When I try to execute BibTeX, I get the following error message:
INFO - This is Biber 2.8
INFO - Logfile is 'test.blg'
INFO - Reading 'test.bcf'
INFO - Found 1 citekeys in bib section 0
INFO - Processing section 0
INFO - Looking for bibtex format file 'H:/PhD/Work/Papers/library.bib' for section 0
ERROR - Data file 'H:/PhD/Work/Papers/library.bib' cannot be read in encoding 'ascii': ascii "\xE2" does not map to Unicode at C:\Users\rp1513\AppData\Local\Temp\par-727031353133\cache-72ca3f5324b5c5d2fae0b0f98af3c6b7e3920161\inc\lib/File/Slurper.pm line 63.
INFO - ERRORS: 1
The library.bib file is automatically generated by Mendeley. I have no problem if I change the backend to “bibtex” and then change the bibtex execution to bibtex as well.
Here is an MWE using my library.bib
file:
% preamble to define document settings
% basic page setup
\documentclass[a4paper,12pt,oneside]{book}
% bibliography settings
\usepackage[backend=biber, style=authoryear, citestyle=authoryear]{biblatex}
\bibliography{H:/PhD/Work/Papers/library}
\begin{document}
\tableofcontents
Here is a reference to one of the papers in my Mendeley library (\cite{Cancer2011}).
\printbibliography[heading=bibintoc]
\end{document}
The .bib
file is automatically generated by Mendeley, but here is the head:
Automatically generated by Mendeley Desktop 1.17.11
Any changes to this file will be lost if it is regenerated by Mendeley.
BibTeX export options can be customized via Options -> BibTeX in Mendeley Desktop
@article{Kim2013,
abstract = {Despite the advances in biomedical research and clinical applications, cancer remains a leading cause of death worldwide. Given the limitations of conventional chemotherapeutics, including serious toxicities and reduced quality of life for patients, the development of safe and efficacious alternatives with known mechanism of action is much needed. Prevention of cancer through dietary intervention may hold promise and has been investigated extensively in the recent years. AMP-activated protein kinase (AMPK) is an energy sensor that plays a key role in the regulation of protein and lipid metabolism in response to changes in fuel availability. When activated, AMPK promotes energy-producing catabolic pathways while inhibiting anabolic pathways, such as cell growth and proliferation - thereby antagonizing carcinogenesis. Other anti-cancer effects of AMPK may include promoting autophagy and DNA repair upon UVB damage. In the last decade, interest in AMPK has grown extensively as it emerged as an attractive target molecule for cancer prevention and treatment. Among the latest developments is the activation of AMPK by naturally occurring dietary constituents and plant products - termed phytochemicals. Owing to their efficacy and safety, phytochemicals are considered as an alternative to the conventional harmful chemotherapy. The rising popularity of using phytochemicals for cancer prevention and therapy is supported by a substantial progress in identifying the molecular pathways involved, including AMPK. In this article, we review the recent progress in this budding field that suggests AMPK as a new molecular target in the prevention and treatment of cancer by phytochemicals.},
author = {Kim, Inyoung and He, Yu-Ying},
doi = {10.3389/fonc.2013.00175},
file = {:C$\backslash$:/Users/rp1513/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Kim, He - 2013 - Targeting the AMP-Activated Protein Kinase for Cancer Prevention and Therapy.pdf:pdf},
issn = {2234-943X},
journal = {Frontiers in oncology},
keywords = {AMPK,DNA repair,ampk,apoptosis,cancer prevention,dna repair,phytochemicals,proliferation},
number = {175},
pages = {1--12},
pmid = {23875169},
title = {{Targeting the AMP-Activated Protein Kinase for Cancer Prevention and Therapy.}},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3711071{\&}tool=pmcentrez{\&}rendertype=abstract},
volume = {3},
year = {2013}
}
@article{Ostrom2014,
abstract = {Gliomas are the most common primary intracranial tumor, representing 81{\%} of malignant brain tumors. Although relatively rare, they cause significant mortality and morbidity. Glioblastoma, the most common glioma histology (∼45{\%} of all gliomas), has a 5-year relative survival of ∼5{\%}. A small portion of these tumors are caused by Mendelian disorders, including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome. Genomic analyses of glioma have also produced new evidence about risk and prognosis. Recently discovered biomarkers that indicate improved survival include O⁶-methylguanine-DNA methyltransferase methylation, isocitrate dehydrogenase mutation, and a glioma cytosine-phosphate-guanine island methylator phenotype. Genome-wide association studies have identified heritable risk alleles within 7 genes that are associated with increased risk of glioma. Many risk factors have been examined as potential contributors to glioma risk. Most significantly, these include an increase in risk by exposure to ionizing radiation and a decrease in risk by history of allergies or atopic disease(s). The potential influence of occupational exposures and cellular phones has also been examined, with inconclusive results. We provide a “state of the science” review of current research into causes and risk factors for gliomas in adults.},
author = {Ostrom, Quinn T. and Bauchet, Luc and Davis, Faith G. and Deltour, Isabelle and Fisher, James L. and Langer, Chelsea Eastman and Pekmezci, Melike and Schwartzbaum, Judith A. and Turner, Michelle C. and Walsh, Kyle M. and Wrensch, Margaret R. and Barnholtz-Sloan, Jill S.},
doi = {10.1093/neuonc/nou087},
file = {:/icnas3.cc.ic.ac.uk/rp1513/PhD/Work/Papers/nou087.pdf:pdf},
isbn = {1523-5866 (Electronic)$\backslash$r1522-8517 (Linking)},
issn = {15235866},
journal = {Neuro-Oncology},
keywords = {brain tumors,epidemiology,genome-wide association studies,glioma,risk factors},
number = {7},
pages = {896--913},
pmid = {24842956},
title = {{The epidemiology of glioma in adults: A state of the science review}},
volume = {16},
year = {2014}
}
Any help would be greatly appreciated!
.tex
and.bib
file.\documentclass[a4paper,12pt,oneside]{report}
I'm using pdflatex to generate the file, and I think the encoding is UTF-8 (shown in bottom right corner)..bib
file you posted does not reproduce the problem for me. As far as I can see it only contains ASCII chars, so is uncritical. Try to isolate the problematic entry in your.bib
file using binary search (delete one half of the file, see if the error persist, etc. You will have to delete temporary files (.bbl
,.bcf
) between compilations to make sure no problematic content is left in the aux files. Also search for non-ASCII chars explicitly.). Can you check that the.bib
file is really UTF8?