Molecular Memory and Processing Devices in Solution and on Surfaces

Author(s):  
Andrew N. Shipway ◽  
Eugenii Katz ◽  
Itamar Willner
Keyword(s):  

2004 ◽  
Vol 30 (4) ◽  
pp. 545-561 ◽  
Author(s):  
A.S. Dvornikov ◽  
Y.C. Liang ◽  
P.M. Rentzepis


2008 ◽  
Vol 22 (12) ◽  
pp. 1183-1202 ◽  
Author(s):  
QILIANG LI

As CMOS technology extends beyond the current technology node, many challenges to conventional MOSFET were raised. Non-classical CMOS to extend and fundamentally new technologies to replace current CMOS technology are under intensive investigation to meet these challenges. The approach of hybrid silicon/molecular electronics is to provide a smooth transition technology by integrating molecular intrinsic scalability and diverse properties with the vast infrastructure of traditional MOS technology. Here we discuss: (1) the integration of redox-active molecules into Si -based structures, (2) characterization and modeling of the properties of these Si /molecular systems, (3) single and multiple states of Si /molecular memory, and (4) applications based on hybrid Si /molecular electronic system.



2014 ◽  
Vol 117 (11) ◽  
pp. 1262-1277 ◽  
Author(s):  
Anna Tetievsky ◽  
Miri Assayag ◽  
Rotem Ben-Hamo ◽  
Sol Efroni ◽  
Gal Cohen ◽  
...  

Faster reinduction of heat acclimation (AC) after its decline indicates “AC memory.” Our previous results revealed involvement of epigenetic mechanisms of transcriptional regulation. We hypothesized that the decline of AC (DeAC) is a period of “dormant memory” during which many processes are alerted to enable rapid reacclimation (ReAC). Using a genomewide approach we studied the AC, DeAC, and ReAC transcriptomes, to uncover hallmark pathways linked to “molecular memory” in the cardioacclimatome. Fifty rats subjected to heat acclimation [34°C for 2d (AC2d) or 30d (AC30)], DeAC (24°C, 30 days), ReAC (34°C, 2 days), and untreated controls were used. The GeneChip Rat Gene 1.0 ST Array was employed for left ventricular (cardiac) mRNA hybridization. Three independent bioinformatic analyses showed that 1) during AC2d enrichment of DNA impair/repair-linked genes is seen, and this is the molecular on-switch of acclimation; 2) genes activated in AC30 underlie the qualitative physiological adaptations of cardiac performance; 3) particular molecular programs encompassing constitutive upregulation of p38 MAPK, Jak/Stat, and Akt pathways and targets are specifically activated during DeAC and ReAC; and 4) epigenetic markers such as linker histones (histones H1 cluster), associated with nucleosome spacing, transcriptional chromatin modifiers, poly-(ADP-ribose) polymerase-1 (PARP1) linked to chromatin compaction, and microRNAs are only altered during DeAC/ReAC. The latter are newcomers to the AC/DeAC puzzle. We suggest that these transcriptional responses maintain euchromatin and proteostasis and enable faster physiological recovery upon ReAC by rapidly reestablishing the protected acclimated cardiophenotype. We propose that the cardiac AC model can be applied to acclimation processes in general.



2012 ◽  
Vol 32 (6) ◽  
pp. 919-941 ◽  
Author(s):  
Gavin R. Owen ◽  
Elisabeth Anne Brenner


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