JerMa88/TPR_Peer_Reviews huggingface dataset:
Peer review of: The RNA quality control pathway nonsense-mediated mRNA decay targets cellular and viral (2020)



REVIEWERS' COMMENTS: 

 

Reviewer #1 (Remarks to the Author): 

 

Overall, the authors have addressed my concerns. They have included additional results, controls, 
and analysis. My enthusiasm for this manuscript has improved with these additions and it is clear 
that this work will lead to future interesting studies. 

 

1. The authors now include new information in Sup. Fig. 5 and lines 175-186 that addresses my 
previous comment. 

2. The additional plots are useful additions. 

3. The GEO accession number has been updated, but was not available to reviewers. 

4. It seems worth mentioning that UPF1 plays a role in multiple decay pathways. This could be done 
without giving away current plans about Staufen-mediated decay. 

5. The validation data now included in Sup. Fig. 8 is useful. 

6. The authors claim that stating whether certain non-coding RNAs have been reported in other 
ribosome-associated reports is beyond the scope of this work. It appears to this reviewer that 
context of their finding would be helpful to readers. 

7. The authors include additional negative controls in their assays, which strengthens their previous 
conclusion. 

8. The authors have now added relevant information about the context of XBP1 in B cell 
development to the Discussion Section. 

 

 

 

Reviewer #2 (Remarks to the Author): 

 

This is good work with broad interest to the virology field. The authors have addressed all of my 
concerns. I found two typos: 

 

1. "rending" line 85 

2. "preformed" line 290.
Peer review of: Rational flux-tuning of Halomonas bluephagenesis for co-production of bioplastic PHB and (2020)



REVIEWERS' COMMENTS: 

Reviewer #1: unavailable. 

Reviewer #2 (Remarks to the Author): 

The authors have done a nice job responding to my (somewhat lengthy comments). I only have 2 
points that I don’t feel were adequately addressed but which can be quite easily: 

1. Original comment, now Lines 153-155 – “The medium named “60MME” has 60 g/L NaCl by 
definition. Therefore, why was there a “factorial analysis” to find the optimized concentration?” 

The authors responded that the NaCl concentration in the 60MME medium was determined from the 
factorial analysis. The only problem with this is that as written, it sounds like the 60MME medium 
already existed and then a new analysis was done. To clarify, I suggest the authors simply change the 
first instance of “60MME” on line 154 to “MME.” This way, in the subsequent sentence, it becomes 
clear that “60MME” was defined AFTER this factorial experiment. 

2. Original comment, now Line 156, Figure 3c – “60 g/L was noted to give the “highest” concentration 
at 2.82 g/L. Is this really significantly different from what was achieved with 80 g/L?” 

The authors responded that the difference was not significant but that higher NaCl concentrations are 
undesirable. The authors should revise the sentence that follows to acknowledge this in the 
manuscript. It currently reads “Since a higher NaCl concentration failed to improve ectoine 
accumulation, simultaneously inhibiting the cell growth.” I note that this is not a complete sentence. I 
suggest revising to read something like: 
“The titer was comparable at higher NaCl concentration, but cell growth was inhibited.” 

Reviewer #3 (Remarks to the Author): 

Dear Authors, 

your manuscript was carefully revised, and the comments were appropriatey addressed. It can now be 
accepted for publication. 

Reviewer #4 (Remarks to the Author): 

Authors have addressed the suggestions. No more comments.
Peer review of: Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes (2020)

Reviewers' Comments:
Reviewer #2:
Remarks to the Author:
No further suggestions. However, there is still a major worry that there is still no way to interpret
the lack of consistent "directionality" of BBB-related genes in the mouse versus human data sets
and the non-BBB actions of exenatide. Ultimately, there is a lot of data. But it remains unclear
whether this study can really show a clear conclusion about the use of exenatide to treat AD via a
BBB mechanism.
Peer review of: Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes (2020)


Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
Zhao et al. have provided a thorough and thoughtful reply to the comments of both reviewers. I 
appreciate the considerable extra effort to validate changes to brain endothelial cells with other 
methods, and the qPCR, western blot, and FISH provide considerable evidence to back up changes 
observed by scRNAseq, particularly during this time. The flow of the article is also much improved 
with the additional acknowledgement of recent publications by the Wyss-Coray lab, and this work 
provides an excellent complement to their work detailing changes to brain endothelium during 
aging. Finally, the additional analysis of microglia activation, and discussion around mechanistic 
aspects of GLP1R treatment provide greater context. This is timely and exciting work that provides 
exquisite details of changes to the neurovasculature during aging, as well as potential therapeutic 
avenues, and I recommend its acceptance. 
 
 
 
Reviewer #2: 
Remarks to the Author: 
To Authors: This is a study with lots of data. Much of the data may replicate what has been 
published in the literature in terms of aging vascular signatures (e.g. Boisvert, Cell Rep 2018; 
Olah, Nat Comm 2018; Guo Neurobiol Dis 2019; Tabula Muris Consortium, BioRchiv 2019). There 
are some remaining concerns. 
 
1. The authors still appear to conclude the major response in the aging vascular system is 
centered on the BBB, and that exenatide efficacy is mediated by BBB rescue. One may still worry 
that the data might not fully support these two major conclusions. Many other non-BBB pathways 
are affected. Exenatide surely affects non-BBB/non-endothelial targets in vivo. 
 
2. There may still be several inconsistent findings. Many BBB genes move in opposite directions in 
aged mouse versus aged humans. Overall, the aged normal mouse is more similar to the aged AD 
human but not the normal aged human. Why? 
 
3. Finally, a minor technical question please. The authors replotted Fig 5b as the new Fig 4b. The 
original Fig 5b stated that “n=9 image stacks from 3 mice for each group”. If it is true that this 
meant 3 image stacks from each mouse, and 3 mice total, then it was pointed out that calculating 
means and SEM from n=9 data points was incorrect. What should be done is to first calculate a 
mean of 3 image stacks per mouse, and then calculate the group average with only n=3 data 
points. If so, shouldn’t the SEM (SD divided by square root of n) be very different for n=9 versus 
n=3? It is surprising that the replotted means and SEM are almost exactly the same.
Peer review of: Interneuron-specific plasticity at parvalbumin and somatostatin inhibitory synapses onto (2019)


 

Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
The authors have provided new experiments (Suppl Fig 4) and addressed my main concerns. The 
argumentation regarding the clamping remains a bit puzzling. I take it that the 0mV clamp experiment 
was in part done to isolate inhibitory currents and prevent APs. Now, the authors argue that this did 
not prevent involvement of T-type VGCCs since the clamp is likely to be incomplete. But then one 
expects this to impact the iLTP in the distal dendrites as well since the inhibitory currents will likely be 
very weak. Nonetheless, the authors convinced me with pharmacology experiment, which now clearly 
demonstrates that T-type VGCCs are engaged in this plasticity. 
I have no further requests or suggestions. 
ANTHONY HOLTMAAT 
 
 
 
Reviewer #2: 
Remarks to the Author: 
The authors have provided reasonable responses to the criticisms.
Peer review of: Plasticity of muscle synergies through fractionation and merging during development and (2020)



Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
The ms has been thoroughly revised following the reviewers’ recommendations. The answer to the 
question of the potential effect of speed on muscle synergies is convincing. The authors’ 
hypothesis that “It is plausible that when running at the self-selected preferred speed, one 
employs a set of designated, default mode synergies” is interesting, although it deserves further 
scrutiny. 
 
The authors did not pursue much further biomechanical analysis, as we asked in the first round. 
Nevertheless, their approach to the problem is satisfactory. They used a complex metric to 
highlight a simple landing-take off asymmetry, the hysteresis (only depending on potential energy) 
corresponds per se to the modification of the COM position at foot-contact and toe-off. This is a 
good way to illustrate the deviation from an elastic rebound. 
 
 
 
 
 
Reviewer #3: 
Remarks to the Author: 
The authors have answered for all my comments perfectly.
Peer review of: A spike-timing-dependent plasticity rule for dendritic spines (2018)



Reviewers' Comments: 
 
Reviewer #2: 
Remarks to the Author: 
The authors have addressed several of my comments. However, my major point 1 remains 
unaddressed. I continue to think that it is important to know whether the present findings hold in 
mature circuits in older animals. Furthermore, I don't think the limitations of studies published more 
than 20 years ago should be used as an argument. Obviously, we have better techniques and 
accordingly set the bar higher, not lower. Finally, while the Corona pandemic may be an argument for 
giving the authors more time for a careful revision, it is definitely not an argument for omitting 
important experiments.
Peer review of: A spike-timing-dependent plasticity rule for dendritic spines (2018)



Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
The authors have satisfactorily responded to my comments and the manuscript is significantly 
improved. 
 
 
 
Reviewer #2: 
Remarks to the Author: 
The paper by Tazerart et al. has been improved, but requires further revision. 
 
Major points: 
1. The fact that all results are obtained from young animals remains an issue. The authors argue that 
LTD is missing in older animals (Verhoog et al., 2013), but this is exactly my point. Readers will be 
primarily interested in phenomena occurring in the mature brain. If the conclusions do not hold in the 
mature brain, the manuscript should be published in a more specialized journal. 
 
2. The authors claim that potentiation is independent of the distance from the soma (line 450), but 
this dependence is not properly analyzed. Figure S14 is off the point. One would like to see a figure in 
which t-LTP or t-LTD is plotted against distance. 
 
3. The authors argue that only the DMSO-dissolved latrunculin affects t-LTP. This argument is difficult 
to follow, because DMSO only facilitates the distribution in the aqueous phase. This raises the question 
whether (1) DMSO has an effect on its own, and (2) latrunculin in ACSF lacks an effect simply because 
the substance does not dissolve. Clarification is needed. 
 
4. It is disappointing that the authors cannot pinpoint the relation between Ca2+ transients and t-LTD. 
The apologetic statements on p. 18 should be better replaced by additional experiments (4 neurons is 
probably not enough to detect small differences). 
 
5. Traces of Ca2+ transients (deltaG / R as a function of time) should be shown in the main figures 
(e.g. Figure 6). 
 
6. The paper is still too long in relation to the new information it contains. It should be substantially 
shortened. 
 
 
Minor points: 
Line 67: “performed a protocol during which we perform” sounds awkward. 
Line 115: The complete statistics for these findings should be given in main text. 
Line 140: “postsynaptic voltage at the postsynaptic site” is redundant. 
Line 450: “did not find any correlation …” – the authors should refer to Figure S14 here and extend 
the analysis. 
Line 750: “Mann-Whitney” is misspelled. 
Supplement line 185: “physiological temperatures” should read “near-physiological temperature".
Peer review of: Reduced serial dependence suggests deficits in synaptic potentiation in anti-NMDAR (2020)

Reviewers' Comments:
Reviewer #2:
 Remarks to the Author:
 I very much enjoyed reading this revised version of the work as well as your replies. Hypotheses 1
 and 3 have been clarified, and new analyses on angular preference and bias changes with recovery in
 NMDAR encephalitis patients really strengthen the findings. I have no further comment or request.
Peer review of: Preventing and treating PTSD-like memory by trauma contextualization (2020)



Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
1. The authors have adequately described the differences between familiar (a 20 cm diameter round) chamber vs. 
conditioning (a 20 x 20 cm square) chamber. However, now all figures show familiar and conditioning chambers as being 
square (if I am not mistaken, I think they were all shown as round previously). I recommend familiar chambers to be 
represented as round and conditioning chambers depicted as square in all figures. 
 
Related to the above, the authors state on Pg. 11: “A squared conditioning chamber (20 x 20 cm)…The floor of the 
chamber consisted of 30 stainless-steel rods (5 mm diameter), spaced 5 mm apart…” I do not see how 30 rods (5 mm 
diameter, 5 mm apart) can fit inside 20 x 20 cm square chamber. 
 
 
2. I remain steadfast for the third time that the immediate post-training cort injection producing PTSD-like effects require 
some explanation. The claim that post-training cort is causally involved in PTSD-like memory formation via inducing 
contextual amnesia needs to be supported by facts and not mere conjectures. Whether the authors’ argument that “the 
post-training optogenetic inhibition of dCA1 does not necessarily recapitulate the deleterious effect of post-training 
injection of cort on the dHPC-dependent contextualized fear memory” is valid or not won’t be known unless such 
experiment has been performed. If cort effects are due to affecting the memory consolidation process that occurs during a 
critical time window after aversive experience, this can be tested optogenetically as was done during fear conditioning. I 
believe such post-training manipulations are typical in memory consolidation experiments.
Peer review of: Behavioral and neuronal underpinnings of safety in numbers in fruit flies (2019)


 

 

Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
This is a strong review that addresses both my and the other reviewers' comments adequately, 
through new experiments and some wise toning down of conclusions where certain experimental 
results have (unavoidable) caveats. 
 
 
 
Reviewer #2: 
Remarks to the Author: 
In this revised version of the manuscript by by Ferreira and Moita, authors have added useful 
behavioral experiments that clarified most of the confusion I have with the paper. They have also 
significantly improved the description of the behavior experiments, and provided necessary controls. 
After the substantial changes done in the text, I think the data provided supports the conclusions of 
the paper. I thank the authors for their hard work. I have no further comments, and I recommend 
publication of the manuscript with no further edits. 
 
 
 
Reviewer #3: 
Remarks to the Author: 
Thank you for the revisions, which addressed most of my points. Two minor points remain. 
 
It is still unclear, what boxplots within your violin plots represent. Whiskers of boxplots may represent 
1.5 IQR, or 10%/90%, or 5%/95%. In your rebuttal letter you say IQR, but this information does not 
appear in the legends of the manuscript. 
 
New point: 
Please reconsider Line 255 in the discussion section saying “insects can only use short range auditory 
signals”. This is certainly not true for crickets, grasshoppers and other insect auditory-communication 
specialists. Their auditory signaling range goes far beyond their visual range.
Peer review of: Rapid Bayesian learning in the mammalian olfactory system (2019)



Reviewers' Comments: 

Reviewer #1: 
Remarks to the Author: 
The authors have addressed comments to my satisfaction. 

Sincerely, 
Matt Smear 

Reviewer #2: 
Remarks to the Author: 
The authors have included more clarity as to what is learned and why and the paper is easier to read. 
I do have one request which is to not refer to receptor affinities as weights because this is confusing, 
why not use the correct term? While I still think this is a bit remote from the biological system, this is 
a fascinating paper with a number of interesting ideas which will certainly change my thinking about 
the first stage of olfactory learning. 

Reviewer #3: 
Remarks to the Author: 
The authors did a solid job at answering my concerns. I am happy to support publication.
Peer review of: Purine metabolism regulates DNA repair and therapy resistance in glioblastoma (2020)


REVIEWERS' COMMENTS: 

Reviewer #1 (Remarks to the Author): 

The authors have adequately addressed my comments and criticisms 

Reviewer #2 (Remarks to the Author): 

The authors have responded well to my comments and suggestions. Particularly the new data 
confirming the results with orthotopic PDX models has greatly increased the value of this study. 

Reviewer #3 (Remarks to the Author): 

The revised manuscript is acceptable for publication. We look forward to the next paper in the 
series. 

Reviewer #4 (Remarks to the Author): 

I am satisfied with the revised ms that all my comments have been addressed.
Peer review of: Placebos without deception reduce self-report and neural measures of emotional distress (2020)



Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
The authors have done an excellent job in addressing all my concerns. Notably, they have 
added substantial power to their analysis by significantly enlarging their sample. This not 
only strengthens confidence into the main findings of the study (on the placebo effect on 
the late LPP) but it also led to the elimination or reduction of placebo effects on the early 
LPP, which appeared inconsistent or implausible in the first version of the manuscript. This 
further underlines the importance of sufficiently powered samples. 
 
I believe that this is now a very solid and at the same time very important paper, and I 
strongly recommend publication. 
 
One little detail, which I think can be addressed without further involvement of reviewers: 
In L152, the authors announce to “discuss in more detail below” effects of placebos on 
reactivity to both neutral and negative emotional stimuli, referring to similar observations in 
other studies. I could not find such a discussion, though, in the remainder of the paper. I 
think it would be important to add it, such that the reader has a chance to integrate the 
current findings into a broader picture. 
 
 
 
 
 
Reviewer #2: 
Remarks to the Author: 
The authors should be applauded for replicating their work. Unfortunately, this did not 
address my concerns, which have in fact been aggravated by their responses. Most 
importantly, given the sensitivity of the brain potential to regulation strategies, it seems it is 
now conceptually impossible to know if the brain potential amplitude (susceptible to 
cognitive elaboration) and self-report (susceptible to elaboration as well) both just reflect 
demand characteristics. This seems to broadly limit the ability of the data to address the 
research question. It is a hard question to tackle, and maybe the present measures are not 
sufficient to come to a clear conclusion. In addition, it may not be appropriate to refer to a 
time range up to 1000 ms post-stimulus as reflecting "early attention".
Peer review of: Gasdermin-D-dependent IL-1α release from microglia promotes protective immunity during (2021)


REVIEWERS' COMMENTS: 

Reviewer #1 (Remarks to the Author): 

The authors have satisfactorily addressed the reviewers concerns. This is a much improved 
manuscript that presents important new information. This manuscript contains new insights into 
the differential roles of microglia and macrophages to propagate inflammation and contributes new 
information on the roles of microglia and the alarmin IL-1a, to promote neuroinflammation and 
parasite control in the brain. This information will be of interest to the parasite community and 
contributes to the understanding of the immune response to Toxoplasma gondii in the brain. 

Reviewer #2 (Remarks to the Author): 

Thank you for addressing all of my questions raised and making the corrections requested.
Peer review of: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated (2020)



REVIEWER COMMENTS 

 

Reviewer #1 (Remarks to the Author): 

 

Thank you for a thoughtful response to critique. The new data has greatly improved the manuscript. 

 

 

Reviewer #2 (Remarks to the Author): 

 

This is an extensive revision. All points have been addressed and the manuscript has improved. This 
is an important study that further contributes to the understanding of CaMKII in cardiac 
pathophysiology. I have no further questions. 

Johannes Backs 

 

 

Reviewer #3 (Remarks to the Author): 

 

The authors have extensively revised their manusript, addressed all points raised by this and the 
other reviewers and have added new experiments to support their data and conclusions. 

 

I have no further questions. 

 

Christoph Maack 

 

 

Reviewer #4 (Remarks to the Author): 

 

The Authors present a three-compartment mitochondrial model, based on previous work, that 
incorporates major processes in addition to the Creatine-Phosphocreatine system that regenerates 
ADP, both in cytoplasmic and periplasmic spaces. 

The Authors simulate the metabolic phenotype of the mitochondrial CaMKII (mtCaMKII) and 
mitochondrial CK overexpressors by, e.g., decreasing complex I activity or mitochondrial CK, 
increasing the activity of TCA cycle enzymes (Fig. 7). 

 

Two important remarks that the Authors should address: 

 

1) They simulate the cycle of ATP hydrolysis occurring during the heart cycle of systole-diastole (their 
Fig. S6). However, they do not do the same with the cytoplasmic Ca2+ (Cai), and they should, 
otherwise it won’t be a realistic simulation since Ca2+ also oscillates during the cycle of contraction-
relaxation of the heart. Apparently, the Authors left Cai constant, as a parameter, after inspection of 
the model equations (in Gitlab) by this Reviewer. As a result, the mitochondrial Ca2+ (Camito) 
appears not to change (or very little) which has metabolic consequences for the flux through the TCA 
cycle, respiration and ATP synthesis, all relevant for the present work. 

 

2) Although the simulation approach utilized is correct, its reliability depends on the model 
parameterization under conditions as close as possible to the experimental situation being 
simulated, to validate the model behavior under those conditions. This should be accompanied by a 
Supplementary Table with the parameters utilized in the simulations and their references for 
justification. 

Do the Authors have simulations of relevant experimental results from this work or the work of 
others, independently from what they are trying to simulate, e.g., ATP/ADP or ATP/PCr ratio? If so, 
please, include in Supplement.
Peer review of: The kallikrein–kinin pathway as a mechanism for auto-control of brown adipose tissue (2020)


 

Reviewers' Comments: 
 
Reviewer #1: 
Remarks to the Author: 
The authors have addressed all my comments and concerns sufficiently well, and the manuscript 
has been improved significantly. 
 
 
 
Reviewer #3: 
Remarks to the Author: 
the authors addressed all my concerns, I would suggest to accept the paper for publications