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32,559 results on '"Dávid S"'

1. Climate, food and humans predict communities of mammals in the United States

Author

Kays, Roland, Snider, Matthew H., Hess, George, Cove, Michael V., Jensen, Alex, Shamon, Hila, McShea, William J., Rooney, Brigit, Allen, Maximilian L., Pekins, Charles E., Wilmers, Christopher C., Pendergast, Mary E., Green, Austin M., Suraci, Justin, Leslie, Matthew S., Nasrallah, Sophie, Farkas, Dan, Jordan, Mark, Grigione, Melissa, LaScaleia, Michael C., Davis, Miranda L., Hansen, Chris, Millspaugh, Josh, Lewis, Jesse S., Havrda, Michael, Long, Robert, Remine, Kathryn R., Jaspers, Kodi J., Lafferty, Diana J. R., Hubbard, Tru, Studds, Colin E., Barthelmess, Erika L., Andy, Katherine, Romero, Andrea, O'Neill, Brian J., Hawkins, Melissa T. R., Lombardi, Jason V., Sergeyev, Maksim, Fisher-Reid, M. Caitlin, Rentz, Michael S., Nagy, Christopher, Davenport, Jon M., Rega-Brodsky, Christine C., Appel, Cara L., Lesmeister, Damon B., Giery, Sean T., Whittier, Christopher A., Alston, Jesse M., Sutherland, Chris, Rota, Christopher, Murphy, Thomas, Lee, Thomas E., Mortelliti, Alessio, Bergman, Dylan L., Compton, Justin A., Gerber, Brian D., Burr, Jess, Rezendes, Kylie, DeGregorio, Brett A., Wehr, Nathaniel H., Benson, John F., O’Mara, M. Teague, Jachowski, David S., Gray, Morgan, Beyer, Dean E., Belant, Jerrold L., Horan, Robert V., Lonsinger, Robert C., Kuhn, Kellie M., Hasstedt, Steven C. M., Zimova, Marketa, Moore, Sophie M., Herrera, Daniel J., Fritts, Sarah, Edelman, Andrew J., Flaherty, Elizabeth A., Petroelje, Tyler R., Neiswenter, Sean A., Risch, Derek R., Iannarilli, Fabiola, van der Merwe, Marius, Maher, Sean P., Farris, Zach J., Webb, Stephen L., Mason, David S., Lashley, Marcus A., Wilson, Andrew M., Vanek, John P., Wehr, Samuel R., Conner, L. Mike, Beasley, James C., Bontrager, Helen L., Baruzzi, Carolina, Ellis-Felege, Susan N., Proctor, Mike D., Schipper, Jan, Weiss, Katherine C. B., Darracq, Andrea K., Barr, Evan G., Alexander, Peter D., Şekercioğlu, Çağan H., Bogan, Daniel A., Schalk, Christopher M., Fantle-Lepczyk, Jean E., Lepczyk, Christopher A., LaPoint, Scott, Whipple, Laura S., Rowe, Helen Ivy, Mullen, Kayleigh, Bird, Tori, Zorn, Adam, Brandt, LaRoy, Lathrop, Richard G., McCain, Craig, Crupi, Anthony P., Clark, James, and Parsons, Arielle

Published
2024

2. Fluorescence-Based Real-Time Analysis of Osteoclast Development

Author

Áron Pánczél, Simon P. Nagy, János Farkas, Zoltán Jakus, Dávid S. Győri, and Attila Mócsai

Subjects
osteoclasts, cell fusion, fluorescence microscopy, Cre recombinase, myeloid cell differentiation, fluorescent Cre-reporter, Biology (General), QH301-705.5
Abstract

Osteoclasts are multinucleated cells of hematopoietic origin which are critically involved in physiological and pathological bone resorption. They develop from myeloid progenitors through characteristic gene expression changes and intercellular fusion. This process is directed by M-CSF and RANKL which are also able to trigger osteoclast development from bone marrow cells in vitro. Osteoclasts are conventionally visualized by histochemical staining followed by manual counting, which hinders kinetic studies and automated quantification. Here we describe two fluorescence-based assays for the real-time analysis of myeloid cell to osteoclast development (FRAMCO) in primary mouse bone marrow cell cultures. Both assays rely on red-to-green fluorescence conversion of the membrane-targeted tdTomato/membrane-targeted eGFP (mTmG) transgene by Cre recombinase driven by the osteoclast-specific cathepsin K promoter (Ctsk-Cre). In the first assay (FRAMCO1.1), osteoclast-specific gene expression triggers red-to-green color conversion of cells carrying both the Ctsk-Cre and mTmG transgenes. In the second assay (FRAMCO1.2), red-to-green fluorescence conversion is triggered by fusion of neighboring co-cultured bone marrow cells separately carrying either the Ctsk-Cre or the mTmG transgenes. The two assays were tested using a high-content confocal fluorescence imaging system, followed by automated quantification. The FRAMCO1.1 assay showed robust red-to-green fluorescence conversion of more than 50% of the culture (including mononuclear cells) within 3 days under osteoclastogenic conditions. The FRAMCO1.2 assay showed a less robust but still readily measurable red-to-green color conversion in multinuclear cells within 5 days of differentiation. The assays required both the Ctsk-Cre and the mTmG transgenes and gave no signals in parallel macrophage cultures. The proper functioning of the two assays was also confirmed at the DNA, mRNA and bulk protein level. The assay systems were validated using lisophosphatidylcholine, a previously reported inhibitor of preosteoclast fusion. Taken together, our assays allow high-throughput automated real-time analysis of two critical aspects of osteoclast development, facilitating the screening for novel drug candidates for the pharmacological control of osteoclast-mediated bone resorption.

Published
2021
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3. Osteoclast Signal Transduction During Bone Metastasis Formation

Author

Dávid S. Győri and Attila Mócsai

Subjects
osteoclast (OC), signaling/signaling pathways, tumor, bone metastases (BM), osteolysis, Biology (General), QH301-705.5
Abstract

Osteoclasts are myeloid lineage-derived bone-resorbing cells of hematopoietic origin. They differentiate from myeloid precursors through a complex regulation process where the differentiation of preosteoclasts is followed by intercellular fusion to generate large multinucleated cells. Under physiological conditions, osteoclastogenesis is primarily directed by interactions between CSF-1R and macrophage colony-stimulating factor (M-CSF, CSF-1), receptor activator of nuclear factor NF-κB (RANK) and RANK ligand (RANKL), as well as adhesion receptors (e.g., integrins) and their ligands. Osteoclasts play a central role in physiological and pathological bone resorption and are also required for excessive bone loss during osteoporosis, inflammatory bone and joint diseases (such as rheumatoid arthritis) and cancer cell-induced osteolysis. Due to the major role of osteoclasts in these diseases the better understanding of their intracellular signaling pathways can lead to the identification of potential novel therapeutic targets. Non-receptor tyrosine kinases and lipid kinases play major roles in osteoclasts and small-molecule kinase inhibitors are emerging new therapeutics in diseases with pathological bone loss. During the last few years, we and others have shown that certain lipid (such as phosphoinositide 3-kinases PI3Kβ and PI3Kδ) and tyrosine (Src−family and Syk) kinases play a critical role in osteoclast differentiation and function in humans and mice. Some of these signaling pathways shows similarity to immunoreceptor-like receptor signaling and involves important other enzymes (e.g., PLCγ2) and adapter proteins (such as the ITAM−bearing adapters DAP12 and the Fc-receptor γ-chain). Here, we review recently identified osteoclast signaling pathways and their role in osteoclast differentiation and function as well as pathological bone loss associated with osteolytic tumors of the bone. A better understanding of osteoclast signaling may facilitate the design of novel and more efficient therapies for pathological bone resorption and osteolytic skeletal metastasis formation.

Published
2020
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4. Hematopoietic or Osteoclast-Specific Deletion of Syk Leads to Increased Bone Mass in Experimental Mice

Author

Dániel Csete, Edina Simon, Ahmad Alatshan, Petra Aradi, Csaba Dobó-Nagy, Zoltán Jakus, Szilvia Benkő, Dávid S. Győri, and Attila Mócsai

Subjects
SYK (spleen tyrosine kinase), tyrosine kinase, osteoclasts, Cre-Lox, in vivo, mice, Immunologic diseases. Allergy, RC581-607
Abstract

Syk is a non-receptor tyrosine kinase critically involved in signaling by various immunoreceptors including B-cell-receptors and activating Fc-receptors. We have previously shown that Syk also mediates immunoreceptor-like signals required for the in vitro development and function of osteoclasts. However, the perinatal lethality of Syk−/− mice precluded the analysis of the role of Syk in in vivo bone metabolism. To overcome that problem, we generated mice with osteoclast-specific (SykΔOC) or hematopoietic (SykΔHaemo) Syk deficiency by conditional deletion of Syk using Cre recombinase expressed under the control of the Ctsk or Vav1 promoter, respectively. Micro-CT analysis revealed increased bone trabecular density in both SykΔOC and SykΔHaemo mice, although hematopoietic Syk deficiency caused a more severe phenotype than osteoclast-specific Syk deficiency. Osteoclast-specific Syk deficiency reduced, whereas hematopoietic Syk deficiency completely blocked in vitro development of osteoclasts. Both interventions inhibited the resorptive activity of osteoclasts and osteoclast-specific gene expression. Kinetic analysis of Syk protein levels, Cre expression and the genomic deletion of the Sykflox allele revealed complete and early deletion of Syk from SykΔHaemo osteoclasts whereas Syk was incompletely deleted at a later stage of osteoclast development from SykΔOC cultures. Those results provide an explanation for the in vivo and in vitro difference between the SykΔOC and SykΔHaemo mutant strains and suggest late activation of, and incomplete target gene deletion upon, osteoclast-specific Cre expression driven by the Ctsk promoter. Taken together, our results indicate that Syk plays an indispensable role in osteoclast-mediated in vivo bone resorption and suggest that Syk-specific inhibitors may provide therapeutic benefit in inflammatory and other diseases characterized by excessive osteoclast-mediated bone resorption.

Published
2019
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19. Results of a randomized phase II trial of paclitaxel and carboplatin versus bleomycin, etoposide and cisplatin for newly diagnosed and recurrent Chemonaive stromal ovarian tumors: An NRG oncology/gynecologic oncology group study14

Author

Brown, Jubilee, Miller, Austin, Holman, Laura L., Backes, Floor, Nagel, Christa, Bender, David, Miller, David S., Powell, Matthew A., Westin, Shannon N., Bonebrake, Albert, Muller, Carolyn Y., Secord, Angeles Alvarez, Crane, Erin, Schorge, John, Tew, William P., Sood, Anil K., Bookman, Michael A., Aghajanian, Carol, and Gershenson, David M.

Published
2024
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29. SWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis

Author

Yavas, Aslihan, Ozcan, Kerem, Adsay, N. Volkan, Balci, Serdar, Tarcan, Zeynep C., Hechtman, Jaclyn F., Luchini, Claudio, Scarpa, Aldo, Lawlor, Rita T., Mafficini, Andrea, Reid, Michelle D., Xue, Yue, Yang, Zhaohai, Haye, Kester, Bellizzi, Andrew M., Vanoli, Alessandro, Benhamida, Jamal, Balachandran, Vinod, Jarnagin, William, Park, Wungki, O’Reilly, Eileen M., Klimstra, David S., and Basturk, Olca

Published
2024
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40. Association of nirmatrelvir–ritonavir with post-acute sequelae and mortality in patients admitted to hospital with COVID-19: a retrospective cohort study

Author

Wang, Huwen, Wei, Yuchen, Hung, Chi Tim, Lin, Guozhang, Jiang, Xiaoting, Li, Conglu, Jia, Katherine Min, Yam, Carrie Ho Kwan, Chow, Tsz Yu, Ho, Janice Ying-en, Wang, Yawen, Zhao, Shi, Guo, Zihao, Li, Kehang, Yang, Aimin, Mok, Chris Ka Pun, Hui, David S C, Yeoh, Eng Kiong, and Chong, Ka Chun

Published
2024
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