Institution
Case Western Reserve University
Education•Cleveland, Ohio, United States•
About: Case Western Reserve University is a education organization based out in Cleveland, Ohio, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 54617 authors who have published 106568 publications receiving 5071613 citations. The organization is also known as: Case & Case Western.
Topics: Population, Cancer, Health care, Medicine, Transplantation
Papers published on a yearly basis
Papers
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Karolinska Institutet1, University of Oxford2, University of Toronto3, Centre national de la recherche scientifique4, University of California, Berkeley5, Los Alamos National Laboratory6, Tsinghua University7, University of Science and Technology of China8, Weizmann Institute of Science9, Scripps Research Institute10, Novartis11, Argonne National Laboratory12, Yeshiva University13, Brookhaven National Laboratory14, Rutgers University15, Case Western Reserve University16, University of California, San Francisco17, Columbia University18, Max Delbrück Center for Molecular Medicine19, New York University20
TL;DR: This review presents methods that could be applied at the outset of any project, a prioritized list of alternate strategies and a list of pitfalls that trip many new investigators.
Abstract: In selecting a method to produce a recombinant protein, a researcher is faced with a bewildering array of choices as to where to start. To facilitate decision-making, we describe a consensus 'what to try first' strategy based on our collective analysis of the expression and purification of over 10,000 different proteins. This review presents methods that could be applied at the outset of any project, a prioritized list of alternate strategies and a list of pitfalls that trip many new investigators.
778 citations
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TL;DR: It is demonstrated that KS/CS-PG is inhibitory to embryonic dorsal root ganglia neurites in vitro and that complete inhibition requires contributions from both KS and CS moieties.
777 citations
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TL;DR: Policy makers need to look beyond such areas as health information technology to shape a coordinated and focused national policy in support of patient-centered care.
Abstract: The phrase “patient-centered care” is in vogue, but its meaning is poorly understood. This article describes patient-centered care, why it matters, and how policy makers can advance it in practice. Ultimately, patient-centered care is determined by the quality of interactions between patients and clinicians. The evidence shows that patient-centered care improves disease outcomes and quality of life, and that it is critical to addressing racial, ethnic, and socioeconomic disparities in health care and health outcomes. Policy makers need to look beyond such areas as health information technology to shape a coordinated and focused national policy in support of patient-centered care. This policy should help health professionals acquire and maintain skills related to patient-centered care, and it should encourage organizations to cultivate a culture of patient-centeredness.
777 citations
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TL;DR: Green tea may protect against cancer by causing cell cycle arrest and inducing apoptosis, and needs to be evaluated in human trials.
Abstract: Background and Purpose: The polyphenolic compounds present in green tea show cancer chemopreventive effects in many animal tumor models. Epidemiologic studies have also suggested that green tea consumption might be effective in the prevention of certain human cancers. We investigated the effect of green tea polyphenols and the major constituent, epigallocatechin-3-gallate, on the induction of apoptosis (programmed cell death) and regulation of cell cycle in human and mouse carcinoma cells. Methods: Human epidermoid carcinoma cells (cell line A431), human carcinoma keratinocyte (cell line HaCaT), human prostate carcinoma cells (cell line DU145), mouse lymphoma cells (cell line L5178Y), and normal human epidermal keratinocytes (NHEKs) were used. Apoptosis was assessed by 1) the formation of internucleosomal DNA fragments by agarose gel electrophoresis, 2) confocal microscopy, and 3) flow cytometry after tagging the DNA fragments by fluorescence label. The distribution of cells in different phases of the cell cycle was analyzed by flow cytometry. Results: Treatment of A431 cells with green tea polyphenols and its components, epigallocatechin-3-gallate, epigallocatechin, and epicatechin-3-gallate, resulted in the formation of internucleo-somal DNA fragments, characteristic of apoptosis. Treatment with epigallocatechin-3-gallate also resulted in apoptosis in HaCaT, L5178Y, and DU145 cells, but not in NHEK. Confocal microscopy and flow cytometry confirmed the findings. The DNA cell cycle analysis showed that in A431 cells, epigallocatechin-3-gallate treatment resulted in arrest in the G 0 -G 1 phase of the cell cycle and a dose-dependent apoptosis. Conclusions: Green tea may protect against cancer by causing cell cycle arrest and inducing apoptosis. It needs to be evaluated in human trials.
776 citations
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TL;DR: The arguments for a causal role for either amyloid deposition or cerebrovascular pathology as the primary trigger in the development of non-genetic AD are summarised.
Abstract: The cause of Alzheimer's disease (AD) is unknown. This gap in knowledge has created a stumbling block in the search for a genuinely effective treatment or cure for this dementia. This article summarises the arguments for a causal role for either amyloid deposition or cerebrovascular pathology as the primary trigger in the development of non-genetic AD. A bare-bones survey of the published research reveals no compelling evidence that amyloid deposition is neurotoxic in human beings or that it results in neurodegenerative changes involving synaptic, metabolic, or neuronal loss in human or transgenic-mouse brains. By contrast, the data supporting AD as a primary vascular disorder are more convincing. Findings suggesting a vascular cause of AD come from epidemiological, neuroimaging, pathological, pharmacotherapeutic, and clinical studies. The consensus of these studies indicates that chronic brain hypoperfusion is linked to AD risk factors, AD preclinical detection and pharmacotherapeutic action of AD symptoms.
776 citations
Authors
Showing all 54953 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert Langer | 281 | 2324 | 326306 |
Bert Vogelstein | 247 | 757 | 332094 |
Zhong Lin Wang | 245 | 2529 | 259003 |
John Q. Trojanowski | 226 | 1467 | 213948 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
Peter Libby | 211 | 932 | 182724 |
David Baltimore | 203 | 876 | 162955 |
Carlo M. Croce | 198 | 1135 | 189007 |
Ronald Klein | 194 | 1305 | 149140 |
Eric J. Topol | 193 | 1373 | 151025 |
Paul M. Thompson | 183 | 2271 | 146736 |
Yusuke Nakamura | 179 | 2076 | 160313 |
Dennis J. Selkoe | 177 | 607 | 145825 |
David L. Kaplan | 177 | 1944 | 146082 |
Evan E. Eichler | 170 | 567 | 150409 |