Baseband Radio over Fiber Aided Millimeter-Wave Distributed Antenna for Optical/Wireless Integration

A Baseband Radio Over Fiber (BROF) architecture is proposed, where upto four Radio Frequency (RF) carriers can be generated, while using the heterodyne photo-detection of only two optical signals. This proposed BROF architecture has a star-like structure and it is composed of six Radio Access Units (RAUs), where data is transmitted from the Central Unit (CU) to the Base Station (BS) and from the BS to the RAU over a distance of 20 Km and 0.3 Km, respectively, at a rate of 768 Mbps. The performance of the system supporting four carrier frequencies drops by at most 1dB, at a BER of 10-9, compared to conventional heterodyne photo-detection

A Full-Duplex Diversity-Assisted Hybrid Analogue/Digitized Radio Over Fibre for Optical/Wireless Integration

A duplex Radio Over Fibre (ROF) ring architecture is proposed taking into account the constraints imposed by the cost of fibre laying and of the optical/electronic components, as well as the spectral efficiency and the duplex link performance. It has been shown that relying on Analogue ROF (AROF) and state-of-the-art Digitized ROF (DROF) architectures for downlink and uplink transmission, respectively, attains a high-integrity duplex performance. A sophisticated amalgam of Optical Carrier Suppression (OCS), Code Division Multiplexing (CDM), optical frequency multiplexing, Optical Carrier Reuse (OCR) and distributed antennas is conceived

Performance improvement and cost reduction techniques for radio over fiber communications

Advanced cost reduction and performance improvement techniques conceived for Radio Over Fiber (ROF) communications are considered. ROF techniques are expected to form the backbone of the future 5G generation of wireless networks. The achievable link performance and the associated deployement cost constitute the most salient metrics of a ROF architecture. In this paper, we commence by providing a rudimentary overview of the ROF architecture and then elaborate on ROF techniques designed for improving the attainable system performance. We conclude by describing the ROF techniques conceived for reducing the ROF system installation costs

Radio-over-Fiber Aided Base Station Coordination for OFDM

This proceding at: IEEE 80th Vehicular Technology Conference (VTC)Fall. Took place 2014, September 15-19, in Vancouver (Canada).Radio over Fiber (RoF) distribution aided co-operation of Remote Access Points (RAPs) is proposed for jointly transmitting data to the users in the downlink (DL) of a Multiple Input Multiple Output Orthogonal Frequency Division Multiplexing (MIMO-OFDM) system. Joint transmission is performed with the aid of Block Diagonalization (BD), where the transmitted signal is pre-distorted in order to overcome the non-linearity imposed by the optical modulator. We demonstrate that with adequate design, the users can obtain high data rates with very small degradation introduced by the RoF transmission. Quantitatively, when M=7 RAPs, each equipped with t=2 transmit antennas (TAs) each, cooperate to serve N=7 simultaneous users, also equipped with r=2 receive antennas (RAs), the SNR degradation is kept below 0.1 dB compared to a system assuming a perfect RoF channel. On the other hand, the SNR performance degradation is around 1.2 dB, when the number of antennas at the transmitters and the receivers is increased to t=r=8.This work was supported by projects CSD2008-00010, TEC2011-29006- C03-03 and by a mobility grant of Spanish Ministry of Education. The financial support of the UK Government’s Engineering & Physical Sciences Research Council (EPSRC) as well as that of the Research Councils UK (RCUK) and of the European Research Council’s Senior Research Fellow Grant is also gratefully acknowledged.Publicad

Error vector magnitude analysis of fading SIMO channels relying on MRC reception

We analytically characterize the data-aided Error Vector Magnitude (EVM) performance of a Single Input Multiple Output (SIMO) communication system relying on Maximal Ratio Combining (MRC) having either independent or correlated branches that are non-identically distributed. In particular, exact closed form expressions are derived for the EVM in -? fading and -? shadowed fading channels and these expressions are validated by simulations. The derived expressions are expressed in terms of Lauricella’s function of the fourth kind F(N) D (.), which can be easily computed. Furthermore, we have simplified the derived expressions for various special cases such as independent and identically distributed branches, Rayleigh fading, Nakagamim fading and -? fading. Additionally, a parametric study of the EVM performance of the wireless system is presented

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570