Implementation and Electrical Characterization of Shallow Trench Isolation

Shallow trench isolation (STI) planarized with chemical mechanical polishing (CMP) has replaced LOCOS as the conventional isolation technique for sub-micron devices 171. The implementation and feasibility of STI has been examined for future device fabrication at RIT. STI test structures have been fabricated to investigate leakage currents between adjacent NMOS transistors in a p-substrate. Trenches were dry etched to a target depth of 2 μm to isolate n+ regions with a junction depth of 0.89 μm. Trench Refill was done with LTO planarized by chemical mechanical polishing (CMP). By testing source/drain n+ regions isolated by two trenches, leakage current of 36.8 pA/μm was measured for a 3.3 V on drain. It is evident that continued experimentation with STI should be implemented with a twin well process to subdue the possible effect of punch through

Cooling electrons by magnetic-field tuning of Andreev reflection

A solid-state cooling principle based on magnetic-field-driven tunable suppression of Andreev reflection in superconductor/two-dimensional electron gas nanostructures is proposed. This cooling mechanism can lead to very large heat fluxes per channel up to 10^4 times greater than currently achieved with superconducting tunnel junctions. This efficacy and its availability in a two-dimensional electron system make this method of particular relevance for the implementation of quantum nanostructures operating at cryogenic temperatures.Comment: 4 pages, 4 figures, published versio

Association of a homozygous GCK missense mutation with mild diabetes

Background: Homozygous inactivating GCK mutations have been repeatedly reported to cause severe hyperglycemia, presenting as permanent neonatal diabetes mellitus (PNDM). Conversely, only two cases of GCK homozygous mutations causing mild hyperglycemia have been so far described. We here report a novel GCK mutation (c.1116G>C, p.E372D), in a family with one homozygous member showing mild hyperglycemia. Methods: GCK mutational screening was carried out by Sanger sequencing. Computational analyses to investigate pathogenicity and molecular dynamics (MD) were performed for GCK-E372D and for previously described homozygous mutations associated with mild (n = 2) or severe (n = 1) hyperglycemia, used as references. Results: Of four mildly hyperglycemic family-members, three were heterozygous and one, diagnosed in the adulthood, was homozygous for GCK-E372D. Two nondiabetic family members carried no mutations. Fasting glucose (p = 0.016) and HbA1c (p = 0.035) correlated with the number of mutated alleles (0–2). In-silico predicted pathogenicity was not correlated with the four mutations’ severity. At MD, GCK-E372D conferred protein structure flexibility intermediate between mild and severe GCK mutations. Conclusions: We present the third case of homozygous GCK mutations associated with mild hyperglycemia, rather than PNDM. Our in-silico analyses support previous evidences suggesting that protein stability plays a role in determining clinical severity of GCK mutations