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1. Long-Term Effects of Sotatercept on Right Ventricular Function

Author: Gomberg-Maitland, Mardi, McLaughlin, Vallerie V., Badesch, David B., Ghofrani, Hossein-Ardeschir, Hoeper, Marius M., Humbert, Marc, Preston, Ioana R., Souza, Rogerio, Waxman, Aaron B., de Oliveira Pena, Janethe, Lu, Jonathan T., Manimaran, Solaiappan, and Gibbs, J. Simon R.
Published: 2023
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2. Association of Variants in the SPTLC1 Gene With Juvenile Amyotrophic Lateral Sclerosis

Author: Johnson, Janel O., Chia, Ruth, Miller, Danny E., Li, Rachel, Kumaran, Ravindran, Abramzon, Yevgeniya, Alahmady, Nada, Renton, Alan E., Topp, Simon D., Gibbs, J. Raphael, Cookson, Mark R., Sabir, Marya S., Dalgard, Clifton L., Troakes, Claire, Jones, Ashley R., Shatunov, Aleksey, Iacoangeli, Alfredo, Al Khleifat, Ahmad, Ticozzi, Nicola, Silani, Vincenzo, Gellera, Cinzia, Blair, Ian P., Dobson-Stone, Carol, Kwok, John B., Bonkowski, Emily S., Palvadeau, Robin, Tienari, Pentti J., Morrison, Karen E., Shaw, Pamela J., Al-Chalabi, Ammar, Brown, Robert H., Calvo, Andrea, Mora, Gabriele, Al-Saif, Hind, Gotkine, Marc, Leigh, Fawn, Chang, Irene J., Perlman, Seth J., Glass, Ian, Scott, Anna I., Shaw, Christopher E., Basak, A. Nazli, Landers, John E., Chiò, Adriano, Crawford, Thomas O., Smith, Bradley N., Traynor, Bryan J., Smith, Bradley N., Ticozzi, Nicola, Fallini, Claudia, Gkazi, Athina Soragia, Topp, Simon D., Scotter, Emma L., Kenna, Kevin P., Keagle, Pamela, Tiloca, Cinzia, Vance, Caroline, Troakes, Claire, Colombrita, Claudia, King, Andrew, Pensato, Viviana, Castellotti, Barbara, Baas, Frank, ten Asbroek, Anneloor L. M. A., McKenna-Yasek, Diane, McLaughlin, Russell L., Polak, Meraida, Asress, Seneshaw, Esteban-Pérez, Jesús, Stevic, Zorica, D’Alfonso, Sandra, Mazzini, Letizia, Comi, Giacomo P., Del Bo, Roberto, Ceroni, Mauro, Gagliardi, Stella, Querin, Giorgia, Bertolin, Cinzia, van Rheenen, Wouter, Rademakers, Rosa, van Blitterswijk, Marka, Lauria, Giuseppe, Duga, Stefano, Corti, Stefania, Cereda, Cristina, Corrado, Lucia, Sorarù, Gianni, Williams, Kelly L., Nicholson, Garth A., Blair, Ian P., Leblond-Manry, Claire, Rouleau, Guy A., Hardiman, Orla, Morrison, Karen E., Veldink, Jan H., van den Berg, Leonard H., Al-Chalabi, Ammar, Pall, Hardev, Shaw, Pamela J., Turner, Martin R., Talbot, Kevin, Taroni, Franco, García-Redondo, Alberto, Wu, Zheyang, Glass, Jonathan D., Gellera, Cinzia, Ratti, Antonia, Brown, Robert H., Silani, Vincenzo, Shaw, Christopher E., Landers, John E., Dalgard, Clifton L., Adeleye, Adelani, Soltis, Anthony R., Alba, Camille, Viollet, Coralie, Bacikova, Dagmar, Hupalo, Daniel N., Sukumar, Gauthaman, Pollard, Harvey B., Wilkerson, Matthew D., Martinez, Elisa McGrath, Abramzon, Yevgeniya, Ahmed, Sarah, Arepalli, Sampath, Baloh, Robert H., Bowser, Robert, Brady, Christopher B., Brice, Alexis, Broach, James, Campbell, Roy H., Camu, William, Chia, Ruth, Cooper-Knock, John, Ding, Jinhui, Drepper, Carsten, Drory, Vivian E., Dunckley, Travis L., Eicher, John D., England, Bryce K., Faghri, Faraz, Feldman, Eva, Floeter, Mary Kay, Fratta, Pietro, Geiger, Joshua T., Gerhard, Glenn, Gibbs, J. Raphael, Gibson, Summer B., Glass, Jonathan D., Hardy, John, Harms, Matthew B., Heiman-Patterson, Terry D., Hernandez, Dena G., Jansson, Lilja, Kirby, Janine, Kowall, Neil W., Laaksovirta, Hannu, Landeck, Natalie, Landi, Francesco, Le Ber, Isabelle, Lumbroso, Serge, MacGowan, Daniel J. L., Maragakis, Nicholas J., Mora, Gabriele, Mouzat, Kevin, Murphy, Natalie A., Myllykangas, Liisa, Nalls, Mike A., Orrell, Richard W., Ostrow, Lyle W., Pamphlett, Roger, Pickering-Brown, Stuart, Pioro, Erik P., Pletnikova, Olga, Pliner, Hannah A., Pulst, Stefan M., Ravits, John M., Renton, Alan E., Rivera, Alberto, Robberecht, Wim, Rogaeva, Ekaterina, Rollinson, Sara, Rothstein, Jeffrey D., Scholz, Sonja W., Sendtner, Michael, Shaw, Pamela J., Sidle, Katie C., Simmons, Zachary, Singleton, Andrew B., Smith, Nathan, Stone, David J., Tienari, Pentti J., Troncoso, Juan C., Valori, Miko, Van Damme, Philip, Van Deerlin, Vivianna M., Van Den Bosch, Ludo, Zinman, Lorne, Landers, John E., Chiò, Adriano, Traynor, Bryan J., Angelocola, Stefania M., Ausiello, Francesco P., Barberis, Marco, Bartolomei, Ilaria, Battistini, Stefania, Bersano, Enrica, Bisogni, Giulia, Borghero, Giuseppe, Brunetti, Maura, Cabona, Corrado, Calvo, Andrea, Canale, Fabrizio, Canosa, Antonio, Cantisani, Teresa A., Capasso, Margherita, Caponnetto, Claudia, Cardinali, Patrizio, Carrera, Paola, Casale, Federico, Chiò, Adriano, Colletti, Tiziana, Conforti, Francesca L., Conte, Amelia, Conti, Elisa, Corbo, Massimo, Cuccu, Stefania, Dalla Bella, Eleonora, D’Errico, Eustachio, DeMarco, Giovanni, Dubbioso, Raffaele, Ferrarese, Carlo, Ferraro, Pilar M., Filippi, Massimo, Fini, Nicola, Floris, Gianluca, Fuda, Giuseppe, Gallone, Salvatore, Gianferrari, Giulia, Giannini, Fabio, Grassano, Maurizio, Greco, Lucia, Iazzolino, Barbara, Introna, Alessandro, La Bella, Vincenzo, Lattante, Serena, Lauria, Giuseppe, Liguori, Rocco, Logroscino, Giancarlo, Logullo, Francesco O., Lunetta, Christian, Mandich, Paola, Mandrioli, Jessica, Manera, Umberto, Manganelli, Fiore, Marangi, Giuseppe, Marinou, Kalliopi, Marrosu, Maria Giovanna, Martinelli, Ilaria, Messina, Sonia, Moglia, Cristina, Mora, Gabriele, Mosca, Lorena, Murru, Maria R., Origone, Paola, Passaniti, Carla, Petrelli, Cristina, Petrucci, Antonio, Pozzi, Susanna, Pugliatti, Maura, Quattrini, Angelo, Ricci, Claudia, Riolo, Giulia, Riva, Nilo, Russo, Massimo, Sabatelli, Mario, Salamone, Paolina, Salivetto, Marco, Salvi, Fabrizio, Santarelli, Marialuisa, Sbaiz, Luca, Sideri, Riccardo, Simone, Isabella, Simonini, Cecilia, Spataro, Rossella, Tanel, Raffaella, Tedeschi, Gioacchino, Ticca, Anna, Torriello, Antonella, Tranquilli, Stefania, Tremolizzo, Lucio, Trojsi, Francesca, Vasta, Rosario, Vacchiano, Veria, Vita, Giuseppe, Volanti, Paolo, Zollino, Marcella, and Zucchi, Elisabetta
Abstract: IMPORTANCE: Juvenile amyotrophic lateral sclerosis (ALS) is a rare form of ALS characterized by age of symptom onset less than 25 years and a variable presentation. OBJECTIVE: To identify the genetic variants associated with juvenile ALS. DESIGN, SETTING, AND PARTICIPANTS: In this multicenter family-based genetic study, trio whole-exome sequencing was performed to identify the disease-associated gene in a case series of unrelated patients diagnosed with juvenile ALS and severe growth retardation. The patients and their family members were enrolled at academic hospitals and a government research facility between March 1, 2016, and March 13, 2020, and were observed until October 1, 2020. Whole-exome sequencing was also performed in a series of patients with juvenile ALS. A total of 66 patients with juvenile ALS and 6258 adult patients with ALS participated in the study. Patients were selected for the study based on their diagnosis, and all eligible participants were enrolled in the study. None of the participants had a family history of neurological disorders, suggesting de novo variants as the underlying genetic mechanism. MAIN OUTCOMES AND MEASURES: De novo variants present only in the index case and not in unaffected family members. RESULTS: Trio whole-exome sequencing was performed in 3 patients diagnosed with juvenile ALS and their parents. An additional 63 patients with juvenile ALS and 6258 adult patients with ALS were subsequently screened for variants in the SPTLC1 gene. De novo variants in SPTLC1 (p.Ala20Ser in 2 patients and p.Ser331Tyr in 1 patient) were identified in 3 unrelated patients diagnosed with juvenile ALS and failure to thrive. A fourth variant (p.Leu39del) was identified in a patient with juvenile ALS where parental DNA was unavailable. Variants in this gene have been previously shown to be associated with autosomal-dominant hereditary sensory autonomic neuropathy, type 1A, by disrupting an essential enzyme complex in the sphingolipid synthesis pathway. CONCLUSIONS AND RELEVANCE: These data broaden the phenotype associated with SPTLC1 and suggest that patients presenting with juvenile ALS should be screened for variants in this gene.
Published: 2021
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3. Switching to riociguat versus maintenance therapy with phosphodiesterase-5 inhibitors in patients with pulmonary arterial hypertension (REPLACE): a multicentre, open-label, randomised controlled trial.

Author: Hoeper, Marius M, Al-Hiti, Hikmet, Benza, Raymond L, Chang, Sung-A, Corris, Paul A, Gibbs, J Simon R, Grünig, Ekkehard, Jansa, Pavel, Klinger, James R, Langleben, David, McLaughlin, Vallerie V, Meyer, Gisela M B, Ota-Arakaki, Jaquelina, Peacock, Andrew J, Pulido, Tomás, Rosenkranz, Stephan, Vizza, Carmine Dario, Vonk-Noordegraaf, Anton, White, R James, and Chang, Mikyung
Subjects: PULMONARY hypertension, PHOSPHODIESTERASE-5 inhibitors, INTERACTIVE voice response (Telecommunication), RESPIRATORY infections, BRAIN natriuretic factor, ENDOTHELIN receptors, OBSTRUCTIVE lung diseases
Abstract: Riociguat and phosphodiesterase-5 inhibitors (PDE5i), approved for the treatment of pulmonary arterial hypertension (PAH), act on the same pathway via different mechanisms. Riociguat might be an alternative option for patients with PAH who do not respond sufficiently to treatment with PDE5i, but comparisons of the potential benefits of riociguat and PDE5i in these patients are needed. The aim of this trial was to assess the effects of switching to riociguat from PDE5i therapy versus continued PDE5i therapy in patients with PAH at intermediate risk of 1-year mortality. Riociguat rEplacing PDE5i therapy evaLuated Against Continued PDE5i thErapy (REPLACE) was an open-label, randomised controlled trial in 81 hospital-based pulmonary hypertension centres in 22 countries. The study enrolled patients aged 18–75 years with symptomatic PAH at intermediate risk of 1-year mortality (based on the European Society for Cardiology–European Respiratory Society guideline thresholds for WHO functional class and 6-min walk distance [6MWD]) who were receiving treatment with a PDE5i with or without an endothelin receptor antagonist for at least 6 weeks before randomisation. Patients were excluded if they had been previously treated with riociguat, had used prostacyclin analogues or prostacyclin receptor agonists within 30 days before randomisation, had clinically significant restrictive or obstructive parenchymal lung disease, or had left heart disease. Patients were randomly assigned (1:1) to remain on PDE5i treatment (oral sildenafil [≥60 mg per day] or oral tadalafil [20–40 mg per day]; the PDE5i group) or to switch to oral riociguat (up to 2·5 mg three times per day; the riociguat group), using an interactive voice and web response system, stratified by cause of PAH. The primary endpoint was clinical improvement by week 24, defined as an absence of clinical worsening and prespecified improvements in at least two of three variables (6MWD, WHO functional class, and N -terminal prohormone of brain natriuretic peptide), analysed using last observation carried forward in all randomly assigned patients with observed values at baseline and week 24 who received at least one dose of study medication (the full analysis set). Secondary endpoints included clinical worsening events. The trial has been completed and is registered with ClinicalTrials.gov , NCT02891850. Between Jan 11, 2017, and July 31, 2019, 293 patients were screened, of which 226 patients were randomly assigned to the riociguat group (n=111) or to the PDE5i group (n=115). 211 patients completed the study and 14 patients discontinued (seven in each group). One patient assigned to the PDE5i group did not receive treatment, so 225 patients were included in the safety analysis, and one further patient in the PDE5i group had missing components of the composite primary endpoint at baseline, so 224 patients were included in the full analysis set. The primary endpoint was met by 45 (41%) of 111 patients in the riociguat group and 23 (20%) of 113 patients in the PDE5i group; odds ratio [OR] 2·78 (95% CI 1·53–5·06; p=0·0007). Clinical worsening events occurred in one (1%) of 111 patients in the riociguat group (hospitalisation due to worsening PAH) and 10 (9%) of 114 patients in the PDE5i group (hospitalisation due to worsening PAH [n=9]; disease progression [n=1]; OR 0·10 [0·01–0·73]; p=0·0047). The most frequently occurring adverse events were hypotension (15 [14%]), headache (14 [13%]), and dyspepsia (10 [9%]) in the riociguat group, and headache (eight [7%]), cough (seven [6%]), and upper respiratory tract infection (seven [6%]) in the PDE5i group. Serious adverse events were reported in eight (7%) of 111 patients in the riociguat group and 19 (17%) of 114 patients in the PDE5i group. During the study, four patients died in the PDE5i group, one of them during the safety follow-up period. Switching to riociguat from PDE5i treatment, both of which act via the nitric oxide–soluble guanylate cyclase–cyclic guanosine monophosphate pathway, could be a strategic option for treatment escalation in patients with PAH at intermediate risk of 1-year mortality. Bayer AG, Merck Sharp & Dohme. [ABSTRACT FROM AUTHOR]
Published: 2021
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4. A Phase 2b randomized trial of lorecivivint, a novel intra-articular CLK2/DYRK1A inhibitor and Wnt pathway modulator for knee osteoarthritis.

Author: Yazici, Y., McAlindon, T.E., Gibofsky, A., Lane, N.E., Lattermann, C., Skrepnik, N., Swearingen, C.J., Simsek, I., Ghandehari, H., DiFrancesco, A., Gibbs, J., Tambiah, J.R.S., Hochberg, M.C., and Tambiah, J
Abstract: Objective: Lorecivivint (LOR; SM04690), an investigational Wnt pathway modulator, previously demonstrated patient-reported and radiographic outcome improvements vs placebo in clinically relevant subjects with moderate to severe knee osteoarthritis (OA). This study's objective was to identify effective LOR doses.Design: Subjects in this 24-week, Phase 2b, multicenter, randomized, double-blind, placebo (PBO)-controlled trial received an intra-articular injection of 2 mL LOR (0.03, 0.07, 0.15, or 0.23 mg), PBO, or dry-needle sham. The primary efficacy endpoints were changes in Pain NRS [0-10], WOMAC Pain [0-100], WOMAC Function [0-100], and radiographic mJSW outcomes, which were measured using baseline-adjusted analysis of covariance at Week 24. Multiple Comparison Procedure-Modeling (MCP-Mod) was performed for dose modeling.Results: In total, 695/700 subjects were treated. Pain NRS showed significant improvements vs PBO after treatment with 0.07 mg and 0.23 mg LOR at Weeks 12 (-0.96, 95% CI [-1.54, -0.37], P = 0.001; -0.78 [-1.39, -0.17], P = 0.012) and 24 (-0.70 [-1.34, -0.06], P = 0.031; -0.82 [-1.51, -0.12], P = 0.022). Additionally, 0.07 mg LOR significantly improved WOMAC Pain and Function subscores vs PBO at Week 12 (P = 0.04, P = 0.021), and 0.23 mg LOR significantly improved both WOMAC subscores at Week 24 (P = 0.031, P = 0.017). No significant differences from PBO were observed for other doses. No radiographic progression was observed in any group at Week 24. MCP-Mod identified 0.07 mg LOR as the lowest effective dose.Conclusion: This 24-week Phase 2b trial demonstrated the efficacy of LOR on PROs in knee OA subjects. The optimal dose for future studies was identified as 0.07 mg LOR. [ABSTRACT FROM AUTHOR]
Published: 2021
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5. Switching to riociguat versus maintenance therapy with phosphodiesterase-5 inhibitors in patients with pulmonary arterial hypertension (REPLACE): a multicentre, open-label, randomised controlled trial

Author: Hoeper, Marius M, Al-Hiti, Hikmet, Benza, Raymond L, Chang, Sung-A, Corris, Paul A, Gibbs, J Simon R, Grünig, Ekkehard, Jansa, Pavel, Klinger, James R, Langleben, David, McLaughlin, Vallerie V, Meyer, Gisela M B, Ota-Arakaki, Jaquelina, Peacock, Andrew J, Pulido, Tomás, Rosenkranz, Stephan, Vizza, Carmine Dario, Vonk-Noordegraaf, Anton, White, R James, Chang, Mikyung, Kleinjung, Frank, Meier, Christian, Paraschin, Karen, Ghofrani, Hossein Ardeschir, Simonneau, Gérald, Olschewski, H, Delcroix, M, Andrade-Lima, M, de Amorim Corrêac, R, Figueiredo Campos, F, Ota Arakaki, J, Meyer, G, De Souza, R, Langleben, D, Al-Hiti, H, Jansa, P, Mellemkjær, S, Bauer, F, Montani, D, Simonneau, G, Drömann, D, Ghofrani, H-A, Grünig, E, Halank, M, Held, M, Hoeper, MM, Klose, H, Kneidinger, N, Leuchte, H, Opitz, C, Rosenkranz, S, Wilkens, H, Wirtz, H, Karvounis, H, Pitsiou, G, Orfanos, S, D'Alto, M, Ghio, S, Vizza, CD, Vitulo, P, Nakayama, T, Maki, H, Tatebe, S, de los Rios Ibarra, M, Pulido, T, Van Dijk, A, Vonk-Noordegraaf, A, Roleder, T, Castro, G, Loureiro, MJ, Robalo-Martins, S, Barberá, JA, Lázaro, M, Perez-Penate, GM, Román, A, Cheng, C-C, Hsu, C-H, Hsu, H-H, Atahan, E, Mogulkoc Bishop, N, Okumus, NG, Onen, Z, Chang, H-J, Chang, S-A, Lee, J-S, Kim, H-K, Coghlan, JG, Corris, PA, Church, AC, Condliffe, R, Gibbs, JSR, Peacock, AJ, Wort, S, Allen, R, Allen, S, Awdish, R, Benza, RL, DeSouza, S, Feldman, J, Johri, S, Klinger, JR, Layish, D, McConnell, J, McLaughlin, VV, Migliore, C, Rahaghi, F, Rischard, F, Robbins, I, Satterwhite, L, Shah, T, Sulica, R, and White, RJ
Abstract: Riociguat and phosphodiesterase-5 inhibitors (PDE5i), approved for the treatment of pulmonary arterial hypertension (PAH), act on the same pathway via different mechanisms. Riociguat might be an alternative option for patients with PAH who do not respond sufficiently to treatment with PDE5i, but comparisons of the potential benefits of riociguat and PDE5i in these patients are needed. The aim of this trial was to assess the effects of switching to riociguat from PDE5i therapy versus continued PDE5i therapy in patients with PAH at intermediate risk of 1-year mortality.
Published: 2021
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6. Rediscovery of the Rare Bee Epeoloides pilosulus in Manitoba (Hymenoptera: Apidae).

Author: Gibbs, J., Hanuschuk, E. J., and Shukla-Bergen, S.
Subjects: APIDAE, HYMENOPTERA, PRIMULACEAE, BEES, SPECIES
Abstract: Epeoloides pilosulus (Cresson) (Hymenoptera: Apidae) is an exceptionally rare bee of conservation concern. Epeoloides are cleptoparasites of the oil-collecting bees Macropis (Hymenoptera: Melittidae), which specialize on oil-producing species in the genus Lysimachia (Ericales: Primulaceae). We report on the first records of E. pilosulus in Manitoba in 95-years, and only the fifth through eighth specimens for Canada since 1960. Manitoban records of Macropis are also provided. [ABSTRACT FROM AUTHOR]
Published: 2020
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7. Assessing Health and Safety Concerns and Psychological Stressors among Agricultural Workers in the U.S. Midwest.

Author: Arora, K., Cheyney, M., Gerr, F., Bhagianadh, D., Gibbs, J., and Anthony, T. R.
Subjects: AGRICULTURAL laborers, AGRICULTURAL safety, FARM management, NEEDS assessment, MONETARY incentives, MEDICAL care surveys
Abstract: There is limited research exploring agricultural workers' own perspectives on the relative importance of the hazards and stressors they experience. There is also a lack of evidence on whether this reporting differs by method of elicitation. Finally, very little research exists on how to improve mail survey response rates among agricultural workers. We examined health and safety concerns and psychological stressors among Midwestern farmers. We assessed whether these reports varied by survey mode (mail survey versus inperson survey). The efficacy of two different types of incentives to enhance mail survey response rates among agricultural workers was also investigated. In 2018, a needs assessment survey was developed and mailed to a random sample of farm owner-operators in Iowa, Ohio, and Missouri, with randomly assigned prepaid or promised monetary incentives. In-person surveys were conducted among farm owner-operators and hired workers at three regional farm shows in Iowa, Minnesota, and Nebraska. The mail survey response rates were compared by incentive type. Content analysis was used to generate themes associated with health and safety concerns and psychological stressors, which were then ranked by frequency counts. Chi-square tests were used to analyze variation in the distribution of these themes by survey mode. The response rate for the $1 prepaid incentive was double that of the $10 promised incentive. Content analysis identified 13 health and safety concerns and eight psychological stressors. Chemicals, equipment/tools, and health outcomes were the most frequently noted health and safety concerns. Finances, climate/weather, and farm workload and management were the most frequently noted psychological stressors. Although there was considerable overlap in survey responses across mail and in-person respondents, important differences by sample and survey mode characteristics were observed. The results can support a variety of stakeholders in prioritizing and developing interventions and educational resources to address health and safety concerns and psychological stressors among Midwestern farmers. Our findings also contribute to the evidence base on primary data collection methods for agricultural workers. [ABSTRACT FROM AUTHOR]
Published: 2020
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8. Detecting and managing pulmonary hypertension.

Author: Gibbs, J. Simon R. and Charalampopoulos, Athanasios
Subjects: PULMONARY hypertension, PERSISTENT fetal circulation syndrome, CONGENITAL heart disease
Abstract: The article focuses on the detection and management of a type of high blood pressure, pulmonary hypertension (PH). Topics include the causes of PH including left heart disease and parenchymal lung disease; its prevalence among aged 65 and over; and rare forms including pulmonary arterial hypertension (PAH), and chronic thromboembolic pulmonary hypertension (CTEPH).
Published: 2019

9. Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture

Author: Chia, Ruth, Sabir, Marya S., Bandres-Ciga, Sara, Saez-Atienzar, Sara, Reynolds, Regina H., Gustavsson, Emil, Walton, Ronald L., Ahmed, Sarah, Viollet, Coralie, Ding, Jinhui, Makarious, Mary B., Diez-Fairen, Monica, Portley, Makayla K., Shah, Zalak, Abramzon, Yevgeniya, Hernandez, Dena G., Blauwendraat, Cornelis, Stone, David J., Eicher, John, Parkkinen, Laura, Ansorge, Olaf, Clark, Lorraine, Honig, Lawrence S., Marder, Karen, Lemstra, Afina, St George-Hyslop, Peter, Londos, Elisabet, Morgan, Kevin, Lashley, Tammaryn, Warner, Thomas T., Jaunmuktane, Zane, Galasko, Douglas, Santana, Isabel, Tienari, Pentti J., Myllykangas, Liisa, Oinas, Minna, Cairns, Nigel J., Morris, John C., Halliday, Glenda M., Van Deerlin, Vivianna M., Trojanowski, John Q., Grassano, Maurizio, Calvo, Andrea, Mora, Gabriele, Canosa, Antonio, Floris, Gianluca, Bohannan, Ryan C., Brett, Francesca, Gan-Or, Ziv, Geiger, Joshua T., Moore, Anni, May, Patrick, Krüger, Rejko, Goldstein, David S., Lopez, Grisel, Tayebi, Nahid, Sidransky, Ellen, Norcliffe-Kaufmann, Lucy, Palma, Jose-Alberto, Kaufmann, Horacio, Shakkottai, Vikram G., Perkins, Matthew, Newell, Kathy L., Gasser, Thomas, Schulte, Claudia, Landi, Francesco, Salvi, Erika, Cusi, Daniele, Masliah, Eliezer, Kim, Ronald C., Caraway, Chad A., Monuki, Edwin S., Brunetti, Maura, Dawson, Ted M., Rosenthal, Liana S., Albert, Marilyn S., Pletnikova, Olga, Troncoso, Juan C., Flanagan, Margaret E., Mao, Qinwen, Bigio, Eileen H., Rodríguez-Rodríguez, Eloy, Infante, Jon, Lage, Carmen, González-Aramburu, Isabel, Sanchez-Juan, Pascual, Ghetti, Bernardino, Keith, Julia, Black, Sandra E., Masellis, Mario, Rogaeva, Ekaterina, Duyckaerts, Charles, Brice, Alexis, Lesage, Suzanne, Xiromerisiou, Georgia, Barrett, Matthew J., Tilley, Bension S., Gentleman, Steve, Logroscino, Giancarlo, Serrano, Geidy E., Beach, Thomas G., McKeith, Ian G., Thomas, Alan J., Attems, Johannes, Morris, Christopher M., Palmer, Laura, Love, Seth, Troakes, Claire, Al-Sarraj, Safa, Hodges, Angela K., Aarsland, Dag, Klein, Gregory, Kaiser, Scott M., Woltjer, Randy, Pastor, Pau, Bekris, Lynn M., Leverenz, James B., Besser, Lilah M., Kuzma, Amanda, Renton, Alan E., Goate, Alison, Bennett, David A., Scherzer, Clemens R., Morris, Huw R., Ferrari, Raffaele, Albani, Diego, Pickering-Brown, Stuart, Faber, Kelley, Kukull, Walter A., Morenas-Rodriguez, Estrella, Lleó, Alberto, Fortea, Juan, Alcolea, Daniel, Clarimon, Jordi, Nalls, Mike A., Ferrucci, Luigi, Resnick, Susan M., Tanaka, Toshiko, Foroud, Tatiana M., Graff-Radford, Neill R., Wszolek, Zbigniew K., Ferman, Tanis, Boeve, Bradley F., Hardy, John A., Topol, Eric J., Torkamani, Ali, Singleton, Andrew B., Ryten, Mina, Dickson, Dennis W., Chiò, Adriano, Ross, Owen A., Gibbs, J. Raphael, Dalgard, Clifton L., Traynor, Bryan J., and Scholz, Sonja W.
Abstract: The genetic basis of Lewy body dementia (LBD) is not well understood. Here, we performed whole-genome sequencing in large cohorts of LBD cases and neurologically healthy controls to study the genetic architecture of this understudied form of dementia, and to generate a resource for the scientific community. Genome-wide association analysis identified five independent risk loci, whereas genome-wide gene-aggregation tests implicated mutations in the gene GBA. Genetic risk scores demonstrate that LBD shares risk profiles and pathways with Alzheimer’s disease and Parkinson’s disease, providing a deeper molecular understanding of the complex genetic architecture of this age-related neurodegenerative condition.
Published: 2021
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10. SWITCHING TO RIOCIGUAT IN PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION NOT AT TREATMENT GOAL WITH PHOSPHODIESTERASE TYPE-5 INHIBITORS: SUBGROUP ANALYSIS RESULTS OF THE REPLACE STUDY

Author: Hoeper, Marius, Ghofrani, Hossein, Al-Hiti, Hikmet, Benza, Raymond, Chang, Sung A., Corris, Paul, Gibbs, J. Simon, Grünig, Ekkehard, Jansa, Pavel, Klinger, James, Langleben, David, McLaughlin, Vallerie, Meyer, Gisela, Ota-Arakaki, Jaquelina, Peacock, Andrew, Pulido, Tomas, Rosenkranz, Stephan, Vizza, Carmine Dario, Noordegraaf, Anton Vonk, White, R., Chang, Mikyung, Kleinjung, Frank, Meier, Christian, Paraschin, Karen, and Simonneau, Gerald
Published: 2020
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11. High diversity of native plants and vegetation types in the Morialta Conservation Park and the threat of invasive species

Author: Anderson, J., Keppel, G., Thomson, S.-M., Gibbs, J., and Brunetti, G.
Abstract: ABSTRACTMorialta Conservation Park is a scenic protected area that contains important vegetation remnants of the Mount Lofty Ranges. Here we investigate the vegetation ecology, soils and plant diversity of the park. Using a stratified, quantitative survey of woody vegetation and topsoils throughout the park within forty-five 10 × 10 m plots, we identified ten distinct vegetation types, nine being native and the other being dominated by the invasive European olive (Olea europaea). Soil conductivity and fertility, as well as aspect, were significant predictors of species composition, indicating that high environmental heterogeneity in soils and topography are important in facilitating the high biodiversity in the Morialta Conservation Park. The European olive and Boneseed (Chrysanthemoides moniliferassp. monilifera) are widespread in the park and a threat to native vegetation. Using published plant lists and the Atlas of Living Australia, we report 486 native (and 300 introduced) plant taxa from the park and its immediate surrounds, including species considered endangered at either the state or national level, or the IUCN Red List. Therefore, the park is highly important for conservation and the threat posed by the European olive, Boneseed and other invasive species should be effectively managed.
Published: 2020
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12. Update of screening and diagnostic modalities for connective tissue disease-associated pulmonary arterial hypertension.

Author: Young, Amber, Nagaraja, Vivek, Basilious, Mark, Habib, Mirette, Townsend, Whitney, Gladue, Heather, Badesch, David, Gibbs, J Simon R, Gopalan, Deepa, Manes, Alessandra, Oudiz, Ronald, Satoh, Toru, Torbicki, Adam, Torres, Fernando, McLaughlin, Vallerie, and Khanna, Dinesh
Abstract: Pulmonary arterial hypertension (PAH) has high morbidity and mortality in connective tissue diseases (CTDs), especially systemic sclerosis (SSc). In this systematic review, we provide an update on screening measures for early detection of PAH in CTD. Manuscripts published between July 2012 and October 2017, which incorporated screening measures to identify patients with PAH by right heart catheterization, were identified. Risk of bias was assessed using the QUADAS-2 tool. The systematic review resulted in 1514 unique citations and 22 manuscripts were included for final review; the majority of manuscripts had a lower risk of bias based on the QUADAS-2 tool. There were 16 SSc cohort studies and 6 case-control studies (SSc 4, SLE 2). Four SSc cohort studies evaluated transthoracic echocardiography (TTE) only. Eight SSc cohort studies evaluated composite measures including ASIG, DETECT, and a combination of tricuspid regurgitation velocity (TRV) and PFT variables. DETECT and ASIG had greater sensitivity and negative predictive value (NPV) compared to the 2009 ESC/ERS guidelines in different cohorts. The addition of PFT variables, such as DLCO or FVC/ DLCO ratio, to TRV, resulted in greater sensitivity and NPV compared to TRV alone. Current screening for PAH in CTDs is centered on SSc. Data continues to support the use of TTE and provides additional evidence for use of composite measures. [ABSTRACT FROM AUTHOR]
Published: 2019
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13. Limited phenological and dietary overlap between bee communities in spring flowering crops and herbaceous enhancements.

Author: Wood, T. J., Gibbs, J., Rothwell, N., Wilson, J. K., Gut, L., Brokaw, J., and Isaacs, R.
Subjects: POLLINATION, VACCINIUM corymbosum, SOUR cherry, BIODIVERSITY, BEES
Abstract: Abstract: Wild bee populations have undergone declines in recent years across much of the Western world, and these declines have the potential to limit yield in pollination‐dependent crops. Highbush blueberry, Vaccinium corymbosum, and tart cherry, Prunus cerasus, are spring‐blooming crops that rely on the movement of pollen by bees and other insects for pollination. Wild bee populations can be increased on farmland by providing floral resources, but whether the addition of these plants translates into increased pollinator density on crop flowers has not been documented in most cropping systems. To determine the importance of providing additional floral resources for wild bee pollinator communities, we selected blueberry fields and tart cherry orchards with and without herbaceous floral enhancements in western Michigan, USA. The bee communities visiting crop flowers, enhancements and control grassy field margins were sampled over a 5‐yr period. In addition, the pollen diets of the most abundant wild bee crop pollinators were quantified across Michigan to better understand their foraging niches and to identify potentially important alternative host plants. The presence of floral enhancements did not increase the abundance of wild bees on either blueberry or cherry flowers during bloom. The bee community visiting blueberry was evenly composed of short‐season bees that fly only during the spring and long‐season bees that fly in both spring and summer. In contrast, the bee community visiting cherry was dominated by short‐season spring bees. The majority of pollen collected by the wild bee communities visiting blueberry and cherry was from spring‐flowering woody plants, with limited use of the herbaceous enhancements. Enhancements attracted greater abundance and species richness of bees compared to control areas, including twice as many floral specialists. Conserving summer‐flying, grassland‐associated bees is an appropriate goal for pollinator conservation programs. However, herbaceous enhancements may not provide adequate resources for the wild bees that pollinate spring‐flowering crops. This study demonstrates that an examination of the pollen collected by wild bees across their flight periods can identify plant species to help them persist in intensively managed landscapes. [ABSTRACT FROM AUTHOR]
Published: 2018
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14. Genetic determinants of risk in pulmonary arterial hypertension: international genome-wide association studies and meta-analysis

Author: Rhodes, Christopher J, Batai, Ken, Bleda, Marta, Haimel, Matthias, Southgate, Laura, Germain, Marine, Pauciulo, Michael W, Hadinnapola, Charaka, Aman, Jurjan, Girerd, Barbara, Arora, Amit, Knight, Jo, Hanscombe, Ken B, Karnes, Jason H, Kaakinen, Marika, Gall, Henning, Ulrich, Anna, Harbaum, Lars, Cebola, Inês, Ferrer, Jorge, Lutz, Katie, Swietlik, Emilia M, Ahmad, Ferhaan, Amouyel, Philippe, Archer, Stephen L, Argula, Rahul, Austin, Eric D, Badesch, David, Bakshi, Sahil, Barnett, Christopher, Benza, Raymond, Bhatt, Nitin, Bogaard, Harm J, Burger, Charles D, Chakinala, Murali, Church, Colin, Coghlan, John G, Condliffe, Robin, Corris, Paul A, Danesino, Cesare, Debette, Stéphanie, Elliott, C Gregory, Elwing, Jean, Eyries, Melanie, Fortin, Terry, Franke, Andre, Frantz, Robert P, Frost, Adaani, Garcia, Joe G N, Ghio, Stefano, Ghofrani, Hossein-Ardeschir, Gibbs, J Simon R, Harley, John, He, Hua, Hill, Nicholas S, Hirsch, Russel, Houweling, Arjan C, Howard, Luke S, Ivy, Dunbar, Kiely, David G, Klinger, James, Kovacs, Gabor, Lahm, Tim, Laudes, Matthias, Machado, Rajiv D, MacKenzie Ross, Robert V, Marsolo, Keith, Martin, Lisa J, Moledina, Shahin, Montani, David, Nathan, Steven D, Newnham, Michael, Olschewski, Andrea, Olschewski, Horst, Oudiz, Ronald J, Ouwehand, Willem H, Peacock, Andrew J, Pepke-Zaba, Joanna, Rehman, Zia, Robbins, Ivan, Roden, Dan M, Rosenzweig, Erika B, Saydain, Ghulam, Scelsi, Laura, Schilz, Robert, Seeger, Werner, Shaffer, Christian M, Simms, Robert W, Simon, Marc, Sitbon, Olivier, Suntharalingam, Jay, Tang, Haiyang, Tchourbanov, Alexander Y, Thenappan, Thenappan, Torres, Fernando, Toshner, Mark R, Treacy, Carmen M, Vonk Noordegraaf, Anton, Waisfisz, Quinten, Walsworth, Anna K, Walter, Robert E, Wharton, John, White, R James, Wilt, Jeffrey, Wort, Stephen J, Yung, Delphine, Lawrie, Allan, Humbert, Marc, Soubrier, Florent, Trégouët, David-Alexandre, Prokopenko, Inga, Kittles, Richard, Gräf, Stefan, Nichols, William C, Trembath, Richard C, Desai, Ankit A, Morrell, Nicholas W, and Wilkins, Martin R
Abstract: Rare genetic variants cause pulmonary arterial hypertension, but the contribution of common genetic variation to disease risk and natural history is poorly characterised. We tested for genome-wide association for pulmonary arterial hypertension in large international cohorts and assessed the contribution of associated regions to outcomes.
Published: 2019
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15. Reduced plasma levels of small HDL particles transporting fibrinolytic proteins in pulmonary arterial hypertension

Author: Harbaum, Lars, Ghataorhe, Pavandeep, Wharton, John, Jiménez, Beatriz, Howard, Luke S G, Gibbs, J Simon R, Nicholson, Jeremy K, Rhodes, Christopher J, and Wilkins, Martin R
Abstract: BackgroundAberrant lipoprotein metabolism has been implicated in experimental pulmonary hypertension, but the relevance to patients with pulmonary arterial hypertension (PAH) is inconclusive.ObjectiveTo investigate the relationship between circulating lipoprotein subclasses and survival in patients with PAH.MethodsUsing nuclear magnetic resonance spectroscopy, 105 discrete lipoproteins were measured in plasma samples from two cohorts of patients with idiopathic or heritable PAH. Data from 1124 plasma proteins were used to identify proteins linked to lipoprotein subclasses. The physical presence of proteins was confirmed in plasma lipoprotein subfractions separated by ultracentrifugation.ResultsPlasma levels of three lipoproteins from the small high-density lipoprotein (HDL) subclass, termed HDL-4, were inversely related to survival in both the discovery (n=127) and validation (n=77) cohorts, independent of exercise capacity, comorbidities, treatment, N-terminal probrain natriuretic peptide, C reactive protein and the principal lipoprotein classes. The small HDL subclass rich in apolipoprotein A-2 content (HDL-4-Apo A-2) exhibited the most significant association with survival. None of the other lipoprotein classes, including principal lipoprotein classes HDL and low-density lipoprotein cholesterol, were prognostic. Three out of nine proteins identified to associate with HDL-4-Apo A-2 are involved in the regulation of fibrinolysis, namely, the plasmin regulator, alpha-2-antiplasmin, and two major components of the kallikrein–kinin pathway (coagulation factor XI and prekallikrein), and their physical presence in the HDL-4 subfraction was confirmed.ConclusionReduced plasma levels of small HDL particles transporting fibrinolytic proteins are associated with poor outcomes in patients with idiopathic and heritable PAH.
Published: 2019
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16. Plasma proteome analysis in patients with pulmonary arterial hypertension: an observational cohort study.

Author: Rhodes, Christopher J, Wharton, John, Ghataorhe, Pavandeep, Watson, Geoffrey, Girerd, Barbara, Howard, Luke S, Gibbs, J Simon R, Condliffe, Robin, Elliot, Charles A, Kiely, David G, Simonneau, Gerald, Montani, David, Sitbon, Olivier, Gall, Henning, Schermuly, Ralph T, Ghofrani, H Ardeschir, Lawrie, Allan, Humbert, Marc, and Wilkins, Martin R
Subjects: PULMONARY hypertension, BIOLOGICAL assay, BLOOD proteins, APTAMERS, MORTALITY, PROGNOSIS
Abstract: Summary Background Idiopathic and heritable pulmonary arterial hypertension form a rare but molecularly heterogeneous disease group. We aimed to measure and validate differences in plasma concentrations of proteins that are associated with survival in patients with idiopathic or heritable pulmonary arterial hypertension to improve risk stratification. Methods In this observational cohort study, we enrolled patients with idiopathic or heritable pulmonary arterial hypertension from London (UK; cohorts 1 and 2), Giessen (Germany; cohort 3), and Paris (France; cohort 4). Blood samples were collected at routine clinical appointment visits, clinical data were collected within 30 days of blood sampling, and biochemical data were collected within 7 days of blood sampling. We used an aptamer-based assay of 1129 plasma proteins, and patient clinical details were concealed to the technicians. We identified a panel of prognostic proteins, confirmed with alternative targeted assays, which we evaluated against the established prognostic risk equation for pulmonary arterial hypertension derived from the REVEAL registry. All-cause mortality was the primary endpoint. Findings 20 proteins differentiated survivors and non-survivors in 143 consecutive patients with idiopathic or heritable pulmonary arterial hypertension with 2 years' follow-up (cohort 1) and in a further 75 patients with 2·5 years' follow-up (cohort 2). Nine proteins were both prognostic independent of plasma NT-proBNP concentrations and confirmed by targeted assays. The functions of these proteins relate to myocardial stress, inflammation, pulmonary vascular cellular dysfunction and structural dysregulation, iron status, and coagulation. A cutoff-based score using the panel of nine proteins provided prognostic information independent of the REVEAL equation, improving the C statistic from area under the curve 0·83 (for REVEAL risk score, 95% CI 0·77–0·89; p<0·0001) to 0·91 (for panel and REVEAL 0·87–0·96; p<0·0001) and improving reclassification indices without detriment to calibration. Poor survival was preceded by an adverse change in panel score in paired samples from 43 incident patients with pulmonary arterial hypertension in cohort 3 (p=0·0133). The protein panel was validated in 93 patients with idiopathic or heritable pulmonary arterial hypertension in cohort 4, with 4·4 years' follow-up and improved risk estimates, providing complementary information to the clinical risk equation. Interpretation A combination of nine circulating proteins identifies patients with pulmonary arterial hypertension with a high risk of mortality, independent of existing clinical assessments, and might have a use in clinical management and the evaluation of new therapies. Funding National Institute for Health Research, Wellcome Trust, British Heart Foundation, Assistance Publique-Hôpitaux de Paris, Inserm, Université Paris-Sud, and Agence Nationale de la Recherche. [ABSTRACT FROM AUTHOR]
Published: 2017
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17. Clinical and genetic analyses of familial and sporadic frontotemporal dementia patients in Southern Italy.

Author: Capozzo, Rosa, Sassi, Celeste, Hammer, Monia B., Arcuti, Simona, Zecca, Chiara, Barulli, Maria R., Tortelli, Rosanna, Gibbs, J. Raphael, Crews, Cynthia, Seripa, Davide, Carnicella, Francesco, Dell'Aquila, Claudia, Rossi, Marco, Tamma, Filippo, Valluzzi, Francesco, Brancasi, Bruno, Panza, Francesco, Singleton, Andrew B., and Logroscino, Giancarlo
Abstract: Introduction We investigated the clinical differences between familial and sporadic frontotemporal dementia (FTD), screening for mutations in known FTD genes. Methods We diagnosed 22 affected individuals belonging to eight families and 43 sporadic cases with FTD in Apulia, Southern Italy, in 2 years. Mutations in common causative FTD genes ( GRN , MAPT , VCP , and TARDBP ) and C9ORF72 expansions were screened. Results Behavioral variant of FTD was the most common clinical subtype (50% and 69% in familial and sporadic cases, respectively). Social conduct impairment/disinhibition, loss of insight, and inflexibility were the most frequent clinical features observed at onset. One new mutation was identified in GRN in family A. Discussion Disease onset in sporadic FTD was more frequently characterized by a clustering of behavioral symptoms with apathy and loss of personal hygiene. Mutations in common causative FTD genes are not a major cause of familial and sporadic FTD in the Southern Italian population. [ABSTRACT FROM AUTHOR]
Published: 2017
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18. RATIONALE AND DESIGN OF THE PRIMEX TRIAL: A STUDY OF 2 DOSES OF ORAL CXA-10 IN PULMONARY ARTERIAL HYPERTENSION (PAH)

Author: Simon, Marc, Machado, Roberto, Badesch, David, Benza, Raymond, Gibbs, J. Simon, Gomberg-Maitland, Mardi, Hemnes, Anna, Kawut, Steven, Oudiz, Ronald, Danoff, Theodore, Brien, Gerald O., and Gladwin, Mark
Published: 2020
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19. Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry

Author: Sawhney, Jitendra PS., Kothiwale, Veerappa A., Bisne, Vikas, Durgaprasad, Rajashekhar, Jadhav, Praveen, Chopda, Manoj, Vanajakshamma, Velam, Meena, Ramdhan, Vijayaraghavan, Govindan, Chawla, Kamaldeep, Allu, Jagan, Pieper, Karen S., John Camm, A., Kakkar, Ajay K., Kakkar, Ajay K., Bassand, Jean-Pierre, John Camm, A., Fitzmaurice, David A., Goldhaber, Samuel Z., Goto, Shinya, Haas, Sylvia, Hacke, Werner, Mantovani, Lorenzo G., Misselwitz, Frank, Pieper, Karen S., Turpie, Alexander G.G., van Eickels, Martin, Verheugt, Freek W.A., John Camm, A., Bassand, Jean-Pierre, Goldhaber, Samuel Z., Haas, Sylvia, Kayani, Gloria, Mantovani, Lorenzo G., Fox, Keith A.A., Gersh, Bernard J., Luciardi, Hector Lucas, Gibbs, Harry, Brodmann, Marianne, Cools, Frank, Barretto, Antonio Carlos Pereira, Connolly, Stuart J., Spyropoulos, Alex, Eikelboom, John, Corbalan, Ramon, Hu, Dayi, Jansky, Petr, Nielsen, Jørn Dalsgaard, Ragy, Hany, Raatikainen, Pekka, Le Heuzey, Jean-Yves, Darius, Harald, Keltai, Matyas, Kakkar, Sanjay, Sawhney, Jitendra Pal Singh, Agnelli, Giancarlo, Ambrosio, Giuseppe, Koretsune, Yukihiro, Sánchez Díaz, Carlos Jerjes, Ten Cate, Hugo, Atar, Dan, Stepinska, Janina, Panchenko, Elizaveta, Lim, Toon Wei, Jacobson, Barry, Oh, Seil, Viñolas, Xavier, Rosenqvist, Marten, Steffel, Jan, Angchaisuksiri, Pantep, Oto, Ali, Parkhomenko, Alex, Al Mahmeed, Wael, Fitzmaurice, David, Goldhaber, Samuel Z., Hu, D.Y., Chen, K.N., Zhao, Y.S., Zhang, H.Q., Chen, J.Z., Cao, S.P., Wang, D.W., Yang, Y.J., Li, W.H., Yin, Y.H., Tao, G.Z., Yang, P., Chen, Y.M., He, S.H., Wang, Ying, Wang, Yong, Fu, G.S., Li, X., Wu, T.G., Cheng, X.S., Yan, X.W., Zhao, R.P., Chen, M.S., Xiong, L.G., Chen, P., Jiao, Y., Guo, Y., Xue, L., Wang, F.Z., Li, H., Yang, Z.M., Bai, C.L., Chen, J., Chen, J.Y., Chen, X., Feng, S., Fu, Q.H., Gao, X.J., Guo, W.N., He, R.H., He, X.A., Hu, X.S., Huang, X.F., Li, B., Li, J., Li, L., Li, Y.H., Liu, T.T., Liu, W.L., Liu, Y.Y., Lu, Z.C., Luo, X.L., Ma, T.Y., Peng, J.Q., Sheng, X., Shi, X.J., Sun, Y.H., Tian, G., Wang, K., Wang, L., Wu, R.N., Xie, Q., Xu, R.Y., Yang, J.S., Yang, L.L., Yang, Q., Yang, Y.J., Ye, Y., Yu, H.Y., Yu, J.H., Yu, T., Zhai, H., Zhan, Q., Zhang, G.S., Zhang, Q., Zhang, R., Zhang, Y., Zheng, W.Y., Zhou, B., Zhou, Z.H., Zhu, X.Y., Kakkar, S., Sawhney, J.P.S., Jadhav, P., Durgaprasad, R., Ravi Shankar, A.G., Rajput, R.K., Bhargava, K., Sarma, R., Srinivas, A., Roy, D., Nagamalesh, U.M., Chopda, M., Kishore, R., Kulkarni, G., Chandwani, P., Pothiwala, R.A., Padinhare Purayil, M., Shah, S., Chawla, K., Kothiwale, V.A., Raghuraman, B., Vijayaraghavan, G., Vijan, V.M., Bantwal, G., Bisne, V., Khan, A., Gupta, J.B., Kumar, S., Jain, D., Abraham, S., Adak, D., Barai, A., Begum, H., Bhattacharjee, P., Dargude, M., Davies, D., Deshpande, B., Dhakrao, P., Dhyani, V., Duhan, S., Earath, M., Ganatra, A., Giradkar, S., Jain, V., Karthikeyan, R., Kasala, L., Kaur, S., Krishnappa, S., Lawande, A., Lokesh, B., Madarkar, N., Meena, R., More, P., Naik, D., Prashanth, K., Rao, M., Rao, N.M., Sadhu, N., Shah, D., Sharma, M., Shiva, P., Singhal, S., Suresh, S., Vanajakshamma, V., Panse, S.G., Koretsune, Y., Kanamori, S., Yamamoto, K., Kumagai, K., Katsuda, Y., Sadamatsu, K., Toyota, F., Mizuno, Y., Misumi, I., Noguchi, H., Ando, S., Suetsugu, T., Minamoto, M., Oda, Hiroshi, Shiraishi, K., Adachi, S., Chiba, K., Norita, H., Tsuruta, M., Koyanagi, T., Yamamoto, K., Ando, H., Higashi, T., Okada, K., Azakami, S., Komaki, S., Kumeda, K., Murayama, T., Matsumura, J., Oba, Y., Sonoda, R., Goto, K., Minoda, K., Haraguchi, Y., Suefuji, H., Miyagi, H., Kato, H., Nakamura, Tadashi, Nakamura, Tsugihiro, Nandate, H., Zaitsu, R., Fujiura, Yoshihisa, Yoshimura, A., Numata, H., Ogawa, J., Tatematsu, H., Kamogawa, Y., Murakami, K., Wakasa, Y., Yamasawa, M., Maekawa, H., Abe, S., Kihara, H., Tsunoda, S., Saito, Katsumi, Saito, Kazuyuki, Fudo, T., Obunai, K., Tachibana, H., Oba, I., Kuwahata, T., Higa, S., Gushiken, M., Eto, T., Yoshida, H., Ikeda, D., Fujiura, Yoshitake, Ishizawa, M., Nakatsuka, M., Murata, K., Ogurusu, C., Shimoyama, M., Akutsu, M., Takamura, I., Hoshino, F., Yokota, N., Iwao, T., Tsuchida, K., Takeuchi, M., Hatori, Y., Kitami, Y., Nakamura, Yoichi, Oyama, R., Ageta, M., Oda, Hiroyuki, Go, Y., Mishima, K., Unoki, T., Morii, S., Shiga, Yuhei, Sumi, H., Nagatomo, T., Sanno, K., Fujisawa, K., Atsuchi, Y., Nagoshi, T., Seto, T., Tabuchi, T., Kameko, M., Nii, K., Oshiro, K., Takezawa, H., Nagano, S., Miyamoto, N., Iwaki, M., Nakamura, Yuichiro, Fujii, M., Okawa, M., Abe, Masahiko, Abe, Masatake, Abe, Mitsunori, Saito, T., Mito, T., Nagao, K., Minami, J., Mita, T., Sakuma, I., Taguchi, T., Marusaki, S., Doi, H., Tanaka, M., Fujito, T., Matsuta, M., Kusumoto, T., Kakinoki, S., Ashida, K., Yoshizawa, N., Agata, J., Arasaki, O., Manita, M., Ikemura, M., Fukuoka, S., Murakami, H., Matsukawa, S., Hata, Y., Taniguchi, T., Ko, T., Kubo, H., Imamaki, M., Akiyama, M., Inagaki, M., Odakura, H., Ueda, T., Katsube, Y., Nakata, A., Watanabe, H., Techigawara, M., Igarashi, M., Taga, K., Kimura, T., Tomimoto, S., Shibuya, M., Nakano, M., Ito, K., Seo, T., Hiramitsu, S., Hosokawa, H., Hoshiai, M., Hibino, M., Miyagawa, K., Horie, Hajime, Sugishita, N., Shiga, Yukio, Soma, A., Neya, K., Yoshida, Tetsuro, Yoshida, Tomoki, Mizuguchi, M., Ishiguro, M., Minagawa, T., Wada, M., Mukawa, H., Okuda, F., Nagasaka, S., Abe, Y., Adachi, Sen, Adachi, Susumu, Adachi, T., Akahane, K., Amano, T., Aoki, K., Aoyama, T., Arai, H., Arima, S., Arino, T., Asano, H., Asano, T., Azuma, J., Baba, T., Betsuyaku, T., Chibana, H., Date, H., Doiuchi, J., Emura, Y., Endo, M., Fujii, Y., Fujiki, R., Fujisawa, A., Fujisawa, Y., Fukuda, T., Fukui, T., Furukawa, N., Furukawa, T., Furumoto, W., Goto, T., Hamaoka, M., Hanazono, N., Hasegawa, K., Hatsuno, T., Hayashi, Y., Higuchi, K., Hirasawa, K., Hirayama, H., Hirose, M., Hirota, S., Honda, M., Horie, Hideki, Ido, T., Iiji, O., Ikeda, H., Ikeda, K., Ikeoka, K., Imaizumi, M., Inaba, H., Inoue, T., Iseki, F., Ishihara, A., Ishioka, N., Ito, N., Iwase, T., Kakuda, H., Kamata, J., Kanai, H., Kanda, H., Kaneko, M., Kano, H., Kasai, T., Kato, T., Kato, Y., Kawada, Y., Kawai, K., Kawakami, K., Kawakami, S., Kawamoto, T., Kawano, S., Kim, J., Kira, T., Kitazawa, H., Kitazumi, H., Kito, T., Kobayashi, T., Koeda, T., Kojima, J., Komatsu, H., Komatsu, I., Koshibu, Y., Kotani, T., Kozuka, T., Kumai, Y., Kumazaki, T., Maeda, I., Maeda, K., Maruyama, Y., Matsui, S., Matsushita, K., Matsuura, Y., Mineoi, K., Mitsuhashi, H., Miura, N., Miyaguchi, S., Miyajima, S., Miyamoto, H., Miyashita, A., Miyata, S., Mizuguchi, I., Mizuno, A., Mori, T., Moriai, O., Morishita, K., Murai, O., Nagai, Sho, Nagai, Shunichi, Nagata, E., Nagata, H., Nakagomi, A., Nakahara, S., Nakamura, M., Nakamura, R., Nakanishi, N., Nakayama, T., Nakazato, R., Nanke, T., Nariyama, J., Niijima, Y., Niinuma, H., Nishida, Y., Nishihata, Y., Nishino, K., Nishioka, H., Nishizawa, K., Niwa, I., Nomura, K., Nomura, S., Nozoe, M., Ogawa, T., Ohara, N., Okada, M., Okamoto, K., Okita, H., Okuyama, M., Ono, H., Ono, T., Onuki Pearce, Y., Oriso, S., Ota, A., Otaki, E., Saito, Y., Sakai, H., Sakamoto, N., Sakamoto, Y., Samejima, Y., Sasagawa, Y., Sasaguri, H., Sasaki, A., Sasaki, T., Sato, Kazuki, Sato, Kiyoharu, Sawano, M., Seki, S., Sekine, Y., Seta, Y., Sezaki, K., Shibata, N., Shiina, Y., Shimono, H., Shimoyama, Y., Shindo, T., Shinohara, H., Shinohe, R., Shinozuka, T., Shirai, T., Shiraiwa, T., Shozawa, Y., Suga, T., Sugimoto, C., Suzuki, Kazuo, Suzuki, Keita, Suzuki, Shu, Suzuki, Shunji, Suzuki, Susumu, Suzuki, Y., Tada, M., Taguchi, A., Takagi, T., Takagi, Y., Takahashi, K., Takahashi, S., Takai, H., Takanaka, C., Take, S., Takeda, H., Takei, K., Takenaka, K., Tana, T., Tanabe, G., Taya, K., Teragawa, H., Tohyo, S., Toru, S., Tsuchiya, Y., Tsuji, T., Tsuzaki, K., Uchiyama, H., Ueda, O., Ueda, T., Ueyama, Y., Wakaki, N., Wakiyama, T., Washizuka, T., Watanabe, M., Yamada, T., Yamagishi, T., Yamaguchi, H., 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Robertson, C., Sage, A., Sanghera, T., Shaw, P., Shoemaker, J., Smith, K., Stephanie, B., Thatcher, A., Theobald, H., Thompson, N., Treasure, L., Tripti, T., Verdi, C., and Worthy, V.
Abstract: The Global Anticoagulant Registry in the FIELD–Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry.
Published: 2018
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20. Frequency of Loss of Function Variants in LRRK2 in Parkinson Disease

Author: Blauwendraat, Cornelis, Reed, Xylena, Kia, Demis A., Gan-Or, Ziv, Lesage, Suzanne, Pihlstrøm, Lasse, Guerreiro, Rita, Gibbs, J. Raphael, Sabir, Marya, Ahmed, Sarah, Ding, Jinhui, Alcalay, Roy N., Hassin-Baer, Sharon, Pittman, Alan M., Brooks, Janet, Edsall, Connor, Hernandez, Dena G., Chung, Sun Ju, Goldwurm, Stefano, Toft, Mathias, Schulte, Claudia, Bras, Jose, Wood, Nicholas W., Brice, Alexis, Morris, Huw R., Scholz, Sonja W., Nalls, Mike A., Singleton, Andrew B., and Cookson, Mark R.
Abstract: IMPORTANCE: Pathogenic variants in LRRK2 are a relatively common genetic cause of Parkinson disease (PD). Currently, the molecular mechanism underlying disease is unknown, and gain and loss of function (LOF) models of pathogenesis have been postulated. LRRK2 variants are reported to result in enhanced phosphorylation of substrates and increased cell death. However, the double knockout of Lrrk2 and its homologue Lrrk1 results in neurodegeneration in a mouse model, suggesting that disease may occur by LOF. Because LRRK2 inhibitors are currently in development as potential disease-modifying treatments in PD, it is critical to determine whether LOF variants in LRRK2 increase or decrease the risk of PD. OBJECTIVE: To determine whether LRRK1 and LRRK2 LOF variants contribute to the risk of developing PD. DESIGN, SETTING, AND PARTICIPANTS: To determine the prevailing mechanism of LRRK2-mediated disease in human populations, next-generation sequencing data from a large case-control cohort (>23 000 individuals) was analyzed for LOF variants in LRRK1 and LRRK2. Data were generated at 5 different sites and 5 different data sets, including cases with clinically diagnosed PD and neurologically normal control individuals. Data were collected from 2012 through 2017. MAIN OUTCOMES AND MEASURES: Frequencies of LRRK1 and LRRK2 LOF variants present in the general population and compared between cases and controls. RESULTS: Among 11 095 cases with PD and 12 615 controls, LRRK1 LOF variants were identified in 0.205% of cases and 0.139% of controls (odds ratio, 1.48; SE, 0.571; 95% CI, 0.45-4.44; P = .49) and LRRK2 LOF variants were found in 0.117% of cases and 0.087% of controls (odds ratio, 1.48; SE, 0.431; 95% CI, 0.63-3.50; P = .36). All association tests suggested lack of association between LRRK1 or LRRK2 variants and PD. Further analysis of lymphoblastoid cell lines from several heterozygous LOF variant carriers found that, as expected, LRRK2 protein levels are reduced by approximately half compared with wild-type alleles. CONCLUSIONS AND RELEVANCE: Together these findings indicate that haploinsufficiency of LRRK1 or LRRK2 is neither a cause of nor protective against PD. Furthermore, these results suggest that kinase inhibition or allele-specific targeting of mutant LRRK2 remain viable therapeutic strategies in PD.
Published: 2018
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21. Fractal Analysis of Right Ventricular Trabeculae in Pulmonary Hypertension

Author: Dawes, Timothy J. W., Cai, Jiashen, Quinlan, Marina, Marvao, Antonio de, Ostrowski, Philip J., Tokarczuk, Paweł F., Watson, Geoffrey M. J., Wharton, John, Howard, Luke S. G. E., Gibbs, J. Simon R., Cook, Stuart A., Wilkins, Martin R., and O’Regan, Declan P.
Abstract: Fractal analysis of the right ventricle is practical and reproducible in both healthy subjects and patients with disease, offering insights into cardiac efficiency, hemodynamic adaptation, and tissue characterization in right-sided heart failure; however, it does not provide incremental benefit in predicting survival.
Published: 2018
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22. Efficacy of Exome-Targeted Capture Sequencing to Detect Mutations in Known Cerebellar Ataxia Genes

Author: Coutelier, Marie, Hammer, Monia B., Stevanin, Giovanni, Monin, Marie-Lorraine, Davoine, Claire-Sophie, Mochel, Fanny, Labauge, Pierre, Ewenczyk, Claire, Ding, Jinhui, Gibbs, J. Raphael, Hannequin, Didier, Melki, Judith, Toutain, Annick, Laugel, Vincent, Forlani, Sylvie, Charles, Perrine, Broussolle, Emmanuel, Thobois, Stéphane, Afenjar, Alexandra, Anheim, Mathieu, Calvas, Patrick, Castelnovo, Giovanni, de Broucker, Thomas, Vidailhet, Marie, Moulignier, Antoine, Ghnassia, Robert T., Tallaksen, Chantal, Mignot, Cyril, Goizet, Cyril, Le Ber, Isabelle, Ollagnon-Roman, Elisabeth, Pouget, Jean, Brice, Alexis, Singleton, Andrew, and Durr, Alexandra
Abstract: IMPORTANCE: Molecular diagnosis is difficult to achieve in disease groups with a highly heterogeneous genetic background, such as cerebellar ataxia (CA). In many patients, candidate gene sequencing or focused resequencing arrays do not allow investigators to reach a genetic conclusion. OBJECTIVES: To assess the efficacy of exome-targeted capture sequencing to detect mutations in genes broadly linked to CA in a large cohort of undiagnosed patients and to investigate their prevalence. DESIGN, SETTING, AND PARTICIPANTS: Three hundred nineteen index patients with CA and without a history of dominant transmission were included in the this cohort study by the Spastic Paraplegia and Ataxia Network. Centralized storage was in the DNA and cell bank of the Brain and Spine Institute, Salpetriere Hospital, Paris, France. Patients were classified into 6 clinical groups, with the largest being those with spastic ataxia (ie, CA with pyramidal signs [n = 100]). Sequencing was performed from January 1, 2014, through December 31, 2016. Detected variants were classified as very probably or definitely causative, possibly causative, or of unknown significance based on genetic evidence and genotype-phenotype considerations. MAIN OUTCOMES AND MEASURES: Identification of variants in genes broadly linked to CA, classified in pathogenicity groups. RESULTS: The 319 included patients had equal sex distribution (160 female [50.2%] and 159 male patients [49.8%]; mean [SD] age at onset, 27.9 [18.6] years). The age at onset was younger than 25 years for 131 of 298 patients (44.0%) with complete clinical information. Consanguinity was present in 101 of 298 (33.9%). Very probable or definite diagnoses were achieved for 72 patients (22.6%), with an additional 19 (6.0%) harboring possibly pathogenic variants. The most frequently mutated genes were SPG7 (n = 14), SACS (n = 8), SETX (n = 7), SYNE1 (n = 6), and CACNA1A (n = 6). The highest diagnostic rate was obtained for patients with an autosomal recessive CA with oculomotor apraxia–like phenotype (6 of 17 [35.3%]) or spastic ataxia (35 of 100 [35.0%]) and patients with onset before 25 years of age (41 of 131 [31.3%]). Peculiar phenotypes were reported for patients carrying KCND3 or ERCC5 variants. CONCLUSIONS AND RELEVANCE: Exome capture followed by targeted analysis allows the molecular diagnosis in patients with highly heterogeneous mendelian disorders, such as CA, without prior assumption of the inheritance mode or causative gene. Being commonly available without specific design need, this procedure allows testing of a broader range of genes, consequently describing less classic phenotype-genotype correlations, and post hoc reanalysis of data as new genes are implicated in the disease.
Published: 2018
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23. Discovery and functional prioritization of Parkinson’s disease candidate genes from large-scale whole exome sequencing

Author: Jansen, Iris, Ye, Hui, Heetveld, Sasja, Lechler, Marie, Michels, Helen, Seinstra, Renée, Lubbe, Steven, Drouet, Valérie, Lesage, Suzanne, Majounie, Elisa, Gibbs, J., Nalls, Mike, Ryten, Mina, Botia, Juan, Vandrovcova, Jana, Simon-Sanchez, Javier, Castillo-Lizardo, Melissa, Rizzu, Patrizia, Blauwendraat, Cornelis, Chouhan, Amit, Li, Yarong, Yogi, Puja, Amin, Najaf, van Duijn, Cornelia, Morris, Huw, Brice, Alexis, Singleton, Andrew, David, Della, Nollen, Ellen, Jain, Shushant, Shulman, Joshua, and Heutink, Peter
Abstract: Whole-exome sequencing (WES) has been successful in identifying genes that cause familial Parkinson’s disease (PD). However, until now this approach has not been deployed to study large cohorts of unrelated participants. To discover rare PD susceptibility variants, we performed WES in 1148 unrelated cases and 503 control participants. Candidate genes were subsequently validated for functions relevant to PD based on parallel RNA-interference (RNAi) screens in human cell culture and Drosophilaand C. elegansmodels. Assuming autosomal recessive inheritance, we identify 27 genes that have homozygous or compound heterozygous loss-of-function variants in PD cases. Definitive replication and confirmation of these findings were hindered by potential heterogeneity and by the rarity of the implicated alleles. We therefore looked for potential genetic interactions with established PD mechanisms. Following RNAi-mediated knockdown, 15 of the genes modulated mitochondrial dynamics in human neuronal cultures and four candidates enhanced α-synuclein-induced neurodegeneration in Drosophila. Based on complementary analyses in independent human datasets, five functionally validated genes—GPATCH2L, UHRF1BP1L, PTPRH, ARSB, and VPS13C—also showed evidence consistent with genetic replication. By integrating human genetic and functional evidence, we identify several PD susceptibility gene candidates for further investigation. Our approach highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies.
Published: 2017
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24. A global view of pulmonary hypertension.

Author: Hoeper, Marius M, Humbert, Marc, Souza, Rogerio, Idrees, Majdy, Kawut, Steven M, Sliwa-Hahnle, Karen, Jing, Zhi-Cheng, and Gibbs, J Simon R
Subjects: DISEASES in older people, PULMONARY hypertension, SCHISTOSOMIASIS
Abstract: Summary Pulmonary hypertension is a substantial global health issue. All age groups are affected with rapidly growing importance in elderly people, particularly in countries with ageing populations. Present estimates suggest a pulmonary hypertension prevalence of about 1% of the global population, which increases up to 10% in individuals aged more than 65 years. In almost all parts of the world, left-sided heart and lung diseases have become the most frequent causes of pulmonary hypertension. About 80% of affected patients live in developing countries, where pulmonary hypertension is frequently associated with congenital heart disease and various infectious disorders, including schistosomiasis, HIV, and rheumatic heart disease. These forms of pulmonary hypertension occur predominantly in those younger than 65 years. Independently of the underlying disease, the development of pulmonary hypertension is associated with clinical deterioration and a substantially increased mortality risk. Global research efforts are needed to establish preventive strategies and treatments for the various types of pulmonary hypertension. [ABSTRACT FROM AUTHOR]
Published: 2016
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25. Plasma proteome analysis in patients with pulmonary arterial hypertension: an observational cohort study

Author: Rhodes, Christopher J, Wharton, John, Ghataorhe, Pavandeep, Watson, Geoffrey, Girerd, Barbara, Howard, Luke S, Gibbs, J Simon R, Condliffe, Robin, Elliot, Charles A, Kiely, David G, Simonneau, Gerald, Montani, David, Sitbon, Olivier, Gall, Henning, Schermuly, Ralph T, Ghofrani, H Ardeschir, Lawrie, Allan, Humbert, Marc, and Wilkins, Martin R
Abstract: Idiopathic and heritable pulmonary arterial hypertension form a rare but molecularly heterogeneous disease group. We aimed to measure and validate differences in plasma concentrations of proteins that are associated with survival in patients with idiopathic or heritable pulmonary arterial hypertension to improve risk stratification.
Published: 2017
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26. Genome-wide Pleiotropy Between Parkinson Disease and Autoimmune Diseases

Author: Witoelar, Aree, Jansen, Iris E., Wang, Yunpeng, Desikan, Rahul S., Gibbs, J. Raphael, Blauwendraat, Cornelis, Thompson, Wesley K., Hernandez, Dena G., Djurovic, Srdjan, Schork, Andrew J., Bettella, Francesco, Ellinghaus, David, Franke, Andre, Lie, Benedicte A., McEvoy, Linda K., Karlsen, Tom H., Lesage, Suzanne, Morris, Huw R., Brice, Alexis, Wood, Nicholas W., Heutink, Peter, Hardy, John, Singleton, Andrew B., Dale, Anders M., Gasser, Thomas, Andreassen, Ole A., and Sharma, Manu
Abstract: IMPORTANCE: Recent genome-wide association studies (GWAS) and pathway analyses supported long-standing observations of an association between immune-mediated diseases and Parkinson disease (PD). The post-GWAS era provides an opportunity for cross-phenotype analyses between different complex phenotypes. OBJECTIVES: To test the hypothesis that there are common genetic risk variants conveying risk of both PD and autoimmune diseases (ie, pleiotropy) and to identify new shared genetic variants and their pathways by applying a novel statistical framework in a genome-wide approach. DESIGN, SETTING, AND PARTICIPANTS: Using the conjunction false discovery rate method, this study analyzed GWAS data from a selection of archetypal autoimmune diseases among 138 511 individuals of European ancestry and systemically investigated pleiotropy between PD and type 1 diabetes, Crohn disease, ulcerative colitis, rheumatoid arthritis, celiac disease, psoriasis, and multiple sclerosis. NeuroX data (6927 PD cases and 6108 controls) were used for replication. The study investigated the biological correlation between the top loci through protein-protein interaction and changes in the gene expression and methylation levels. The dates of the analysis were June 10, 2015, to March 4, 2017. MAIN OUTCOMES AND MEASURES: The primary outcome was a list of novel loci and their pathways involved in PD and autoimmune diseases. RESULTS: Genome-wide conjunctional analysis identified 17 novel loci at false discovery rate less than 0.05 with overlap between PD and autoimmune diseases, including known PD loci adjacent to GAK, HLA-DRB5, LRRK2, and MAPT for rheumatoid arthritis, ulcerative colitis and Crohn disease. Replication confirmed the involvement of HLA, LRRK2, MAPT, TRIM10, and SETD1A in PD. Among the novel genes discovered, WNT3, KANSL1, CRHR1, BOLA2, and GUCY1A3 are within a protein-protein interaction network with known PD genes. A subset of novel loci was significantly associated with changes in methylation or expression levels of adjacent genes. CONCLUSIONS AND RELEVANCE: The study findings provide novel mechanistic insights into PD and autoimmune diseases and identify a common genetic pathway between these phenotypes. The results may have implications for future therapeutic trials involving anti-inflammatory agents.
Published: 2017
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27. Machine Learning of Three-dimensional Right Ventricular Motion Enables Outcome Prediction in Pulmonary Hypertension: A Cardiac MR Imaging Study

Author: Dawes, Timothy J. W., Marvao, Antonio de, Shi, Wenzhe, Fletcher, Tristan, Watson, Geoffrey M. J., Wharton, John, Rhodes, Christopher J., Howard, Luke S. G. E., Gibbs, J. Simon R., Rueckert, Daniel, Cook, Stuart A., Wilkins, Martin R., and O’Regan, Declan P.
Abstract: Applying machine learning of complex motion phenotypes obtained from cardiac MR images allows more accurate prediction of patient outcomes in pulmonary hypertension.
Published: 2017
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28. Plasma Metabolomics Implicates Modified Transfer RNAs and Altered Bioenergetics in the Outcomes of Pulmonary Arterial Hypertension

Author: Rhodes, Christopher J., Ghataorhe, Pavandeep, Wharton, John, Rue-Albrecht, Kevin C., Hadinnapola, Charaka, Watson, Geoffrey, Bleda, Marta, Haimel, Matthias, Coghlan, Gerry, Corris, Paul A., Howard, Luke S., Kiely, David G., Peacock, Andrew J., Pepke-Zaba, Joanna, Toshner, Mark R., Wort, S. John, Gibbs, J. Simon R., Lawrie, Allan, Gräf, Stefan, Morrell, Nicholas W., and Wilkins, Martin R.
Abstract: Supplemental Digital Content is available in the text.
Published: 2017
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29. Novel genetic loci underlying human intracranial volume identified through genome-wide association

Author: Adams, Hieab H H, Hibar, Derrek P, Chouraki, Vincent, Stein, Jason L, Nyquist, Paul A, Rentería, Miguel E, Trompet, Stella, Arias-Vasquez, Alejandro, Seshadri, Sudha, Desrivières, Sylvane, Beecham, Ashley H, Jahanshad, Neda, Wittfeld, Katharina, Van der Lee, Sven J, Abramovic, Lucija, Alhusaini, Saud, Amin, Najaf, Andersson, Micael, Arfanakis, Konstantinos, Aribisala, Benjamin S, Armstrong, Nicola J, Athanasiu, Lavinia, Axelsson, Tomas, Beiser, Alexa, Bernard, Manon, Bis, Joshua C, Blanken, Laura M E, Blanton, Susan H, Bohlken, Marc M, Boks, Marco P, Bralten, Janita, Brickman, Adam M, Carmichael, Owen, Chakravarty, M Mallar, Chauhan, Ganesh, Chen, Qiang, Ching, Christopher R K, Cuellar-Partida, Gabriel, Braber, Anouk Den, Doan, Nhat Trung, Ehrlich, Stefan, Filippi, Irina, Ge, Tian, Giddaluru, Sudheer, Goldman, Aaron L, Gottesman, Rebecca F, Greven, Corina U, Grimm, Oliver, Griswold, Michael E, Guadalupe, Tulio, Hass, Johanna, Haukvik, Unn K, Hilal, Saima, Hofer, Edith, Hoehn, David, Holmes, Avram J, Hoogman, Martine, Janowitz, Deborah, Jia, Tianye, Kasperaviciute, Dalia, Kim, Sungeun, Klein, Marieke, Kraemer, Bernd, Lee, Phil H, Liao, Jiemin, Liewald, David C M, Lopez, Lorna M, Luciano, Michelle, Macare, Christine, Marquand, Andre, Matarin, Mar, Mather, Karen A, Mattheisen, Manuel, Mazoyer, Bernard, McKay, David R, McWhirter, Rebekah, Milaneschi, Yuri, Mirza-Schreiber, Nazanin, Muetzel, Ryan L, Maniega, Susana Muñoz, Nho, Kwangsik, Nugent, Allison C, Loohuis, Loes M Olde, Oosterlaan, Jaap, Papmeyer, Martina, Pappa, Irene, Pirpamer, Lukas, Pudas, Sara, Pütz, Benno, Rajan, Kumar B, Ramasamy, Adaikalavan, Richards, Jennifer S, Risacher, Shannon L, Roiz-Santiañez, Roberto, Rommelse, Nanda, Rose, Emma J, Royle, Natalie A, Rundek, Tatjana, Sämann, Philipp G, Satizabal, Claudia L, Schmaal, Lianne, Schork, Andrew J, Shen, Li, Shin, Jean, Shumskaya, Elena, Smith, Albert V, Sprooten, Emma, Strike, Lachlan T, Teumer, Alexander, Thomson, Russell, Tordesillas-Gutierrez, Diana, Toro, Roberto, Trabzuni, Daniah, Vaidya, Dhananjay, Van der Grond, Jeroen, Van der Meer, Dennis, Van Donkelaar, Marjolein M J, Van Eijk, Kristel R, Van Erp, Theo G M, Van Rooij, Daan, Walton, Esther, Westlye, Lars T, Whelan, Christopher D, Windham, Beverly G, Winkler, Anderson M, Woldehawariat, Girma, Wolf, Christiane, Wolfers, Thomas, Xu, Bing, Yanek, Lisa R, Yang, Jingyun, Zijdenbos, Alex, Zwiers, Marcel P, Agartz, Ingrid, Aggarwal, Neelum T, Almasy, Laura, Ames, David, Amouyel, Philippe, Andreassen, Ole A, Arepalli, Sampath, Assareh, Amelia A, Barral, Sandra, Bastin, Mark E, Becker, Diane M, Becker, James T, Bennett, David A, Blangero, John, van Bokhoven, Hans, Boomsma, Dorret I, Brodaty, Henry, Brouwer, Rachel M, Brunner, Han G, Buckner, Randy L, Buitelaar, Jan K, Bulayeva, Kazima B, Cahn, Wiepke, Calhoun, Vince D, Cannon, Dara M, Cavalleri, Gianpiero L, Chen, Christopher, Cheng, Ching-Yu, Cichon, Sven, Cookson, Mark R, Corvin, Aiden, Crespo-Facorro, Benedicto, Curran, Joanne E, Czisch, Michael, Dale, Anders M, Davies, Gareth E, De Geus, Eco J C, De Jager, Philip L, de Zubicaray, Greig I, Delanty, Norman, Depondt, Chantal, DeStefano, Anita L, Dillman, Allissa, Djurovic, Srdjan, Donohoe, Gary, Drevets, Wayne C, Duggirala, Ravi, Dyer, Thomas D, Erk, Susanne, Espeseth, Thomas, Evans, Denis A, Fedko, Iryna O, Fernández, Guillén, Ferrucci, Luigi, Fisher, Simon E, Fleischman, Debra A, Ford, Ian, Foroud, Tatiana M, Fox, Peter T, Francks, Clyde, Fukunaga, Masaki, Gibbs, J Raphael, Glahn, David C, Gollub, Randy L, Göring, Harald H H, Grabe, Hans J, Green, Robert C, Gruber, Oliver, Gudnason, Vilmundur, Guelfi, Sebastian, Hansell, Narelle K, Hardy, John, Hartman, Catharina A, Hashimoto, Ryota, Hegenscheid, Katrin, Heinz, Andreas, Le Hellard, Stephanie, Hernandez, Dena G, Heslenfeld, Dirk J, Ho, Beng-Choon, Hoekstra, Pieter J, Hoffmann, Wolfgang, Hofman, Albert, Holsboer, Florian, Homuth, Georg, Hosten, Norbert, Hottenga, Jouke-Jan, Pol, Hilleke E Hulshoff, Ikeda, Masashi, Ikram, M Kamran, Jack, Clifford R, Jenkinson, Mark, Johnson, Robert, Jönsson, Erik G, Jukema, J Wouter, Kahn, René S, Kanai, Ryota, Kloszewska, Iwona, Knopman, David S, Kochunov, Peter, Kwok, John B, Lawrie, Stephen M, Lemaître, Hervé, Liu, Xinmin, Longo, Dan L, Longstreth, W T, Lopez, Oscar L, Lovestone, Simon, Martinez, Oliver, Martinot, Jean-Luc, Mattay, Venkata S, McDonald, Colm, McIntosh, Andrew M, McMahon, Katie L, McMahon, Francis J, Mecocci, Patrizia, Melle, Ingrid, Meyer-Lindenberg, Andreas, Mohnke, Sebastian, Montgomery, Grant W, Morris, Derek W, Mosley, Thomas H, Mühleisen, Thomas W, Müller-Myhsok, Bertram, Nalls, Michael A, Nauck, Matthias, Nichols, Thomas E, Niessen, Wiro J, Nöthen, Markus M, Nyberg, Lars, Ohi, Kazutaka, Olvera, Rene L, Ophoff, Roel A, Pandolfo, Massimo, Paus, Tomas, Pausova, Zdenka, Penninx, Brenda W J H, Pike, G Bruce, Potkin, Steven G, Psaty, Bruce M, Reppermund, Simone, Rietschel, Marcella, Roffman, Joshua L, Romanczuk-Seiferth, Nina, Rotter, Jerome I, Ryten, Mina, Sacco, Ralph L, Sachdev, Perminder S, Saykin, Andrew J, Schmidt, Reinhold, Schofield, Peter R, Sigurdsson, Sigurdur, Simmons, Andy, Singleton, Andrew, Sisodiya, Sanjay M, Smith, Colin, Smoller, Jordan W, Soininen, Hilkka, Srikanth, Velandai, Steen, Vidar M, Stott, David J, Sussmann, Jessika E, Thalamuthu, Anbupalam, Tiemeier, Henning, Toga, Arthur W, Traynor, Bryan J, Troncoso, Juan, Turner, Jessica A, Tzourio, Christophe, Uitterlinden, Andre G, Hernández, Maria C Valdés, Van der Brug, Marcel, Van der Lugt, Aad, Van der Wee, Nic J A, Van Duijn, Cornelia M, Van Haren, Neeltje E M, Van ′t Ent, Dennis, Van Tol, Marie-Jose, Vardarajan, Badri N, Veltman, Dick J, Vernooij, Meike W, Völzke, Henry, Walter, Henrik, Wardlaw, Joanna M, Wassink, Thomas H, Weale, Michael E, Weinberger, Daniel R, Weiner, Michael W, Wen, Wei, Westman, Eric, White, Tonya, Wong, Tien Y, Wright, Clinton B, Zielke, H Ronald, Zonderman, Alan B, Deary, Ian J, DeCarli, Charles, Schmidt, Helena, Martin, Nicholas G, De Craen, Anton J M, Wright, Margaret J, Launer, Lenore J, Schumann, Gunter, Fornage, Myriam, Franke, Barbara, Debette, Stéphanie, Medland, Sarah E, Ikram, M Arfan, and Thompson, Paul M
Abstract: Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five previously unknown loci for intracranial volume and confirmed two known signals. Four of the loci were also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (ρgenetic= 0.748), which indicates a similar genetic background and allowed us to identify four additional loci through meta-analysis (Ncombined= 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, and Parkinson's disease, and were enriched near genes involved in growth pathways, including PI3K-AKT signaling. These findings identify the biological underpinnings of intracranial volume and their link to physiological and pathological traits.
Published: 2016
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30. Echocardiographic and Hemodynamic Predictors of Survival in Precapillary Pulmonary Hypertension: Seven-Year Follow-Up.

Author: Grapsa, Julia, Pereira Nunes, Maria Carmo, Tan, Timothy C., Cabrita, Ines Zimbarra, Coulter, Taryn, Smith, Benjamin C. F., Dawson, David, Gibbs, J. Simon R., and Nihoyannopoulos, Petros
Published: 2015
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31. Biventricular Function at High Altitude: Implications for Regulation of Stroke Volume in Chronic Hypoxia.

Author: Back, Nathan, Cohen, Irun R., Lajtha, Abel N.S., Lambris, John D., Paoletti, Rodolfo, Roach, Robert C., Wagner, Peter D., Hackett, Peter H., and Gibbs, J Simon R
Abstract: The myocardium is well protected against chronic hypoxia. In chronic hypoxia stroke volume falls both at rest and on exercise. The fall in stroke volume is associated with reduction in left ventricular dimensions and filling pressure. An obvious explanation for this is the reduction in plasma volume observed at high altitude, but this does not appear to be the whole story. Neither is left ventricular systolic function abnormal even at the summit of Mount Everest. Hypoxia itself may have a direct effect on impairing myocardial relaxation. Increased pulmonary vascular resistance leads to right ventricular pressure overload. This may impair right ventricular function, and reduce stroke volume and venous return to the left atrium. Interaction between the right and left ventricles, which share a common septum and are potentially constrained in volume by the pericardium, may impair diastolic left ventricular filling as a consequence of right ventricular pressure overload, and hence reduce stroke volume. It is questionable how clinically significant is this left ventricular diastolic dysfunction. The relative importance of different mechanisms which reduce stroke volume probably depends whether hemodynamics are measured at rest or on exercise. Intervention with sildenafil to ameliorate hypoxic pulmonary vasoconstriction is associated with both an increase in exercise capacity and stroke volume in hypoxia. Whether these have a causal association remains to be demonstrated. [ABSTRACT FROM AUTHOR]
Published: 2008
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32. A Pathway to Clinician-Led Culture Change in the Operating Theatre

Author: Gibbs, J and Smith, P
Abstract: Noise in the operating theatre environment has remained a persistent and unresolved problem (Szalma & Hancock 2011). The problem currently lacks an effective solution (Schafer et al 2012). In order to partially resolve this issue, the authors created a behavioural noise reduction tool called ‘Below Ten Thousand’. This study identifies a potential solution to the problem of behavioural noise in the operating theatre, and indicates further research must be undertaken to identify the full scale of benefits this technique can deliver to the team environment in the operating theatre.
Published: 2016
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33. A global view of pulmonary hypertension

Author: Hoeper, Marius M, Humbert, Marc, Souza, Rogerio, Idrees, Majdy, Kawut, Steven M, Sliwa-Hahnle, Karen, Jing, Zhi-Cheng, and Gibbs, J Simon R
Abstract: Pulmonary hypertension is a substantial global health issue. All age groups are affected with rapidly growing importance in elderly people, particularly in countries with ageing populations. Present estimates suggest a pulmonary hypertension prevalence of about 1% of the global population, which increases up to 10% in individuals aged more than 65 years. In almost all parts of the world, left-sided heart and lung diseases have become the most frequent causes of pulmonary hypertension. About 80% of affected patients live in developing countries, where pulmonary hypertension is frequently associated with congenital heart disease and various infectious disorders, including schistosomiasis, HIV, and rheumatic heart disease. These forms of pulmonary hypertension occur predominantly in those younger than 65 years. Independently of the underlying disease, the development of pulmonary hypertension is associated with clinical deterioration and a substantially increased mortality risk. Global research efforts are needed to establish preventive strategies and treatments for the various types of pulmonary hypertension.
Published: 2016
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34. mRNA expression, splicing and editing in the embryonic and adult mouse cerebral cortex

Author: Dillman, Allissa A, Hauser, David N, Gibbs, J Raphael, Nalls, Michael A, McCoy, Melissa K, Rudenko, Iakov N, Galter, Dagmar, and Cookson, Mark R
Abstract: The complexity of the adult brain is a result of both developmental processes and experience-dependent circuit formation. One way to look at the differences between embryonic and adult brain is to examine gene expression. Previous studies have used microarrays to address this in a global manner. However, the transcriptome is more complex than gene expression levels alone, as alternative splicing and RNA editing generate a diverse set of mature transcripts. Here we report a high-resolution transcriptome data set of mouse cerebral cortex at embryonic and adult stages using RNA sequencing (RNA-Seq). We found many differences in gene expression, splicing and RNA editing between embryonic and adult cerebral cortex. Each data set was validated technically and biologically, and in each case we found our RNA-Seq observations to have predictive validity. We provide this data set and analysis as a resource for understanding gene expression in the embryonic and adult cerebral cortex.
Published: 2016
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35. Review article: Anti-embolism stockings.

Author: Patel, N, Khakha, R, Gibbs, J, Patel, Nimesh, Khakha, Raghbir, and Gibbs, James
Published: 2013

36. Association of a Novel ACTA1 Mutation With a Dominant Progressive Scapuloperoneal Myopathy in an Extended Family

Author: Zukosky, Kristen, Meilleur, Katherine, Traynor, Bryan J., Dastgir, Jahannaz, Medne, Livija, Devoto, Marcella, Collins, James, Rooney, Jachinta, Zou, Yaqun, Yang, Michele L., Gibbs, J. Raphael, Meier, Markus, Stetefeld, Joerg, Finkel, Richard S., Schessl, Joachim, Elman, Lauren, Felice, Kevin, Ferguson, Toby A., Ceyhan-Birsoy, Ozge, Beggs, Alan H., Tennekoon, Gihan, Johnson, Janel O., and Bönnemann, Carsten G.
Abstract: IMPORTANCE: New genomic strategies can now be applied to identify a diagnosis in patients and families with previously undiagnosed rare genetic conditions. The large family evaluated in the present study was described in 1966 and now expands the phenotype of a known neuromuscular gene. OBJECTIVE: To determine the genetic cause of a slowly progressive, autosomal dominant, scapuloperoneal neuromuscular disorder by using linkage and exome sequencing. DESIGN, SETTING, AND PARTICIPANTS: Fourteen affected individuals in a 6-generation family with a progressive scapuloperoneal disorder were evaluated. Participants were examined at pediatric, neuromuscular, and research clinics from March 1, 2005, to May 31, 2014. Exome and linkage were performed in genetics laboratories of research institutions. MAIN OUTCOMES AND MEASURES: Examination and evaluation by magnetic resonance imaging, ultrasonography, electrodiagnostic studies, and muscle biopsies (n = 3). Genetic analysis included linkage analysis (n = 17) with exome sequencing (n = 7). RESULTS: Clinical findings included progressive muscle weakness in an initially scapuloperoneal and distal distribution, including wrist extensor weakness, finger and foot drop, scapular winging, mild facial weakness, Achilles tendon contractures, and diminished or absent deep tendon reflexes. Both age at onset and progression of the disease showed clinical variability within the family. Muscle biopsy specimens demonstrated type I fiber atrophy and trabeculated fibers without nemaline rods. Analysis of exome sequences within the linkage region (4.8 megabases) revealed missense mutation c.591C>A p.Glu197Asp in a highly conserved residue in exon 4 of ACTA1. The mutation cosegregated with disease in all tested individuals and was not present in unaffected individuals. CONCLUSIONS AND RELEVANCE: This family defines a new scapuloperoneal phenotype associated with an ACTA1 mutation. A highly conserved protein, ACTA1 is implicated in multiple muscle diseases, including nemaline myopathy, actin aggregate myopathy, fiber-type disproportion, and rod-core myopathy. To our knowledge, mutations in Glu197 have not been reported previously. This residue is highly conserved and located in an exposed position in the protein; the mutation affects the intermolecular and intramolecular electrostatic interactions as shown by structural modeling. The mutation in this residue does not appear to lead to rod formation or actin accumulation in vitro or in vivo, suggesting a different molecular mechanism from that of other ACTA1 diseases.
Published: 2015
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37. A Genome-Wide Association Study of Myasthenia Gravis

Author: Renton, Alan E., Pliner, Hannah A., Provenzano, Carlo, Evoli, Amelia, Ricciardi, Roberta, Nalls, Michael A., Marangi, Giuseppe, Abramzon, Yevgeniya, Arepalli, Sampath, Chong, Sean, Hernandez, Dena G., Johnson, Janel O., Bartoccioni, Emanuela, Scuderi, Flavia, Maestri, Michelangelo, Gibbs, J. Raphael, Errichiello, Edoardo, Chiò, Adriano, Restagno, Gabriella, Sabatelli, Mario, Macek, Mark, Scholz, Sonja W., Corse, Andrea, Chaudhry, Vinay, Benatar, Michael, Barohn, Richard J., McVey, April, Pasnoor, Mamatha, Dimachkie, Mazen M., Rowin, Julie, Kissel, John, Freimer, Miriam, Kaminski, Henry J., Sanders, Donald B., Lipscomb, Bernadette, Massey, Janice M., Chopra, Manisha, Howard, James F., Koopman, Wilma J., Nicolle, Michael W., Pascuzzi, Robert M., Pestronk, Alan, Wulf, Charlie, Florence, Julaine, Blackmore, Derrick, Soloway, Aimee, Siddiqi, Zaeem, Muppidi, Srikanth, Wolfe, Gil, Richman, David, Mezei, Michelle M., Jiwa, Theresa, Oger, Joel, Drachman, Daniel B., and Traynor, Bryan J.
Abstract: IMPORTANCE: Myasthenia gravis is a chronic, autoimmune, neuromuscular disease characterized by fluctuating weakness of voluntary muscle groups. Although genetic factors are known to play a role in this neuroimmunological condition, the genetic etiology underlying myasthenia gravis is not well understood. OBJECTIVE: To identify genetic variants that alter susceptibility to myasthenia gravis, we performed a genome-wide association study. DESIGN, SETTING, AND PARTICIPANTS: DNA was obtained from 1032 white individuals from North America diagnosed as having acetylcholine receptor antibody–positive myasthenia gravis and 1998 race/ethnicity-matched control individuals from January 2010 to January 2011. These samples were genotyped on Illumina OmniExpress single-nucleotide polymorphism arrays. An independent cohort of 423 Italian cases and 467 Italian control individuals were used for replication. MAIN OUTCOMES AND MEASURES: We calculated P values for association between 8 114 394 genotyped and imputed variants across the genome and risk for developing myasthenia gravis using logistic regression modeling. A threshold P value of 5.0 × 10−8 was set for genome-wide significance after Bonferroni correction for multiple testing. RESULTS: In the overall case-control cohort, we identified association signals at CTLA4 (rs231770; P = 3.98 × 10−8; odds ratio, 1.37; 95% CI, 1.25-1.49), HLA-DQA1 (rs9271871; P = 1.08 × 10−8; odds ratio, 2.31; 95% CI, 2.02 - 2.60), and TNFRSF11A (rs4263037; P = 1.60 × 10−9; odds ratio, 1.41; 95% CI, 1.29-1.53). These findings replicated for CTLA4 and HLA-DQA1 in an independent cohort of Italian cases and control individuals. Further analysis revealed distinct, but overlapping, disease-associated loci for early- and late-onset forms of myasthenia gravis. In the late-onset cases, we identified 2 association peaks: one was located in TNFRSF11A (rs4263037; P = 1.32 × 10−12; odds ratio, 1.56; 95% CI, 1.44-1.68) and the other was detected in the major histocompatibility complex on chromosome 6p21 (HLA-DQA1; rs9271871; P = 7.02 × 10−18; odds ratio, 4.27; 95% CI, 3.92-4.62). Association within the major histocompatibility complex region was also observed in early-onset cases (HLA-DQA1; rs601006; P = 2.52 × 10−11; odds ratio, 4.0; 95% CI, 3.57-4.43), although the set of single-nucleotide polymorphisms was different from that implicated among late-onset cases. CONCLUSIONS AND RELEVANCE: Our genetic data provide insights into aberrant cellular mechanisms responsible for this prototypical autoimmune disorder. They also suggest that clinical trials of immunomodulatory drugs related to CTLA4 and that are already Food and Drug Administration approved as therapies for other autoimmune diseases could be considered for patients with refractory disease.
Published: 2015
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38. Guía de práctica clínica de la ESC 2014 sobre el diagnóstico y el tratamiento de la embolia pulmonar aguda

Author: Konstantinides, Stavros, Torbicki, Adam, Agnelli, Giancarlo, Danchin, Nicolas, Fitzmaurice, David, Galiè, Nazzareno, R. Gibbs, J. Simon, Huisman, Menno, Humbert, Marc, Kucher, Nils, Lang, Irene, Lankeit, Mareike, Lekakis, John, Maack, Christoph, Mayer, Eckhard, Meneveau, Nicolas, Perrier, Arnaud, Pruszczyk, Piotr, Rasmussen, Lars H., Schindler, Thomas H., Svitil, Pavel, Noordegraaf, Anton Vonk, Zamorano, José Luis, and Zompatori, Maurizio
Abstract: Comité de la ESC para la elaboración de Guías de Práctica Clínica (CPG): José Luis Zamorano (Presidente) (España), Stephan Achenbach (Alemania), Helmut Baumgartner (Alemania), Jeroen J. Bax (Países Bajos), Héctor Bueno (España), Veronica Dean (Francia), Christi Deaton (Reino Unido), Çetin Erol (Turquía), Robert Fagard (Bélgica), Roberto Ferrari (Italia), David Hasdai (Israel), Arno Hoes (Países Bajos), Paulus Kirchhof (Alemania/Reino Unido), Juhani Knuuti (Finlandia), Philippe Kolh (Bélgica), Patrizio Lancellotti (Bélgica), Ales Linhart (República Checa), Petros Nihoyannopoulos (Reino Unido), Massimo F. Piepoli (Italia), Piotr Ponikowski (Polonia), Per Anton Sirnes (Noruega), Juan Luis Tamargo (España), Michal Tendera (Polonia), Adam Torbicki (Polonia), William Wijns (Bélgica), Stephan Windecker (Suiza)
Published: 2015
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39. Response to Pulmonary Arterial Hypertension Drug Therapies in Patients with Pulmonary Arterial Hypertension and Cardiovascular Risk Factors

Author: Charalampopoulos, Athanasios, Howard, Luke S., Tzoulaki, Ioanna, Gin-Sing, Wendy, Grapsa, Julia, Wilkins, Martin R., Davies, Rachel J., Nihoyannopoulos, Petros, Connolly, Susan B., and Gibbs, J. Simon R.
Abstract: The age at diagnosis of pulmonary arterial hypertension (PAH) and the prevalence of cardiovascular (CV) risk factors are increasing. We sought to determine whether the response to drug therapy was influenced by CV risk factors in PAH patients. We studied consecutive incident PAH patients (n= 146) between January 1, 2008, and July 15, 2011. Patients were divided into two groups: the PAH–No CV group included patients with no CV risk factors (obesity, systemic hypertension, type 2 diabetes mellitus, permanent atrial fibrillation, mitral and/or aortic valve disease, and coronary artery disease), and the PAH-CV group included patients with at least one. The response to PAH treatment was analyzed in all the patients who received PAH drug therapy. The PAH–No CV group included 43 patients, and the PAH-CV group included 69 patients. Patients in the PAH–No CV group were younger than those in the PAH-CV group (P< 0.0001). In the PAH–No CV group, 16 patients (37%) improved on treatment and 27 (63%) did not improve, compared with 11 (16%) and 58 (84%) in the PAH-CV group, respectively (P= 0.027 after adjustment for age). There was no difference in survival at 30 months (P= 0.218). In conclusion, in addition to older age, CV risk factors may predict a reduced response to PAH drug therapy in patients with PAH.
Published: 2014
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40. Can my patient with CVD travel to high altitude?

Author: Hoigné, Philipp and Gibbs, J Simon R
Abstract: Patients with borderline health should consult a physican before travelling to altitude. The physician will need to know the duration of the trip, ascent profile and how much exercise the patient plans to undertake. The presence of comorbid diseases which reduce oxygenation and ventilation should also be taken into account. Every patient must be assessed on an individual basis, there are no clinical investigations which reliably predict outcome at altitude. Complex cases may require advice from the patient's cardiologist. Travelling from sea level to an altitude of 2,500 m causes a 20% reduction in the partial pressure of inspired oxygen. There is an initial net increase in myocardial oxygen consumption during the first 3-5 days, this then falls as cardiac output on exercise is reduced. During this time patients with angina pectoris may become symptomatic at a lower level of exercise than at sea level and should be advised to reduce their activity. After five days at 2,500 m, the exertion threshold returns to sea level values. Patients should not travel to high altitude immediately after an acute coronary syndrome. Most patients with stable coronary artery disease with a sufficiently high exercise capacity at sea level can go as high as 3,000-3,500 m with only a minimally increased risk. Patients with heart failure have a greater reduction in exercise performance than healthy people at altitude. Patients with mild to moderately impaired systolic LVF and mild symptoms may travel up to 3,000-3,500 m for a day trip. Patients with poorly controlled hypertension should not travel to high altitude. Those with controlled hypertension should consider taking their own blood pressure during a stay at altitude. [ABSTRACT FROM AUTHOR]
Published: 2013

41. Can my patient with CVD travel to high altitude?

Author: Hoigné, Philipp and Gibbs, J. Simon R.
Subjects: PATIENTS, CARDIOVASCULAR diseases, PHYSICIANS, PHYSIOLOGY, TRAVEL, HYPOXEMIA
Abstract: The article focuses on high altitude travel for people with cardiovascular disease (CVD). The severity of a patient's underlying cardiovascular disease will be the basis of his/her tolerance to altitude. The length of time of the trip, the ascent profile, and the effort that the patient plans to undergo are cited as the factors a physician must consider in order to provide appropriate advice. Patients with CVD may reportedly aggravate their condition when experiencing high altitude illnesses.
Published: 2013

42. Diagnosing and managing pulmonary hypertension.

Author: Charalampopoulos, Athanasios, Raphael, Claire, Gin-Sing, Wendy, and Gibbs, J. Simon R.
Subjects: PULMONARY hypertension diagnosis, PULMONARY hypertension treatment, ETIOLOGY of diseases, DRUG side effects, DRUG interactions
Abstract: The article discusses the diagnosis and management of pulmonary hypertension (PH). It describes its underlying causes, the manifestations of the condition and its treatment options. It explains that accurate diagnosis is important since it is a potentially lethal disease but is treatable. It presents tables on the most causes of PH, an updated clinical classification of the disease and the specific therapies for each, as well as the main side effects and interactions of PH medications.
Published: 2012

43. Exome sequencing in an SCA14 family demonstrates its utility in diagnosing heterogeneous diseases.

Author: Sailer A, Scholz SW, Gibbs JR, Tucci A, Johnson JO, Wood NW, Plagnol V, Hummerich H, Ding J, Hernandez D, Hardy J, Federoff HJ, Traynor BJ, Singleton AB, Houlden H, Sailer, Anna, Scholz, Sonja W, Gibbs, J Raphael, Tucci, Arianna, and Johnson, Janel O
Published: 2012
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44. Exome sequencing in an SCA14 family demonstrates its utility in diagnosing heterogeneous diseases.

Author: Sailer, Anna, Scholz, Sonja W., Gibbs, J. Raphael, Tucci, Arianna, Johnson, Janel O., Wood, Nicholas W., Plagnol, Vincent, Hummerich, Holger, Ding, Jinhui, Hernandez, Dena, Hardy, John, Federoff, Howard J., Traynor, Bryan J., Singleton, Andrew B., and Houlden, Henry
Published: 2012
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45. Documenting Persistence of Most Eastern North American Bee Species (Hymenoptera: Apoidea: Anthophila) to 1990-2009.

Author: Colla, S. R., Ascher, J. S., Arduser, M., Cane, J., Devrup, M., Droege, S., Gibbs, J., Griswold, T., Hall, H. G., Henne, C., Neff, J., Jean, R. P., Rightmyer, M. G., Sheffield, C., Veit, M., and Wolf, A.
Subjects: BEES, CLASSIFICATION of insects, SPECIES distribution, STATISTICAL sampling
Abstract: The article discusses a study on the persistence of all bee species known historically from eastern North America by bringing together scientific expertise and data from bee collections which resulted in a list of species that have and have not been detected in the past two decades. A list of bees happening east of the Mississippi River in the U.S. and east of Manitoba in Canada was extracted from Discover Life Bee Species Guide and World Checklist made up of 770 species. The list of undetected species are largely made of bees that were uncommon before 1990 which are hard to identify, have parasitic life styles and limited distributions. The results emphasize the need for additional taxonomic and life history studies of many groups as well as the need to use diverse sampling methods.
Published: 2012
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46. Recurrence risk of epilepsy and mental retardation in females due to parental mosaicism of PCDH19 mutations.

Author: Dibbens LM, Kneen R, Bayly MA, Heron SE, Arsov T, Damiano JA, Desai T, Gibbs J, McKenzie F, Mulley JC, Ronan A, and Scheffer IE
Published: 2011
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47. Perchlorate and Nitrate in Leafy Vegetables of North America.

Author: Sanchez, C. A., K. S. Crump, Krieger, R. I., Khandaker, N. R., and Gibbs, J. P.
Published: 2005
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48. Association of a common genetic variant with Parkinson’s disease is mediated by microglia

Author: Langston, Rebekah G., Beilina, Alexandra, Reed, Xylena, Kaganovich, Alice, Singleton, Andrew B., Blauwendraat, Cornelis, Gibbs, J. Raphael, and Cookson, Mark R.
Abstract: Studies of multiple neurodegenerative disorders have identified many genetic variants that are associated with risk of disease throughout a lifetime. For example, Parkinson’s disease (PD) risk is attributed in part to both coding mutations in the leucine-rich repeat kinase 2 (LRRK2) gene and to a common noncoding variation in the 5′ region of the LRRK2locus, as identified by genome-wide association studies (GWAS). However, the mechanisms linking GWAS variants to pathogenicity are largely unknown. Here, we found that the influence of PD-associated noncoding variation on LRRK2expression is specifically propagated through microglia and not by other cell types that express LRRK2in the human brain. We find microglia-specific regulatory chromatin regions that modulate the LRRK2expression in human frontal cortex and substantia nigra and confirm these results in a human-induced pluripotent stem cell–derived microglia model. We showed, using a large-scale clustered regularly interspaced short palindromic repeats interference (CRISPRi) screen, that a regulatory DNA element containing the single-nucleotide variant rs6581593 influences the LRRK2expression in microglia. Our study demonstrates that cell type should be considered when evaluating the role of noncoding variation in disease pathogenesis and sheds light on the mechanism underlying the association of the 5′ region of LRRK2 with PD risk.
Published: 2022
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49. Medical Laser Safety Hazard Evaluation.

Author: Edwards, Ben E., Barnes, L. K., Gibbs, J. B., and Nguyen, G. B.
Abstract: Health care laser systems offer general laser hazards and additional specific concerns unique to the clinical environment. A formal laser hazard evaluation procedure provides an efficient mechanism for identifying potential laser safety hazards. This paper outlines such a medical laser hazard evaluation program and highlights the unique characteristics of medical lasers. [ABSTRACT FROM AUTHOR]
Published: 2002
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50. HISPANIC STUDIES: LITERATURE, 1490-1700

Author: GIBBS, J., GIBBS, J., and GIBBS, J.
Published: 1957
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