73 research outputs found

    DUT Temperature Coefficient and Power Cycles to Failure

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    We demonstrated power cycling tests with different temperature coefficient samples and shown that cycles to failure strongly depends upon the coefficient. The test samples are investigated by SAT before and after the failure. As a result, we clarified the relationship between the DUT temperature coefficient and failure mechanism. The temperature coefficient is extremely important as a parameter for power cycle tests. High temperature coefficient can lead shorter cycles to failure by thermal runaway before bonding wire disconnection. We also proposed a new method to control temperature coefficient of DUT with gate voltage clamping to drain voltage.33rd International Symposium on Power Semiconductor Devices and ICs (ISPSD 2021), 30th of May and 3rd of June, 2021, Full Virtual Conferenc

    Systems Analysis of ATF3 in Stress Response and Cancer Reveals Opposing Effects on Pro-Apoptotic Genes in p53 Pathway

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    Stress-inducible transcription factors play a pivotal role in cellular adaptation to environment to maintain homeostasis and integrity of the genome. Activating transcription factor 3 (ATF3) is induced by a variety of stress and inflammatory conditions and is over-expressed in many kinds of cancer cells. However, molecular mechanisms underlying pleiotropic functions of ATF3 have remained elusive. Here we employed systems analysis to identify genome-wide targets of ATF3 that is either induced by an alkylating agent methyl methanesulfonate (MMS) or over-expressed in a prostate tumour cell line LNCaP. We show that stress-induced and cancer-associated ATF3 is recruited to 5,984 and 1,423 targets, respectively, in the human genome, 89% of which are common. Notably, ATF3 targets are highly enriched for not only ATF/CRE motifs but also binding sites of several other stress-inducible transcription factors indicating an extensive network of stress response factors in transcriptional regulation of target genes. Further analysis of effects of ATF3 knockdown on these targets revealed that stress-induced ATF3 regulates genes in metabolic pathways, cell cycle, apoptosis, cell adhesion, and signalling including insulin, p53, Wnt, and VEGF pathways. Cancer-associated ATF3 is involved in regulation of distinct sets of genes in processes such as calcium signalling, Wnt, p53 and diabetes pathways. Notably, stress-induced ATF3 binds to 40% of p53 targets and activates pro-apoptotic genes such as TNFRSF10B/DR5 and BBC3/PUMA. Cancer-associated ATF3, by contrast, represses these pro-apoptotic genes in addition to CDKN1A/p21. Taken together, our data reveal an extensive network of stress-inducible transcription factors and demonstrate that ATF3 has opposing, cell context-dependent effects on p53 target genes in DNA damage response and cancer development

    Tilt Angle and Theoretical Target Strength of the Japanese Sandeel, Ammodytes personatus Captured on the Northern Coast of Hokkaido, Japan.

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    The tilt angle, i.e., the angle from horizontal made by the fish body as its head dives down or up, affects the readings on fish echo soundings. We measured the tilt angle of Japanese sandeels (Ammodytes personatus Girard) in a water tank, and calculated the acoustic target strength (TS) using a theoretical scattering model. This study examined the TS of sandeels from the northern coast of Hokkaido, which have a larger body size than those in other regions in Japan. TS values for sandeels, a swimbladderless fish, were estimated using a distorted-wave Born approximation (DWBA) model at two frequencies: 38 and 120 kHz. The mean tilt angle was 20.4?? (S.D. = 18.5??), which differed slightly from that of the lesser sandeel, Ammodytes marinus. The regression equations of the average TS values were TS38kHz = 8.2 log10SL ??? 74.2 and TS120kHz = 20.9 log10SL ??? 92.6, respectively. At 120 kHz, the slope was close to 20, suggesting that the acoustic backscattering strength was proportional to the square of the body length. This value was smaller at 38 kHz, suggesting that the acoustic backscattering strength was stable to differences in body length. We obtained a small discrepancy for both frequencies (??TS = TS120kHz???TS38kHz) were TS120kHz < TS38kHz. Discrepancies of ???1.3 dB for the maximum TS, and ???1.8 dB for averaged TS were found in 72 fish samples, which would be useful for identifying sandeel schools in practical analysis using TS differences

    A Model of Ischemia-Induced Neuroblast Activation in the Adult Subventricular Zone

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    We have developed a rat brain organotypic culture model, in which tissue slices contain cortex-subventricular zone-striatum regions, to model neuroblast activity in response to in vitro ischemia. Neuroblast activation has been described in terms of two main parameters, proliferation and migration from the subventricular zone into the injured cortex. We observed distinct phases of neuroblast activation as is known to occur after in vivo ischemia. Thus, immediately after oxygen/glucose deprivation (6–24 hours), neuroblasts reduce their proliferative and migratory activity, whereas, at longer time points after the insult (2 to 5 days), they start to proliferate and migrate into the damaged cortex. Antagonism of ionotropic receptors for extracellular ATP during and after the insult unmasks an early activation of neuroblasts in the subventricular zone, which responded with a rapid and intense migration of neuroblasts into the damaged cortex (within 24 hours). The process is further enhanced by elevating the production of the chemoattractant SDf-1α and may also be boosted by blocking the activation of microglia. This organotypic model which we have developed is an excellent in vitro system to study neurogenesis after ischemia and other neurodegenerative diseases. Its application has revealed a SOS response to oxygen/glucose deprivation, which is inhibited by unfavorable conditions due to the ischemic environment. Finally, experimental quantifications have allowed us to elaborate a mathematical model to describe neuroblast activation and to develop a computer simulation which should have promising applications for the screening of drug candidates for novel therapies of ischemia-related pathologies
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