A Novel VLSI Design On CSKA Of Binary Tree Adder With Compaq Area And High Throughput

Addition is one of the most basic operations performed in all computing units, including microprocessors and digital signal processors. It is also a basic unit utilized in various complicated algorithms of multiplication and division. Efficient implementation of an adder circuit usually revolves around reducing the cost to propagate the carry between successive bit positions. Multi-operand adders are important arithmetic design blocks especially in the addition of partial products of hardware multipliers. The multi-operand adders (MOAs) are widely used in the modern low-power and high-speed portable very-large-scale integration systems for image and signal processing applications such as digital filters, transforms, convolution neural network architecture. Hence, a new high-speed and area efficient adder architecture is proposed using pre-compute bitwise addition followed by carry prefix computation logic to perform the three-operand binary addition that consumes substantially less area, low power and drastically reduces the adder delay. Further, this project is enhanced by using Modified carry bypass adder to further reduce more density and latency constraints. Modified carry skip adder introduces simple and low complex carry skip logic to reduce parameters constraints. In this proposal work, designed binary tree adder (BTA) is analyzed to find the possibilities for area minimization. Based on the analysis, critical path of carry is taken into the new logic implementation and the corresponding design of CSKP are proposed for the BTA with AOI, OAI

Analysis of the CD1 Antigen Presenting System in Humanized SCID Mice

CD1 molecules are glycoproteins that present lipids and glycolipids for recognition by T cells. CD1-dependent immune activation has been implicated in a wide range of immune responses, however, our understanding of the role of this pathway in human disease remains limited because of species differences between humans and other mammals: whereas humans express five different CD1 gene products (CD1a, CD1b, CD1c, CD1d, and CD1e), muroid rodents express only one CD1 isoform (CD1d). Here we report that immune deficient mice engrafted with human fetal thymus, liver, and CD34+ hematopoietic stem cells develop a functional human CD1 compartment. CD1a, b, c, and d isoforms were highly expressed by human thymocytes, and CD1a+ cells with a dendritic morphology were present in the thymic medulla. CD1+ cells were also detected in spleen, liver, and lungs. APCs from spleen and liver were capable of presenting bacterial glycolipids to human CD1-restricted T cells. ELISpot analyses of splenocytes demonstrated the presence of CD1-reactive IFN-γ producing cells. CD1d tetramer staining directly identified human iNKT cells in spleen and liver samples from engrafted mice, and injection of the glycolipid antigen α-GalCer resulted in rapid elevation of human IFN-γ and IL-4 levels in the blood indicating that the human iNKT cells are biologically active in vivo. Together, these results demonstrate that the human CD1 system is present and functionally competent in this humanized mouse model. Thus, this system provides a new opportunity to study the role of CD1-related immune activation in infections to human-specific pathogens

Primaquine in vivax malaria: an update and review on management issues

Primaquine was officially licensed as an anti-malarial drug by the FDA in 1952. It has remained the only FDA licensed drug capable of clearing the intra-hepatic schizonts and hypnozoites of Plasmodium vivax. This update and review focuses on five major aspects of primaquine use in treatment of vivax malaria, namely: a) evidence of efficacy of primaquine for its current indications; b) potential hazards of its widespread use, c) critical analysis of reported resistance against primaquine containing regimens; d) evidence for combining primaquine with artemisinins in areas of chloroquine resistance; and e) the potential for replacement of primaquine with newer drugs