Institution
University of Basel
Education•Basel, Basel-Stadt, Switzerland•
About: University of Basel is a education organization based out in Basel, Basel-Stadt, Switzerland. It is known for research contribution in the topics: Population & Gene. The organization has 25084 authors who have published 52975 publications receiving 2388002 citations. The organization is also known as: Universität Basel & Basel University.
Topics: Population, Gene, Medicine, Context (language use), Transplantation
Papers published on a yearly basis
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TL;DR: Results indicate that the sister of P-glycoprotein is the major canalicular bile salt export pump of mammalian liver.
911 citations
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TL;DR: It is shown that the von Hippel–Lindau tumour suppressor protein pVHL negatively regulates CX CR4 expression owing to its capacity to target hypoxia-inducible factor (HIF) for degradation under normoxic conditions, resulting in HIF-dependent CXCR4 activation.
Abstract: Organ-specific metastasis is governed, in part, by interactions between chemokine receptors on cancer cells and matching chemokines in target organs. For example, malignant breast cancer cells express the chemokine receptor CXCR4 and commonly metastasize to organs that are an abundant source of the CXCR4-specific ligand stromal cell-derived factor-1α (ref. 1). It is still uncertain how an evolving tumour cell is reprogrammed to express CXCR4, thus implementing the tendency to metastasize to specific organs. Here we show that the von Hippel–Lindau tumour suppressor protein pVHL negatively regulates CXCR4 expression owing to its capacity to target hypoxia-inducible factor (HIF) for degradation under normoxic conditions. This process is suppressed under hypoxic conditions, resulting in HIF-dependent CXCR4 activation. An analysis of clear cell renal carcinoma that manifests mutation of the VHL gene in most cases revealed an association of strong CXCR4 expression with poor tumour-specific survival. These results suggest a mechanism for CXCR4 activation during tumour cell evolution and imply that VHL inactivation acquired by incipient tumour cells early in tumorigenesis confers not only a selective survival advantage but also the tendency to home to selected organs.
906 citations
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TL;DR: It turns out that the important contribution of PTI to disease resistance is masked by pathogen virulence effectors that have evolved to suppress it.
Abstract: For many years, research on a suite of plant defense responses that begin when plants are exposed to general microbial elicitors was underappreciated, for a good reason: There has been no critical experimental demonstration of their importance in mediating plant resistance during pathogen infection. Today, these microbial elicitors are named pathogen- or microbe-associated molecular patterns (PAMPs or MAMPs) and the plant responses are known as PAMP-triggered immunity (PTI). Recent studies provide an elegant explanation for the difficulty of demonstrating the role of PTI in plant disease resistance. It turns out that the important contribution of PTI to disease resistance is masked by pathogen virulence effectors that have evolved to suppress it.
900 citations
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University of Basel1, Swiss Tropical and Public Health Institute2, Fudan University3, University of Melbourne4, University of California, San Francisco5, Wellcome Trust Sanger Institute6, Veterinary Laboratories Agency7, King's College London8, University of Ghana9, Centers for Disease Control and Prevention10, Addis Ababa University11, Imperial College London12, National Institute for Medical Research13
TL;DR: Coalescent analyses indicate that MTBC emerged about 70,000 years ago, accompanied migrations of anatomically modern humans out of Africa and expanded as a consequence of increases in human population density during the Neolithic period, consistent with MTBC displaying characteristics indicative of adaptation to both low and high host densities.
Abstract: Tuberculosis caused 20% of all human deaths in the Western world between the seventeenth and nineteenth centuries and remains a cause of high mortality in developing countries. In analogy to other crowd diseases, the origin of human tuberculosis has been associated with the Neolithic Demographic Transition, but recent studies point to a much earlier origin. We analyzed the whole genomes of 259 M. tuberculosis complex (MTBC) strains and used this data set to characterize global diversity and to reconstruct the evolutionary history of this pathogen. Coalescent analyses indicate that MTBC emerged about 70,000 years ago, accompanied migrations of anatomically modern humans out of Africa and expanded as a consequence of increases in human population density during the Neolithic period. This long coevolutionary history is consistent with MTBC displaying characteristics indicative of adaptation to both low and high host densities.
894 citations
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TL;DR: It is recommended that all renal transplant recipients should be screened for BKV replication in the urine every three months during the first two years posttransplant; and if PVAN and concurrent acute rejection is diagnosed, antirejection treatment should be considered, coupled with subsequently reducing immunosuppression.
Abstract: Polyomavirus-associated nephropathy (PVAN) is an emerging cause of kidney transplant failure affecting 1-10% of patients. As uncertainty exists regarding risk factors, diagnosis, and intervention, an independent panel of experts reviewed the currently available evidence and prepared this report. Most cases of PVAN are elicited by BK virus (BKV) in the context of intense immunosuppression. No specific immunosuppressive drug is exclusively associated with PVAN, but most cases reported to date arise while the patient is on triple immunosuppressive combinations, often comprising tacrolimus and/or mycophenolate mofetil plus corticosteroids. Immunologic control of polyomavirus replication can be achieved by reducing, switching, and/or discontinuing components of the immunosuppressive regimen, but the individual's risk of rejection should be considered. The success rate of this intervention is increased with earlier diagnosis. Therefore, it is recommended that all renal transplant recipients should be screened for BKV replication in the urine: 1) every three months during the first two years posttransplant; 2) when allograft dysfunction is noted; and 3) when allograft biopsy is performed. A positive screening result should be confirmed in <4 weeks and assessed by quantitative assays (e.g. BKV DNA or RNA load in plasma or urine). Definitive diagnosis of PVAN requires allograft biopsy. If PVAN and concurrent acute rejection is diagnosed, antirejection treatment should be considered, coupled with subsequently reducing immunosuppression. The antiviral cidofovir is not approved for PVAN, but investigational use at low doses (0.25-0.33 mg/kg intravenously biweekly) without probenicid should be considered for refractory cases. Retransplantation after renal allograft loss to PVAN remains a treatment option for patients clearing polyomavirus replication.
886 citations
Authors
Showing all 25374 results
Name | H-index | Papers | Citations |
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Yang Yang | 171 | 2644 | 153049 |
Martin Karplus | 163 | 831 | 138492 |
Frank J. Gonzalez | 160 | 1144 | 96971 |
Paul Emery | 158 | 1314 | 121293 |
Matthias Egger | 152 | 901 | 184176 |
Don W. Cleveland | 152 | 444 | 84737 |
Ashok Kumar | 151 | 5654 | 164086 |
Kurt Wüthrich | 143 | 739 | 103253 |
Thomas J. Smith | 140 | 1775 | 113919 |
Robert Huber | 139 | 671 | 73557 |
Peter Robmann | 135 | 1438 | 97569 |
Ernst Detlef Schulze | 133 | 670 | 69504 |
Michael Levine | 129 | 586 | 55963 |
Claudio Santoni | 129 | 1027 | 80598 |
Pablo Garcia-Abia | 126 | 989 | 78690 |