Institution
Hebron University
Education•Hebron, Palestinian Territory•
About: Hebron University is a education organization based out in Hebron, Palestinian Territory. It is known for research contribution in the topics: Population & Cancer. The organization has 2714 authors who have published 4180 publications receiving 163736 citations.
Papers published on a yearly basis
Papers
More filters
••
TL;DR: This paper aims to demonstrate the efforts towards in-situ applicability of EMMARM, as to provide real-time information about concrete mechanical properties such as E-modulus and compressive strength.
Abstract: Safia Hussain, BSc, Dorottya M Berki, BSc, Siew-Eng Choon, MRCP, A David Burden, MD, FRCP, Michael H Allen, PhD, Juan I Arostegui, MD, PhD, Antonio Chaves, MD, Michael Duckworth, Alan D Irvine, MD, Maja Mockenhaupt, MD, PhD, Alexander A Navarini, MD, PhD, Marieke MB Seyger, MD, PhD, Pere Soler-Palacin, MD, PhD, Christa Prins, MD, Laurence Valeyrie-Allanore, MD, M Asuncion Vicente, MD, Richard C Trembath, FMedSci, Catherine H Smith, MD, FRCP, Jonathan N Barker, MD, FRCP,* Francesca Capon, PhD,*
97 citations
••
TL;DR: This study analyzed the effect of intensity domain adaptation on the recently proposed CNN-based MS lesion segmentation method and found the effectiveness of the proposed model in adapting previously acquired knowledge to new image domains, even when a reduced number of training samples was available in the target dataset.
97 citations
••
University of Colorado Boulder1, Yonsei University2, Samsung Medical Center3, National Taiwan University4, Chungbuk National University5, Seoul National University Hospital6, University of Oldenburg7, Hebron University8, National Health Service9, University of Manchester10, Yale Cancer Center11, University of Parma12, Takeda Pharmaceutical Company13, The Royal Marsden NHS Foundation Trust14
TL;DR: In this article, the authors reported the final efficacy, safety, and exploratory results of the ALTA-1L trial, which is a study of brigatinib in ALK inhibitor-naive advanced ALK-positive NSCLC.
97 citations
••
TL;DR: In this paper, the authors reported whole genome transcript analysis validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and correlated with immunohistological observations for four Type 1 diabetes patients and for purified islets from two of them.
Abstract: Type 1 diabetes (T1D) is caused by the selective destruction of the insulin-producing beta cells of the pancreas by an autoimmune response. Due to ethical and practical difficulties, the features of the destructive process are known from a small number of observations, and transcriptomic data are remarkably missing. Here we report whole genome transcript analysis validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and correlated with immunohistological observations for four T1D pancreases (collected 5 days, 9 months, 8 and 10 years after diagnosis) and for purified islets from two of them. Collectively, the expression profile of immune response and inflammatory genes confirmed the current views on the immunopathogenesis of diabetes and showed similarities with other autoimmune diseases; for example, an interferon signature was detected. The data also supported the concept that the autoimmune process is maintained and balanced partially by regeneration and regulatory pathway activation, e.g. non-classical class I human leucocyte antigen and leucocyte immunoglobulin-like receptor, subfamily B1 (LILRB1). Changes in gene expression in islets were confined mainly to endocrine and neural genes, some of which are T1D autoantigens. By contrast, these islets showed only a few overexpressed immune system genes, among which bioinformatic analysis pointed to chemokine (C-C motif) receptor 5 (CCR5) and chemokine (CXC motif) receptor 4) (CXCR4) chemokine pathway activation. Remarkably, the expression of genes of innate immunity, complement, chemokines, immunoglobulin and regeneration genes was maintained or even increased in the long-standing cases. Transcriptomic data favour the view that T1D is caused by a chronic inflammatory process with a strong participation of innate immunity that progresses in spite of the regulatory and regenerative mechanisms.
97 citations
••
Spanish National Research Council1, Bellvitge University Hospital2, University of Barcelona3, Aarhus University Hospital4, Hebron University5, Wellcome Trust Sanger Institute6, National Institutes of Health7, Massachusetts Institute of Technology8, Harvard University9, Catalan Institution for Research and Advanced Studies10
TL;DR: The presence of promoter CpG island hypermethylation-linked inactivation of DERL3 (Derlin-3) is demonstrated, a key gene in the endoplasmic reticulum-associated protein degradation pathway, in human tumours and highlights the tumour suppressor features of the gene.
Abstract: Cancer cells possess aberrant proteomes that can arise by the disruption of genes involved in physiological protein degradation. Here we demonstrate the presence of promoter CpG island hypermethylation-linked inactivation of DERL3 (Derlin-3), a key gene in the endoplasmic reticulum-associated protein degradation pathway, in human tumours. The restoration of in vitro and in vivo DERL3 activity highlights the tumour suppressor features of the gene. Using the stable isotopic labelling of amino acids in cell culture workflow for differential proteome analysis, we identify SLC2A1 (glucose transporter 1, GLUT1) as a downstream target of DERL3. Most importantly, SLC2A1 overexpression mediated by DERL3 epigenetic loss contributes to the Warburg effect in the studied cells and pinpoints a subset of human tumours with greater vulnerability to drugs targeting glycolysis.
97 citations
Authors
Showing all 2723 results
Name | H-index | Papers | Citations |
---|---|---|---|
José Baselga | 156 | 707 | 122498 |
M. I. Martínez | 134 | 1251 | 79885 |
Josep Tabernero | 111 | 803 | 68982 |
Jordi Rello | 103 | 694 | 35994 |
Xavier Montalban | 95 | 762 | 52842 |
James M. Downey | 91 | 381 | 29506 |
Enriqueta Felip | 83 | 622 | 53364 |
Joaquim Bellmunt | 82 | 660 | 41472 |
Joan Montaner | 80 | 489 | 22413 |
Marc Miravitlles | 76 | 651 | 25671 |
David H. Salat | 75 | 241 | 36779 |
Eduard Gratacós | 75 | 531 | 20178 |
Alex Rovira | 74 | 356 | 19586 |
Ramon Bataller | 72 | 283 | 19316 |
Maria Buti | 71 | 493 | 26596 |