Institution
Wake Forest University
Education•Winston-Salem, North Carolina, United States•
About: Wake Forest University is a education organization based out in Winston-Salem, North Carolina, United States. It is known for research contribution in the topics: Population & Diabetes mellitus. The organization has 21499 authors who have published 48731 publications receiving 2246027 citations. The organization is also known as: Wake Forest College.
Topics: Population, Diabetes mellitus, Cancer, Medicine, Blood pressure
Papers published on a yearly basis
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TL;DR: In this paper, the authors studied the possible correlations between defects and photoluminescence spectra in ZnO nanoparticles of sizes ranging from 43 nm to 73 nm in diameter.
Abstract: We studied the possible correlations between defects and photoluminescence spectra in ZnO nanoparticles of sizes ranging from 43 nm to 73 nm in diameter. The defects and impurity contents were characterized by Fourier-transform infrared (FTIR) spectroscopy. The results show fewer carboxylate and hydroxyl impurities for particles of larger sizes. No significant variation in oxygen vacancy content was found among samples. Annealing in vacuum at 300 °C significantly reduces the carboxylate and hydroxyl impurities in the samples. The total luminescence intensity (UV + visible) increases as the particle size grows for both the unannealed and annealed samples. This suggests that both types of luminescence are subject to non-radiative quenching by near surface defect centers, possibly carboxylate and hydroxyl impurities. There may be quenching due to intrinsic lattice defects too. It is found that annealing in vacuum enhances the visible luminescence both absolutely and relative to the UV exciton luminescence. In addition to the 2.5 eV green luminescence peak, a peak centered at 2.8 eV can also be resolved, espeically for the 43 nm sample. (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)
400 citations
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TL;DR: The insulin-modified frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis provides estimates of insulin sensitivity that correlate significantly with those from the glucose clamp, however, in NIDDM.
Abstract: An insulin-modified frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis was compared with the glucose clamp in 11 subjects with normal glucose tolerance (NGT), 20 with impaired glucose tolerance (IGT), and 24 with non-insulin-dependent diabetes mellitus (NIDDM). The insulin sensitivity index (SI) was calculated from FSIGTT using 22- and 12-sample protocols (SI(22) and SI(12), respectively). Insulin sensitivity from the clamp was expressed as SI(clamp) and SIP(clamp). Minimal model parameters were similar when calculated with SI(22) and SI(12). SI could not be distinguished from 0 in approximately 50% of diabetic patients with either protocol. SI(22) correlated significantly with SI(clamp) in the whole group (r = 0.62), and in the NGT (r = 0.53), IGT (r = 0.48), and NIDDM (r = 0.41) groups (P < 0.05 for each). SI(12) correlated significantly with SI(clamp) in the whole group (r = 0.55, P < 0.001) and in the NGT (r = 0.53, P = 0.046) and IGT (r = 0.58, P = 0.008) but not NIDDM (r = 0.30, P = 0.085) groups. When SI(22), SI(clamp), and SIP(clamp) were expressed in the same units, SI(22) was 66 +/- 5% (mean +/- SE) and 50 +/- 8% lower than SI(clamp) and SIP(clamp), respectively. Thus, minimal model analysis of the insulin-modified FSIGTT provides estimates of insulin sensitivity that correlate significantly with those from the glucose clamp. The correlation was weaker, however, in NIDDM. The insulin-modified FSIGTT can be used as a simple test for assessment of insulin sensitivity in population studies involving nondiabetic subjects. Additional studies are needed before using this test routinely in patients with NIDDM.
400 citations
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University of Oxford1, Johns Hopkins University2, The George Institute for Global Health3, Colef4, University of Edinburgh5, University College London6, Imperial College London7, Boston University8, University of South Florida9, University of Washington10, University of California, San Francisco11, University of Gothenburg12, Wake Forest University13, Kyushu University14, Group Health Cooperative15, National Cheng Kung University16, NHS Scotland17, Norwegian Institute of Public Health18, Tianjin Medical University19, Stockholm University20, University of Sydney21, Curtin University22
TL;DR: A meta-analysis of unpublished data to estimate the sex-specific relationship between women and men with diabetes with incident dementia found individuals with type 2 diabetes are at ∼60% greater risk for the development of dementia compared with those without diabetes.
Abstract: OBJECTIVE Type 2 diabetes confers a greater excess risk of cardiovascular disease in women than in men. Diabetes is also a risk factor for dementia, but whether the association is similar in women and men remains unknown. We performed a meta-analysis of unpublished data to estimate the sex-specific relationship between women and men with diabetes with incident dementia. RESEARCH DESIGN AND METHODS A systematic search identified studies published prior to November 2014 that had reported on the prospective association between diabetes and dementia. Study authors contributed unpublished sex-specific relative risks (RRs) and 95% CIs on the association between diabetes and all dementia and its subtypes. Sex-specific RRs and the women-to-men ratio of RRs (RRRs) were pooled using random-effects meta-analyses. RESULTS Study-level data from 14 studies, 2,310,330 individuals, and 102,174 dementia case patients were included. In multiple-adjusted analyses, diabetes was associated with a 60% increased risk of any dementia in both sexes (women: pooled RR 1.62 [95% CI 1.45–1.80]; men: pooled RR 1.58 [95% CI 1.38–1.81]). The diabetes-associated RRs for vascular dementia were 2.34 (95% CI 1.86–2.94) in women and 1.73 (95% CI 1.61–1.85) in men, and for nonvascular dementia, the RRs were 1.53 (95% CI 1.35–1.73) in women and 1.49 (95% CI 1.31–1.69) in men. Overall, women with diabetes had a 19% greater risk for the development of vascular dementia than men (multiple-adjusted RRR 1.19 [95% CI 1.08–1.30]; P CONCLUSIONS Individuals with type 2 diabetes are at ∼60% greater risk for the development of dementia compared with those without diabetes. For vascular dementia, but not for nonvascular dementia, the additional risk is greater in women.
400 citations
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TL;DR: Both LDL subclasses were significantly associated with subclinical atherosclerosis, with small LDL confounding the association of large LDL with atherosclerotic risk.
399 citations
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TL;DR: Molecular mechanisms potentially underlying the memory-enhancing and neuroprotective effects of intranasal insulin are presented and an overview of neuroimaging studies indicating that disturbances in insulin metabolism and altered brain responses to insulin are linked to decreased cerebral volume and especially to hippocampal atrophy is provided.
Abstract: Research in animals and humans has associated Alzheimer’s disease (AD) with decreased cerebrospinal fluid levels of insulin in combination with decreased insulin sensitivity (insulin resistance) in the brain. This phenomenon is accompanied by attenuated receptor expression of insulin and insulin-like growth factor, enhanced serine phosphorylation of insulin receptor substrate-1, and impaired transport of insulin across the blood-brain barrier. Moreover, clinical trials have demonstrated that intranasal insulin improves both memory performance and metabolic integrity of the brain in patients suffering from AD or its prodrome, mild cognitive impairment. These results, in conjunction with the finding that insulin mitigates hippocampal synapse vulnerability to beta amyloid, a peptide thought to be causative in the development of AD, provide a strong rationale for hypothesizing that pharmacological strategies bolstering brain insulin signaling, such as intranasal administration of insulin, could have significant potential in the treatment and prevention of AD. With this view in mind, the review at hand will present molecular mechanisms potentially underlying the memory-enhancing and neuroprotective effects of intranasal insulin. Then, we will discuss the results of intranasal insulin studies that have demonstrated that enhancing brain insulin signaling improves memory and learning processes in both cognitively healthy and impaired humans. Finally, we will provide an overview of neuroimaging studies indicating that disturbances in insulin metabolism—such as insulin resistance in obesity, type 2 diabetes and AD—and altered brain responses to insulin are linked to decreased cerebral volume and especially to hippocampal atrophy.
399 citations
Authors
Showing all 21721 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
David J. Hunter | 213 | 1836 | 207050 |
Ronald Klein | 194 | 1305 | 149140 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Russel J. Reiter | 169 | 1646 | 121010 |
David R. Jacobs | 165 | 1262 | 113892 |
Barbara E.K. Klein | 160 | 856 | 93319 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
Steven R. Cummings | 158 | 579 | 104007 |
David Cella | 156 | 1258 | 106402 |
Jack M. Guralnik | 148 | 453 | 83701 |