradiation-induced hypoglycemia on the fourth day after intervention. Islets collected at this time showed an impaired insulin secretion without affecting insulin content. This impairment persisted after one month follow-up with reduced number of beta-cells in morphological examination.

Abdomen↗