1,721 research outputs found

    Direct charge measurement in Floating Gate transistors of Flash EEPROM using Scanning Electron Microscopy

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    We present a characterization methodology for fast direct measurement of the charge accumulated on Floating Gate (FG) transistors of Flash EEPROM cells. Using a Scanning Electron Microscope (SEM) in Passive Voltage Contrast (PVC) mode we were able to distinguish between '0' and '1' bit values stored in each memory cell. Moreover, it was possible to characterize the remaining charge on the FG; thus making this technique valuable for Failure Analysis applications for data retent ion measurements in Flash EEPROM. The technique is at least two orders of magnitude faster than state-of-the-art Scanning Probe Microscopy (SPM) methods. Only a relatively simple backside sample preparation is necessary for accessing the FG of memory transistors. The technique presented was successfully implemented on a 0.35 ÎŒm technology node microcontroller and a 0.21 ÎŒm smart card integrated circuit. We also show the ease of such technique to cover all cells of a memory (using intrinsic features of SEM) and to automate memory cells characterization using standard image processing technique

    Broad white matter impairment in multiple system atrophy.

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    Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by the widespread aberrant accumulation of α-synuclein (α-syn). MSA differs from other synucleinopathies such as Parkinson's disease (PD) in that α-syn accumulates primarily in oligodendrocytes, the only source of white matter myelination in the brain. Previous MSA imaging studies have uncovered focal differences in white matter. Here, we sought to build on this work by taking a global perspective on whole brain white matter. In order to do this, in vivo structural imaging and diffusion magnetic resonance imaging were acquired on 26 MSA patients, 26 healthy controls, and 23 PD patients. A refined whole brain approach encompassing the major fiber tracts and the superficial white matter located at the boundary of the cortical mantle was applied. The primary observation was that MSA but not PD patients had whole brain deep and superficial white matter diffusivity abnormalities (p < .001). In addition, in MSA patients, these abnormalities were associated with motor (Unified MSA Rating Scale, Part II) and cognitive functions (Mini-Mental State Examination). The pervasive whole brain abnormalities we observe suggest that there is widespread white matter damage in MSA patients which mirrors the widespread aggregation of α-syn in oligodendrocytes. Importantly, whole brain white matter abnormalities were associated with clinical symptoms, suggesting that white matter impairment may be more central to MSA than previously thought

    Decision process in large-scale crisis management

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    International audienceThis paper deals with the decision-aiding process in large-scale crisis such as natural disasters. It consists in four phases: decision context characterization, system modelling, aggregation and integration. The elements of the context, such as crisis level, risk situation, decision-maker problem issue are defined through the characterization phase. At the feared event occurrence, these elements will interact on a target system. Through the model on this system, the consequences to stakes could be assessed or estimated. The presented aggregation approaches will allow taking the right decisions. The architecture of a Decision Support System is presented in the integration phase

    Phase 3 Trial of 177Lu-Dotatate for Midgut Neuroendocrine Tumors

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    Background Patients with advanced midgut neuroendocrine tumors who have had disease progression during first-line somatostatin analogue therapy have limited therapeutic options. This randomized, controlled trial evaluated the efficacy and safety of lutetium-177 (177Lu)-Dotatate in patients with advanced, progressive, somatostatin-receptor-positive midgut neuroendocrine tumors. Methods We randomly assigned 229 patients who had well-differentiated, metastatic midgut neuroendocrine tumors to receive either 177Lu-Dotatate (116 patients) at a dose of 7.4 GBq every 8 weeks (four intravenous infusions, plus best supportive care including octreotide long-acting repeatable [LAR] administered intramuscularly at a dose of 30 mg) (177Lu-Dotatate group) or octreotide LAR alone (113 patients) administered intramuscularly at a dose of 60 mg every 4 weeks (control group). The primary end point was progression-free survival. Secondary end points included the objective response rate, overall survival, safety, and the side-effect profile. The final analysis of overall survival will be conducted in the future as specified in the protocol; a prespecified interim analysis of overall survival was conducted and is reported here. Results At the data-cutoff date for the primary analysis, the estimated rate of progression-free survival at month 20 was 65.2% (95% confidence interval [CI], 50.0 to 76.8) in the 177Lu-Dotatate group and 10.8% (95% CI, 3.5 to 23.0) in the control group. The response rate was 18% in the 177Lu-Dotatate group versus 3% in the control group (P<0.001). In the planned interim analysis of overall survival, 14 deaths occurred in the 177Lu-Dotatate group and 26 in the control group (P=0.004). Grade 3 or 4 neutropenia, thrombocytopenia, and lymphopenia occurred in 1%, 2%, and 9%, respectively, of patients in the 177Lu-Dotatate group as compared with no patients in the control group, with no evidence of renal toxic effects during the observed time frame. Conclusions Treatment with 177Lu-Dotatate resulted in markedly longer progression-free survival and a significantly higher response rate than high-dose octreotide LAR among patients with advanced midgut neuroendocrine tumors. Preliminary evidence of an overall survival benefit was seen in an interim analysis; confirmation will be required in the planned final analysis. Clinically significant myelosuppression occurred in less than 10% of patients in the 177Lu-Dotatate group. (Funded by Advanced Accelerator Applications; NETTER-1 ClinicalTrials.gov number, NCT01578239 ; EudraCT number 2011-005049-11
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