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E Robin

Publications and source records attributed to E Robin.

At least 19 recordsLinked to original sources

[Is entropy a monitor for the guidance of intraoperative analgesia?].

OBJECTIVE: Comparison between BIS (Bispectral Index) and state (SE) and response (RE) entropy during laparotomy for inflammatory bowel disease patients (IBD) and evaluation of the variations of RE and SE during nociceptive stimulation. STUDY DESIGN: Prospective, observational study. PATIENTS AND METHODS: Fourteen IBD's patients undergoing laparotomy were included. Anaesthesia aimed to maintain BIS between 40 and 60 by isoflurane and nitrous oxide. Analgesia was performed by sufentanil bolus administrated according to an increase of 20% of systolic blood pressure (SBP) and heart rate compared with the baseline values. BIS, RE and SE were measured at each nociceptive stimulation. A variance analysis (Anova) was used to assess BIS, RE and SE variations throughout surgery (p<0.05 as significant). Relationship between BIS, RE and SE was assessed by Pearson correlation (p<0.01 as significant). The ability for SE and RE to predict depth of anaesthesia and intraoperative analgesia was performed by calculating area under the receiver operated curves (AUC). RESULTS: BIS and entropy parameters had strictly the same evolution during anaesthesia. SBP increased significantly during nociceptive stimulation while no variation of RE was observed. A significant correlation was shown between BIS, RE and SE. The evaluation of anaesthesia depth was good for RE (AUC: 0.932+/-0.26) and SE (AUC: 0.926+/-0.27). There was however no difference between RE and SE to predict analgesic requirement. CONCLUSION: Because RE includes muscular frequency analysis, it does not allow analgesic requirement evaluation in paralyzed patients.

Adult↗

Non-invasive prediction of fluid responsiveness during major hepatic surgery.

BACKGROUND: The aim of this study was to evaluate potential predictors of fluid responsiveness obtained during major hepatic surgery. The predictors studied were invasive monitoring of intravascular pressures (radial and pulmonary artery catheter), including direct measurement of respiratory variation in arterial pulse pressure (PPVart), transoesophageal echocardiography (TOE), and non-invasive estimates of PPVart from the infrared photoplethysmography waveform from the Finapres (PPVfina) and the pulse oximetry waveform (PPVsat). METHODS: We conducted a prospective study of 54 fluid challenges (250 ml colloid) given for haemodynamic instability in eight patients undergoing hepatic resection. Fluid responsiveness was defined as an increase in stroke volume index (SVI) >or=10%. The following variables were recorded before each fluid challenge: right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), PPVart, PPVfina, PPVsat, and the TOE-derived variables left ventricular end-diastolic area index (LVEDAI), early/late (E/A) diastolic filling wave ratio, deceleration time of the E wave (MDT) of mitral flow and the systolic fraction of the pulmonary venous flow (SF). RESULTS: Only PPVfina, PPVart (both P<0.001), PPVsat (P=0.02), LVEDAI and MDT (both P=0.04) were different in responder vs non-responder fluid challenges. The areas under the receiver operating characteristic (ROC) curves were 0.81 (PPVfina), 0.79 (PPVart), 0.70 (LVEDAI), 0.68 (PPVsat and MDT), 0.63 (RAP), 0.62 (E/A), 0.55 (PAOP) and 0.42 (SF). The areas under the ROC curves for RAP, E/A, PAOP and SF were significantly less than that for PPVfina (P<0.05 in each case). Only PPVart (r=0.59, P=0.0001) and PPVfina (r=0.56, P=0.0001) correlated with the fluid challenge-induced changes in SVI. CONCLUSIONS: PPVart and PPVfina predict fluid responsiveness during major hepatic surgery. This suggests that intraoperative monitoring of fluid responsiveness may be implemented simply and non-invasively.

Aged↗

Predictive factors for rhabdomyolysis after bariatric surgery.

BACKGROUND: Prevalence of obesity is increasing internationally. Obesity is also incriminated in the development of postoperative rhabdomyolysis (RML). Its major risk is the development of renal failure which is associated with high mortality. The aim of this study was to determine the risk factors for RML in patients undergoing bariatric surgery. METHODS: Over a 12-month period, 49 consecutive patients were studied. They underwent gastric banding (n=32) or intestinal or gastric bypass (n=17) for morbid obesity (BMI >40 kg/m(2)). Surgery was performed in the supine position with a lumbar pad placed for intestinal shunt. The duration of surgery, persistent postoperative muscular pain, and pre- and postoperative creatine kinase (CK) were recorded. RML was defined as postoperative CK >1000 IU. L(-1) (5 times the normal value). Patients were retrospectively divided into 2 groups according to the presence or not of RML. In order to assess the role of BMI, it was decided to conduct an additional analysis in a group of consecutive non-obese patients who were matched for other risk characteristics. RESULTS: In the 49 patients included in the study 13 developed RML (26.5%). Surgery >4 hours, presence of diabetes and patient ASA physical status III or IV were identified as factors associated with higher risk of RML. In the matched group (9 patients), no one developed postoperative RML. CONCLUSIONS: After surgery for obesity, the risk of RML increases with prolonged surgery (>4 hours) and in diabetic obese patients with BMI >40 kg/m(2). In such patients, CK could be systematically measured to verify the presence of muscle injuries.

Adult↗

[Inhaled nitric oxide in the peroperative period and recovery].

OBJECTIVE: To analyse the current knowledge concerning use of inhaled NO (iNO) in anaesthesia and intensive care. DATA SOURCE: References were obtained from Medline, recent review articles, the library of the department and personal files. STUDY SELECTION: All categories of articles on this topic have been selected. DATA EXTRACTION: Articles have been analysed for history, biochemistry, pharmacology, toxicity and clinical use of iNO. DATA SYNTHESIS: Nitric oxide (NO) is a potent endothelium-dependent vasodilator. Because of its selective action on pulmonary circulation and the lack of effect on the systemic circulation due to its inactivation by haemoglobin, iNO has been presented as a new therapeutic agent in most diseases with pulmonary hypertension. During heart transplantation or surgical correction of congenital heart disease, iNO decreases pulmonary hypertension and improves altered right ventricular function. Studies included however small numbers of patients. Preliminary pharmacological studies demonstrated that iNO was able to decrease pulmonary hypertension and improve systemic oxygenation in adult respiratory distress syndrome. To date, none of the three multicentric studies performed was able to show any significant effect on duration of mechanical ventilation, morbidity or mortality. Finally, the sole demonstrated indication for iNO which remains is the persistent pulmonary hypertension of the newborn. Two multicentric studies have evidenced an improvement in systemic oxygenation and a reduced need for extracorporeal membrane oxygenation. In these two studies global mortality was however unchanged. CONCLUSION: Persistent pulmonary hypertension is the sole demonstrated indication for iNO. Inhaled nitric oxide may be efficient in pulmonary hypertension, right ventricular dysfunction and severe hypoxemia. Inhaled nitric oxide must be considered as a rescue therapy or needs to be part of research protocols.

Administration, Inhalation↗

Gastric tonometry.

Explore the source record for details and available documents.

Carbon Dioxide↗

[Patients with alcoholic liver disease hospitalized in gastroenterology. A national multicenter study].

OBJECTIVES: To describe the characteristics of in-patients with alcoholic liver disease in Hepatogastroenterology and to evaluate whether geographic location was a risk factor for cirrhosis. METHODS: A French, national, multicenter, prospective investigation was performed in the last quarter of 1997. To be included in the study, patients had to have drunk at least 50 g of alcohol per day for the past year or to have cirrhosis. RESULTS: Seventeen centers included 802 patients, 20% had histologically proven cirrhosis or probable cirrhosis. Thirty-five percent had undergone liver biopsy. Twenty five percent of these patients had cirrhosis without acute alcoholic hepatitis and 37% had cirrhosis with acute alcoholic hepatitis. After dividing France along a Bordeaux-Strasbourg axis, there was more histologically proven or probable cirrhosis in the North (46%) than in the South (36%) (P<0.005) while daily alcohol intake was greater the South (150 +/- 6 g) than in the North (129 +/- 4 g) (P<0.0001). When the six variables (age, sex, daily consumption of alcohol over the past 5 years, presence of hepatitis B surface antigen and antibodies to hepatitis C virus, total duration of alcohol abuse) were considered together in stepwise logistic regression analysis, geographic location changed the prediction of cirrhosis. The odds ratio for cirrhosis in patients living to the North of the Bordeaux-Strasbourg axis was 1.9 (95% confidence interval range 1.1-3.2) (P<0.02), suggesting the role of nutritional factors.

Age Distribution↗

Patients with myelodysplastic syndromes benefit from palliative therapy with amifostine, pentoxifylline, and ciprofloxacin with or without dexamethasone.

Thirty-five patients with myelodysplastic syndrome (MDS) were registered on protocol MDS 96-02 and were receiving continuous therapy with pentoxifylline 800 mg 3 times a day and ciprofloxacin 500 mg twice a day by mouth; dexamethasone was added to the regimen for the partial responders and the nonresponders after 12 weeks at a dose of 4 mg by mouth every morning for 4 weeks. Amifostine was administered intravenously 3 times a week at 3 dose levels (200 mg/M(2), 300 mg/M(2), and 400 mg/M(2)) to cohorts of 10 patients each. Therapy has been continued for 1 year in responders. Twenty-nine have completed at least 12 weeks of therapy and are available for response evaluation. Of the 21 men and 8 women (median age, 67 years), 20 had refractory anemia (RA), 3 had RA with ringed sideroblasts (RARS), 5 had RA with excess blasts (RAEB), and 1 had chronic myelomonocytic leukemia (CMMoL). Five had secondary MDS. No differences were noted in response rates among the 3 dose levels. Seven patients did not respond at all, and 22 showed an improvement in cytopenias (76%). Three had a triple lineage response, 10 had a double lineage response, and 9 had a single lineage response (8 of 9 in absolute neutrophil count [ANC] and 1 had more than a 50% reduction in packed red blood cell transfusions). Fifteen patients responded only after the addition of dexamethasone, whereas 7 responded before. When examined by lineage, 19 of 22 showed improved ANC, 11 of 22 demonstrated more than 50% reduction in blood transfusions, improved Hb levels, or both, and 7 of 22 showed improvement in platelet counts. Interestingly, the responses were frequently slow to appear, and continued improvement in counts was seen up to 12 months of therapy and beyond. This study supports the feasibility of treating patients with MDS with the unique approach of cytoprotection and anticytokine therapies as well as the principle that prolonged commitment to treatment is desirable when noncytotoxic agents are administered. (Blood. 2000;95:1580-1587)

Adult↗

Frequent loss of 1p32 region but no mutation of the p18 tumor suppressor gene in meningiomas.

After chromosome 22 and NF2 inactivation, the loss of chromosome 1p is one of the most frequent abnormalities encountered in meningiomas. However the putative tumor suppressor gene located on 1p inactivated in meningiomas has still to be identified. We screened 68 meningiomas for LOH on chromosome 22 and 1. We found 34 LOH on the NF2 region on chromosome 22 (50%) and 19 LOH on 1p (28%), 16 being associated with loss of chromosome 22. Partial deletions delimited a candidate region located between D1S234 and D1S2797. The p18INK4C tumor suppressor gene, a member of the genes family coding for inhibitors of cyclin-dependent kinases, is located in this region. To determine whether p18 is involved in development of meningiomas, we performed a mutation analysis of the p18 gene and a search for homozygous deletion in the 19 meningiomas with 1p loss. Sequencing analysis of the p18 gene revealed one polymorphism, but no somatic mutations and no homozygous deletions were found. These results confirm that the loss of chromosome 1p32 is a frequent feature in meningiomas, however the p18 tumor suppressor gene which is located in this region, does not seem to be involved.

Alleles↗

Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance.

A low dose (0.5 mg/kg) of lipopolysaccharide (LPS), administered 72 hours before 60-minute middle cerebral artery occlusion, induced a delayed neuroprotection proven by the significant decrease (-35%) of brain infarct volume in comparison with control, whereas infarct volumes remained unchanged in rats treated 12, 24, or 168 hours before ischemia. This delayed neuroprotective effect of LPS was induced only with low doses (0.25 to 1 mg/kg), whereas this effect disappeared with a higher dose (2 mg/kg). The delayed neuroprotection of LPS was induced in the cortical part of the infarcted zone, not in the subcortical part. The beneficial effect of LPS on consequences of middle cerebral artery occlusion was suppressed by dexamethasone (3 mg/kg) and indomethacin (3 mg/ kg) administered 1 hour before LPS, whereas both drugs had no direct effect on infarct volume by themselves, suggesting that activation of inflammatory pathway is involved in the development of LPS-induced brain ischemic tolerance. Preadministration of cycloheximide, an inhibitor of protein synthesis, also blocked LPS-induced brain ischemic tolerance suggesting that a protein synthesis is also necessary as a mediating mechanism. Superoxide dismutase (SOD) could be one of the synthesized proteins because lipopolysaccharide increased SOD brain activity 72 hours, but not 12 hours, after its administration, which paralleled the development of brain ischemic tolerance. In contrast, catalase brain activity remained unchanged after LPS administration. The LPS-induced delayed increase in SOD brain content was suppressed by a previous administration of indomethacin. These data suggest that the delayed neuroprotective effect of low doses of LPS is mediated by an increased synthesis of brain SOD that could be triggered by activation of inflammatory pathway.

Adaptation, Physiological↗

Effect of L-arginine on endothelial injury and hemostasis in rabbit endotoxin shock.

To investigate whether impaired endothelial function was related to alteration of nitric oxide (NO) formation during endotoxic shock, we studied the effects of supplementation of L-arginine (L-Arg), D-arginine (D-Arg), and N(G)-nitro-L-arginine methyl ester (L-NAME), on endothelial function and structure in a rabbit model. Endotoxic shock was induced by a single lipopolysaccharide bolus (0.5 mg/kg i.v., Escherichia coli endotoxin). Coagulation factors and expression of monocyte tissue factor were determined by functional assays. Endothelium-dependent vascular relaxation was assessed by in vitro vascular reactivity. Immunohistochemical staining (CD31) was performed to assess damaged endothelial cell surface of the abdominal aorta. These parameters were studied 5 days after the onset of endotoxic shock and were compared under three conditions: in absence of treatment, with L-Arg or D-Arg supplementation, or with L-NAME. Both L-Arg and D-Arg significantly improved endothelium-dependent relaxation and endothelial morphological injury. L-NAME did not alter endothelial histological injury induced by lipopolysaccharide. These data indicate that arginine supplementation nonspecifically prevents endothelial dysfunction and histological injury in rabbit endotoxic shock. Moreover, L-Arg has no effect on coagulation activation and expression of monocyte tissue factor induced by endotoxic shock.

Acetylcholine↗

Suppression of telomerase activity and cytokine messenger RNA levels in acute myelogenous leukemia cells in vivo in patients by amifostine and interleukin 4.

High levels of telomerase activity and high rates of cell proliferation are associated with a poor prognosis in acute myelogenous leukemia. Furthermore, cytokine production by leukemia cells is believed to play an important role in determining the proliferative characteristics of leukemia. The in vivo effects of two noncytotoxic agents on these parameters were determined in 33 acute myelogenous leukemia patients. Three daily doses of interleukin (IL) 4 or a single dose of amifostine reduced telomerase activity in the leukemia marrow cells in 7 of 9 and 11 of 13 patients, respectively. The administration of a single dose of amifostine resulted in a reduction in tumor necrosis factor alpha and IL-6 transcript levels in the marrow cells of 10 of 13 and 12 of 13 patients in which these transcripts were present. The administration of only three doses of IL-4 or a single dose of amifostine has a significant effect on leukemia cell parameters, which are believed to have a significant impact on the in vivo biology of the disease and on its response to remission induction therapy.

Adult↗

Low dose of lipopolysaccharide induces a delayed enhanced nitric oxide-mediated relaxation in rat aorta.

Delayed effect on vascular reactivity of isolated aorta was studied after injection of a single low dose of lipopolysaccharide (0.5 mg/kg i.p.). The maximal vascular effect was observed 72 h after lipopolysaccharide administration with an increase in maximal endothelium-dependent relaxing response to acetylcholine and parallelly a decrease in contractile response to phenylephrine. The change in contractile response was nullified by endothelium removal as well by in vitro aortic rings incubation with N(omega)-monomethyl-L-arginine but not with indomethacin. A low dose of lipopolysaccharide induces a delayed enhanced nitric oxide-mediated vascular relaxation which could contribute to its delayed anti-ischemic properties in ischemic tolerance phenomenon.

Acetylcholine↗

Germline mutations of p53 but not p16/CDKN2 or PTEN/MMAC1 tumor suppressor genes predispose to gliomas. The ANOCEF Group. Association des NeuroOncologues d'Expression Française.

Constitutional DNA from 44 selected patients suspected of being genetically predisposed to develop astrocytic tumors was analyzed for germline mutations of the p53, p16, and PTEN genes. Six constitutional missense mutations of the p53 gene were identified (13.6%), but no mutations of the p16 and PTEN genes were found, suggesting that (1) germline p53 mutations contribute to a small portion of astrocytic tumors, (2) inherited mutations of the p16 and PTEN gene do not predispose to the development of gliomas, and (3) other genes are involved in glioma predisposition.

Amino Acid Substitution↗

Biologic characteristics of patients with hypocellular myelodysplastic syndromes.

Rates of proliferation and apoptosis as well as expression of tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta) and the number of macrophages were measured in bone marrow (BM) biopsies of 33 patients who presented with hypocellular (cellularity < 30%) myelodysplastic syndromes (MDS). Results showed that 2/3 of the patients had high apoptosis, high cytokine levels and large number of macrophages in their biopsies while 1/3 did not. Apoptosis and TNF-alpha levels were directly related (r = 0.583, P = 0.003, n = 24) as was apoptosis and the degree of anemia (P = 0.033, n = 18). A subgroup of patients with abnormalities of chromosomes 5 or 7 had higher platelets (P = 0.026) and higher apoptosis (P = 0.038) when compared with the rest of the group. Eight patients had no evidence of apoptosis and almost no detectable TNF-alpha in their biopsies. We conclude that within the hypocellular variant of MDS, there may be two distinct sub-groups of patients, one who present with high cytokine-mediated intramedullary apoptosis and the other who may be better characterized as having a stem-cell failure defect since they showed no evidence of apoptosis.

Adolescent↗

Relationship between inward rectifier potassium current impairment and brain injury after cerebral ischemia/reperfusion.

Functional alterations of barium-sensitive potassium inward rectifier (KIR) current, which is involved in the vasodilation of middle cerebral arteries (MCA) in rat brain, have been described during brain ischemia/reperfusion (I/R). The authors investigate the effects of I/R on KIR current recorded in isolated myocytes from MCA of control rats and from contralateral and ipsilateral MCA of ischemic rats by the whole-cell patch-clamp technique, and the relationship between its alteration and the severity of brain injury. The vascular smooth muscle cells exhibited similar morphologic features in all conditions, and the KIR was present in the three groups of myocytes, exhibiting a characteristic inward rectification and a normal external potassium dependence. The KIR density was significantly reduced in cell of MCA ipsilateral to occlusion with a maximum at -135 mV, whereas there was no difference between control and contralateral cells. This alteration in KIR density in occluded MCA was significantly correlated with severity of brain injury and brain edema. These results suggest that the alteration of KIR density in MCA myocytes after I/R and the consecutive impaired dilation of MCA may contribute to aggravation of the brain injury.

Animals↗

Spontaneous down-regulation of Fas-associated phosphatase-1 may contribute to excessive apoptosis in myelodysplastic marrows.

In this study, we examined the role of Fas-signaling in the apoptotic pathway in myelodysplastic syndromes (MDS). Ficoll-separated mononuclear cells from 18 bone marrow aspirate specimens obtained from 17 MDS patients, 4 normal healthy donors, and 3 acute myeloid leukemia patients transformed from MDS (t-AML) were studied for mRNA expression of Fas-L, Fas, and the effectors of their signaling, Caspase 1 and Caspase 3, using reverse transcriptase polymerase chain reaction. Fas-L, Fas, and Caspase 1 were detectable in all of the samples in the three groups. Caspase 3 was detectable both in MDS and t-AML specimens but was negligible in normal cells. The apoptotic index (AI%) determined by in situ end labeling of fragmented DNA in 4-hour cultures of mononuclear cells was significantly higher in MDS cells compared to normal or t-AML cells (mean +/- SEM: 2.3% +/- 0.4% in MDS, n = 10 vs. 0.6% +/- 0.2%, n = 4, P = 0.014 in normal cells, and 0.2% +/- 0.2%, n = 3, P = 0.007 in t-AML cells). Treatment of MDS cells with anti-Fas-L antibody suppressed apoptosis (AI%: 2.1% +/- 0.6% in untreated vs. 1.37% +/- 0.5% in treated, n = 6, P = 0.02), indicating functional participation of Fas-signaling in MDS. Further, it was found that Fas-L, Fas, and Caspase 1 mRNA expression remained unchanged in 4 hours. Caspase 3 expression appeared in normal cells after 4 hours and was present at both 0 and 4 hours in MDS and t-AML cells. In contrast to persistent expression in normal and t-AML cells, cells from the 5 MDS patients studied consistently showed significantly lowered or undetectable expression of a negative regulator of Fas, called Fas-associated phosphatase-1 (Fap-1) after 4 hours. Thus, the high AI% in MDS corresponds to a rapid decline in Fap-1. Furthermore, in tumor necrosis factor alpha (TNF-alpha) treated HL60 promyelocytic cells, a definite periodicity in the expression of different mRNAs was observed with upregulation of TNF-alpha itself at 30 minutes, increased expression of Fas and the appearance of Fas-L after 2 hours, and a decrease in Fap-1 expression after 8 hours. These results suggest that TNF-alpha not only induces the effectors of Fas-signaling but also may downregulate the inhibitor. We conclude that a spontaneous and rapid down-regulation of Fap-1, possibly induced by TNF-alpha, a cytokine shown to be present in excess in MDS marrows, may underlie the increased apoptotic death of hematopoietic cells in these patients. Interference with Fap-1 turnover may provide a new therapeutic modality for MDS.

Apoptosis↗

A needs index for mental health care.

The study aimed to develop a mental illness needs index to help local managers, district purchasers and national policy makers in allocating resources. Formulae were developed by regression analysis using 1991 census data to predict the period prevalence of acute psychiatric admission from electoral wards. Census variables used were chosen on the basis of an established association with mental illness rates. Data from one English Health Service region were analysed for patterns common to wards at hospital catchment area level and patterns common to district health authorities at regional level. The North East Thames region was chosen as the setting for the study, with 7096 patients being admitted during 1991. In most, but not all, catchment areas reasonable prediction of the pattern of admission prevalence was possible using the variables chosen. However, different population characteristics predicted admission prevalence in rural and urban areas. Prediction methods based on one or two variables are thus unlikely to work in both settings. A Mental Illness Needs Index (MINI) based on social isolation, poverty, unemployment, permanent sickness and temporary and insecure housing predicted differences in admission prevalence between wards at catchment area level better than Jarman's Underprivileged Area (UPA) score [1] and between districts at regional level better than the UPA score and comparably to the York Psychiatric Index [2] (adjusted r2 at regional level (MINI 0.82, UPA 0.53, York index 0.70). District admission prevalence rates vary by a factor of three between rural and inner city areas; this difference may not fully reflect the variation in the cost of providing care. It did not prove possible to incorporate factors related to bed availability in the models used; reasons for this are discussed. Data covering other aspects of mental health care in addition to hospital admission are needed for more satisfactory modelling.

Adolescent↗