Institution
Loma Linda University
Education•Loma Linda, California, United States•
About: Loma Linda University is a education organization based out in Loma Linda, California, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 9220 authors who have published 13485 publications receiving 447094 citations. The organization is also known as: University of Loma Linda.
Topics: Population, Medicine, Poison control, Transplantation, Health care
Papers published on a yearly basis
Papers
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TL;DR: Allium sativum (garlic) has been recognized not only as a spice but also as a substance which exerts a control on microorganisms which holds a promising position as a broad-spectrum therapeutic agent.
146 citations
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TL;DR: Open partial trapeziectomy and interpositional arthroplasty have proven to be effective in ameliorating the symptoms of carpometacarpal joint arthritis of the thumb.
Abstract: Open partial trapeziectomy and interpositional arthroplasty have proven to be effective in ameliorating the symptoms of carpometacarpal joint arthritis of the thumb. Surgical technique of arthroscopic partial resection of the trapezium and interpositional arthroplasty is described. Thirty-three interpositional arthroplasties were carried out arthroscopically. Autogenous tendon graft. Gortex (WL Gore & Associates, Inc. Flagstaff, AZ) and fascia lata allograft were used as interpositional material; 87.8% of patients got relief from pain. Average postoperative pinch strength was 11 lbs. No ligament reconstruction was required because the capsule was left intact. The procedures were done on an outpatient basis and all patients were discharged the same day. There were no complications associated with radial sensory nerve.
146 citations
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TL;DR: Less than half of eyes treated for DME with intravitreous ranibizumab have persistent central-involved DME through 24 weeks after initiating treatment, and longer-term visual acuity outcomes appear to be slightly worse than in the 60% in which DME does not persist.
Abstract: Importance The prevalence of persistent diabetic macular edema (DME) after months of anti–vascular endothelial growth factor therapy and its effect on visual acuity are unknown. Objective To assess subsequent outcomes of eyes with DME persisting for 24 weeks after initiating treatment with 0.5 mg of ranibizumab. Design, Setting, and Participants We performed post hoc, exploratory analyses of a randomized clinical trial from March 20, 2007, through January 29, 2014, from 117 of 296 eyes (39.5%) randomly assigned to receive ranibizumab with persistent DME (central subfield thickness ≥250 μm on time domain optical coherence tomography) through the 24-week visit. Interventions Four monthly intravitreous injections of ranibizumab and then as needed per protocol. Main Outcomes and Measures Cumulative 3-year probabilities of chronic persistent DME (failure to achieve a central subfield thickness Results The probability of chronic persistent DME among eyes with persistent DME at the 24-week visit decreased from 100% at the 32-week visit to 81.1% (99% CI, 69.6%-88.6%), 55.8% (99% CI, 42.9%-66.9%), and 40.1% (99% CI, 27.4%-52.4%) at the 1-, 2-, and 3-year visits, respectively. At 3 years, visual acuity improved in eyes with and without chronic persistent DME through the follow-up period, respectively, by a mean of 7 letters and 13 letters from baseline. Among 40 eyes with chronic persistent edema through 3 years, 17 (42.5%) (99% CI, 23.1%-63.7%) gained 10 letters or more from baseline, whereas 5 (12.5%) (99% CI, 2.8%-31.5%) lost 10 letters or more from baseline. Conclusions and Relevance These data suggest less than half of eyes treated for DME with intravitreous ranibizumab have persistent central-involved DME through 24 weeks after initiating treatment. Among the 40% that then have chronic persistent central-involved DME through 3 years, longer-term visual acuity outcomes appear to be slightly worse than in the 60% in which DME does not persist. Nevertheless, when following the treatment protocol used in this trial among eyes with vision impairment from DME, long-term improvement in visual acuity from baseline is typical and substantial (≥2-line) loss of visual acuity is likely uncommon through 3 years, even when central-involved DME chronically persists.
146 citations
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Wake Forest University1, Loma Linda University2, University of Nebraska Medical Center3, Children's National Medical Center4, Yeshiva University5, Boston Children's Hospital6, Emory University7, University of Southern California8, Riley Hospital for Children9, Cleveland Clinic10, Bristol-Myers Squibb11, University of Louisville12, Cornell University13, McGill University14, Wright State University15
TL;DR: The 1987 pediatric brain death guidelines were reviewed and revised and recommendations were developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system.
Abstract: Objective:To review and revise the 1987 pediatric brain death guidelines.Methods:Relevant literature was reviewed. Recommendations were developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system.Conclusions and Recommendations:1) Determination of brain death
146 citations
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TL;DR: Clinical data demonstrate that let-7 can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival, and it is made the case that assessing its tumor presence is crucial when choosing therapy.
Abstract: Abnormal regulation and expression of microRNAs (miRNAs) has been documented in various diseases including cancer. The miRNA let-7 (MIRLET7) family controls developmental timing and differentiation. Let-7 loss contributes to carcinogenesis via an increase in its target oncogenes and stemness factors. Let-7 targets include genes regulating the cell cycle, cell signaling, and maintenance of differentiation. It is categorized as a tumor suppressor because it reduces cancer aggressiveness, chemoresistance, and radioresistance. However, in rare situations let-7 acts as an oncogene, increasing cancer migration, invasion, chemoresistance, and expression of genes associated with progression and metastasis. Here, we review let-7 function as tumor suppressor and oncogene, considering let-7 as a potential diagnostic and prognostic marker, and a therapeutic target for cancer treatment. We explain the complex regulation and function of different let-7 family members, pointing to abnormal processes involved in carcinogenesis. Let-7 is a promising option to complement conventional cancer therapy, but requires a tumor specific delivery method to avoid toxicity. While let-7 therapy is not yet established, we make the case that assessing its tumor presence is crucial when choosing therapy. Clinical data demonstrate that let-7 can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival.
145 citations
Authors
Showing all 9287 results
Name | H-index | Papers | Citations |
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Bruce L. Miller | 163 | 1153 | 115975 |
Jonathan I. Epstein | 138 | 1121 | 80975 |
Tony L. Yaksh | 123 | 806 | 60898 |
David M. Livingston | 118 | 312 | 58142 |
William B. Isaacs | 117 | 521 | 58187 |
Alan W. Partin | 111 | 710 | 54213 |
David N. Herndon | 108 | 1227 | 54888 |
Edward R. Laws | 105 | 722 | 39822 |
David C. Bellinger | 98 | 452 | 35449 |
Pedram Argani | 97 | 372 | 35607 |
Michael W. Steffes | 96 | 341 | 43260 |
Gary K. Steinberg | 94 | 529 | 31259 |
Michael S. Gazzaniga | 92 | 372 | 35305 |
David J. Baylink | 90 | 425 | 29109 |
Jesse B. Jupiter | 90 | 543 | 26480 |