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Design Issues in Magnetic Field Coupled Array: Clock Structure, Fabrication Defects and Dipolar CouplingKumari, Anita 01 January 2011 (has links)
Even though silicon technology is dominant today, the physics (quantum electron tunneling effect), design (power dissipation, wire delays) and the manufacturing (lithography resolution) limitations of CMOS technology are pushed towards the scaling end. These issues motivated us towards a new paradigm that contributes to a continued advancement
in terms of performance, density, and cost. The magnetic field coupled computing (MFC) paradigm, which is one of the regimes where we leverage and utilize the neighbor interaction of the nanomagnets to order the single-domain magnetic cells to perform computational tasks. The most important and attractive features of this technology are: 1) room
temperature operation, which has been a limitation in electrostatic field coupled devices, 2) high density and nonetheless 3) low static power dissipation. It will be intriguing to address queries like, what are the challenges posed by the technology with such exotic features? Answer to such questions would become the focus of this doctoral research.
The fundamental problem with magnetic field coupled devices is the directional flow of information from input to output. In this work, we have proposed a novel spatially moving Landauer clock system for MFC nanomagnet array which has an advantage over existing adiabatic clock system. Extensive simulation studies were done to model and validate the clock for different length, size, and shape of nanomagnet array.
Another key challenge is the manufacturing defect, which leads to uncertainty and unreliability issues. We studied the different dominant types of geometric defects (missing material, missing cell, spacing, bulge, and merging) in array (used as interconnects) based on our fabrication experiments. We also studied effect of these defects on different segments (locations) of the array with spatially moving clock. The study concluded that a spatially moving clock scheme constitutes a robust MFC architecture as location of defect and length of arrays does not play any role in error masking as opposed to conventional
clock.
Finally, the work presents the study on the 2D nanomagnet array for boolean logic computation and vision logic computation. The effect of dipole-dipole interaction on magnetization state transition in closely spaced 2D array of ferromagnetic circular nanomagnet was explored. The detailed design space to demarcate the boundary between single domain state and vortex state reveals that the single domain state space is desirable for Boolean logic computation while the space around the boundary would be appropriate for vision logic computing.
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The Peripheral Clock Regulates Human PigmentationHardman, J.A., Tobin, Desmond J., Haslam, I.S., Farjo, N.P., Farjo, B.K., Al-Nuaimi, Y., Grimaldi, B., Paus, R. 2014 September 1924 (has links)
No / Although the regulation of pigmentation is well characterized, it remains unclear whether cell-autonomous controls regulate the cyclic on–off switching of pigmentation in the hair follicle (HF). As human HFs and epidermal melanocytes express clock genes and proteins, and given that core clock genes (PER1, BMAL1) modulate human HF cycling, we investigated whether peripheral clock activity influences human HF pigmentation. We found that silencing BMAL1 or PER1 in human HFs increased HF melanin content. Furthermore, tyrosinase expression and activity, as well as TYRP1 and TYRP2 mRNA levels, gp100 protein expression, melanocyte dendricity, and the number gp100+ HF melanocytes, were all significantly increased in BMAL1 and/or PER1-silenced HFs. BMAL1 or PER1 silencing also increased epidermal melanin content, gp100 protein expression, and tyrosinase activity in human skin. These effects reflect direct modulation of melanocytes, as BMAL1 and/or PER1 silencing in isolated melanocytes increased tyrosinase activity and TYRP1/2 expression. Mechanistically, BMAL1 knockdown reduces PER1 transcription, and PER1 silencing induces phosphorylation of the master regulator of melanogenesis, microphthalmia-associated transcription factor, thus stimulating human melanogenesis and melanocyte activity in situ and in vitro. Therefore, the molecular clock operates as a cell-autonomous modulator of human pigmentation and may be targeted for future therapeutic strategies.
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