[R] (Solved] Re: pubmed.mineR
David Winsemius
dwinsemius at comcast.net
Fri Aug 5 17:48:20 CEST 2016
> On Aug 4, 2016, at 9:52 PM, Mehdi Najafi <sm.najafi92 at gmail.com> wrote:
>
> ---------- Forwarded message ----------
> From: Mehdi Najafi <sm.najafi92 at gmail.com>
> Date: Fri, Aug 5, 2016 at 9:17 AM
> Subject: pubmed.mineR
> To: ramu at igib.in
>
>
> Hi dear helper, it has been a pleasure to read magnificat paper titled
> "pubmed.mineR: An R package with text-mining algorithms to analyse PubMed
> abstracts".
> I encuntered a problem using it.I wish you could help me with that.
> favorite
> <http://stackoverflow.com/questions/38781115/cant-find-objects-using-pubmed-miner-package#>
>
I think it would have been courteous of you to post a solved message since you did so 10 hours ago on the crossposting.
Also please realize that crossposting is specifically deprecated on Rhelp.
--
David.
>
> I have downloaded abstracts of interest from pubmed.com then read them
> using pubmed.mineR package with readabs() function, which is supposed to
> create object of class "Abstracs", but when I type in ls(), it gives me
> character(0), which as far as i know implies that there is no object in the
> memory. I want to search abstracts using searchabsL(x,include="term"), Here
> x is the object of class Abstracts containing data.though i don't know how?
>
> after readabs() i face these lines:
>
>> readabs("b.txt")
>
> An object of class "Abstracts"
>
> Slot "Journal":
>
> [1] "1. Alzheimers Res Ther. 2015 Dec 18;7(1):75. doi:
> 10.1186/s13195-015-0159-5."
>
> [2] "2. J Cereb Blood Flow Metab. 2016 Mar;36(3):621-8. doi:
> 10.1177/0271678X15606141."
>
>
> Slot "Abstract":
>
> [1] " Diagnostic value of cerebrospinal fluid Aβ ratios in preclinical
> Alzheimer's disease. Adamczuk K(1,)(2), Schaeverbeke J(3,)(4),
> Vanderstichele HM(5), Lilja J(6,)(7), Nelissen N(8,)(9), Van Laere
> K(10,)(11), Dupont P(12,)(13), Hilven K(14), Poesen K(15,)(16),
> Vandenberghe R(17,)(18,)(19). Author information: (1)Laboratory for
> Cognitive Neurology, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> kate.adamczuk at med.kuleuven.be. (2)Alzheimer Research Centre KU Leuven,
> Leuven Institute of Neuroscience and Disease, Herestraat 49, 3000, Leuven,
> Belgium. kate.adamczuk at med.kuleuven.be. (3)Laboratory for Cognitive
> Neurology, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> jolien.schaeverbeke at med.kuleuven.be. (4)Alzheimer Research Centre KU
> Leuven, Leuven Institute of Neuroscience and Disease, Herestraat 49, 3000,
> Leuven, Belgium. jolien.schaeverbeke at med.kuleuven.be. (5)ADx NeuroSciences,
> Technologiepark 4, 9052, Gent, Belgium. hugo.vanderstichele@
> adxneurosciences.com. (6)GE Healthcare, Björkgatan 30, 751 25, Uppsala,
> Sweden. johan.lilja at radiol.uu.se. (7)Nuclear Medicine and PET, Department
> of Surgical Sciences, Uppsala University, 751 85, Uppsala, Sweden.
> johan.lilja at radiol.uu.se. (8)Laboratory for Cognitive Neurology, KU
> Leuven, Herestraat 49, 3000, Leuven, Belgium. natalie.nelissen at psych.ox.ac.
> uk. (9)Department of Psychiatry, Oxford University, Oxford, OX3 7JX, UK.
> natalie.nelissen at psych.ox.ac.uk. (10)Alzheimer Research Centre KU Leuven,
> Leuven Institute of Neuroscience and Disease, Herestraat 49, 3000, Leuven,
> Belgium. koen.vanlaere at uzleuven.be. (11)Nuclear Medicine and Molecular
> Imaging Department, KU Leuven and University Hospitals Leuven, Herestraat
> 49, 3000, Leuven, Belgium. koen.vanlaere at uzleuven.be. (12)Laboratory for
> Cognitive Neurology, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> patrick.dupont at med.kuleuven.be. (13)Alzheimer Research Centre KU Leuven,
> Leuven Institute of Neuroscience and Disease, Herestraat 49, 3000, Leuven,
> Belgium. patrick.dupont at med.kuleuven.be. (14)Laboratory for
> Neuroimmunology, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> kelly.hilven at med.kuleuven.be. (15)Laboratory for Molecular Neurobiomarker
> Research, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> koen.poesen at uzleuven.be. (16)Laboratory Medicine, UZ Leuven, Herestraat 49,
> 3000, Leuven, Belgium. koen.poesen at uzleuven.be. (17)Laboratory for
> Cognitive Neurology, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.
> rik.vandenberghe at uz.kuleuven.ac.be. (18)Alzheimer Research Centre KU
> Leuven, Leuven Institute of Neuroscience and Disease, Herestraat 49, 3000,
> Leuven, Belgium. rik.vandenberghe at uz.kuleuven.ac.be. (19)Neurology
> Department, University Hospitals Leuven, Herestraat 49, 3000, Leuven,
> Belgium. rik.vandenberghe at uz.kuleuven.ac.be. INTRODUCTION: In this study
> of preclinical Alzheimer's disease (AD) we assessed the added diagnostic
> value of using cerebrospinal fluid (CSF) Aβ ratios rather than Aβ42 in
> isolation for detecting individuals who are positive on amyloid positron
> emission tomography (PET). METHODS: Thirty-eight community-recruited
> cognitively intact older adults (mean age 73, range 65-80 years) underwent
> (18)F-flutemetamol PET and CSF measurement of Aβ1-42, Aβ1-40, Aβ1-38,
> and total tau (ttau). (18)F-flutemetamol retention was quantified using
> standardized uptake value ratios in a composite cortical region (SUVRcomp)
> with reference to cerebellar grey matter. Based on a prior autopsy
> validation study, the SUVRcomp cut-off was 1.57. Sensitivities,
> specificities and cut-offs were defined based on receiver operating
> characteristic analysis with CSF analytes as variables of interest and
> (18)F-flutemetamol positivity as the classifier. We also determined
> sensitivities and CSF cut-off values at fixed specificities of 90Â % and
> 95Â %. RESULTS: Seven out of 38 subjects (18Â %) were positive on amyloid
> PET. Aβ42/ttau, Aβ42/Aβ40, Aβ42/Aβ38, and Aβ42 had the highest
> accuracy to identify amyloid-positive subjects (area under the curve
> (AUC) ≥ 0.908). Aβ40 and Aβ38 had significantly lower
> discriminative power (AUC = 0.571). When specificity was fixed at 90 %
> and 95 %, Aβ42/ttau had the highest sensitivity among the different CSF
> markers (85.71 % and 71.43 %, respectively). Sensitivity of Aβ42 alone
> was significantly lower under these conditions (57.14Â % and 42.86Â %,
> respectively). CONCLUSION: For the CSF-based definition of preclinical AD,
> if a high specificity is required, our data support the use of Aβ42/ttau
> rather than using Aβ42 in isolation. DOI: 10.1186/s13195-015-0159-5
> PMCID: PMC4683859"
>
> [2] "Epub 2015 Sep 30. Cerebrospinal fluid profiles with increasing number
> of cerebral microbleeds in a continuum of cognitive impairment. Shams
> S(1), Granberg T(2), Martola J(2), Li X(3), Shams M(2), Fereshtehnejad
> SM(3), Cavallin L(2), Aspelin P(2), Kristoffersen-Wiberg M(2), Wahlund
> LO(3). Author information: (1)Department of Clinical Science,
> Intervention, and Technology, Division of Medical Imaging and Technology,
> Karolinska Institutet, Stockholm, Sweden Department of Radiology,
> Karolinska University Hospital, Stockholm, Sweden sara.shams at ki.se.
> (2)Department of Clinical Science, Intervention, and Technology, Division
> of Medical Imaging and Technology, Karolinska Institutet, Stockholm, Sweden
> Department of Radiology, Karolinska University Hospital, Stockholm, Sweden.
> (3)Department of Neurobiology, Care Sciences, and Society, Karolinska
> Institutet, Stockholm, Sweden Division of Clinical Geriatrics, Karolinska
> University Hospital, Stockholm, Sweden. Cerebral microbleeds (CMBs) are
> hypothesised to have an important yet unknown role in the dementia disease
> pathology. In this study we analysed increasing number of CMBs and their
> independent associations with routine cerebrospinal fluid (CSF) biomarkers
> in a continuum of cognitive impairment. A total of 1039 patients undergoing
> dementia investigation were analysed and underwent lumbar puncture, and an
> MRI scan. CSF samples were analysed for amyloid β (Aβ) 42, total tau
> (T-tau), tau phosphorylated at threonine 18 (P-tau) and CSF/serum albumin
> ratios. Increasing number of CMBs were independently associated with low
> Aβ42 levels, in the whole cohort, Alzheimer's disease and mild cognitive
> impairment (p < 0.05). CSF/serum albumin ratios were high with multiple
> CMBs (p < 0.001), reflecting accompanying blood-brain barrier
> dysfunction. T-tau and P-tau levels were lower in Alzheimer's patients with
> multiple CMBs when compared to zero CMBs, but did not change in the rest of
> the cohort. White matter hyperintensities were associated with low Aβ42
> in the whole cohort and Alzheimer's disease (p < 0.05). Aβ42 is the
> routine CSF-biomarker mainly associated with CMBs in cognitive impairment,
> and there is an accumulative effect with increasing number of CMBs. © The
> Author(s) 2015. DOI: 10.1177/0271678X15606141 PMCID: PMC4794093
> [Available on 2017-03-01]"
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> Slot "PMID":
>
> [1] 26677842 26661151
> I would be glad to hear from you. sincerely,Mehdi Najafi.
>
> [[alternative HTML version deleted]]
>
> ______________________________________________
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David Winsemius
Alameda, CA, USA
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