Analytical Investigation on a New Approach for Achieving Deep Penetration in a Lossy Medium: The Lossy Prism, Journal of Telecommunications and Information Technology, 2017, nr 3

Recent studies highlighted deep-penetration prop-erties of inhomogeneous waves at the interface between a loss-less and a lossy medium. Such waves can be generated bymeans of radiating structures known as Leaky-Wave Anten-nas (LWAs). Here, a different approach is proposed basedon the use of a lossy prism capable to generate an inhomo-geneous wave when illuminated by a homogeneous wave. Thelossy prism is conceived and designed thinking of Ground-Penetrating Radar (GPR). The results achieved by the lossyprism will be compared with those obtained by means of a pre-viously designed LWA that was created with the identical ob-jective. The approach of this paper is purely theoretical, andit aims at providing basic ideas and preliminary results usefulfor an innovative LWA design

Verification of the electromagnetic deep-penetration effect in the real world

The deep penetration of electromagnetic waves into lossy media can be obtained by properly generating inhomogeneous waves. In this work, for the very first time, we demonstrate the physical implementation and the practical relevance of this phenomenon. A thorough numerical investigation of the deep-penetration effects has been performed by designing and comparing three distinct practical radiators, emitting either homogeneous or inhomogeneous waves. As concerns the latter kind, a typical Menzel microstrip antenna is first used to radiate improper leaky waves. Then, a completely new approach based on an optimized 3-D horn TEM antenna applied to a lossy prism is described, which may find applications even at optical frequencies. The effectiveness of the proposed radiators is measured using different algorithms to consider distinct aspects of the propagation in lossy media. We finally demonstrate that the deep penetration is possible, by extending the ideal and theoretical evidence to practical relevance, and discuss both achievements and limits obtained through numerical simulations on the designed antennas

Numerical Evaluation of Electromagnetic-wave Penetration at Normal Incidence through an Inhomogeneous-wave Approach, Journal of Telecommunications and Information Technology, 2018, nr 2

This paper presents numerical scenarios concerning penetration in a lossy medium that can be obtained by radiating inhomogeneous electromagnetic waves. Former papers approached this problem, both analytically and numerically, finding requirements and limits of the so-called “deeppenetration” condition, which consists of a wave transmitted in a lossy medium having an attenuation vector whose direction forms the angle of ninety degrees with the normal to the separation surface. The deep-penetration condition always requires an oblique incidence, therefore is not practical in many applications. For this reason, we are interested here in finding whether an inhomogeneous wave guarantees larger penetration than the one obtainable with homogeneous waves, even when the incident wave is normal to the separation surface between two media, i.e. when the deep-penetration condition is not satisfied. We are also interested in verifying numerically whether the lossy-prism structure may achieve larger penetration than the one obtainable through traditional leakywave antennas, and we also wish to propose a lossy-prism design more realistic than the one previously presented in the literature

HMG20B stabilizes association of LSD1 with GFI1 on chromatin to confer transcription repression and leukemia cell differentiation block

Pharmacologic inhibition of LSD1 induces molecular and morphologic differentiation of blast cells in acute myeloid leukemia (AML) patients harboring MLL gene translocations. In addition to its demethylase activity, LSD1 has a critical scaffolding function at genomic sites occupied by the SNAG domain transcription repressor GFI1. Importantly, inhibitors block both enzymatic and scaffolding activities, in the latter case by disrupting the protein:protein interaction of GFI1 with LSD1. To explore the wider consequences of LSD1 inhibition on the LSD1 protein complex we applied mass spectrometry technologies. We discovered that the interaction of the HMG-box protein HMG20B with LSD1 was also disrupted by LSD1 inhibition. Downstream investigations revealed that HMG20B is co-located on chromatin with GFI1 and LSD1 genome-wide; the strongest HMG20B binding co-locates with the strongest GFI1 and LSD1 binding. Functional assays demonstrated that HMG20B depletion induces leukemia cell differentiation and further revealed that HMG20B is required for the transcription repressor activity of GFI1 through stabilizing LSD1 on chromatin at GFI1 binding sites. Interaction of HMG20B with LSD1 is through its coiled-coil domain. Thus, HMG20B is a critical component of the GFI1:LSD1 transcription repressor complex which contributes to leukemia cell differentiation block

Histone Modifications Drive Aberrant Notch3 Expression/Activity and Growth in T-ALL

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood cancer caused by the deregulation of key T-cell developmental pathways, including Notch signaling. Aberrant Notch signaling in T-ALL occurs by NOTCH1 gain-of-function mutations and by NOTCH3 overexpression. Although NOTCH3 is assumed as a Notch1 target, machinery driving its transcription in T-ALL is undefined in leukemia subsets lacking Notch1 activation. Here, we found that the binding of the intracellular Notch3 domain, as well as of the activated Notch1 fragment, to the NOTCH3 gene locus led to the recruitment of the H3K27 modifiers JMJD3 and p300, and it was required to preserve transcriptional permissive/active H3K27 marks and to sustain NOTCH3 gene expression levels. Consistently, pharmacological inhibition of JMJD3 by GSKJ4 treatment or of p300 by A-485 decreased the levels of expression of NOTCH3, NOTCH1 and of the Notch target genes DELTEX1 and c-Myc and abrogated cell viability in both Notch1- and Notch3-dependent T-cell contexts. Notably, re-introduction of exogenous Notch1, Notch3 as well as c-Myc partially rescued cells from anti-growth effects induced by either treatment. Overall our findings indicate JMJD3 and p300 as general Notch1 and Notch3 signaling co-activators in T-ALL and suggest further investigation on the potential therapeutic anti-leukemic efficacy of their enzymatic inhibition in Notch/c-Myc axis-related cancers and diseases

Enhancer recruitment of a RUNX1, HDAC1 and TLE3 co-repressor complex by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia

Tissue-inappropriate expression of FOXC1 (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes