Institution
University College Cork
Education•Cork, Ireland•
About: University College Cork is a education organization based out in Cork, Ireland. It is known for research contribution in the topics: Population & Irish. The organization has 12056 authors who have published 28452 publications receiving 958414 citations. The organization is also known as: Coláiste na hOllscoile Corcaigh & National University of Ireland, Cork.
Topics: Population, Irish, Gut flora, Microbiome, Casein
Papers published on a yearly basis
Papers
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TL;DR: Progress in this area will be facilitated by optimising strain, dose and product formulations, including protective commensal species; matching these formulations with selectively responsive subpopulations; and identifying ways to manipulate diet to modify bacterial profiles and metabolism.
Abstract: Probiotics are derived from traditional fermented foods, from beneficial commensals or from the environment. They act through diverse mechanisms affecting the composition or function of the commensal microbiota and by altering host epithelial and immunological responses. Certain probiotic interventions have shown promise in selected clinical conditions where aberrant microbiota have been reported, such as atopic dermatitis, necrotising enterocolitis, pouchitis and possibly irritable bowel syndrome. However, no studies have been conducted that can causally link clinical improvements to probiotic-induced microbiota changes. Whether a disease-prone microbiota pattern can be remodelled to a more robust, resilient and disease-free state by probiotic administration remains a key unanswered question. Progress in this area will be facilitated by: optimising strain, dose and product formulations, including protective commensal species; matching these formulations with selectively responsive subpopulations; and identifying ways to manipulate diet to modify bacterial profiles and metabolism.
437 citations
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University of Oxford1, University of Leicester2, University of Texas Health Science Center at San Antonio3, Duke University4, Novartis5, Moscow State University6, University of North Carolina at Chapel Hill7, University College Cork8, Federal University of São Paulo9, National Taiwan University10, The Chinese University of Hong Kong11, University of California, San Francisco12, Veterans Health Administration13, University of Bern14, University of California, San Diego15, Tulane University16, University of Sydney17, Medical University of Warsaw18, Harvard University19, Istanbul University20, University of Oslo21, University of Washington22, Monash University23, University of Eastern Finland24, University of Toronto25, University of Cape Town26, National University of Cordoba27, University of Illinois at Chicago28, Lahey Hospital & Medical Center29, Massachusetts Institute of Technology30, National and Kapodistrian University of Athens31, Utrecht University32, Umeå University33, Dresden University of Technology34, University of Liège35, Aarhus University36, University of Buenos Aires37, Masaryk University38, University of Copenhagen39, Semmelweis University40, Mario Negri Institute for Pharmacological Research41, University of Helsinki42
TL;DR: Among persons with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors, assignment to nateglinide for 5 years did not reduce the incidence of diabetes or the coprimary composite cardiovascular outcomes.
Abstract: After adjustment for multiple testing, nateglinide, as compared with placebo, did not significantly reduce the cumulative incidence of diabetes (36% and 34%, respectively; hazard ratio, 1.07; 95% confidence interval [CI], 1.00 to 1.15; P = 0.05), the core composite cardiovascular outcome (7.9% and 8.3%, respectively; hazard ratio, 0.94, 95% CI, 0.82 to 1.09; P = 0.43), or the extended composite cardiovascular outcome (14.2% and 15.2%, respectively; hazard ratio, 0.93, 95% CI, 0.83 to 1.03; P = 0.16). Nateglinide did, however, increase the risk of hypoglycemia. Conclusions Among persons with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors, assignment to nateglinide for 5 years did not reduce the incidence of diabetes or the coprimary composite cardiovascular outcomes. (ClinicalTrials.gov number, NCT00097786.)
436 citations
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TL;DR: The data suggest that low-pH conditions may have the potential to select for L. monocytogenes mutants with increased natural acid tolerance and increased virulence.
Abstract: The ability of Listeria monocytogenes to tolerate low-pH environments is of particular importance because the pathogen encounters such environments in vivo, both during passage through the stomach and within the macrophage phagosome. In our study, L. monocytogenes was shown to exhibit a significant adaptive acid tolerance response following a 1-h exposure to mild acid (pH 5.5), which is capable of protecting cells from severe acid stress (pH 3.5). Susceptibility to pH 3.5 acid is growth phase dependent. Stationary-phase Listeria cultures are naturally resistant to the challenge pH (pH 3.5), while exponential-phase cultures require adaptation at pH 5.5 to induce acid tolerance. Adaptation requires protein synthesis, since treatment with chloramphenicol prevents the development of acid tolerance. Induction of the acid tolerance response also protects L. monocytogenes against the effect of other environmental stresses. Acid-adapted cells demonstrate increased tolerance toward thermal stress, osmotic stress, crystal violet, and ethanol. Following prolonged exposure of L. monocytogenes to pH 3.5, we isolated mutants which constitutively demonstrate increased acid tolerance at all stages of the growth cycle. These mutants do not display full acid tolerance, but their resistance to low pH can be further increased following adaptation to mild-acid conditions. The mutants demonstrated increased lethality for mice relative to that of the wild type when inoculated by the intraperitoneal route. When administered as lower inocula, the mutants reached higher levels in the spleens of infected mice than did the wild type. The data suggest that low-pH conditions may have the potential to select for L. monocytogenes mutants with increased natural acid tolerance and increased virulence.
433 citations
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TL;DR: In this paper, the authors use the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) to improve and expand the quantification of personal health-care access and quality for 195 countries and territories from 1990 to 2015.
427 citations
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TL;DR: In this article, Proteolysis in cheese during ripening is investigated. But it is not shown to be present in the case of sourdough, and the results are limited.
Abstract: (1996). Proteolysis in cheese during ripening. Food Reviews International: Vol. 12, No. 4, pp. 457-509.
427 citations
Authors
Showing all 12300 results
Name | H-index | Papers | Citations |
---|---|---|---|
Stephen J. O'Brien | 153 | 1062 | 93025 |
James J. Collins | 151 | 669 | 89476 |
J. Wouter Jukema | 124 | 785 | 61555 |
John F. Cryan | 124 | 723 | 58938 |
Fergus Shanahan | 117 | 705 | 51963 |
Timothy G. Dinan | 116 | 689 | 60561 |
John M. Starr | 116 | 695 | 48761 |
Gordon G. Wallace | 114 | 1267 | 69095 |
Colin Hill | 112 | 693 | 54484 |
Robert Clarke | 111 | 512 | 90049 |
Douglas B. Kell | 111 | 634 | 50335 |
Thomas Bein | 109 | 677 | 42800 |
Steven C. Hayes | 106 | 450 | 51556 |
Åke Borg | 105 | 444 | 53835 |
Eamonn Martin Quigley | 103 | 685 | 39585 |