Institution
Houston Methodist Hospital
Healthcare•Houston, Texas, United States•
About: Houston Methodist Hospital is a healthcare organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 9825 authors who have published 18872 publications receiving 779830 citations. The organization is also known as: The Methodist Hospital.
Topics: Population, Cancer, Medicine, Transplantation, Breast cancer
Papers published on a yearly basis
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TL;DR: It is shown here, however, that substrata coated with an isolated cell‐binding domain of fibronectin are not sufficient for complete cell adhesion; cells attach and spread but, unlike those adhering to intact fibronECTin, they do not form stress fibres terminating in focal adhesions.
Abstract: Fibronectin has been shown previously to promote complete cell adhesion in the absence of other serum components or de novo protein synthesis. Recently a sequence of four amino acids from the cell-binding domain of fibronectin has been termed the 'cell recognition site' of this multidomain molecule since it mediates cell attachment and inhibits cell adhesion to intact fibronectin. We show here, however, that substrata coated with an isolated cell-binding domain of fibronectin are not sufficient for complete cell adhesion; cells attach and spread but, unlike those adhering to intact fibronectin, they do not form stress fibres terminating in focal adhesions. An additional external stimulus is needed for this cytoskeletal reorganisation and may be provided by one of two heparin-binding fragments of fibronectin. The two 'signals' required for complete adhesion need not be provided simultaneously since focal adhesion formation can be promoted by stimulating cells pre-spread on a cell-binding fragment of fibronectin with a soluble heparin-binding fragment. This second stimulation may involve cell membrane heparan sulphate proteoglycans.
426 citations
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TL;DR: Observations in several regions of interest in limbic and paralimbic brain regions in emotional responding are reviewed, to determine if common or segregated patterns of activations exist in different emotions and across various emotional tasks.
Abstract: Neuroimaging studies with positron emission tomography and functional magnetic resonance imaging have begun to describe the functional neuroanatomy of human emotion. Taken separately, specific studies vary in task dimensions and in type(s) of emotion studied, and are limited by statistical power and sensitivity. By examining findings across studies in a meta-analysis, we sought to determine if common or segregated patterns of activations exist in different emotions and across various emotional tasks. We surveyed over 55 positron emission tomography and functional magnetic resonance imaging activation studies, which investigated emotion in healthy subjects. This paper will review observations in several regions of interest in limbic (eg, amygdala, anterior cingulate cortex) and paralimbic (eg, medial prefrontal cortex, insula) brain regions in emotional responding.
424 citations
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TL;DR: In this review, the most recent and important multiscale cancer modeling works that have successfully established a mechanistic link between different biological scales are introduced and biophysical, biochemical, and biomechanical factors are considered in these models.
Abstract: Simulating cancer behavior across multiple biological scales in space and time, i.e., multiscale cancer modeling, is increasingly being recognized as a powerful tool to refine hypotheses, focus experiments, and enable more accurate predictions. A growing number of examples illustrate the value of this approach in providing quantitative insights in the initiation, progression, and treatment of cancer. In this review, we introduce the most recent and important multiscale cancer modeling works that have successfully established a mechanistic link between different biological scales. Biophysical, biochemical, and biomechanical factors are considered in these models. We also discuss innovative, cutting-edge modeling methods that are moving predictive multiscale cancer modeling toward clinical application. Furthermore, because the development of multiscale cancer models requires a new level of collaboration among scientists from a variety of fields such as biology, medicine, physics, mathematics, engineering, and computer science, an innovative Web-based infrastructure is needed to support this growing community.
423 citations
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TL;DR: It is demonstrated for the first time in a model of chronic neurodegeneration that morphological activation of microglia and astroglia does not predict glial function, and that the presence of CD4+ T cells provides supportive neuroprotection by modulating the trophic/cytotoxic balance of glia.
Abstract: Neuroinflammation, marked by gliosis and infiltrating T cells, is a prominent pathological feature in diverse models of dominantly inherited neurodegenerative diseases. Recent evidence derived from transgenic mice ubiquitously overexpressing mutant Cu2+/Zn2+ superoxide dismutase (mSOD1), a chronic neurodegenerative model of inherited amyotrophic lateral sclerosis (ALS), indicates that glia with either a lack of or reduction in mSOD1 expression enhance motoneuron protection and slow disease progression. However, the contribution of T cells that are present at sites of motoneuron injury in mSOD1 transgenic mice is not known. Here we show that when mSOD1 mice were bred with mice lacking functional T cells or CD4+ T cells, motoneuron disease was accelerated, accompanied by unexpected attenuated morphological markers of gliosis, increased mRNA levels for proinflammatory cytokines and NOX2, and decreased levels of trophic factors and glial glutamate transporters. Bone marrow transplants reconstituted mice with T cells, prolonged survival, suppressed cytotoxicity, and restored glial activation. These results demonstrate for the first time in a model of chronic neurodegeneration that morphological activation of microglia and astroglia does not predict glial function, and that the presence of CD4+ T cells provides supportive neuroprotection by modulating the trophic/cytotoxic balance of glia. These glial/T-cell interactions establish a novel target for therapeutic intervention in ALS and possibly other neurodegenerative diseases.
422 citations
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TL;DR: This chapter discusses the development of Guidelines, further preoperative testing to Assess Coronary Risk, and management of Specific Preoperative Cardiovascular Condition.
Abstract: Table of ContentsI. IntroductionA. Development of GuidelinesB. General ApproachC. Preoperative Clinical EvaluationII. Further Preoperative Testing to Assess Coronary RiskA. Clinical MarkersB. Functional CapacityC. Surgery-Specific RiskIII. Management of Specific Preoperative Cardiovascular Condition
421 citations
Authors
Showing all 9852 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Nancy A. Jenkins | 155 | 741 | 101587 |
Neal G. Copeland | 154 | 726 | 100130 |
Joseph Jankovic | 153 | 1146 | 93840 |
Christopher P. Cannon | 151 | 1118 | 108906 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Peter B. Jones | 145 | 1857 | 94641 |
Stephen F. Badylak | 133 | 530 | 57083 |
Christie M. Ballantyne | 132 | 1012 | 77651 |
Jeremiah Stamler | 127 | 655 | 70751 |
Kamyar Kalantar-Zadeh | 118 | 1025 | 56187 |
Shahrokh F. Shariat | 118 | 1637 | 58900 |
Stephen Safe | 116 | 784 | 60588 |