Long noncoding RNAs (lncRNAs) have emerged as critical regulators of cellular functions including maintenance of cellular homeostasis as well as the onset and progression of disease. LncRNAs often exhibit cell-, tissue-, and disease-specific expression patterns, making them desirable therapeutic targets. LncRNAs are commonly targeted using oligonucleotide therapeutics, and advances in oligonucleotide chemistry including C2 ribose sugar modifications such as 2'-fluoro, 2'-O-methyl, and 2-O-methoxyethyl modifications; 2'4'-constrained nucleotides such as locked nucleic acids and constrained 2'-O-ethyl (cEt) nucleotides; and phosphorothioate bonds have dramatically improved efficacy of oligonucleotide therapies. Novel delivery platforms such as viral vectors and nanoparticles have also improved pharmacokinetic properties of oligonucleotides targeting lncRNAs. Accumulating pre-clinical studies have utilized these strategies to therapeutically target lncRNAs and alter progression of many different disease states including Snhg12 and Chast in cardiovascular disease, Mirt2 and HOTTIP in sepsis and autoimmune disease, and Malat1 and HOXB-AS3 in cancer. Emerging oligonucleotide conjugation methods including the use of peptide nucleic acids hold promise to facilitate targeting to specific tissue types. Here, we review recent advances in lncRNA therapeutics and provide examples of how lncRNAs have been successfully targeted in pre-clinical models of disease. Finally, we detail remaining challenges facing the lncRNA field and how advances in delivery platforms and oligonucleotide chemistry might help overcome these barriers to catalyze the translation of pre-clinical studies to successful pharmaceutical development.

A major unresolved challenge in miRNA biology is the capacity to monitor the spatiotemporal activity of miRNAs expressed in animal disease models. We recently reported that the miRNA-ON monitoring system called RILES (RNAi-inducible expression Luciferase system) implanted in lentivirus expression system (LentiRILES) offers unique opportunity to decipher the kinetics of miRNA activity in vitro, in relation with their intracellular trafficking in glioblastoma cells. In this study, we describe in detail the method for the production of LentiRILES stable cell lines and employed it in several applications in the field of miRNA biology and therapy. We show that LentiRILES is a robust, highly specific and sensitive miRNA sensor system that can be used in vitro as a single-cell miRNA monitoring method, cell-based screening platform for miRNA therapeutics and as a tool to analyse the structure-function relationship of the miRNA duplex. Furthermore, we report the kinetics of miRNA activity upon the intracranial delivery of miRNA mimics in an orthotopic animal model of glioblastoma. This information is exploited to evaluate the tumour suppressive function of miRNA-200c as locoregional therapeutic modality to treat glioblastoma. Our data provide evidence that LentiRILES is a robust system, well suited to resolve the activity of endogenous and exogenously expressed miRNAs from basic research to gene and cell therapy.

Objective: Vascular smooth muscle cell (VSMC) plasticity plays a critical role in the development of atherosclerosis. Long noncoding RNAs (lncRNAs) are emerging as important regulators in the vessel wall and impact cellular function through diverse interactors. However, the role of lncRNAs in regulating VSMCs plasticity and atherosclerosis remains unclear. Approach and Results: We identified a VSMC-enriched lncRNA cardiac mesoderm enhancer-associated noncoding RNA (CARMN) that is dynamically regulated with progression of atherosclerosis. In both mouse and human atherosclerotic plaques, CARMN colocalized with VSMCs and was expressed in the nucleus. Knockdown of CARMN using antisense oligonucleotides in Ldlr −/− mice significantly reduced atherosclerotic lesion formation by 38% and suppressed VSMCs proliferation by 45% without affecting apoptosis. In vitro CARMN gain- and loss-of-function studies verified effects on VSMC proliferation, migration, and differentiation. TGF-β1 (transforming growth factor-beta) induced CARMN expression in a Smad2/3-dependent manner. CARMN regulated VSMC plasticity independent of the miR143/145 cluster, which is located in close proximity to the CARMN locus. Mechanistically, lncRNA pulldown in combination with mass spectrometry analysis showed that the nuclear-localized CARMN interacted with SRF (serum response factor) through a specific 600–1197 nucleotide domain. CARMN enhanced SRF occupancy on the promoter regions of its downstream VSMC targets. Finally, knockdown of SRF abolished the regulatory role of CARMN in VSMC plasticity. Conclusions: The lncRNA CARMN is a critical regulator of VSMC plasticity and atherosclerosis. These findings highlight the role of a lncRNA in SRF-dependent signaling and provide implications for a range of chronic vascular occlusive disease states.

The current design of the CBM-TOF inner wall is based on double stack multi-strip, multi-gap resistive plate counters (MSMGRPCs) with 2 x 5 gas gaps, equipped with low resistivity glass electrodes. Three types of MSMGRPC, with different granularity as a function of polar angle are used for a full coverage of the active area of the inner wall. A MSMGRPC prototype with the highest granularity of the CBM-TOF wall and 200 mu m gap size was tested in the Detector Laboratory of Hadron Physics Department of IFIN-HH with cosmic rays and 60Co radioactive source. The obtained performances in terms of time resolution, efficiency and its uniformity across the active area of the detector are reported in this paper.

Latest results of the R&D activity devoted to the development of the multi-strip multi-gap resistive plate counter (MSMGRPC) prototype with the highest granularity of the Time of Flight (TOF) subsystem of the Compressed Baryonic Matter (CBM) experiment are reported in this contribution. The new designed MSMGRPC fulfills simultaneously the granularity requirement and the optimum matching of the characteristic impedance of the signal transmission line to the input impedance of the front-end electronics, exploiting the special architecture of the high voltage and signal electrodes. The results in terms of the efficiency and time resolution, obtained in the laboratory cosmic ray test using a triggered data acquisition system and in heavy ion in-beam test based on a free streaming readout in mCBM setup at SIS18/GSI Darmstadt, are reported.

Long noncoding RNAs (lncRNAs) play important roles in regulating diverse cellular processes in the vessel wall, including atherosclerosis. RNA-Seq profiling of intimal lesions revealed a lncRNA, VINAS (Vascular INflammation and Atherosclerosis lncRNA Sequence), that is enriched in the aortic intima and regulates vascular inflammation. Aortic intimal expression of VINAS fell with atherosclerotic progression and rose with regression. VINAS knockdown reduced atherosclerotic lesion formation by 55% in LDL receptor–deficient (LDLR–/–) mice, independent of effects on circulating lipids, by decreasing inflammation in the vessel wall. Loss- and gain-of-function studies in vitro demonstrated that VINAS serves as a critical regulator of inflammation by modulating NF-κB and MAPK signaling pathways. VINAS knockdown decreased the expression of key inflammatory markers, such as MCP-1, TNF-α, IL-1β, and COX-2, in endothelial cells (ECs), vascular smooth muscle cells, and bone marrow–derived macrophages. Moreover, VINAS silencing decreased expression of leukocyte adhesion molecules VCAM-1, E-selectin, and ICAM-1 and reduced monocyte adhesion to ECs. DEP domain containing 4 (DEPDC4), an evolutionary conserved human ortholog of VINAS with approximately 74% homology, showed similar regulation in human and pig atherosclerotic specimens. DEPDC4 knockdown replicated antiinflammatory effects of VINAS in human ECs. These findings reveal a potentially novel lncRNA that regulates vascular inflammation, with broad implications for vascular diseases.

Long noncoding RNAs (lncRNAs) are emerging regulators of biological processes in the vessel wall; however, their role in atherosclerosis remains poorly defined. We used RNA sequencing to profile lncRNAs derived specifically from the aortic intima of Ldlr -/- mice on a high-cholesterol diet during lesion progression and regression phases. We found that the evolutionarily conserved lncRNA small nucleolar host gene-12 (SNHG12) is highly expressed in the vascular endothelium and decreases during lesion progression. SNHG12 knockdown accelerated atherosclerotic lesion formation by 2.4-fold in Ldlr -/- mice by increased DNA damage and senescence in the vascular endothelium, independent of effects on lipid profile or vessel wall inflammation. Conversely, intravenous delivery of SNHG12 protected the tunica intima from DNA damage and atherosclerosis. LncRNA pulldown in combination with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis showed that SNHG12 interacted with DNA-dependent protein kinase (DNA-PK), an important regulator of the DNA damage response. The absence of SNHG12 reduced the DNA-PK interaction with its binding partners Ku70 and Ku80, abrogating DNA damage repair. Moreover, the anti-DNA damage agent nicotinamide riboside (NR), a clinical-grade small-molecule activator of NAD+, fully rescued the increases in lesional DNA damage, senescence, and atherosclerosis mediated by SNHG12 knockdown. SNHG12 expression was also reduced in pig and human atherosclerotic specimens and correlated inversely with DNA damage and senescent markers. These findings reveal a role for this lncRNA in regulating DNA damage repair in the vessel wall and may have implications for chronic vascular disease states and aging.

The Time-of-Flight (TOF) subsystem, one of the core detectors of the CBM experiment, is dedicated to the identification of all charged hadrons produced in beam-target interaction. The targeted system time resolution of 80 ps and an efficiency above 90% should be maintained at a particle flux up to 30 kHz/cm2 in the region of low polar angles. In order to cope with these challenging requirements, CBM-TOF wall will be equipped with Multi-Gap Resistive Plate Counters with Multi-Strip readout (MSMGRPC). Our R&D activity has been focused on the development of a MSMGRPC prototype for the most demanding region of the CBM-TOF wall, the region of low polar angles (from 2.5° to ∼12° around the beam pipe). The results obtained in heavy ion in-beam tests have demonstrated the performances of the developed prototypes in conditions of exposure of the whole active area to high flux and high multiplicity reaction products. The latest developed prototypes have an optimized design which fulfills simultaneously two important requirements for MSMGRPCs, the granularity for the inner zone of the CBM-TOF subdetector and the impedance matching to the front-end electronics. Based on the obtained in-beam test results and the architecture of the developed prototypes, a modular structure of 12 units called modules is proposed. A total number of 470 MSMGRPCs (~30000 readout channels) assures an uniform coverage of the active area.

Introduction: Long non-coding RNAs (lncRNAs) are emerging regulators of biological processes in the vessel wall; however, their role in vascular inflammation remains poorly understood. Hypothesis: Identification of inflammation-responsive lncRNAs expressed in the aortic intima may provide novel mechanistic insights in vascular inflammation. Methods: Using RNA-Seq profiling to identify a lncRNA derived specifically from the aortic intima of atherosclerotic mice, we discovered an inflammation-responsive lncRNA, lncRNA-MAP3K4, and evaluated its role in the mechanisms mediating vascular cell inflammation. Results: Aortic expression of lncRNA-MAP3K4 , an intima-enriched and polyadenylated lncRNA , was reduced by 50% with atherosclerotic progression and by 75% following LPS-induced endotoxemia in mice. GapmeR-mediated silencing of lncRNA-MAP3K4 potently reduced mRNA and protein expression of adhesion molecules or chemokines (e.g. ICAM-1, E-selectin, MCP-1) in endothelial cells via a p38-MAPK pathway, and decreased PBMC adhesion to endothelium by 40%. Moreover, lncRNA-MAP3K4 knockdown also reduced inflammatory markers in vascular smooth muscle cells and macrophages. Analyzing the lncRNA-MAP3K4 locus, we found MAP3K4, an upstream kinase of the MAPK cascade, shared the promoter region with lncRNA-MAP3K4. In vitro and in vivo, lncRNA-MAP3K4 and MAP3K4 showed parallel inflammation-responsive expression patterns. lncRNA-MAP3K4 knockdown reduced mRNA and protein expression of MAP3K4 in cis in vessel wall cell types. ChIP-seq data showed chromatin modifications and bidirectional promoter characteristics in the lncRNA-MAP3K4/ MAP3K4 promoter region. MAP3K4 knockdown showed a similar anti-inflammation phenotype as lncRNA-MAP3K4 via a p38-MAPK pathway and cooperativity with lncRNA-MAP3K4 . Conclusions: Deficiency of lncRNA-MAP3K4 markedly reduced inflammation in vascular cells via a p38-MAPK pathway and cis -regulation of MAP3K4 from a shared bidirectional promoter. This study illustrated a divergently transcribed lncRNA/protein-coding gene pair involved in vascular inflammation and more broadly informs a better understanding of mammalian genome regulatory mechanisms in vascular disease states.

MicroRNA (miRNA) oligonucleotides therapeutics are potent and attractive drugs for cancer treatment, but the kinetics of their intracellular trafficking, RISC processing and interaction with their mRNA targets in the cells are still not well understood. Moreover, the absence of efficient carriers impairs their translation into the clinic. Here, we compare the kinetics of miRNA-133a activity after transfection of U87MG glioblastoma cells with either a home-made lipopolyplexes (LPRi) or with the RNAiMax transfection reagent. For this purpose, we combined miRNA intracellular trafficking studies by confocal microscopy with our previously described RILES miRNA-ON reporter system subcloned here in a lentivirus expression vector (LentiRILES) for longitudinal analysis of miRNA activity in transfected cells. Using the LentiRILES system, we report significant differences in terms of miRNA delivery kinetics performed by these two transfection regents. We decipher the mechanisms of miRNA delivery by LPRi and investigate the main steps of miRNA internalization and cytosolic processing. We demonstrate that LPRi preferentially uses caveolae-mediated endocytosis as the main internalization pathway, releases miRNA into the cytosol after the first 3 h of incubation, and addresses the cytosolic miRNAs to P-bodies, while a fraction of miRNAs are exported to the extracellular space through exosomes which were found fully capable to re-transfect the cells. We implanted the LentiRILES cells in the brain of mice and infused the tumours with LPRi.miRNA using the convection-enhanced delivery method. Bioluminescence imaging of the live mice revealed efficient delivery of miRNAs in glioblastoma tumours, attesting successful miRNA uptake, internalization and RISC activation in vivo. Overall, our study provides a comprehensive overview of miRNA intracellular trafficking and processing in a glioblastoma context and highlights the potential use of LPRi for miRNA-based therapy.

Long non-coding RNAs (lncRNAs) are emerging regulators of pathophysiological processes including atherosclerosis. Using RNA-seq profiling of the intima of lesions, here we identify a macrophage-specific lncRNA MAARS (Macrophage-Associated Atherosclerosis lncRNA Sequence). Aortic intima expression of MAARS increases by 270-fold with atherosclerotic progression and decreases with regression by 60%. MAARS knockdown reduces atherosclerotic lesion formation by 52% in LDLR −/− mice, largely independent of effects on lipid profile and inflammation, but rather by decreasing macrophage apoptosis and increasing efferocytosis in the vessel wall. MAARS interacts with HuR/ELAVL1, an RNA-binding protein and important regulator of apoptosis. Overexpression and knockdown studies verified MAARS as a critical regulator of macrophage apoptosis and efferocytosis in vitro, in an HuR-dependent manner. Mechanistically, MAARS knockdown alters HuR cytosolic shuttling, regulating HuR targets such as p53, p27, Caspase-9, and BCL2. These findings establish a mechanism by which a macrophage-specific lncRNA interacting with HuR regulates apoptosis, with implications for a broad range of vascular disease states.

Chronic vascular inflammation plays a key role in the pathogenesis of atherosclerosis. Long non-coding RNAs (lncRNAs) have emerged as essential inflammation regulators. We identify a novel lncRNA termed lncRNA-MAP3K4 that is enriched in the vessel wall and regulates vascular inflammation. In the aortic intima, lncRNA-MAP3K4 expression was reduced by 50% during the progression of atherosclerosis (chronic inflammation) and 70% during endotoxemia (acute inflammation). lncRNA-MAP3K4 knockdown reduced the expression of key inflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascular smooth muscle cells and decreased monocytes adhesion to endothelium, as well as reducing TNF-α, IL-1β, COX2 expression in macrophages. Mechanistically, lncRNA-MAP3K4 regulates inflammation through the p38 MAPK signaling pathway. lncRNA-MAP3K4 shares a bidirectional promoter with MAP3K4, an upstream regulator of the MAPK signaling pathway, and regulates its transcription in cis. lncRNA-MAP3K4 and MAP3K4 show coordinated expression in response to inflammation in vivo and in vitro. Similar to lncRNA-MAP3K4, MAP3K4 knockdown reduced the expression of inflammatory factors in several different vascular cells. Furthermore, lncRNA-MAP3K4 and MAP3K4 knockdown showed cooperativity in reducing inflammation in endothelial cells. Collectively, these findings unveil the role of a novel lncRNA in vascular inflammation by cis-regulating MAP3K4 via a p38 MAPK pathway.

Rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19), has led to a global pandemic, failures of local health care systems, and global economic recession. MicroRNAs (miRNAs) have recently emerged as important regulators of viral pathogenesis, particularly among RNA viruses, but the impact of host miRNAs on SARS-CoV-2 infectivity remains unknown. In this study, we utilize the combination of powerful bioinformatic prediction algorithms and miRNA profiling to predict endogenous host miRNAs that may play important roles in regulating SARS-CoV-2 infectivity. We provide a collection of high-probability miRNA binding sites within the SARS-CoV-2 genome as well as within mRNA transcripts of critical viral entry proteins ACE2 and TMPRSS2 and their upstream modulators, the interferons (IFN). By utilizing miRNA profiling datasets of SARS-CoV-2-resistant and -susceptible cell lines, we verify the biological plausibility of the predicted miRNA–target RNA interactions. Finally, we utilize miRNA profiling of SARS-CoV-2-infected cells to identify predicted miRNAs that are differentially regulated in infected cells. In particular, we identify predicted miRNA binders to SARS-CoV-2 ORFs (miR-23a (1ab), miR-29a, -29c (1ab, N), miR-151a, -151b (S), miR-4707-3p (S), miR-298 (5′-UTR), miR-7851-3p (5′-UTR), miR-8075 (5′-UTR)), ACE2 3′-UTR (miR-9-5p, miR-218-5p), TMPRSS2 3′-UTR (let-7d-5p, -7e-5p, miR-494-3p, miR-382-3p, miR-181c-5p), and IFN-α 3′-UTR (miR-361-5p, miR-410-3p). Overall, this study provides insight into potential novel regulatory mechanisms of SARS-CoV-2 by host miRNAs and lays the foundation for future investigation of these miRNAs as potential therapeutic targets or biomarkers.

: The progress in small-interfering RNA (siRNA) therapeutics depends on the development of suitable nanocarriers to perform specific and effective delivery to dysfunctional cells. In this paper, we questioned whether P-selectin, a cell adhesion molecule specifically expressed on the surface of activated endothelial cells (EC) could be employed as a target for nanotherapeutic intervention. To this purpose, we developed and characterized P-selectin targeted PEGylated cationic liposomes able to efficiently pack siRNA and to function as efficient vectors for siRNA delivery to tumour necrosis factor-α (TNF-α) activated EC. Targeted cationic liposomes were obtained by coupling a peptide with high affinity for P-selectin to a functionalized PEGylated phospholipid inserted in the liposomes' bilayer (Psel-lipo). As control, scrambled peptide coupled cationic liposomes (Scr-lipo) were used. The lipoplexes obtained by complexation of Psel-lipo with siRNA (Psel-lipo/siRNA) were taken up specifically and at a higher extent by TNF-α activated b.End3 endothelial cells as compared to non-targeted Scr-lipo/siRNA. The Psel-lipo/siRNA delivered with high efficiency siRNA into the cells. The lipoplexes were functional as demonstrated by the down-regulation of the selected gene (GAPDH). The results demonstrate an effective targeted delivery of siRNA into cultured activated endothelial cells using P-selectin directed PEGylated cationic liposomes, which subsequently knock-down the desired gene.

Introduction: Accumulating studies indicate that long non-coding RNAs (lncRNAs) play important roles in the regulation of diverse biological processes in health and disease. There is increasing appreciation that altered expression of lncRNAs associates with stage-specific cardiovascular diseases. Methods: Using RNA-Seq profiling to identify lncRNAs derived specifically from the aortic intima of LDLR -/- mice during lesion progression and regression phases, we discovered a lncRNA that is highly regulated in atherosclerosis. Results: Aortic intima expression of AIR ( A therosclerosis and I nflammation-associated lnc R NA) was reduced with atherosclerotic progression (by 60%) and increased with regression (by 35%). AIR, a polyadenylated lncRNA, does not encode for a protein or peptide and is expressed in both the cytoplasm and the nucleus. AIR is enriched in the aortic intima compared to the media/adventitia. Furthermore, AIR is expressed higher in endothelial cells (ECs) compared to vascular smooth muscle cells, fibroblasts, or macrophages. Expression of AIR is reduced in ECs exposed to TNF-α and IL1β. GapmeR silencing of AIR in activated ECs decreased mRNA and protein levels of VCAM-1, E-selectin, MCP-1, COX-2, and IL1βin a NF-Kβ and p38MAPK-dependent manner. Moreover, ECs deficient in AIR reduced PBMCs adhesion to TNFα-stimulated ECs by 38%. AIR knockdown increased the expression of a downstream protein, I Kappa-B Kinase-Interacting Protein (IKBIP), suggesting a cis -regulatory mechanism. In vivo AIR knockdown using GapmeRs dramatically decreased atherosclerotic lesion formation by 67% ( p=0.0001 ) in the aortic sinus of LDLR -/- mice fed with high cholesterol diet for 12 weeks compared to controls. Decreased levels of ICAM-1, E-selectin and IL1β were observed in the aortic intima in response to AIR inhibition. Finally, AIR inhibition significantly reduced levels of inflammatory markers MCP-1, COX-2, and IL1β in bone marrow, lungs, and the liver. Conclusions: Deficiency of lncRNA AIR significantly reduced the expression of key inflammatory markers in ECs in a NF-Kβ and p38MAPK-dependent manner andinhibitedatherosclerotic plaque formation by reducing vessel wall inflammation, establishing new insights for anti-inflammatory therapies.

The free streaming readout concept of the CBM experiment imposes to the Multi-Strip Multi-Gap RPCs (MSMGRPCs) developed for the CBM-TOF wall a very good matching of the characteristic impedance of the signal transmission line (corresponding to a single strip) to the input impedance of the front-end electronics in order to reduce fake signals produced by reflections. The design of the MSMGRPC prototype described here exploits in an innovative way the advantage of a strip structure for the readout and the high voltage electrodes, the impedance of the signal transmission line being adjusted independent of the detector granularly. The new design allows to built MSMGRPCs with the impedance corresponding to a single strip matched to the input impedance of the front end electronics. The prototype was tested in-beam at CERN-SPS with reaction products of a 30.A GeV Pb beam colliding onto a Pb target, in conditions rather similar in terms of energy and multiplicity with those expected at SIS100/FAIR. The obtained performance of 62 +/- 3 ps system time resolution and 97% efficiency shows that the new developed prototype meets the challenging requirements for the inner zone of the CBM-TOF wall.

The FOPI Collaboration at the GSI SIS-18 synchrotron measured charged kaons from central and semicentral collisions of Ni+Ni at a beam energy of 1.91A GeV. We present the distribution of the K-/K+ ratio on the energy vs polar angle plane in the nucleon-nucleon center-of-mass frame, with and without subtraction of the contribution of phi(1020) meson decays to the K- yield. The acceptance of the current experiment is substantially wider compared to the previous measurement of the same colliding system. The ratio of K- to K+ energy spectra is expected to be sensitive to the in-medium modifications of basic kaon properties like mass. Recent results obtained by the HADES Collaboration at 1.23A and 1.76A GeV indicate that after inclusion of the phi meson decay contribution to the K- production no difference between the slopes of the K- and K+ energy spectra is observed within uncertainties. For our data a linear fit to this ratio obtained after subtraction of the phi meson contribution still shows a decrease with kinetic energy, although a constant value cannot be rejected. The contribution of A(1520) -> pK(-) decays estimated from fitting the thermal model to the experimental yields appears to be another factor of moderate relevance.

Piasecki, K.; Tyminski, Z.; Herrmann, N.; Averbeck, R.; Andronic, A.; Barret, V.; Basrak, Z.; Bastid, N.; Benabderrahmane, M. L.; Berger, M.; Buehler, P.; Cargnelli, M.; Caplar, R.; Cordier, E.; Crochet, P.; Czerwiakowa, O.; Deppner, I.; Dupieux, P.; Dzelalija, M.; Fabbietti, L.; Fodor, Z.; Gasik, P.; Gasparic, I.; Grishkin, Y.; Hartmann, O. N.; Hildenbrand, K. D.; Hong, B.; Kang, T. I.; Kecskemeti, J.; Kim, Y. J.; Kirejczyk, M.; Kis, M.; Koczon, P.; Korolija, M.; Kotte, R.; Lebedev, A.; Leifels, Y.; Le Fevre, A.; Liu, J. L.; Lopez, X.; Mangiarotti, A.; Manko, V.; Marton, J.; Matulewicz, T.; Merschmeyer, M.; Münzer, R.; Pelte, D.; Petrovici, M.; Rami, F.; Reischl, A.; Reisdorf, W.; Ryu, M. S.; Schmidt, P.; Schüttauf, A.; Seres, Z.; Sikora, B.; Sim, K. S.; Simion, V.; SiwekWilczynska, K.; Smolyankin, V.; Stoicea, G.; Suzuki, K.; Wagner, P.; Weber, I.; Widmann, E.; Wisniewski, K.; Xiao, Z. G.; Xu, H. S.; Yushmanov, I.; Zhang, Y.; Zhilin, A.; Zinyuk, V.; Zmeskal, J.;

K. Piasecki, ∗ N. Herrmann, R. Averbeck, A. Andronic, V. Barret, Z. Basrak, N. Bastid, M.L. Benabderrahmane, M. Berger, 7 P. Buehler, M. Cargnelli, R. Čaplar, E. Cordier, P. Crochet, O. Czerwiakowa, † I. Deppner, P. Dupieux, M. Dželalija, L. Fabbietti, 7 Z. Fodor, P. Gasik, 6, 7 I. Gašparić, Y. Grishkin, O.N. Hartmann, K.D. Hildenbrand, B. Hong, T.I. Kang, J. Kecskemeti, Y.J. Kim, M. Kirejczyk, † M. Kǐs, 5 P. Koczon, M. Korolija, R. Kotte, A. Lebedev, Y. Leifels, A. Le Fèvre, J.L. Liu, 14 X. Lopez, A. Mangiarotti, V. Manko, J. Marton, T. Matulewicz, M. Merschmeyer, R. Münzer, 7 D. Pelte, M. Petrovici, F. Rami, A. Reischl, W. Reisdorf, M.S. Ryu, P. Schmidt, A. Schüttauf, Z. Seres, B. Sikora, K.S. Sim, V. Simion, K. Siwek-Wilczyńska, V. Smolyankin, G. Stoicea, K. Suzuki, Z. Tymiński, † P. Wagner, I. Weber, E. Widmann, K. Wísniewski, Z.G. Xiao, H.S. Xu, I. Yushmanov, Y. Zhang, A. Zhilin, V. Zinyuk, and J. Zmeskal