Multi-terminal memtransistors from polycrystalline monolayer molybdenum disulfide

Sangwan, Vinod K.,Lee, Hong-Sub,Bergeron, Hadallia,Balla, Itamar,Beck, Megan E.,Chen, Kan-Sheng,Hersam, Mark C. Nature Publishing Group 2018 Nature Vol. No.

Memristors are two-terminal passive circuit elements that have been developed for use in non-volatile resistive random-access memory and may also be useful in neuromorphic computing. Memristors have higher endurance and faster read/write times than flash memory and can provide multi-bit data storage. However, although two-terminal memristors have demonstrated capacity for basic neural functions, synapses in the human brain outnumber neurons by more than a thousandfold, which implies that multi-terminal memristors are needed to perform complex functions such as heterosynaptic plasticity. Previous attempts to move beyond two-terminal memristors, such as the three-terminal Widrow–Hoff memristor and field-effect transistors with nanoionic gates or floating gates, did not achieve memristive switching in the transistor. Here we report the experimental realization of a multi-terminal hybrid memristor and transistor (that is, a memtransistor) using polycrystalline monolayer molybdenum disulfide (MoS<SUB>2</SUB>) in a scalable fabrication process. The two-dimensional MoS<SUB>2</SUB> memtransistors show gate tunability in individual resistance states by four orders of magnitude, as well as large switching ratios, high cycling endurance and long-term retention of states. In addition to conventional neural learning behaviour of long-term potentiation/depression, six-terminal MoS<SUB>2</SUB> memtransistors have gate-tunable heterosynaptic functionality, which is not achievable using two-terminal memristors. For example, the conductance between a pair of floating electrodes (pre- and post-synaptic neurons) is varied by a factor of about ten by applying voltage pulses to modulatory terminals. In situ scanning probe microscopy, cryogenic charge transport measurements and device modelling reveal that the bias-induced motion of MoS<SUB>2</SUB> defects drives resistive switching by dynamically varying Schottky barrier heights. Overall, the seamless integration of a memristor and transistor into one multi-terminal device could enable complex neuromorphic learning and the study of the physics of defect kinetics in two-dimensional materials.

Three Divergent Forms of Critical Thinking : Their Implications for Our Teaching

M. Neil Browne,J. Kevin Quinn,Suzanne Bergeron 대한사고개발학회 1995 The International Journal of Creativity & Problem Vol.5 No.1

Akt promotes chemoresistance in human ovarian cancer cells by modulating cisplatin-induced, p53-dependent ubiquitination of FLICE-like inhibitory protein

Abedini, M R,Muller, E J,Bergeron, R,Gray, D A,Tsang, B K Macmillan Publishers Limited 2010 Oncogene Vol.29 No.1

Although Akt is a determinant of cisplatin (cis-diaminedichloroplatinum (CDDP)) resistance in ovarian cancer cells, which is related in part to its inhibitory action on p53 activation, precisely how Akt confers CDDP resistance is unclear. In this study, we show that CDDP induced p53-dependent Fas-associated death domain-like interleukin-1β-converting enzyme (FLICE)-like inhibitory protein (FLIP) degradation in chemosensitive ovarian cancer cells but not their resistant counterparts. CDDP induced FLIP–p53–Itch interaction, colocalization and FLIP ubiquitination in chemosensitive but not chemoresistant ovarian cancer cells. Moreover, although activated Akt inhibited CDDP-induced FLIP degradation and apoptosis in sensitive cells, these responses were facilitated by dominant-negative Akt expression in chemoresistant cells. Inhibition of Akt function also facilitated p53–FLIP interaction and FLIP ubiquitination, which were attenuated by p53 silencing. These results suggest that Akt confers resistance, in part, by modulating CDDP-induced, p53-dependent FLIP ubiquitination. Understanding the precise etiology of chemoresistance may improve treatment for ovarian cancer.

Anthocyanin-Rich Black Currant Extract and Cyanidin-3-O-Glucoside Have Cytoprotective and Anti-Inflammatory Properties

Jacynthe Desjardins,Shinichi Tanabe,Chantal Bergeron,Stefan Gafner,Daniel Grenier 한국식품영양과학회 2012 Journal of medicinal food Vol.15 No.12

Periodontal diseases are a group of multifactorial polymicrobial infections characterized by a progressive inflammatory destruction of the periodontium. Flavonoids, including anthocyanins, are receiving increasing attention because of their promising human health benefits. The aim of our study was to investigate the effect of anthocyanins, pure or as part of a standardized black currant extract, on nicotine-induced cytotoxicity and lipopolysaccharide (LPS)-induced inflammatory responses in human cells. Using a colorimetric assay that measures cell viability, it was found that a pretreatment with an anthocyanin-rich black currant extract or cyanidin-3-O-glucoside neutralized the cytotoxic effect of nicotine on epithelial cells and fibroblasts in a dose-dependent manner. The black currant extract and cyanidin-3-O-glucoside also inhibited the LPSinduced secretion of interleukin-6 by human macrophages. The results of the present study suggest that black currant extract and cyanidin-3-O-glucoside may be promising candidates for the development of novel therapies to prevent and/or to treat smoking-related periodontal diseases.

Performance and cycling efficiency after supra-maximal interval training in trained cross-country mountain bikers

( Philippe Gendron ),( Pascal Dufresne ),( Louis Laurencelle ),( Francois Trudeau ),( Simon Bergeron-vaillancourt ),( Anthony Bonal ),( Claude Lajoie ) 한국스포츠정책과학원(구 한국스포츠개발원) 2016 International Journal of Applied Sports Sciences Vol.28 No.1

The purpose was to examine improvements of performance and different physiological parameters in ten trained male cross-country mountain bikers after a supra-maximal interval training (SMIT) program of 8 sessions. Each session comprised 60 to 90 repeated 1-minute bouts consisting of a 20-s effort at 115% of maximal aerobic power (MAP), followed by 40-s recovery at 50% of MAP. Performance time to complete the virtual time-trial performance test was reduced significantly by -4.2%. Pulmonary sub-maximal oxygen consumption and deoxyhemoglobin in vastus lateralis decreased significantly by .4.7% and -21.9% respectively during the MAP test. Our findings suggest that SMIT program might improve performance and cycling efficiency in XC mountain bikers.

P73 regulates cisplatin-induced apoptosis in ovarian cancer cells via a calcium/calpain-dependent mechanism

Al-Bahlani, S,Fraser, M,Wong, A Y C,Sayan, B S,Bergeron, R,Melino, G,Tsang, B K Nature Publishing Group 2011 Oncogene Vol.30 No.41

<P>P73 is important in drug-induced apoptosis in some cancer cells, yet its role in the regulation of chemosensitivity in ovarian cancer (OVCA) is poorly understood. Furthermore, if and how the deregulation of p73-mediated apoptosis confers resistance to cisplatin (CDDP) treatment is unclear. Here we demonstrate that TAp73α over-expression enhanced CDDP-induced PARP cleavage and apoptosis in both chemosensitive (OV2008 and A2780s) and their resistant counterparts (C13* and A2780cp) and another chemoresistant OVCA cells (Hey); in contrast, the effect of ΔNp73α over-expression was variable. P73α downregulation attenuated CDDP-induced PUMA and NOXA upregulation and apoptosis in OV2008 cells. CDDP decreased p73α steady-state protein levels in OV2008, but not in C13*, although the mRNA expression was identical. CDDP-induced p73α downregulation was mediated by a calpain-dependent pathway. CDDP induced calpain activation and enhanced its cytoplasmic interaction and co-localization with p73α in OV2008, but not C13* cells. CDDP increased the intracellular calcium concentration ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) in OV2008 but not C13* whereas cyclopiazonic acid (CPA), a Ca<SUP>2+</SUP>-ATPase inhibitor, caused this response and calpain activation, p73α processing and apoptosis in both cell types. CDDP-induced [Ca<SUP>2+</SUP>]<SUB>i</SUB> increase in OV2008 cells was not effected by the elimination of extracellular Ca<SUP>2+</SUP>, but this was attenuated by the depletion of internal Ca<SUP>2+</SUP> store, indicating that mobilization of intracellular Ca<SUP>2+]</SUP> stores was potentially involved. These findings demonstrate that p73α and its regulation by the Ca<SUP>2+</SUP>-mediated calpain pathway are involved in CDDP-induced apoptosis in OVCA cells and that dysregulation of Ca<SUP>2+</SUP>/calpain/p73 signaling may in part be the pathophysiology of CDDP resistance. Understanding the cellular and molecular mechanisms of chemoresistance will direct the development of effective strategies for the treatment of chemoresistant OVCA.</P>

In utero exposure to electronic-cigarette aerosols decreases lung fibrillar collagen content, increases Newtonian resistance and induces sex-specific molecular signatures in neonatal mice

Cahill Kerin M.,Gartia Manas R.,Sahu Sushant,Bergeron Sarah R.,Heffernan Linda M.,Paulsen Daniel B.,Penn Arthur L.,Noël Alexandra 한국독성학회 2022 Toxicological Research Vol.38 No.2

Approximately 7% of pregnant women in the United States use electronic-cigarette (e-cig) devices during pregnancy. There is, however, no scientific evidence to support e-cig use as being ‘safe’ during pregnancy. Little is known about the effects of fetal exposures to e-cig aerosols on lung alveologenesis. In the present study, we tested the hypothesis that in utero exposure to e-cig aerosol impairs lung alveologenesis and pulmonary function in neonates. Pregnant BALB/c mice were exposed 2 h a day for 20 consecutive days during gestation to either filtered air or cinnamon-flavored e-cig aerosol (36 mg/ mL of nicotine). Lung tissue was collected in offspring during lung alveologenesis on postnatal day (PND) 5 and PND11. Lung function was measured at PND11. Exposure to e-cig aerosol in utero led to a significant decrease in body weights at birth which was sustained through PND5. At PND5, in utero e-cig exposures dysregulated genes related to Wnt signaling and epigenetic modifications in both females (~ 120 genes) and males (40 genes). These alterations were accompanied by reduced lung fibrillar collagen content at PND5—a time point when collagen content is close to its peak to support alveoli formation. In utero exposure to e-cig aerosol also increased the Newtonian resistance of offspring at PND11, suggesting a narrowing of the conducting airways. At PND11, in females, transcriptomic dysregulation associated with epigenetic alterations was sustained (17 genes), while WNT signaling dysregulation was largely resolved (10 genes). In males, at PND11, the expression of only 4 genes associated with epigenetics was dysregulated, while 16 Wnt related-genes were altered. These data demonstrate that in utero exposures to cinnamon-flavored e-cig aerosols alter lung structure and function and induce sex-specific molecular signatures during lung alveologenesis in neonatal mice. This may reflect epigenetic programming affecting lung disease development later in life.

The rapidly pulsating subdwarf B star PG 1325+101. II. Structural parameters from asteroseismology

Charpinet, S.,Silvotti, R.,Bonanno, A.,Fontaine, G.,Brassard, P.,Chayer, P.,Green, E. M.,Bergeron, P.,Bernabei, S.,Leccia, S. EDP Sciences 2006 Astronomy and astrophysics Vol.459 No.2

Large contribution of human papillomavirus in vaginal neoplastic lesions: A worldwide study in 597 samples

HPV VVAP study group,Alemany, L.,Saunier, M.,Tinoco, L.,Quiros, B.,Alvarado-Cabrero, I.,Alejo, M.,Joura, E.A.,Maldonado, P.,Klaustermeier, J.,Salmeron, J.,Bergeron, C.,Petry, K.U.,Guimera, N.,Clavero, Pergamon Press 2014 European journal of cancer Vol.50 No.16

Aim: This work describes the human papillomavirus (HPV) prevalence and the HPV type distribution in a large series of vaginal intraepithelial neoplasia (VAIN) grades 2/3 and vaginal cancer worldwide. Methods: We analysed 189 VAIN 2/3 and 408 invasive vaginal cancer cases collected from 31 countries from 1986 to 2011. After histopathological evaluation of sectioned formalin-fixed paraffin-embedded samples, HPV DNA detection and typing was performed using the SPF-10/DNA enzyme immunoassay (DEIA)/LiPA<SUB>25</SUB> system (version 1). A subset of 146 vaginal cancers was tested for p16<SUP>INK4a</SUP> expression, a cellular surrogate marker for HPV transformation. Prevalence ratios were estimated using multivariate Poisson regression with robust variance. Results: HPV DNA was detected in 74% (95% confidence interval (CI): 70-78%) of invasive cancers and in 96% (95% CI: 92-98%) of VAIN 2/3. Among cancers, the highest detection rates were observed in warty-basaloid subtype of squamous cell carcinomas, and in younger ages. Concerning the type-specific distribution, HPV16 was the most frequently type detected in both precancerous and cancerous lesions (59%). p16<SUP>INK4a</SUP> overexpression was found in 87% of HPV DNA positive vaginal cancer cases. Conclusions: HPV was identified in a large proportion of invasive vaginal cancers and in almost all VAIN 2/3. HPV16 was the most common type detected. A large impact in the reduction of the burden of vaginal neoplastic lesions is expected among vaccinated cohorts.