A CMOS-compatible poly-Si nanowire device with hybrid sensor/memory characteristics for System-on-Chip applications.

This paper reports a versatile nano-sensor technology using "top-down" poly-silicon nanowire field-effect transistors (FETs) in the conventional Complementary Metal-Oxide Semiconductor (CMOS)-compatible semiconductor process. The nanowire manufacturing technique reduced nanowire width scaling to 50 nm without use of extra lithography equipment, and exhibited superior device uniformity. These n type polysilicon nanowire FETs have positive pH sensitivity (100 mV/pH) and sensitive deoxyribonucleic acid (DNA) detection ability (100 pM) at normal system operation voltages. Specially designed oxide-nitride-oxide buried oxide nanowire realizes an electrically V(th)-adjustable sensor to compensate device variation. These nanowire FETs also enable non-volatile memory application for a large and steady V(th) adjustment window (>2 V Programming/Erasing window). The CMOS-compatible manufacturing technique of polysilicon nanowire FETs offers a possible solution for commercial System-on-Chip biosensor application, which enables portable physiology monitoring and in situ recording.

Selective insertion of oxygen and selenium into an electron-precise paramagnetic selenium-manganese carbonyl cluster [Se(6)Mn(6)(CO)(18)](4-).

The facile synthesis of a novel electron-precise paramagnetic hexamanganese carbonyl selenide cluster [Se(6)Mn(6)(CO)(18)](4-) (1) was discovered, which demonstrates contrasting reactivity toward O(2) and Se(8) under markedly mild conditions to afford the O- and Se-inserted clusters [Se(6)Mn(6)(CO)(18)(O)](4-) (2) and [Se(10)Mn(6)(CO)(18)](4-) (3), respectively. Clusters 1-3 represent the first examples of electron-precise paramagnetic main-group transition metal carbonyl clusters, and their formation and bonding properties are further elucidated by theoretical calculations.

Inhibition of hepatitis C virus replication by arsenic trioxide.

Hepatitis C virus (HCV) is a serious global problem, and present therapeutics are inadequate to cure HCV infection. In the present study, various antiviral assays show that As2O3 at submicromolar concentrations is capable of inhibiting HCV replication. The 50% effective concentration (EC50) of As2O3 required to inhibit HCV replication was 0.35 microM when it was determined by a reporter-based HCV replication assay, and the EC50 was below 0.2 microM when it was determined by quantitative reverse transcription-PCR analysis. As2O3 did not cause cellular toxicity at this concentration, as revealed by an MTS [3-(4,5-dimethylthiozol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] assay. A combination of As2O3 and alpha interferon exerted synergistic effects against HCV, as revealed by a multiple linear logistic model and isobologram analysis. Furthermore, in an alternative HCV antiviral system that may recapitulate additional steps involved in HCV infection and replication, As2O3 at 0.3 microM totally abolished the HCV signal, whereas alpha interferon at a high dose (5,000 IU/ml) only partially suppressed the HCV signal. The study highlights the indications for use of a novel class of anti-HCV agent. Further elucidation of the exact antiviral mechanism of As2O3 may lead to the development of agents with potent activities against HCV or related viruses.