Institution
University of Alabama at Birmingham
Education•Birmingham, Alabama, United States•
About: University of Alabama at Birmingham is a education organization based out in Birmingham, Alabama, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 38523 authors who have published 86775 publications receiving 3930642 citations. The organization is also known as: UAB & The University of Alabama at Birmingham.
Topics: Population, Medicine, Cancer, Poison control, Health care
Papers published on a yearly basis
Papers
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University of Texas MD Anderson Cancer Center1, University of Chicago2, Roswell Park Cancer Institute3, Seattle Cancer Care Alliance4, University of Southern Denmark5, University of New South Wales6, Jikei University School of Medicine7, University of Oklahoma8, Kaplan Medical Center9, University of Utah10, Texas Oncology11, University of Pennsylvania12, University of Ulsan13, University of Alabama at Birmingham14, University of Oxford15, Washington University in St. Louis16, Kaiser Permanente17, Memorial Sloan Kettering Cancer Center18, AbbVie19
TL;DR: Across all trial populations, a regimen of carboplatin, paclitaxel, and veliparib induction therapy followed by veliporib maintenance therapy led to significantly longer progression-free survival than carboplati plus pac Litaxel induction therapy alone.
Abstract: Background Data are limited regarding the use of poly(adenosine diphosphate [ADP]–ribose) polymerase inhibitors, such as veliparib, in combination with chemotherapy followed by maintenance...
557 citations
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University of Gothenburg1, Florey Institute of Neuroscience and Mental Health2, University of Newcastle3, University of Wisconsin-Madison4, University of Bonn5, Washington University in St. Louis6, University of Alabama at Birmingham7, University of Amsterdam8, Utrecht University9, Royal Netherlands Academy of Arts and Sciences10, University of California11
TL;DR: It is argued that targeting astrocytes may represent an effective therapeutic strategy for Alexander disease, neurotrauma, stroke, epilepsy and Alzheimer’s disease as well as other neurodegenerative diseases.
Abstract: The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases. As this concept is changing, so is also the perceived role of astrocytes in the healthy and diseased brain and spinal cord. We have started to unravel the different signalling mechanisms that trigger specific molecular, morphological and functional changes in reactive astrocytes that are critical for repairing tissue and maintaining function in CNS pathologies, such as neurotrauma, stroke, or neurodegenerative diseases. An increasing body of evidence shows that the effects of astrogliosis on the neural tissue and its functions are not uniform or stereotypic, but vary in a context-specific manner from astrogliosis being an adaptive beneficial response under some circumstances to a maladaptive and deleterious process in another context. There is a growing support for the concept of astrocytopathies in which the disruption of normal astrocyte functions, astrodegeneration or dysfunctional/maladaptive astrogliosis are the primary cause or the main factor in neurological dysfunction and disease. This review describes the multiple roles of astrocytes in the healthy CNS, discusses the diversity of astroglial responses in neurological disorders and argues that targeting astrocytes may represent an effective therapeutic strategy for Alexander disease, neurotrauma, stroke, epilepsy and Alzheimer's disease as well as other neurodegenerative diseases.
557 citations
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TL;DR: The clinical manifestations, recent molecular and genetic findings, and current and developing therapies for managing clinical problems associated with neurofibromatosis type 1 are described.
Abstract: Neurofibromatosis type 1 (NF1) is an autosomal dominant condition with a worldwide incidence of 1 per 2500 to 3000 individuals. Caused by a germ-line‐ inactivating mutation in the NF1 gene on chromosome 17, the disease is associated with increased morbidity and mortality. In the past several years, significant progress has been made in standardizing management of the major clinical features of neurofibromatosis type 1. Moreover, improved understanding of how the neurofibromatosis type 1 protein, neurofibromin, regulates cell growth recently provided insight into the pathogenesis of the disease and has led to the development of new therapies. In this review, we describe the clinical manifestations, recent molecular and genetic findings, and current and developing therapies for managing clinical problems associated with neurofibromatosis type 1. Pediatrics 2009;123:124‐133
555 citations
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TL;DR: It is suggested that Wnt/β-catenin signaling in osteoblasts coordinates postnatal bone acquisition by controlling the differentiation and activity of both osteoblast and osteoclasts.
554 citations
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TL;DR: The CES-DC showed poor reliability and validity in the children alone but had good psychometric properties for the adolescents, and more validational research is required before standard clinical use can be recommended.
Abstract: Psychometric characteristics of the Center for Epidemiological Studies Depression Scale for Children (CES-DC) were evaluated with 148 child and adolescent psychiatric inpatients. Test-retest reliability, internal consistency, and concurrent validity were adequate. Principal components analysis identified three distinct factors: behavioral and cognitive components of depression and a happiness dimension. However, subsequent factor scores and CES-DC total scores were unable to discriminate DSM-III diagnoses, including depressive and nondepressive categories. The CES-DC showed poor reliability and validity in the children alone but had good psychometric properties for the adolescents. More validational research is required before standard clinical use can be recommended.
554 citations
Authors
Showing all 38940 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rudolf Jaenisch | 206 | 606 | 178436 |
Joel Schwartz | 183 | 1149 | 109985 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
Gregg L. Semenza | 168 | 502 | 130316 |
David R. Jacobs | 165 | 1262 | 113892 |
Hua Zhang | 163 | 1503 | 116769 |
David R. Holmes | 161 | 1624 | 114187 |
David Cella | 156 | 1258 | 106402 |
Elaine S. Jaffe | 156 | 828 | 112412 |
Michael A. Matthay | 151 | 998 | 98687 |
Lawrence Corey | 146 | 773 | 78105 |
Barton F. Haynes | 144 | 911 | 79014 |
Douglas D. Richman | 142 | 633 | 82806 |
Kjell Fuxe | 142 | 1479 | 89846 |