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2. 3:00 PM Abstract No. 141 Interventional radiology patient throughput: application of lean sigma methodology and real-time delay dashboard to improve operations and patient experience

Author

Owens, A., primary, Demmert, A., additional, Abdollahian, D., additional, Werner, J., additional, Dinicola, J., additional, Parduba, W., additional, Denker, S., additional, Dawson, M., additional, Prigel, C., additional, Lara, E., additional, Hester, A., additional, and Hong, K., additional

Published
2018
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5. Image processing and control of a programmable spatial light modulator for spatial beam shaping

Author

Awwal, Abdul A. S., primary, Orth, Charles, additional, Tse, Eddy, additional, Matone, JoAnn, additional, Paul, Mitanu, additional, Hardy, Carla, additional, Brunton, Gordon, additional, Hermann, Mark, additional, Yang, Steve, additional, DiNicola, J. M. M., additional, Rever, Matt, additional, Dixit, Sham, additional, and Heebner, John, additional

Published
2013
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6. Assembly of High-Areal-Density Deuterium-Tritium Fuel from Indirectly Driven Cryogenic Implosions

Author

Mackinnon, A. J., primary, Kline, J. L., additional, Dixit, S. N., additional, Glenzer, S. H., additional, Edwards, M. J., additional, Callahan, D. A., additional, Meezan, N. B., additional, Haan, S. W., additional, Kilkenny, J. D., additional, Döppner, T., additional, Farley, D. R., additional, Moody, J. D., additional, Ralph, J. E., additional, MacGowan, B. J., additional, Landen, O. L., additional, Robey, H. F., additional, Boehly, T. R., additional, Celliers, P. M., additional, Eggert, J. H., additional, Krauter, K., additional, Frieders, G., additional, Ross, G. F., additional, Hicks, D. G., additional, Olson, R. E., additional, Weber, S. V., additional, Spears, B. K., additional, Salmonsen, J. D., additional, Michel, P., additional, Divol, L., additional, Hammel, B., additional, Thomas, C. A., additional, Clark, D. S., additional, Jones, O. S., additional, Springer, P. T., additional, Cerjan, C. J., additional, Collins, G. W., additional, Glebov, V. Y., additional, Knauer, J. P., additional, Sangster, C., additional, Stoeckl, C., additional, McKenty, P., additional, McNaney, J. M., additional, Leeper, R. J., additional, Ruiz, C. L., additional, Cooper, G. W., additional, Nelson, A. G., additional, Chandler, G. G. A., additional, Hahn, K. D., additional, Moran, M. J., additional, Schneider, M. B., additional, Palmer, N. E., additional, Bionta, R. M., additional, Hartouni, E. P., additional, LePape, S., additional, Patel, P. K., additional, Izumi, N., additional, Tommasini, R., additional, Bond, E. J., additional, Caggiano, J. A., additional, Hatarik, R., additional, Grim, G. P., additional, Merrill, F. E., additional, Fittinghoff, D. N., additional, Guler, N., additional, Drury, O., additional, Wilson, D. C., additional, Herrmann, H. W., additional, Stoeffl, W., additional, Casey, D. T., additional, Johnson, M. G., additional, Frenje, J. A., additional, Petrasso, R. D., additional, Zylestra, A., additional, Rinderknecht, H., additional, Kalantar, D. H., additional, Dzenitis, J. M., additional, Di Nicola, P., additional, Eder, D. C., additional, Courdin, W. H., additional, Gururangan, G., additional, Burkhart, S. C., additional, Friedrich, S., additional, Blueuel, D. L., additional, Bernstein, l. A., additional, Eckart, M. J., additional, Munro, D. H., additional, Hatchett, S. P., additional, Macphee, A. G., additional, Edgell, D. H., additional, Bradley, D. K., additional, Bell, P. M., additional, Glenn, S. M., additional, Simanovskaia, N., additional, Barrios, M. A., additional, Benedetti, R., additional, Kyrala, G. A., additional, Town, R. P. J., additional, Dewald, E. L., additional, Milovich, J. L., additional, Widmann, K., additional, Moore, A. S., additional, LaCaille, G., additional, Regan, S. P., additional, Suter, L. J., additional, Felker, B., additional, Ashabranner, R. C., additional, Jackson, M. C., additional, Prasad, R., additional, Richardson, M. J., additional, Kohut, T. R., additional, Datte, P. S., additional, Krauter, G. W., additional, Klingman, J. J., additional, Burr, R. F., additional, Land, T. A., additional, Hermann, M. R., additional, Latray, D. A., additional, Saunders, R. L., additional, Weaver, S., additional, Cohen, S. J., additional, Berzins, L., additional, Brass, S. G., additional, Palma, E. S., additional, Lowe-Webb, R. R., additional, McHalle, G. N., additional, Arnold, P. A., additional, Lagin, L. J., additional, Marshall, C. D., additional, Brunton, G. K., additional, Mathisen, D. G., additional, Wood, R. D., additional, Cox, J. R., additional, Ehrlich, R. B., additional, Knittel, K. M., additional, Bowers, M. W., additional, Zacharias, R. A., additional, Young, B. K., additional, Holder, J. P., additional, Kimbrough, J. R., additional, Ma, T., additional, La Fortune, K. N., additional, Widmayer, C. C., additional, Shaw, M. J., additional, Erbert, G. V., additional, Jancaitis, K. S., additional, DiNicola, J. M., additional, Orth, C., additional, Heestand, G., additional, Kirkwood, R., additional, Haynam, C., additional, Wegner, P. J., additional, Whitman, P. K., additional, Hamza, A., additional, Dzenitis, E. G., additional, Wallace, R. J., additional, Bhandarkar, S. D., additional, Parham, T. G., additional, Dylla-Spears, R., additional, Mapoles, E. R., additional, Kozioziemski, B. J., additional, Sater, J. D., additional, Walters, C. F., additional, Haid, B. J., additional, Fair, J., additional, Nikroo, A., additional, Giraldez, E., additional, Moreno, K., additional, Vanwonterghem, B., additional, Kauffman, R. L., additional, Batha, S., additional, Larson, D. W., additional, Fortner, R. J., additional, Schneider, D. H., additional, Lindl, J. D., additional, Patterson, R. W., additional, Atherton, L. J., additional, and Moses, E. I., additional

Published
2012
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7. Cryogenic thermonuclear fuel implosions on the National Ignition Facility

Author

Glenzer, S. H., primary, Callahan, D. A., additional, MacKinnon, A. J., additional, Kline, J. L., additional, Grim, G., additional, Alger, E. T., additional, Berger, R. L., additional, Bernstein, L. A., additional, Betti, R., additional, Bleuel, D. L., additional, Boehly, T. R., additional, Bradley, D. K., additional, Burkhart, S. C., additional, Burr, R., additional, Caggiano, J. A., additional, Castro, C., additional, Casey, D. T., additional, Choate, C., additional, Clark, D. S., additional, Celliers, P., additional, Cerjan, C. J., additional, Collins, G. W., additional, Dewald, E. L., additional, DiNicola, P., additional, DiNicola, J. M., additional, Divol, L., additional, Dixit, S., additional, Döppner, T., additional, Dylla-Spears, R., additional, Dzenitis, E., additional, Eckart, M., additional, Erbert, G., additional, Farley, D., additional, Fair, J., additional, Fittinghoff, D., additional, Frank, M., additional, Frenje, L. J. A., additional, Friedrich, S., additional, Gatu Johnson, M., additional, Gibson, C., additional, Giraldez, E., additional, Glebov, V., additional, Glenn, S., additional, Guler, N., additional, Haan, S. W., additional, Haid, B. J., additional, Hammel, B. A., additional, Hamza, A. V., additional, Haynam, C. A., additional, Heestand, G. M., additional, Hermann, M., additional, Hermann, H. W., additional, Hicks, D. G., additional, Hinkel, D. E., additional, Holder, J. P., additional, Holunda, D. M., additional, Horner, J. B., additional, Hsing, W. W., additional, Huang, H., additional, Izumi, N., additional, Jackson, M., additional, Jones, O. S., additional, Kalantar, D. H., additional, Kauffman, R., additional, Kilkenny, J. D., additional, Kirkwood, R. K., additional, Klingmann, J., additional, Kohut, T., additional, Knauer, J. P., additional, Koch, J. A., additional, Kozioziemki, B., additional, Kyrala, G. A., additional, Kritcher, A. L., additional, Kroll, J., additional, La Fortune, K., additional, Lagin, L., additional, Landen, O. L., additional, Larson, D. W., additional, LaTray, D., additional, Leeper, R. J., additional, Le Pape, S., additional, Lindl, J. D., additional, Lowe-Webb, R., additional, Ma, T., additional, McNaney, J., additional, MacPhee, A. G., additional, Malsbury, T. N., additional, Mapoles, E., additional, Marshall, C. D., additional, Meezan, N. B., additional, Merrill, F., additional, Michel, P., additional, Moody, J. D., additional, Moore, A. S., additional, Moran, M., additional, Moreno, K. A., additional, Munro, D. H., additional, Nathan, B. R., additional, Nikroo, A., additional, Olson, R. E., additional, Orth, C. D., additional, Pak, A. E., additional, Patel, P. K., additional, Parham, T., additional, Petrasso, R., additional, Ralph, J. E., additional, Rinderknecht, H., additional, Regan, S. P., additional, Robey, H. F., additional, Ross, J. S., additional, Rosen, M. D., additional, Sacks, R., additional, Salmonson, J. D., additional, Saunders, R., additional, Sater, J., additional, Sangster, C., additional, Schneider, M. B., additional, Séguin, F. H., additional, Shaw, M. J., additional, Spears, B. K., additional, Springer, P. T., additional, Stoeffl, W., additional, Suter, L. J., additional, Thomas, C. A., additional, Tommasini, R., additional, Town, R. P. J., additional, Walters, C., additional, Weaver, S., additional, Weber, S. V., additional, Wegner, P. J., additional, Whitman, P. K., additional, Widmann, K., additional, Widmayer, C. C., additional, Wilde, C. H., additional, Wilson, D. C., additional, Van Wonterghem, B., additional, MacGowan, B. J., additional, Atherton, L. J., additional, Edwards, M. J., additional, and Moses, E. I., additional

Published
2012
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8. 64 Timepiece

Author

Dinicola, J.

Subjects
Computer Graphics, Video Games, Strategy Game, Computer Game, Programs
Published
1983

11. Pediatric Hepatitis C Screening by Maternal Hepatitis C Infection Status During Pregnancy.

Author

DiNicola J, Lentscher A, Liu H, Chappell CA, and Rick AM

Subjects
Humans, Female, Pregnancy, Retrospective Studies, Infant, Newborn, Infant, Adult, Viral Load, Male, Neonatal Screening, Mass Screening, Hepacivirus genetics, Pregnancy Complications, Infectious diagnosis, Pregnancy Complications, Infectious virology, Hepatitis C diagnosis, Infectious Disease Transmission, Vertical
Abstract

Background: Screening for perinatal hepatitis C virus (HCV) infections remains low despite increases in the number of at-risk infants. It is unknown if pediatric screening varies by maternal HCV infection status during pregnancy., Methods: Using a retrospective cohort of mother-infant pairs born from 2015 to 2019, we identified women with HCV and classified their infection status during pregnancy as active, probable, or previous based on HCV RNA testing obtained during pregnancy. We used logistic regression to assess odds ratio (OR) of infant screening based on maternal HCV infection status., Results: Of the 503 HCV-exposed infants, 137 (27%) were born to women with previous infection, 106 (21%) to women with probable infection, and 260 (52%) to women with active infection. Completion of pediatric screening varied by maternal infection status (43% previous infection; 49% probable infection; 58% active; P = 0.014). Pediatric HCV infection ranged from 1.7 to 7.7% by maternal viral load (VL) status. Infants born to women with active infection were 2.5 times more likely (95% confidence intervals [CI]: 1.5-4.4) to have a screening test ordered versus infants of previously infected women; there was no difference for infants of women with probable infection (OR:1.6; 95% CI: 0.9-3.2). Test ordering was also associated with maternal smoking status, a visit at ≥18 months of age, and outpatient documentation of HCV exposure. If a test was ordered, there was no difference in test completion by maternal infection status. However, test completion was associated with living with a nonbiologic parent and earlier birth year., Conclusion: Infants born to women with active infection are more likely to be screened for HCV, but many children continue to be unscreened and pediatric HCV infections are going undetected. New Centers for Disease Control and Prevention pediatric HCV screening guidelines recommending earlier screening may improve screening rates., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Journal of the Pediatric Infectious Diseases Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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12. In vivo measurement of RBC survival in patients with sickle cell disease before or after hematopoietic stem cell transplantation.

Author

Leonard AK, Furstenau D, Inam Z, Luckett C, Chu R, Demirci S, Essawi K, Gudmundsdottir B, Hinds M, DiNicola J, Li Q, Eaton WA, Cellmer T, Wang X, Thein SL, Macari ER, VanNest S, Hsieh MM, Bonner M, Pierciey FJ, and Tisdale JF

Subjects
Humans, Biotin, Erythrocytes pathology, Hemoglobins, Anemia, Sickle Cell pathology, Hematopoietic Stem Cell Transplantation adverse effects, Hematopoietic Stem Cell Transplantation methods
Abstract

Abstract: Stable, mixed-donor-recipient chimerism after allogeneic hematopoietic stem cell transplantation (HSCT) for patients with sickle cell disease (SCD) is sufficient for phenotypic disease reversal, and results from differences in donor/recipient-red blood cell (RBC) survival. Understanding variability and predictors of RBC survival among patients with SCD before and after HSCT is critical for gene therapy research which seeks to generate sufficient corrected hemoglobin to reduce polymerization thereby overcoming the red cell pathology of SCD. This study used biotin labeling of RBCs to determine the lifespan of RBCs in patients with SCD compared with patients who have successfully undergone curative HSCT, participants with sickle cell trait (HbAS), and healthy (HbAA) donors. Twenty participants were included in the analysis (SCD pre-HSCT: N = 6, SCD post-HSCT: N = 5, HbAS: N = 6, and HbAA: N = 3). The average RBC lifespan was significantly shorter for participants with SCD pre-HSCT (64.1 days; range, 35-91) compared with those with SCD post-HSCT (113.4 days; range, 105-119), HbAS (126.0 days; range, 119-147), and HbAA (123.7 days; range, 91-147) (P<.001). RBC lifespan correlated with various hematologic parameters and strongly correlated with the average final fraction of sickled RBCs after deoxygenation (P<.001). No adverse events were attributable to the use of biotin and related procedures. Biotin labeling of RBCs is a safe and feasible methodology to evaluate RBC survival in patients with SCD before and after HSCT. Understanding differences in RBC survival may ultimately guide gene therapy protocols to determine hemoglobin composition required to reverse the SCD phenotype as it relates directly to RBC survival. This trial was registered at www.clinicaltrials.gov as #NCT04476277., (Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution.)

Published
2024
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13. Sustained fetal hemoglobin induction in vivo is achieved by BCL11A interference and coexpressed truncated erythropoietin receptor.

Author

Uchida N, Ferrara F, Drysdale CM, Yapundich M, Gamer J, Nassehi T, DiNicola J, Shibata Y, Wielgosz M, Kim YS, Bauler M, Throm RE, Haro-Mora JJ, Demirci S, Bonifacino AC, Krouse AE, Linde NS, Donahue RE, Ryu B, and Tisdale JF

Subjects
Animals, Erythroid Cells, Macaca mulatta, Mice, Repressor Proteins, Fetal Hemoglobin genetics, Receptors, Erythropoietin genetics
Abstract

Hematopoietic stem cell gene therapy for hemoglobin disorders, including sickle cell disease, requires high-efficiency lentiviral gene transfer and robust therapeutic globin expression in erythroid cells. Erythropoietin is a key cytokine for erythroid proliferation and differentiation (erythropoiesis), and truncated human erythropoietin receptors (thEpoR) have been reported in familial polycythemia. We reasoned that coexpression of thEpoR could enhance the phenotypic effect of a therapeutic vector in erythroid cells in xenograft mouse and autologous nonhuman primate transplantation models. We generated thEpoR by deleting 40 amino acids from the carboxyl terminus, allowing for erythropoietin-dependent enhanced erythropoiesis of gene-modified cells. We then designed lentiviral vectors encoding both thEpoR and B cell lymphoma/leukemia 11A ( BCL11A )-targeting microRNA-adapted short hairpin RNA (shmiR BCL11A) driven by an erythroid-specific promoter. thEpoR expression enhanced erythropoiesis among gene-modified cells in vitro. We then transplanted lentiviral vector gene-modified CD34 + cells with erythroid-specific expression of both thEpoR and shmiR BCL11A and compared to cells modified with shmiR BCL11A only. We found that thEpoR enhanced shmiR BCL11A-based fetal hemoglobin (HbF) induction in both xenograft mice and rhesus macaques, whereas HbF induction with shmiR BCL11A only was robust, yet transient. thEpoR/shmiR BCL11A coexpression allowed for sustained HbF induction at 20 to 25% in rhesus macaques for 4 to 8 months. In summary, we developed erythroid-specific thEpoR/shmiR BCL11A-expressing vectors, enhancing HbF induction in xenograft mice and rhesus macaques. The sustained HbF induction achieved by addition of thEpoR and shmiR BCL11A may represent a viable gene therapy strategy for hemoglobin disorders., (Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Published
2021
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14. Cas9 protein delivery non-integrating lentiviral vectors for gene correction in sickle cell disease.

Author

Uchida N, Drysdale CM, Nassehi T, Gamer J, Yapundich M, DiNicola J, Shibata Y, Hinds M, Gudmundsdottir B, Haro-Mora JJ, Demirci S, and Tisdale JF

Abstract

Gene editing with the CRISPR-Cas9 system could revolutionize hematopoietic stem cell (HSC)-targeted gene therapy for hereditary diseases, including sickle cell disease (SCD). Conventional delivery of editing tools by electroporation limits HSC fitness due to its toxicity; therefore, efficient and non-toxic delivery remains crucial. Integrating lentiviral vectors are established for therapeutic gene delivery to engraftable HSCs in gene therapy trials; however, their sustained expression and size limitation preclude their use for CRISPR-Cas9 delivery. Here, we developed a Cas9 protein delivery non-integrating lentiviral system encoding guide RNA and donor DNA, allowing for transient endonuclease function and inclusion of all editing tools in a single vector (all-in-one). We demonstrated efficient one-time correction of the SCD mutation in the endogenous βs-globin gene up to 42% at the protein level (p < 0.01) with the Cas9 protein delivery non-integrating lentiviral all-in-one system without electroporation. Our findings improve prospects for efficient and safe genome editing., Competing Interests: The authors declare no competing interests.

Published
2021
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15. SMAD7 enhances adult β-cell proliferation without significantly affecting β-cell function in mice.

Author

Sehrawat A, Shiota C, Mohamed N, DiNicola J, Saleh M, Kalsi R, Zhang T, Wang Y, Prasadan K, and Gittes GK

Subjects
Animals, Female, Glucose pharmacology, Male, Mice, Mice, Knockout, Signal Transduction, Sweetening Agents pharmacology, Transforming Growth Factor beta genetics, Cell Proliferation, Insulin physiology, Insulin Secretion drug effects, Insulin-Secreting Cells cytology, Insulin-Secreting Cells physiology, Smad7 Protein physiology, Transforming Growth Factor beta metabolism
Abstract

The interplay between the transforming growth factor β (TGF-β) signaling proteins, SMAD family member 2 (SMAD2) and 3 (SMAD3), and the TGF-β-inhibiting SMAD, SMAD7, seems to play a vital role in proper pancreatic endocrine development and also in normal β-cell function in adult pancreatic islets. Here, we generated conditional SMAD7 knockout mice by crossing insulin1 Cre mice with SMAD7 fx/fx mice. We also created a β cell-specific SMAD7-overexpressing mouse line by crossing insulin1 Dre mice with HPRT-SMAD7/RosaGFP mice. We analyzed β-cell function in adult islets when SMAD7 was either absent or overexpressed in β cells. Loss of SMAD7 in β cells inhibited proliferation, and SMAD7 overexpression enhanced cell proliferation. However, alterations in basic glucose homeostasis were not detectable following either SMAD7 deletion or overexpression in β cells. Our results show that both the absence and overexpression of SMAD7 affect TGF-β signaling and modulates β-cell proliferation but does not appear to alter β-cell function. Reversible SMAD7 overexpression may represent an attractive therapeutic option to enhance β-cell proliferation without negative effects on β-cell function., (© 2020 Sehrawat et al.)

Published
2020
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