Holographic MIMO Communications: Theoretical Foundations, Enabling Technologies, and Future Directions

Future wireless systems are envisioned to create an endogenously holography-capable, intelligent, and programmable radio propagation environment, that will offer unprecedented capabilities for high spectral and energy efficiency, low latency, and massive connectivity. A potential and promising technology for supporting the expected extreme requirements of the sixth-generation (6G) communication systems is the concept of the holographic multiple-input multiple-output (HMIMO), which will actualize holographic radios with reasonable power consumption and fabrication cost. The HMIMO is facilitated by ultra-thin, extremely large, and nearly continuous surfaces that incorporate reconfigurable and sub-wavelength-spaced antennas and/or metamaterials. Such surfaces comprising dense electromagnetic (EM) excited elements are capable of recording and manipulating impinging fields with utmost flexibility and precision, as well as with reduced cost and power consumption, thereby shaping arbitrary-intended EM waves with high energy efficiency. The powerful EM processing capability of HMIMO opens up the possibility of wireless communications of holographic imaging level, paving the way for signal processing techniques realized in the EM-domain, possibly in conjunction with their digital-domain counterparts. However, in spite of the significant potential, the studies on HMIMO communications are still at an initial stage, its fundamental limits remain to be unveiled, and a certain number of critical technical challenges need to be addressed. In this survey, we present a comprehensive overview of the latest advances in the HMIMO communications paradigm, with a special focus on their physical aspects, their theoretical foundations, as well as the enabling technologies for HMIMO systems. We also compare the HMIMO with existing multi-antenna technologies, especially the massive MIMO, present various...Comment: double column, 58 page

A transgenic macrophage-based platform to assess the efficacy and specificity of HuR modulators in inflammation

RNA-binding proteins (RBPs) are essential controllers of RNA metabolism, and their deregulation can cause various pathologies.Human Antigen R (HuR) is an RBP engaged in the nuclear and cytoplasmic regulation of critical RNAs involved in cellularhomeostasis. Conversely, its deregulation leads to tissue degeneration, cancer and immunopathology, fueling efforts for itsexploitation as a target for relevant therapeutics. An expanding list of natural and synthetic compounds has been generatedthat disrupt HuR’s affinity for RNA, block its subcellular movements or debilitate its expression. The use of such HuR-inhibitorsshows promise in the management of several cancers. However, the divergent functions of HuR on inflammatory degenerations– as revealed in animal models of HuR’s obligatory and tissue-specific ablation – raise skepticism on the use of HuRinhibitorsagainst inflammatory reactions – including those associated with tumors. In many cases, this is due to the poorintegration of appropriate cell-based assays to provide insights into applicability for controlling inflammatory reactions.Here, we present a transgenic macrophage-based platform for the functional assessment of HuR inhibitors that considersthe context of HuR activities in inflammation that fail when HuR is lost. We employ this platform to assess the specificityand efficacy of three publicly available and prototypical HuR disruptors and two anti-inflammatory compounds known toalter HuR’s subcellular localization. We demonstrate that only one HuR-disruptor possesses HuR-dependent and selectiveanti-inflammatory activities, which do not extend the pathologic side effects incurred by the complete obliteration of HuRin immune cells. Our data provide a proof-of-principle case on appropriately assessing the modulators of HuR, highlightingthe need to exploit context-specific cell-based assays for the preclinical evaluation of RBP inhibitors

Total pancreatectomy for pancreatic carcinoma. when, why, and what are the outcomes? Results of a systematic review

The role of total pancreatectomy (TP) to treat pancreatic carcinoma is still debated. The aims of this study were to systematically review the previous literature and to summarize the indications and results of TP for pancreatic carcinoma. A systematic search was performed to identify all studies published up to November 2018 analyzing the survival of patients undergoing TP for pancreatic carcinoma. Clinical effectiveness was synthetized through a narrative review with full tabulation of results. Six studies published between 2009 and 2016 were retrieved, including 316 patients. The major indication was positive pancreatic margin at frozen section during partial pancreatectomy. The overall morbidity ranged from 36% to 69%, and mortality from 0% to 27%. Overall survival ranged from 52.7% to 67% at 1 year, from 20% to 42% at 3 years of follow-up, whereas the 5-year estimated overall survival ranged from 4.5% to 21.9%. Total pancreatectomy has an important role in the armamentarium of pancreatic surgeons. Postoperative morbidity and mortality are not negligible, but a trend for better postoperative outcomes in recent years is noticed. Mortality related to difficult glycemic control is rare. Long-term survival is comparable with survival after partial pancreatectomy for carcinoma

Complement C3 inhibition in severe COVID-19 using compstatin AMY-101

Complement C3 activation contributes to COVID-19 pathology, and C3 targeting has emerged as a promising therapeutic strategy. We provide interim data from ITHACA, the first randomized trial evaluating a C3 inhibitor, AMY-101, in severe COVID-19 (PaO2/FiO2 <= 300 mmHg). Patients received AMY-101 (n = 16) or placebo (n = 15) in addition to standard of care. AMY-101 was safe and well tolerated. Compared to placebo (8 of 15, 53.3%), a higher, albeit nonsignificant, proportion of AMY-101-treated patients (13 of 16, 81.3%) were free of supplemental oxygen at day 14. Three nonresponders and two placebo-treated patients succumbed to disease-related complications. AMY-101 significantly reduced CRP and ferritin and restrained thrombin and NET generation. Complete and sustained C3 inhibition was observed in all responders. Residual C3 activity in the three nonresponders suggested the presence of a convertase-independent C3 activation pathway overriding the drug's inhibitory activity. These findings support the design of larger trials exploring the potential of C3-based inhibition in COVID-19 or other complement-mediated diseases