Institution
University of Gothenburg
Education•Gothenburg, Sweden•
About: University of Gothenburg is a education organization based out in Gothenburg, Sweden. It is known for research contribution in the topics: Population & Poison control. The organization has 23855 authors who have published 65241 publications receiving 2606327 citations. The organization is also known as: Göteborg University & Gothenburg University.
Topics: Population, Poison control, Health care, Implant, Dementia
Papers published on a yearly basis
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Duke University1, Cleveland Clinic2, University of Alberta3, Stavanger University Hospital4, Pierre-and-Marie-Curie University5, University of California, San Francisco6, Veterans Health Administration7, University of Glasgow8, Université de Montréal9, University of Gothenburg10, University of North Carolina at Chapel Hill11, Charité12, University of Oslo13, Rabin Medical Center14, Johnson & Johnson15, Emory University16, Universidade Federal do Rio Grande do Sul17, Pontifical Catholic University of Chile18, Linköping University19, MetroHealth20, University of California, Los Angeles21, Janssen Pharmaceutica22, University of Maryland, Baltimore23, University of Florida24, University of Pennsylvania25, Dalhousie University26, Ford Motor Company27, Monash University28, Vilnius University29, University of Washington30, Mexican Social Security Institute31, University of Brescia32, Seoul National University33, Mayo Clinic34, Wrocław Medical University35, Mahidol University36, University of Otago37, University of Groningen38, Thomas Jefferson University39
TL;DR: In this article, Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization and had a small, nonsignificant effect on dyspnea when used in combination with other therapies.
Abstract: A b s t r ac t Background Nesiritide is approved in the United States for early relief of dyspnea in patients with acute heart failure. Previous meta-analyses have raised questions regarding renal toxicity and the mortality associated with this agent. Methods We randomly assigned 7141 patients who were hospitalized with acute heart failure to receive either nesiritide or placebo for 24 to 168 hours in addition to standard care. Coprimary end points were the change in dyspnea at 6 and 24 hours, as measured on a 7-point Likert scale, and the composite end point of rehospitalization for heart failure or death within 30 days. Results Patients randomly assigned to nesiritide, as compared with those assigned to placebo, more frequently reported markedly or moderately improved dyspnea at 6 hours (44.5% vs. 42.1%, P = 0.03) and 24 hours (68.2% vs. 66.1%, P = 0.007), but the prespecified level for significance (P≤0.005 for both assessments or P≤0.0025 for either) was not met. The rate of rehospitalization for heart failure or death from any cause within 30 days was 9.4% in the nesiritide group versus 10.1% in the placebo group (absolute difference, −0.7 percentage points; 95% confidence interval [CI], −2.1 to 0.7; P = 0.31). There were no significant differences in rates of death from any cause at 30 days (3.6% with nesiritide vs. 4.0% with placebo; absolute difference, −0.4 percentage points; 95% CI, −1.3 to 0.5) or rates of worsening renal function, defined by more than a 25% decrease in the estimated glomerular filtration rate (31.4% vs. 29.5%; odds ratio, 1.09; 95% CI, 0.98 to 1.21; P = 0.11). Conclusions Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization and had a small, nonsignificant effect on dyspnea when used in combination with other therapies. It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension. On the basis of these results, nesiritide cannot be recommended for routine use in the broad population of patients with acute heart failure. (Funded by Scios; ClinicalTrials.gov number, NCT00475852.)
1,046 citations
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TL;DR: It is shown that human subcutaneous adipose cells, like 3T3-L1 cells, are target cells for IL-6 and that it may act in concert with other cytokines that also are up-regulated in adipose Cells in insulin resistance.
1,046 citations
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TL;DR: The hypothesis that new connective tissue attachment may form on a previously periodontitis involved root surface provided cells originating from the periodontal ligament are enabled to repopulate the root surface during healing is tested and the concept that theperiodontitis affected root surface is a major preventive factor for new attachment is invalid.
Abstract: The present experiment was undertaken to test the hypothesis that new connective tissue attachment may form on a previously periodontitis involved root surface provided cells originating from the periodontal ligament are enabled to repopulate the root surface during healing. A mandibular incisor with advanced periodontal disease of long standing (the distance between the cemento-enamel junction and the alveolar bone crest was 9 mm) was subjected to periodontal surgery using a technique which during healing prevented the dentogingival epithelium and the gingival connective tissue from reaching contact with the curetted root surface. Preference was hereby given to the periodontal ligament cells to repopulate the previously diseased root surface. After 3 months of healing a block biopsy containing the incisor and surrounding tissue was sampled. The histological analysis revealed that new cementum with inserting principal fibers had formed on the previously diseased root surface. This new attachment extended in coronal direction to a level 5 mm coronal to the alveolar bone crest. This finding suggests that new attachment can be achieved by cells originating from the periodontal ligament and demonstrates that the concept that the periodontitis affected root surface is a major preventive factor for new attachment is invalid.
1,040 citations
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TL;DR: How technological advances have enabled the detection of neurofilament proteins in the blood is considered, and how these proteins consequently have the potential to be easily measured biomarkers of neuroaxonal injury in various neurological conditions are discussed.
Abstract: Neuroaxonal damage is the pathological substrate of permanent disability in various neurological disorders. Reliable quantification and longitudinal follow-up of such damage are important for assessing disease activity, monitoring treatment responses, facilitating treatment development and determining prognosis. The neurofilament proteins have promise in this context because their levels rise upon neuroaxonal damage not only in the cerebrospinal fluid (CSF) but also in blood, and they indicate neuroaxonal injury independent of causal pathways. First-generation (immunoblot) and second-generation (enzyme-linked immunosorbent assay) neurofilament assays had limited sensitivity. Third-generation (electrochemiluminescence) and particularly fourth-generation (single-molecule array) assays enable the reliable measurement of neurofilaments throughout the range of concentrations found in blood samples. This technological advancement has paved the way to investigate neurofilaments in a range of neurological disorders. Here, we review what is known about the structure and function of neurofilaments, discuss analytical aspects and knowledge of age-dependent normal ranges of neurofilaments and provide a comprehensive overview of studies on neurofilament light chain as a marker of axonal injury in different neurological disorders, including multiple sclerosis, neurodegenerative dementia, stroke, traumatic brain injury, amyotrophic lateral sclerosis and Parkinson disease. We also consider work needed to explore the value of this axonal damage marker in managing neurological diseases in daily practice.
1,038 citations
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TL;DR: It is hypothesized that free fatty acids and testosterone might provide a background not only to a defense reaction and primary hypertension, suggested previously, but also to a defeat reaction, which contributes to an endocrine aberration leading to metabolic aberrations and visceral fat accumulation, which in turn leads to disease.
Abstract: Insulin resistance is the cornerstone for the development of non-insulin-dependent diabetes mellitus (NIDDM). Free fatty acids (FFAs) cause insulin resistance in muscle and liver and increase hepatic gluconeogenesis and lipoprotein production and perhaps decrease hepatic clearance of insulin. It is suggested that the depressing effect of insulin on circulating FFA concentration is dependent on the fraction derived from visceral adipocytes, which have a low responsiveness to the antilipolytic effect of insulin. Elevated secretion of cortisol and/or testosterone induces insulin resistance in muscle. This also seems to be the case for low testosterone concentrations in men. In addition, cortisol increases hepatic gluconeogenesis. Cortisol and testosterone have “permissive” effect on adipose lipolysis and therefore amplify lipolytic stimulation; FFA, cortisol, and testosterone thus have powerful combined effects, resulting in insulin resistance and increased hepatic gluconeogenesis. All these factors promoting insulin resistance are active in abdominal visceral obesity, which is closely associated with insulin resistance, NIDDM, and the “ metabolic syndrome.” In addition, the endocrine aberrations may provide a cause for visceral fat accumulation, probably due to regional differences in steroid-hormone-receptor density. In addition to the increased activity along the adrenocorticosteroid axis, there also seem to be signs of increased activity from the central sympathetic nervous system. These are the established endocrine consequences of hypothalamic arousal in the defeat and defense reactions. There is some evidence that suggests an increased prevalence of psychosocial stress factors is associated with visceral distribution of body fat. Therefore, it is hypothesized that such factors might provide a background not only to a defense reaction and primary hypertension, suggested previously, but also to a defeat reaction, which contributes to an endocrine aberration leading to metabolic aberrations and visceral fat accumulation, which in turn leads to disease.
1,033 citations
Authors
Showing all 24120 results
Name | H-index | Papers | Citations |
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Peter J. Barnes | 194 | 1530 | 166618 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Richard H. Friend | 169 | 1182 | 140032 |
Napoleone Ferrara | 167 | 494 | 140647 |
Timothy A. Springer | 167 | 669 | 122421 |
Anders Björklund | 165 | 769 | 84268 |
Hua Zhang | 163 | 1503 | 116769 |
Kaj Blennow | 160 | 1845 | 116237 |
Leif Groop | 158 | 919 | 136056 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Johan G. Eriksson | 156 | 1257 | 123325 |
Naveed Sattar | 155 | 1326 | 116368 |
Paul Elliott | 153 | 773 | 103839 |
Claude Bouchard | 153 | 1076 | 115307 |
Hakon Hakonarson | 152 | 968 | 101604 |