Design of Hybrid Full Adder using 6T-XOR-Cell for High Speed Processor Designs Applications

Hybrid-logic implementation is highly suitable in the design of a full adder circuit to attain high-speed low-power consumption, which helps to design n any high speed ALUs that can be used in varies processors and applicable for high speed IoT- Application. XOR/XNOR-cell, Hybrid Full Adder (HFA) are the fundamental building block to perform any arithmetic operation. In this paper, different types of high-speed, low-power 6T-XOR/XNOR-cell designs are being proposed and simulated results are presented. The proposed HFA is simulated using a cadence virtuoso environment in a 45nm technology with supply voltage as 0.8V at 1GHz. The proposed HFA consumes a power of 1.555uw, and the delay is 36.692ns.  Layout designs are drawn for both 6T-XOR/XNOR-cell, and 1- bit HFA designs. XOR/XNOR-cells are designed based on the combination of normal CMOS-inverter and Pass Transistor Logic (PTL). Which is used in the design of high end device processors such as ALU that can be implemented for the IoT- design applications

Excessive reactive oxygen species induce transcription-dependent replication stress.

Elevated levels of reactive oxygen species (ROS) reduce replication fork velocity by causing dissociation of the TIMELESS-TIPIN complex from the replisome. Here, we show that ROS generated by exposure of human cells to the ribonucleotide reductase inhibitor hydroxyurea (HU) promote replication fork reversal in a manner dependent on active transcription and formation of co-transcriptional RNA:DNA hybrids (R-loops). The frequency of R-loop-dependent fork stalling events is also increased after TIMELESS depletion or a partial inhibition of replicative DNA polymerases by aphidicolin, suggesting that this phenomenon is due to a global replication slowdown. In contrast, replication arrest caused by HU-induced depletion of deoxynucleotides does not induce fork reversal but, if allowed to persist, leads to extensive R-loop-independent DNA breakage during S-phase. Our work reveals a link between oxidative stress and transcription-replication interference that causes genomic alterations recurrently found in human cancer. [Abstract copyright: © 2023. The Author(s).

Excessive reactive oxygen species induce transcription-dependent replication stress

Elevated levels of reactive oxygen species (ROS) reduce replication fork velocity by causing dissociation of the TIMELESS-TIPIN complex from the replisome. Here, we show that ROS generated by exposure of human cells to the ribonucleotide reductase inhibitor hydroxyurea (HU) promote replication fork reversal in a manner dependent on active transcription and formation of co-transcriptional RNA:DNA hybrids (R-loops). The frequency of R-loop-dependent fork stalling events is also increased after TIMELESS depletion or a partial inhibition of replicative DNA polymerases by aphidicolin, suggesting that this phenomenon is due to a global replication slowdown. In contrast, replication arrest caused by HU-induced depletion of deoxynucleotides does not induce fork reversal but, if allowed to persist, leads to extensive R-loop-independent DNA breakage during S-phase. Our work reveals a link between oxidative stress and transcription-replication interference that causes genomic alterations recurrently found in human cancer

Excessive reactive oxygen species induce transcription-dependent replication stress

Excessive oxidative stress is widely perceived as a key factor in cancer progression. Here, the authors reveal that oxidative stress induces transcription-dependent replication fork stalling that appears to be a major source of chromosomal rearrangements found in human cancers