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 & Transplantation. 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, Transplantation, Gene, Poison control, Quantum dot
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University of California, San Francisco1, University of Basel2, University of British Columbia3, McGill University4, Vita-Salute San Raffaele University5, Queen Mary University of London6, University of Düsseldorf7, Icahn School of Medicine at Mount Sinai8, University of Miami9, Hoffmann-La Roche10, Genentech11, Baylor College of Medicine12
TL;DR: Among patients with primary progressive multiple sclerosis, ocrelizumab was associated with lower rates of clinical and MRI progression than placebo; there was no clinically significant difference between groups in the rates of serious adverse events and serious infections.
Abstract: BackgroundAn evolving understanding of the immunopathogenesis of multiple sclerosis suggests that depleting B cells could be useful for treatment. We studied ocrelizumab, a humanized monoclonal antibody that selectively depletes CD20-expressing B cells, in the primary progressive form of the disease. MethodsIn this phase 3 trial, we randomly assigned 732 patients with primary progressive multiple sclerosis in a 2:1 ratio to receive intravenous ocrelizumab (600 mg) or placebo every 24 weeks for at least 120 weeks and until a prespecified number of confirmed disability progression events had occurred. The primary end point was the percentage of patients with disability progression confirmed at 12 weeks in a time-to-event analysis. ResultsThe percentage of patients with 12-week confirmed disability progression was 32.9% with ocrelizumab versus 39.3% with placebo (hazard ratio, 0.76; 95% confidence interval [CI], 0.59 to 0.98; P=0.03). The percentage of patients with 24-week confirmed disability progression w...
1,220 citations
TL;DR: It is hypothesized that the life form “tree” is limited at treeline altitudes by the potential investment, rather than production, of assimilates (growth as such,rather than photosynthesis or the carbon balance, being limited), and root zone temperature, though largely unknown, is likely to be most critical.
Abstract: In this review I first compile data for the worldwide position of climate-driven alpine treelines. Causes for treeline formation are then discussed with a global perspective. Available evidence suggests a combination of a general thermal boundary for tree growth, with regionally variable “modulatory” forces, including the presence of certain taxa. Much of the explanatory evidence found in the literature relates to these modulatory aspects at regional scales, whereas no good explanations emerged for the more fundamental global pattern related to temperature per se, on which this review is focused. I hypothesize that the life form “tree” is limited at treeline altitudes by the potential investment, rather than production, of assimilates (growth as such, rather than photosynthesis or the carbon balance, being limited). In shoots coupled to a cold atmosphere, meristem activity is suggested to be limited for much of the time, especially at night. By reducing soil heat flux during the growing season the forest canopy negatively affects root zone temperature. The lower threshold temperature for tissue growth and development appears to be higher than 3°C and lower than 10°C, possibly in the 5.5–7.5°C range, most commonly associated with seasonal means of air temperature at treeline positions. The physiological and developmental mechanisms responsible have yet to be analyzed. Root zone temperature, though largely unknown, is likely to be most critical.
1,218 citations
TL;DR: To identify other miRNA genes in pathogenic viruses, a new miRNA gene prediction method with small-RNA cloning from several virus-infected cell types was combined and predicted miRNAs in several large DNA viruses.
Abstract: Epstein-Barr virus (EBV or HHV4), a member of the human herpesvirus (HHV) family, has recently been shown to encode microRNAs (miRNAs). In contrast to most eukaryotic miRNAs, these viral miRNAs do not have close homologs in other viral genomes or in the genome of the human host. To identify other miRNA genes in pathogenic viruses, we combined a new miRNA gene prediction method with small-RNA cloning from several virus-infected cell types. We cloned ten miRNAs in the Kaposi sarcoma-associated virus (KSHV or HHV8), nine miRNAs in the mouse gammaherpesvirus 68 (MHV68) and nine miRNAs in the human cytomegalovirus (HCMV or HHV5). These miRNA genes are expressed individually or in clusters from either polymerase (pol) II or pol III promoters, and share no substantial sequence homology with one another or with the known human miRNAs. Generally, we predicted miRNAs in several large DNA viruses, and we could neither predict nor experimentally identify miRNAs in the genomes of small RNA viruses or retroviruses.
1,208 citations
University of Alabama at Birmingham1, College of Health Sciences, Bahrain2, University of Hohenheim3, Jimma University4, Queensland Government5, University of Queensland6, Mekelle University7, Institute for Health Metrics and Evaluation8, University of Cartagena9, Komfo Anokye Teaching Hospital10, University of Manitoba11, University of Gondar12, University of São Paulo13, Aga Khan University14, New Generation University College15, Public Health Foundation of India16, Duy Tan University17, Centers for Disease Control and Prevention18, Bielefeld University19, Imperial College London20, University of Basel21, Swiss Tropical and Public Health Institute22, Boston Children's Hospital23, Baylor College of Medicine24, Yonsei University25, Tehran University of Medical Sciences26, Jordan University of Science and Technology27, University of London28, University of Melbourne29, Aintree University Hospitals NHS Foundation Trust30, University of Liverpool31, Martin Luther University of Halle-Wittenberg32, United Nations Population Fund33, Iran University of Medical Sciences34, University of Ulm35, University of Sydney36, University of Porto37, University of British Columbia38, A.T. Still University39, Golestan University40, Harvard University41, Case Western Reserve University42, Marshall University43, University of KwaZulu-Natal44, AIIMS, New Delhi45, Utkal University46, Haramaya University47, Queensland University of Technology48, Jagiellonian University Medical College49, Wrocław Medical University50, Johns Hopkins University51, Hanoi Medical University52, National Research University – Higher School of Economics53, Norwegian Institute of Public Health54, University of Bergen55, University of Tromsø56, Karolinska Institutet57, Kyoto University58, Jackson State University59, Wuhan University60, University of Washington61
TL;DR: In this article, the authors report results of the Global Burden of Disease (GBD) 2015 study on primary liver cancer incidence, mortality, and disability-adjusted life-years (DALYs) for 195 countries or territories from 1990 to 2015, and present global, regional, and national estimates on the burden of liver cancer attributable to hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol, and an “other” group that encompasses residual causes.
Abstract: Importance Liver cancer is among the leading causes of cancer deaths globally. The most common causes for liver cancer include hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol use. Objective To report results of the Global Burden of Disease (GBD) 2015 study on primary liver cancer incidence, mortality, and disability-adjusted life-years (DALYs) for 195 countries or territories from 1990 to 2015, and present global, regional, and national estimates on the burden of liver cancer attributable to HBV, HCV, alcohol, and an “other” group that encompasses residual causes. Design, Settings, and Participants Mortality was estimated using vital registration and cancer registry data in an ensemble modeling approach. Single-cause mortality estimates were adjusted for all-cause mortality. Incidence was derived from mortality estimates and the mortality-to-incidence ratio. Through a systematic literature review, data on the proportions of liver cancer due to HBV, HCV, alcohol, and other causes were identified. Years of life lost were calculated by multiplying each death by a standard life expectancy. Prevalence was estimated using mortality-to-incidence ratio as surrogate for survival. Total prevalence was divided into 4 sequelae that were multiplied by disability weights to derive years lived with disability (YLDs). DALYs were the sum of years of life lost and YLDs. Main Outcomes and Measures Liver cancer mortality, incidence, YLDs, years of life lost, DALYs by etiology, age, sex, country, and year. Results There were 854 000 incident cases of liver cancer and 810 000 deaths globally in 2015, contributing to 20 578 000 DALYs. Cases of incident liver cancer increased by 75% between 1990 and 2015, of which 47% can be explained by changing population age structures, 35% by population growth, and −8% to changing age-specific incidence rates. The male-to-female ratio for age-standardized liver cancer mortality was 2.8. Globally, HBV accounted for 265 000 liver cancer deaths (33%), alcohol for 245 000 (30%), HCV for 167 000 (21%), and other causes for 133 000 (16%) deaths, with substantial variation between countries in the underlying etiologies. Conclusions and Relevance Liver cancer is among the leading causes of cancer deaths in many countries. Causes of liver cancer differ widely among populations. Our results show that most cases of liver cancer can be prevented through vaccination, antiviral treatment, safe blood transfusion and injection practices, as well as interventions to reduce excessive alcohol use. In line with the Sustainable Development Goals, the identification and elimination of risk factors for liver cancer will be required to achieve a sustained reduction in liver cancer burden. The GBD study can be used to guide these prevention efforts.
1,208 citations
TL;DR: All human solid tumor cells require CD47 expression to suppress phagocytic innate immune surveillance and elimination, showing that CD47 is a commonly expressed molecule on all cancers, its function to blockphagocytosis is known, and blockade of its function leads to tumor cell phagcytosis and elimination.
Abstract: CD47, a "don't eat me" signal for phagocytic cells, is expressed on the surface of all human solid tumor cells Analysis of patient tumor and matched adjacent normal (nontumor) tissue revealed that CD47 is overexpressed on cancer cells CD47 mRNA expression levels correlated with a decreased probability of survival for multiple types of cancer CD47 is a ligand for SIRPα, a protein expressed on macrophages and dendritic cells In vitro, blockade of CD47 signaling using targeted monoclonal antibodies enabled macrophage phagocytosis of tumor cells that were otherwise protected Administration of anti-CD47 antibodies inhibited tumor growth in orthotopic immunodeficient mouse xenotransplantation models established with patient tumor cells and increased the survival of the mice over time Anti-CD47 antibody therapy initiated on larger tumors inhibited tumor growth and prevented or treated metastasis, but initiation of the therapy on smaller tumors was potentially curative The safety and efficacy of targeting CD47 was further tested and validated in immune competent hosts using an orthotopic mouse breast cancer model These results suggest all human solid tumor cells require CD47 expression to suppress phagocytic innate immune surveillance and elimination These data, taken together with similar findings with other human neoplasms, show that CD47 is a commonly expressed molecule on all cancers, its function to block phagocytosis is known, and blockade of its function leads to tumor cell phagocytosis and elimination CD47 is therefore a validated target for cancer therapies
1,206 citations
Authors
Showing all 25374 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| 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 |