Institution
University of Modena and Reggio Emilia
Education•Modena, Italy•
About: University of Modena and Reggio Emilia is a education organization based out in Modena, Italy. It is known for research contribution in the topics: Population & Transplantation. The organization has 8179 authors who have published 22418 publications receiving 671337 citations. The organization is also known as: Università degli Studi di Modena e Reggio Emilia & Universita degli Studi di Modena e Reggio Emilia.
Topics: Population, Transplantation, Stem cell, Cancer, Breast cancer
Papers published on a yearly basis
Papers
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TL;DR: In patients with chronic hepatitis C with or without cirrhosis, peginterferon alfa‐2a (relative to IFN) significantly reduced fibrosis, and the beneficial effects of peginerferon on liver histology are closely related to virologic response.
226 citations
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Seton Medical Center1, Saint Francis University2, Queen Mary University of London3, University of Illinois at Chicago4, Veterans Health Administration5, University of Toronto6, National and Kapodistrian University of Athens7, University Hospitals of Leicester NHS Trust8, University of Colorado Denver9, Katholieke Universiteit Leuven10, University of Modena and Reggio Emilia11, Maastricht University12
TL;DR: The findings demonstrate large differences among pulmonary rehabilitation programmes across continents for all aspects, including the setting, the case mix of individuals with a chronic respiratory disease, composition of the pulmonary rehabilitation team, completion rates, methods of referral and types of reimbursement.
Abstract: The aim was to study the overall content and organisational aspects of pulmonary rehabilitation programmes from a global perspective in order to get an initial appraisal on the degree of heterogeneity worldwide. A 12-question survey on content and organisational aspects was completed by representatives of pulmonary rehabilitation programmes that had previously participated in the European Respiratory Society (ERS) COPD Audit. Moreover, all ERS members affiliated with the ERS Rehabilitation and Chronic Care and/or Physiotherapists Scientific Groups, all members of the American Association of Cardiovascular and Pulmonary Rehabilitation, and all American Thoracic Society Pulmonary Rehabilitation Assembly members were asked to complete the survey via multiple e-mailings. The survey has been completed by representatives of 430 centres from 40 countries. The findings demonstrate large differences among pulmonary rehabilitation programmes across continents for all aspects that were surveyed, including the setting, the case mix of individuals with a chronic respiratory disease, composition of the pulmonary rehabilitation team, completion rates, methods of referral and types of reimbursement. The current findings stress the importance of future development of processes and performance metrics to monitor pulmonary rehabilitation programmes, to be able to start international benchmarking, and to provide recommendations for international standards based on evidence and best practice.
226 citations
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TL;DR: The mechanisms responsible for producing abnormal spermatozoa in the ejaculate are relatively unknown as discussed by the authors. But many studies have shown the presence of nuclear DNA strand breaks in human ejaculated spermatoza and the abnormal persistence of apoptotic marker proteins.
Abstract: The mechanisms responsible for producing abnormal spermatozoa in the ejaculate are relatively unknown. Numerous studies have now shown the presence of nuclear DNA strand breaks in human ejaculated spermatozoa and the abnormal persistence of apoptotic marker proteins. The reason why human spermatozoa, in particular from men with abnormal semen parameters, possess these abnormalities is still not clear. Two processes that have been linked to the presence of nuclear DNA strand breaks in spermatozoa are anomalies in apoptosis during spermatogenesis or problems in the replacement of histones with protamines during spermiogenesis. Understanding the mechanisms responsible for producing abnormal spermatozoa in the human will improve knowledge about certain causes of male infertility.
225 citations
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TL;DR: The results suggest that FSHD results from inappropriate overexpression of FRG1 in skeletal muscle, which leads to abnormal alternative splicing of specific pre-mRNAs.
Abstract: Facioscapulohumeral muscular dystrophy is a human muscle disorder linked to deletions of a repeat unit on chromosome 4 An experiment in which transgenic mice were engineered to overexpress three skeletal muscle genes linked to this deletion shows that overexpression of one of them, FRG1, causes the signs of muscular dystrophy Too much FRG1 leads to abnormal splicing of pre-mRNAs in skeletal muscle Future studies will explore how this leads to abnormal spine curvature and other symptoms And the availability of a mouse model for this type of muscular dystrophy will be of value in evaluating therapeutic strategies Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant neuromuscular disorder that is not due to a classical mutation within a protein-coding gene1,2 Instead, almost all FSHD patients carry deletions of an integral number of tandem 33-kilobase repeat units, termed D4Z4, located on chromosome 4q35 (ref 3) D4Z4 contains a transcriptional silencer whose deletion leads to inappropriate overexpression in FSHD skeletal muscle of 4q35 genes located upstream of D4Z4 (ref 4) To identify the gene responsible for FSHD pathogenesis, we generated transgenic mice selectively overexpressing in skeletal muscle the 4q35 genes FRG1, FRG2 or ANT1 We find that FRG1 transgenic mice develop a muscular dystrophy with features characteristic of the human disease; by contrast, FRG2 and ANT1 transgenic mice seem normal FRG1 is a nuclear protein and several lines of evidence suggest it is involved in pre-messenger RNA splicing5,6,7 We find that in muscle of FRG1 transgenic mice and FSHD patients, specific pre-mRNAs undergo aberrant alternative splicing Collectively, our results suggest that FSHD results from inappropriate overexpression of FRG1 in skeletal muscle, which leads to abnormal alternative splicing of specific pre-mRNAs
225 citations
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TL;DR: It is concluded that, ghrelin is produced by well-defined cell types, which in the past had been labelled differently in various mammals mostly because of the different size of their secretory granule.
Abstract: Ghrelin is a new gastric peptide involved in food intake control and growth hormone release. We aimed to assess its cell localisation in man during adult and fetal life and to clarify present interspecies inconsistencies of gastric endocrine cell types. A specific serum generated against amino acids 13–28 of ghrelin was tested on fetal and adult gastric mucosa and compared with ghrelin in situ hybridisation. Immunogold electron microscopy was performed on normal human, rat and dog adult stomach. Ghrelin cells were detected in developing gut, pancreas and lung from gestational week 10 and in adult human, rat and dog gastric mucosa. By immunogold electron microscopy, gastric ghrelin cells showed distinctive morphology and hormone reactivity in respect to histamine enterochromaffin-like, somatostatin D, glucagon A or serotonin enterochromaffin cells. Ghrelin cells were characterised by round, compact, electron-dense secretory granules of P/D1 type in man (mean diameter 147±30 nm), A-like type in the rat (183±37 nm) and X type in the dog (273±49 nm). It is concluded that, ghrelin is produced by well-defined cell types, which in the past had been labelled differently in various mammals mostly because of the different size of their secretory granule. In man ghrelin cells develop during early fetal life.
225 citations
Authors
Showing all 8322 results
Name | H-index | Papers | Citations |
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Carlo M. Croce | 198 | 1135 | 189007 |
Gregory Y.H. Lip | 169 | 3159 | 171742 |
Geoffrey Burnstock | 141 | 1488 | 99525 |
Peter M. Rothwell | 134 | 779 | 67382 |
Claudio Franceschi | 120 | 856 | 59868 |
Lorenzo Galluzzi | 118 | 477 | 71436 |
Leonardo M. Fabbri | 109 | 566 | 60838 |
David N. Reinhoudt | 107 | 1082 | 48814 |
Stefano Pileri | 100 | 635 | 43369 |
Andrea Bizzeti | 99 | 1168 | 46880 |
Brian K. Shoichet | 98 | 281 | 40313 |
Dante Gatteschi | 97 | 727 | 48729 |
Roberta Sessoli | 95 | 424 | 41458 |
Thomas A. Buchholz | 93 | 494 | 33409 |
Pier Luigi Zinzani | 92 | 857 | 35476 |