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
Papers
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TL;DR: One hundred sixty-four participants recounted situations in which their feelings had been hurt (victim accounts) or in which they had hurt another person's feelings (perpetrator accounts) and then completed a questionnaire as mentioned in this paper.
Abstract: One hundred sixty-four participants recounted situations in which their feelings had been hurt (victim accounts) or in which they had hurt another person's feelings (perpetrator accounts) and then completed a questionnaire. Hurt feelings were precipitated by events that connoted relational devaluation, and the victims' distress correlated strongly with feelings of rejection. Victims were typically hurt by people whom they knew well, suggesting that familiarity or closeness played a role. Analyses of the subjective experience revealed that hurt feelings are characterized by undifferentiated negative affect that is often accompanied by emotions such as anxiety and hostility. Victims' responses to the event were related to their attributions for the perpetrators' actions, and hurtful episodes typically had negative repercussions for the relationships between perpetrators and victims.
422 citations
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Colorado School of Public Health1, Wake Forest University2, University of North Carolina at Chapel Hill3, Cincinnati Children's Hospital Medical Center4, Centers for Disease Control and Prevention5, National Institutes of Health6, Kaiser Permanente7, University of Washington8, University of Michigan9
TL;DR: The prevalence of complications and comorbidities was higher among teenagers and young adults who had been diagnosed with type 2 diabetes compared with type 1, but frequent in both groups, and these findings support early monitoring of youth with diabetes for development of complications.
Abstract: Importance The burden and determinants of complications and comorbidities in contemporary youth-onset diabetes are unknown. Objective To determine the prevalence of and risk factors for complications related to type 1 diabetes vs type 2 diabetes among teenagers and young adults who had been diagnosed with diabetes during childhood and adolescence. Design, Setting, and Participants Observational study from 2002 to 2015 in 5 US locations, including 2018 participants with type 1 and type 2 diabetes diagnosed at younger than 20 years, with single outcome measures between 2011 and 2015. Exposures Type 1 and type 2 diabetes and established risk factors (hemoglobin A 1c level, body mass index, waist-height ratio, and mean arterial blood pressure). Main Outcomes and Measures Diabetic kidney disease, retinopathy, peripheral neuropathy, cardiovascular autonomic neuropathy, arterial stiffness, and hypertension. Results Of 2018 participants, 1746 had type 1 diabetes (mean age, 17.9 years [SD, 4.1]; 1327 non-Hispanic white [76.0%]; 867 female patients [49.7%]), and 272 had type 2 (mean age, 22.1 years [SD, 3.5]; 72 non-Hispanic white [26.5%]; 181 female patients [66.5%]). Mean diabetes duration was 7.9 years (both groups). Patients with type 2 diabetes vs those with type 1 had higher age-adjusted prevalence of diabetic kidney disease (19.9% vs 5.8%; absolute difference [AD], 14.0%; 95% CI, 9.1%-19.9%; P P = .02), peripheral neuropathy (17.7% vs 8.5%; AD, 9.2%; 95% CI, 4.8%-14.4%; P P P P = .62). After adjustment for established risk factors measured over time, participants with type 2 diabetes vs those with type 1 had significantly higher odds of diabetic kidney disease (odds ratio [OR], 2.58; 95% CI, 1.39-4.81; P =.003), retinopathy (OR, 2.24; 95% CI, 1.11-4.50; P = .02), and peripheral neuropathy (OR, 2.52; 95% CI, 1.43-4.43; P = .001), but no significant difference in the odds of arterial stiffness (OR, 1.07; 95% CI, 0.63-1.84; P = .80) and hypertension (OR, 0.85; 95% CI, 0.50-1.45; P = .55). Conclusions and Relevance Among teenagers and young adults who had been diagnosed with diabetes during childhood or adolescence, the prevalence of complications and comorbidities was higher among those with type 2 diabetes compared with type 1, but frequent in both groups. These findings support early monitoring of youth with diabetes for development of complications.
422 citations
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TL;DR: Severe reductions in CD4 counts in patients with newly diagnosed HGG treated with radiation and temozolomide treatment are common, treatment-related, long-lasting, and associated with early death from tumor progression.
Abstract: Purpose: Patients with high-grade gliomas (HGG) routinely receive radiation, temozolomide, and glucocorticoids. As each of these is immunosuppressive, we conducted a prospective, multicenter study to follow CD4 counts over time and determine whether low CD4 counts were associated with adverse outcomes. Experimental Design: Patients with newly diagnosed HGG had CD4 counts drawn before initiating standard therapy and monthly thereafter for 1 year. Information on hospitalizations, infections, glucocorticoid use, survival, and cause of death were also collected. Results: Ninety-six evaluable patients were accrued [85% glioblastoma, median age of 57, median Karnofsky performance status (KPS) = 90]. The median CD4 count before radiation and temozolomide treatment was 664 cells/mm 3 . The CD4 count nadir occurred 2 months after initiating therapy when 73% of patients had CD4 counts less than 300 cells/mm 3 and 40% had less than 200 cells/mm 3 . CD4 counts remained low throughout the year of follow-up. Patients with CD4 counts less than 200 cells/mm 3 at 2 months had shorter survival than those with higher counts (median: 13.1 vs. 19.7 months, P = 0.002). Median survival was related to CD4 toxicity grades (I = 23.8 months, II = 19.7 months, III–IV = 13.1 months, P = 0.009). The adjusted HR for death attributable to 2-month CD4 count below 200 was 1.66 ( P = 0.03). Eighty-eight percent of deaths resulted from disease progression, whereas only 2.5% were due to infection. Conclusions: Severe reductions in CD4 counts in patients with newly diagnosed HGG treated with radiation and temozolomide treatment are common, treatment-related, long-lasting, and associated with early death from tumor progression. Clin Cancer Res; 17(16); 5473–80. ©2011 AACR .
421 citations
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TL;DR: These data provide the first direct evidence that MCKD2 and FJHN arise from mutation of the UMOD gene and are allelic disorders.
Abstract: Introduction: Medullary cystic kidney disease 2 (MCKD2) and familial juvenile hyperuricaemic nephropathy (FJHN) are both autosomal dominant renal diseases characterised by juvenile onset of hyperuricaemia, gout, and progressive renal failure. Clinical features of both conditions vary in presence and severity. Often definitive diagnosis is possible only after significant pathology has occurred. Genetic linkage studies have localised genes for both conditions to overlapping regions of chromosome 16p11-p13. These clinical and genetic findings suggest that these conditions may be allelic. Aim: To identify the gene and associated mutation(s) responsible for FJHN and MCKD2. Methods: Two large, multigenerational families segregating FJHN were studied by genetic linkage and haplotype analyses to sublocalise the chromosome 16p FJHN gene locus. To permit refinement of the candidate interval and localisation of candidate genes, an integrated physical and genetic map of the candidate region was developed. DNA sequencing of candidate genes was performed to detect mutations in subjects affected with FJHN (three unrelated families) and MCKD2 (one family). Results: We identified four novel uromodulin ( UMOD) gene mutations that segregate with the disease phenotype in three families with FJHN and in one family with MCKD2. Conclusion: These data provide the first direct evidence that MCKD2 and FJHN arise from mutation of the UMOD gene and are allelic disorders. UMOD is a GPI anchored glycoprotein and the most abundant protein in normal urine. We postulate that mutation of UMOD disrupts the tertiary structure of UMOD and is responsible for the clinical changes of interstitial renal disease, polyuria, and hyperuricaemia found in MCKD2 and FJHN.
420 citations
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TL;DR: A new measure of work—family balance is developed and discriminant validity is established between it, work— family conflict, and work-family enrichment and results suggest that balance explains variance beyond that explained by traditional measures of conflict and enrichment.
Abstract: This study deepens our theoretical and practical understanding of work-family balance, defined as the 'accomplishment of role-related expectations that are negotiated and shared between an individual and his/her role-related partners in the work and family domains' (Grzywacz & Carlson, 2007: 458). We develop a new measure of work-family balance and establish discriminant validity between it, work-family conflict, and work-family enrichment. Further, we examine the relationship of work-family balance with six key work and family outcomes. Results suggest that balance explains variance beyond that explained by traditional measures of conflict and enrichment for five of six outcomes tested: job satisfaction, organizational commitment, family satisfaction, family performance, and family functioning. We conclude with a discussion of the applications of our work.
420 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 |