Sensitivity of Localized Surface Plasmon Resonances to Bulk and Local Changes in the Optical Environment

This document is the Accepted Manuscript version of a Published Work that appeared in final form in Journal of Physical Chemistry C copyright © 2009 American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://dx.doi.org/10.1021/jp810322qSingle rod-shaped and disk-shaped gold nanoparticles with sizes ranging from 60 to 162 nm were analyzed using dark-field scattering spectroscopy. The sensitivity of the localized surface plasmon resonance (LSPR) of each nanoparticle to both a bulk and a local change in the refractive index of the environment was obtained by monitoring the change in the spectral position of the LSPR. It was found that the rods were more sensitive to changes in both the local environment and the bulk environment, in particular rods with a length > 110 nm. This behavior was confirmed by finite element modeling of the structures that clearly indicated a saturation of the relative wavelength shift for the disks as the diameter increased whereas the sensitivity of the rods continued to increase linearly with increasing length. This disparity in the behavior of the two types of nanoparticle may in part be attributed to two principal effects associated with the presence of the substrate: first, that the proportion of the surface area of the nanoparticle in contact with the substrate is larger for the disk than for the rod; second, that the LSPR electromagnetic field is more concentrated within the superstrate for the rod compared to the disk. Further analysis of data obtained from modeling a changing local environment indicates that, although the rods are more sensitive, both rods and disks exhibit a similar field confinement

OpenDPD: An Open-Source End-to-End Learning & Benchmarking Framework for Wideband Power Amplifier Modeling and Digital Pre-Distortion

With the rise in communication capacity, deep neural networks (DNN) for digital pre-distortion (DPD) to correct non-linearity in wideband power amplifiers (PAs) have become prominent. Yet, there is a void in open-source and measurement-setup-independent platforms for fast DPD exploration and objective DPD model comparison. This paper presents an open-source framework, OpenDPD, crafted in PyTorch, with an associated dataset for PA modeling and DPD learning. We introduce a Dense Gated Recurrent Unit (DGRU)-DPD, trained via a novel end-to-end learning architecture, outperforming previous DPD models on a digital PA (DPA) in the new digital transmitter (DTX) architecture with unconventional transfer characteristics compared to analog PAs. Measurements show our DGRU-DPD achieves an ACPR of -44.69/-44.47 dBc and an EVM of -35.22 dB for 200 MHz OFDM signals. OpenDPD code, datasets, and documentation are publicly available at https://github.com/lab-emi/OpenDPD.Comment: To be published at the 2024 IEEE International Symposium on Circuits and Systems (ISCAS), Singapor

The Impact of Mutation of Myelodysplasia-Related Genes in De Novo Acute Myeloid Leukemia Carrying NPM1 Mutation

Background: The impact of gene mutations typically associated with myelodysplastic syndrome (MDS) in acute myeloid leukemia (AML) with NPM1 mutation is unclear. Methods: Using a cohort of 107 patients with NPM1-mutated AML treated with risk-adapted therapy, we compared survival outcomes of patients without MDS-related gene mutations (group A) with those carrying concurrent FLT3-ITD (group B) or with MDS-related gene mutations (group C). Minimal measurable disease (MMD) status assessed by multiparameter flow cytometry (MFC), polymerase chain reaction (PCR), and/or next-generation sequencing (NGS) were reviewed. Results: Among the 69 patients treated intensively, group C showed significantly inferior progression-free survival (PFS, p \u3c 0.0001) but not overall survival (OS, p = 0.055) compared to group A. Though groups A and C had a similar MMD rate, group C patients had a higher relapse rate (p = 0.016). Relapse correlated with MMD status at the end of cycle 2 induction (p = 0.023). Survival of group C patients was similar to that of group B. Conclusion: MDS-related gene mutations are associated with an inferior survival in NPM1-mutated AML

Myeloid- and Epithelial-Derived HBEGF Promotes Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a poorly understood, progressive lethal lung disease with no known cure. In addition to alveolar epithelial cell (AEC) injury and excessive deposition of extracellular matrix proteins, chronic inflammation is a hallmark of IPF. Literature suggests that the persistent inflammation seen in IPF primarily consists of monocytes and macrophages. Recent work demonstrates that monocyte-derived alveolar macrophages (moAMs) drive lung fibrosis, but further characterization of critical moAM cell attributes is necessary. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is an important EGFR (epidermal growth factor receptor) ligand that has essential roles in angiogenesis, wound healing, keratinocyte migration, and epithelial-mesenchymal transition. Our past work has shown HB-EGF is a primary marker of profibrotic M2 macrophages, and this study seeks to characterize myeloid-derived HB-EGF and its primary mechanism of action in bleomycin-induced lung fibrosis using Hbegff/f;Lyz2Cre+ mice. Here, we show that IPF patients and fibrotic mice have increased expression of HB-EGF and that lung macrophages and transitional alveolar epithelial cells of fibrotic mice and humans all express HB-EGF. We also show that Hbegff/f;Lyz2Cre+ mice are protected from bleomycin-induced fibrosis and that this protection is likely multifactorial, caused by decreased CCL2-dependent monocyte migration, decreased fibroblast migration, and decreased contribution of HB-EGF from AEC sources when HB-EGF is removed under the Lyz2Cre promoter

The histone deacetylase Hdac7 supports LPS-inducible glycolysis and Il-1β production in murine macrophages via distinct mechanisms

Abstract TLRs reprogram macrophage metabolism, enhancing glycolysis and promoting flux through the tricarboxylic acid cycle to enable histone acetylation and inflammatory gene expression. The histone deacetylase (HDAC) family of lysine deacetylases regulates both TLR-inducible glycolysis and inflammatory responses. Here, we show that the TLR4 agonist LPS, as well as agonists of other TLRs, rapidly increase enzymatic activity of the class IIa HDAC family (HDAC4, 5, 7, 9) in both primary human and murine macrophages. This response was abrogated in murine macrophages deficient in histone deacetylase 7 (Hdac7), highlighting a selective role for this specific lysine deacetylase during immediate macrophage activation. With the exception of the TLR3 agonist polyI:C, TLR-inducible activation of Hdac7 enzymatic activity required the MyD88 adaptor protein. The rapid glycolysis response, as assessed by extracellular acidification rate, was attenuated in Hdac7-deficient mouse macrophages responding to submaximal LPS concentrations. Surprisingly however, reconstitution of these cells with either wild-type or an enzyme-dead mutant of Hdac7 enhanced LPS-inducible glycolysis, whereas only the former promoted production of the inflammatory mediators Il-1β and Ccl2. Thus, Hdac7 enzymatic activity is required for TLR-inducible production of specific inflammatory mediators, whereas it acts in an enzyme-independent fashion to reprogram metabolism in macrophages responding to submaximal LPS concentrations. Hdac7 is thus a bifurcation point for regulated metabolism and inflammatory responses in macrophages. Taken together with existing literature, our findings support a model in which submaximal and maximal activation of macrophages via TLR4 instruct glycolysis through distinct mechanisms, leading to divergent biological responses.</jats:p