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Institution

University College Cork

EducationCork, 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
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Journal ArticleDOI
TL;DR: The generation and sources of ROS within tumour cells, the regulation of ROS by antioxidant defence systems, as well as the effect of elevated ROS production on their signalling targets in cancer are discussed.

1,100 citations

Journal ArticleDOI
01 May 2000-Lait
TL;DR: The principal pathways for the formation of flavour compounds in cheese (glycolysis, lipolysis and proteolysis) are reviewed in this article, where the authors present a detailed review of the principal pathways.
Abstract: The principal pathways for the formation of flavour compounds in cheese (glycolysis, lipolysis and proteolysis) are reviewed. Depending on variety, microflora and ripening conditions, lac- tate may be metabolized by a number of pathways to various compounds which contribute to cheese flavour or off-flavours. Citrate metabolism by citrate-positive lactococci or Leuconostoc spp. is important in certain varieties (e.g., Dutch cheeses). Lipolysis results directly in the formation of flavour compounds by liberating free fatty acids (FFA). FFA may also be metabolized to alkan-2-ones and fatty acid lactones. Proteolysis of the caseins to a range of small- and intermediate-sized peptides and free amino acids (FAA) probably only contributes to the background flavour of most cheese varieties, but FAA are important precursors for a range of poorly-understood catabolic reactions which produce volatile compounds essential for flavour.

1,091 citations

Journal ArticleDOI
TL;DR: The current status of research into developing appropriate tests for assessing depression- and anxiety-related behaviours in mice is assessed.
Abstract: Psychiatry has proven to be among the least penetrable clinical disciplines for the development of satisfactory in vivo model systems for evaluating novel treatment approaches. However, mood and anxiety disorders remain poorly understood and inadequately treated. With the explosion in the use of genetically modified mice, enormous research efforts have been focused on developing mouse models of psychiatric disorders. The success of this approach is largely contingent on the usefulness of available behavioural models of depression- and anxiety-related behaviours in mice. Here, we assess the current status of research into developing appropriate tests for assessing such behaviours.

1,084 citations

Journal ArticleDOI
TL;DR: Light is shed on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility and within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways.
Abstract: Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 × 10(-8)). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 × 10(-4), Bonferroni corrected), of which six reached P < 5 × 10(-8), including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility.

1,076 citations


Authors

Showing all 12300 results

NameH-indexPapersCitations
Stephen J. O'Brien153106293025
James J. Collins15166989476
J. Wouter Jukema12478561555
John F. Cryan12472358938
Fergus Shanahan11770551963
Timothy G. Dinan11668960561
John M. Starr11669548761
Gordon G. Wallace114126769095
Colin Hill11269354484
Robert Clarke11151290049
Douglas B. Kell11163450335
Thomas Bein10967742800
Steven C. Hayes10645051556
Åke Borg10544453835
Eamonn Martin Quigley10368539585
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202381
2022400
20212,153
20201,927
20191,679
20181,618