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Acknowledgements (amended) (Stefanie Biehl, 03 December 2013)

The authors wish to thank Sebastian Michelmann for his help with data collection. Portions of the research in this paper use the FERET database of facial images collected under the FERET program. This research was supported by the Deutsche Forschungsgemeinschaft (DFG, grants HE 4531/1-1, KFO 125, and RTG 1253/1). This publication was funded by the German Research Foundation (DFG) and the University of Wuerzburg in the funding program `Open Access Publishing┬┐. The authors also wish to thank everyone involved in the review process for very helpful suggestions on how to improve the manuscript. read full comment

Comment on: Biehl et al. BMC Neuroscience, 14:107

Longer journal paper on this topic (Tony Lindeberg, 26 September 2013)

A longer journal version of this work has been published in:

Lindeberg T (2013) Invariance of visual operations at the level of receptive fields. PLoS ONE 8(7): e66990. doi:10.1371/journal.pone.0066990 read full comment

Comment on: Lindeberg BMC Neuroscience, 14:P242

Omission (Shiree Heath, 28 May 2013)

It has come to the authors' attention that several entries have been inadvertently omitted from Table 2 'Behavioral results for participants with aphasia' during the formatting procedures for online publication. Column 3 'P03' should contain the following CAT results:

- naming = 49*
- fluency = 16
- reading = 59*
- spoken picture description = 19* read full comment

Comment on: Heath et al. BMC Neuroscience, 13:98

Glutamate and locomotory control in amphioxus larvae (Thurston Lacalli, 08 March 2013)

As the investigator responsible for the EM-level reconstructions [1] used as a point of reference by Candiani et al. in this new study, I am gratified at the degree to which their neurochemical map of the amphioxus larval CNS matches our morphological one. An unexpected result, for me at any rate, is that Candiani et al. find only a single pair of glutaminergic neurons in the anterior nerve cord, in contrast with the cholinergic, GABAergic and glycinergic neurons, which occur in greater numbers over multiple segments. The authors conclude that their single glutaminergic pair corresponds to the third pair of Large Paired Neurons (LPN3s) identified by EM. The location supports this, as does the nature of the LPN3s themselves: they are essentially unique, being by far the largest interneurons... read full comment

Comment on: Candiani et al. BMC Neuroscience, 13:59

Iron, CCSVI, and Autoimmunity (Sara Kreindler, 02 September 2011)

The finding that iron deposition may not be causally linked to MS raises an intriguing question: Might CCSVI trigger MS in a way that does not depend on iron deposition? It occurs to me that a possible answer might be found by treating the autoimmune and vascular accounts of MS not as competing theories but as different pieces of the puzzle.

Consider the dominant animal model for MS – experimental allergic encephalomyelitis. This model depends on an intracerebral injection of antibodies, as antibodies generated in the body will not cross an intact blood-brain barrier (BBB). There is evidence that the BBB of MS patients is damaged, but it is not yet known why or at what point this damage occurs. The mechanism of venous reflux proposed by the vascular theory constitutes... read full comment

Comment on: Zivadinov et al. BMC Neuroscience, 12:60

Queries re: sample and interpretation of findings (Belinda Lennox, 31 May 2011)

I was fascinated to read your study that seems to show a very robust difference in levels of cytokines in unmedicated first episode patients with schizophrenia. I have 2 queries, relating to the subjects tested, and the measures of inflammation.

Firstly, can you clarify for me the nature of the patients that you studied and how the patients were recruited and from what setting? What was the length of untreated illness in the patients and were they never medicated, or just unmedicated at the time of testing? Only 10 of the 51 patients were subsequently treated with antipsychotics, which would suggest to me that they were not acutely unwell. They do not seem like a typical cohort of first episode psychosis patients in my experience. The diagnosis at first presentation of... read full comment

Comment on: Reale et al. BMC Neuroscience, 12:13

Clarification (Lars Edvinsson, 10 November 2010)



In results page 2, line 18; we would like to clarify our results by adding:

“The information on infarct volume and neurology score after MCAO was taken from our previous study in BMC Neuroscience [18].”

read full comment

Comment on: Maddahi et al. BMC Neuroscience, 10:56

Hebb happy! (paul adams, 12 May 2010)

Wouldn't one expect this if connections are Hebbian? read full comment

Comment on: Fares et al. BMC Neuroscience, 10:O19

The modulation of corticospinal excitability during the foreperiod (Craig Sinclair, 28 July 2008)

I was interested by your findings presented in this paper.I found the observation of a significant Precue x Time interaction in the prime mover APB muscle to be interesting. In particular, the fact that the MEP amplitude appeared to decline across the foreperiod when the precued movement was one which maximally engaged the APB muscle (180, 225, or 270 degrees movements) as opposed to when the precued movement was not requiring such strong abduction/flexion (90, 135 degrees movements). I wonder if this might reflect a movement specific suppression of MEP amplitude in the prime mover muscle during the foreperiod? If so, do you think that this might involve a different inhibitory mechanism to the more generalized suppression seen in the non-involved FDI muscle regardless of the precued... read full comment

Comment on: van Elswijk et al. BMC Neuroscience, 9:51

Incorrect citation in article (Anne Hart, 18 June 2007)

The final version of the article says: "We did not detect any overt cell fate changes or morphological defects in any of these or other neurons in lin-12(lf), lin-12(gfcs) or lin-12(n137gf) mutant animals (data not shown), consistent with a previous report [47] and supporting our conclusion that lin-12 mediated behavioral changes were not due to developmental defects."This sentence should cite to reference #41 by Altun-Gultekin, et al. which also finds that altering lin-12 Notch activity does not change neuronal morphology. read full comment

Comment on: Chao et al. BMC Neuroscience, 6:45

Updated contact information for corresponding author (David Sherry, 21 May 2007)

Since this paper was published the corresponding author has moved. The new contact information is:Dave SherryOUHSCDepartment of Cell Biology940 Stanton L Young BlvdOklahoma City, OK 73104USAe-mail: david-sherry@ouhsc.edu read full comment

Comment on: Sherry et al. BMC Neuroscience, 7:54

Web access to data (Daniel A. Wagenaar, 09 March 2007)

All raw data used for this report may be obtained from the web, at http://potterlab.bme.gatech.edu/development-data.Analogues of Figure 1 for each of the 58 cultures studied are available at the same location. Requests for access may be sent to Steve Potter (steve.potter@bme.gatech.edu). read full comment

Comment on: Wagenaar et al. BMC Neuroscience, 7:11

Access to These Data (Steve Potter, 10 January 2007)

Access is free to all of the data described in this article. In addition, we provide codelets to help process it in batch mode, as well as help files, and format descriptions. The total size of the data sets is over 45GB. For your access code, please send a request to me:Prof. Steve Potter <steve.potter@bme.gatech.edu> read full comment

Comment on: Wagenaar et al. BMC Neuroscience, 7:11

Comparison with earlier version (Don L. Jewett, 03 August 2006)

The final version of this article was posted about June 26, 2006. If you looked earlier than this date, you would have seen the preliminary version. The final version is the one that should be quoted or referred to, should such an eventuality occur. read full comment

Comment on: Jewett et al. BMC Neuroscience, 7:18

neuroprotective?? (Harvey Mace, 15 June 2006)

This must be the strangest paper I have read so far. As I thought everyone knows, all the antipsychotics are NEUROTOXIC, not neuroprotective, hence the millions of sufferers of acute and tardive motor dysfunctions, not to mention tardive dementia, caused by them. Why do the authors consider schizophrenia is caused by something modelled by growth medium deficiency, and if so would it not suggest attempts to reverse the deficiency as more likely to be therapeutic? read full comment

Comment on: Bastianetto et al. BMC Neuroscience, 7:28

The ADD/ADHD and Alzheimer's disease connection (Lynn Spina, 23 May 2006)

Although I am not a professional in this field, I'd consider myself a case study. Upon researching any relationship between ADD/ADHD and Alzheimer's disease, I came upon your site in search for answers. I do think there is viable evidence to continue research along this vein. I hope that there continues to be some interest in this connection, as I think it can be invaluable in the treatment/prevention of many neural diseases such as Alzheimer's and Neiman-Picks disease and it's relationship to ADD/ADHD. Thank you, ~Lynn Spina read full comment

Comment on: Fossella et al. BMC Neuroscience, 3:14

Statistics (Timothy Dixon, 20 February 2006)

What statistics are used in this study? The presences of an 'F' value combined with the experimental design would indicate ANOVA. However, any ANOVA F statistic below 1 can never be significant. As I am not involved in this area of research I am probably missing some different significance test. read full comment

Comment on: Iannone et al. BMC Neuroscience, 7:13

Melatonin, Mammalian Evolution, and Brain Size... (James Howard, 03 November 2004)

I found this interesting. In 2001, I published a paper dealing with the influence of melatonin on evolution of mammals and their large brains (Hormones in Mammalian Evolution, Rivista di Biologia / Biology Forum 2001; 94: 177-184). read full comment

Comment on: Niles et al. BMC Neuroscience, 5:41

A Basis of Consciousness... (James Howard, 03 November 2004)

I thought this might be of interest to this idea.A Basis of ConsciousnessCopyright 2003, James Michael HowardI define "consciousness" as one brain mechanism having to inhibit or enhance another. This makes one mechanism "aware" of the other. Now this may be magnified into any level of complexity of "on off" mechanisms monitored by other "on off" mechanisms. This is a form of "consciousness."However, I suggest the real key to "consciousness" is awareness of "need." When the above scenario is connected with a mechanism which generates "need," the interaction reaches the level of self awareness. Hence, hunger, thirst, etc. and sex produce "self awareness" in their satisfaction or deferral. (The memories of how these needs were met are stored in the association areas which refine the... read full comment

Comment on: Tononi BMC Neuroscience, 5:42

New contact information (Thomas Hughes, 19 August 2004)

To contact us about reagents, maps, and sequence files, please note that our server address has changed to:http://momotion.cns.montana.eduNew email address is: thughesgfp@mac.com read full comment

Comment on: Sheridan et al. BMC Neuroscience, 3:7