PubMed

Grant described the vessels of Wearn in 1926.

In 1929 Grant and Viko assessed hearts for the presence of the vessels of Wearn, but noted they were identified. The reason for this negative study is not entirely clear. It may be explained that some of the vessels of Wearn are greater than 10um but less than 40 um. 40um was the smallest lumen diameter of a vessel which the specific dye would enter.

Vessels of Wearn identified by Grant in 1926:

1. https://twitter.com/BrettSnodgrass1/status/420281076070637568

For additional commentary and reference to Grant's 1929 study, please see:

1. http://bit.ly/1929Grant

2. http://scholar.google.com/scholar?cluster=5189678684113164458&hl=en&as_sdt=0,26&sciodt=0,26

3. https://twitter.com/BrettSnodgrass1/status/410929217170206721

4. http://bit.ly/ThebesianVeins

5. http://bit.ly/vasaThebesii

Comments and suggestions are welcome. If this comment is not helpful, please consider adding a comment about how it may be improved.

Thank you kindly.

Please be aware that KB is NOT an oral squamous cell carcinoma (OSCC). The cell line is cross-contaminated, as shown by Gartler in 1967 (PMID 4864103). For a database of cross-contaminated or otherwise misidentified cell lines, see http://iclac.org/databases/cross-contaminations/.

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/

GPHMM authors comment on their project home page (http://bioinformatics.ustc.edu.cn/gphmm/) on the performance of GPHMM in this comparison:

"We would like to point out critical errors found in a recently paper "Comparison of methods to detect copy number alterations in cancer using simulated and real genotyping data" published in BMC Bioinformatics with PMID 22870940, which was trying to compare different computational approaches including the GPHMM method.

As demonstrated in the GPHMM paper, we showed the superior performance of GPHMM on a cell-line dataset (see Figure 1,2,3 and Table 2 in the paper). However in this BMC paper, we found that the authors evaluated our method with the same dataset, but claimed that GPHMM failed to recognize the alteration pattern in the cell-line samples. Astonished by this apparent contradiction, we contacted them and later it became clear that during the test they WRONGLY replaced an important data file (“hhall.hg18_m.pfb”) in the tool package with another file used in their study.

Given the fact that this is a survey paper trying to accurately compare different methods and provide unbiased guidance to readers and the conclusion they made will pose influence on user's final choice of method in their studies, we suggested them to retest GPHMM and update their results. Unfortunately, except an ambiguous statement in the text saying “the baseline shift can be correctly estimated if a PFB with a modified specification is used”, we found the results and conclusion were not changed at all in the final version of this paper. Therefore, we argue that the performance of GPHMM is significantly underestimated in this paper."

This CBT model appears useful in patients with Dhat syndrome.

Dear Authors,

Thank you very much for the excellent publication and acknowledging that the connections between the coronary arteries and left ventricle were not probably not veins.

These connections may represent the vessels of Wearn, which appear unusually prominent.

An applicable ICD9 code might be 746.85, coronary artery anomaly, as it may meet the clinical criteria for the definition of fistulae.

Referring to these arterial connections as Thebesian veins has caused me much confusion when I was trying to understand the simple relationship of pulmonary atresia with intact ventricular septum and the coronary arteriopathy seen in PAIVS. With the growth of social media, and electronic data storage, I think that we may now be able to address the diffuse distribution of ambiguous or misleading nomenclature that fills as least half of related publications.

Dr. Paul Lurie's plea for collaboration in this regard has motivated me to take several steps in an effort to try to help produce accurate, simple, precise anatomic nomenclature and include:

1. I collaborated with Elsevier to help get the article by Wearn et al. changed to open-access. http://bit.ly/JTWearn

2. I obtained the original article (through ArtRieve http://www.artrieve.com/) written by Thebesius and uploaded the first digital copy. http://bit.ly/Thebesius

3. I published or wrote in the American Journal of Cardiology, Cardiovascular Pathology, Twitter, Facebook, Google Plus, and directly E-mailed several authors that were publishing related content.

4. I have posted numerous PubMed Commons comments. I regret that they may not always be helpful to every user, but I echo Dr. Lurie’s plea for collaboration in this regard. The PubMed Commons commentary is a welcome means with significant potential to vastly improve the peer review process.

My aim is that researchers in the future will probably not need to read more than 30 articles before they realize that myocardial sinusoids indeed exist, they were defined by Wearn, and that Thebesian veins are not arteries.

Please see

1. http://bit.ly/JTWearn

2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933738/

3. http://bit.ly/vasaThebesii

4. http://bit.ly/ThebesianByPratt

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

Comments and suggestions are welcome.

Thank you very much.

A series of analogies between vitamin D and adiponectin, isn't it? The most intriguing for me (at this point) seems to be the (auto)immune disease and the (common ?) gene-related pathways ! Comments? Thanks.

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

The authors report an interesting study in regards to sustained hypoxia and respiratory neural control during a critical period of development in rats. However it may have no relation to the phenomenon of human sudden infant death syndrome (SIDS). It has been shown that human SIDS occur between birth and 3.5 years with a 4-parameter lognormal age distribution (Johnson SB) Mage DT, 2009. This distribution is continuous and has no discontinuities between fore and aft portions of the age distribution on either side of "a critical period of development." The SIDS community seems to have forgotten that the operative definiton of modern SIDS as being restricted to under one year from birth was made for research purposes only Willinger M, 1991 and the triple risk model for SIDS cited by these authors does not predict a 50% male excess for SIDS Mage DT, 2013.

Further details are in Jargin SV. Dermatopathology: Practical & Conceptual 2007;13(1):20 continued in 2008;14(2), 2009;15(1), 15(2), 15(4), 2010;16(1), 16(2), 16(3). Unfortunately, the journal Dermatopathology: Practical & Conceptual is currently unavailable on-line.

This paper describes an amazing work and links the CD4 T cell responses against H1N1 with those against orexin. This paper has received a lot of mainstream media attention (see here for example) where it has been described as the demonstration that narcolepsy is an autoimmune disease. Although the study provides interesting data re-inforcing the autoimmune hypothesis of narcolepsy, it does not demonstrate so and it's not the first study to suggest the autoimmune hypothesis, as authors correctly point in the discussion. A brief comment summarizing the study and providing context to those mainstream media headlines has been published here

Nobody can deny the importance of social media, but the doctor has to strike a balance between his professional demands and the urge to check the latest facebook post or reply to a tweet ASAP. All social media have the option of customization and if a physician chooses wisely he will be able to have latest knowledge and information from the social media at his finger tips ( literally)

In addition doctors are humans too. We need to socialize and a little bit of socialization on FB, Twitter or G+ might not hurt if we keep a track of the time we need to spend of these social media sites

And who would the 'heroes' be? Those for whom the compensation is most likely to compensate them for the loss of their organ (i.e. the poor).

Here in the UK, when one mentions a hero it is usually in reference to a soldier. The hero narrative is rampant. So who joins the army? In a cursory glance at the literature I find few data for the UK, but plenty for the US. For one, it seems that people are less likely to enlist if they have college educated parents. Why else would the British Army choose to focus its recruitment efforts in the poorest of schools? One wonders whether the (largely) privately educated graduates of Sandhurst will face the same danger to life as their soldier counterparts. Are we really comfortable with our heroes being less well educated than the beneficiaries of their heroism? I, for one, am not.

There is every reason to suspect that the same would apply to living organ donation. The hero narrative is only "appropriate and useful" as a means of dispelling guilt.

The authors note the incidence of SIDS < 1 year has declined but the proportion of neonates < 7 days has increased. This may be because the number of neonate SIDS has remained constant while the number of post neonates (7 < age < 365 days) has decreased. Using U.S. CDC data (wonder.cdc.gov) from 1999 to 2010 for ICDR95 SIDS the number of neonate SIDS per year has held constant at an average of 34 per year while total SIDS has decreased from 2616 to 2036.

In the list of collaborators, the exact name of Helmi BEN SAAD is "BEN SAAD H" not "SAAD HB".

The second author name is "BEN SAAD H" not "BENSAAD H"

Dear Authors.

Thank you for publishing this excellent article that provides quantitative data related to the venular connections to the right atrium.

The following terms are used to describe the connections between the heart chambers and coronary veins.

1. Venoluminal*

2. Venosinusoidal*

3. Thebesian vessels

4. Thebesian veins

5. vasa Thebesii

*There may be some distinction between the listed venoluminal and venosinusoidal connections. The reported morphometric study of the Thebesian veins did not contain the same amount of granularity that Wearn reported for the arteriosinusoidal and arterioluminal vessels. See vessel diameter ranges in the collapsed and open state. http://bit.ly/JTWearn

Wearn indeed studied the Thebesian veins, see heart 11. http://bit.ly/JTWearn

Although some veins were noted to connect to myocardial sinusoids, Wearn did not quantitatively distinguish between venosinusoidal and venoluminal connections as he did for the arteriosinusoidal and arterioluminal vessels.

They are different from the arterial connections to the heart chambers. The arterial connections that connect directly to the heart chambers are not venular, and they were reportedly not studied by Thebesius. http://bit.ly/vasaThebesii

Wearn used a translator for his literature review. Wearn detailed the the vessels named after him, the vessels of Wearn. http://bit.ly/JTWearn

The vessels of Wearn consist of the i. Arteriosinusoidal vessels ii. Arterioluminal vessels

These two vessels types were described by Wearn http://bit.ly/JTWearn and connect arteries to the heart chambers exclusive of the capillary bed.

Wearn studied the connections using India ink, which did enter the capillary beds, and subsequently entered the heart chambers. The Thebesian veins probably facilitate entry of the coronary artery-injected India ink into the heart chambers through Arterio-capillary-venular-cameral connections.

It may be possible that arterio-capillary-cameral connections exist.

In addition, Wearn studied different hearts using celloidin injection into the coronary arteries. This celloidin was chilled by placing the heart in cold water. The chilled celloidin appeared too thick to enter the capillaries. For clarity, there are two distinguishable types of vessels that have been identified connecting from the coronary arteries to the heart chambers and the term vessels of Wearn encompasses them both. They are not referred to as arteries because they have been noted to lose their internal elastic lamina as they approach the heart chamber, thus becoming a "vessel," and no longer fulfilling the histologic definition of an artery.

For additional commentary, please see

https://twitter.com/BrettSnodgrass1/status/418890181509263360

http://bit.ly/ThebesianByPratt

https://twitter.com/BrettSnodgrass1/status/417363766204825600

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

Comments and suggestions are welcome.

Thank you kindly.

This article was corrected in 2006, but does not appear to be linked in PubMed. Correction: Are fast food restaurants an environmental risk factor for obesity? http://www.ijbnpa.org/content/pdf/1479-5868-3-35.pdf

This article was cited in: Jargin SV. Asbestos-Related Policies: Revaluation Needed. Molodoi Uchenyi 2013;(7):514-517. http://www.moluch.ru/archive/54/7325/