Anti-CSK (aa 1-100) polyclonal antibody

Aggressive scaling of single-gate CMOS device face greater challenge in nanometre technology as sub-threshold and gate-oxide leakage currents increase exponentially with reduction of channel length. This paper discusses a double-gate FinFET (DGFET) technology which mitigates leakage current and higher ON state current when scaling is done beyond 32nm. Here 8 and 16 input OR gate domino logic circuits are simulated on 32nm FinFET Predictive technology model (PTM) on HSPICE. Simulation results of different 8 input OR gate domino logic circuits like Current-mirror footed domino (CMFD), High-speed clock-delayed (HSCD), Modified-HSCD (M-HSCD), Conditional evaluation domino logic (CEDL) and Conditional stacked keeper domino logic (CSK-DL), all operated in Short Gate (SG) and Low Power (LP) mode, shows tremendous reduction in average power consumption and delay. In this paper, domino logic-based circuit Ultra-Low Power Stack Dual-Phase Clock (ULPS-DPC) is proposed for both CMOS and FinFET (SG and LP modes). Proposed circuit shows maximum reduction in average power consumption of 84.04% when compared with CSK-DL circuit and maximum reduction in delay of 75.4% when compared with M-HSCD circuit at 10MHz frequency when these circuits are simulated in SG mode.

Glioblastoma multiforme (GBM) is the most aggressive human brain tumor, and GBM stem cells (GSC) may be responsible for its recurrence and therapeutic resistance. Toll-like receptors (TLRs), which recognize multiple ligands (endogenous and pathogen-associated) and trigger the immune response of mature immune cells, are also expressed by hematopoietic stem and progenitor cells, where their activation results in the differentiation of these cells into myeloid cells. Since TLR expression has been recently described in neural cells, including neural stem cells, we studied TLR expression by GSCs and the effect of stimulation by TLR ligands on promoting GSC differentiation into mature GBM cells. First, our results showed heterogeneous TLR expression by GBM cells from human tumors and, for the first time, by human GSCs defined by their CD133(+) and CD44(+) phenotypes. Next, the effect of TLR ligands was studied in in vitro cell cultures of neurospheres and CD44(+) cells obtained from two GBM cell lines (U-87 and U-118). The expression of GSC markers diminished in the presence of Pam(3)CSK(4) or LPS (TLR2 and TLR4 ligands, respectively), thus indicating TLR-dependent differentiation. Interestingly, simultaneous treatment with Pam(3)CSK(4) plus temozolomide (TMZ), the reference drug in GBM treatment, significantly increased cell death compared to the effect of the ligand alone, which showed no toxicity, or TMZ alone. These results suggest a synergistic effect between Pam(3)CSK(4) and TMZ based on the induction of TLR-dependent GSC differentiation towards mature GBM cells, which exhibited increased sensitivity to chemotherapy, and provide new perspectives in GBM therapy.