Institution
JDRF
Nonprofit•Toronto, Ontario, Canada•
About: JDRF is a nonprofit organization based out in Toronto, Ontario, Canada. It is known for research contribution in the topics: Type 1 diabetes & Diabetes mellitus. The organization has 305 authors who have published 278 publications receiving 26517 citations. The organization is also known as: Juvenile Diabetes Research Foundation.
Papers published on a yearly basis
Papers
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TL;DR: It is shown that pluripotent stem cells can be derived from the late epiblast layer of post-implantation mouse and rat embryos using chemically defined, activin-containing culture medium that is sufficient for long-term maintenance of human embryonic stem cells.
Abstract: Although the first mouse embryonic stem (ES) cell lines were derived 25 years ago using feeder-layer-based blastocyst cultures, subsequent efforts to extend the approach to other mammals, including both laboratory and domestic species, have been relatively unsuccessful. The most notable exceptions were the derivation of non-human primate ES cell lines followed shortly thereafter by their derivation of human ES cells. Despite the apparent common origin and the similar pluripotency of mouse and human embryonic stem cells, recent studies have revealed that they use different signalling pathways to maintain their pluripotent status. Mouse ES cells depend on leukaemia inhibitory factor and bone morphogenetic protein, whereas their human counterparts rely on activin (INHBA)/nodal (NODAL) and fibroblast growth factor (FGF). Here we show that pluripotent stem cells can be derived from the late epiblast layer of post-implantation mouse and rat embryos using chemically defined, activin-containing culture medium that is sufficient for long-term maintenance of human embryonic stem cells. Our results demonstrate that activin/Nodal signalling has an evolutionarily conserved role in the derivation and the maintenance of pluripotency in these novel stem cells. Epiblast stem cells provide a valuable experimental system for determining whether distinctions between mouse and human embryonic stem cells reflect species differences or diverse temporal origins.
1,945 citations
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Ljubljana University Medical Centre1, King's College London2, Vita-Salute San Raffaele University3, Stanford University4, American Diabetes Association5, University of Padua6, Harvard University7, University of Amsterdam8, University of Sydney9, University of Colorado Denver10, University of Sheffield11, University of Washington12, University of Cambridge13, Shanghai Jiao Tong University14, University of Virginia15, JDRF16, Katholieke Universiteit Leuven17, University of East Anglia18, San Antonio River Authority19, Steno Diabetes Center20, University of Montpellier21, University of Florida22, Nihon University23, Yale University24, Tel Aviv University25
TL;DR: This article summarizes the ATTD consensus recommendations for relevant aspects of CGM data utilization and reporting among the various diabetes populations.
Abstract: Improvements in sensor accuracy, greater convenience and ease of use, and expanding reimbursement have led to growing adoption of continuous glucose monitoring (CGM). However, successful utilization of CGM technology in routine clinical practice remains relatively low. This may be due in part to the lack of clear and agreed-upon glycemic targets that both diabetes teams and people with diabetes can work toward. Although unified recommendations for use of key CGM metrics have been established in three separate peer-reviewed articles, formal adoption by diabetes professional organizations and guidance in the practical application of these metrics in clinical practice have been lacking. In February 2019, the Advanced Technologies & Treatments for Diabetes (ATTD) Congress convened an international panel of physicians, researchers, and individuals with diabetes who are expert in CGM technologies to address this issue. This article summarizes the ATTD consensus recommendations for relevant aspects of CGM data utilization and reporting among the various diabetes populations.
1,776 citations
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TL;DR: The many new candidate genes suggested by these results include IL10, IL19, IL20, GLIS3, CD69 and IL27.
Abstract: Type 1 diabetes (T1D) is a common autoimmune disorder that arises from the action of multiple genetic and environmental risk factors. We report the findings of a genome-wide association study of T1D, combined in a meta-analysis with two previously published studies. The total sample set included 7,514 cases and 9,045 reference samples. Forty-one distinct genomic locations provided evidence for association with T1D in the meta-analysis (P < 10(-6)). After excluding previously reported associations, we further tested 27 regions in an independent set of 4,267 cases, 4,463 controls and 2,319 affected sib-pair (ASP) families. Of these, 18 regions were replicated (P < 0.01; overall P < 5 × 10(-8)) and 4 additional regions provided nominal evidence of replication (P < 0.05). The many new candidate genes suggested by these results include IL10, IL19, IL20, GLIS3, CD69 and IL27.
1,547 citations
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San Antonio River Authority1, Ljubljana University Medical Centre2, University of Amsterdam3, University of Colorado Denver4, University of Washington5, King's College London6, Vita-Salute San Raffaele University7, Stanford University8, University of Padua9, Harvard University10, University of Sheffield11, University of Cambridge12, Shanghai Jiao Tong University13, Princess Margaret Hospital for Children14, University of Virginia15, JDRF16, University of East Anglia17, Copenhagen University Hospital18, University of Montpellier19, Yale University20
TL;DR: This article summarizes the ATTD consensus recommendations and represents the current understanding of how CGM results can affect outcomes.
Abstract: Measurement of glycated hemoglobin (HbA1c) has been the traditional method for assessing glycemic control. However, it does not reflect intra- and interday glycemic excursions that may lead to acute events (such as hypoglycemia) or postprandial hyperglycemia, which have been linked to both microvascular and macrovascular complications. Continuous glucose monitoring (CGM), either from real-time use (rtCGM) or intermittently viewed (iCGM), addresses many of the limitations inherent in HbA1c testing and self-monitoring of blood glucose. Although both provide the means to move beyond the HbA1c measurement as the sole marker of glycemic control, standardized metrics for analyzing CGM data are lacking. Moreover, clear criteria for matching people with diabetes to the most appropriate glucose monitoring methodologies, as well as standardized advice about how best to use the new information they provide, have yet to be established. In February 2017, the Advanced Technologies & Treatments for Diabetes (ATTD) Congress convened an international panel of physicians, researchers, and individuals with diabetes who are expert in CGM technologies to address these issues. This article summarizes the ATTD consensus recommendations and represents the current understanding of how CGM results can affect outcomes.
1,173 citations
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TL;DR: There is now an increasing body of data to suggest that strategies involving a more targeted antioxidant approach, using agents that penetrate specific cellular compartments, may be the elusive additive therapy required to further optimize renoprotection in diabetes.
Abstract: It is postulated that localized tissue oxidative stress is a key component in the development of diabetic nephropathy. There remains controversy, however, as to whether this is an early link between hyperglycemia and renal disease or develops as a consequence of other primary pathogenic mechanisms. In the kidney, a number of pathways that generate reactive oxygen species (ROS) such as glycolysis, specific defects in the polyol pathway, uncoupling of nitric oxide synthase, xanthine oxidase, NAD(P)H oxidase, and advanced glycation have been identified as potentially major contributors to the pathogenesis of diabetic kidney disease. In addition, a unifying hypothesis has been proposed whereby mitochondrial production of ROS in response to chronic hyperglycemia may be the key initiator for each of these pathogenic pathways. This postulate emphasizes the importance of mitochondrial dysfunction in the progression and development of diabetes complications including nephropathy. A mystery remains, however, as to why antioxidants per se have demonstrated minimal renoprotection in humans despite positive preclinical research findings. It is likely that the utility of current study approaches, such as vitamin use, may not be the ideal antioxidant strategy in human diabetic nephropathy. There is now an increasing body of data to suggest that strategies involving a more targeted antioxidant approach, using agents that penetrate specific cellular compartments, may be the elusive additive therapy required to further optimize renoprotection in diabetes.
1,032 citations
Authors
Showing all 305 results
Name | H-index | Papers | Citations |
---|---|---|---|
Mark E. Cooper | 158 | 1463 | 124887 |
John A. Todd | 121 | 515 | 67413 |
Mikael Knip | 105 | 784 | 40829 |
Chantal Mathieu | 102 | 753 | 43596 |
Paola Allavena | 89 | 309 | 54251 |
Daniel Pipeleers | 84 | 339 | 24157 |
Ezio Bonifacio | 82 | 357 | 22157 |
Jorma Ilonen | 82 | 569 | 27414 |
Olli Simell | 82 | 481 | 24415 |
Bart O. Roep | 73 | 317 | 17667 |
Neil Walker | 72 | 340 | 35414 |
Vincent Plagnol | 71 | 221 | 24649 |
Merlin C. Thomas | 71 | 351 | 18143 |
Suvi M. Virtanen | 67 | 389 | 18321 |
Heikki Hyöty | 65 | 332 | 15602 |