ECO-CHIP: Estimation of Carbon Footprint of Chiplet-based Architectures for Sustainable VLSI

Decades of progress in energy-efficient and low-power design have successfully reduced the operational carbon footprint in the semiconductor industry. However, this has led to an increase in embodied emissions, encompassing carbon emissions arising from design, manufacturing, packaging, and other infrastructural activities. While existing research has developed tools to analyze embodied carbon at the computer architecture level for traditional monolithic systems, these tools do not apply to near-mainstream heterogeneous integration (HI) technologies. HI systems offer significant potential for sustainable computing by minimizing carbon emissions through two key strategies: ``reducing" computation by reusing pre-designed chiplet IP blocks and adopting hierarchical approaches to system design. The reuse of chiplets across multiple designs, even spanning multiple generations of integrated circuits (ICs), can substantially reduce embodied carbon emissions throughout the operational lifespan. This paper introduces a carbon analysis tool specifically designed to assess the potential of HI systems in facilitating greener VLSI system design and manufacturing approaches. The tool takes into account scaling, chiplet and packaging yields, design complexity, and even carbon overheads associated with advanced packaging techniques employed in heterogeneous systems. Experimental results demonstrate that HI can achieve a reduction of embodied carbon emissions up to 70\% compared to traditional large monolithic systems. These findings suggest that HI can pave the way for sustainable computing practices, contributing to a more environmentally conscious semiconductor industry.Comment: Under review at HPCA2

Mechanism of action of potential anticancer drugs

Traditionally, inoperable or metastatic cancers have been treated by causing massive DNA damage in order to induce self-destruction (apoptosis) of the rapidly multiplying cancer cells. Initially, this strategy works for many cancers, in particular those which express normal p53 tumor suppressor protein. However, most cancers eventually aquire mutations in either p53 or other signaling molecules and fail to initiate apoptosis in response to severe DNA damage. During this study three types of compounds were investigated for their DNA damaging and anticancer effects: a pair of novel metal containing compounds, a pair of natural products, and a known synthetic drug which had been used many years ago for completely different indication. It was shown that all stop the growth of cancer cells and that the latter two classes do not require functional p53 because they work equally well in cells with normal (wildtype), mutant or no p53. The two nickel complexes investigated in this dissertation, differ in their ability to cause DNA damage and cell death. The oxidized form of the nickel complex, [Ni(CR-2H)] 2+ causes DNA damage and cell death at a much lower concentration than its reduced counterpart [Ni(CR)] 2+ . The phenanthridine alkaloids, Sanguinarine and Chelerythine cause high levels of DNA strand breaks and extremely rapid apoptosis which is not due to DNA damage because the quick onset precludes extensive signaling. The effects of the phenanthridines were linked to production of large amounts of reactive oxygen species (ROS), in particular hydrogen peroxide (H 2 O 2 ). The importance of ROS for the action of anticancer drugs as well as antibiotics is increasingly being recognized. In addition we also investigated the thioxanthone Lucanthone or Miracil D (which was used for the treatment of parasitic worms more than 50 years ago). It causes DNA strand breaks and apoptosis. Apoptosis occurs on a timescale consistent with signaling. However, p53 does not seem to be involved and alternative mechanisms are being investigated. This work provides new directions for designing novel anticancer drugs that are not subject to the limitations of DNA damaging agents

Mechanism of action of potential anticancer drugs

Traditionally, inoperable or metastatic cancers have been treated by causing massive DNA damage in order to induce self-destruction (apoptosis) of the rapidly multiplying cancer cells. Initially, this strategy works for many cancers, in particular those which express normal p53 tumor suppressor protein. However, most cancers eventually aquire mutations in either p53 or other signaling molecules and fail to initiate apoptosis in response to severe DNA damage. During this study three types of compounds were investigated for their DNA damaging and anticancer effects: a pair of novel metal containing compounds, a pair of natural products, and a known synthetic drug which had been used many years ago for completely different indication. It was shown that all stop the growth of cancer cells and that the latter two classes do not require functional p53 because they work equally well in cells with normal (wildtype), mutant or no p53. The two nickel complexes investigated in this dissertation, differ in their ability to cause DNA damage and cell death. The oxidized form of the nickel complex, [Ni(CR-2H)] 2+ causes DNA damage and cell death at a much lower concentration than its reduced counterpart [Ni(CR)] 2+ . The phenanthridine alkaloids, Sanguinarine and Chelerythine cause high levels of DNA strand breaks and extremely rapid apoptosis which is not due to DNA damage because the quick onset precludes extensive signaling. The effects of the phenanthridines were linked to production of large amounts of reactive oxygen species (ROS), in particular hydrogen peroxide (H 2 O 2 ). The importance of ROS for the action of anticancer drugs as well as antibiotics is increasingly being recognized. In addition we also investigated the thioxanthone Lucanthone or Miracil D (which was used for the treatment of parasitic worms more than 50 years ago). It causes DNA strand breaks and apoptosis. Apoptosis occurs on a timescale consistent with signaling. However, p53 does not seem to be involved and alternative mechanisms are being investigated. This work provides new directions for designing novel anticancer drugs that are not subject to the limitations of DNA damaging agents

Distribution of Zn, Cu, Mn & Fe in Bombay Harbour Bay

35-40Concentrations of biologically significant trace elements-Zn, Cu, Mn and Fe in sea waters, sediments and some organisms (fish,prawns and crab) of Bombay Harbour bay were studied by spectrophotometric methods. All the reagents used in the estimation were subjected to analysis of these metals and the contamination of samples was minimised by purifying the reagents wherever necessary. Accumulation of these metals in flesh of the 3 species was also estimated. Distribution coefficients (Kd) in suspended silt and bottom sediments were higher than in organisms by order of magnitude and were in the order Zn < Cu < Mn < Fe and the average values were in the ratio of 1:3:20:600. While Zn and Fe showed preferential accumulation in finer fractions of sediments higher concentrations of Cu and Mn were indicated in coarser fractions of sediments