Catalyst preparation for CMOS-compatible silicon nanowire synthesis

Metallic contamination was key to the discovery of semiconductor nanowires, but today it stands in the way of their adoption by the semiconductor industry. This is because many of the metallic catalysts required for nanowire growth are not compatible with standard CMOS (complementary metal oxide semiconductor) fabrication processes. Nanowire synthesis with those metals which are CMOS compatible, such as aluminium and copper, necessitate temperatures higher than 450 C, which is the maximum temperature allowed in CMOS processing. Here, we demonstrate that the synthesis temperature of silicon nanowires using copper based catalysts is limited by catalyst preparation. We show that the appropriate catalyst can be produced by chemical means at temperatures as low as 400 C. This is achieved by oxidizing the catalyst precursor, contradicting the accepted wisdom that oxygen prevents metal-catalyzed nanowire growth. By simultaneously solving material compatibility and temperature issues, this catalyst synthesis could represent an important step towards real-world applications of semiconductor nanowires.Comment: Supplementary video can be downloaded on Nature Nanotechnology websit

Acute immune signatures and their legacies in severe acute respiratory syndrome coronavirus-2 infected cancer patients

Given the immune system’s importance for cancer surveillance and treatment, we have investigated how it may be affected by SARS-CoV-2 infection of cancer patients. Across some heterogeneity in tumor type, stage, and treatment, virus-exposed solid cancer patients display a dominant impact of SARS-CoV-2, apparent from the resemblance of their immune signatures to those for COVID-19+ non-cancer patients. This is not the case for hematological malignancies, with virus-exposed patients collectively displaying heterogeneous humoral responses, an exhausted T cell phenotype and a high prevalence of prolonged virus shedding. Furthermore, while recovered solid cancer patients’ immunophenotypes resemble those of nonvirus-exposed cancer patients, recovered hematological cancer patients display distinct, lingering immunological legacies. Thus, while solid cancer patients, including those with advanced disease, seem no more at risk of SARS-CoV-2-associated immune dysregulation than the general population, hematological cancer patients show complex immunological consequences of SARS-CoV-2 exposure that might usefully inform their care

CELL SURFACE INTERLEUKIN-1 alpha, WHICH DRIVES THE SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE (SASP), IS TETHERED VIA IL-1R2 OR GPI-ANCHORED

Atherosclerosis is instigated, driven and worsened by inflammation. However, the processes that drive this and cause chronic inflammation are not well understood, but likely involve interplay between macrophages, endothelial cells (ECs) and vascular smooth muscle (VSMCs). Macrophages, ECs and VSMCs all undergo senescence in advanced plaques, which results in the establishment of the senescence-associated secretory phenotype (SASP). The SASP is driven by membrane-bound IL-1α that drives the perpetual secretion of IL-6, IL-8, MCP-1 and numerous other inflammatory cytokines and growth factors that likely potentiate plaque growth. However, how the cytokine IL-1α, which lacks a signal peptide or a transmembrane domain, is tethered to the cell surface is unknown. Using flow cytometry we show that senescent fibroblasts bear IL-1α on the cell surface. Similarly, resting human and murine macrophages express IL-1α on the cell surface, with expression significantly upregulated upon LPS treatment. However, significant false-positive staining can occur without the use of a robust dead cell gate. Furthermore, the level of membrane IL-1α is significantly lower in IL-1R1-/- or IL-1R2-/- macrophages compared to wild-type, indicating that cell surface IL-1α may in fact be tethered to its cognate receptors IL-1R1 and IL-1R2. In addition, we find human and mouse macrophages do not respond to IL-1α or IL-1β treatment, despite expression of IL-1R1 and response to LPS that shares the same signalling pathway. We believe the SASP could be a key driver of the chronic inflammation witnessed in vascular disease. Therefore, the elucidation of mechanisms that control SASPs are important to help identify new targets that could specifically target vascular inflammation whilst sparing normal host defence

Acute immune signatures and their legacies in severe acute respiratory syndrome coronavirus-2 infected cancer patients

Given the immune system's importance for cancer surveillance and treatment, we have investigated how it may be affected by SARS-CoV-2 infection of cancer patients. Across some heterogeneity in tumor type, stage, and treatment, virus-exposed solid cancer patients display a dominant impact of SARS-CoV-2, apparent from the resemblance of their immune signatures to those for COVID-19+ non-cancer patients. This is not the case for hematological malignancies, with virus-exposed patients collectively displaying heterogeneous humoral responses, an exhausted T cell phenotype and a high prevalence of prolonged virus shedding. Furthermore, while recovered solid cancer patients' immunophenotypes resemble those of non-virus-exposed cancer patients, recovered hematological cancer patients display distinct, lingering immunological legacies. Thus, while solid cancer patients, including those with advanced disease, seem no more at risk of SARS-CoV-2-associated immune dysregulation than the general population, hematological cancer patients show complex immunological consequences of SARS-CoV-2 exposure that might usefully inform their care