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7. Thresholds for adding degraded tropical forest to the conservation estate

Author

Ewers, Robert M., Orme, C. David L., Pearse, William D., Zulkifli, Nursyamin, Yvon-Durocher, Genevieve, Yusah, Kalsum M., Yoh, Natalie, Yeo, Darren C. J., Wong, Anna, Williamson, Joseph, Wilkinson, Clare L., Wiederkehr, Fabienne, Webber, Bruce L., Wearn, Oliver R., Wai, Leona, Vollans, Maisie, Twining, Joshua P., Turner, Edgar C., Tobias, Joseph A., Thorley, Jack, Telford, Elizabeth M., Teh, Yit Arn, Tan, Heok Hui, Swinfield, Tom, Svátek, Martin, Struebig, Matthew, Stork, Nigel, Sleutel, Jani, Slade, Eleanor M., Sharp, Adam, Shabrani, Adi, Sethi, Sarab S., Seaman, Dave J. I., Sawang, Anati, Roxby, Gabrielle Briana, Rowcliffe, J. Marcus, Rossiter, Stephen J., Riutta, Terhi, Rahman, Homathevi, Qie, Lan, Psomas, Elizabeth, Prairie, Aaron, Poznansky, Frederica, Pillay, Rajeev, Picinali, Lorenzo, Pianzin, Annabel, Pfeifer, Marion, Parrett, Jonathan M., Noble, Ciar D., Nilus, Reuben, Mustaffa, Nazirah, Mullin, Katherine E., Mitchell, Simon, Mckinlay, Amelia R., Maunsell, Sarah, Matula, Radim, Massam, Michael, Martin, Stephanie, Malhi, Yadvinder, Majalap, Noreen, Maclean, Catherine S., Mackintosh, Emma, Luke, Sarah H., Lewis, Owen T., Layfield, Harry J., Lane-Shaw, Isolde, Kueh, Boon Hee, Kratina, Pavel, Konopik, Oliver, Kitching, Roger, Kinneen, Lois, Kemp, Victoria A., Jotan, Palasiah, Jones, Nick, Jebrail, Evyen W., Hroneš, Michal, Heon, Sui Peng, Hemprich-Bennett, David R., Haysom, Jessica K., Harianja, Martina F., Hardwick, Jane, Gregory, Nichar, Gray, Ryan, Gray, Ross E. J., Granville, Natasha, Gill, Richard, Fraser, Adam, Foster, William A., Folkard-Tapp, Hollie, Fletcher, Robert J., Fikri, Arman Hadi, Fayle, Tom M., Faruk, Aisyah, Eggleton, Paul, Edwards, David P., Drinkwater, Rosie, Dow, Rory A., Döbert, Timm F., Didham, Raphael K., Dickinson, Katharine J. M., Deere, Nicolas J., de Lorm, Tijmen, Dawood, Mahadimenakbar M., Davison, Charles W., Davies, Zoe G., Davies, Richard G., Dančák, Martin, Cusack, Jeremy, Clare, Elizabeth L., Chung, Arthur, Chey, Vun Khen, Chapman, Philip M., Cator, Lauren, Carpenter, Daniel, Carbone, Chris, Calloway, Kerry, Bush, Emma R., Burslem, David F. R. P., Brown, Keiron D., Brooks, Stephen J., Brasington, Ella, Brant, Hayley, Boyle, Michael J. W., Both, Sabine, Blackman, Joshua, Bishop, Tom R., Bicknell, Jake E., Bernard, Henry, Basrur, Saloni, Barclay, Maxwell V. L., Barclay, Holly, Atton, Georgina, Ancrenaz, Marc, Aldridge, David C., Daniel, Olivia Z., Reynolds, Glen, and Banks-Leite, Cristina

Published
2024
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11. Regional impacts of warming on biodiversity and biomass in high latitude stream ecosystems across the Northern Hemisphere

Author

Jackson, Michelle C., Friberg, Nikolai, Moliner Cachazo, Luis, Clark, David R., Mutinova, Petra Thea, O’Gorman, Eoin J., Kordas, Rebecca L., Gallo, Bruno, Pichler, Doris E., Bespalaya, Yulia, Aksenova, Olga V., Milner, Alexander, Brooks, Stephen J., Dunn, Nicholas, Lee, K.W.K., Ólafsson, Jón S., Gíslason, Gísli M., Millan, Lucia, Bell, Thomas, Dumbrell, Alex J., and Woodward, Guy

Published
2024
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13. Correspondence: Striking the Balance

Author

Art, Robert J, Brooks, Stephen G., Wohlforth, William Curti, Lieber, Keir A. (Keir Alexander), and Alexander, Gerard

Published
2006

18. Spleen tyrosine kinase inhibition restores myeloid homeostasis in COVID-19

Author

Wigerblad, Gustaf, Warner, Seth A, Ramos-Benitez, Marcos J, Kardava, Lela, Tian, Xin, Miao, Rui, Reger, Robert, Chakraborty, Mala, Wong, Susan, Kanthi, Yogendra, Suffredini, Anthony F, Dell’Orso, Stefania, Brooks, Stephen, King, Christopher, Shlobin, Oksana, Nathan, Steven D, Cohen, Jonathan, Moir, Susan, Childs, Richard W, Kaplan, Mariana J, Chertow, Daniel S, and Strich, Jeffrey R

Subjects
Biomedical and Clinical Sciences, Immunology, Clinical Research, Clinical Trials and Supportive Activities, Prevention, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Humans, Syk Kinase, COVID-19, Oxazines, HLA-DR Antigens, Homeostasis
Abstract

Spleen tyrosine kinase (SYK) is a previously unidentified therapeutic target that inhibits neutrophil and macrophage activation in coronavirus disease 2019 (COVID-19). Fostamatinib, a SYK inhibitor, was studied in a phase 2 placebo-controlled randomized clinical trial and was associated with improvements in many secondary end points related to efficacy. Here, we used a multiomic approach to evaluate cellular and soluble immune mediator responses of patients enrolled in this trial. We demonstrated that SYK inhibition was associated with reduced neutrophil activation, increased circulation of mature neutrophils (CD10+CD33-), and decreased circulation of low-density granulocytes and polymorphonuclear myeloid-derived suppressor cells (HLA-DR-CD33+CD11b-). SYK inhibition was also associated with normalization of transcriptional activity in circulating monocytes relative to healthy controls, an increase in frequency of circulating nonclassical and HLA-DRhi classical monocyte populations, and restoration of interferon responses. Together, these data suggest that SYK inhibition may mitigate proinflammatory myeloid cellular and soluble mediator responses thought to contribute to immunopathogenesis of severe COVID-19.

Published
2023

23. Constitutively active Lyn kinase causes a cutaneous small vessel vasculitis and liver fibrosis syndrome

Author

de Jesus, Adriana A., Chen, Guibin, Yang, Dan, Brdicka, Tomas, Ruth, Natasha M., Bennin, David, Cebecauerova, Dita, Malcova, Hana, Freeman, Helen, Martin, Neil, Svojgr, Karel, Passo, Murray H., Bhuyan, Farzana, Alehashemi, Sara, Rastegar, Andre T., Uss, Katsiaryna, Kardava, Lela, Marrero, Bernadette, Duric, Iris, Omoyinmi, Ebun, Peldova, Petra, Lee, Chyi-Chia Richard, Kleiner, David E., Hadigan, Colleen M., Hewitt, Stephen M., Pittaluga, Stefania, Carmona-Rivera, Carmelo, Calvo, Katherine R., Shah, Nirali, Balascakova, Miroslava, Fink, Danielle L., Kotalova, Radana, Parackova, Zuzana, Peterkova, Lucie, Kuzilkova, Daniela, Campr, Vit, Sramkova, Lucie, Biancotto, Angelique, Brooks, Stephen R., Manes, Cameron, Meffre, Eric, Harper, Rebecca L., Kuehn, Hyesun, Kaplan, Mariana J., Brogan, Paul, Rosenzweig, Sergio D., Merchant, Melinda, Deng, Zuoming, Huttenlocher, Anna, Moir, Susan L., Kuhns, Douglas B., Boehm, Manfred, Skvarova Kramarzova, Karolina, and Goldbach-Mansky, Raphaela

Published
2023
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24. Genetically programmed alternative splicing of NEMO mediates an autoinflammatory disease phenotype

Author

Lee, Younglang, Wessel, Alex W, Xu, Jiazhi, Reinke, Julia G, Lee, Eries, Kim, Somin M, Hsu, Amy P, Zilberman-Rudenko, Jevgenia, Cao, Sha, Enos, Clinton, Brooks, Stephen R, Deng, Zuoming, Lin, Bin, de Jesus, Adriana A, Hupalo, Daniel N, Piotto, Daniela GP, Terreri, Maria T, Dimitriades, Victoria R, Dalgard, Clifton L, Holland, Steven M, Goldbach-Mansky, Raphaela, Siegel, Richard M, and Hanson, Eric P

Subjects
Infectious Diseases, Genetics, Pediatric, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Alternative Splicing, Child, Hereditary Autoinflammatory Diseases, Humans, I-kappa B Kinase, Immunologic Deficiency Syndromes, Male, NF-kappa B, Phenotype, Genetic diseases, Immunology, Inflammation, Innate immunity, Signal transduction, Medical and Health Sciences
Abstract

Host defense and inflammation are regulated by the NF-κB essential modulator (NEMO), a scaffolding protein with a broad immune cell and tissue expression profile. Hypomorphic mutations in inhibitor of NF-κB kinase regulatory subunit gamma (IKBKG) encoding NEMO typically present with immunodeficiency. Here, we characterized a pediatric autoinflammatory syndrome in 3 unrelated male patients with distinct X-linked IKBKG germline mutations that led to overexpression of a NEMO protein isoform lacking the domain encoded by exon 5 (NEMO-Δex5). This isoform failed to associate with TANK binding kinase 1 (TBK1), and dermal fibroblasts from affected patients activated NF-κB in response to TNF but not TLR3 or RIG-I-like receptor (RLR) stimulation when isoform levels were high. By contrast, T cells, monocytes, and macrophages that expressed NEMO-Δex5 exhibited increased NF-κB activation and IFN production, and blood cells from these patients expressed a strong IFN and NF-κB transcriptional signature. Immune cells and TNF-stimulated dermal fibroblasts upregulated the inducible IKK protein (IKKi) that was stabilized by NEMO-Δex5, promoting type I IFN induction and antiviral responses. These data revealed how IKBKG mutations that lead to alternative splicing of skipping exon 5 cause a clinical phenotype we have named NEMO deleted exon 5 autoinflammatory syndrome (NDAS), distinct from the immune deficiency syndrome resulting from loss-of-function IKBKG mutations.

Published
2022

25. A CTCF-binding site in the Mdm1-Il22-Ifng locus shapes cytokine expression profiles and plays a critical role in early Th1 cell fate specification

Author

Liu, Chunhong, Nagashima, Hiroyuki, Fernando, Nilisha, Bass, Victor, Gopalakrishnan, Jaanam, Signorella, Sadie, Montgomery, Will, Lim, Ai Ing, Harrison, Oliver, Reich, Lauren, Yao, Chen, Sun, Hong-Wei, Brooks, Stephen R., Jiang, Kan, Nagarajan, Vijayaraj, Zhao, Yongbing, Jung, Seolkyoung, Phillips, Rachael, Mikami, Yohei, Lareau, Caleb A., Kanno, Yuka, Jankovic, Dragana, Aryee, Martin J., Pękowska, Aleksandra, Belkaid, Yasmine, O’Shea, John, and Shih, Han-Yu

Published
2024
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28. Concentrations and predictors of select nutrients in Canadian human milk samples from the Maternal-Infant Research on Environmental Chemicals pregnancy cohort

Author

Hopperton, Kathryn E, O’Neill, Erica, Chakrabarti, Subhadeep, Stanton, Melanie, Parnel, Sophie, Arbuckle, Tye E, Ashley-Martin, Jillian, Bertinato, Jesse, Bouchard, Maryse F, Borghese, Michael M, Brooks, Stephen, Cockell, Kevin, Dabeka, Robert, Joung, Meong Jin, Lanphear, Bruce P, Lapointe, Pascal, MacFarlane, Amanda J, MacPherson, Susan, Krzeczkowski, John, Rawn, Dorothea F K, von Dadelszen, Peter, Weiler, Hope A, Xiao, Chao Wu, and Fisher, Mandy

Published
2024
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31. Distinct interferon signatures and cytokine patterns define additional systemic autoinflammatory diseases

Author

de Jesus, Adriana A, Hou, Yangfeng, Brooks, Stephen, Malle, Louise, Biancotto, Angelique, Huang, Yan, Calvo, Katherine R, Marrero, Bernadette, Moir, Susan, Oler, Andrew J, Deng, Zuoming, Montealegre Sanchez, Gina A, Ahmed, Amina, Allenspach, Eric, Arabshahi, Bita, Behrens, Edward, Benseler, Susanne, Bezrodnik, Liliana, Bout-Tabaku, Sharon, Brescia, AnneMarie C, Brown, Diane, Burnham, Jon M, Caldirola, Maria Soledad, Carrasco, Ruy, Chan, Alice Y, Cimaz, Rolando, Dancey, Paul, Dare, Jason, DeGuzman, Marietta, Dimitriades, Victoria, Ferguson, Ian, Ferguson, Polly, Finn, Laura, Gattorno, Marco, Grom, Alexei A, Hanson, Eric P, Hashkes, Philip J, Hedrich, Christian M, Herzog, Ronit, Horneff, Gerd, Jerath, Rita, Kessler, Elizabeth, Kim, Hanna, Kingsbury, Daniel J, Laxer, Ronald M, Lee, Pui Y, Lee-Kirsch, Min Ae, Lewandowski, Laura, Li, Suzanne, Lilleby, Vibke, Mammadova, Vafa, Moorthy, Lakshmi N, Nasrullayeva, Gulnara, O'Neil, Kathleen M, Onel, Karen, Ozen, Seza, Pan, Nancy, Pillet, Pascal, Piotto, Daniela Gp, Punaro, Marilynn G, Reiff, Andreas, Reinhardt, Adam, Rider, Lisa G, Rivas-Chacon, Rafael, Ronis, Tova, Rösen-Wolff, Angela, Roth, Johannes, Ruth, Natasha Mckerran, Rygg, Marite, Schmeling, Heinrike, Schulert, Grant, Scott, Christiaan, Seminario, Gisella, Shulman, Andrew, Sivaraman, Vidya, Son, Mary Beth, Stepanovskiy, Yuriy, Stringer, Elizabeth, Taber, Sara, Terreri, Maria Teresa, Tifft, Cynthia, Torgerson, Troy, Tosi, Laura, Van Royen-Kerkhof, Annet, Wampler Muskardin, Theresa, Canna, Scott W, and Goldbach-Mansky, Raphaela

Subjects
Genetics, Clinical Research, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Autoimmune Diseases, Female, Humans, Interferon Type I, Interleukin-18, Macrophage Activation Syndrome, Male, Mutation, Panniculitis, Pulmonary Alveolar Proteinosis, Genetic diseases, Immunology, Inflammation, Innate immunity, Monogenic diseases, Medical and Health Sciences
Abstract

BACKGROUNDUndifferentiated systemic autoinflammatory diseases (USAIDs) present diagnostic and therapeutic challenges. Chronic interferon (IFN) signaling and cytokine dysregulation may identify diseases with available targeted treatments.METHODSSixty-six consecutively referred USAID patients underwent underwent screening for the presence of an interferon signature using a standardized type-I IFN-response-gene score (IRG-S), cytokine profiling, and genetic evaluation by next-generation sequencing.RESULTSThirty-six USAID patients (55%) had elevated IRG-S. Neutrophilic panniculitis (40% vs. 0%), basal ganglia calcifications (46% vs. 0%), interstitial lung disease (47% vs. 5%), and myositis (60% vs. 10%) were more prevalent in patients with elevated IRG-S. Moderate IRG-S elevation and highly elevated serum IL-18 distinguished 8 patients with pulmonary alveolar proteinosis (PAP) and recurrent macrophage activation syndrome (MAS). Among patients with panniculitis and progressive cytopenias, 2 patients were compound heterozygous for potentially novel LRBA mutations, 4 patients harbored potentially novel splice variants in IKBKG (which encodes NF-κB essential modulator [NEMO]), and 6 patients had de novo frameshift mutations in SAMD9L. Of additional 12 patients with elevated IRG-S and CANDLE-, SAVI- or Aicardi-Goutières syndrome-like (AGS-like) phenotypes, 5 patients carried mutations in either SAMHD1, TREX1, PSMB8, or PSMG2. Two patients had anti-MDA5 autoantibody-positive juvenile dermatomyositis, and 7 could not be classified. Patients with LRBA, IKBKG, and SAMD9L mutations showed a pattern of IRG elevation that suggests prominent NF-κB activation different from the canonical interferonopathies CANDLE, SAVI, and AGS.CONCLUSIONSIn patients with elevated IRG-S, we identified characteristic clinical features and 3 additional autoinflammatory diseases: IL-18-mediated PAP and recurrent MAS (IL-18PAP-MAS), NEMO deleted exon 5-autoinflammatory syndrome (NEMO-NDAS), and SAMD9L-associated autoinflammatory disease (SAMD9L-SAAD). The IRG-S expands the diagnostic armamentarium in evaluating USAIDs and points to different pathways regulating IRG expression.TRIAL REGISTRATIONClinicalTrials.gov NCT02974595.FUNDINGThe Intramural Research Program of the NIH, NIAID, NIAMS, and the Clinical Center.

Published
2020

32. Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C

Author

Pal-Ghosh, Sonali, Karpinski, Beverly A., Datta Majumdar, Himani, Ghosh, Trisha, Thomasian, Julie, Brooks, Stephen R., Sawaya, Andrew P., Morasso, Maria I., Scholand, Kaitlin K., de Paiva, Cintia S., Galletti, Jeremias G., and Stepp, Mary Ann

Published
2023
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33. SOX2 Epidermal Overexpression Promotes Cutaneous Wound Healing via Activation of EGFR/MEK/ERK Signaling Mediated by EGFR Ligands.

Author

Uchiyama, Akihiko, Nayak, Subhashree, Graf, Rose, Cross, Michael, Hasneen, Kowser, Gutkind, J, Brooks, Stephen, and Morasso, Maria

Subjects
Animals, Cell Proliferation, Cells, Cultured, ErbB Receptors, Female, Heparin-binding EGF-like Growth Factor, Keratinocytes, Ligands, MAP Kinase Signaling System, Male, Mice, Models, Animal, Primary Cell Culture, RNA-Seq, SOXB1 Transcription Factors, Signal Transduction, Skin, Up-Regulation, Wound Healing
Abstract

Oral mucosa contains a unique transcriptional network that primes oral wounds for rapid resolution in humans. Our previous work identified genes that were consistently upregulated in the oral mucosa and demonstrated that induction of one of the identified genes, transcription factor SOX2, promoted cutaneous wound healing in mice. In this study, we investigated the molecular and cellular mechanisms by which SOX2 accelerates wound healing in skin. RNA-sequencing analysis showed that SOX2 induced a proliferative and wound-activated phenotype in skin keratinocytes prior to wounding. During wound healing, SOX2 induced proliferation of epithelial and connective tissue cells and promoted angiogenesis. Chromatin immunoprecipitation assay revealed that SOX2 directly regulates expression of EGFR ligands, resulting in activation of EGFR. In vitro, skin keratinocytes overexpressing SOX2 promoted cell migration via the EGFR/MEK/ERK pathway. We conclude that induction of SOX2 in skin keratinocytes accelerates cutaneous wound healing by promoting keratinocyte migration and proliferation, and enhancement of angiogenesis via upregulation of EGFR ligands and activation of EGFR/MEK/ERK pathway. Through the identification of putative cutaneous SOX2 targets, such as HBEGF, this study opens venues to determine clinical targets for treatment of skin wounds.

Published
2019

34. Perspective: Human Milk Composition and Related Data for National Health and Nutrition Monitoring and Related Research

Author

Ahuja, Jaspreet K C, Casavale, Kellie O, Li, Ying, Hopperton, Kathryn E, Chakrabarti, Subhadeep, Hines, Erin P, Brooks, Stephen P J, Bondy, Genevieve S, MacFarlane, Amanda J, Weiler, Hope A, Wu, Xianli, Borghese, Michael M, Ahluwalia, Namanjeet, Cheung, Winnie, Vargas, Ashley J, Arteaga, Sonia, Lombo, Tania, Fisher, Mandy M, Hayward, Deborah, and Pehrsson, Pamela R

Published
2022
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36. Warming reduces trophic diversity in high‐latitude food webs.

Author

Jackson, Michelle C., O'Gorman, Eoin J., Gallo, Bruno, Harpenslager, Sarah F., Randall, Kate, Harris, Danielle N., Prentice, Hannah, Trimmer, Mark, Sanders, Ian, Dumbrell, Alex J., Cameron, Tom C., Layer‐Dobra, Katrin, Bespalaya, Yulia, Aksenova, Olga, Friberg, Nikolai, Moliner Cachazo, Luis, Brooks, Stephen J., and Woodward, Guy

Subjects
GLOBAL warming, FOOD chains, INVERTEBRATE communities, ARCTIC climate, FRESHWATER invertebrates
Abstract

The physical effects of climate warming have been well documented, but the biological responses are far less well known, especially at the ecosystem level and at large (intercontinental) scales. Global warming over the next century is generally predicted to reduce food web complexity, but this is rarely tested empirically due to the dearth of studies isolating the effects of temperature on complex natural food webs. To overcome this obstacle, we used 'natural experiments' across 14 streams in Iceland and Russia, with natural warming of up to 20°C above the coldest stream in each high‐latitude region, where anthropogenic warming is predicted to be especially rapid. Using biomass‐weighted stable isotope data, we found that community isotopic divergence (a universal, taxon‐free measure of trophic diversity) was consistently lower in warmer streams. We also found a clear shift towards greater assimilation of autochthonous carbon, which was driven by increasing dominance of herbivores but without a concomitant increase in algal stocks. Overall, our results support the prediction that higher temperatures will simplify high‐latitude freshwater ecosystems and provide the first mechanistic glimpses of how warming alters energy transfer through food webs at intercontinental scales. [ABSTRACT FROM AUTHOR]

Published
2024
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38. A Multiomic Analysis to Identify Drivers of Subclinical Vascular Disease in Systemic Lupus Erythematosus.

Author

Oliveira, Christopher, Temesgen‐Oyelakin, Yenealem, Naqi, Mohammad, Davis, Michael, Naz, Faiza, Dell'Orso, Stefania, Brooks, Stephen, Kuhn, Skyler, Hill, Tom, Li, Xiaobai, Patel, Nidhi, Parel, Philip, Gadina, Massimo, Gupta, Sarthak, Mehta, Nehal, Hasni, Sarfaraz A., and Kaplan, Mariana J.

Subjects
RISK assessment, PROTEINS, RESEARCH funding, RADIOPHARMACEUTICALS, MULTIOMICS, DEOXY sugars, SYSTEMIC lupus erythematosus, DESCRIPTIVE statistics, CARDIOVASCULAR disease diagnosis, PROTEOMICS, EMISSION-computed tomography, VASCULAR diseases, DISEASE progression, BIOMARKERS, SEQUENCE analysis, INTERLEUKINS, TUMOR necrosis factors, EVALUATION, DISEASE risk factors
Abstract

Objective: Systemic lupus erythematosus (SLE) increases cardiovascular disease (CVD) risk, and this is not explained by traditional risk factors. Characterization of blood immunologic signatures that associate with subclinical CVD and predict its progression has been challenging and may help identify subgroups at risk. Methods: Patients with SLE (n = 77) and healthy controls (HCs) (n = 27) underwent assessments of arterial stiffness, vascular wall inflammation, and coronary atherosclerosis burden with cardio‐ankle vascular index (CAVI); fluorodeoxyglucose–positron emission tomography/computed tomography (CT) (target‐to‐background ratio [TBR]); and coronary CT angiography. Whole blood bulk RNA sequencing was performed in a subset of study participants (HC n = 10, SLE n = 20). In a partially overlapping subset (HC n = 24, SLE n = 64), serum inflammatory protein biomarkers were quantified with an Olink platform. Results: CAVI, TBR, and noncalcified coronary plaque burden (NCB) were increased in patients with SLE compared to HCs. When comparing patients with SLE with high CAVI scores to those with low CAVI scores or to HCs, there was a down‐regulation of genes in pathways involved in the cell cycle and differentially regulated pathways related to metabolism. Distinct serum proteins associated with increased CAVI (CCL23, colony‐stimulating factor 1, latency‐activating peptide transforming growth factor β1, interleukin 33 [IL‐33], CD8A, and IL‐12B), NCB (monocyte chemotactic protein 4 and FMS‐like tyrosine kinase 3 ligand [Flt3L]), and TBR (CD5, IL‐1α, AXIN1, cystatin D [CST5], and tumor necrosis factor receptor superfamily 9; P < 0.05). Conclusion: Blood gene expression patterns and serum proteins that associate with worse vascular phenotypes suggest dysregulated immune and metabolic pathways linked to premature CVD. Cytokines and chemokines identified in associations with arterial stiffness, inflammation, and NCB in SLE may allow for characterization of new CVD biomarkers in lupus. [ABSTRACT FROM AUTHOR]

Published
2024
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39. Transcriptional signature primes human oral mucosa for rapid wound healing

Author

Iglesias-Bartolome, Ramiro, Uchiyama, Akihiko, Molinolo, Alfredo A, Abusleme, Loreto, Brooks, Stephen R, Callejas-Valera, Juan Luis, Edwards, Dean, Doci, Colleen, Asselin-Labat, Marie-Liesse, Onaitis, Mark W, Moutsopoulos, Niki M, Gutkind, J Silvio, and Morasso, Maria I

Subjects
Genetics, Dental/Oral and Craniofacial Disease, 1.1 Normal biological development and functioning, Aetiology, 2.1 Biological and endogenous factors, Underpinning research, Skin, Biopsy, Humans, Keratinocytes, Mouth Mucosa, Transcription Factors, Wound Healing, Biological Sciences, Medical and Health Sciences
Abstract

Oral mucosal wound healing has long been regarded as an ideal system of wound resolution. However, the intrinsic characteristics that mediate optimal healing at mucosal surfaces are poorly understood, particularly in humans. We present a unique comparative analysis between human oral and cutaneous wound healing using paired and sequential biopsies during the repair process. Using molecular profiling, we determined that wound-activated transcriptional networks are present at basal state in the oral mucosa, priming the epithelium for wound repair. We show that oral mucosal wound-related networks control epithelial cell differentiation and regulate inflammatory responses, highlighting fundamental global mechanisms of repair and inflammatory responses in humans. The paired comparative analysis allowed for the identification of differentially expressed SOX2 (sex-determining region Y-box 2) and PITX1 (paired-like homeodomain 1) transcriptional regulators in oral versus skin keratinocytes, conferring a unique identity to oral keratinocytes. We show that SOX2 and PITX1 transcriptional function has the potential to reprogram skin keratinocytes to increase cell migration and improve wound resolution in vivo. Our data provide insights into therapeutic targeting of chronic and nonhealing wounds based on greater understanding of the biology of healing in human mucosal and cutaneous environments.

Published
2018

47. Forest-linked livelihoods in a globalized world

Author

Oldekop, Johan A., Rasmussen, Laura Vang, Agrawal, Arun, Bebbington, Anthony J., Meyfroidt, Patrick, Bengston, David N., Blackman, Allen, Brooks, Stephen, Davidson-Hunt, Iain, Davies, Penny, Dinsi, Stanley C., Fontana, Lorenza B., Gumucio, Tatiana, Kumar, Chetan, Kumar, Kundan, Moran, Dominic, Mwampamba, Tuyeni H., Nasi, Robert, Nilsson, Margareta, Pinedo-Vasquez, Miguel A., Rhemtulla, Jeanine M., Sutherland, William J., Watkins, Cristy, and Wilson, Sarah J.

Published
2020
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50. Phase 1 double-blind randomized safety trial of the Janus kinase inhibitor tofacitinib in systemic lupus erythematosus

Author

Hasni, Sarfaraz A., Gupta, Sarthak, Davis, Michael, Poncio, Elaine, Temesgen-Oyelakin, Yenealem, Carlucci, Philip M., Wang, Xinghao, Naqi, Mohammad, Playford, Martin P., Goel, Rishi R., Li, Xiaobai, Biehl, Ann J., Ochoa-Navas, Isabel, Manna, Zerai, Shi, Yinghui, Thomas, Donald, Chen, Jinguo, Biancotto, Angélique, Apps, Richard, Cheung, Foo, Kotliarov, Yuri, Babyak, Ashley L., Zhou, Huizhi, Shi, Rongye, Stagliano, Katie, Tsai, Wanxia Li, Vian, Laura, Gazaniga, Nathalia, Giudice, Valentina, Lu, Shajia, Brooks, Stephen R., MacKay, Meggan, Gregersen, Peter, Mehta, Nehal N., Remaley, Alan T., Diamond, Betty, O’Shea, John J., Gadina, Massimo, and Kaplan, Mariana J.

Published
2021
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