[R] Fwd: pubmed.mineR

[Mehdi Najafi]

---------- 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 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]"































Slot "PMID":

[1] 26677842 26661151
I would be glad to hear from you. sincerely,Mehdi Najafi.

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