Institution
University of Paris
Education•Paris, France•
About: University of Paris is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Medicine. The organization has 102426 authors who have published 174180 publications receiving 5041753 citations. The organization is also known as: Sorbonne.
Topics: Population, Medicine, Context (language use), Transplantation, Gene
Papers published on a yearly basis
Papers
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TL;DR: A-type granites have long been recognized as a distinct group of granites, the term A-type was coined first less than thirty years ago as discussed by the authors, and they are fairly common at shallower depths, especially at the subvolcanic level where they form ring complexes rooting caldera volcanoes.
1,071 citations
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15 Feb 2018TL;DR: It is shown that a bilingual dictionary can be built between two languages without using any parallel corpora, by aligning monolingual word embedding spaces in an unsupervised way.
1,068 citations
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TL;DR: Novel beta-AR agonists having high thermogenic, antiobesity, and antidiabetic activities in animal models are among the most potent stimulators of the beta 3-AR.
Abstract: Since the classification of beta-adrenergic receptors (beta-ARs) into beta 1 and beta 2 subtypes, additional beta-ARs have been implicated in the control of various metabolic processes by catecholamines. A human gene has been isolated that encodes a third beta-AR, here referred to as the "beta 3-adrenergic receptor." Exposure of eukaryotic cells transfected with this gene to adrenaline or noradrenaline promotes the accumulation of adenosine 3',5'-monophosphate; only 2 of 11 classical beta-AR blockers efficiently inhibited this effect, whereas two others behaved as beta 3-AR agonists. The potency order of beta-AR agonists for the beta 3-AR correlates with their rank order for stimulating various metabolic processes in tissues where atypical adrenergic sites are thought to exist. In particular, novel beta-AR agonists having high thermogenic, antiobesity, and antidiabetic activities in animal models are among the most potent stimulators of the beta 3-AR.
1,066 citations
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Brown University1, University of New South Wales2, University of Barcelona3, Columbia University4, Harvard University5, International AIDS Society6, Stanford University7, University of British Columbia8, University of California, San Diego9, University of Alabama at Birmingham10, Federal University of Rio de Janeiro11, University of Colorado Denver12, Istituto Superiore di Sanità13, University of Paris14, University of California, San Francisco15
TL;DR: The availability of new antiretroviral drugs has expanded treatment choices and the importance of adherence, emerging long-term complications of therapy, recognition and management of antireTroviral failure, and new monitoring tools are addressed.
Abstract: Objective To update recommendations for antiretroviral therapy for adult human
immunodeficiency virus type 1 (HIV-1) infection, based on new information
and drugs that are available.
Participants
A 17-member international physician panel with antiretroviral research
and HIV patient care experience initially convened by the International AIDS
Society–USA in December 1995.
Evidence
Available clinical and basic science data including phase 3 controlled
trials; data on clinical, virologic, and immunologic end points; research
conference reports; HIV pathogenesis data; and panel expert opinion. Recommendations
were limited to therapies available (US Food and Drug Administration approved)
in 1999.
Consensus Process
The panel assesses new research reports and interim results and regularly
meets to consider how the new data affect therapy recommendations. Recommendations
are updated via full-panel consensus. Guidelines are presented as recommendations
if the supporting evidence warrants routine use in the particular situation
and as considerations if data are preliminary or incomplete but suggestive.
Conclusions
The availability of new antiretroviral drugs has expanded treatment
choices. The importance of adherence, emerging long-term complications of
therapy, recognition and management of antiretroviral failure, and new monitoring
tools are addressed. Optimal care requires individualized management and ongoing
attention to relevant scientific and clinical information in the field.
1,066 citations
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TL;DR: Evidence is presented that a gene encoding myosin VIIA is responsible for USH1B and that USH IB appears as a primary cytoskeletal protein defect, which implicate the genes encoding other unconventional myosins and their interacting proteins as candidates for other genetic forms of Usher syndrome.
Abstract: USHER syndrome represents the association of a hearing impairment with retinitis pigmentosa1 and is the most frequent cause of deaf–blindness in humans. It is inherited as an autosomal recessive trait which is clinically and genetically heterogeneous2,3. Some patients show abnormal organization of microtubules in the axoneme of their photoreceptors cells (connecting cilium)4–6, nasal ciliar cells7 and sperm cells5, as well as widespread degeneration of the organ of Corti8. Usher syndrome type 1 (USH1) is characterized by a profound congenital sensorineural hearing loss, constant vestibular dysfunction and prepubertal onset of retinitis pigmentosa. Of three different genes responsible for USH19–11,USH1B maps to 11q13.5 (ref. 10) and accounts for about 75% of USH1 patients2,3. The mouse deafness shaker-1 (shl) mutation has been localized to the homologous murine region12,13. Taking into account the cytoskeletal abnormalities in USH patients, the identification of a gene encoding an unconventional myosin as a candidate for shaker-1(ref. 14) led us to consider the human homo-logue as a good candidate for the gene that is defective in USH1B. Here we present evidence that a gene encoding myosin VIIA is responsible for USH1B. Two different premature stop codons, a six-base-pair deletion and two different missense mutations were detected in five unrelated families. In one of these families, the mutations were identified in both alleles. These mutations, which are located at the amino-terminal end of the motor domain of the protein, are likely to result in the absence of a functional protein. Thus USH IB appears as a primary cytoskeletal protein defect. These results implicate the genes encoding other unconventional myosins and their interacting proteins as candidates for other genetic forms of Usher syndrome.
1,063 citations
Authors
Showing all 102613 results
Name | H-index | Papers | Citations |
---|---|---|---|
Guido Kroemer | 236 | 1404 | 246571 |
David H. Weinberg | 183 | 700 | 171424 |
Paul M. Thompson | 183 | 2271 | 146736 |
Chris Sander | 178 | 713 | 233287 |
Sophie Henrot-Versille | 171 | 957 | 157040 |
Richard H. Friend | 169 | 1182 | 140032 |
George P. Chrousos | 169 | 1612 | 120752 |
Mika Kivimäki | 166 | 1515 | 141468 |
Martin Karplus | 163 | 831 | 138492 |
William J. Sandborn | 162 | 1317 | 108564 |
Darien Wood | 160 | 2174 | 136596 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Paul Emery | 158 | 1314 | 121293 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Joao Seixas | 153 | 1538 | 115070 |