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Ou JHJ, Kuhn RJ, Lopez S, Rice CM
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Biographical Feature: James H. Strauss, Jr. (1938-2021)
JOURNAL OF VIROLOGY 2022 MAY 11; 96(9):?
David A, Parkinson N, Peacock TP, Pairo-Castineira E, Khanna T, Cobat A, Tenesa A, Sancho-Shimizu V, Casanova JL, Abel L, Barclay WS, Baillie JK, Sternberg MJE
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A common TMPRSS2 variant has a protective effect against severe COVID-19
CURRENT RESEARCH IN TRANSLATIONAL MEDICINE 2022 MAY; 70(2):? Article 103333
Background: The human protein transmembrane protease serine type 2 (TMPRSS2) plays a key role in SARS-CoV-2 infection, as it is required to activate the virus' spike protein, facilitating entry into target cells. We hypothesized that naturally-occurring TMPRSS2 human genetic variants affecting the structure and function of the TMPRSS2 protein may modulate the severity of SARS-CoV-2 infection. Methods: We focused on the only common TMPRSS2 non-synonymous variant predicted to be damaging (rs12329760 C>T, p.V160M), which has a minor allele frequency ranging from 0.14 in Ashkenazi Jewish to 0.38 in East Asians. We analysed the association between the rs12329760 and COVID-19 severity in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units recruited as part of the GenOMICC (Genetics Of Mortality In Critical Care) study. Logistic regression analyses were adjusted for sex, age and deprivation index. For in vitro studies, HEK293 cells were co-transfected with ACE2 and either TMPRSS2 wild type or mutant (TMPRSS2(V160M)). A SARS-CoV-2 pseudovirus entry assay was used to investigate the ability of TMPRSS2(V160M) to promote viral entry. Results: We show that the T allele of rs12329760 is associated with a reduced likelihood of developing severe COVID-19 (OR 0.87, 95%CI:0.79-0.97, p = 0.01). This association was stronger in homozygous individuals when compared to the general population (OR 0.65, 95%CI:0.50-0.84, p = 1.3 x 10(-3)). We demonstrate in vitro that this variant, which causes the amino acid substitution valine to methionine, affects the catalytic activity of TMPRSS2 and is less able to support SARS-CoV-2 spike-mediated entry into cells. Conclusion: TMPRSS2 rs12329760 is a common variant associated with a significantly decreased risk of severe COVID-19. Further studies are needed to assess the expression of TMPRSS2 across different age groups. Moreover, our results identify TMPRSS2 as a promising drug target, with a potential role for camostat mesilate, a drug approved for the treatment of chronic pancreatitis and postoperative reflux esophagitis, in the treatment of COVID-19. Clinical trials are needed to confirm this. (C) 2022 The Authors. Published by Elsevier Masson SAS.
Hosfelt J, Richards A, Zheng M, Adura C, Nelson B, Yang A, Fay A, Resager W, Ueberheide B, Glickman JF, Lupoli TJ
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Article An allosteric inhibitor of bacterial Hsp70 chaperone potentiates antibiotics and mitigates resistance
CELL CHEMICAL BIOLOGY 2022 MAY 19; 29(5):854-+
DnaK is the bacterial homolog of Hsp70, an ATP-dependent chaperone that helps cofactor proteins to catalyze nascent protein folding and salvage misfolded proteins. In the pathogen Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), DnaK and its cofactors are proposed antimycobacterial targets, yet few small-molecule inhibitors or probes exist for these families of proteins. Here, we describe the repurposing of a drug called telaprevir that is able to allosterically inhibit the ATPase activity of DnaK and to prevent chaperone function by mimicking peptide substrates. In mycobacterial cells, telaprevir disrupts DnaK-and cofactor-mediated cellular proteostasis, resulting in enhanced efficacy of aminoglycoside antibiotics and reduced resistance to the frontline TB drug rifampin. Hence, this work contributes to a small but growing collection of protein chaperone inhibitors, and it demonstrates that these molecules disrupt bacterial mechanisms of survival in the presence of different antibiotic classes.
Meednu N, Rangel-Moreno J, Zhang F, Escalera-Rivera K, Corsiero E, Prediletto E, DiCarlo E, Goodman S, Donlin LT, Raychauduri S, Bombardieri M, Pitzalis C, Orange DE, McDavid A, Anolik JH
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Dynamic spectrum of ectopic lymphoid B cell activation and hypermutation in the RA synovium characterized by NR4A nuclear receptor expression
CELL REPORTS 2022 MAY 3; 39(5):? Article 110766
Ectopic lymphoid structures (ELS) can develop in rheumatoid arthritis (RA) synovial tissue, but the precise pathways of B cell activation and selection are not well understood. Here, we identify a synovial B cell population characterized by co-expression of a family of orphan nuclear receptors (NR4A1-3), which is highly enriched in RA synovial tissue. A transcriptomic profile of NR4A synovial B cells significantly overlaps with germinal center light zone B cells and an accrual of somatic hypermutation that correlates with loss of naive B cell state. NR4A B cells co-express lymphotoxins a and b and IL-6, supporting functions in ELS promotion. Expanded and shared clones between synovial NR4A B cells and plasma cells and the rapid upregulation with BCR stimulation point to in situ differentiation. Together, we identify a dynamic progression of B cell activation in RA synovial ELS, with NR4A transcription factors having an important role in local adaptive immune responses.
Ahmed Z, Agha N, Trunk A, Berger M, Gail A
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Universal Guide for Skull Extraction and Custom-Fitting of Implants to Continuous and Discontinuous Skulls
ENEURO 2022 MAY-JUN; 9(3):? Article 0028-22.2022
Intracranial neurophysiological recordings require chronic implants to provide transcranial access to the brain. Especially in larger animals, which participate in experiments over extended periods of time, implants should match the skull curvature to promote osseointegration and avoid tissue and bacterial ingress over time. Proposed CAD methods for designing implants to date have focused on naive animals with continuous and even skull surfaces and calculate Boolean differences between implant and skull surface to fit the implant to the skull curvature. However, custom-fitting by calculating the difference fails, if a discontinuous skull surface needs to be matched. Also, the difference method does not allow designs with constant material thickness along the skull curvature, e.g., to allow fixed screw lengths. We present a universal step-by-step guide for custom-fitting implants which overcomes these limitations. It is suited for unusual skull conditions, like surface discontinuities or irregularities and includes virtual bending as a process to match skull surfaces while maintaining implant thickness. We demonstrate its applicability for a wide spectrum of scenarios, ranging from complex-shaped single-pieced implants to detailed multicomponent implant systems built on even or discontinuous skull. The guide uses only a few software tools and the final virtual product can be manufactured using CNC milling or 3D printing. A detailed description of this process is available on GitHub including step-by-step video instructions suitable for users without any prior knowledge in CAD programming. We report the experience with these implants over several years in 11 rhesus monkeys.
Bernatowska E, Pac M, Heropolitanska-Pliszka E, Pietrucha B, Dabrowska-Leonik N, Skomska-Pawliszak M, Bernat-Sitarz K, Krzysztopa-Grzybowska K, Wolska-Kusnierz B, Bohynikova N, Augustynowicz E, Augustynowicz-Kopec E, Korzeniewska-Kosela M, Wieteska-Klimczak A, Ksiazyk J, Jackowska T, van den Burg M, Casanova JL, Picard C, Mikoluc B
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BCG Moreau Polish Substrain Infections in Patients With Inborn Errors of Immunity: 40 Years of Experience in the Department of Immunology, Children's Memorial Health Institute, Warsaw
FRONTIERS IN PEDIATRICS 2022 MAY 19; 10(?):? Article 839111
ObjectiveWe aimed to assess BCG (Bacillus Calmette-Guerin) complications in patients with Inborn Errors of Immunity (IEI), according to the inherited disorders and associated immunological defects, as well as the different BCG substrains. MaterialWe studied adverse reactions to the locally-produced BCG Moreau vaccine, analyzed in patients with IEI diagnosed between 1980 and 2020 in the Department of Immunology, Children's Memorial Health Institute (CMHI), Warsaw. These results were compared with previously published studies. ResultsSignificantly fewer disseminated BCG infections (BCGosis) were found in 11 of 72 (15%) SCID (Severe Combined Immunodeficiency) NK (Natural Killer)-phenotype patients, when compared with the 119 out of 349 (34%) (p = 0.0012) patients with SCID with BCG in other countries. Significantly fewer deaths caused by BCGosis were observed (p = 0.0402). A significantly higher number of hematopoietic stem cell transplantations (HSCTs) were performed in the CMHI study (p = 0.00001). BCGosis was found in six patients with Mendelian susceptibility to mycobacterial diseases (MSMD). Other patients with IEI prone to BCG complications, such as CGD (Chronic Granulomatous Disease), showed no case of BCGosis. ConclusionThe BCG Moreau substrain vaccine, produced in Poland since 1955, showed genetic differences with its parental Brazilian substrain together with a superior clinical safety profile in comparison with the other BCG substrains, with no BCGosis in patients with IEI other than SCID and MSMD. Our data also confirmed significantly fewer cases of BCGosis and deaths caused by BCG infection in patients with SCID with this vaccine substrain. Finally, they confirmed the protecting role of NK cells, probably via their production of IFN-gamma.
Blauvelt A, Guttman-Yassky E, Paller AS, Simpson EL, Cork MJ, Weisman J, Browning J, Soong W, Sun X, Chen Z, Kosloski MP, Kamal MA, Delevry D, Chuang CC, O'Malley JT, Bansal A
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Long-Term Efficacy and Safety of Dupilumab in Adolescents with Moderate-to-Severe Atopic Dermatitis: Results Through Week 52 from a Phase III Open-Label Extension Trial (LIBERTY AD PED-OLE)
AMERICAN JOURNAL OF CLINICAL DERMATOLOGY 2022 MAY; 23(3):365-383
Background For adolescent patients (aged >= 12 to <18 years) with uncontrolled moderate-to-severe atopic dermatitis (AD), 16 weeks of treatment with dupilumab resulted in substantial clinical benefit compared with placebo, with an acceptable safety profile. However, long-term data on the approved dose regimens of dupilumab in adolescents with AD are lacking. Objectives This open-label extension study (LIBERTY AD PED-OLE, NCT02612454) reports the long-term safety, efficacy, and pharmacokinetics of dupilumab in adolescents with moderate-to-severe AD who had participated in dupilumab parent trials. Methods Patients enrolled under the original study protocol received subcutaneous dupilumab according to a weight-based regimen (2 or 4 mg/kg every week). Following protocol amendment, patients were switched to subcutaneous dupilumab 300 mg every 4 weeks (q4w) irrespective of weight, and newly enrolled patients were started on dupilumab 300 mg q4w. Patients with an inadequate clinical response (Investigator's Global Assessment [IGA] score of 0/1 was not reached) to the q4w regimen could be uptitrated to the approved dupilumab dose regimens of 200 or 300 mg every 2 weeks (body weight <60 or >= 60 kg, respectively). Patients whose IGA score of 0/1 was maintained continuously for a 12-week period after week 40 were discontinued from dupilumab, monitored for relapse, and re-initiated on dupilumab if required. Results Data for 294 patients (mean age 14.7 years) were analyzed, 102 (34.7%) of whom had completed the 52-week visit at the database lock. The dupilumab long-term safety profile was comparable to that seen in adults and consistent with the known safety profile. Most treatment-emergent adverse events were mild/moderate. By week 52, 42.7% of patients had an IGA score of 0/1 (clear/almost clear), and 93.1%, 81.2%, and 56.4%, respectively, had at least a 50%, 75%, or 90% improvement in Eczema Area and Severity Index (EASI). Most (70.9%) patients required uptitration to the approved dupilumab dose regimen. The proportions of uptitrated patients with an IGA score of 0/1 or 75% improvement in EASI increased over time, reaching 35.7% and 51.9%, respectively, 48 weeks after the first uptitration visit. By week 52, 29.4% of patients had clear/almost clear skin sustained for 12 weeks and had stopped medication; 56.7% relapsed and were subsequently re-initiated on treatment, with a mean time to re-initiation of 17.5 (+/- standard deviation 17.3) weeks. Conclusions Consistent with results seen with short-term treatment, long-term treatment with dupilumab showed an acceptable safety profile while providing incremental clinical benefit with continued treatment over time. The high proportion of patients who needed uptitration because of inadequate response to q4w dosing supports the q2w dose regimen as optimal for this age group. Finally, the majority of patients who stopped medication after having clear/almost clear skin sustained over 12 weeks experienced disease recurrence, suggesting the need for continued dupilumab dosing to maintain efficacy.
Chen HF, Hu B, Horth C, Bareke E, Rosenbaum P, Kwon SY, Sirois J, Weinberg DN, Robison FM, Garcia BA, Lu C, Pastor WA, Majewski J
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H3K36 dimethylation shapes the epigenetic interaction landscape by directing repressive chromatin modifications in embryonic stem cells
GENOME RESEARCH 2022 MAY; 32(5):825-837
Epigenetic modifications on the chromatin do not occur in isolation. Chromatin-associated proteins and their modification products form a highly interconnected network, and disturbing one component may rearrange the entire system. We see this increasingly clearly in epigenetically dysregulated cancers. It is important to understand the rules governing epigenetic interactions. Here, we use the mouse embryonic stem cell (mESC) model to describe in detail the relationships within the H3K27-H3K36-DNA methylation subnetwork. In particular, we focus on the major epigenetic reorganization caused by deletion of the histone 3 lysine 36 methyltransferase NSD1, which in mESCs deposits nearly all of the intergenic H3K36me2. Although disturbing the H3K27 and DNA methylation (DNAme) components also affects this network to a certain extent, the removal of H3K36me2 has the most drastic effect on the epigenetic landscape, resulting in full intergenic spread of H3K27me3 and a substantial decrease in DNAme. By profiling DNMT3A and CHH methylation (mCHH), we show that H3K36me2 loss upon Nsd1-KO leads to a massive redistribution of DNMT3A and mCHH away from intergenic regions and toward active gene bodies, suggesting that DNAme reduction is at least in part caused by redistribution of de novo methylation. Additionally, we show that pervasive acetylation of H3K27 is regulated by the interplay of H3K36 and H3K27 methylation. Our analysis highlights the importance of H3K36me2 as a major determinant of the developmental epigenome and provides a framework for further consolidating our knowledge of epigenetic networks.
Tumasyan A, Adam W, Andrejkovic JW, Bergauer T, Chatterjee S, Damanakis K, Dragicevic M, Del Valle AE, Fruhwirth R, Jeitler M, Krammer N, Lechner L, Liko D, Mikulec I, Paulitsch P, Pitters FM, Schieck J, Schofbeck R, Schwarz D, Templ S, Waltenberger W, Wulz CE, Chekhovsky V, Litomin A, Makarenko V, Darwish MR, De Wolf EA, Janssen T, Kello T, Lelek A, Sfar HR, Van Mechelen P, Van Putte S, Van Remortel N, Bols ES, D'Hondt J, De Moor A, Delcourt M, El Faham H, Lowette S, Moortgat S, Morton A, Muller D, Sahasransu AR, Tavernier S, Van Doninck W, Vannerom D, Beghin D, Bilin B, Clerbaux B, De Lentdecker G, Favart L, Kalsi AK, Lee K, Mahdavikhorrami M, Makarenko I, Moureaux L, Paredes S, Petre L, Popov A, Postiau N, Starling E, Thomas L, Vanden Bemden M, Vander Velde C, Vanlaer P, Cornelis T, Dobur D, Knolle J, Lambrecht L, Mestdach G, Niedziela M, Rendon C, Roskas C, Samalan A, Skovpen K, Tytgat M, Van den Bossche N, Vermassen B, Wezenbeek L, Benecke A, Bethani A, Bruno G, Bury F, Caputo C, David P, Delaere C, Donertas IS, Giammanco A, Jaffel K, Jain S, Lemaitre V, Mondal K, Prisciandaro J, Taliercio A, Teklishyn M, Tran TT, Vischia P, Wertz S, Alves GA, Hensel C, Moraes A, Teles PR, Alda WL, Pereira MAG, Ferreira MB, Malbouisson HB, Carvalho W, Chinellato J, Da Costa EM, Da Silveira GG, Damiao DD, Sousa VD, De Souza SF, Herrera CM, Amarilo KM, Mundim L, Nogima H, Santoro A, Do Amaral SMS, Sznajder A, Thiel M, De Araujo FTD, Pereira AV, Bernardes CA, Calligaris L, Tomei TRFP, Gregores EM, Lemos DS, Mercadante PG, Novaes SF, Padula SS, Aleksandrov A, Antchev G, Hadjiiska R, Iaydjiev P, Misheva M, Rodozov M, Shopova M, Sultanov G, Dimitrov A, Ivanov T, Litov L, Pavlov B, Petkov P, Petrov A, Cheng T, Javaid T, Mittal M, Yuan L, Ahmad M, Bauer G, Dozen C, Hu Z, Martins J, Wang Y, Yi K, Chapon E, Chen GM, Chen HS, Chen M, Iemmi F, Kapoor A, Leggat D, Liao H, Liu ZA, Milosevic V, Monti F, Sharma R, Tao J, Thomas-Wilsker J, Wang J, Zhang H, Zhao J, Agapitos A, An Y, Ban Y, Chen C, Levin A, Li Q, Lyu X, Mao Y, Qian SJ, Wang D, Xiao J, Yang H, Lu M, You Z, Gao X, Okawa H, Zhang Y, Lin Z, Xiao M, Avila C, Cabrera A, Florez C, Fraga J, Guisao JM, Ramirez F, Alvarez JDR, Giljanovic D, Godinovic N, Lelas D, Puljak I, Antunovic Z, Kovac M, Sculac T, Brigljevic V, Ferencek D, Majumder D, Roguljic M, Starodumov A, Susa T, Attikis A, Christoforou K, Kole G, Kolosova M, Konstantinou S, Mousa J, Nicolaou C, Ptochos F, Razis PA, Rykaczewski H, Saka H, Finger M, Finger M, Kveton A, Ayala E, Jarrin EC, Abdelalim AA, Elgammal S, Lotfy A, Mahmoud MA, Bhowmik S, Dewanjee RK, Ehataht K, Kadastik M, Nandan S, Nielsen C, Pata J, Raidal M, Tani L, Veelken C, Eerola P, Kirschenmann H, Osterberg K, Voutilainen M, Bharthuar S, Brucken E, Garcia F, Havukainen J, Kim MS, Kinnunen R, Lampen T, Lassila-Perini K, Lehti S, Linden T, Lotti M, Martikainen L, Myllymaki M, Ott J, Rantanen MM, Siikonen H, Tuominen E, Tuominiemi J, Luukka P, Petrow H, Tuuva T, Amendola C, Besancon M, Couderc F, Dejardin M, Denegri D, Faure JL, Ferri F, Ganjour S, Gras P, de Monchenault GH, Jarry P, Lenzi B, Malcles J, Rander J, Rosowsky A, Sahin MO, Savoy-Navarro A, Simkina P, Titov M, Yu GB, Ahuja S, Beaudette F, Bonanomi M, Perraguin AB, Busson P, Cappati A, Charlot C, Davignon O, Diab B, Falmagne G, Alves BAFS, Ghosh S, de Cassagnac RG, Hakimi A, Kucher I, Motta J, Nguyen M, Ochando C, Paganini P, Rembser J, Salerno R, Sarkar U, Sauvan JB, Sirois Y, Tarabini A, Zabi A, Zghiche A, Agram JL, Andrea J, Apparu D, Bloch D, Bourgatte G, Brom JM, Chabert EC, Collard C, Darej D, Fontaine JC, Goerlach U, Grimault C, Le Bihan AC, Nibigira E, Van Hove P, Asilar E, Beauceron S, Bernet C, Boudoul G, Camen C, Carle A, Chanon N, Contardo D, Depasse P, El Mamouni H, Fay J, Gascon S, Gouzevitch M, Ille B, Laktineh IB, Lattaud H, Lesauvage A, Lethuillier M, Mirabito L, Perries S, Shchablo K, Sordini V, Touquet G, Vander Donckt M, Viret S, Khvedelidze A, Lomidze I, Tsamalaidze Z, Botta V, Feld L, Klein K, Lipinski M, Meuser D, Pauls A, Rowert N, Schulz J, Teroerde M, Dodonova A, Eliseev D, Erdmann M, Fackeldey P, Fischer B, Hebbeker T, Hoepfner K, Ivone F, Mastrolorenzo L, Merschmeyer M, Meyer A, Mocellin G, Mondal S, Mukherjee S, Noll D, Novak A, Pozdnyakov A, Rath Y, Reithler H, Schmidt A, Schuler SC, Sharma A, Vigilante L, Wiedenbeck S, Zaleski S, Dziwok C, Flugge G, Ahmad WH, Hlushchenko O, Kress T, Nowack A, Pooth O, Roy D, Stahl A, Ziemons T, Zotz A, Petersen HA, Martin MA, Asmuss P, Baxter S, Bayatmakou M, Behnke O, Martinez AB, Bhattacharya S, Bin Anuar AA, Blekman F, Borras K, Brunner D, Campbell A, Cardini A, Cheng C, Colombina F, Rodriguez SC, Silva GC, De Silva M, Didukh L, Eckerlin G, Eckstein D, Banos LIE, Filatov O, Gallo E, Geiser A, Giraldi A, Greau G, Grohsjean A, Guthoff M, Jafari A, Jomhari NZ, Jung H, Kasem A, Kasemann M, Kaveh H, Kleinwort C, Kogler R, Krucker D, Lange W, Lipka K, Lohmann W, Mankel R, Melzer-Pellmann IA, Morentin MM, Metwally J, Meyer AB, Meyer M, Mnich J, Mussgiller A, Nurnberg A, Otarid Y, Adan DP, Pitzl D, Raspereza A, Lopes BR, Rubenach J, Saggio A, Saibel A, Savitskyi M, Scham M, Scheurer V, Schnake S, Schutze P, Schwanenberger C, Shchedrolosiev M, Ricardo RES, Stafford D, Tonon N, Van De Klundert M, Vazzoler F, Walsh R, Walter D, Wang Q, Wen Y, Wichmann K, Wiens L, Wissing C, Wuchterl S, Aggleton R, Albrecht S, Bein S, Benato L, Connor P, De Leo K, Eich M, El Morabit K, Feindt F, Frohlich A, Garbers C, Garutti E, Gunnellini P, Hajheidari M, Haller J, Hinzmann A, Kasieczka G, Klanner R, Kramer T, Kutzner V, Lange J, Lange T, Lobanov A, Malara A, Matthies C, Mehta A, Nigamova A, Rodriguez KJP, Rieger M, Rieger O, Schleper P, Schroder M, Schwandt J, Sonneveld J, Stadie H, Steinbruck G, Tews A, Zoi I, Bechtel J, Brommer S, Burkart M, Butz E, Caspart R, Chwalek T, De Boer W, Dierlamm A, Droll A, Faltermann N, Giffels M, Gosewisch JO, Gottmann A, Hartmann F, Heidecker C, Husemann U, Keicher P, Koppenhofer R, Maier S, Mitra S, Muller T, Neukum M, Quast G, Rabbertz K, Rauser J, Savoiu D, Schnepf M, Seith D, Shvetsov I, Simonis HJ, Ulrich R, Van der Linden J, Von Cube RF, Wassmer M, Weber M, Wieland S, Wolf R, Wozniewski S, Wunsch S, Anagnostou G, Daskalakis G, Kyriakis A, Loukas D, Stakia A, Diamantopoulou M, Karasavvas D, Kontaxakis P, Koraka CK, Manousakis-Katsikakis A, Panagiotou A, Papavergou I, Saoulidou N, Theofilatos K, Tziaferi E, Vellidis K, Vourliotis E, Bakas G, Kousouris K, Papakrivopoulos I, Tsipolitis G, Zacharopoulou A, Adamidis K, Bestintzanos I, Evangelou I, Foudas C, Gianneios P, Katsoulis P, Kokkas P, Manthos N, Papadopoulos I, Strologas J, Csanad M, Farkas K, Gadallah MMA, Lokos S, Major P, Mandal K, Pasztor G, Radl AJ, Suranyi O, Veres GI, Bartok M, Bencze G, Hajdu C, Horvath D, Sikler F, Veszpremi V, Czellar S, Fasanella D, Fienga F, Karancsi J, Molnar J, Szillasi Z, Teyssier D, Raics P, Trocsanyi ZL, Ujvari B, Csorgo T, Nemes F, Novak T, Bahinipati S, Kar C, Mal P, Mishra T, Bindhu VKMN, Nayak A, Saha P, Sur N, Swain SK, Vats D, Bansal S, Beri SB, Bhatnagar V, Chaudhary G, Chauhan S, Dhingra N, Gupta R, Kaur A, Kaur H, Kaur M, Kumari P, Meena M, Sandeep K, Singh JB, Virdi AK, Ahmed A, Bhardwaj A, Choudhary BC, Gola M, Keshri S, Kumar A, Naimuddin M, Priyanka P, Ranjan K, Saumya S, Shah A, Bharti M, Bhattacharya R, Bhattacharya S, Bhowmik D, Dutta S, Dutta S, Gomber B, Maity M, Palit P, Rout PK, Saha G, Sahu B, Sarkar S, Sharan M, Behera PK, Behera SC, Kalbhor P, Komaragiri JR, Kumar D, Muhammad A, Panwar L, Pradhan R, Pujahari PR, Sharma A, Sikdar AK, Tiwari PC, Naskar K, Aziz T, Dugad S, Kumar M, Banerjee S, Chudasama R, Guchait M, Karmakar S, Kumar S, Majumder G, Mazumdar K, Mukherjee S, Alpana A, Dube S, Kansal B, Laha A, Pandey S, Rastogi A, Sharma S, Bakhshiansohi H, Khazaie E, Zeinali M, Chenarani S, Etesami SM, Khakzad M, Najafabadi MM, Grunewald M, Abbrescia M, Aly R, Aruta C, Colaleo A, Creanza D, De Filippis N, De Palma M, Di Florio A, Di Pilato A, Elmetenawee W, Errico F, Fiore L, Iaselli G, Ince M, Lezki S, Maggi G, Maggi M, Margjeka I, Mastrapasqua V, My S, Nuzzo S, Pellecchia A, Pompili A, Pugliese G, Ramos D, Ranieri A, Selvaggi G, Silvestris L, Simone FM, Venditti R, Verwilligen P, Abbiendi G, Battilana C, Bonacorsi D, Borgonovi L, Brigliadori L, Campanini R, Capiluppi P, Castro A, Cavallo FR, Ciocca C, Cuffiani M, Dallavalle GM, Diotalevi T, Fabbri F, Fanfani A, Giacomelli P, Giommi L, Grandi C, Guiducci L, Lo Meo S, Lunerti L, Marcellini S, Masetti G, Navarria FL, Perrotta A, Primavera F, Rossi AM, Rovelli T, Siroli GP, Albergo S, Costa S, Di Mattia A, Potenza R, Tricomi A, Tuve C, Barbagli G, Cassese A, Ceccarelli R, Ciulli V, Civinini C, D'Alessandro R, Focardi E, Latino G, Lenzi P, Lizzo M, Meschini M, Paoletti S, Seidita R, Sguazzoni G, Viliani L, Benussi L, Bianco S, Piccolo D, Bozzo M, Ferro F, Mulargia R, Robutti E, Tosi S, Benaglia A, Boldrini G, Brivio F, Cetorelli F, De Guio F, Dinardo ME, Dini P, Gennai S, Ghezzi A, Govoni P, Guzzi L, Lucchini MT, Malberti M, Malvezzi S, Massironi A, Menasce D, Moroni L, Paganoni M, Pedrini D, Pinolini BS, Ragazzi S, Redaelli N, de Fatis TT, Valsecchi D, Zuolo D, Buontempo S, Carnevali F, Cavallo N, De Iorio A, Fabozzi F, Iorio AOM, Lista L, Meola S, Paolucci P, Rossi B, Sciacca C, Azzi P, Bacchetta N, Bisello D, Bortignon P, Bragagnolo A, Carlin R, Checchia P, Dorigo T, Dosselli U, Gasparini F, Gasparini U, Grosso G, Layer L, Lusiani E, Margoni M, Marini F, Meneguzzo AT, Pazzini J, Ronchese P, Rossin R, Simonetto F, Strong G, Tosi M, Yarar H, Zanetti M, Zotto P, Zucchetta A, Zumerle G, Aime C, Braghieri A, Calzaferri S, Fiorina D, Montagna P, Ratti SP, Re V, Riccardi C, Salvini P, Vai I, Vitulo P, Asenov P, Bilei GM, Ciangottini D, Fano L, Magherini M, Mantovani G, Mariani V, Menichelli M, Moscatelli F, Piccinelli A, Presilla M, Rossi A, Santocchia A, Spiga D, Tedeschi T, Azzurri P, Bagliesi G, Bertacchi V, Bianchini L, Boccali T, Bossini E, Castaldi R, 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Search for invisible decays of the Higgs boson produced via vector boson fusion in proton-proton collisions at root s=13 TeV
PHYSICAL REVIEW D 2022 MAY 20; 105(9):? Article 092007
A search for invisible decays of the Higgs boson produced via vector boson fusion (VBF) has been performed with 101 fb(-1) of proton-proton collisions delivered by the LHC at root s = 13 TeV and collected by the CMS detector in 2017 and 2018. The sensitivity to the VBF production mechanism is enhanced by constructing two analysis categories, one based on missing transverse momentum and a second based on the properties of jets. In addition to control regions with Z and W boson candidate events, a highly populated control region, based on the production of a photon in association with jets, is used to constrain the dominant irreducible background from the invisible decay of a Z boson produced in association with jets. The results of this search arc combined with all previous measurements in the VBF topology, based on data collected in 2012 (at root s = 8 TeV), 2015, and 2016, corresponding to integrated luminosities of 19.7, 2.3, and 36.3 fb(-1), respectively. The observed (expected) upper limit on the invisible branching fraction of the Higgs boson is found to be 0.18 (0.10) at the 95% confidence level, assuming the standard model production cross section. The results are also interpreted in the context of Higgs-portal models.
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Observation of B-0 ->psi(2S)K-S(0)pi(+)pi(-) and B-s(0)->psi(2S)K-S(0) decays
EUROPEAN PHYSICAL JOURNAL C 2022 MAY 31; 82(5):? Article 499
Using a data sample of root s = 13 TeV protonproton collisions collected by the CMS experiment at the LHC in 2017 and 2018 with an integrated luminosity of 103 fb(-1), the B-s(0) -> psi(2S)K-S(0) and B-0 -> psi(2S)K-S(0) pi(+) pi(-) decays are observed with significances exceeding 5 standard deviations. The resulting branching fraction ratios, measured for the first time, correspond to B(B-s(0) -> psi(2S)K-S(0))/B(B-0 Zeta -> psi(2S)K-S(0)) = (3.33 +/- 0.69(stat) +/- 0.11 (syst) +/- 0.34 (f(s)/f(d))) x 10(-2) and B(B-0 -> psi(2S)K-S(0) pi(+) pi(-))/B(B-0 -> psi(2S)K-S(0)) = 0.480 +/- 0.013 (stat) +/- 0.032 (syst), where the last uncertainty in the first ratio is related to the uncertainty in the ratio of production cross sections of B-s(0) and B-0 mesons, f(s)/f(d).