Search

Your search keyword '"Hackam, David J."' showing total 706 results
Start Over Author "Hackam, David J."
706 results on '"Hackam, David J."'

1. List of Contributors

Author

Agrawal, Pankaj B., primary, Akhtar, Yasmin, additional, Alallah, Jubara, additional, Alhassen, Ziad, additional, Altit, Gabriel, additional, AlZubaidi, Abbas, additional, Amlani, Lahin M., additional, Antelo, Martin, additional, Athalye-Jape, Gayatri, additional, Badarch, Jargalsaikhan, additional, Baer, Gerri, additional, Bagga, Nitasha, additional, Bahr, Timothy M., additional, Bar-Cohen, Yaniv, additional, M. Barr, Stephanie, additional, Bauer, Andrew J., additional, Bearer, Cynthia F., additional, Beckman, Ross M., additional, Beltempo, Marc, additional, Bembea, Melania M., additional, Berlin, Sheila, additional, Berry, Shandeigh N., additional, Bhandari, Vineet, additional, Bhatia, Shaifali, additional, Bhombal, Shazia, additional, Bigelow, Elaine O., additional, Blevins, Carley, additional, Boppana, Suresh, additional, Boss, Renee, additional, Brooks, Sandra, additional, Buonocore, Giuseppe, additional, Burnsed, Jennifer, additional, Calabria, Andrew C., additional, Carrasco, Melisa, additional, Carter, Brian S., additional, Chandrasekharan, Praveen, additional, Chavez-Valdez, Raul, additional, Choleva, Lauryn, additional, Christensen, Robert D., additional, Chung, Wendy K., additional, Coggins, Sarah A., additional, Cooke, David W., additional, Cummings, Laura, additional, Currie, Erin R., additional, Davidson, Joanne O., additional, Davis, Jonathan M., additional, Day-Richardson, Colby L., additional, De Leon, Diva D., additional, Dedhia, Kavita, additional, Dendi, Alvaro, additional, Deshpande, Anita, additional, Dionne, Janis M., additional, Donda, Keyur, additional, Donohue, Lee, additional, Doyle, Jefferson J., additional, Dulkerian, Susan J., additional, Dumpa, Vikramaditya, additional, Duncan, Andrea F., additional, Dunham, Alexandra M., additional, Ecret, DiAnn, additional, Ellis, Kelstan, additional, El-Metwally, Dina, additional, Etchill, Eric W., additional, Ethawi, Yahya, additional, Everett, Allen D., additional, Fabres, Jorge, additional, Felling, Ryan J., additional, Fenton, Tanis R., additional, Flannery, Dustin D., additional, Flynn, Joseph T., additional, Fredenburg, Michaelene, additional, Fuqua, John, additional, Garcia, Alejandro V., additional, Garzon, Steven, additional, Gauda, Estelle B., additional, Thompson, Marisa Gilstrop, additional, Goldenberg, Barton, additional, Salazar, Andres J. Gonzalez, additional, Goodwin, Julie E., additional, Goudy, Steven L., additional, Graham, Ernest, additional, Grauerholz, Kathryn, additional, Groves, Mari L., additional, Guillot, Mireille, additional, Gunn, Alistair J., additional, Gupta, Arjun, additional, Hackam, David J., additional, Hidalgo, Joaquin, additional, Honcharuk, Erin, additional, Htun, Zeyar, additional, Hudak, Mark L., additional, Driscoll, Colleen A. Hughes, additional, Huisman, Thierry A.G.M., additional, Jabroun, Mireille, additional, Jackson, Eric M., additional, Jain, Naveen, additional, Jain, Rajesh, additional, Jelin, Angie, additional, Jelin, Eric, additional, Juul, Sandra E., additional, Kaufman, David A., additional, BMBS, Alison Kent,, additional, Khuder, Sundos, additional, Kovler, Mark L., additional, Kraus, Courtney L., additional, Krishnamurthy, Ganga, additional, Kukora, Stephanie K., additional, Kumar, Ashok, additional, Kunisaki, Shaun M., additional, Kuper-Sassé, Margaret, additional, Kwiatkowski, David M., additional, Lakshminrusimha, Satyan, additional, Laventhal, Naomi T., additional, Lawrence, Shelley M., additional, Lee-Winn, Angela E., additional, Leuthner, Steven, additional, Lewallen, Laura, additional, Lewis, Tamorah R., additional, Liken, Hillary B., additional, Liubšys, Arūnas, additional, Lui, Kei, additional, Maheshwari, Akhil, additional, Maitre, Nathalie L., additional, Makker, Kartikeya, additional, Mammen, Cherry, additional, J. Martin, Richard, additional, Mattos Castellano, María, additional, Maxwell, Jessie R., additional, McFarlane, Renske, additional, McLemore, Gabrielle, additional, McNelis, Kera M., additional, McPherson, Christopher, additional, Mietzsch, Ulrike, additional, Milante, Rachel R., additional, Miller, Jena L., additional, Mukhopadhyay, Sagori, additional, Mynak, Mimi L., additional, Nasr, Isam W., additional, Natarajan, Niranjana, additional, Navaneethan, Hema, additional, Nees, Shannon N., additional, Nguyen, Mai, additional, Noori, Shahab, additional, Odackal, Namrita J., additional, Ohls, Robin K., additional, Ostrander, Betsy E., additional, Pammi, Mohan, additional, Parimi, Prabhu S., additional, Park, Albert, additional, Patil, Monika S., additional, Pereira, Elaine M., additional, Premkumar, Muralidhar H., additional, Price-Douglas, Webra, additional, Puopolo, Karen M., additional, Rabe, Heike, additional, M. Rahman, Mohammad, additional, Reber, Kristina, additional, Kallem, Venkat Reddy, additional, Repka, Michael X., additional, Rhee, Daniel S., additional, Ringle, Megan L., additional, Rohrer, Allison, additional, Romero, Christopher J., additional, Ryan, Marisa A., additional, Sampah, Maame E.S., additional, Sanchez-Valle, Amarilis, additional, Sant’Anna, Guilherme M., additional, Saugstad, Ola D., additional, RobertH., Anne and, additional, Schacht, John P., additional, Schelonka, Robert L., additional, Schofield, Erin E., additional, Selewski, David T., additional, Shah, Prakesh S., additional, Shih, Jessica G., additional, Sibinga, Erica M.S., additional, Sigal, Winnie, additional, Sims, Brian, additional, Singh, Rachana, additional, Singh, Srijan, additional, Snyder, Donna, additional, Sobrero, Helena, additional, Sponseller, Paul D., additional, Stafstrom, Carl E., additional, Steflik, Heidi J., additional, Sun, Lisa R., additional, Sundararajan, Sripriya, additional, Taylor, Sarah N., additional, Terrin, Norma, additional, Thacker, Prolima G., additional, Thébaud, Bernard, additional, Toms, Rune, additional, Torres, Benjamin A., additional, Tunkel, David E., additional, Umandap, Christine H., additional, Chaves, Diana Vargas, additional, Vento, Maximo, additional, Walsh, Jonathan, additional, Walter, Jolan, additional, Weaver, Meaghann S., additional, Weimer, Kristin, additional, Weller, Jennine, additional, Winter, Lindy W., additional, Wu, Tai-Wei, additional, and Yau, Mabel, additional

Published
2024
Full Text
View/download PDF

2. Necrotizing Enterocolitis

Author

Weller, Jennine, primary, Sampah, Maame E.S., additional, Salazar, Andres J. Gonzalez, additional, and Hackam, David J., additional

Published
2024
Full Text
View/download PDF

5. Age-dependent regulation of SARS-CoV-2 cell entry genes and cell death programs correlates with COVID-19 severity.

Author

Inde, Zintis, Croker, Ben A, Yapp, Clarence, Joshi, Gaurav N, Spetz, Johan, Fraser, Cameron, Qin, Xingping, Xu, Le, Deskin, Brian, Ghelfi, Elisa, Webb, Gabrielle, Carlin, Aaron F, Zhu, Yanfang Peipei, Leibel, Sandra L, Garretson, Aaron F, Clark, Alex E, Duran, Jason M, Pretorius, Victor, Crotty-Alexander, Laura E, Li, Chendi, Lee, Jamie Casey, Sodhi, Chhinder, Hackam, David J, Sun, Xin, Hata, Aaron N, Kobzik, Lester, Miller, Jeffrey, Park, Jin-Ah, Brownfield, Douglas, Jia, Hongpeng, and Sarosiek, Kristopher A

Subjects
Lung, Cells, Cultured, Vero Cells, Animals, Mice, Inbred C57BL, Humans, Severity of Illness Index, Gene Expression Profiling, Age Factors, Apoptosis, Aged, Middle Aged, Infant, Female, Male, Virus Internalization, Chlorocebus aethiops, COVID-19, Angiotensin-Converting Enzyme 2, SARS-CoV-2, Vaccine Related, Pneumonia & Influenza, Emerging Infectious Diseases, Biodefense, Pneumonia, Infectious Diseases, Prevention, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being
Abstract

Novel coronavirus disease 2019 (COVID-19) severity is highly variable, with pediatric patients typically experiencing less severe infection than adults and especially the elderly. The basis for this difference is unclear. We find that mRNA and protein expression of angiotensin-converting enzyme 2 (ACE2), the cell entry receptor for the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes COVID-19, increases with advancing age in distal lung epithelial cells. However, in humans, ACE2 expression exhibits high levels of intra- and interindividual heterogeneity. Further, cells infected with SARS-CoV-2 experience endoplasmic reticulum stress, triggering an unfolded protein response and caspase-mediated apoptosis, a natural host defense system that halts virion production. Apoptosis of infected cells can be selectively induced by treatment with apoptosis-modulating BH3 mimetic drugs. Notably, epithelial cells within young lungs and airways are more primed to undergo apoptosis than those in adults, which may naturally hinder virion production and support milder COVID-19 severity.

Published
2021

16. Genetic and Pharmacologic Manipulation of TLR4 Has Minimal Impact on Ethanol Consumption in Rodents

Author

Harris, R Adron, Bajo, Michal, Bell, Richard L, Blednov, Yuri A, Varodayan, Florence P, Truitt, Jay M, de Guglielmo, Giordano, Lasek, Amy W, Logrip, Marian L, Vendruscolo, Leandro F, Roberts, Amanda J, Roberts, Edward, George, Olivier, Mayfield, Jody, Billiar, Timothy R, Hackam, David J, Mayfield, R Dayne, Koob, George F, Roberto, Marisa, and Homanics, Gregg E

Subjects
Alcoholism, Alcohol Use and Health, Basic Behavioral and Social Science, Neurosciences, Behavioral and Social Science, Substance Misuse, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Mental health, Oral and gastrointestinal, Stroke, Good Health and Well Being, Alcohol Drinking, Alcoholism, Animals, Body Weight, Conditioning, Operant, Female, Gene Knockout Techniques, Lipopolysaccharides, Male, Mice, Mice, Knockout, Naloxone, Narcotic Antagonists, Nucleus Accumbens, Rats, Receptors, GABA-A, Toll-Like Receptor 4, (+)-naloxone, chronic intermittent ethanol vapor, drinking-in-the-dark, lipopolysaccharide, operant self-administration, Toll-like receptor 4 knock-out, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery
Abstract

Toll-like receptor 4 (TLR4) is a critical component of innate immune signaling and has been implicated in alcohol responses in preclinical and clinical models. Members of the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium tested the hypothesis that TLR4 mediates excessive ethanol drinking using the following models: (1) Tlr4 knock-out (KO) rats, (2) selective knockdown of Tlr4 mRNA in mouse nucleus accumbens (NAc), and (3) injection of the TLR4 antagonist (+)-naloxone in mice. Lipopolysaccharide (LPS) decreased food/water intake and body weight in ethanol-naive and ethanol-trained wild-type (WT), but not Tlr4 KO rats. There were no consistent genotypic differences in two-bottle choice chronic ethanol intake or operant self-administration in rats before or after dependence. In mice, (+)-naloxone did not decrease drinking-in-the-dark and only modestly inhibited dependence-driven consumption at the highest dose. Tlr4 knockdown in mouse NAc did not decrease drinking in the two-bottle choice continuous or intermittent access tests. However, the latency to ethanol-induced loss of righting reflex increased and the duration decreased in KO versus WT rats. In rat central amygdala neurons, deletion of Tlr4 altered GABAA receptor function, but not GABA release. Although there were no genotype differences in acute ethanol effects before or after chronic intermittent ethanol exposure, genotype differences were observed after LPS exposure. Using different species and sexes, different methods to inhibit TLR4 signaling, and different ethanol consumption tests, our comprehensive studies indicate that TLR4 may play a role in ethanol-induced sedation and GABAA receptor function, but does not regulate excessive drinking directly and would not be an effective therapeutic target.Significance statementToll-like receptor 4 (TLR4) is a key mediator of innate immune signaling and has been implicated in alcohol responses in animal models and human alcoholics. Members of the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium participated in the first comprehensive study across multiple laboratories to test the hypothesis that TLR4 regulates excessive alcohol consumption in different species and different models of chronic, dependence-driven, and binge-like drinking. Although TLR4 was not a critical determinant of excessive drinking, it was important in the acute sedative effects of alcohol. Current research efforts are directed at determining which neuroimmune pathways mediate excessive alcohol drinking and these findings will help to prioritize relevant pathways and potential therapeutic targets.

Published
2017

17. The human milk oligosaccharides 2’-fucosyllactose and 6’-sialyllactose protect against the development of necrotizing enterocolitis by inhibiting toll-like receptor 4 signaling

Author

Sodhi, Chhinder P., Wipf, Peter, Yamaguchi, Yukihiro, Fulton, William B., Kovler, Mark, Niño, Diego F., Zhou, Qinjie, Banfield, Emilyn, Werts, Adam D., Ladd, Mitchell R., Buck, Rachael H., Goehring, Karen C., Prindle, Jr, Thomas, Wang, Sanxia, Jia, Hongpeng, Lu, Peng, and Hackam, David J.

Published
2021
Full Text
View/download PDF

33. Human milk oligosaccharides reduce necrotizing enterocolitis induced-neuroinflammation and cognitive impairment in mice

Author

Sodhi, Chhinder P., primary, Ahmad, Raheel, additional, Fulton, William B., additional, Lopez, Carla, additional, Eke, Benjamin, additional, Scheese, Daniel, additional, Duess, Johannes, additional, Steinway, Steven, additional, Raouf, Zachariah, additional, Moore, Hannah, additional, Tsuboi, Koichi, additional, Sampah, Maame, additional, Jang, Hee-Seong, additional, Buck, Rachael H., additional, Hill, David R., additional, Niemiro, Grace M., additional, Prindle, Thomas, additional, Wang, Sanxia, additional, Wang, Meghan, additional, Jia, Hongpeng, additional, Catazaro, Jonathan, additional, Lu, Peng, additional, and Hackam, David J., additional

Published
2023
Full Text
View/download PDF

42. Insights image for “The human milk oligosaccharides 2’-fucosyllactose and 6’-sialyllactose protect against the development of necrotizing enterocolitis by inhibiting toll-like receptor 4 signaling.”

Author

Sodhi, Chhinder P., Wipf, Peter, Yamaguchi, Yukihiro, Fulton, William B., Kovler, Mark, Niño, Diego F., Zhou, Qinjie, Banfield, Emilyn, Werts, Adam D., Ladd, Mitchell R., Buck, Rachael H., Goehring, Karen C., Prindle, Jr, Thomas, Wang, Sanxia, Jia, Hongpeng, Lu, Peng, and Hackam, David J.

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results