Showing papers by "Yang Li published in 2020"

Pan-cancer analysis of whole genomes

Abstract: Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1,2,3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10,11,12,13,14,15,16,17,18.

Combined measurements of Higgs boson production and decay using up to 80 fb− 1 of proton-proton collision data at √s=13 TeV collected with the ATLAS experiment

Abstract: Combined measurements of Higgs boson production cross sections and branching fractions arc presented. The combination is based on the analyses of the Higgs boson decay modes H -> gamma gamma, ZZ ...

Patterns of somatic structural variation in human cancer genomes

Abstract: A key mutational process in cancer is structural variation, in which rearrangements delete, amplify or reorder genomic segments that range in size from kilobases to whole chromosomes1-7. Here we develop methods to group, classify and describe somatic structural variants, using data from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), which aggregated whole-genome sequencing data from 2,658 cancers across 38 tumour types8. Sixteen signatures of structural variation emerged. Deletions have a multimodal size distribution, assort unevenly across tumour types and patients, are enriched in late-replicating regions and correlate with inversions. Tandem duplications also have a multimodal size distribution, but are enriched in early-replicating regions-as are unbalanced translocations. Replication-based mechanisms of rearrangement generate varied chromosomal structures with low-level copy-number gains and frequent inverted rearrangements. One prominent structure consists of 2-7 templates copied from distinct regions of the genome strung together within one locus. Such cycles of templated insertions correlate with tandem duplications, and-in liver cancer-frequently activate the telomerase gene TERT. A wide variety of rearrangement processes are active in cancer, which generate complex configurations of the genome upon which selection can act.

SARS-CoV-2 Orf9b suppresses type I interferon responses by targeting TOM70.

Abstract: COVID-19 is caused by SARS-CoV-2. As of July 16th, 2020, there were 13,579,581 diagnosed cases and 584,782 deaths attributed to COVID-19 reported globally (https://coronavirus.jhu.edu/map. html). Unfortunately, there is still no effective drug or vaccine for treating this disease. To accelerate drug development, there is an urgent need to identify critical molecular targets and the role they play in infection. Herein, we reported that Orf9b localizes on the membrane of mitochondria and suppresses type I interferon (IFN-I) responses through association with TOM70, and TOM70 overexpression could largely rescue this inhibition. Our results suggest the potential of targeting Orf9b-TOM70 interaction as a novel therapeutic strategy of COVID-19. Induction of IFN-I is a central event of the immune defense against viral infection. Upon exposure to RNA viruses, an intracellular antiviral response is initiated by activation of RIG-I like receptors. In particular, when RIG-I/MDA5 detects viral RNA, they trigger a signaling complex on the mitochondrial outer membrane, including the adapter proteins MAVS/TRAF3/TRAF6/TOM70, which ultimately leads to IFN-β production and induction of a host antiviral state. Recent studies have shown that the most prominent feature of SARS-CoV-2, in terms of immune responses as compared to that of other viruses such as influenza A, is that it triggers a very low level of IFN-I. In addition, it has also been found that the chemical, Liquiritin, can inhibit SARS-CoV-2 by mimicking IFN-I. Thus, understanding how SARS-CoV-2 suppresses IFN-I responses may be a particularly promising approach to devise therapeutic strategies to counteract SARS-CoV-2 infections. Previous studies have shown that SARS-CoV Orf9b, an alternative open reading frame within the nucleocapsid (N) gene, can significantly inhibit IFN-I production as a result of targeting mitochondria. In addition, antibodies against Orf9b were present in the sera of convalescent SARS-CoV. or SARS-CoV-2 patients. Therefore, we speculate that SARS-CoV-2 Orf9b may play a critical role in coronavirus-host interactions, particularly via an effect on IFN-I production. To explore the role of Orf9b in host–pathogen interaction, we employed a biotin-streptavidin affinity purification mass spectrometry approach to identify the human proteins that physically interact with Orf9b (Supplementary Fig. 1a). We found that TOM70 scored the highest among all of the identified interactions (Supplementary Table 1). To validate this interaction, we performed co-immunoprecipitation (co-IP) and found that HA-TOM70 coprecipitated with Orf9b (Fig. 1a) and Orf9b could be pulled down with biotinylated TOM70 (Supplementary Fig. 1b). To quantify the binding strength of this interaction, we performed Biolayer Interferometry (BLI) and found that the Kd is indeed relatively low (44.9 nM) (Fig. 1b). Considering the high homology of Orf9b in SARS-like coronaviruses (Fig. 1c), we also tested whether SARS-CoV Orf9b interacts with TOM70. Interestingly, we found that SARS-CoV Orf9b exhibits a similar binding strength as SARS-CoV-2 Orf9b, indicating that the interaction may be conserved across the SARS-like coronavirus family (Supplementary Fig. 1c). To further pinpoint the region of TOM70 that is required for the interaction with Orf9b, TOM70 was divided into individual domains according to the known functions of the regions (Fig. 1d). We found that only the construct consisting of residues 235–608 (TOM70235-608) that contained both the core and C-terminal domains precipitated with biotinylated Orf9b, and this interaction was comparable with that of the fulllength TOM70 (Fig. 1e, Supplementary Fig. 1d). This suggests that the core and C-terminal domains of TOM70 are essential for this interaction, while the transmembrane and clamp domains are not required. Since TOM70 is located in the outer membrane of mitochondria, we hypothesized that SARS-CoV-2 Orf9b may also localize to the outer membrane of mitochondria through interaction with TOM70. Indeed, immunostaining of Orf9b-Flag expressing HEK 293T cells revealed that both SARS-CoV and SARS-CoV-2 Orf9b localize to the membrane of mitochondria (Supplementary Fig. 2a) and colocalize with TOM70 (Fig. 1f). Further, we expressed TOM70ΔTM, a construct without the N-terminal transmembrane domain of TOM70, to investigate whether it would change the mitochondria localization of Orf9b. Despite the presence of endogenous TOM70 in the cells, TOM70ΔTM overexpression indeed partially disrupted the association of SARS-CoV or SARS-CoV-2 Orf9b with mitochondria (Fig. 1g, Supplementary Fig. 2b). Considering the critical role of mitochondria and TOM70 in IFN-I responses, we next investigated whether Orf9b impacted antiviral IFN-I signaling. We monitored human interferon-β (IFN-β) promoter activity in the presence or absence of SARS-CoV-2 Orf9b using a dual luciferase reporter assay. We observed that Orf9b significantly reduced the activation of IFN-β as compared to that of the vehicle controls. The vehicle controls were prepared by co-transfecting with poly(I:C) (Fig. 1h) or MAVS overexpression (Fig. 1i). Next, we examined whether overexpression of TOM70 can counteract the Orf9b-mediated inhibition of IFN-I responses. We observed that

SARS-CoV-2 proteome microarray for global profiling of COVID-19 specific IgG and IgM responses

Abstract: We still know very little about how the human immune system responds to SARS-CoV-2. Here we construct a SARS-CoV-2 proteome microarray containing 18 out of the 28 predicted proteins and apply it to the characterization of the IgG and IgM antibodies responses in the sera from 29 convalescent patients. We find that all these patients had IgG and IgM antibodies that specifically bind SARS-CoV-2 proteins, particularly the N protein and S1 protein. Besides these proteins, significant antibody responses to ORF9b and NSP5 are also identified. We show that the S1 specific IgG signal positively correlates with age and the level of lactate dehydrogenase (LDH) and negatively correlates with lymphocyte percentage. Overall, this study presents a systemic view of the SARS-CoV-2 specific IgG and IgM responses and provides insights to aid the development of effective diagnostic, therapeutic and vaccination strategies. Currently very little is known about how our immune system responds to SARS-CoV-2 infection. Here the authors generate a SARS-CoV-2 proteome microarray for profiling of IgG and IgM responses to COVID-19 in patients and find significant responses to ORF9b and NSP5, as well as the S1 and N proteins.

Different longitudinal patterns of nucleic acid and serology testing results based on disease severity of COVID-19 patients.

Abstract: Effective strategy to mitigate the ongoing pandemic of 2019 novel coronavirus (COVID-19) require a comprehensive understanding of humoral responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the emerging virus causing COVID-19. The dynamic profile of viral replication and shedding along with viral antigen specific antibody responses among COVID-19 patients started to be reported but there is no consensus on their patterns. Here, we conducted a serial investigation on 21 individuals infected with SARS-CoV-2 in two medical centres from Jiangsu Province, including 11 non-severe COVID-19 patients, and 5 severe COVID-19 patients and 5 asymptomatic carriers based on nucleic acid test and clinical symptoms. The longitudinal swab samples and sera were collected from these people for viral RNA testing and antibody responses, respectively. Our data revealed different pattern of seroconversion among these groups. All 11 non-severe COVID-19 patients and 5 severe COVID-19 patients were seroconverted during hospitalization or follow-up period, suggesting that serological testing is a complementary assay to nucleic acid test for those symptomatic COVID-19 patients. Of note, immediate antibody responses were identified among severe cases, compared to non-severe cases. On the other hand, only one were seroconverted for asymptomatic carriers. The SARS-CoV-2 specific antibody responses were well-maintained during the observation period. Such information is of immediate relevance and would assist COVID-19 clinical diagnosis, prognosis and vaccine design.

Pan-cancer analysis of whole genomes identifies driver rearrangements promoted by LINE-1 retrotransposition.

Abstract: About half of all cancers have somatic integrations of retrotransposons. Here, to characterize their role in oncogenesis, we analyzed the patterns and mechanisms of somatic retrotransposition in 2,954 cancer genomes from 38 histological cancer subtypes within the framework of the Pan-Cancer Analysis of Whole Genomes (PCAWG) project. We identified 19,166 somatically acquired retrotransposition events, which affected 35% of samples and spanned a range of event types. Long interspersed nuclear element (LINE-1; L1 hereafter) insertions emerged as the first most frequent type of somatic structural variation in esophageal adenocarcinoma, and the second most frequent in head-and-neck and colorectal cancers. Aberrant L1 integrations can delete megabase-scale regions of a chromosome, which sometimes leads to the removal of tumor-suppressor genes, and can induce complex translocations and large-scale duplications. Somatic retrotranspositions can also initiate breakage–fusion–bridge cycles, leading to high-level amplification of oncogenes. These observations illuminate a relevant role of L1 retrotransposition in remodeling the cancer genome, with potential implications for the development of human tumors. An analysis of 2,954 genomes from 38 cancer subtypes identified 19,166 retrotransposition events in 35% of samples. Aberrant LINE-1 retrotranspositions can lead to the deletion of tumor-suppressor genes as well as the amplification of oncogenes.

Observation of structure in the J/ψ-pair mass spectrum

Abstract: Using proton-proton collision data at centre-of-mass energies of $\sqrt{s} = 7$, $8$ and $13\mathrm{\,TeV}$ recorded by the LHCb experiment at the Large Hadron Collider, corresponding to an integrated luminosity of $9\mathrm{\,fb}^{-1}$, the invariant mass spectrum of $J/\psi$ pairs is studied. A narrow structure around $6.9\mathrm{\,GeV/}c^2$ matching the lineshape of a resonance and a broad structure just above twice the $J/\psi$ mass are observed. The deviation of the data from nonresonant $J/\psi$-pair production is above five standard deviations in the mass region between $6.2$ and $7.4\mathrm{\,GeV/}c^2$, covering predicted masses of states composed of four charm quarks. The mass and natural width of the narrow $X(6900)$ structure are measured assuming a Breit--Wigner lineshape.

Performance of electron and photon triggers in ATLAS during LHC Run 2

Abstract: Electron and photon triggers covering transverse energies from 5 GeV to several TeV are essential for the ATLAS experiment to record signals for a wide variety of physics: from Standard Model processes to searches for new phenomena in both proton–proton and heavy-ion collisions. To cope with a fourfold increase of peak LHC luminosity from 2015 to 2018 (Run 2), to 2.1×1034cm-2s-1, and a similar increase in the number of interactions per beam-crossing to about 60, trigger algorithms and selections were optimised to control the rates while retaining a high efficiency for physics analyses. For proton–proton collisions, the single-electron trigger efficiency relative to a single-electron offline selection is at least 75% for an offline electron of 31 GeV, and rises to 96% at 60 GeV; the trigger efficiency of a 25 GeV leg of the primary diphoton trigger relative to a tight offline photon selection is more than 96% for an offline photon of 30 GeV. For heavy-ion collisions, the primary electron and photon trigger efficiencies relative to the corresponding standard offline selections are at least 84% and 95%, respectively, at 5 GeV above the corresponding trigger threshold.

Disruption of chromatin folding domains by somatic genomic rearrangements in human cancer

Abstract: Chromatin is folded into successive layers to organize linear DNA. Genes within the same topologically associating domains (TADs) demonstrate similar expression and histone-modification profiles, and boundaries separating different domains have important roles in reinforcing the stability of these features. Indeed, domain disruptions in human cancers can lead to misregulation of gene expression. However, the frequency of domain disruptions in human cancers remains unclear. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), which aggregated whole-genome sequencing data from 2,658 cancers across 38 tumor types, we analyzed 288,457 somatic structural variations (SVs) to understand the distributions and effects of SVs across TADs. Notably, SVs can lead to the fusion of discrete TADs, and complex rearrangements markedly change chromatin folding maps in the cancer genomes. Notably, only 14% of the boundary deletions resulted in a change in expression in nearby genes of more than twofold.

Erratum: The Belle II Physics Book (Progress of Theoretical and Experimental Physics (2019) 2019 (123C01) DOI: 10.1093/ptep/ptz106)

Abstract: In the original version of this manuscript, an error was introduced on pp352. '2.7nb:1.6nb' has been corrected to '2.4nb:1.3nb' in the current online and printed version. doi:10.1093/ptep/ptz106.

Hsp27 chaperones FUS phase separation under the modulation of stress-induced phosphorylation

Abstract: Protein phase separation drives the assembly of membraneless organelles, but little is known about how these membraneless organelles are maintained in a metastable liquid- or gel-like phase rather than proceeding to solid aggregation. Here, we find that human small heat-shock protein 27 (Hsp27), a canonical chaperone that localizes to stress granules (SGs), prevents FUS from undergoing liquid-liquid phase separation (LLPS) via weak interactions with the FUS low complexity (LC) domain. Remarkably, stress-induced phosphorylation of Hsp27 alters its activity, leading Hsp27 to partition with FUS LC to preserve the liquid phase against amyloid fibril formation. NMR spectroscopy demonstrates that Hsp27 uses distinct structural mechanisms for both functions. Our work reveals a fine-tuned regulation of Hsp27 for chaperoning FUS into either a polydispersed state or a LLPS state and suggests an essential role for Hsp27 in stabilizing the dynamic phase of stress granules.

A comprehensive, longitudinal analysis of humoral responses specific to four recombinant antigens of SARS-CoV-2 in severe and non-severe COVID-19 patients.

Abstract: There is an urgent need for effective treatment and preventive vaccine to contain this devastating global pandemic, which requires a comprehensive understanding of humoral responses specific to SARS-CoV-2 during the disease progression and convalescent phase of COVID-19 patients. We continuously monitored the serum IgM and IgG responses specific to four SARS-CoV-2 related antigens, including the nucleoprotein (NP), receptor binding domain (RBD), S1 protein, and ectodomain (ECD) of the spike protein among non-severe and severe COVID-19 patients for seven weeks since disease onset. Most patients generated humoral responses against NP and spike protein-related antigens but with their distinct kinetics profiles. Combined detection of NP and ECD antigens as detecting antigen synergistically improved the sensitivity of the serological assay, compared to that of using NP or RBD as detection antigen. 80.7% of convalescent sera from COVID-19 patients revealed that the varying extents of neutralization activities against SARS-CoV-2. S1-specific and ECD-specific IgA responses were strongly correlated with the neutralization activities in non-severe patients, but not in severe patients. Moreover, the neutralizing activities of the convalescent sera were shown to significantly decline during the period between 21 days to 28 days after hospital discharge, accompanied by a substantial drop in RBD-specific IgA response. Our data provide evidence that are crucial for serological testing, antibody-based intervention, and vaccine design of COVID-19.

Study of the lineshape of the χc1 (3872) state

Abstract: A study of the lineshape of the χc1(3872) state is made using a data sample corresponding to an integrated luminosity of 3 fb-1 collected in pp collisions at center-of-mass energies of 7 and 8 TeV with the LHCb detector. Candidate χc1(3872) and ψ(2S) mesons from b-hadron decays are selected in the J/ψπ+π- decay mode. Describing the lineshape with a Breit-Wigner function, the mass splitting between the χc1(3872) and ψ(2S) states, Δm, and the width of the χc1(3872) state, ΓBW, are determined to be Δm=185.598±0.067±0.068 MeV,ΓBW=1.39±0.24±0.10 MeV, where the first uncertainty is statistical and the second systematic. Using a Flatte-inspired model, the mode and full width at half maximum of the lineshape are determined to be mode=3871.69-0.04-0.13+0.00+0.05 MeV,FWHM=0.22-0.06-0.13+0.07+0.11 MeV. An investigation of the analytic structure of the Flatte amplitude reveals a pole structure, which is compatible with a quasibound D0D¯*0 state but a quasivirtual state is still allowed at the level of 2 standard deviations.

A DNAH17 missense variant causes flagella destabilization and asthenozoospermia.

Abstract: Asthenozoospermia is a common cause of male infertility, but its etiology remains incompletely understood. We recruited three Pakistani infertile brothers, born to first-cousin parents, displaying idiopathic asthenozoospermia but no ciliary-related symptoms. Whole-exome sequencing identified a missense variant (c.G5408A, p.C1803Y) in DNAH17, a functionally uncharacterized gene, recessively cosegregating with asthenozoospermia in the family. DNAH17, specifically expressed in testes, was localized to sperm flagella, and the mutation did not alter its localization. However, spermatozoa of all three patients showed higher frequencies of microtubule doublet(s) 4-7 missing at principal piece and end piece than in controls. Mice carrying a homozygous mutation (Dnah17M/M) equivalent to that in patients recapitulated the defects in patients' sperm tails. Further examinations revealed that the doublets 4-7 were destabilized largely due to the storage of sperm in epididymis. Altogether, we first report that a homozygous DNAH17 missense variant specifically induces doublets 4-7 destabilization and consequently causes asthenozoospermia, providing a novel marker for genetic counseling and diagnosis of male infertility.

EuPRAXIA Conceptual Design Report

Abstract: This report presents the conceptual design of a new European research infrastructure EuPRAXIA. The concept has been established over the last four years in a unique collaboration of 41 laboratories within a Horizon 2020 design study funded by the European Union. EuPRAXIA is the first European project that develops a dedicated particle accelerator research infrastructure based on novel plasma acceleration concepts and laser technology. It focuses on the development of electron accelerators and underlying technologies, their user communities, and the exploitation of existing accelerator infrastructures in Europe. EuPRAXIA has involved, amongst others, the international laser community and industry to build links and bridges with accelerator science — through realising synergies, identifying disruptive ideas, innovating, and fostering knowledge exchange. The Eu-PRAXIA project aims at the construction of an innovative electron accelerator using laser- and electron-beam-driven plasma wakefield acceleration that offers a significant reduction in size and possible savings in cost over current state-of-the-art radiofrequency-based accelerators. The foreseen electron energy range of one to five gigaelectronvolts (GeV) and its performance goals will enable versatile applications in various domains, e.g. as a compact free-electron laser (FEL), compact sources for medical imaging and positron generation, table-top test beams for particle detectors, as well as deeply penetrating X-ray and gamma-ray sources for material testing. EuPRAXIA is designed to be the required stepping stone to possible future plasma-based facilities, such as linear colliders at the high-energy physics (HEP) energy frontier. Consistent with a high-confidence approach, the project includes measures to retire risk by establishing scaled technology demonstrators. This report includes preliminary models for project implementation, cost and schedule that would allow operation of the full Eu-PRAXIA facility within 8—10 years.

Global profiling of SARS-CoV-2 specific IgG/ IgM responses of convalescents using a proteome microarray

Abstract: COVID-19 is caused by SARS-CoV-2, and has become a global pandemic. There is no highly effective medicine or vaccine, most of the patients were recovered by their own immune response, especially the virus specific IgG and IgM responses. However, the IgG/ IgM responses is barely known. To enable the global understanding of SARS-CoV-2 specific IgG/ IgM responses, a SARS-CoV-2 proteome microarray with 18 out of the 28 predicted proteins was constructed. The microarray was applied to profile the IgG/ IgM responses with 29 convalescent sera. The results suggest that at the convalescent phase 100% of patients had IgG/ IgM responses to SARS-CoV-2, especially to protein N, S1 but not S2. S1 purified from mammalian cell demonstrated the highest performance to differentiate COVID-19 patients from controls. Besides protein N and S1, significant antibody responses to ORF9b and NSP5 were also identified. In-depth analysis showed that the level of S1 IgG positively correlate to age and the level of LDH (lactate dehydrogenase), especially for women, while the level of S1 IgG negatively correlate to Ly% (Lymphocyte percentage). This study presents the first whole picture of the SARS-CoV-2 specific IgG/ IgM responses, and provides insights to develop precise immuno-diagnostics, effective treatment and vaccine.

Evidence of a $J/\psi \varLambda$ structure and observation of excited $\varXi^-$ states in the $\varXi_b^-\to J/\psi \varLambda K^-$ decay

Abstract: First evidence of a structure in the $J/\psi \varLambda$ invariant mass distribution is obtained from an amplitude analysis of $\varXi_b^- \to J/\psi \varLambda K^-$ decays. The observed structure is consistent with being due to a charmonium pentaquark with strangeness. Its mass and width are determined to be $4458.8\pm2.9\,^{+4.7}_{-1.1}$MeV and $17.3\pm6.5\,^{+8.0}_{-5.7}$MeV, where the quoted uncertainties are statistical and systematic, respectively. The structure is also consistent with being due to two resonances. In addition, the narrow excited $\varXi^-$ states, $\varXi(1690)^-$ and $\varXi(1820)^-$, are seen for the first time in a $\varXi_b^-$ decay, and their masses and widths are measured with improved precision. The analysis is performed using $pp$ collision data corresponding to a total integrated luminosity of 9fb$^{-1}$, collected with the LHCb experiment at centre-of-mass energies of $7$, $8$ and $13$TeV.

Metal-Free 2D/2D Black Phosphorus and Covalent Triazine Framework Heterostructure for CO2 Photoreduction

Abstract: Photoreduction of CO2 to CH4, which is an 8-electron photoelectrochemical process, represents one of the most appealing approaches that tackles the global warming challenge and fuel crisis. To achi...

Observation of Several Sources of CP Violation in B^{+}→π^{+}π^{+}π^{-} Decays.

Abstract: Observations are reported of different sources of CP violation from an amplitude analysis of B^{+}→π^{+}π^{+}π^{-} decays, based on a data sample corresponding to an integrated luminosity of 3 fb^{-1} of pp collisions recorded with the LHCb detector. A large CP asymmetry is observed in the decay amplitude involving the tensor f_{2}(1270) resonance, and in addition significant CP violation is found in the π^{+}π^{-}S wave at low invariant mass. The presence of CP violation related to interference between the π^{+}π^{-}S wave and the P wave B^{+}→ρ(770)^{0}π^{+} amplitude is also established; this causes large local asymmetries but cancels when integrated over the phase space of the decay. The results provide both qualitative and quantitative new insights into CP -violation effects in hadronic B decays.

Reversible interconversion between methanol-diamine and diamide for hydrogen storage based on manganese catalyzed (de)hydrogenation

Abstract: The development of cost-effective, sustainable, and efficient catalysts for liquid organic hydrogen carrier systems is a significant goal. However, all the reported liquid organic hydrogen carrier systems relied on the use of precious metal catalysts. Herein, a liquid organic hydrogen carrier system based on non-noble metal catalysis was established. The Mn-catalyzed dehydrogenative coupling of methanol and N,N’-dimethylethylenediamine to form N,N’-(ethane-1,2-diyl)bis(N-methylformamide), and the reverse hydrogenation reaction constitute a hydrogen storage system with a theoretical hydrogen capacity of 5.3 wt%. A rechargeable hydrogen storage could be achieved by a subsequent hydrogenation of the resulting dehydrogenation mixture to regenerate the H2-rich compound. The maximum selectivity for the dehydrogenative amide formation was 97%. The development of cost-effective, sustainable, and efficient catalysts for liquid organic hydrogen carrier systems is a significant goal. Herein, authors present a system based on manganese catalysis with a theoretical H2 capacity of 5.3 wt% and high selectivity for the dehydrogenation reaction.

Amplitude analysis of the B + → π + π + π − decay

Abstract: The results of an amplitude analysis of the charmless three-body decay B+→π+π+π-, in which CP-violation effects are taken into account, are reported. The analysis is based on a data sample corresponding to an integrated luminosity of 3 fb-1 of pp collisions recorded with the LHCb detector. The most challenging aspect of the analysis is the description of the behavior of the π+π- S-wave contribution, which is achieved by using three complementary approaches based on the isobar model, the K-matrix formalism, and a quasi-model-independent procedure. Additional resonant contributions for all three methods are described using a common isobar model, and include the ρ(770)0, ω(782) and ρ(1450)0 resonances in the π+π- P-wave, the f2(1270) resonance in the π+π- D-wave, and the ρ3(1690)0 resonance in the π+π- F-wave. Significant CP-violation effects are observed in both S- and D-waves, as well as in the interference between the S- and P-waves. The results from all three approaches agree and provide new insight into the dynamics and the origin of CP-violation effects in B+→π+π+π- decays.

Measurement of $CP$ violation in $B^0\to D^{*\pm} D^{\mp}$ decays

Abstract: The decay-time-dependent CP asymmetry in B$^{0}$→ D$^{∗±}$D$^{∓}$ decays is mea- sured using a data set corresponding to an integrated luminosity of 9 fb$^{−1}$ recorded by the LHCb detector in proton-proton collisions at centre-of-mass energies of 7, 8 and 13 TeV. The CP parameters are measured as$ {\displaystyle \begin{array}{c}{S}_{D\ast D}=-0.861\pm 0.077\left(\mathrm{stat}\right)\pm 0.019\left(\mathrm{syst}\right),\\ {}\varDelta {S}_{D\ast D}=0.019\pm 0.075\left(\mathrm{stat}\right)\pm 0.012\left(\mathrm{syst}\right),\\ {}{C}_{D\ast D}=-0.059\pm 0.092\left(\mathrm{stat}\right)\pm 0.020\left(\mathrm{syst}\right),\\ {}{\varDelta C}_{D\ast D}=-0.031\pm 0.092\left(\mathrm{stat}\right)\pm 0.016\left(\mathrm{syst}\right),\\ {}{\mathcal{A}}_{D\ast D}=\kern0.75em 0.008\pm 0.014\left(\mathrm{stat}\right)\pm 0.006\left(\mathrm{syst}\right).\end{array}} $The analysis provides the most precise single measurement of CP violation in this decay channel to date. All parameters are consistent with their current world average values.[graphic not available: see fulltext]

Angular Analysis of the $B^{+}\rightarrow K^{\ast+}\mu^{+}\mu^{-}$ Decay

Abstract: We present an angular analysis of the $B^{+}\rightarrow K^{\ast+}(\rightarrow K_{S}^{0}\pi^{+})\mu^{+}\mu^{-}$ decay using 9$\,\mbox{fb}^{-1}$ of $pp$ collision data collected with the LHCb experiment. For the first time, the full set of CP-averaged angular observables is measured in intervals of the dimuon invariant mass squared. Local deviations from Standard Model predictions are observed, similar to those in previous LHCb analyses of the isospin-partner $B^{0}\rightarrow K^{\ast0}\mu^{+}\mu^{-}$ decay. The global tension is dependent on which effective couplings are considered and on the choice of theory nuisance parameters.

Study of the ψ 2(3823) and χ c1(3872) states in B+ → (J/ψπ + π −)K+ decays

Abstract: The decays B$^{+}$→ J/ψπ$^{+}$π$^{−}$K$^{+}$ are studied using a data set corresponding to an integrated luminosity of 9 fb$^{−1}$ collected with the LHCb detector in proton-proton collisions between 2011 and 2018. Precise measurements of the ratios of branching fractions with the intermediate ψ$_{2}$(3823), χ$_{c1}$(3872) and ψ(2S) states are reported. The values are$ {\displaystyle \begin{array}{c}\frac{{\mathcal{B}}_{{\mathrm{B}}^{+}\to {\uppsi}_2(3823){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\uppsi_2(3823)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}{{\mathcal{B}}_{{\mathrm{B}}^{+}\to {\upchi}_{\mathrm{c}1}(3872){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\upchi_{\mathrm{c}1}(3872)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}=\left(3.56\pm 0.67\pm 0.11\right)\times {10}^{-2},\\ {}\frac{{\mathcal{B}}_{{\mathrm{B}}^{+}\to {\uppsi}_2(3823){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\uppsi_2(3823)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}{{\mathcal{B}}_{{\mathrm{B}}^{+}\to \uppsi \left(2\mathrm{S}\right){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\uppsi \left(2\mathrm{S}\right)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}=\left(1.31\pm 0.25\pm 0.04\right)\times {10}^{-3},\\ {}\frac{{\mathcal{B}}_{\mathrm{B}+\to {\upchi}_{\mathrm{c}1}(3872){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\upchi_{\mathrm{c}1}(3872)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}{{\mathcal{B}}_{{\mathrm{B}}^{+}\to \uppsi \left(2\mathrm{S}\right){\mathrm{K}}^{+}}\times {\mathcal{B}}_{\uppsi \left(2\mathrm{S}\right)\to \mathrm{J}/{\uppsi \uppi}^{+}{\uppi}^{-}}}=\left(3.69\pm 0.07\pm 0.06\right)\times {10}^{-2},\end{array}} $where the first uncertainty is statistical and the second is systematic. The decay of B$^{+}$→ ψ$_{2}$(3823)K$^{+}$ with ψ$_{2}$(3823) → J/ψπ$^{+}$π$^{−}$ is observed for the first time with a significance of 5.1 standard deviations. The mass differences between the ψ$_{2}$(3823), χ$_{c1}$(3872) and ψ(2S) states are measured to be$ {\displaystyle \begin{array}{c}{m}_{\upchi_{\mathrm{c}1}(3872)}-{m}_{\uppsi_2(3823)}=47.50\pm 0.53\pm 0.13\;\mathrm{MeV}/{c}^2,\\ {}{m}_{\uppsi_2(3823)}-{m}_{\uppsi_2\left(2\mathrm{S}\right)}=137.98\pm 0.53\pm 0.14\;\mathrm{MeV}/{c}^2,\\ {}{m}_{\upchi_{\mathrm{c}1}(3872)}-{m}_{\uppsi_2\left(2\mathrm{S}\right)}=185.49\pm 0.06\pm 0.03\;\mathrm{MeV}/{c}^2,\end{array}} $resulting in the most precise determination of the χ$_{c1}$(3872) mass. The width of the ψ$_{2}$(3823) state is found to be below 5.2 MeV at 90% confidence level. The Breit-Wigner width of the χ$_{c1}$(3872) state is measured to be$ {\Gamma}_{\upchi_{\mathrm{c}1}(3872)}^{\mathrm{BW}}={0.96}_{-0.18}^{+0.19}\pm 0.21\;\mathrm{MeV} $which is inconsistent with zero by 5.5 standard deviations.[graphic not available: see fulltext]

Hsp40 proteins phase separate to chaperone the assembly and maintenance of membraneless organelles.

Abstract: Membraneless organelles contain a wide spectrum of molecular chaperones, indicating their important roles in modulating the metastable conformation and biological function of membraneless organelles. Here we report that class I and II Hsp40 (DNAJ) proteins possess a high ability of phase separation rendered by the flexible G/F-rich region. Different Hsp40 proteins localize in different membraneless organelles. Specifically, human Hdj1 (DNAJB1), a class II Hsp40 protein, condenses in ubiquitin (Ub)-rich nuclear bodies, while Hdj2 (DNAJA1), a class I Hsp40 protein, condenses in nucleoli. Upon stress, both Hsp40 proteins incorporate into stress granules (SGs). Mutations of the G/F-rich region not only markedly impaired Hdj1 phase separation and SG involvement and disrupted the synergistic phase separation and colocalization of Hdj1 and fused in sarcoma (FUS) in cells. Being cophase separated with FUS, Hdj1 stabilized the liquid phase of FUS against proceeding into amyloid aggregation in vitro and alleviated abnormal FUS aggregation in cells. Moreover, Hdj1 uses different domains to chaperone FUS phase separation and amyloid aggregation. This paper suggests that phase separation is an intrinsic property of Hsp40 proteins, which enables efficient incorporation and function of Hsp40 in membraneless organelles and may further mediate the buildup of chaperone network in membraneless organelles.