Institution
Tufts University
Education•Medford, Massachusetts, United States•
About: Tufts University is a education organization based out in Medford, Massachusetts, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 32800 authors who have published 66881 publications receiving 3451152 citations. The organization is also known as: Tufts College & Universitatis Tuftensis.
Topics: Population, Medicine, Health care, Cancer, Context (language use)
Papers published on a yearly basis
Papers
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TL;DR: Nerve fiber layer thickness can be reproducibly measured using OCT; internal is superior to external fixation; each circle diameter tested provides adequate reproducibility.
686 citations
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TL;DR: The findings of the present study suggest that apoptosis may modulate the cellularity of lesions that produce human vascular obstruction, particularly those with evidence of more extensive proliferative activity.
Abstract: Background Apoptosis has been recognized in normal, including rapidly proliferating, cell populations and is inferred to be potentially responsible for the maintenance of stable cell numbers in tissues with various degrees of proliferative activity. Previous studies performed in rats indicated that despite the persistence of a relatively high level of injury-induced proliferative activity, total arterial smooth muscle content at 12 weeks remained unchanged from that measured at 2 weeks, suggesting that accrual of vascular smooth muscle cells is mitigated by cell death. The extent to which apoptosis may be observed in human atherosclerosis and/or restenosis, however, has not been previously established.
Methods and Results We performed immunohistochemical studies on 56 specimens retrieved from patients undergoing directional atherectomy for primary atherosclerotic lesions or recurrent arterial narrowing after percutaneous revascularization (restenosis). Immunohistochemical staining disclosed evidence of apoptosis in 35 (63%) of the 56 specimens studied. When present, immunohistochemical evidence of apoptosis was typically limited to <2% of cells in the specimen. The finding of apoptosis, however, was not distributed equally among four groups of specimens studied. Specimens retrieved from patients with restenosis were more frequently observed to contain foci of apoptosis than specimens retrieved from patients with primary atherosclerotic lesions. Among 14 peripheral arterial specimens from patients with restenosis, 13 (93%) contained foci of apoptosis; in contrast, apoptosis was observed in only 6 (43%) of 14 peripheral specimens from patients with primary lesions ( P =.0046). Among coronary arterial specimens, apoptosis was observed in 12 (86%) of 14 specimens from patients with restenosis versus 6 (29%) of 14 specimens from patients with primary obstructions ( P <.0075).
Conclusions Apoptosis is a feature of human vascular pathology, including restenotic lesions and, to a lesser extent, primary atherosclerotic lesions. The findings of the present study suggest that apoptosis may modulate the cellularity of lesions that produce human vascular obstruction, particularly those with evidence of more extensive proliferative activity.
685 citations
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Tufts University1, San Diego State University2, Kaiser Permanente3, Anschutz Medical Campus4, Pennsylvania State University5, Georgia Institute of Technology6, University of Hawaii7, University of South Florida8, Kraft Foods9, University of North Carolina at Chapel Hill10, Indiana University11, University of Nevada, Reno12
TL;DR: This research highlights the need to understand more fully the rationale behind the rapid decline in physical activity in middle-aged people over a longer period of time.
Abstract: Sarah L. Booth, Ph.D., Vitamin K Laboratory, Jean Mayer USDAHuman Nutrition Research Center on Aging at Tufts University, Boston, MA; James F. Sallis, Ph.D., F.A.C.S.M., Department ofPsychology, San Diego State University, San Diego, CA; Cheryl Ritenbaugh, Ph.D., M.P.H., Kaiser Permanente Center for Health Research, Portland, O R James 0. Hill, Ph.D., Center for Human Nutrition, University of Colorado Health Sciences Center, Denver, CO; Leann L. Birch, Ph.D., Department ofHuman Development and Family Studies, Pennsylvania State University, University Park, PA; Lawrence D. Frank, Ph.D., College OfArchitecture, Georgia Institute of Technology, Atlanta, GA; Karen Glanz, Ph.D., M.P.H., Cancer Research Center of Hawaii, University of Hawaii, Honolulu, HI; David A. Himmelgreen, Ph.D., Department ofAnthropology, University of South Florida, Tampa, FL; Michael Mudd, Corporate Affairs, Kraft Foods, Inc., Northfield, IL; Barry M. Popkin, Ph.D., Department ofNutrition, Carolina Population Center, University of North Carolina, Chapel Hill, NC; Karyl A. Rickard, Ph.D., R.D., C.S.P., F.A.D.A., Nutrition and Dietetics Program, School ofAllied Health Sciences, Indiana University School of Medicine, Indianapolis, IN; Sachiko St. Jeor, Ph.D., R.D., Nutrition Education and Research Program, University of Nevada School of Medicine, Reno, W, Nicholas P. Hays, M.S., Energy Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA.
685 citations
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TL;DR: Overall incidences of ocular and nonocular adverse events and serious adverse events, including the Anti-Platelet Trialists' Collaboration-defined arterial thromboembolic events and vascular deaths, were similar across treatment groups, and IAI was well-tolerated.
684 citations
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TL;DR: Investigation of fibroblasts from SMA patients with various clinical severities of SMA showed a moderate reduction in the amount of SMN protein, particularly in type I (most severe) patients, which is consistent with features of this motor neuron disease.
Abstract: The 38 kDa survival motor neuron (SMN) protein is encoded by two ubiquitously expressed genes: telomeric SMN (SMN(T)) and centromeric SMN (SMN(C)). Mutations in SMN(T), but not SMN(C), cause proximal spinal muscular atrophy (SMA), an autosomal recessive disorder that results in loss of motor neurons. SMN is found in the cytoplasm and nucleus. The nuclear form is located in structures termed gems. Using a panel of anti-SMN antibodies, we demonstrate that the SMN protein is expressed from both the SMN(T) and SMN(C) genes. Western blot analysis of fibroblasts from SMA patients with various clinical severities of SMA showed a moderate reduction in the amount of SMN protein, particularly in type I (most severe) patients. Immunocytochemical analysis of SMA patient fibroblasts indicates a significant reduction in the number of gems in type I SMA patients and a correlation of the number of gems with clinical severity. This correlation to phenotype using primary fibroblasts may serve as a useful diagnostic tool in an easily accessible tissue. SMN is expressed at high levels in brain, kidney and liver, moderate levels in skeletal and cardiac muscle, and low levels in fibroblasts and lymphocytes. In SMA patients, the SMN level was moderately reduced in muscle and lymphoblasts. In contrast, SMN was expressed at high levels in spinal cord from normals and non-SMA disease controls, but was reduced 100-fold in spinal cord from type I patients. The marked reduction of SMN in type I SMA spinal cords is consistent with the features of this motor neuron disease. We suggest that disruption of SMN(T) in type I patients results in loss of SMN from motor neurons, resulting in the degeneration of these neurons.
684 citations
Authors
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Name | H-index | Papers | Citations |
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Walter C. Willett | 334 | 2399 | 413322 |
Frank B. Hu | 250 | 1675 | 253464 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
John Q. Trojanowski | 226 | 1467 | 213948 |
Peter Libby | 211 | 932 | 182724 |
David Baltimore | 203 | 876 | 162955 |
Eric B. Rimm | 196 | 988 | 147119 |
Lewis C. Cantley | 196 | 748 | 169037 |
Bernard Rosner | 190 | 1162 | 147661 |
Charles A. Dinarello | 190 | 1058 | 139668 |
William B. Kannel | 188 | 533 | 175659 |
Scott M. Grundy | 187 | 841 | 231821 |
John P. A. Ioannidis | 185 | 1311 | 193612 |
David H. Weinberg | 183 | 700 | 171424 |
Joel Schwartz | 183 | 1149 | 109985 |