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排序方式: 共有5308条查询结果,搜索用时 15 毫秒
91.
Masateru Takigawa Jatin Relan Ruairidh Martin Steven Kim Takeshi Kitamura Antonio Frontera Ghassen Cheniti Konstantinos Vlachos Grégoire Massoullié Claire A. Martin Nathaniel Thompson Michael Wolf Felix Bourier Anna Lam Josselin Duchateau Nicolas Klotz Thomas Pambrun Arnaud Denis Pierre Jaïs 《Heart rhythm》2018,15(12):1853-1861
92.
93.
Akiyama Shintaro Cohen Nathaniel A. Steinberg Joshua M. Friedberg Scott Cohen Russell D. 《Digestive diseases and sciences》2022,67(3):805-809
Digestive Diseases and Sciences - 相似文献
94.
David A. Talan Sukhjit S. Takhar Anusha Krishnadasan William R. Mower Daniel J. Pallin Manish Garg Jon Femling Richard E. Rothman Johanna C. Moore Alan E. Jones Frank Lovecchio Jonathan Jui Mark T. Steele Amy M. Stubbs William K. Chiang Gregory J. Moran 《Annals of emergency medicine》2021,77(1):32-43
95.
Failure of epoprostenol (prostacyclin, PGI2) to inhibit platelet aggregation and to prevent restenosis after coronary angioplasty: results of a randomised placebo controlled trial. 总被引:2,自引:0,他引:2
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A. H. Gershlick D. Spriggins S. W. Davies Y. D. Syndercombe Court J. Timmins A. D. Timmis M. T. Rothman C. Layton R. Balcon 《Heart (British Cardiac Society)》1994,71(1):7-15
OBJECTIVE--To study the effect of epoprostenol (prostacyclin, PGI2) given before, during, and for 36 h after coronary angioplasty on restenosis at six months and to evaluate the transcardiac gradient of platelet aggregation before and after percutaneous transluminal coronary angioplasty (PTCA) in treated and placebo groups. DESIGN--Double blind placebo controlled randomised study. PATIENTS--135 patients with successful coronary angioplasty. METHODS--Intravenous infusion of PGI2 (4 ng/kg/ml) or buffer was started before balloon angioplasty and continued for 36 hours. Platelet aggregation was measured in blood from the aorta and coronary sinus before and after PTCA in each group. Routine follow up was at six months with repeat angiography and there was quantitative assessment of all angiograms (those undertaken within the follow up period and at routine follow up). PRESENTATION OF RESULTS--Restenosis rates in treated and placebo groups determined according to the National Heart, Lung and Blood Institute definition IV. Comparison at follow up between the effect of treatment on mean absolute luminal diameter and mean absolute follow up diameter in the placebo group. Comparison of acute gain and late loss between groups. RESULTS--Of 125 patients available for assessment 23 were re-admitted because of angina within the follow up period. Quantitative angiography showed restenosis in 15 (10 in the PGI2 group and five in the placebo group). Of 105 patients evaluated at six month angiography there was restenosis in nine more in the PGI2 group and 18 more in the placebo group. Total restenosis rates (for patients) were 29.2% for PGI2 and 38.3% for placebo (NS). The mean absolute gain in luminal diameter was 1.84 (0.76) mm in the PGI2 group and 1.58 (0.56) mm in the placebo group (p = 0.04); the late loss in the PGI2 group was also greater (0.65 (0.94) mm vs 0.62 (0.89) mm (NS) and there was no significant difference in final luminal diameter at follow up between the two groups (1.83 (0.88) mm v 1.59 (0.60) mm). The transcardiac gradient of quantitative platelet aggregation increased after PTCA in both groups, indicating that PGI2 in this dose did not affect angioplasty-induced platelet activation. Mean (SD) platelet activation indices in the PGI2 group were pre PTCA aorta 8.4 (4.1) v coronary sinus 8.8 (4.0) (p = 0.001) and post PTCA aorta 8.9(3.0) v coronary sinus 12.9 (5.7) (p = 0.001). In the placebo group the values were pre PTCA aorta 7.6 (3.3) v coronary sinus 7.4 (3.6) (p = 0.001) and post PTCA aorta 7.6(2.8) v coronary sinus 11.2(4.3) (p = 0.001). CONCLUSION--The dose of PGI2 given was designed to limit side effects and as a short-term infusion did not significantly decrease the six month restenosis rate after PTCA. The sample size, which was determined by the original protocol and chosen because of the potency of the agent being tested, would have detected only a 50% reduction in restenosis rate. There was, however, no effect in the treated patients on the increased platelet aggregation seen in placebo group as a result of angioplasty. Angioplasty is a powerful stimulus to blood factor activation. Powerful agents that prevent local platelet adhesion and aggregation are likely to be required to reduce restenosis. 相似文献
96.
Individuals with diabetes mellitus have cardiovascular disease (CVD) mortality comparable to nondiabetics who have suffered
a myocardial infarction or stroke. Aggressive management of risk factors such as hypertension, dyslipidemia, and platelet
dysfunction in persons with diabetes has been shown to reduce morbidity and mortality in prospective randomized controlled
clinical trials. Accordingly, there are national mandates to lower blood pressure to less than 130/85 mm Hg, reduce low-density
lipoprotein cholesterol to less than 100 mg/dL, and institute aspirin therapy in adult patients with diabetes. Although not
definitively shown to reduce CVD, there are also recommendations to control the level of glycemia, as well. This article discusses
CVD risk factors in the diabetic patient with hypertension. 相似文献
97.
Giulio Innamorati Hamid M. Sadeghi Nathaniel T. Tran Mariel Birnbaumer 《Proceedings of the National Academy of Sciences of the United States of America》1998,95(5):2222-2226
Receptor recycling plays a critical role in the regulation of cellular responsiveness to environmental stimuli. Agonist-promoted phosphorylation of G protein-coupled receptors has been related to their desensitization, internalization, and sequestration. Dephosphorylation of internalized G protein-coupled receptors by cytoplasmic phosphatases has been shown to be pH-dependent, and it has been postulated to be necessary for receptors to recycle to the cell surface. The internalized V2 vasopressin receptor (V2R) expressed in HEK 293 cells is an exception to this hypothesis because it does not recycle to the plasma membrane for hours after removal of the ligand. Because this receptor is phosphorylated only by G protein-coupled receptor kinases (GRKs), the relationship between recycling and GRK-mediated phosphorylation was examined. A nonphosphorylated V2R, truncated upstream of the GRK phosphorylation sites, rapidly returned to the cell surface after removal of vasopressin. Less-drastic truncations of V2R revealed the presence of multiple phosphorylation sites and suggested a key role for a serine cluster present at the C terminus. Replacement of any one of Ser-362, Ser-363, or Ser-364 with Ala allowed quantitative recycling of full-length V2R without affecting the extent of internalization. Examination of the stability of phosphate groups incorporated into the recycling S363A mutant V2Rs revealed that the recycling receptor was dephosphorylated after hormone withdrawal, whereas the wild-type V2R was not, providing molecular evidence for the hypothesis that GRK sites must be dephosphorylated prior to receptor recycling. These experiments uncovered a role for GRK phosphorylation in intracellular sorting and revealed a GRK-dependent anchoring domain that blocks V2R recycling. 相似文献
98.
A Novel KCNJ13 Nonsense Mutation and Loss of Kir7.1 Channel Function Causes Leber Congenital Amaurosis (LCA16)
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Bikash R. Pattnaik Nathaniel York Simran Brar John Chiang De‐Ann M. Pillers Elias I. Traboulsi 《Human mutation》2015,36(7):720-727
Mutations in the KCNJ13 gene that encodes the inwardly rectifying potassium channel Kir7.1 cause snowflake vitreoretinal degeneration (SVD) and leber congenital amaurosis (LCA). Kir7.1 controls the microenvironment between the photoreceptors and the retinal pigment epithelium (RPE) and also contributes to the function of other organs such as uterus and brain. Heterologous expressions of the mutant channel have suggested a dominant‐negative loss of Kir7.1 function in SVD, but parallel studies in LCA16 have been lacking. Herein, we report the identification of a novel nonsense mutation in the second exon of the KCNJ13 gene that leads to a premature stop codon in association with LCA16. We have determined that the mutation results in a severe truncation of the Kir7.1 C‐terminus, alters protein localization, and disrupts potassium currents. Coexpression of the mutant and wild‐type channel has no negative influence on the wild‐type channel function, consistent with the normal clinical phenotype of carrier individuals. By suppressing Kir7.1 function in mice, we were able to reproduce the severe LCA electroretinogram phenotype. Thus, we have extended the observation that Kir7.1 mutations are associated with vision disorders to include novel insights into the molecular mechanism of disease pathobiology in LCA16. 相似文献
99.
Elaine Wethington Christopher Eccleston Geri Gay Rachael Gooberman-Hill Patricia Schofield Elizabeth Bacon Wen Dombrowski Robert Jamison Max Rothman Lauren Meador Cara Kenien Karl Pillemer Corinna Löckenhoff M. Carrington Reid 《The journal of pain》2018,19(12):1416-1423
The rapid growth of mobile health (mHealth) devices holds substantial potential for improving care and care outcomes in all patient populations, including older adults with pain. However, existing research reflects a substantial gap in knowledge about how to design, evaluate, and disseminate devices to optimally address the many challenges associated with managing pain in older persons. Given these knowledge gaps, we sought to develop a set of practice-based research priorities to facilitate innovation in this field. We employed the Cornell Research-Practice Consensus Workshop Model, an evidence-based approach to generating research priorities. Sixty participants attended the conference, where stakeholder groups included older adults with pain and their caregivers, behavioral and social scientists, healthcare providers, pain experts, and specialists in mHealth and health policy. Participants generated 13 recommendations classified into 2 categories: 1) implications for designing research on mHealth among older adults (eg, conduct research on ways to enhance accessibility of mHealth tools among diverse groups of older adults with pain, expand research on mHealth sensing applications), and 2) implementation of mHealth technology into practice and associated regulatory issues (eg, promote research on ways to initiate/sustain patient behavior change, expand research on mHealth cybersecurity and privacy issues).
Perspective
This report highlights a set of research priorities in the area of mHealth and later-life pain derived from the joint perspectives of researchers and key stakeholder groups. Addressing these priorities could help to improve the quality of care delivered to older adults with pain. 相似文献100.