Submited on: 18 Sep 2012 10:38:59 AM GMT
Published on: 18 Sep 2012 12:58:10 PM GMT
 

  • What are the main claims of the paper and how important are they?

    To findout whether the DNA ladder as a signal for apoptosis after neonatel capsaicin treatment using the rat trigeminal ganglion.


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    It is a good attempt to know which is responsible for apoptosis


  • Are the claims properly placed in the context of the previous literature?

    Yes, however they can refer somemore articles.


  • Do the results support the claims? If not, what other evidence is required?

    Yes


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    They have followed the protocol, and also animal ethics committee


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    Yes


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    No Ofcourse


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    Ofcourse, they wanted to confirm whether the cell death is due to Necrosis or Apoptosis and conclude that it is Necrosis rather than Apoptosis.


  • Other Comments:

    They can write basic information of capsaicin, chemical nature, pharmalogical nature, then they may pose the research problem. They can also refer these article.


    Activation of the caspase cascade underlies the rat trigeminal primary neuronal apoptosis induced by neonatal capsaicin administration.

    Jin HWIchikawa HNomura KMukae KTerayama RYamaai TSugimoto T.


    Source      

    Department of Oral Function and Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Japan.


    Abstract

    The systemic administration of capsaicin is known to cause a massive loss of sensory primary neurons in newborn rats. Here we examined the trigeminal ganglion neurons immunohistochemically for the possible induction of activated forms of caspases-9 and -3 following a subcutaneous injection of capsaicin in newborn rats. The DNA fragmentation signal was labeled by a TUNEL method. TUNEL-positive neurons were rare (< 0.5%) at 24 h after injection of the vehicle without capsaicin. After the capsaicin injection, TUNEL-positive neurons began to increase by 12 h, reached a peak at 24 h (11.4%), and returned to the control level by 120 h. Vehicle control levels of caspase- 9-immunoreactive (ir) and caspase-3-ir neurons were low (< 0.5%). Neonatal capsaicin administration induced caspase-9-immunoreactivity (ir) and -3-ir. The temporal distributions of caspase-9-ir and caspase-3-ir neurons were similar to those of TUNEL-positive neurons with peak expressions at 24 h of 13.2 and 11.1%, respectively. A double-stain analysis at 24 h post-injection indicated 72% of TUNEL-positive neurons were caspase-9-ir, and 70% caspase-3-ir. Conversely, 78 and 68% of caspase-9-ir and caspase-3-ir neurons, respectively, were TUNEL-positive. Comparison of two adjacent sections immunostained for the two different antigens revealed the co-expression of the two caspases. These results suggest that neonatal capsaicin triggers the caspase cascade and, thereby, induces trigeminal primary neuronal apoptosis.

    Pain. 1996 Jan;64(1):191-5.


    Capsaicin activated currents in rat dorsal root ganglion cells.

    Liu LWang YSimon SA.


    Source

    Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.


    Abstract

    Capsaicin is a pungent-tasting compound produced by plants in the Capsium family that activates a subset of primary afferent neurons associated with pain and thermoreception. Previous studies from dorsal root ganglion (DRGs) neurons suggest that many of capsaicin's physiological responses are a consequence of its activating a cation-selective current. To further characterize the responses to capsaicin whole-cell patch-clamp measurements were performed on rat DRGs to which 0.1-10 microM capsaicin was continuously applied. The capsaicin-activated currents exhibited marked variability in their thresholds, amplitude (to 15 nA), rates of desensitization, and the number of distinct maxima in the evoked current. Similar responses were found in rat trigeminal ganglion cells. The heterogeneity in the magnitude of the currents evoked by 0.1 microM capsaicin likely reflects different types of capsaicin-sensitive neurons; a result consistent with in vitro extracellular recordings from capsaicin-sensitive sensory afferents (Seno and Dray 1993).

    Arch Histol Cytol. 2005 Dec;68(4):301-10.

  • Competing interests:
    No, only teaching the subjects
  • Invited by the author to review this article? :
    No
  • Have you previously published on this or a similar topic?:
    No
  • References:
  • Experience and credentials in the specific area of science:

    Scholarly Reviewer

  • How to cite:  Anonymous.Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis[Review of the article 'Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis ' by Nakagawa H].WebmedCentral 2012;3(9):WMCRW002249
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  • What are the main claims of the paper and how important are they?

    Study claimed that capsiacin at the dosages tested caused necrosis rather that apoptotic death in neuronal cells. I view this submission as speculation rather than factual statments. The fact that DNA ladder formation was not observed do not mean death occurred by necrosis. The study observed absence of DNA ladder formation in cells treated with capsaicin at 50 mg/kg. There was no variation in concentration of capsaicin used to allow for such conclusion. Moreso, study did not report any parameters consistent with necrotic death. Therefore I find it unacceptable the conclusion of authors that capsaicin caused cell death in neurons by necrotic process.


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    Study is original and scholarly. But the methods employed did not permit full exploration of the study objectives. Data presented are limited in scope.


  • Are the claims properly placed in the context of the previous literature?

    Partially.


  • Do the results support the claims? If not, what other evidence is required?

    1. There are no data indicating presence of necrosis in cells treated with capsiacin. Though if data presented rule out apoptotic death of treated cells, autophagic or necrotic may play role but any submission needs to be supported by facts.

    2. The concentrations of capsiascin was not varied in this study.


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    NA


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    The methodolgy are explicit enough to permit reproduction of experiments.


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    Yes. More data could be provided to eliminate apoptosis and reveal presence of necrosis. Authors could subject treated cells to apoptotic/necrotic staining.


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    Data presented are preliminary. Further studies are needed to draw valid conclusion


  • Other Comments:

    No

  • Competing interests:
    No
  • Invited by the author to review this article? :
    No
  • Have you previously published on this or a similar topic?:
    No
  • References:
  • Experience and credentials in the specific area of science:

    I have been involved with cellular studies where apoptotic or necrotic processes are determined.

  • How to cite:  Anonymous.Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis[Review of the article 'Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis ' by Nakagawa H].WebmedCentral 2012;3(9):WMCRW002248
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Necrosis or Apoptosis-DNA laddering as a tool
Posted by Dr. Joseph M Antony on 19 Sep 2012 05:51:23 PM GMT

  • What are the main claims of the paper and how important are they?

    The main claim of this article is that capsaicin-induced apoptosis of trigeminal neurons cannot be detected using DNA ladder formation as a tool.


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    While the claim is novel, it does so without any merit, based on published data available. Taking particular note of their conclusion that capsaicin causes necrosis rather than apoptosis, I would suggest that based on the paper by Sugimoto et al (1999) (PMID  9914448), it appears that DNA laddering might not be the most effective way of determining capsaicin-induced apoptosis in trigeminal neurons. Perhaps Hiura et al., might consider using EM and nick end labeling to determine apopotsis, which has been performed earlier. DNA laddering is a very insensitive tool in this context. Just because DNA fragmentation is not visible on agarose gel, it does not mean that there is no apopotosis. Further, treating trigeminal neurons in culture (in vitro) might have indicated a different result as was done with the Saos-2 cel line treated with okadaic acid. In conlusion, a technical challenge must not be the deciding factor in determining a cellular mechanism, at least when there is evidence in terms of published literature.


  • Are the claims properly placed in the context of the previous literature?

    Somewhat


  • Do the results support the claims? If not, what other evidence is required?

    No. Please refer to the previous section


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    No


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    Somewhat satisfactory


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    Yes, as explained in the previous section


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    No


  • Other Comments:

    None

  • Competing interests:
    None
  • Invited by the author to review this article? :
    No
  • Have you previously published on this or a similar topic?:
    No
  • References:
  • Experience and credentials in the specific area of science:

    Have worked on neuronal cells

  • How to cite:  Antony J M.Necrosis or Apoptosis-DNA laddering as a tool[Review of the article 'Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis ' by Nakagawa H].WebmedCentral 2012;3(9):WMCRW002245
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  • What are the main claims of the paper and how important are they?

    To Findout Whether DNA Ladder as a Signal For Apoptosis In Trigeminal Ganglion Using Rat Model System


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    It is an good attempt to check whether Necrosis or Apoptosis is happening in this phenomena


  • Are the claims properly placed in the context of the previous literature?

    Yes,However,They can refer some papers inorder to visuvalize the molecular mechanism.

    Chu-Sook Kim, Won-Hyung Park, Jun-Young Park, Ji-Hye Kang, Mi-Ock Kim, Teruo Kawada, Hoon Yoo, In-Seob Han, and Rina Yu. Journal of Medicinal Food. Fall 2004, 7(3): 267-273. doi:10.1089/jmf.2004.7.267.

    Published in Volume: 7 Issue 3: September 24, 2004

    Article

    Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells

    Chin-Lin Hsu and Gow-Chin Yen *

    Department of Food Science and Biotechnology, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan


  • Do the results support the claims? If not, what other evidence is required?

    Their results are intersting and support their claim, however they can reconfirm by further experiments.


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    Suffcient protocol is given, they have followed animal ethics committee also.


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    Yes, valid


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    They can still refer the molecular mechanism of apoptosis and necrosis


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    It is a good approach


  • Other Comments:

    Their findings indicates that at low concentration of Oa induces apoptosis but at higher concentration of OA results in necrosis. This Implicate that the concentration of OA play the role in inducing either apoptosis or necrosis. The compound may react with DNA which results switching over of any one mechanism.

  • Competing interests:
    Scholarly Reviewer
  • Invited by the author to review this article? :
    No
  • Have you previously published on this or a similar topic?:
    No
  • References:
  • Experience and credentials in the specific area of science:

    Teaching

  • How to cite:  Anonymous.Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis[Review of the article 'Analysis of DNA Extracted From the Trigeminal Ganglion Cells After Neonatal Capsaicin Treatment by Agarose Gel Electrophoresis ' by Nakagawa H].WebmedCentral 2012;3(9):WMCRW002244
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