On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Human Islet Autotransplantation" DOI 10.1007/978-94-007-6884-0_21-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Immunology of β-Cell Destruction". DOI 10.1007/978-94-007-6884-0_18-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"β-Cell Function in Obese-Hyperglycemic Mice (ob /ob Mice)". DOI 10.1007/978-94-007-6884-0_15-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Mechanisms of Pancreatic β-Cell Apoptosis in Diabetes and Its Therapies". DOI 10.1007/978-94-007-6884-0_14-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Proteomics and Islet Research" DOI 10.1007/978-94-007-6884-0_12-1

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Electrical, Calcium, and Metabolic Oscillations in Pancreatic Islets". DOI 10.1007/978-94-007-6884-0_10-3

On 2015 May 10, Md. Shahidul Islam commented:

This review was published in 2010. In 2014, an updated version of this review has been published (DOI 10.1007/978-94-007-6686-0_9).

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. "Basement Membrane in Pancreatic Islet Function". Online ISBN: 978-94-007-6884-0. DOI 10.1007/978-94-007-6884-0_8-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Role of Mitochondria in β-Cell Function and Dysfunction". DOI 10.1007/978-94-007-6884-0_7-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"ATP-Sensitive Potassium Channels in Health and Disease" DOI 10.1007/978-94-007-6884-0_6-3

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Electrophysiology of Islet Cells" DOI 10.1007/978-94-007-6884-0_5-2

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015 (with a different title). Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"(Dys)Regulation of Insulin Secretion by Macronutrients" DOI 10.1007/978-94-007-6884-0_4-3

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"High-Fat Programming of β-Cell Dysfunction". DOI 10.1007/978-94-007-6884-0_3-6

On 2015 Jul 26, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015 (with a different title). Islets of Langerhans, 2nd ed. Springer. Online ISBN: 978-94-007-6884-0.

"Regulation of Pancreatic Islet Formation". DOI 10.1007/978-94-007-6884-0_36-2

On 2015 Jul 25, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. "The Comparative Anatomy of Islets" R. Scott Heller. in "Islets of Langerhans" ISBN-13: 978-9400766853 ISBN-10: 9400766858. Springer. 10.1007/978-94-007-6686-0_2

On 2015 Jul 25, Md. Shahidul Islam commented:

An updated version of this paper has been published in 2015. "Microscopic Anatomy of the Human Islet of Langerhans" Islets of Langerhans 2nd ed. 2015 Edition. Springer. PP 19-38. ISBN-13: 978-9400766853 ISBN-10: 9400766858 DOI 10.1007/978-94-007-6884-0_1-2

On 2015 Mar 13, Martine Crasnier-Mednansky commented:

Escherichia coli cells growing on excess glucose (Fig. 3, Environment G) do not consume acetate after glucose depletion (the acetate switch occurs before glucose is fully depleted). In fact, cells utilize both glucose and acetate during entry into the stationary phase of growth (see Fig. 1A in Wolfe AJ, 2005). Failure to assimilate acetate before glucose depletion was reported for a specific mutant strain and resulted in a diauxic type of growth (Nyström T, 1993).

Acetate utilization by acetate-adapted cells is not diminished by glucose addition (Lowry OH, 1971). Furthermore glucose utilization by acetate-adapted cells is inhibited by acetate. It is therefore questionable whether acetate-adapted cells are `adapting´ to glucose when transferred to a medium containing a large excess of acetate (Fig. 3, Environment GA). In this context, the reversible phosphotransfer reaction between phosphoacetate kinase and the phosphotransferase system (PTS), originally proposed by Fox DK, 1986 but never established in vivo, should be physiologically relevant as to regulate the rate of sugar transport by the PTS and thus the cAMP level.

On 2013 Oct 23, ANDREW SU commented:

!MOVED http://biogps.org

The URL in the original abstract has now been retired. This data set (together with other gene expression data sets) are now hosted at http://biogps.org.

On 2016 Apr 22, Morten Oksvold commented:

Please note that this article has been retracted.

On 2013 Nov 24, John Sotos commented:

In his letter describing recently-introduced Congressional legislation to establish “healthcare innovation zones” (1), Dr. Kirch of the Association of American Medical Colleges (AAMC) listed his financial disclosures as “none.” I believe this is misleading.

Dr. Kirch did not disclose that the AAMC proposed such zones (2). As a federally registered lobbying organization that has spent $100,000-$400,000 annually on lobbying activities since 1999 (3), common sense dictates that one of the AAMC’s “products” is legislation.

Thus, Dr. Kirch should have disclosed his organization’s role in the product his letter described, just as he would have disclosed if his organization had invented a new drug or device expected to benefit the organization or its affiliates. At the very least, such disclosure would have helped the JAMA editors realize he was hyping something his organization helped create.

(1) Kirch DG. The Healthcare Innovation Zone: a platform for true reform. JAMA. 2010 Mar 3;303(9):874-875. Pubmed 20197534. doi: 10.1001/jama.2010.224.

(2) “Rep. Schwartz introduces legislation to establish AAMC-proposed health care innovation zones.” Press Release, Association of American Medical Colleges, July 10, 2009. Online at: http://www.aamc.org/newsroom/pressrel/2009/090710.htm — accessed April 4, 2010.

(3) Lobbying Disclosure Act Database: http://soprweb.senate.gov/index.cfm?event=choosefields — Searched on “registrant name” = “association of american medical colleges” on April 4, 2010.

On 2016 Jul 01, Anne Niknejad commented:

'It has been shown that apoptotic stimuli induce nuclear accumulation of GSK3β colocalising it with p53 [15]. This study reported that there was no nuclear accumulation of GSK3β after DNA damage (induced by camptothecin treatment) but rather an exclusive activation of the nuclear pool with no activation of cytosolic pools. The authors showed that p53 coimmunoprecipitates with GSK3β from nuclear fractions after camptothecin treatment.'

Actually the reference 15 is wrong, no 'p53' mention, no camptothecin treatment (but staurosporine treatment)

http://www.ncbi.nlm.nih.gov/pubmed/?term=11495916

The correct reference could be

http://www.ncbi.nlm.nih.gov/pubmed/?term=12048243

(not cited in References)

On 2014 Jan 08, Tom Kindlon commented:

Early diagnosis of CFS/ME has been shown to lead to a better prognosis

It was interesting to see the various views expressed by GPs in this paper[1]. However I think a couple of useful points could have been added. There is much discussion in the paper about whether a label of CFS/ME is useful or not. The authors refer to NICE guidelines which "emphasise the importance of a definitive diagnosis"[2]. However, I think it would have been useful to add some direct evidence on this issue.

For example, research published by the Centres for Disease Control and Prevention (CDC) which found that an earlier diagnosis led to a better prognosis[3]. This prompted the CDC to launch a two-pronged awareness drive aimed at both health professionals and the general public - the tag line for the latter was, "Get informed. Get diagnosed. Get help."[4].

A UK study found that the longer the interval between a patient falling ill and getting a diagnosis, the greater the likelihood that they would become severely affected. [5]

The authors mention the issue of CFS/ME being managed in primary care. It is important for GPs to know that GPs encouraging patients to do a graded exercise programme is associated with a higher rate of adverse reactions. For example, a survey which asked patients about their experiences of treatments over the previous three years found that 45% reported being made worse by a graded exercise therapy (GET) programme overseen by their GP, compared to 31% who reported being made worse by a GET under a NHS specialist and 29% of those who did a GET in other circumstances[6]. The NICE guidelines do not recommend that a GP oversee such an approach[2].

References:

[1] Chew-Graham C, Dowrick C, Wearden A, Richardson V, Peters S. Making the diagnosis of Chronic Fatigue Syndrome/Myalgic Encephalitis in primary care: a qualitative study. BMC Fam Pract. 2010 Feb 23;11:16.

[2] NICE CG 53 Chronic fatigue syndrome/Myalgic encephalomyelitis (or encephalopathy) guideline.

[3] Nisenbaum R, Jones JF, Unger ER, Reyes M and Reeves WC. A population-based study of the clinical course of chronic fatigue syndrome. Health and Quality of Life Outcomes 2003;1:49-58.

[4] CDC Chronic Fatigue Syndrome Awareness Campaign. http://cdc.gov/cfs/awareness.htm [Last accessed: 31 March, 2010]

[5] Pheby D and Saffron L. Risk factors for severe ME/CFS. Biology and Medicine (2009); 1 (4):50-74. http://biolmedonline.com/Articles/vol1_4_50-74.pdf [Last accessed: 31 March, 2010]

[6] Action for M.E. and AYME Survey 2008 Results http://afme.wordpress.com/5-treatments-and-symptoms/ [Last accessed: 31 March, 2010]

On 2017 Jun 27, Andy Collings commented:

A subset of experimental results from this study were the focus of a replication attempt as part of the Reproducibility Project: Cancer Biology (https://osf.io/e81xl/wiki/home/). The experimental designs and protocols were reviewed and approved in a Registered Report (http://dx.doi.org/10.7554/eLife.12626) and the results of the experiments were published in a Replication Study (http://dx.doi.org/10.7554/eLife.26030).

On 2016 May 10, Morten Oksvold commented:

Please pay attention to the following report by ORI (Office of Research Integrity) before reading this article:

https://ori.hhs.gov/content/case-summary-pastorino-john-g

On 2014 Nov 19, Amanda Capes-Davis commented:

Cell lines that are known to be misidentified are now also hosted in the NCBI BioSample database at http://www.ncbi.nlm.nih.gov/biosample/.

The list of known misidentified cell lines continues to be updated by ICLAC and has a dedicated webpage at http://iclac.org/databases/cross-contaminations/.

Many thanks to Tanya Barrett and NCBI staff for their work in making the data more widely accessible.

On 2014 Jul 29, Amanda Capes-Davis commented:

Neil, in answer to your question, we have been distributing our list of misidentified cell lines since 2009. Initially we did not have a dedicated website for distribution and I was concerned about the security of the data when people could not come back to check the data against a primary source. We now have a website up and running as a primary distribution point so an open source approach is much more feasible.

The committee is a voluntary one, so we offer the data using whatever tools we have available. Hosting in the NCBI BioSample database is a fantastic step forward for us.

On 2014 Jul 29, Neil Saunders commented:

Good to know that something (somewhat) better than PDF is available, but why not simply post that at the ICLAC site rather than via email? Also good to hear about BioSample.

On 2014 Jul 29, Casey A Ydenberg commented:

If you send me the spreadsheet, I would be happy to create a more human-and-computer friendly version which you could then add to the ICLAC website (for free). ydenberg AT gmail DOT com.

On 2014 Jul 29, Tanya Barrett commented:

In addition, the ICLAC cross-contaminated and misidentified cell lines will soon be hosted in the NCBI BioSample database - watch out for a link on the homepage at http://www.ncbi.nlm.nih.gov/biosample/

On 2014 Jul 29, Amanda Capes-Davis commented:

Neil, the database itself is maintained as an Excel spreadsheet. Copies are available on request - just let me know your email and I can send through to you.

On 2014 Jul 28, Neil Saunders commented:

This looks like a very useful resource. I'm sure it would be used and known more widely if the data were provided in an open, usable format. A PDF is most certainly not a database. Perhaps someone at the ICLAC could look into providing the data in a delimited plain text format such as CSV.

On 2014 Jan 13, Amanda Capes-Davis commented:

This list of cross-contaminated or misidentified cell lines is now curated by the International Cell Line Authentication Committee (ICLAC). You can download the latest version at http://iclac.org/databases/cross-contaminations/

On 2014 Jan 14, Sergei Jargin commented:

More details: Jargin SV. Some aspects of dental caries prevention and treatment in children: a view from Russia. Pesq Bras Odontoped Clin Integr, João Pessoa 2010; 10(2):297-300. http://revista.uepb.edu.br/index.php/pboci/article/viewFile/959/464

On 2014 Dec 11, Ibrahim Masoodi commented:

Ulcerative colitis has remitting and relapsing course and is affecting millions around the globe.The biomarkers can predict the severity in a non invasive manner .There is a growing need to identify more useful biomarkers in order to predict an impending relapse . We found serum CRP and fecal markers MPO , Lactoferrin very useful.These correlated with endoscopic severity and disease activity

On 2014 Sep 07, Ivan Oransky commented:

The authors of this retracted study are returning a $275,000 (AU)grant because of "misleaing and incorrect" information: http://retractionwatch.com/2014/08/29/australian-university-to-repay-275k-grant-because-of-misleading-and-incorrect-information/

On 2014 May 20, Ivan Oransky commented:

This study has been retracted: http://retractionwatch.com/2014/05/19/seventh-retraction-appears-for-author-who-tampered-with-investigation/

On 2016 Apr 22, Morten Oksvold commented:

Please note that this article has been retracted due to plagiarism.

On 2017 Jul 07, Morten Oksvold commented:

This article should have been retracted after an investigation by The University of Maryland found this article to contain "compromised" data (a total of 26 articles in 11 journals were affected). The journal Cancer Research was informed in August 2016, according to Retraction Watch.

http://retractionwatch.com/2017/04/26/university-asked-numerous-retractions-eight-months-later-three-journals-done-nothing/

On 2014 Jan 07, Brett Snodgrass commented:

Dear Author,

Thank you for the excellent article.

Please provide your kind attention to the distinction between the Thebesian veins and the vessels of Wearn.

Please consider the following post and associated links to PubMed related to the heart's vasculature. https://twitter.com/BrettSnodgrass1/status/417049983028690944

Comments and suggestions are welcome.

Thank you kindly.

On 2014 Jul 14, Sally Gore commented:

Required reading for our library fellows as they work through their rotation in research and scholarly communication services.

On 2014 Jan 11, I-Chen Tsai commented:

Wow. PubMed now opens for comments, called PubMed commons!!

On 2014 Oct 06, Anders von Heijne commented:

Wonderful!. This is a must read for all diagnosticians. But don´t miss Stanley DE, Campos DG. The logic of medical diagnosis. Perspect Biol Med. 2013 Spring;56(2):300-15 that takes the argument one step further.

On 2016 Nov 28, David Juurlink commented:

I thank Dr. Tucker for this comment. Upon re-examination, the quote above (taken from Vowles KE, 2015) does not accurately reflect the methodology of the Cochrane review. I have shared this observation with the quote's author. I remain concerned, however, about the generalizability of the review's conclusions regarding the risk of iatrogenic opioid addiction, which are at odds not only with a large body of clinical experience but also with two recent, comprehensive systematic reviews (Chou R, 2015, Vowles KE, 2015) that conclude opioid addiction occurs far more frequently than this review suggests.

On 2016 Nov 26, John Tucker commented:

There is an old saying "If it sounds too good (bad) to be true, it probably isn't". Thus my curiosity was raised when Dr. Juurlink, quoting a third party rather than the Cochrane Review itself, implied that the low rate of addiction reported in this review is an artifact of arbitrarily imputing zero addiction rate to studies in which it was not reported.

Reference to the original text shows that Dr. Juurlink's statement and the letter he quotes are both incorrect.

The actual content of the review is below:

"Six studies [of 26 total] specifically stated that no cases of addiction were observed, and 18 studies did not report whether addiction was observed.... Among the studies where addiction or addiction and abuse rates are specifically reported, the total event rate is 0.27% (7/ 2613)."

The Review further states that if the rate in the remaining trials (which were much smaller) is assumed to be zero, the addiction rate falls by about half.

Thus in contrast to Dr. Juurlink's implied statement, the conclusion of this meta analysis, that addiction rates in chronic pain are quite low among appropriately screened patients, is NOT contingent upon unrealistic assumptions.

On 2016 Nov 06, David Juurlink commented:

Regarding the risk of addiction during chronic opioid therapy, readers of this review are directed to the correspondence associated with Vowles KE, 2015, in which the authors note: "Importantly, of the 26 studies reviewed by Noble et al., only 2 (7.7%) reported rates of opioid addiction and those authors imputed (page 8) an addiction rate of zero in the other 24 studies (92.3%). Although there is clear utility in their broader findings, we would urge caution in assuming absence of any particular phenomenon simply because it is not reported."

On 2013 Nov 24, John Sotos commented:

Medical educators I’ve known have often cited the case histories in the Journal‘s CPCs as model presentations of clinical information.

Unfortunately, case 2-2010 jeopardizes this reputation by saying the patient experienced “an episode of pain in his left arm … that radiated to his heart” (1).

Medical trainees should not emulate this statement, for three reasons:

First, it is not believable. The complex innervation of thoracic structures prevents localization of pain to any internal organ.

Second, it is ambiguous. Many patients believe pain near the left breast is “heart pain” (2), whereas physicians generally associate retrosternal discomfort with cardiac ischemia.

Third, even if this statement were a direct quote from the patient, it violates the precept to “question [the patient] until sufficient details are obtained to categorize the symptom in medical terms” (3).

No institution of medical education can rest on its laurels. I hope The Journal will re-dedicate itself to maintaining its pre-eminence in this vital field.

(1) Isselbacher EM, Kligerman SJ, Lam KM, Hurtado RM. Case records of the Massachusetts General Hospital. Case 2-2010. A 47-year-old man with abdominal and flank pain. N Engl J Med. 2010 Jan 21;362(3):254-62. Pubmed 20089976 doi: 10.1056/NEJMcpc0905548.

(2) Wood P. Diseases of the Heart and Circulation. 2nd ed. London: Eyre and Spottiswoode, 1956. Page 4.

(3) DeGowin RL. DeGowin & DeGowin’s Bedside Diagnostic Examination. 5th ed. New York: Macmillan, 1987. Page 24.

On 2016 Aug 08, Stuart RAY commented:

The single line "Erratum in Correction [Hepatology. 2015]" above does not capture the complex recent history of this publication. That correction notes a 12-fold (person-years vs. person-months) calculation error that, once corrected, eliminates any statistical difference in HCC rates between those with HBsAg loss and those with HCC persistence.

Fortunately, an alert and astute reader (Chee-Kiat Tan, Singapore General Hospital) called attention to the important implications of this error in a Letter to the Editor [which, I hope, will be linked from this Pubmed record]. The authors provided a fairly terse reply.

In a notably rare Editorial response to Tan's letter, Michael Nathanson and Norah Terrault note that a key conclusion of the report is arguably strengthened by the correction: that HCC can occur in persons even after HBsAg loss, even in the absence of cirrhosis.

The importance of vigilance for HCC in persons with HBV infection (even in the absence of detectable HBsAg) is amplified by this correction; careful reading of the literature is also emphasized.

On 2014 Apr 10, Alexander Klabnik commented:

I recommend

On 2016 Feb 18, Kristina Hanspers commented:

The interactome in figure 1b is available in the "Open Access Publication" collection at WikiPathways: http://www.wikipathways.org/index.php/Pathway:WP2916. This pathway can be downloaded for use in network analysis tools such as Cytoscape and PathVisio.

On 2014 Feb 07, Saša Branković commented:

This theory is a (probably unintentional) plagiarism. Because, Manfred Velden (1974) had introduced the uncertainty (entropy) processing hypothesis of the orienting response and Saša Branković (2001) implemented the model into the theory of motivation, which has been called the theory of informational needs.

On 2014 Mar 15, Jonathan Eisen commented:

Carl Zimmer wrote an article in the New York Times about this paper. See Scientists Start a Genomic Catalog of Earth’s Abundant Microbes

On 2014 Mar 13, Jonathan Eisen commented:

I am the senior author on this paper and I have written a detailed blog post describing some of the history behind the project and other details. See "Story Behind the Nature Paper on 'A phylogeny driven genomic encyclopedia of bacteria & archaea'"

On 2013 Nov 01, Darren L Dahly commented:

I am currently drafting a paper following from this work that uses mixture modelling to cluster study participants based on these socio-economic indicators. A poster of the preliminary work can be found here. http://f1000.com/posters/browse/summary/1089836 It offers a different perspective from this previous paper that focused on results from linear models.

On 2015 Oct 07, Peter Good commented:

Shaw recently presented compelling evidence that acetaminophen (Tylenol) depletes glutathione in autism, asthma, and other disorders: “The characteristic loss of Purkinje cells in the brains of people with autism is consistent with depletion of brain glutathione due to excess acetaminophen usage, which leads to premature brain Purkinje cell death.”[1] Shaw observed that Cuba vaccinates all their children, especially against measles, yet their autism incidence is only 1/300th of ours in the U.S. What’s the difference, according to Shaw? Cuba prohibits over-the-counter acetaminophen, and only rarely allows acetaminophen prescribed for vaccinations, because acetaminophen is limited by the embargo. Deth noted that acetaminophen (like mercury) readily binds selenium-containing proteins that underlie the glutathione system [2]. By depleting glutathione, acetaminophen may effectively deplete glutamine because glutamine enters cells more easily than glutamate, thus often provides glutamate to synthesize glutathione [3].

As Shaw noted, Bauer and Kriebel reported recommendations that acetaminophen (paracetamol in the UK) be given before and after circumcision: “These guidelines include the suggestion of a first dose . . . two hours prior to the procedure, and doses every 4–6 hours for 24 hours following the procedure. Thus newborn males often receive 5–7 doses . . . during the developmentally vulnerable initial days of life.” They also cited evidence that may explain the increased number of children born autistic: “In the early 1980’s about 42% of women used paracetamol during the first trimester of pregnancy. The rate climbed to over 65% in the early 1990’s, where it has essentially remained through 2004.”[4]

For further evidence of glutathione depletion in autism, see: Chronic neurochemical asymmetry and dysconnection in autism. Implications of a personal trial of oral citrulline + taurine – published at <http:/www.autismstudies.net>

references 1. Shaw W. Evidence that increased acetaminophen use in genetically vulnerable children appears to be a major cause of the epidemics of autism, attention deficit with hyperactivity, and asthma. J Restorative Medicine 2013;2:1–16. 2. Deth R (PhD). Personal communication 2010. 3. Hong RW, Rounds JD, Helton SW, Robinson MK, Wilmore DW. Glutamine preserves liver glutathione after lethal hepatic injury. Ann Surg 1992;215:114–119. 4. Bauer AZ, Kriebel D. Prenatal and perinatal analgesic exposure and autism: an ecological link. Environ Health 2013;12:41.

On 2014 Jul 02, Balázs Győrffy commented:

Our paper described the analysis tool as it was at the time of publication. For a more up-to-date description please check either the homepage (www.kmplot.com) or our latest publication (http://www.ncbi.nlm.nih.gov/pubmed/?term=24367507).

On 2014 Mar 12, Diana Frame commented:

The full text link provided for this article does not work, but full text can be found here: http://www.annalsoftransplantation.com/download/index/idArt/880549 . Note that it's only "free full text" if you choose the personal copy option.

On 2014 Aug 01, Mark Yarchoan commented:

Overall, this study raises interest in a link between metabolic derangements and Alzheimer’s disease (AD). However, one concern I have is that in evaluating a possible association between low circulating leptin and incident dementia, the authors adjusted for current BMI, but not amount or direction of recent weight change. It is well known (and reiterated in this article) that, “Although midlife obesity is associated with an increased risk of AD, late-life weight loss is known to precede the onset of clinical AD.” Therefore, it is to be expected that the AD and normal groups might have similar overall weight and BMI, but a different direction and rate of BMI change (AD group rapidly losing weight, normal aging group keeping or gaining weight). Leptin levels are correlated with current body fat mass, but appear to be even more significantly affected by direction of weight change. For example, 14% intentional weight loss in human subjects results in a 64.5% reduction in leptin levels (Sumithran et al. NEJM 2014/ PMID: 22029981). Therefore, I am concerned that the observed differences in leptin levels in this study may simply be a consequence of the significant and early weight loss seen in AD.

On 2015 Oct 15, Nanjiang Shu commented:

Link to the web-server has been changed to http://frag1d.bioshu.se

On 2014 Jan 15, Patricia Duffel commented:

Considerable changes to PubMed have taken place since this was written. I suggest taking a look at https://www.ncbi.nlm.nih.gov/books/NBK3827/

On 2015 Dec 01, S A Ostroumov commented:

DOI:10.1134/S0012496609050159; In the presence of this aquatic, submerged, free-floating higher plant (rigid hornwort) in water system, it was occured that a decrease in concentrations of the four heavy metals (cadmium; copper; lead; zinc; Cu, Zn, Cd, and Pb) in the water medium accelerated. The aquatic macrophytes served as a factor to speed up the water purification (decontamination) process in the aquatic system. The method for measuring the heavy metals was stripping voltammetry. This paper is in the database of the United States Environmental Protection Agency (U.S.EPA), titled: Health & Environmental Research Online (HERO): http://hero.epa.gov/index.cfm?action=reference.details&reference_id=362778; FULL TEXT ONLINE FREE: https://www.researchgate.net/publication/40481671; KEYWORDS: the additional keywords for this paper in the database HERO: phytoremediation; polluted water; water pollution; water quality; Ceratophyllum demersum; Ceratophyllum; Ceratophyllaceae; Nymphaeales; dicotyledons; angiosperms; Spermatophyta; plants; eukaryotes; water composition and quality; Aquatic Biology and Ecology (MM300); Water Resources (PP200); Pollution and Degradation (PP600); Industrial Wastes and Effluents. The additional keywords: decontamination, aquatic, submerged, free-floating, higher plant, phytotechnology, ecotechnology, macrophytes, environmental toxicology, environmental chemistry, hornwort, rigid hornwort, coontail, coon's tail, stripping voltammetry; **

On 2014 Nov 19, Kaccie Li commented:

The authors of this study generalized the subjects from the United States to be white/Caucasian which is a serious oversight. A cursory look at US demographics would reveal that just over 75 percent of the population is white which is probably already questionable to generalize the entire group as white, but a closer look reveals even more concerning factors. Consider the populations in the studies classified under "white" in Table 2 of this article where the first two entries were studies done by Wang and colleagues (ref 13) and Porter and colleagues (ref 14). The first study was done at Baylor College of Medicine where a meager 43 percent of the student population is white. Suppose subject recruitment was done in the city Houston in general, the conclusions of Lim's study can be further put under scrutiny since only about 25 percent of Houston's population is white (non-hispanic). Similar things could be stated about individuals recruited in Porter's study (ref 14) at the University of Rochester where only about 76 percent of the student body is white. Lim and Fam does not mention the possibility of the presence of significant African and Asian Americans being an unknown factor that could have affected their results and conclusions.

On 2014 Oct 15, Amanda Capes-Davis commented:

More recent work has shown that hTERT-EEC is misidentified and is actually MCF-7. So hTERT-EEC cells are from breast carcinoma, not immortalized endothelium.

It's important to test cell lines to confirm they correspond to the expected donor and are not cross-contaminated, using a consensus technique such as STR profiling. Journals are increasingly requiring testing as a prerequisite before publication and this will help to address the widespread use of misidentified cell lines in the scientific literature.

It's also a good idea to check before using a cell line to see if others have documented a problem previously. ICLAC maintains a list of known misidentified cell lines at http://iclac.org/databases/cross-contaminations/.

On 2017 Aug 20, Daniel Weiss commented:

This paper shows the insensitivity of two tiered testing for Lyme disease. Patients were “categorized as having Lyme disease, and met the CDC surveillance criteria for diagnosis”, i.e. positive serology or positive culture. Nonetheless, only “two-thirds of patients with acute neuroborreliosis or carditis … were seropositive by two-tier testing”. Therefore, one third were negative.

These authors also state that “IgM testing in Lyme disease has been problematic” and the CDC requirement that “IgM criteria should only be used to support the diagnosis of early LD in persons with illness of <1 month duration” “reduces the sensitivity of serologic testing” in certain patient groups.

This is one of many papers that argue against the reliance on serologic tests to rule out Lyme disease.

On 2017 May 31, David Nunan commented:

Readers may not be aware of the notice of concern raised with this paper and another paper (Paterna S, 2008) by the same group published in Clinical Science in 2008, both of which were included in a 2012 systematic review published in BMJ Open Heart which was subsequently retracted. Whilst there is a link above to the notice of concern, here I've provided the contents of that notice. This paper has not been retracted.

Concern has been raised regarding a paper published in the Journal of Cardiac Failure: “Long-Term Effects of Dietary Sodium Intake on Cytokines and Neurohumoral Activation in Patients With Recently Compensated Heart Failure,” by Parrinello et al, J Card Fail 2009;15:864–73. The paper contains a dataset identical to that published by the same authors in Clinical Science 2008;114:221–30. The corresponding author, Dr di Pasquale of Palermo, Italy, has indicated that an error was made during a “cut and paste” process, and a table from the 2008 Clinical Science paper was mistakenly reproduced in the 2009 Journal of Cardiac Failure paper. Dr di Pasquale also coauthored an online manuscript in Heart, August 21, 2012, using a meta-analysis of 6 earlier papers, and that online report also includes the duplicated data. When questioned about the data, Dr di Pasquale reported that by unintentional error he had inserted the table from the earlier 2008 paper (Clinical Science) into the 2009 paper (Journal of Cardiac Failure). The Dean of the Medical School at the University of Palermo was notified and asked to investigate the matter. It was reported that Dr di Pasquale lost the raw data owing to a “computer crash” without having made backup files. The data are therefore not verifiable. Based on the information at hand, we have been unable to independently determine with certainty the cause of duplication of the dataset. Given the fact that there are duplicate data published, and there is no way to validate or verify the veracity of the data, readers should be cautioned in the application of the findings reported in these manuscripts to their clinical practice.

Gary S. Francis, MD Professor of Medicine, University of Minnesota Editor-in-Chief, Journal of Cardiac Failure http://dx.doi.org/10.1016/j.cardfail.2013.05.015

On 2013 Oct 31, John Cannell commented:

I congratulate the authors on a fine study. I wonder if they know that a recent meta-analysis found the the risk of preeclampsia is inversely related to maternal 25(OH)D levels?

Tabesh M, 2013

If not, it shows how little communication is occurring between autism spectrum disorder (ASD) scientists and the broader scientific realm. Each ASD scientist seems to be immersed in his or her own research interest but seemingly oblivious to the larger body of science research.

Thus the vitamin D theory of ASD (vitamin D deficiency being the environmental risk factor for this highly heritable disorder) is consistent with the authors work. Three recent studies, using community controls, have found 25(OH)D levels are significantly lower in children with ASD. Two of the studies below (Mostafa et al and Gong et al) also found ASD severity, as rated on standard ASD rating scales, is inversely correlated with 25(OH)D levels. Mostafa et al found an R value of -.86 for the association of serum 25(OH)D with ASD severity.

Gong ZL, Luo CM, Wang L, Shen L, Wei F, Tong RJ, Liu Y. Serum 25-hydroxyvitamin D levels in Chinese children with autism spectrum disorders. Neuroreport. 2013 Oct 1. Gong ZL, 2014

Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D in Egyptian children with autism. J Altern Complement Med. 2010 Jun;16(6):641-5. Meguid NA, 2010

Mostafa GA, Al-Ayadhi LY.Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation. 2012 Aug 17;9:201. Mostafa GA, 2012

There is a plethora of basic science explaining why low gestational or early childhood 25(OH)D levels would adversely effect brain development.

DeLuca GC, Kimball SM, Kolasinski J, Ramagopalan SV, Ebers GC. Review: the role of vitamin D in nervous system health and disease. Neuropathol Appl Neurobiol. 2013 Aug;39(5):458-84. doi: 10.1111/nan.12020. DeLuca GC, 2013

Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH. Developmental vitamin D deficiency causes abnormal brain development. Psychoneuroendocrinology. 2009 Dec;34 Suppl 1:S247-57. doi: 10.1016/j.psyneuen.2009.04.015. Epub . Review. Eyles DW, 2009

Furthermore, the vitamin D theory of autism explains most of the epidemiological facts of ASD.

Cannell JJ. On the aetiology of autism. Acta Paediatr. 2010 Aug;99(8):1128-30. Cannell JJ, 2010

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9. Cannell JJ, 2008

70% of American toddlers do not take the American Pediatric Association's recommended vitamin D supplement of 400 IU/day. As milk consumption has fallen, so have toddler’s vitamin D levels.

Cannell JJ. Autism, will vitamin D treat core symptoms? Medical Hypotheses. 2013 Aug;81(2):195-8. Cannell JJ, 2013

Some autism researchers seem cognizant of the entire body of autism research. For example, a group of well-known European autism researchers, including Professor Christopher Gillberg of the Gillberg Neuropsychiatric Institute, have recently called for the need for “urgent research” into the vitamin D deficiency theory of ASD.

Kočovská E, Fernell E, Billstedt E, Minnis H, Gillberg C. Vitamin D and autism: clinical review. Res Dev Disabil. 2012 Sep-Oct;33(5):1541-50. doi: 10.1016/j.ridd.2012.02.015. Epub 2012 Apr 21.Kočovská E, 2012

However, these scientists appear to be in the minority. Until all autism researchers become cognizant of the wider body of scientific research, we will continue to wonder how to prevent - and perhaps even treat - this modern day plague.

John J Cannell, MD

Vitamin D Council

http://www.vitamindcouncil.org

On 2014 Nov 30, Diego Mauricio Riaño-Pachón commented:

Some of the fl-cDNA sequences appear to have originated from mice/rat instead of maize. Genbank had started to remove some of these entries.

On 2013 Dec 30, Keizo Takao commented:

The raw data of behavioral tests, which are not described in this paper, are shown in the Mouse Phenotype Database (http://www.mouse-phenotype.org/). "ImageTM", image analysis application software used in this article, is now freely available from http://www.mouse-phenotype.org/software.html.

On 2014 Jul 04, Ferenc Zsila commented:

In page 583, the authors claim that "We also examined anthocyanidin–DNA interactions spectrophotometrically at pH 7.5 but were unable to demonstrate significant or consistent shifts in l max or maximum absorbance that would indicate the interaction between the two at this pH as has been observed for other flavonoids (Webb and Ebeler 2004)."

However, all details of the spectrophotometric measurements are missing from the experimental section. Name and concentration of the tested anthocyanidin(s), concentration of the DNA, temperature, solvent, optical pathlength, wavelength range, and the type of the instrument used all remain unknown. Additionally, the absorption spectra are not shown either.

On 2013 Oct 23, ANDREW SU commented:

!MOVED http://biogps.org

The URL in the original abstract has now been retired. This data set (together with other gene expression data sets) are now hosted at http://biogps.org.

On 2016 Oct 03, Morten Oksvold commented:

Please note that after an investigation at the University of Cologne, six articles where T. Wenz figures as first or senior author were found to contain questionable data due to scientific misconduct. This article is one of these six articles.

The conclusion from the report was ready June 28, 2016, please see the link (in German):

http://www.portal.uni-koeln.de/9015.html?&tx_news_pi1[news]=4335&tx_news_pi1[controller]=News&tx_news_pi1[action]=detail&cHash=1deb8399d7f796d65ca9f6ae4764a1ce

On 2015 Aug 21, Bill Cayley commented:

A good example of when the simpler approach is just as good or better (when less is more) - for more on this, see: https://lessismoreebm.wordpress.com/

On 2016 Jan 12, Peter Gøtzsche commented:

The odds ratio for death was 1.95 (95% confidence interval 1.21 to 3.14), when psychotic patients received 3 or more antipsychotics simultaneously instead of one, thus doubling the mortality. However, the authors adjusted for somatic comedication and the adjusted odds ratio was 1.16 (0.68 to 2.00). This is a fatal error. The death rate soared, the more drugs for somatic illnesses, the patients received (27 times if they received at least 10), and the use of, for example, cardiovascular drugs were 37% and 16% among those who died and those who survived (controls), respectively. The use of diabetes drugs was 12% and 6%, respectively. Since increased doses and the use of several antipsychotics simultaneously increase the incidence of somatic illnesses, it is blatantly wrong to adjust for the use of somatic comedication, as this is part of the causal chain from psychosis to death. In this manner, the adjustment removes a relation between polypharmacy and death that actually exists.

Better studies have shown that polypharmacy with antipsychotics increases deaths, as expected. Some of these studies are mentioned in the current study’s Discussion section.

Peter C Gøtzsche, Professor and Director, Nordic Cochrane Centre

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 NCT002289835. We believe the correct ID, which we have found by hand searching, is NCT00289835.

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 Mar 17, Ivan Oransky commented:

This paper has been retracted, the second retraction by the same group: http://retractionwatch.com/2015/03/17/cell-biologists-in-south-korea-retract-two-papers/

On 2014 Mar 05, Gwinyai Masukume commented:

In the introduction of this article, the authors state: “We report the largest case series of advanced abdominal pregnancies from sub-Saharan Africa from 1976 to 2006.” This case series has 20 patients.

In 1989, in the article below originating from Africa, South of the Sahara, 23 cases were described. This would thus be the ‘largest case series of advanced abdominal pregnancy from sub-Saharan Africa between 1976 and 2006’.

White RG. Advanced abdominal pregnancy--a review of 23 cases. Ir J Med Sci. 1989; 158(4):77-8. White RG, 1989

On 2014 Mar 12, George W Hinkal commented:

None

On 2014 Feb 27, George W Hinkal commented:

The National Cancer Institute has been investing in the development of an online webportal of curated cancer nanotechnology data called caNanoLab. The numerical data, nanomaterial characterizations and composition information for the ten nanoparticles related to this publication have been added to the database and can be found at:

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161216&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161218&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161217&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161226&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161221&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161222&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33685522&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161224&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161225&page=0&tab=ALL

https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=34766848&page=0&tab=ALL

The left navigation links on these pages provide information about each sample (under Navigation Tree).

For general information on how to use caNanoLab, please visit https://cananolab.nci.nih.gov/caNanoLab/home.jsp

On 2014 Jan 07, Brett Snodgrass commented:

Dear Author,

Thank you for the excellent article. Although the fistula closed without a specific ligation procedure, the three procedures probably altered the hemodynamics of the right ventricle and permitted the vessel of Wearn to become less prominent and/or close. The closure may be physiologic or anatomic, and I do not think we have sufficient information to make a definitive determination. The closure would probably be considered anatomic if the vessel lumen became fibrosed.

Please consider viewing the following post related to this article.

https://twitter.com/BrettSnodgrass1/status/415904348074287105

Comments and feedback are welcome.

Thank you kindly.

On 2016 Aug 30, Ben Goldacre commented:

This trial has the wrong trial registry ID associated with it on PubMed. The ID given is NCT0019256. The correct ID is NCT00192556. This has been corrected in a subsequent correction published in the originating journal, but not in the PubMed metadata.

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 and this ID has already been corrected in the originating journal; we hope that this trial’s text and metadata can also be corrected in PubMed.

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 Nov 01, Michael Axtell commented:

The URL given in this paper for some large supplemental files, http://www.bio.psu.edu/people/faculty/Axtell/AxtellLab/Data.html , is no longer active.

Instead, these data may now be found at https://psu.app.box.com/v/axtelldata , in the directory called 'AddoQuayeetal2009_RNA'

Thanks, Mike Axtell

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 Apr 23, Philippe Coulon commented:

philippe.coulon at seattlechildrens.org; coulon at uni-muenster.de

On 2014 Mar 03, lin XIAO commented:

This work open a new avenue to understand the white matter function and brings new conception about motor skill learning.

On 2015 Feb 26, Frank Twisk commented:

The article below is a formal response to the article above

BMC Med. 2010 Jun 15;8:35. doi: 10.1186/1741-7015-8-35. Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways. Maes M, Twisk FNM.

Abstract

BACKGROUND:

In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present.

METHODS:

Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IO&NS) pathways are key elements.

DISCUSSION:

Although human and animal studies have established that the pathophysiology of ME/CFS includes IO&NS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IO&NS pathways is known to induce fatigue and somatic (F&S) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IO&NS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors.

CONCLUSIONS:

In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IO&NS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IO&NS pathophysiology by applying laboratory tests that examine the pathways involved.

PMID: 20550693

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901228/pdf/1741-7015-8-35.pdf

On 2014 Oct 28, David Vaux commented:

In Figure 5A of this paper, the upper part of the panel showing the SKBR3 cells with the FoxM1 plasmid (FC) looks very similar to the panel of MCF-7 cells in Figure 5C of the paper in the Journal of Cellular Biochemistry 108:916-925 published in 2009.

In Fig. 6C, the bottom of the panel showing control (NS) SUM149 cells on the left, looks very similar to the upper part of the panel of UC/FS SUM149 cells on the right.

As some of these panels therefore do not appear to be correctly labelled, the conclusions might not be correct.

On 2014 Mar 25, Valter Silva commented:

Focusing on abdominal obesity

Although the paper of Alberti KG, 2009¹ is very cited (more than 2000 times) and is very helpful for managing metabolic syndrome, there are some gaps in the diagnosis of abdominal obesity. We discussed this gaps in our review,² and also, we offered solutions such as "What is the best available evidence for measuring waist circumference?"

Valter Silva, Research assistant, Universidade Federal de São Paulo, SP, Brazil

Competing interests: None declared.

Reference:

1. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009;120(16):1640-5.

2. Silva V, Stanton KR, Grande AJ. Harmonizing the diagnosis of metabolic syndrome--focusing on abdominal obesity. Metab Syndr Relat Disord. 2013;11(2):102-8.

On 2014 Jan 06, Tom Kindlon commented:

Why are we only given information on 3 out of the 8 SF-36 subscales?

Reading this paper, one could be forgiven for thinking that the SF-36 questionnaire only has 3 subscales: Physical Functioning, Mental Health and Social Functioning as that is all we are given information on. In fact, of course, the SF-36 questionnaire has 8 subscales: Physical function, Role physical, Bodily pain, General health, Vitality, Social function, Role emotional and Mental health[1]. The authors use the empiric definition for CFS[2] which requires at a minimum that the "role physical" and "role emotional" subscales also be measured. We also know that all 8 subscales were measured in this cohort[3]. So why was the information not given?

If one was not giving the authors the benefit of the doubt, one could speculate that it was because Table 4 would not look as good, as the Chi-squared calculations would not reach statistical significance for the missing data. But that would be speculation - there could be other reasons for the missing information.

Perhaps the authors could post the relevant data now.

I am not simply being mischievous - I would be interested in particular to see what are the scores for Classes 1 and 2 which include nearly all of the CFS patients (88/92, 95.7%).

References:

[1] Ware JE, Sherbourne CD: The MOS 36-item short form health survey (SF-36): conceptual framework and item selection. Med Care 1992, 30:473-483.

[2] Reeves WC, Wagner D, Nisenbaum R, Jones JF, Gurbaxani B, Solomon L, Papanicolaou DA, Unger ER, Vernon SD, Heim C: Chronic fatigue syndrome--a clinically empirical approach to its definition and study. BMC Medicine 2005, 3:19.

[3] An evaluation of exclusionary medical/psychiatric conditions in the definition of chronic fatigue syndrome. Jones JF, Lin JM, Maloney EM, Boneva RS, Nater UM, Unger ER, Reeves WC. BMC Med. 2009 Oct 12;7(1):57. - see Tables 5 and 6.

On 2014 Jan 06, Tom Kindlon commented:

There has been criticism of how CFS is defined in this study

I thought it would be useful to point out that there is controversy [1,2] with regard to the criteria [3] used in this study to define Chronic Fatigue Syndrome (CFS).

For example, the criteria for CFS used in this study do not even require a patient to have fatigue. The authors say: “We used the Multidimensional Fatigue Inventory (MFI-20) [4] to measure characteristics of fatigue” but they do not give the thresholds. Given the MFI-20 has five subscales: (General fatigue, Physical fatigue, Mental fatigue, Activity reduction and Motivation reduction), one would probably suspect that a patient would have to score poorly on one of the headings which have fatigue in their title. But the actual criteria are: a patient needs to score >=13 on MFI general fatigue or >=10 on reduced activity. Note, one could score >=10 on the MFI reduced activity questions without necessarily being fatigued (one could be depressed or even lazy) (only current major depressive disorder with melancholic features (MDDm) is an exclusion for this definition of CFS).

This is despite the fact that in the current paper, the authors say: “Chronic fatigue syndrome (CFS) is a common, debilitating illness whose hallmark symptoms involve fatigue and fatigability”. Many other questions have been raised about the criteria for CFS that were used in this study. For example, the authors only considered current MDDm to be exclusionary for CFS while the International CFS Study group recommended that conditions (including MDDm) were considered exclusions unless they had been “resolved for more than 5 years before the onset of the current chronically fatiguing illness”[5].

Prevalence figures show that the criteria, that were used for this cohort, are selecting a broader group than previous criteria for CFS. Based on the figures derived from this cohort, the prevalence of CFS was estimated at 2.54% [6]. Other studies using similar methodology (but which did not operationalize the criteria [7] for the CFS in the same way as this study) estimated the prevalence of CFS to be 0.235% (95% confidence interval, 0.142%-0.327%) and 0.422% (95% confidence interval, 0.29%-0.56%) [8,9].

References:

[1]. Jason LA, & Richman JA. How science can stigmatize: The case of chronic fatigue syndrome. Journal of CFS 2007;14:85-103.

[2]. Jason LA, Najar N, Porter N, Reh C. Evaluating the Centers for Disease Control's empirical chronic fatigue syndrome case definition. Journal of Disability Policy Studies 2009;20;93.

[3]. Reeves WC, Wagner D, Nisenbaum R, Jones JF, Gurbaxani B, Solomon L, Papanicolaou DA, Unger ER, Vernon SD, Heim C: Chronic fatigue syndrome--a clinically empirical approach to its definition and study. BMC Medicine 2005, 3:19.

[4]. Smets EM, Garssen B, Bonke B, De Haes JC. The multidimensional fatigue inventory (MFI) psychometric qualities of an instrument to assess fatigue. J Psychosom Res 1995; 39: 315–25.

[5]. Reeves WC, Lloyd A, Vernon SD, Klimas N, Jason LA, Bleijenberg G, Evengard B, White PD, Nisenbaum R, Unger ER; International Chronic Fatigue Syndrome Study Group. Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution. BMC Health Serv Res. 2003 Dec 31;3(1):25.

[6]. Reeves WC, Jones JF, Maloney E, Heim C, Hoaglin DC, Boneva RS, Morrissey M, Devlin R. Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural Georgia. Popul Health Metr. 2007 Jun 8;5:5.

[7]. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A. The chronic fatigue syndrome; a comprehensive approach to its definition and study. Ann Int Med 1994, 121:953-959.

[8]. Reyes M, Nisenbaum R, Hoaglin DC, Unger ER, Emmons C, Randall B, Stewart JA, Abbey S, Jones JF, Gantz N, Minden S, Reeves WC: Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas. Arch Int Med 2003, 163:1530-1536.

[9]. Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RR, McCready W, Huang CF, Plioplys S. A community-based study of chronic fatigue syndrome. Arch Intern Med. 1999 Oct 11;159(18):2129-37.

On 2014 Jan 06, Tom Kindlon commented:

A more detailed comparison would need to be made before one could say this replicates the previous study

Part of the aim of this study [1] appears to be to compare the classes that were drawn up with a previous cohort[2-4]. However it does not, to my mind, deal with this in a particularly rigorous fashion. The main quantitative comparisons are the percentages that fall in each class (Tables 6 and 7). However, the percentages will be influenced by the quantity and type of non-CFS controls used which are not the same in each cohort [to explain why this is important using an extreme example: if there were 1000 non-CFS cases for everyone one CFS case in one cohort, the percentages in each class would be different than if there was a 1:1 ratio of CFS to non-CFS cases in the other cohort].

The first study involved the following[5]: "This population-based case control study enrolled 227 adults identified from the population of Wichita with: (1) CFS (n = 58); (2) non-fatigued controls matched to CFS on sex, race, age and body mass index (n = 55); (3) persons with medically unexplained fatigue not CFS, which we term ISF (n = 59); (4) CFS accompanied by melancholic depression (n = 27); and (5) ISF plus melancholic depression (n = 28)." This was based on the classification in 1997-2000. These were then assessed during 2003. As one can see in Table 2, in 2003, 6 out of the original 58 CFS patients satisfied the CFS definition[6] as originally operationalized, along with 4 out of the controls. 6 more who had previously been excluded because of previous diagnosis of Major Depressive Disorder with melancholic features (MDDm) were also said to satisfy the original CFS diagnosis. The method for operationalizing the CFS definition[6] was then changed so there was then 43 individuals with CFS (see Table 5). Although the same method[5] of operationalizing the CFS definition[6] is used when comparing the Wichita and Georgia cohorts, it is a very different way to select patients and controls than the current study[1]. So it is questionable how interesting it is to compare the percentages in each class.

A comparison of the percentages of CFS in each class might have been interesting but that was not done.

Also, apart from the percentages, no tables with quantitative information are presented in the current paper to help the reader compare the class groups to see how valid the comparisons are. This is made more difficult because the original study gave much more detailed data on the six class solution rather than the five class solution [2]: "As the five- and six-class solutions produced practically identical classes, with the exception of the fifth group in the five-class solution being divided into the fifth and sixth classes in the six-class solution, only the six-class solution is presented in Table 2."

So in that paper, one has classes which have a median BMI of 32, 30 and 30 which are described in the current paper[1] as obese classes while class 5 would be a combination of classes 5 and 6 which have a median BMI of 26 and 27 are classed as non-obese. So numerical comparisons would have been of more use rather than looking at verbal descriptions - describing two groups which have a median BMI of 30 as obese (so approx 50% would have a BMI under 30, one threshold for obesity) and another group which has a median BMI of around 26.5 as non-obese, seems a bit unsatisfactory. There is a 5 class LCA solution in Figure 1 in one of the Wichita papers which gives some verbal descriptions[4]. As one can see, "obese" is only used to describe two of the five LCA groups: - Obese, hypnoea (27.93%) - Obese, hypnoea and stressed (15.32%) - Interoception (16.22%) - Interoception, depression (19.82%) - Well (20.72%)

However, this does not seem to be the same five class solution for the Wichita cohort as the one described in this paper as the percentages don't match up.

References:

[1]. Aslakson E, Vollmer-Conna U, Reeves WC, White PD. Replication of an empirical approach to delineate the heterogeneity of chronic unexplained fatigue. Popul Health Metr. 2009 Oct 5;7:17.

[2]. Vollmer-Conna U, Aslakson E, White PD: An empirical delineation of the heterogeneity of chronic unexplained fatigue in women. Pharmacogenomics 2006, 7(3):355-364.

[3]. Aslakson E, Vollmer-Conna U, White PD. The validity of an empirical delineation of heterogeneity in chronic unexplained fatigue. Pharmacogenomics. 2006 Apr;7(3):365-73.

[4]. Carmel L, Efroni S, White PD, Aslakson E, Vollmer-Conna U, Rajeevan MS. Gene expression profile of empirically delineated classes of unexplained chronic fatigue. Pharmacogenomics. 2006 Apr;7(3):375-86.

[5]. Reeves WC, Wagner D, Nisenbaum R, Jones JF, Gurbaxani B, Solomon L, Papanicolaou DA, Unger ER, Vernon SD, Heim C. Chronic fatigue syndrome--a clinically empirical approach to its definition and study. BMC Med. 2005 Dec 15;3:19.

[6]. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The chronic fatigue syndrome; a comprehensive approach to its definition and study. Ann Int Med 1994, 121:953-959.

On 2016 Feb 17, Egon Willighagen commented:

Dear Poh et al., could you please inform me about the inhibition effects of the stereochemistry of the allene functionality in NITD448? Did you use a specific stereoisomer, or are they biologically equivalent? Did you measure activity for them separately too? Did docking show differences in binding affinity?

On 2015 Oct 01, ANDREW SU commented:

!MOVED http://biogps.org/circadian

The URL in the original paper has now been retired. The interface described in this paper is now hosted at http://biogps.org/circadian.

On 2013 Dec 29, ROBERT HURST commented:

It is truly amazing that this paper was ever published. First, there is a long history of attempting to correlate IC with infectious agents. Not only is this literature not acknowledged, but the final assessment that the findings represented false positives is not discussed. Amazingly, there are no controls collected from patients without IC but under the same conditions. Thus we do not know whether the alleged "nanobacteria," which may or may not even be living organisms, are even associated with IC, or whether random biopsies from all sorts of disorders might have yielded the same results.

On 2015 May 04, Torsten Seemann commented:

I feel the title of this manuscript is misleading. The "high carbohydrate" diet is 52% and the "low carbohydrate diet" is 45%. This small difference is within measurement error and is not meaningful. The real variables being tested are low versus medium fat, and high versus low fibre.

On 2013 Jul 03, Joshua L Cherry commented:

This review, and the work on which it is based (Webster AJ, 2003, Pagel M, 2006), claim that speciation events are accompanied by bursts of protein sequence evolution. This claim is based on correlations between the total root-to-tip branch length and the number of nodes along this path in phylogenetic trees.

As the authors explain, in such analyses it is critical to account for what they call the node-density artifact. This effect can lead to an apparent correlation for the inferred branch lengths in the absence of a correlation for the true lengths. The authors claim to have accounted for this artifact, but there is reason to doubt this.

The authors attempt to detect the artifact through the concavity of the relationship between number of nodes and path length, and eliminate trees that appear to be affected. There are, however, several reasons to doubt the reliability of their test. The form of the expected relationship is not known. In fact the effect does not depend on only the number of nodes, but also on their position; an additional node in the middle of a long branch will have a large effect on the total calculated length, whereas an additional node near one end of the branch will have a small effect. The authors fit a power law to the data. This family of functions has unrealistic features. The true relationship is expected to approach a horizontal asymptote, whereas the power law increases without bound. Also, the power law artificially forces the curve through the origin. Furthermore, with finite data the downward concavity might not be detected due to chance, even with a perfect model. Because the concavity will be weak under some circumstances, this is an important concern.

I would suggest another type of test. Branch lengths can be recalculated with some species, and hence some nodes, omitted. The true branch lengths and speciation histories of course remain unchanged, but species originally separated from the root by many nodes are now just as vulnerable to branch shortening as species with fewer nodes. If the path shortens as a result, this is evidence of the node-density artifact. I suspect that many additional trees would be shown to suffer from the artifact by this type of test.

On 2014 Jan 11, Brett Snodgrass commented:

Dear Authors,

Thank you for the excellent article.

The image appears to depict an enlarged sinusoid, a structure that was not morphometrically described by Thebesius.

1. http://bit.ly/vasaThebesii

It may be preferable to refer to the sinusoid as "myocardial," instead of attributing it to either Wearn or Thebesius as the meandering sinusoids connect to both the vessels of Wearn and the Thebesian veins. http://bit.ly/JTWearn

Since this appears to be a dilated sinusoid (and possibly its common opening), the fistulae may be vessels of Wearn as they connected to a ventricular chamber to the posterior descending artery, which originated from the right coronary artery.

1. http://bit.ly/JTWearn
2. http://www.ncbi.nlm.nih.gov/pubmed/22704295

Cardiac radiologist Dr. Grollman discusses the vessels of Wearn (arterioluminal & arteriosinusoidal vessels) & the vessels of Thebesius in his insightful letter.

1. http://www.ncbi.nlm.nih.gov/pubmed/9502691

My opinion is that accurate anatomic terminology is a basic principle underlying good medical science, and I ask others to consider whether the aforementioned definitions are appropriate.

If the terms are not appropriate, please consider sharing why through a comment.

If this comment is not helpful, please let me know how it might be improved.

Thank you very much.

On 2014 Aug 27, Jorge H Ramírez commented:

I recently mentioned the RE-LY study in a previous comment yesterday via PubMed Commons. http://www.ncbi.nlm.nih.gov/pubmed/25138329#cm25138329_5938

This will be also my last comment via PubMed commons related to dabigatran or the RE-LY study (the only exception are possible replies to comments related to these posts).

Information about dabigatran & the RE-LY study

1. Cohen Deborah. Concerns over data in key dabigatran trial BMJ 2014; 349:g4747

2. Cohen Deborah. Dabigatran: how the drug company withheld important analyses BMJ 2014; 349:g4670

3. Moore Thomas J, Cohen Michael R, Mattison Donald R. Dabigatran, bleeding, and the regulators BMJ 2014; 349:g4517

4. Charlton Blake, Redberg Rita. The trouble with dabigatran BMJ 2014; 349:g4681

5. Jackson Trevor. Dabigatran and statins: faith, hype, and transparency BMJ 2014; 349:g4793

6. Ramirez, Jorge H (2014): Requested (Jul 29, 2014) & Retracted by the author (Aug 23, 2014): "Conelly S, et al. Dabigatran versus Warfarin in Patients with Atrial Fibrillation. N Engl J Med 2009; 361:1139-1151"] - Question Thread Open. figshare. http://dx.doi.org/10.6084/m9.figshare.1144305

7. Bleeding with dabigatran, rivaroxaban, apixaban. Prescrire Int 2013; 22 (139): 155-159.

8. Dabigatran for atrial fibrillation: why we can not rely on RE-LY http://www.ti.ubc.ca/sites/ti.ubc.ca/files/80.pdf

9. The use, misuse and abuse of dabigatran https://www.mja.com.au/journal/2013/198/7/use-misuse-and-abuse-dabigatran

10. Ramirez, Jorge H (2014): Dabigatran (Pradaxa): 81.4% of registered studies in ClinicalTrials.gov are unpublished. figshare. http://dx.doi.org/10.6084/m9.figshare.1116303

Competing interests: Already declared in previous comment posted in PubMed commons (1st URL above)

On 2014 Jun 01, Ivan Oransky commented:

This paper has been retracted: http://retractionwatch.com/2013/12/09/rats-neuroscientist-notches-third-retraction-this-one-for-using-the-wrong-rnas/ Some of these authors have repeated the study and have republished it: http://retractionwatch.com/2014/05/29/researchers-repeat-retracted-study-republish-in-same-journal-sans-first-author/

On 2015 Oct 02, Simon Young commented:

This is an interesting review but omits some important manuscripts. For example, in the section on the effect of tryptophan loading on mood in healthy volunteers there is no mention of several relevant studies Leathwood PD, 1982, Charney DS, 1982, Greenwood MH, 1974, SMITH B, 1962. The same is true for studies on the effect of tryptophan on sleep Griffiths WJ, 1972, Hartmann E, 1977, Adam K, 1979. The statement in the section 4.1 that “there is little consensus in terms of Trp’s efficacy in treating depression” is not universally accepted. A Cochrane Database Systematic Review concluded that the available evidence suggests that tryptophan is better than placebo at alleviating depression Shaw K, 2002, and tryptophan has been available as a prescription drug for the treatment of depression in a number of countries. The Cochrane Database Systematic Review includes a number of studies not included in the article.

On 2017 Jun 19, Daniele Mengato commented:

Rituximab biosimilar vs rituximab originator in advanced follicular lymphoma

by Daniele Mengato Scuola di Specializzazione in Farmacia Ospedaliera, Dipartimento di Scienze del Farmaco, University of Padua, Padova, Italy

One interesting point of this article by Gao et al. (1) is that the authors have presented a meta-analysis based on the end-point of the overall response rate in which chemotherapy plus rituximab has been compared with chemotherapy alone in patients with advanced follicular lymphoma (AFL). Schulz et al. (2) have conducted a meta-analysis (published in 2007) based on a similar design. In particular, they used the same endpoint obtained from the same RCTs citated in the work by Gao et al. EMA has recently approved a biosimilar of rituximab (called CPT-10) indicated for patients with AFL (3). In documenting the equivalence between CPT-10 and the originator of rituximab, the analysis carried out by EMA has evaluated the randomized trial that directly compared these two agents in the above-mentioned patients. Clinical endpoint investigated in this trial was the same as the one used in the already mentioned meta-analysis: the overall response rate. It has been proposed (4) that an analysis focused on the equivalence between a biosimilar and an originator can be strengthened if a network meta-analysis is performed that includes not only the comparison between biosimilar and originator, but also the comparison between the originator and the old standard of care (i.e. chemotherapy alone). We welcome one such network meta-analysis. For this purpose, as regards the comparison between the originator plus chemotherapy and chemotherapy alone, the 6 trials (5-10) either reported by Gao et al. or by Schulz et al. are suitable for being included in this network meta-analysis.

References

1. Gao G, Liang X, Jiang J, Zhou X, et al. A systematic review and meta-analysis of immunochemotherapy with rituximab for B-cell non-Hodgkin's lymphoma. Acta oncologica. 2010 Jan;49(1):3-12.
2. Schulz H, Bohlius J, Skoetz N, et al. Chemotherapy plus Rituximab versus chemotherapy alone for B-cell non-Hodgkin's lymphoma. The Cochrane database of systematic reviews. 2007 Oct 17(4):Cd003805.
3. EMA European Medicine Agency - Committee for Medicinal Products for Human Use (CHMP). Truxima : EPAR - Public assessment report. http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Public_assessment_report/human/004112/WC500222695.pdf 2016 May;EMA/CHMP/75695/2017
4. Messori A, Trippoli S, Marinai C. Network meta-analysis as a tool for improving the effectiveness assessment of biosimilars based on both direct and indirect evidence: application to infliximab in rheumatoid arthritis. Eur J Clin Pharmacol. 2017 Apr;73(4):513-514. doi:10.1007/s00228-016-2177-z. Epub 2016 Dec 14.
5. Forstpointer R, Dreyling M, Repp R, et al. The addition of rituximab to a combination of fludarabine, cyclophosphamide, mitoxantrone (FCM) significantly increases the response rate and prolongs survival as compared with FCM alone in patients with relapsed and refractory follicular and mantle cell lymphomas: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group. Blood 2004;104(10):3064-3071.
6. Herold M, Pasold R, Srock S, et al. Results of a Prospective Randomised Open Label Phase III Study Comparing Rituximab Plus Mitoxantrone, Chlorambucile, Prednisolone Chemotherapy (R-MCP) Versus MCP Alone in Untreated Advanced Indolent Non-Hodgkin’s Lymphoma (NHL) and MantleCell-Lymphoma (MCL). ASH Annual Meeting Abstracts. 2004; Vol. 104, issue 11:584.
7. Hiddemann W, Kneba B, Dreyling M, et al. Frontline therapy with rituximab added to the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly improves the outcome for patients with advanced-stage follicular lymphoma compared with therapy with CHOP alone: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group. Blood 2005;106(12):3725–3732.
8. Marcus R, Imrie K, Belch A, et al. CVP chemotherapy plus rituximab compared with CVP as first-line treatment for advanced follicular lymphoma. Blood 2005;105(4):1417–1423.
9. Rivas-Vera S, Baez E, Sobrevilla-Calvo P, et al. Is First Line Single Agent Rituximab the Best Treatment for Indolent Non-Hodgkin’s Lymphoma? Update of a Multicentric Study Comparing Rituximab vs CNOP vs Rituximab Plus CNOP. ASH Annual Meeting Abstracts. 2005; Vol. 106, issue 11:2431.
10. van Oers MH, Klasa R, Marcus RE, Wolf M, Kimby E, et al. Rituximab maintenance improves clinical outcome of relapsed/resistant follicular non-Hodgkin lymphoma in patients both with and without rituximab during induction: results of a prospective randomized phase 3 intergroup trial.. Blood 2006;108 (10):3295–301.

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 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 Apr 13, Mark Wewers commented:

Consider the later confirmation of this link between NFKBIZ and interferon gamma in human NK cells at Kannan Y, 2011.

On 2015 Oct 06, S Sundar commented:

The conclusion by Nanda et al on hormonal therapy use for prostate cancer and increased mortality is not only based on a small subset (5%) of a retrospective study but the study population consisted of patients whose primary treatment was Brachytherapy(1). By contrast multiple prospective randomised trials, which have shown significant survival benefits for hormone therapy, utilised external radiation (RT) as the primary treatment modality(2)(3). Hence extreme caution is needed before extrapolating the evidence generated by Nanda et al to routine clinical practice.(1.

Radiobiologically, Brachytherapy is different from external RT. Radiation Doses delivered by Brachytherapy are usually far higher than delivered by external RT. Unlike external RT which is given in daily fractions over many weeks, Seed Brachytherapy delivers continuous radiation and affects repair and repopulation of surrounding normal tissues including vascular structures. Furthermore, a significant proportion of Brachytherapy treated patients have distant vascular migration of radioactive seeds.(4) The long term effect of delivering unnecessary vascular radiation at distant places such as lungs remains to be elucidated.

Independent randomised studies combining modest doses of external RT with adjuvant hormonal therapy have shown substantial overall survival benefit. Hence, unless prospective data confirms the results of data mining by Nanda et al, prostate patients with co-morbidity, who are having external RT as their primary therapy, should not be deprived hormone therapy.

References:

1. Nanda A, Chen M-H, Braccioforte MH, Moran BJ, D’Amico AV. Hormonal therapy use for prostate cancer and mortality in men with coronary artery disease-induced congestive heart failure or myocardial infarction. JAMA. 2009 Aug 26;302(8):866–73.

2. Bolla M, Van Tienhoven G, Warde P, Dubois JB, Mirimanoff R-O, Storme G, et al. External irradiation with or without long-term androgen suppression for prostate cancer with high metastatic risk: 10-year results of an EORTC randomised study. Lancet Oncol. 2010 Nov;11(11):1066–73.

3. Brundage M, Sydes MR, Parulekar WR, Warde P, Cowan R, Bezjak A, et al. Impact of Radiotherapy When Added to Androgen-Deprivation Therapy for Locally Advanced Prostate Cancer: Long-Term Quality-of-Life Outcomes From the NCIC CTG PR3/MRC PR07 Randomized Trial. J Clin Oncol Off J Am Soc Clin Oncol. 2015 Jul 1;33(19):2151–7.

4. Eshleman JS, Davis BJ, Pisansky TM, Wilson TM, Haddock MG, King BF, et al. Radioactive seed migration to the chest after transperineal interstitial prostate brachytherapy: extraprostatic seed placement correlates with migration. Int J Radiat Oncol Biol Phys. 2004 Jun 1;59(2):419–25.

On 2016 Oct 16, Jaime A. Teixeira da Silva commented:

There are concerns about the accuracy of the description related to the mutants in this study. http://imgur.com/7h7RS4p

On 2014 Apr 03, Naresh Kasoju commented:

This work was highlighted as the "Biomaterial of the Month" by the Society for Biomaterials news letter: http://www.biomaterials.org/week/bio43.cfm

On 2014 Nov 23, Harri Hemila commented:

A manuscript version is available at handle