On 2013 Nov 01, Dale D O Martin commented:

An updated list of new post-translationally myristoylated proteins including the anti-apoptotic protein Mcl-1 and the causative agent of Huntington Disease, Huntingtin, can be found here: http://www.ncbi.nlm.nih.gov/pubmed/21965604 Herein, we used a post-translational myristoylation assay, that was dependent on caspase cleavage, to verify previously identified substrates and to identify new post-translationally myristoylated proteins.

On 2014 Feb 07, Dale D O Martin commented:

We have since shown that caspase-cleavage of HTT releases an autophagy-inducing domain that requires its post-translational myristoylation. http://www.ncbi.nlm.nih.gov/pubmed/24459296

Videos can be seen here: http://hmg.oxfordjournals.org/content/early/2014/01/22/hmg.ddu027/suppl/DC1

On 2014 Sep 30, Dale D O Martin commented:

Post-translational myristoylation of both Bap31 and CD-IC2 have recently been confirmed endogenously in Thinon et al found here http://www.ncbi.nlm.nih.gov/pubmed/25255805

On 2014 Feb 01, Jan Tunér commented:

In this study, a 6 mW HeNe laser or a placebo HeNe laser was used to treat leg ulcers twice weekly for 12 weeks. The stated dose was 4 J/cm2. The area of the ulcers varied from 3 cm2 to 32 cm2. To achieve the stated dose, the treatment time of each session of therapy would thus have had to vary from 33 minutes to 6 hours. It is questioned that the patients really would have been treated for 6 hours. The method by which the dose was calculated is therefore questionable. No indication is given of the method of treatment. If a scanning laser with an unexpanded beam was used, the power density would have been about 0.15 W/cm2. If the beam was expanded to a diameter capable of illuminating the whole area of the ulcer at once, the power density when treating the largest ulcer would have been about 0.00019 W/cm2, which is close to the level of moonlight. Unless more parameters are accounted for, it is impossible to evaluate this study. The possibility of performing a double blind study with red light is also questionable. The authors have been reluctant to answer questions on this paper.

On 2014 Aug 24, Ivan Oransky commented:

This study has been retracted: http://retractionwatch.com/2014/07/25/paper-about-widely-touted-but-unapproved-cure-for-cancer-autism-retracted/ It's one of two recent retractions by the group: http://retractionwatch.com/2014/08/21/second-study-of-widely-touted-cancer-and-hiv-cure-retracted/

On 2015 Jul 02, Pedro Silva commented:

The code used to locate the minimum-energy-crossing points in this work is publicly available as:

Silva, Pedro (2015): Program for the computation of MECP using the Firefly Quantum Chemistry program. figshare. http://dx.doi.org/10.6084/m9.figshare.1471648

On 2016 Dec 02, Stephen Strum commented:

This is a landmark publication and should be required reading of all those caring for patients with cancer that involves bone mets. In my medical oncology practice I rarely see attention paid to bone integrity and what is called the the vicious cycle of bone resorption & tumor cell proliferation (VC). The implications of how we assess patients at diagnosis and during the course of their care as it relates to VC and the associated increase in cytokines is of immense prognostic and even diagnostic value. I continue to see men with prostate cancer who never have any lab assessment that relates to bone resorption markers (BRMs). This paper beautifully portrays the importance of bone integrity & the underlying mechanisms of action.

On 2016 Feb 08, Mwidimi Ndosi commented:

My research student Hannah Cumpstey picked this up in the methods section: "A p-value >0.05 was accepted as being statistically different" (Akbari et al, 2007, P.633).

In the results section however, the interpretation of the null hypothesis significance testing seem to follow the conventional significance level, where a p=0.03 is interpreted as significant and p=0.95 not significant (p.634).

Could the authors please comment, just to reassure other readers?

Akbari A, Moodi H, Ghiasi F, Sagheb HM, Rashidi H. (2007) Effects of vacuum-compression therapy on healing of diabetic foot ulcers: randomized controlled trial. J Rehabil Res Dev. 44(5): 631-6.

On 2016 Aug 23, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00535031. We believe the correct ID, which we have found by hand searching, is NCT00535431.

This comment is being posted as part of the OpenTrials.net project^[1] , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

Many thanks,

Jessica Fleminger, Ben Goldacre*

[1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

* Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG

On 2015 May 07, Jeff Kiefer commented:

DAVID is continuously being used as evidenced by its numerous citations in current biomedical literature http://bit.ly/1FS1JgT. However, the data resources used by DAVID appear to not have been updated since 2009 http://david.abcc.ncifcrf.gov/helps/update.html. The fact that DAVID has not been updated going on 5 years calls into question the current utility of using this tool.

On 2016 May 26, Jeff Kiefer commented:

It looks like DAVID has been updated May 2016 https://david-d.ncifcrf.gov/content.jsp?file=release.html.

On 2013 Jun 30, Swapnil Hiremath commented:

This is a fascinating attempt at resolving heterogeneity in this field of contrast nephropathy. The ACT study, done later by Berwanger et al in Circulation 2011 http://www.ncbi.nlm.nih.gov/pubmed/21859972, proved conclusively that NAC is not useful. However, this paper, by trying to resolve the cause of the heterogeneity is a fascinating read beyond just the summary outcome measure. As Prof Stoto would say, while doing a systematic review, try to think, 'What is the Story?'

On 2014 Dec 11, Ibrahim Masoodi commented:

We have found Fecal Lactoferrin an effective biomarker too.This co relates well the UC activity and severity

On 2015 Oct 05, Jan Egger commented:

Videos demonstrating the virtual stenting can be found here: https://www.youtube.com/c/JanEgger/videos

Best wishes, Jan

On 2014 Nov 23, Harri Hemila commented:

A comment is available at: http://hdl.handle.net/10138/25297

On 2014 Dec 10, Kath Wright commented:

Other search filters are available from the InterTASC Information Specialists' Sub-Group Search Filter Resource at https://sites.google.com/a/york.ac.uk/issg-search-filters-resource/home

On 2015 May 04, Raphael Levy commented:

This post is co-authored by Raphael Levy and David Mason.

Note: We contacted Chad Mirkin and EMD Millipore for comments. Chad Mirkin replied but prefers to keep his comments for the peer reviewed literature rather than blogs. EMD Millipore has provided a response (reproduced below) and is keen to further engage in the discussion. They wrote that they "look forward to responding to [the questions you pose at the end of the post] after your blog is posted so other researchers who may have the same questions can follow our discussion online."

To image proteins in cells, biologists have powerful tools based on the Green Fluorescent Protein (GFP) for which Osamu Shimomura, Martin Chalfie and Roger Y. Tsien obtained the 2008 Nobel Prize in Chemistry. RNA molecules play crucial roles in cells such as coding, decoding, regulation, and expression of genes, yet they are much more difficult to study. SmartFlares are nanoparticle-based probes for the detection and imaging of RNA in live cells. Could they become the GFP of the RNA world?

Read more at https://raphazlab.wordpress.com/2015/03/11/how-smart-are-smartflares/

On 2017 Sep 15, Raphael Levy commented:

A new paper confirms that spherical nucleic acids / nano-flares / SmartFlares do no detect mRNA. SmartFlares fail to reflect their target transcripts levels

See also the Guest post by the authors of the above study at my blog.

On 2015 May 12, David Gortler commented:

This trial supports the findings of the older CARDS trials which also showed that "lower is better" when it comes to LDL, and there is additive benefit to driving LDL levels beyond 70mg/dL (the current NECP goal) to even as low as 40mg/dL. Since this publication, it has been additionally shown that elevation of hsCRP is associated with increased risk of type 2 diabetes development in patients with all levels of metabolic syndrome.

In type 1 and type 2 diabetes mellitus, hemoglobin A1c significantly correlates with hsCRP levels and future cardiovascular risk indicating that diabetes has inflammatory fundamentals. Also, hsCRP levels increase with the stage of beta-cell dysfunction and insulin resistance. Non-diabetic drugs that have been shown to reduce hsCRP concentrations include aspirin, statins, cyclooxygenase-2 inhibitors, and fibrates.

On 2014 May 10, Ivan Oransky commented:

This paper has been retracted: http://retractionwatch.com/2014/05/09/more-retractions-for-researcher-who-says-he-will-no-longer-publish/

On 2017 Dec 06, Misha Koksharov commented:

The link to the full text: http://dx.doi.org/10.1139/y91-257

On 2016 Nov 20, Morten Oksvold commented:

An investigation committee at Wayne State University (WSU) recommends that 42 articles from Fazlul Sarkar to be retracted (report finished August 31, 2015). This article represents one of them.

This information was published by Retraction Watch (November 17, 2016) and you can find a link to the full report here:

http://retractionwatch.com/2016/11/17/details-of-investigative-report-into-sarkar-released-by-aclu/

This article should therefore no longer be cited.

On 2015 Jun 18, Bill Cayley commented:

A great example of "Less is More" in Medicine: https://lessismoreebm.wordpress.com/2015/06/17/effect-of-honey-dextromethorphan-and-no-treatment-on-nocturnal-cough-and-sleep-quality-for-coughing-children-and-their-parents/

On 2014 Oct 13, Ivan Oransky commented:

This paper has been retracted, the third retraction of a paper by Nobutu Yamamoto about GcMAF: http://retractionwatch.com/2014/10/10/yet-another-study-of-widely-touted-cancer-cure-retracted/

On 2014 Nov 26, Harri Hemila commented:

A manuscript version is available at handle

On 2013 Oct 23, MARK VRABEL commented:

For the latest evidence on ondansetron, granisetron, other antiemetics, and nonpharmacologic interventions for CINV, see the Oncology Nursing Society Putting Evidence Into Practice http://www.ons.org/Research/PEP/Nausea and http://esource.ons.org/ProductDetails.aspx?sku=INPU0638

On 2016 Aug 23, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT0037. We believe the correct ID, which we have found by hand searching, is NCT00371982.

This comment is being posted as part of the OpenTrials.net project^[1] , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

Many thanks,

Jessica Fleminger, Ben Goldacre*

[1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

* Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG

On 2017 Feb 26, Bill Noble commented:

Please note that the particular strategy proposed here for estimating false discovery rates in the context of tandem mass spectrometry has subsequently been shown to be biased. Evidence for this bias, and discussion of alternative protocols, is given in this paper: https://www.ncbi.nlm.nih.gov/pubmed/26152888

On 2013 Nov 01, Dale D O Martin commented:

It should be noted that N-myristoylation can only occur on N-terminal Glycines, hence the name N-myristoylation. This occurs either co-translationally on the nascent polypeptide following the removal of the initiator Met or it can occur posttranslationally following proteolysis, which exposes a new N-terminal Gly. The latter has only been shown to occur in caspase-cleaved proteins. In this case, the Gly follows an Asp residue where caspase will cleave. The authors here predict internal myristoylation at very unlikely positions. Furthermore, the general consensus sequence for myristoylation is GXXXS/C/T where X is any amino acid, except for large bulky residues, and S/C/T are preferred in position 5 (counting from Gly). The first site they predict is GAAPP and is very unlikely to be myristoylated. Caution should be taken when predicting internal myristoylation sites. Unless it is predicted to be cleaved to expose an N-terminal Gly.

On 2014 Apr 17, Carl Denef commented:

An update of this review is available in an on line database at the following URL:

https://perswww.kuleuven.be/~u0009251/index.htm

This database is updated

On 2014 Dec 10, Kath Wright commented:

Other search filters are available from the InterTASC Information Specialists' Sub-Group Search Filter Resource at https://sites.google.com/a/york.ac.uk/issg-search-filters-resource/home

On 2017 Jan 19, Denise Fernandez-Twinn commented:

I am an author on this paper, however because my name is listed as Twinn DF, I am not getting the cites for this really important paper. Is there something PubMed can do to change the way my name is listed to Fernandez-Twinn DS. I have other collaborative work with some of the other authors on this paper (Ozanne SE and Samuelson AM), so it would be easy to verify my identity and contribution on this paper. Thank you. Kind Regards, Denise S Fernandez-Twinn

On 2014 Nov 17, Raphael Levy commented:

A key paper in the stripy controversy. Discussed here.

More broadly, the evidence behind the structure and special properties of “striped” nanoparticles has been challenged by Cesbron Y, 2012. The publication in 2012 of Cesbron Y, 2012 took three years and has been followed by post-publication peer review of the various existing and new stripy articles on my blog, PubPeer, etc.

A detailed analysis of this body of work is published today in PloS One by Stirling et al; from the abstract: “through a combination of an exhaustive re-analysis of the original data with new experimental measurements of a simple control sample comprising entirely unfunctionalised particles, we conclusively show that all of the STM evidence for striped nanoparticles published to date can instead be explained by a combination of well-known instrumental artefacts, strong observer bias, and/or improper data acquisition/analysis protocols.”

On 2013 Oct 22, DAVID SANDERS commented:

None

On 2013 Oct 25, DAVID SANDERS commented:

This article twice claims that Alvarado J, 2006 hypothesizes that there are two distinct active sites on the E. coli Ppx.

"However, the bifunctional aspect of pppGpp hydrolysis was linked to the presence of two active sites in one study Alvarado J, 2006 but was in favor of a common active site in the other."

"The structural analysis by Alvarado et al. identified domain III as a second PPX active site responsible for pppGpp hydrolysis."Alvarado J, 2006

However, no such statement is made in Alvarado J, 2006.

On 2014 Nov 23, Harri Hemila commented:

Reply to this comment is available at DOI

On 2014 May 12, G L Francis commented:

This paper sought to find a chemically-defined medium to maintain human embryonic stem cells (hESCs) in long-term culture, necessary for expansion of cell numbers to enable production platforms required to provide differentiated cells for the clinical trial of cell-mediated therapeutics and beyond. Although this paper in now six years old the authors raise some important points still relevant today, however, I believe they misinterpreted a key finding for the relative importance of the components of ‘lipid rich albumin’ by underestimating the contribution of the albumin carrier itself. The studies initially utilized KnockOut™ Serum Replacement (KOSR) and then AlbuMAX®, a chromatographically purified lipid-rich bovine serum albumin (BSA) preparation, which they established was the active component in KOSR, moreover, both products are problematic themselves when developing production methods for human clinical products, due to their animal origins . None the less, the importance of the albumin borne lipid components in sustaining pluripotency markers of hESCs, indicating self-renewal over five passages, was correctly established (Fig. 2 & Fig.3). They extend this finding to claim evidence for the exclusive role of lipids, and attribute no role for the associated albumin carrier protein, in supporting the self-renewal of the hESC lines (Fig 3 A-E). It is the latter conclusion I take odds with, and in fact believe the results also support another conclusion - that while lipid components are essential to the action of the lipid-rich albumin preparations used, albumin promotes the action of its lipid ligands, to maximize the response as seen for both KOSR and AlbuMAX®. Indeed careful examination of the data (Fig 3B and Fig3D) reported allows the conclusion that the presence of intact albumin increases the expression of the pluripotency markers TRA-1-60 and NANAOG by around 25%, and only that of OCT4 is unchanged. Also in this series of experiments the authors could have included another control treatment where they mixed the intact AlbuMAX® with trypsin inhibitor before adding the protease trypsin. Next the authors correctly proved that after the repeated passage (X7) of hESCs they actually retained pluripotency and the capacity to differentiate into ectoderm, endoderm, and mesoderm, by displaying the appropriate markers, GFAP & Sox1, Sox17 & Pdx1 (latter not shown), and cardiac Troponin T, respectively (Fig.4A). Differentiation of hESCs passaged under all conditions resulted in a drastic reduction of pluripotency markers Oct4 and NANAOG and the appropriate increase of differentiation marker for each germ layer of the generated embroid bodies (EBs). However, for the AlbuMAX® + Trypsin media passaged hESCs the resulting embroid bodies displayed for each germ layer the relevant markers, but numerically (by inspection) reduced by 47% GFAP and 25% SOX1 (ectoderm), 10% SOX17 and ??% Pdx1 (endoderm), and 42% cardiac Troponin T (mesoderm) compared to EBs derived from hESCs cultured with intact AlbuMAX®. This difference was not addressed by the authors to my knowledge, and if all experimental variables are controlled and assuming these differences are statistically robust - then possibly a more complex role for albumin in facilitating the subsequent differentiation of these cell lines is indicated. Furthermore, the presence of lipid-rich albumin (i.e. BSA present in 10% Fetal Bovine Serum) during hESC differentiation and EB growth suggests the observed marker differences result from earlier genetic or epigenetic modifications to the hESCs during the serial passaging phase. While the possible involvement of other endogenous or exogenous ligands of albumin were considered to no avail, reasonably the authors could not cover the full spectrum of effects that albumin could promote directly or indirectly in mammalian cells, many of which I have reviewed more recently (2010-PMID: 20373019 [PubMed]).<br> I wish to sincerely thank the authors for the wide range of issues they raised in relation to this topic and I hope my comments are of some value to them or others.

On 2016 Feb 18, Kristina Hanspers commented:

The network in figure 2 is available in the "Open Access Publication" collection at WikiPathways: http://www.wikipathways.org/index.php/Pathway:WP2636. This pathway can be downloaded for use in network analysis tools such as Cytoscape and PathVisio.

On 2015 Sep 27, S Sundar commented:

We noticed re-induction of hormone sensitivity in more patients and we presented our experience at the ASCO GU conference in 2008. The conference abstract is unfortunately no longer available from ASCO website.

We have reproduced our submission below for the benefit of clinicians and researchers interested in our manuscript.

Citation:<br> Cox RA, Sundar S. Re-induction of sensitivity to diethylstilbestrol in docetaxel-treated androgen refractory prostate cancer. In: American Society of Clinical Oncology Genitourinary Symposium. 2008. Abstract No: 172. ....................................

Control/Tracking Number: 08-AB-20299-ASCOGU Activity: Abstract Submission Current Date/Time: 1/29/2008 10:04:47 AM

Re-induction of sensitivity to Diethylstilbestrol in Docetaxel treated androgen refractory prostate cancer

Author Block: S. Sundar, R. Cox; Nottingham City Hospital, Nottingham, United Kingdom

Abstract:

Introduction: Diethylstilbestrol (DES) is a standard second line hormone therapy for prostate cancer in the UK. Following introduction of Docetaxel, DES is increasingly being used as third line therapy. We audited our patients (pts) response to DES after treatment with Docetaxel.

Methods: Pts (n=56) who received Docetaxel within an 18-month period were identified from a pharmacy database and the sub-group (n=16) treated with DES after Docetaxel was identified. PSA Response rate (50% decline) to Docetaxel was 60%. All pts had androgen refractory disease and had castrate levels of testosterone (LHRH-agonist therapy/orchidectomy). Pts with a history of ischaemic heart disease, stroke, pulmonary embolism (PE) or thrombosis were not offered DES. Pts were treated with DES 1mg daily with aspirin 75mg daily for thrombotic prophylaxis.

Results: 16 pts subsequently received DES on disease progression following Docetaxel. (1 pt unable to tolerate DES due to nausea was excluded from analysis). Median age of pts given DES after Docetaxel was 70yrs (52-79). 12 of 15 (80%) responded to DES 'after' Docetaxel, with 6 (50%) having a >50% reduction in PSA. Significantly 7 pts were treated with DES 'prior' to Docetaxel. 6 of these 7 pts (86%) who were previously refractory to DES 'prior' to Docetaxel responded to retreatment with DES 'following' Docetaxel chemotherapy. Currently, 6 pts remain on therapy after a median follow up of 2.5 months. 5 pts who progressed, did so after a median treatment duration of 4 months. 1 responding patient stopped after 2 months due to a PE. DES was otherwise very well tolerated. 1 patient stopped treatment after 1 week due to nausea. There were no other documented cardiovascular, cerebrovascular or thrombotic events.

Conclusions: DES is an option for patients with androgen refractory prostate cancer who have relapsed after treatment with Docetaxel. Previous work (Shamash et al, Br.J.Cancer.2005) found re-induction of hormone sensitivity following failure of Chlorambucil and Lomustine chemotherapy. Further investigation of this interesting phenomenon of re-induction of DES sensitivity could provide further insight into molecular mechanisms underlying androgen refractory prostate cancer. : Author Disclosure Information: S. Sundar, None; R. Cox, None. ..........................................................................

On 2015 Jun 28, Erick H Turner commented:

Below are DOIs and links to FDA review documents for the 8 older antidepressant drugs whose reviews are not available on the FDA website Drugs@FDA.

doi:10.6083/M4542M8J Bupropion SR http://digitalcommons.ohsu.edu/fdadrug/21

doi:10.6083/M41C1VJT Fluoxetine http://digitalcommons.ohsu.edu/fdadrug/22

doi:10.6083/M48W3C0Z Mirtazapine http://digitalcommons.ohsu.edu/fdadrug/20

doi:10.6083/M4WM1C2X Nefazodone http://digitalcommons.ohsu.edu/fdadrug/23

doi:10.6083/M4HD7TC4 Paroxetine http://digitalcommons.ohsu.edu/fdadrug/26

doi:10.6083/M4CN72MB Sertraline http://digitalcommons.ohsu.edu/fdadrug/27

doi:10.6083/M4RV0MCN Venlafaxine http://digitalcommons.ohsu.edu/fdadrug/24

doi:10.6083/M4N58K2D Venlafaxine XR http://digitalcommons.ohsu.edu/fdadrug/25

Because they were not acquired directly from the FDA but rather indirectly through colleagues who had obtained them via FOIA requests, the order of the 'hard copy' pages may have been shuffled in some cases. For a 'cleaner' copy, one might need to place a new FOIA request with the FDA (http://www.accessdata.fda.gov/scripts/foi/FOIRequest/requestinfo.cfm).

As for the 4 newer antidepressant drugs, as stated in the article, those reviews are downloadable from Drugs@FDA. If assistance is needed in navigating to and through that site, the "cookbook" article of mine available at http://www.bmj.com/content/347/bmj.f5992 may be useful.

On 2016 Sep 22, Lydia Maniatis commented:

Please see comments on PubPeer.

On 2013 Oct 28, DAVID SANDERS commented:

Identical Env deletions to those described in this article ("The Env truncated at 616 exhibits maximum fusogenicity in cell-to-cell fusion assay. By comparison, full tail Env (632) and the Env truncated to residue 601 mediated fusion at 40%.") are analyzed in Taylor GM, 2003, which is not cited by this article and contains an alternative hypothesis that there is a trimeric coiled coil in the cytoplasmic domain. This hypothesis has gained recent support. Löving R, 2012

Analysis of the effects of Env mutations in Li M, 2001, Yang C, 1997, and Taylor GM, 2003, which is inconsistent with the hypothesis proposed by the authors of this Exp Mol Pathol article, was also ignored by them.

On 2014 Nov 23, Harri Hemila commented:

A manuscript version is available at handle

On 2013 Dec 15, Eduardo Palencia-Herrejón commented:

Surprised with the Le Gall statement against the involvement of family in "hard decisions"... Perhaps the full text provides an adequate explanation, but the bare statement sounds like paternalistic...

On 2015 Jul 02, Pedro Silva commented:

The code used to locate the minimum-energy-crossing points in this work is publicly available as:

Silva, Pedro (2015): Program for the computation of MECP using the Firefly Quantum Chemistry program. figshare. http://dx.doi.org/10.6084/m9.figshare.1471648

On 2013 Oct 26, Graham Coop commented:

The heritable variation in hotspot usage that we found in this article was later mapped to the gene prdm9, see Baudat et al ( Baudat F, 2010 ) and related articles.

On 2014 Nov 24, Claudia Paiva commented:

I think that the possible link between autoimmune thyroiditis and Meniere's disease may be the deposition of antibody+thyroid antigen immune complexes instead of autoimmunity against other antigens. The evidences do not point to hormone levels as the link.

On 2014 Sep 29, Ivan Oransky commented:

This paper has been retracted, one of three studies by the late first author to have been retracted: http://retractionwatch.com/2014/09/26/deceased-researcher-has-two-more-papers-retracted/

On 2017 Oct 14, Eric Yarnell commented:

Authors should be Peng A, Gu Y, Gui DK, Zhu QY, Zhu KY, Lin SY (family and given names have been switched)

On 2015 Oct 15, Nanjiang Shu commented:

Link to the web-server has been changed to http://predzinc.bioshu.se

On 2015 Jun 16, Bill Cayley commented:

A great example of when "Less" is more: https://lessismoreebm.wordpress.com/2015/06/16/systematic-review-of-randomized-controlled-trials-examining-written-action-plans-in-children-what-is-the-plan/

On 2013 Jun 17, Mike Fay commented:

This paper shows an improved way to calculate the variance when using multiple imputation with interval censored data. Huang, Lee and Yu show this is better than calculating the variance by using a correction for multiple imputation developed by Rubin for a different situation, that was used in earlier papers.

Another advantage of this test (not studied in the original paper) is that it retains the type I error fairly well even when the assessment times depend on treatment (see my paper with Joanna Shih Fay MP, 2012).

Software to calculate this test is available in the interval R package, http://cran.r-project.org/web/packages/interval/index.html.

On 2017 May 23, Morten Oksvold commented:

This article was retracted April 27 2017 together with eight other articles from the same group due to data manipulations.

Please note that the retraction notice is visible in the PDF document only.

http://www.jbc.org/content/283/17/11176.full.pdf?sid=a8d5dc2c-dd64-4b19-bf5e-c46f7deb9f49

"This article has been withdrawn by the authors. The authors were recently made aware of issues in Figs. 1A and 2A. In Fig. 1A, the actERK2 panel was manipulated inappropriately, and the GST panel was duplicated in Fig. 1C as the GST panel. In Fig. 2A, the P-Elk panels for ERK2 were duplicated, and the right actERK2 panel for RSK was duplicated in the right actERK2 panel for cFOS. Because the original data are no longer available, in the interest of maintaining accuracy in the published scientific literature, the authors wish to withdraw this article. However, the authors have full confidence in the findings and conclusions of this paper and have replicated the findings in subsequent work."

On 2014 Jan 03, Alexander Lerchl commented:

None

On 2014 Jan 16, Franz Adlkofer commented:

None

On 2014 Feb 11, Franz Adlkofer commented:

Two papers from a research team at the Medical University of Vienna (MUV), the one above and a previous one [1], point to a genotoxic potential of radiofrequency electromagnetic fields. Both papers result from the REFLEX project, a multi-national study on biological effects of electromagnetic fields funded by the European Union, which I coordinated [2]. About three years after REFLEX had been completed all of a sudden the claim was circulated that the Vienna results might have been faked. With this allegation the editors of the two peer-reviewed scientific journals should be forced to retract the respective papers. However, they carried out their own investigations, and in both editorial boards the outcome of a thorough scrutiny led to the conclusion that there is no evidence of fraud.

At the same time, the MUV mandated its Council for Scientific Ethics to investigate in detail how the Vienna REFLEX data were generated. This Council confirmed already at its first meeting and without any investigation the suspected fraud, and recommended the retraction of the two papers. By chance, it turned out that its chairman was a lawyer from the Austrian telecommunication industry. After his replacement the new Council came to the decision that the allegation is unfounded and that there is no reason to further pursue the case. Unhappy with this acquittal, the matter was finally transferred to the newly established Austrian Agency for Research Integrity that after a further scrutiny followed the Council’s decision [3].

Criticism of scientific data is absolutely necessary, but to claim fraud in order to get rid of them is unacceptable, whatever the reasons behind.

1. Diem E, Schwarz C, Adlkofer F, Jahn O, Rüdiger HW (2005) Non-thermal DNA breakage by mobile phone radiation (1800 MHz) in human fibroblasts and transformed GFSH-R17 rat granulosa cells in vitro. Mutat Res 583:178-83.
2. See „REFLEX Final Report“ in http://www.itis.ethz.ch/assets/Downloads/Papers-Reports/Reports/REFLEXFinal-Report171104.pdf
3. See “Part I. A campaign to destroy scientific findings” in http://www.kompetenzinitiative.net/assets/broschuerenreihe_heft-5_eng_screen.pdf

On 2014 Aug 10, Alexander Lerchl commented:

None

On 2014 Nov 26, Harri Hemila commented:

A comment on this study was published in DOI.

A response to that comment was published in DOI.

On 2017 Jul 31, valentina di pietro commented:

Notes: The substitution I226T has never been found in patients affected by Canavan disease. Bioinformatics tools recently deployed to predict mutations did not confirm substitution of I226T as a mutation. According to PredictSNP (https://loschmidt.chemi.muni.cz/predictsnp1/) which combines six different methods (MAPP, Phd-SNP, Poly-phen1, Poly-phen2, SIFT, SNAP) into a consensus classifier, this is a neutral substitution with an 83% level of confidence. Meta-SNP (http://snps.biofold.org/meta-snp/), a meta-predictor which combines the outputs of PANTHER, PhD-SNP, SIFT and SNAP gives a final score of 0.242 . Only a score >0.5 indicates prediction of disease mutations.

On 2015 Feb 15, James Tsung commented:

Link to Focused Cardiac Ultrasound video: https://youtu.be/40tJLGzvmMU?list=PL-HeZidYNe37Rzd6i7OeFHO4Gk3l5NHQP

On 2014 Mar 26, Tom Kindlon commented:

"Actometer readings would have provided more objective data"

My e-letter replying to this paper, "Actometer readings would have provided more objective data", can be read here: http://pediatrics.aappublications.org/content/121/3/e619/reply

On 2015 Aug 01, Jorge H Ramírez commented:

Any reason not to retract this publication?

http://chaoticpharmacology.com/?s=quetiapine

On 2014 Dec 10, Kath Wright commented:

Other search filters are available from the InterTASC Information Specialists' Sub-Group Search Filter Resource at https://sites.google.com/a/york.ac.uk/issg-search-filters-resource/home

On 2015 Mar 25, Sandra Rieger commented:

I would like to know which cells were investigated?

On 2014 Mar 09, Mark Milton commented:

This a good review article. However, the values cited for the vitreal volume of the cynomolgus monkey are incorrect. The source articles were misread. The quoted vitreal volumes (1.5 and 3.2 mL) shouldn't be used when calculating a safety margin based upon the differences in vitreal volume between cynomolgus monkey and man.

On 2014 Aug 08, Yuwei Fan commented:

The equation 2 in Biaxial Flexural Strength Test section seems not correct. Not sure if the data are valid.

On 2015 Jun 02, thomas samaras commented:

Additional information is available on height, body size and longevity from the following publications.

Samaras TT. Evidence from eight different types of studies showing that smaller body size is related to greater longevity. Journal of Scientific Research & Reports. 2014: 3 (16): 2150-2160, 2014; article no. JSRR.2014.16.003.

Samaras TT. Human Scaling and Body Mass Index. In: Samaras TT (ed): Human Body Size and the Laws of Scaling: Physiological Performance, Growth, Longevity and Ecological Ramifications. New York: Nova Science Pub; 2007: pp 17-32.

He Q, Morris BJ, Grove JS, Petrovitch H, Ross W, Masaki KH, et al. Shorter men live longer: Association of height with longevity and FOXO3 genotype in American men of Japanese ancestry. Plos ONE 9(5): e94385. doi:10.1371/journal.pone.0094385.

Salaris L, Poulain M, Samaras TT. Height and survival at older ages among men born in an inland village in Sardinia (Italy), 1866-2006. Biodemography and Social Biology, 58:1, 1-13.

Bartke A. Healthy Aging: Is Smaller better? A mini-review. Gerontology 2012; 58:337-43.

On 2014 Dec 10, Kath Wright commented:

Other search filters are available from the InterTASC Information Specialists' Sub-Group Search Filter Resource at https://sites.google.com/a/york.ac.uk/issg-search-filters-resource/home

On 2013 Nov 04, Laura Williams commented:

Walsh F, 2013 recently investigated the central claim of this article, which is that many soil bacteria are able to grow using different classes of antibiotics as a single carbon source. Contrary to the findings of Dantas et al., Walsh et al. were only able to confirm catabolism of beta-lactam antibiotics, rather than catabolism of multiple classes of antibiotics. Their paper points to the presence of EDTA in the minimal medium used in the original study as a possible source of carbon sufficient for bacterial growth, which would suggest that growth in the media+antibiotic condition is not a indication of catabolism of the antibiotic, but simply antibiotic resistance.

On 2013 Nov 05, Fiona Walsh commented:

The beta-lactams in our study were not 'catabolised' but were digested by the antibiotic resistance enzymes, the beta-lactamases. We used the same strains as the Dantas study i.e. two beta-lactam catabolising bacteria and also identified that the degradation of the beta-lactams was due to the beta-lactamases. These bacteria were either Pseudomonas or Burkholderia species, both of which contain chromosomal beta-lactamases. We identified bacteria which presented with a streptomycin or trimethoprim 'catabolising' phenotype, which we isolated from soil (the original strains from Dantas et al., study with such phenotypes were lost). However, the HPLC experiments clearly showed that these antibiotics were not degraded over 28 days, we concluded based on these and other results that the bacteria did not catabolise the antibiotics. The Dantas study described the HPLC/ chemical degradation studies only for the beta-lactams (carbenicillin and penicillin) and extrapolated these results to all other classes of antibiotics described in the study.

On 2014 Jan 08, Tom Kindlon commented:

More information on what exactly was measured in Reynolds (2004) would have been useful

An important part of this paper is the indirect cost estimates taken from Reynolds et al [1]. It would have been useful to have been given clear information on what was measured in that study.

The current paper says at one point: "Indirect costs include transportation, work productivity losses, disability reimbursements, loss of leisure or duties at home, or services provided by family members, friends, or other informal care providers". However what Reynolds measured was the loss of productivity. It didn't not measure the cost of disability re-imbursements, for example.

This would partly explain differences with some other figures. For example, a report published by Sheffield Halham University in the UK in 2003 estimated the cost to the UK at 3.467 billion pounds Sterling. It calculated the "cost to the nation" by adding together the figure for the lost taxes from people not working plus the cost of paying them disability payments. There could be said to be pluses and minuses with either method of course.

Also, one other minor point: it might have been useful to point out that part of the reason there would be discrepancies between quoted studies is the effect of inflation. For example, we are told "Lloyd and Pender estimated an average cost of $9,436 per patient with ME/CFS, including about AU $2,000 per patient in direct medical costs". But we are not told in the text that the Lloyd and Pender study was published in 1992 (perhaps the figure was increased due to inflation but this has not been made clear).

References:

[1] Reynolds KJ, Vernon SD, Bouchery E, Reeves WC. The economic impact of chronic fatigue syndrome. Cost Eff Resour Alloc. 2004 Jun 21;2(1):4.

[2] Lloyd AR, Pender H. The economic impact of chronic fatigue syndrome. Med J Aust. 1992 Nov 2;157(9):599-601.

On 2017 Jul 11, Daniel Haft commented:

Readers may wish to note that the passenger domain of this autotransporter has multiple copies of repeat that averages about 88 residues in length, with consensus sequence GDNTYAGGTEVEAGTLRVSRDANLGAAAGAVTLDGGALAATASFASARALTLKAAGALDVAAGTTLDWRGAVSGAGKLVKEGAGTLVL. The BatB orthologs discussed in this paper have 17 repeats in Bordetella pertussis and B. bronchiseptica, and 11 repeats in B. parapertussis. The deletion of 531 amino acids in B. parapertussis maps to this repeat region. Additional batB gene translations from Bordetella isolates obtained since this paper show additional examples of changes in the numbers of repeats. Since individual repeats are quite different from each other, these changing repeat copy numbers very likely represent natural variation, not sequencing and assembly errors. Therefore, the shorter form seen in B. parapertussis should not be viewed as non-functional simply because it shows a large deletion relative to B. pertussis.

On 2014 Jan 07, Brett Snodgrass commented:

Dear Reader,

Thank you for providing the excellent report and images. Please provide your kind attention to the distinction between the Thebesian veins and the vessels of Wearn.

http://bit.ly/JTWearn

https://twitter.com/BrettSnodgrass1/status/415908673412530177

A possible name for the title may be: Persistent vessels of Wearn Presenting as Ischemic Heart Disease.

Comments and suggestions are welcome.

Thank you kindly.

On 2016 Mar 10, Kristina Hanspers commented:

The pathways in figures 6-9 are available in the "Open Access Publication" collection at WikiPathways: http://wikipathways.org/index.php/Pathway:WP152, http://wikipathways.org/index.php/Pathway:WP566, http://wikipathways.org/index.php/Pathway:WP341 and http://wikipathways.org/index.php/Pathway:WP211. These pathways can be downloaded for use in network analysis tools such as Cytoscape and PathVisio.

On 2014 Sep 07, Ivan Oransky commented:

This now-retracted paper is one of nine retracted by first author Cory Toth: http://retractionwatch.com/2014/09/02/diabetes-researcher-cory-toth-now-up-to-nine-retractions/

On 2014 Dec 10, Kath Wright commented:

Other search filters are available from the InterTASC Information Specialists' Sub-Group Search Filter Resource at https://sites.google.com/a/york.ac.uk/issg-search-filters-resource/home

On 2013 Oct 24, Tom Kindlon commented:

Extremes In Activity Levels Of Those With Persistent Fatigue Were Not Investigated

I question the claim in Viner et al¹ that "being highly sedentary or highly active independently increased the risk of persistent fatigue, suggesting that divergence in either direction from healthy levels of activity increases the risk for persistent fatigue."

The authors themselves point out that their "definition of being physically active (1 hour of exercise on >=2 days per week) is roughly similar to the current recommendations for adolescents of the President’s Council on Physical Fitness and Sports and the National Association for Sport and Physical Education: “teens should do at least 20 minutes of vigorous activity 3 days a week and 30 minutes of moderate activity 5 days a week”.² So why is this level of activity, which was reported by 48.7% of the young people, being presented as being excessive? If they wanted to investigate being "highly active" (as opposed to simply being “active”), activity levels should not have been dichotomized at level they were in this study.

The question about sedentary activities was: “Outside school hours, on average, how many hours a day do you usually watch TV or videos, play video games, or play on the computer?” If a young person was sedentary for >4 hours a day, it does not mean they was necessarily inactive; indeed in phase 1, 23% of active young people were sedentary for more than 4 hours per day (compared with 30% of inactive young people). Such a lifestyle could be associated with fatigue for other reasons; for example, it could result in a shortage of sleep, rather than it necessarily causing unhealthily low levels of activity.

1 Viner RM, Clark C, Taylor SJ, Bhui K, Klineberg E, Head J, Booy R, Stansfeld SA. Longitudinal risk factors for persistent fatigue in adolescents. Arch Pediatr Adolesc Med. 2008 May;162(5):469-75.

2 Corbin CB, Pangrazi RP, Le Masurier GC. Physical activity for children: current patterns and guidelines. Res Dig. 2004;5(2):1-8.

On 2014 Nov 23, Harri Hemila commented:

A manuscript version is available at handle

On 2014 Apr 07, Muhammad Aslam commented:

This is an interesting study but there is a technical mistake. Hopefully the authors can respond to that. On page 1351 (page 2 of article) the authors state ''Here, we have used 2 such Ras effector mutants to identify selective contributions of Ras effectors of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) or PI3K pathway to vascular phenotypes in vivo. RasV12C40 (G12→V12, T40→C40) binds to and selectively activates PI3K, whereas RasV12S35 (G12→V12, Y35→S35) binds to Raf1 and selectively activates the ERK/MAPK pathway.''

In original H-Ras sequence (NP_001123914.1) there exist no T40 or Y35 rather it is the other way round. In sequence it is T35 and Y40 which is changed to S35 and C40, respectively, as stated by article from Joneson T et al (Science 1996; 271: 810–812).

Regards,

On 2017 Sep 23, Tero Kivelä commented:

Figure 1 in this paper is problematic. It states to show survival curves for uveal melanoma patients. However, while there were 13 patients with uveal melanoma of whom 12 were treated, the figure shows 18 deaths.

On 2016 Mar 29, Jonathan Wren commented:

URL apparently must have ".html" on end to work: http://www.genome.jp/kegg/atlas.html

On 2013 Oct 28, DAVID SANDERS commented:

See the earlier articles "Sulfhydryl involvement in fusion mechanisms" [2000]Sanders DA, 2000 and "Ancient viruses in the fight against HIV" [2003] Sanders DA, 2003 for the prediction of the results published here.

On 2014 Jan 08, Tom Kindlon commented:

Various comments

This paper refers to the use of a re-attribution programme. I thought I would highlight the results of a trial[1] published last year on the topic. It involved testing practice-based training of GPs in reattribution. The method to test the hypothesis was a "cluster randomised controlled trial in 16 practices, 74 GPs and 141 patients with medically unexplained symptoms of 6 hours of reattribution training v. treatment as usual." It found that "Practice-based training in reattribution changed doctor-patient communication without improving outcome of patients with medically unexplained symptoms". Hardly a ringing endorsement of the method.

There has been a lot of hype about the effectiveness of Cognitive Behavioural Therapy (CBT) for Chronic Fatigue Syndrome (CFS). However, a meta-analysis[2] of its efficacy of CBT for CFS published in 2008 might temper some of the enthusiasm. The studies involved a total of 1371 patients. This involved calculating the size of an effect measure, the Cohen's d value. They calculated d using the following method: "Separate mean effect sizes were calculated for each category of outcome variable (e.g., fatigue self-rating) and for each type of outcome variable (mental, physical, and mixed mental and physical). Studies generally included multiple outcome measures. For all analyses except those that compared different categories or types of outcome variables, we used the mean effect size of all the relevant outcome variables of the study."d was calculated to be 0.48. For anyone unfamiliar with Cohen's d values, they are not bounded by 1; also, the higher the score, the bigger the "effect size" i.e. the more "effective" a treatment was found to be. Cohen's d values are considered to be a small effect size at 0.2, a moderate effect size at 0.5, and a large effect size at 0.8[2].

There are now hundreds of studies that have found "physical" abnormalities of one sort or another in Chronic Fatigue Syndrome. Thus I question the placement of "Chronic Fatigue" (which many/most people would read as referring to Chronic Fatigue Syndrome as it is listed beside Fibromyalgia and Irritable Bowel Syndrome) in figure 1, "Hypothetical scatter plot of dysfunction versus pathology in primary care consultations" where "evidence of pathological change" is said to be "absent". The numerous abnormalities found raise questions about the placement on the scatter plot or else the limitations of the concept. Also how "reversible" the "abnormal functioning, either physiological or psychological" is, remains far from clear given the low recovery rates.

References:

[1] Morriss R, Dowrick C, Salmon P, Peters S, Dunn G, Rogers A, Lewis B, Charles-Jones H, Hogg J, Clifford R, Rigby C, Gask L. Cluster randomised controlled trial of training practices in reattribution for medically unexplained symptoms. Br J Psychiatry. 2007 Dec;191:536-42

[2] Malouff, J. M., et al., Efficacy of cognitive behavioral therapy for chronic fatigue syndrome: A meta-analysis. Clinical Psychology Review (2007), doi:10.1016/j.cpr.2007.10.004

[3] Cohen J: Statistical power analysis for the behavioural sciences. Edited by: 2. New Jersey: Lawrence Erlbaum; 1988.

On 2014 Nov 13, Robert Eibl commented:

After contacting the editor in 2008 about some issues with this paper, she suggested considering a “Corrigendum”, but did not publish it. Please find below my updated and slightly modified letter to the editor:

Robert Eibl: Single-receptor adhesion measurements on living cells

Helenius et al. (1) reviewed the use of atomic force microscopy (AFM) for single-cell force spectroscopy (SCFS). They listed in table 1 the references for "receptor-ligand interactions by SCFS using living cells as probes" and pointed to two reports on cell adhesion bonds between integrin alpha4beta1 (very late antigen 4, VLA-4) and its ligand vascular cell adhesion molecule 1 (VCAM-1). Surprisingly, however, Helenius and co-workers have not included the work of Eibl and Benoit (2) in their list, although this original finding on the same integrin to ligand interaction was published well before the two cited references appeared, i.e. 5 and 18 months, respectively, earlier.

In addition to this major exclusion to the very first AFM report on VLA-4/VCAM-1 measurements at the single-molecule level on a living cell, table 1 contains two more mistakes. First, the information stated to be found in a referenced paper is actually not there: Thie et al. (3) serves as reference for the specific measurement of integrin alpha(L)beta2 (leukocyte function antigen 1, LFA-1) on its ligand interstitial cell adhesion molecule 1 (ICAM-1); these authors -- although including one of the co-authors of this review -- never claimed being able to specifically measure any cell adhesion receptor; on the contrary, they state that they could only speculate regarding the cell adhesion receptors involved in their generally unspecific measurements, which might include several integrins and other cell adhesion receptors. This error may also mislead readers with regard to several other aspects of the AFM technique for measuring leukocyte homing receptors with AFM at the single-molecule or single-receptor level, including the original developers of the approach and the time-frame in which it was developed. Second, table 1 also includes a minor, but repeated typing error: “concavalin A” instead of “concanavalin A”.

In my view, a detailed step-by-step protocol in this area could have been included at that time in the review, too (4). For readers interested in an extensive overview of this topic, a book chapter reviews this subject and includes a similar table as well as further protocols for experiments (5). Despite the discussed errors, the review includes a very useful overview on many aspects between physics and biology, and may bring the AFM technology into the scope of cell biologists, i.e. the readers of that journal. The authors are free to use their own nomenclature, like SCFS, very consistently through the review, which may appear to be useful for the beginner, but may not always be specific enough: “single-cell” measurements appear to contradict measurements between two cells, and often SCFS is also used for so-called single-molecule measurements on a cell, but a more precise nomenclature was not in the scope of the review.

REFERENCES

(1) Helenius, J., Heisenberg, C.P., Gaub, H.E., Muller, D.J. (2008). Single-cell force spectroscopy. J. Cell. Sci. 121, 1785-91

(2) Eibl, R.H. and Benoit, M. (2004). Molecular resolution of cell adhesion forces. IEE - Nanobiotechnology 151, 128-132

(3) Thie M, Röspel R, Dettmann W, Benoit M, Ludwig M, Gaub HE, Denker HW (1998). Interactions between trophoblast and uterine epithelium: monitoring of adhesive forces. Hum Reprod. (11):3211-9

(4) Eibl, R.H. and Moy V.T. (2005). Atomic force microscopy measurements of protein-ligand interactions on living cells. In: Protein-Ligand Interactions. (Editor: G.Ulrich Nienhaus), Humana Press, Totowa, NJ, U.S.A., pp. 437-448 ISBN 1588293726

(5) Eibl, R.H. (2013). Single-Molecule Studies of Integrins by AFM-Based Force Spectroscopy on Living Cells. Scanning Probe Microscopy in Nanoscience and Nanotechnology 3: 137-169, ISBN 978-3-642-25414-7_6

On 2014 Nov 17, Raphael Levy commented:

The article has been corrected after re-use of a figure from a previous article had been raised.

There is barely any evidence for the existence of this particular type of stripy nanoparticles blog post, and, more broadly, the evidence behind the structure and special properties of “striped” nanoparticles has been challenged by Cesbron Y, 2012. The publication in 2012 of Cesbron Y, 2012 took three years and has been followed by post-publication peer review of the various existing and new stripy articles on my blog, PubPeer, etc.

A detailed analysis of this body of work is published today in PloS One by Stirling et al; from the abstract: “through a combination of an exhaustive re-analysis of the original data with new experimental measurements of a simple control sample comprising entirely unfunctionalised particles, we conclusively show that all of the STM evidence for striped nanoparticles published to date can instead be explained by a combination of well-known instrumental artefacts, strong observer bias, and/or improper data acquisition/analysis protocols.”

On 2015 Mar 02, Ali Dadban commented:

Couldn't find it in the Archives of the journal's website.

On 2016 Aug 23, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00364963. We believe the correct ID, which we have found by hand searching, is NCT00364936.

This comment is being posted as part of the OpenTrials.net project^[1] , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

Many thanks,

Jessica Fleminger, Ben Goldacre*

[1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

* Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG

On 2016 Aug 19, Morten Oksvold commented:

Please note that this article has been retracted and should therefore not be cited in the future.

http://onlinelibrary.wiley.com/doi/10.1002/ijc.30270/full

On 2017 Aug 20, Daniel Weiss commented:

This paper employs flawed circular reasoning.

The methods section clearly states that “in all patients with neurologic, cardiac or joint involvement, a serologic test positive for B. burgdorferi by ELISA and Western blot was required for case inclusion.”

Then in the results section, the authors state that “among the 44 patients with neurologic, heart or joint abnormalities, all had positive IgM or IgG responses to B. burgdorferi with 2 tier testing”… 2 tier testing had a sensitivity of 100%” .

This often cited manuscript claims that two tier testing has a sensitivity of 100% among those who have positive two tier tests. I urge all to read this paper before citing it.

On 2017 Oct 02, Juliane Bremer commented:

In this review article there is a transposition error in Figure 2, page 444. The F198S-129V mutation in the prion protein that is a cause of Gerstmann-Straussler-Scheinker syndrome, is incorrectly indicated as F189S-129V.

On 2015 Oct 16, David Keller commented:

How did same-sex preference genes persist despite their effects on reproduction?

Evidence suggests the existence of genes which promote homosexual preference. A gene which tends to decrease its own reproduction in this way must have some countervailing effect in order to persist in the gene pool.

If the same mutation which promotes homosexuality in men also increases fecundity in women, it could persist in equilibrium with wild-type alleles. The reduced number of offspring of male carriers would have to be offset by an increased number of offspring in female carriers large enough to avoid the disappearance of the gene which would otherwise occur over time.

Another possibility is that social repression of homosexuality had the paradoxical effect of promoting the survival of same-sex preference genes. Modern society's tolerance, by reducing the social pressure to reproduce, could ironically lead to the gradual disappearance of genes which promote homosexual preference.

On 2016 Nov 20, Morten Oksvold commented:

An investigation committee at Wayne State University (WSU) recommends that 42 articles from Fazlul Sarkar to be retracted (report finished August 31, 2015). This article represents one of them.

This information was published by Retraction Watch (November 17, 2016) and you can find a link to the full report here:

http://retractionwatch.com/2016/11/17/details-of-investigative-report-into-sarkar-released-by-aclu/

This article should therefore no longer be cited.

On 2014 Nov 26, Harri Hemila commented:

A response to this comment was published in DOI.

On 2015 Feb 25, James Tsung commented:

Link to ultrasound videos: https://youtu.be/_4HxdGb1UlY?list=PLHg2xyua_Kjs3tj9InTqEgFkThE4MYm-F

On 2013 Nov 30, GianCarlo Panzica commented:

A following study in the same rat model, demonstrated that also the parvocellular arginine-vasopressin system of the BST and amygdal is altered in Tfm males, suggesting that also this system is depending by androgens for its full differentiation Allieri F, 2013

On 2013 Oct 26, Michael Eisen commented:

Would like to point to a followup paper from our lab: Lusk RW, 2010 used simulations of enhancer evolution to examine one of the conclusions of this paper - that the enrichment and conservation of paired binding sites we observe is the result of selection for paired sites - and found that a selection on binding site composition alone in the presence of a bias for deletions over insertions can result in an enrichment of clustered binding sites that appear (but are not) to be under purifying selection.

On 2013 Dec 30, Tom Kindlon commented:

My published response: "Change in grey matter volume cannot be assumed to be due to cognitive behavioural therapy"

I had a letter published in reply to the authors' response to the Inge Bramsen letter. Among other things, I highlighted that there was no CFS control group in this study, so one shouldn't assume any change was due to CBT e.g. it could be due to the passage of time (plausible given people with CFS, once diagnosed, are more likely to improve than deteriorate, at least in the short term). The letter can be read here: http://brain.oxfordjournals.org/content/132/7/e119.long

On 2016 Aug 23, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00605058. We believe the correct ID, which we have found by hand searching, is NCT00605085.

This comment is being posted as part of the OpenTrials.net project^[1] , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

Many thanks,

Jessica Fleminger, Ben Goldacre*

[1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

* Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG

On 2014 Nov 23, Harri Hemila commented:

A comment is available at: http://hdl.handle.net/10138/16985

On 2015 Jul 20, Salzman Lab Journal Club commented:

This paper provides strong evidence for the dramatic functional change in protein coding enabled by precise RNA editing. An interesting followup would be to see if there are changes in expression levels of the editing guide RNA during the course of trypanosome development. Also, it would be interesting to know the level of expression of the dominant negative AEP1-GFP protein relative to endogenous levels of AEP1.

On 2015 Dec 06, Mark Bolland commented:

There are several errors/inconsistencies in the data related to treatment group numbers and numbers of falls and fractures in this paper. These include:

• 1. The text and Table 1 reports 121 participants in each treatment group, but Table 3 reports 120 for Ca and 122 for CaD.
• 2. Table 3 reports that 75 participants fell with Ca and 49 with CaD, but the breakdown of fallers in Table 3 sums to 71 for Ca and 53 for CaD.
• 3. The text reports the total number of falls as 171 with Ca and 76 with CaD, but Table 3 reports 169 with Ca and 106 with CaD.
• 4. The breakdown of total falls in Table 3 sums to at least 111 with CaD, which is greater than the total falls for CaD reported in the text (76) and Table 3 (106).
• 5. The text reports the mean number of falls per group as 1.41 with Ca and 0.63 with CaD which are incompatible with the reported total number of falls in the text and Table 3.
• 6. The text reports 13 participants with fracture with Ca whereas Table 3 reports 12.

These are discussed in two letters to the editor (Osteoporos Int 2015;26:2713 Bolland MJ, 2015 and Arch Osteoporos. 2015;10:43 Bolland MJ, 2015) with responses by the lead author to each letter (Osteoporos Int. 2015;26:2715-6 Pfeifer M, 2015 and Arch Osteoporos. 2015;10:42 Pfeifer M, 2015).

Given the unwillingness/inability of the author to provide consistent data from the trial, we think it should be excluded from systematic reviews or meta-analyses until consistent data are provided by the authors, with some explanation as to how the errors/inconsistencies occurred.

We have described the full sequence of events in a separate comment.

Mark Bolland, Andrew Grey. University of Auckland

On 2015 Dec 06, Mark Bolland commented:

This comment provides background information to an earlier comment.

We were interested in why different meta-analyses of vitamin D supplements came to different conclusions, and noticed that different meta-analyses used different data from this trial. We identified several errors/inconsistencies in the text and emailed the lead author requesting clarification about the data in March 2014. He responded that the data in the Tables were correct. We replied that there were inconsistencies within the Tables as well and asked for clarification, but he did not respond.

Therefore in April 2014, we contacted the editor of Osteoporosis International advising the editor of the inconsistencies and requested that they be corrected. We felt this is particularly important as it is a highly cited, influential trial reporting benefits of vitamin D supplements on falls, and the inconsistencies occur in the treatment group numbers and the primary and secondary outcomes, so have a major bearing of the interpretation of the trial results. Our primary concern was/is to use the correct data for the trial in meta-analyses. In May 2014, the editor passed on an extract of the lead author’s response and indicated that an erratum would be published. However, we felt the lead author’s response was inadequate because it left a number of uncorrected inconsistencies/errors in the text. We pointed this out to the editor. We are not sure what action the editor took, but no erratum was published. We followed up with 2 further emails to the editor over the next year, and in April 2015, the editor advised that it seemed unlikely that an erratum would be forthcoming.

Therefore, we requested the permission to summarize the issues in a very brief letter. The editor agreed and a short letter summarizing the six errors/inconsistencies in the article was published (Osteoporos Int 2015;26:2713 Bolland MJ, 2015) with a response from the author (Osteoporos Int. 2015;26:2715-6 Pfeifer M, 2015). Unfortunately, in his response the author chose to correct only 2 of the errors identified and introduced a further inconsistency.

In a further letter to the editor, we therefore highlighted the remaining errors/inconsistencies and the consequence of using different possible data combinations from this trial for meta-analyses. The editor indicated that the issues we raised were important but probably irresolvable and offered to publish the letter in Archives of Osteoporosis. We indicated that our preference was that the data were corrected in the original publication rather than our letter being published. We think it quite straightforward to make the simple necessary corrections to two tables and a couple of sentences of text. We feel it is essential that the corrections occur as the errors are in the most important data from the trial: the treatment group numbers and the primary outcome data for falls. The editor considered the issue further and then published our letter (Arch Osteoporos. 2015;10:43 Bolland MJ, 2015) along with a response from the author (Arch Osteoporos. 2015;10:42 Pfeifer M, 2015).

In this second response, the author has still not corrected the identified errors, so, because of the inconsistencies/errors in the data, it is not possible to be sure how many women were in each randomized treatment group, how many women had a fall during the trial, how many total falls occurred in each treatment group, or what is the breakdown of participants by numbers of falls (no falls, 1 fall, 2 falls, etc).

Therefore, we think that the study should be excluded from meta-analyses and systematic reviews and its results viewed with caution until consistent data are provided by the authors with some explanation as to how the errors/inconsistencies occurred.

Mark Bolland, Andrew Grey. University of Auckland

On 2014 Dec 18, Claudia Paiva commented:

Is it possible that the recurrency is overestimated because patients without recurrent events leave the hospital and are excluded from the study? 1334 cases were found and 127 chosen because they could be followed for long term... The rate of recurrency among high-tone controls is 11% (without vertigo) and 17% (without SN), while in the literature the total recurrency among SSNHL sufferers is approximately 2%.

Alternatively, it could be due to a higher rate of recurrency in Japan, since no western studies were made concerning the recurrency rates among low tone hearing loss in western countries. Do you know any broad study in Japan that show the total recurrency rate of SSNHL in Japan and percentages of high x low tone hearing loss among total SSNHL?

It is very important to define the rate of recurrency, so that the patient is aware of the possibility and plot a plan to face it with drs (in case it is high) or can live without the constant burden of "is it going to happen again?" in their heads (in case it is low).

Anyway, these are just considerations made by a worried low tone SSNHL patient and a scientist from another field.

On 2016 Apr 25, Sergio Uribe commented:

Can caries in primary teeth predict caries in permanent teeth in Sweden? Yes considering this paper; No according to https://www.ncbi.nlm.nih.gov/pubmed/23235131

On 2016 Aug 23, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT005725079. We believe the correct ID, which we have found by hand searching, is NCT00572507.

This comment is being posted as part of the OpenTrials.net project^[1] , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

Many thanks,

Jessica Fleminger, Ben Goldacre*

[1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

* Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG