Institution
Lancaster General Hospital
Healthcare•Lancaster, Pennsylvania, United States•
About: Lancaster General Hospital is a healthcare organization based out in Lancaster, Pennsylvania, United States. It is known for research contribution in the topics: Population & Health care. The organization has 310 authors who have published 345 publications receiving 11626 citations.
Topics: Population, Health care, Myocardial infarction, MEDLINE, Cancer
Papers published on a yearly basis
Papers
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TL;DR: Two scales to measure stages of change for exercise behavior and exercise self-efficacy indicated employees who had not yet begun to exercise, in contrast with those who exercised regularly, had little confidence in their ability to exercise.
Abstract: This study examined the application of constructs concerning stage of readiness to change and self-efficacy to exercise. We developed two scales to measure stages of change for exercise behavior. Prevalence information on a sample of 1,063 government employees and 429 hospital employees was then obtained. Next, the ability of a questionnaire measuring exercise self-efficacy to differentiate employees according to stage of readiness to change was tested. Results from both stages-of-change scales revealed that 34–39% of employees were regularly participating in physical activity. Scores on efficacy items significantly differentiated employees at most stages. Results indicated employees who had not yet begun to exercise, in contrast with those who exercised regularly, had little confidence in their ability to exercise. Continued work at understanding the stages of exercise behavior and exercise self-efficacy could yield important information for enhancing exercise adoption and adherence.
1,760 citations
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TL;DR: The CRT improved functional status in patients indicated for an ICD who also have symptomatic HF and intraventricular conduction delay and a subgroup of patients with advanced HF consistently demonstrated improvement across all functional status end points.
707 citations
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Shawnee Mission Medical Center1, Good Samaritan Hospital2, Emory University Hospital3, University of Bonn4, Imperial College London5, Vita-Salute San Raffaele University6, Lancaster General Hospital7, Columbia University8, Rhode Island Hospital9, University of Bern10, London Health Sciences Centre11, Scripps Health12, University of California, San Francisco13
TL;DR: Closing the LAA using the PLAATO system is feasible and can be performed at acceptable risk and may become an alternative in patients with AF and a contraindication for lifelong anticoagulation treatment.
450 citations
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TL;DR: Clinical and immunological investigations of contactin‐associated protein‐like 2 (Caspr2), an autoantigen of encephalitis and peripheral nerve hyperexcitability (PNH) previously attributed to voltage‐gated potassium channels (VGKC), are reported.
Abstract: Objective
To report clinical and immunological investigations of contactin-associated protein-like 2 (Caspr2), an autoantigen of encephalitis and peripheral nerve hyperexcitability (PNH) previously attributed to voltage-gated potassium channels (VGKC).
367 citations
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TL;DR: The results reveal the power of coupling new genotyping technologies to population-specific genetic knowledge and robust clinical data and show evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS.
Abstract: The Clinic for Special Children (CSC) has integrated biochemical and molecular methods into a rural pediatric practice serving Old Order Amish and Mennonite (Plain) children. Among the Plain people, we have used single nucleotide polymorphism (SNP) microarrays to genetically map recessive disorders to large autozygous haplotype blocks (mean = 4.4 Mb) that contain many genes (mean = 79). For some, uninformative mapping or large gene lists preclude disease-gene identification by Sanger sequencing. Seven such conditions were selected for exome sequencing at the Broad Institute; all had been previously mapped at the CSC using low density SNP microarrays coupled with autozygosity and linkage analyses. Using between 1 and 5 patient samples per disorder, we identified sequence variants in the known disease-causing genes SLC6A3 and FLVCR1, and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS. Our results reveal the power of coupling new genotyping technologies to population-specific genetic knowledge and robust clinical data.
280 citations
Authors
Showing all 330 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jacques Devière | 88 | 557 | 25881 |
Jeffrey H. Peters | 67 | 202 | 15675 |
Muhammad Tahir | 65 | 1636 | 23892 |
Alan H. Maurer | 50 | 175 | 7656 |
Frederick B. Rogers | 47 | 173 | 7772 |
Erik G. Puffenberger | 41 | 86 | 6701 |
Kevin A. Strauss | 40 | 106 | 5737 |
Robert MacLaren | 38 | 130 | 4002 |
James F. Spann | 37 | 94 | 4205 |
Anthony A. Gaspari | 37 | 143 | 4638 |
D. Holmes Morton | 35 | 63 | 4585 |
Gregory B. Haber | 34 | 150 | 3539 |
Anthony J. Comerota | 33 | 71 | 5741 |
William E. Dager | 31 | 100 | 2980 |
Robert A. Ganz | 30 | 83 | 3850 |