Nanomagnetic logic based runtime Reconfigurable area efficient and high speed adder design methodology.

In this study, we present a runtime reconfigurable nanomagnetic (RRN) adder design offering significant area efficiency and high speed operations. Subsequently, it is implemented using a micromagnetic simulation tool, by exploiting the reversal magnetization and energy minimization nature of the nanomagnets. We compute the carry and sum of the 1-bit full adder using only two majority gates comprising a total of 7 nanomagnets and single design layout. Consequently, the on-chip clocking schematic for the proposed RRN adder implementation for both horizontal and vertical layouts are introduced. The quantitative analysis of the required resources for higher bit adder architecture using the proposed design is performed and compared with state-of-the art. The proposed design methodology leads to ∼86%, ∼83% and ∼93% reduction in the number of nanomagnets, majority gates and clock cycles respectively resulting in an area efficient and high speed RRN adder architecture.

Imiquimod-induced psoriasis-like inflammation in differentiated Human keratinocytes: Its evaluation using curcumin.

Psoriasis is considered to be a systemic disease of immune dysfunction. It is still unclear what triggers the inflammatory cascade associated with psoriasis but recent evidences suggest the vital role of IL-23/IL-17A cytokine axis in etiology of psoriasis. Several studies have been conducted in psoriatic-like animal models but ethical issues and complexity surrounding it halts the screening of new anti-psoriatic drug candidates. Hence, in this study, we developed a new in-vitro model for psoriasis using imiquimod (IMQ) induced differentiated HaCaT cells which could be used for screening of new anti-psoriatic drug candidates. The differentiated HaCaT cells were treated with IMQ (100µM) to induce psoriatic like inflammation and its effect was investigated using a natural anti-psoriatic compound, curcumin. The proliferation of psoriatic-like cells was inhibited by curcumin at 25 and 50µM concentrations. The psoriatic-like cells decreased in number with increase in apoptotic and dead cells upon curcumin treatment. Curcumin inhibited the proliferation of IMQ-induced differentiated HaCaT cells (Psoriatic-like cells) by down-regulation of pro-inflammatory cytokines, interleukin-17, tumor necrosis factor-α, interferon-γ, and interleukin-6. Apart from this, curcumin significantly enhanced the skin-barrier function by up-regulation of involucrin (iNV) and filaggrin (FLG), the regulators of epidermal skin barrier. The IMQ-induced differentiated HaCaT in vitro model recapitulated some aspects of the psoriasis pathogenesis similar to murine model. Henceforth, we conclude that this model may be used for rapid screening of anti-psoriatic drug candidates and warrant further mechanistic studies.