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1. As fluvastatin shows very promising results towards the treatment of NAFLD, can the results from this experiment and PharmOmics be furthered to clinical trials in humans?2. Can fluvastatin and aspirin be use together to further prevent or treat NALFD?

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1. As fluvastatin shows very promising results towards the treatment of NAFLD, can the results from this experiment and PharmOmics be furthered to clinical trials in humans?2. Can fluvastatin and aspirin be use together to further prevent or treat NALFD?

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1. Why was the percentage of GC content looked into? Is it because genomes with higher GC contents have higher melting temperatures and genes of phages are expected to be more durable?2. In the significance portion, it was mentioned that phage therapy could be used for conditions such as skin acne. How would phage therapy work with hormonal skin acne? 

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1. Why was the percentage of GC content looked into? Is it because genomes with higher GC contents have higher melting temperatures and genes of phages are expected to be more durable?2. In the significance portion, it was mentioned that phage therapy could be used for conditions such as skin acne. How would phage therapy work with hormonal skin acne? 

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Hello Ryan! Very interesting presentation, I've always been curious about what they do with the extra fat in those surgeries.

Here are some of my questions for you

What are the negative side effects of too lean adipose tissue? That is, in conditions of starvation, how does the immune response change?

From my understanding, there are two types of adipose tissue (white and brown). How do the immune response differ between the two?

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1. You mentioned that you provided some specific drugs to replicate exercise, what other factors could you change in order to better replicate exercise?

2. Is low oxygen rates the defining factor for heart attack? Why was low oxygen rates used to replicate heart attack?

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1. You mentioned that you provided some specific drugs to replicate exercise, what other factors could you change in order to better replicate exercise?2. Is low oxygen rates the defining factor for heart attack? Why was low oxygen rates used to replicate heart attack?

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1. You mentioned that you provided some specific drugs to replicate exercise, what other factors could you change in order to better replicate exercise?2. Is low oxygen rates the defining factor for heart attack? Why was low oxygen rates used to replicate heart attack?

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You guys had a beautiful poster, and pairing your presentation with the visual made understanding your research much easier. Just a couple questions for you:

1. This is more of a conceptual question I had while perusing your research, but at what point does the taxonomic or genomic differentiation of various phages become moot? Given the high levels of horizontal gene transfer in the microbial world, what would you designate as a significant difference between very similar strains?

2. In your Future Directions section, you raised the question of whether clusters should be host-genera-based or to allow for multiple hosts under certain clusters. Given your research what would be your inclination, and why?

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I really enjoyed reading about your research and I was very interested in the way that you developed it. I had a couple of questions in regards to your research:

1) In what other ways do you see this research being utilized in that it may prove to be beneficial to the human body?

2) Is there a reason as to why the body experiences mitochondria fission during the event of exercise?

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Hi Ivan! Super nice seeing you again and great job on your project. You did super well. Here are some of my questions.

1. You stated that the broad spectrum between the ratti and stercoralis nematodes were very similar and exhibited barely any differences. Do you think it is possible that these two nematode species recently split off into two different species as they are very similar in the spectrum in response to certain bacterial environments?

2. Could there also be regional differences of the spectrum response to certain bacterial environments based on where the host is residing in and what kind of diet they're intaking? I was just thinking maybe this is possible due to certain mammals containing higher starch diets here in the Americas as compared to other continents.

Great job again! (: Really loved your poster design as well.

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This research was so interesting to me! Thank you for sharing and explaining it to us.

I have few questions : Why did they choose only to test the clustering method on actinobacteriophages ?

what kind of limitations this method creates to test it on other phages ?

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This was a great research project that can possibly have immense clinical significance if it is followed through! I really enjoyed your presentation video as it was easy to follow and understand. I have a few questions that I wanted to ask.

1. What possible effects can mitochondrial fusion have on heart attacks and cardiovascular tissue damage due to hypoxia? Can it be expected that fusion would cause a higher chance of heart attacks and less protection?

2. I have read that aerobic-type exercise such as long-distance running and swimming is more beneficial to the cardiovascular system than anaerobic-type exercises such as short-distance sprinting. Based on this information, could different exercise types/styles have different impacts on the amount of mitochondrial fission in the heart tissue?

3. I am assuming that the Drp1 protein that causes mitochondrial fission does not act on just the heart (correct me if I am wrong). What effects could mitochondrial fission have on other bodily organs and the organism as a whole?

Thank you and great job!

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Hello Roxanne! Awesome presentation, I found it super interesting :) I just have 2 questions for you:

1. What was the purpose of using the pluripotent stem cell line?

2. What would be the next step of this study? Moving onto live mice?

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Congratulations on completing your project. I really liked your presentation and poster, especially the diagrams on the "Abstract" and "Methodology" section.

For future reference, I would recommend you to try to make shorter figure descriptions and make your figures bigger. Since we are looking at them on a computer, there is not much of a problem, but if it was in person, it could cause some issues for your audience.

My questions are the following:

1. Since genome mosaicism is a process on phages, I was wondering if there were specific factors or cues that trigger this process, which could have affected your results? If so, how did you account for such cofounding variable?

2. I thought that a good question to ask was whether or not did you do any comparison between Cluster I and Cluster F of mycobacteriophages? Since both go through lysogenic life cycles, we would expect them to have more similarities than those found with Cluster O, but for that same reason, the small differences that we find between them might actually  say something about why Cluster F was found to overlap more with Cluster O than Cluster I.

3. Since gene exchange happens all the time between microbes, I was wondering if you think whether your novel findings were due to an unaccounted exchange of genetic material?

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Congrats on completing your poster - I wish I could be seeing this and asking questions in person, but you navigated the online format with panache and ease. Just a couple questions on future

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I would like to congratulate you. You did an amazing job. I truly enjoyed reading and watching your presentation. Keep up the good work.

My questions are the following:

1. Since it has been known that in nature structure defines function, I was wondering if the difference in shape between the SV endothelial cells and the Control endothelial cells told you anything new about SV CHD or CHD in general?

2. Given that as everyone gets older, their cells start to slowly deteriorate. I was wondering if you knew how age affects each of these differences found in SV endothelial cells in comparison to the cells of a healthy individual?

3. Also, could you explain in a little more detail what is the importance of NOTCH1 proteins in having a healthy heart?

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Hello Roxanne and et. , what a very interesting and comprehensive presentation. As someone who started taking exercise more seriously through quarantine, this really made me think about the inner workings of my body cells. I had a few questions about the study, though.

1. What are the most realistic applications that you could foresee for humans, with the experimental results you have obtained + the experiments that you plan to run in the future?

2. Was there a specific reason besides safety that live mices/rats could not be used for the experiment? It seems plausible to be able to measure activity levels of these animals by making them exercise and then extracted cells afterwards, but was there another obstacle to this?

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Hi Jennifer! Great presentation and poster!
Here are my questions for your presentation:

1.  Could this possibly be a viable treatment moving forward with further research even if the morphology observed after the overactivation of YAP causing transit amplifying cells (TAC) to proliferate into ameloblasts? I wonder if other mammals with a similar HIPPO system for dental growth would experience something similar.

2.  Could there be some repercussive effects of the TACs proliferating into the ameloblasts and not being able to differentiate between such cells?

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This was a superb project that I really enjoyed! The presentation was clear and informative, and the poster was easy to understand and had great information. I have a few questions that I wanted to ask you.

1. Do you think that these bacteria are absolutely necessary for this nematode parasite to be able to survive in an environment? For example, if the nematode was introduced to a region where all conditions of living were perfect for it to grow and spread but the soil/feces bacteria were not those that it uses for chemotaxis during the two life stages that were covered in the experiment, would this have a significant effect?

2. Could some sort of soil treatment be used to disrupt the life cycle of the nematode? Possibly using a chemical (if it is discovered) that can inhibit the chemotaxis of the iL3 towards the soil bacteria?

3. As I understand, this mechanism of using bacteria for chemotaxis can be found in a wide range of organisms. How many of these research results can be generalized to other organisms with similar life cycles?

Thanks, and once again great job!

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Really enjoyed your presentation- definitely interesting research! I also thought it was well organized and easy to follow.
I did have some questions regarding the two species of parasitic nematodes used:
Was there a particular reason as to why you chose those two species of strongyloides? And although you didn't find any significant differences in their responses to bacteria in the adult stage and iL3 stage, could there perhaps be differences in their responses to bacteria during other or more specific parts of their life cycles?
I was also wondering, and I apologize if you answered this question already, about the significance of the repulsion from bacteria during the short term and how this might inform future health measures?

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Hey y'all; loved your presentation! I really enjoyed getting into the details of your genomic analyses, it was awesome. Just a few questions for you!

1. Is it possible this method could be expanded to learn more about viruses in general, not just phages?

2. Outside of phage isolation, what other uses will finding these genetic differences be put towards?

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Hi Jennifer, this was a very interesting project and as a pre-dental student it was great to see worlds collide in MIMG and dental research! I just had a few questions about the implications about the study.

1. Since the morphology was found to be irregular in the mouse dentition, would there be a possibility that this same effect could occur in humans? How would we avoid that?

2. Potentially, is there a way to stop differentiation and/or proliferation once the inhibitor is removed? If the inhibitor is a large factor of how much YAP is produced, would adding Large Tumor Suppressor Kinase 1/2 to an environment subsequently slow down or even hinder cell growth, potentially making this a possible treatment for some forms of oral cancer?

Thank you very much for the presentation!

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How do you identify the disease gene signatures and drug gene signatures?Can you explain more on how PharmOmics works?

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How do you identify the disease gene signatures and drug gene signatures?Can you explain more on how PharmOmics works?

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Hi LeAnn,
I really like the topic of your work. I would like to know more about that. First, I would like to know how would you confirm that the structure you have obtained is the pre-fusion of gB but not other protein? What was the change in the structure before and after the host-virus structure that you were able to discover through 3D image? Thank you so much!

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I observed that in the result that mature natural killer cells and type 2 innate lymphoid cells decrease, I just wonder if you happen to know why these 2 type of population decrease while others increase? Have you suggested any treatment based on your finding?

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I observed that in the result that mature natural killer cells and type 2 innate lymphoid cells decrease, I just wonder if you happen to know why these 2 type of population decrease while others increase? Have you suggested any treatment based on your finding?

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Hi; I really enjoyed your research presentation! I thought it was interesting how you found unexpected clustering in many groups. I have a couple questions about your research:
1) How would selecting a gene that codes for a different protein rather than DNA helicase make an impact on the phylogeny you created?

2) You mentioned that high similarities and intercluster conservation in Myoviridae Arthrobacter clusters may be explained by constant horizontal gene transfer. If this wasn't the case, is there another explanation for these similarities?

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Hi Christopher, thanks for the great presentation! I did have a few questions regarding your research.

1. How do hypoxic conditions activate HIF genes exactly? For instance, does hypoxia result in signaling of certain messengers that suppress the expression of a gene that typically inactivates these HIF genes when in normal oxygen level conditions?

2. What other HIF genes and cells besides the ones mentioned in t heir research study, if any, are associated with tumor progression and chemotherapy resistance?

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Quick question, when these connections between GCS and differences In length are being compared, how did you account for the reasoning that the GC% content would increase with length? Were comparisons made for a consistently measured stretch of genome length?

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Quick question, when these connections between GCS and differences In length are being compared, how did you account for the reasoning that the GC% content would increase with length? Were comparisons made for a consistently measured stretch of genome length?

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Hi Ryan! Great job on the presentation and the poster! This is really an interesting topic that grabs my attention right away! I was impressed and learned a lot from your experiment, and here are some of my questions after reading  through it.
1. In terms of the choice of the sample in this experiment, why female and adipose tissue from abdominoplasty specifically? I know BMI is a measure of your height and weight that is usually used for determine the degree of obesity. But it doesn’t tell where the fats accumulate in the body. So will the location of excess weight matter?
2. The experiment proves that excess weight is an established risk factor for type 2 diabetes, but why many obese individuals do not develop type 2 diabetes. Is the reverse still reasonable?
3. Yet there’s no cure for type 2 diabetes, based on what u get from this experiment what are some future approaches that can help benefit prevention, interventions, and overall patient care.

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Hi! I thought you did a great presentation and your poster was very well organized. I just had a couple questions for you:
-Do you have any ideas on why DN1S increased editing compared to the other constructs you introduced?
-Why does unequal expression in  K562 cells not give you a fair comparison?
-It almost seems as though the inhibition of the NHEJ is more feasible/more efficient than promotion of the HDR, would this be a correct assesment of the data?

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1. What are other possible reasons for the conservation of certain conserved genes?2.  If phamerator map analysis shows that there is conservation of genes even when they are infecting different hosts, what it a commonality between these phages that could explain this?

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1. What are other possible reasons for the conservation of certain conserved genes?2.  If phamerator map analysis shows that there is conservation of genes even when they are infecting different hosts, what it a commonality between these phages that could explain this?

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What's up Ryan! So I have a few questions about your work. 

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What's up Ryan! So I have a few questions about your work. 

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It's well known that BMI is a fairly inaccurate measure of body fat. Is there any chance that this might have been a confounding variable in your study and are there plans to better address this at a later time?

Also, you mentioned that there are a few potential pathways through which insulin resistance may be affected. Is there a plan to identify which pathway specifically should be targeted by therapeutics?

Great presentation by the way!

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Hello Anhyo! I really enjoyed your presentation. I think you did a really good job presenting the background and the experiment. I  just have a couple of questions.
1. How would this affect our future treatment for single ventricle congenital heart disease?
2. How will this finding help obstetricians performing prenatal care?

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Hi Ryan! I thought your research presentation was very interesting! I do have a couple of questions that I was wondering if you could answer:

1) All the samples of adipose tissue came from women, whom have different immunological responses than men. Women are actually known to have faster immune responses that evolved to protect developing fetuses. Knowing this, do you think the findings would have changed in adipose samples were also taken from men?

2) You stated that innate lymphoid cell, natural killer cells, and macrophages were present in adipose tissues as predisposition to the link between obesity and diabetes. I was wondering if these are also found in other types of tissues, such as skeletal muscle tissue?

Thank you!

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Hi Jennifer, I have some questions would like to ask you. The first question I would like to ask is how would we test that those regenerated cell would differentiate into ameloblasts that secret enamel?Another question is could you elaborate what is dedifferentiate since it's the first time I have heard about that. Also how would you perform the experiment to study cell dedifferentiate ?

Thank you so much. And looking forward for your future study!

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Your presentation/poster were very interesting and well put together. I especially enjoyed how well you explained the background information for your research. A few of the questions that I devised while studying your project were:

1. What is the significance of being able to view bacteriophages in terms of both inter- and intra-cluster relationships?

2. Do you expect Seurat to be effective for all mycobacteriophages or are there any limitations to analyzing these phages?

3. Could any changes or adaptations be made to the Seurat tool in order to give you more comprehensive results for analyzing genomic diversity?

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Hi Ryan, great presentation and research poster! I did have a few questions about your research.

1. Is there a specific reason why you guys used BMI rather than body fat composition? I know that BMI is usually not as accurate since people with a greater amount of muscle mass would have a greater BMI compared to even those with a greater amount of adipose tissue. How do you think the results would be affected if you guys used body fat composition instead of BMI?

2. I don't have a lot of experience with research and research methods, so I was wondering how you managed to extract the human  immune cells?

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Hi Jessica! This was such an interesting research topic, and both your presentation and poster was amazing! I have some questions about your research:

1. Is there a reason why male mice were used instead of female mice? Do you think the gender of the mice would’ve affected the results at all?

2. Is there a reason as to why the drug treatment was done for 10 weeks? Do you think a longer treatment could’ve caused any side effects?

3. What is the difference in the mechanism of action between fluvastatin and aspirin? Why can aspirin only be used for preventative measures?

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Hi Jennifer
Your presentation is really interesting. I really enjoyed your presentation. I just have a couple questions.
1. What would the next step of the experiment be?
2. What other steps are needed before it can be used to treat tooth loss in humans?
3. Can the treatment potentially induce tumor?

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Hi Jennifer
Your presentation is really interesting. I really enjoyed your presentation. I just have a couple questions.
1. What would the next step of the experiment be?
2. What other steps are needed before it can be used to treat tooth loss in humans?
3. Can the treatment potentially induce tumor?

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Hi, I really enjoyed your presentation and your poster looks very well put together. I was wondering if you could clarify a couple things about your experiments: I understand that you were looking at similarities and differences between the myovirdae, but what exactly constitutes a "cluster" versus a "singleton"? In addition, what experiemnts would you think of next in order to further analyze the clustering and design better parameters?

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Hi Yash!
Great job on your presentations and I just had couple of questions after looking at your poster and abstract.

1) Did any of your data suggest any method of binding, it seems from your expected data (unconfirmed) that it binds at the hinge region by I wanted to know more about what makes this hinge region so important in that binding?

2) And my second question is there information as to why this binding is being intiated to begin with?

3) And finally in your abstract you talk about how limiting cholesterol biosynthesis can increase STING activity but is there any suggestion as to how an increased or decreased intake of cholesterol in our foods can have an effect on this STING, interferon pathway?

Great job again!

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Hi guys! Amazing presentation, I just have a few questions:
1. Could you potentially explain a little more in depth about how the whole genome nucleotide sequence dot plot works? What does the boldness of certain spots signify?

2. Why did the clustering system guidelines change? Was it missing essential information?

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Hey Ryan! You did such a good job on your poster presentation and the whole research was very informative. I have a few questions for you regarding your experiment.
1) As BMI is a body mass index which measures the body fat based on height and weight You did the experiment using BMI to compare the lean and obese adipose tissues and to see immune cells and their activities trends with BMI. Do you think it will affect the accuracy of results or provide limitations as it is not an accurate body fat measurement? Or do you think these slight changes will not make any difference.
2) For your experiment you used adipose tissue samples which were derived from predominantly female patients between the age of 30-50 years. Was there a specific reason of selecting female patients or was it an unconscious decision. if there was a reason what was it? if not, then do you think doing this experiment on male and female would give similar results or slightly different results?

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Hi Yash! Your introduction video was very clear and concise, making it very easy for me to follow along!
Here are some questions I have for you.
1. Are the proteins from the STING pathways specific proteins involved in just this pathway only or can they be involved in other pathways?
2. Assuming that the translocation of the STING proteins lead to releasing of the type I interferons, why are IFNs released in the Golgi instead of the ER?

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Hello, I always find computer analysis to be intriguing. Good work on your project and presentation. The figures were interesting as well. Just a some questions:

1. Are there other programs that could be used to help make connections between different genomes, and how did you choose Seurat specifically?

2. Not as related to the research itself, but do you believe that with the ever changing genomes of phages and increase use of digital media, a 2D diagram will eventually be replaced in accurately showing viral clusters? (is there a more viable way in your opinion).
Thank you and nice work!

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Hi, thank you for your presentation, I have a few questions.

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Hi, thank you for your presentation, I have a few questions.

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1) Do you know if smooth muscles in the congenital heart disease phenotypes have altered morphologies like the epithelial cells?

2) Will you consider testing the various subtypes of the single ventricle phenotype?

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Hi Jessica!

This is amazing research that you are conducting and it is so refreshing to see as NAFLD is something the quite prevalent in my family spanning many generations.
This leads me to my first question:
1) Did you research provide any insight to how these course of drugs may have different efficacy levels in those with the genetic form of NAFDL rather than induced (with I assume is to mimic weight gain in human populations)?

2) We hear a lot about how excess use of aspirin can be a detriment to our livers, with much of by family being told be doctors to avoid the use of aspirin, ibuprofen, and acetaminophen. I was wondering from your research or in future you plan to do, did you see any detrimental effects of taking aspirin as a preventative measure for NAFDL?

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Hello Lilibeth, great job on your project! I think it is very relevant to modern medicine. I have a few questions based off your abstract video.
1. What causes poor gene editing within the Cas 9 system? Is their other systems that produces the same editing?
2. Can gene editing happen at any part of the cell cycle?

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Hello Yash! Very interesting topic your project is on. I had a few quick questions based on your abstract video.
1. Why does the cell need to build up their immune defenses against other cells?
2. What is immune fatigue?

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Hello,  I thought the research done was very interesting, especially how you showed how current schemes of phage categorization could use some improvement. Just some questions:
1. Is there a proposed method of better categorizing phages that show such similarities than those conventionally used?

2. Do you happen to know of other phages showing similar bridges as the ones mentioned in your research that could also be studied?
Thank you!

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Hi Andres! You had an awesome research topic and presentation! I personally know how much time and effort it takes to make all the figures (and not to mention to do the actual research project), so good job!

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Hi Sunjum, this was a very thorough presentation and poster! Prior to this, I have never heard of or was aware of the importance of characterizing single gene mutation detection systems.

1) Were the mutagens used to characterize the rpoB gene the same as the mutagens for thyA?

2) Is there a reason why you chose to look at mutagen that caused more mutations via transversions of CG >> GC? Were there other mutagens that caused transversions at AT sites?

Thank you!

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Hi I enjoyed your presentation and found it interesting. I have two questions I'm curious about.

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Hi I enjoyed your presentation and found it interesting. I have two questions I'm curious about.

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1) What drove you to test these specific fusion constructs over others?

2)  Have you considered performing assays of isolated fusion proteins to possibly work around the problems of cells not properly expression the fusion proteins?

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I really enjoyed your project. As I was looking over your poster and watching your video abstract, I developed a few questions.
1. Is there a reason that the project focused only on nucleotide, amino acid, and protein level similarities to differentiate the phage clusters?

2. It is mentioned that further research could involve more Myoviridae phages. How do you anticipate these other phages to fit into the phylogeny and SplitsTree that you built for the Myoviridae family?

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Hey Ruchal! I enjoyed your presentation, and I had no clue you were in research! I have a few questions, if that is alright.
1. The data that follows the contents of the exosomes is still unknown and needs to be gathered from the proteomics that will be ran on the exosomes. If you expect the contents of the exosomes to be the PD-L1 that suppresses immune activity, is there a way for the endogenous immune system to actually recognize the exosomes before they are able to release the PD-L1 to cause immunosuppression? Do you think that the lack of this recognition is what leads to the immunosuppression, or is it because it acts on the immune cells themselves?

2. Are there any current anti-cancer treatments that target this mechanism of excretion in order to combat the effects of the immunosuppression? If you are able to confirm the presence of the PD-L1 in the exosomes, what are the next steps for you? Will you attempt to find a mechanism to halt the export, or will you further analyze the cancer cells?

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Thank you guys for preparing and sharing this information. I have a few questions about the research: 1. In the abstract you mention about the NS and GCS of the two phages, and say "supporting the reclustering of the two into a single cluster." What did you mean by reclustering? Are you referring to their evolutionary history in the sense that they came from a common ancestor and after time diverged, but are now converging?
2. When beginning this research, was it already decided that these two phages would be compared, or was it only after comparing the nucleotide similarity that the research question and hypothesis were created?

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Hey Jennifer! You did a great job and it was really interesting to see your work. The topic was very new to me which I found very engaging and interesting. I have a few questions regarding your experiment.
1) While doing the research and designing your experiment, what methods did you choose to select the controls to compare results in fig 2,3,4 and 5. Did you have to conduct several experiments to find out the results and trying different controls? I am interested in knowing how did you go about the controls and how challenging was it?
2) What do you think will happen if you did the same experiment on humans? Do you think there will be more limitations in finding the results in humans? What challenges would you expect in comparison to your study on mouse.
Good luck for your future studies.

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Hi Ami! I enjoyed your presentation and the topic was really interesting. I have a few questions about your project:

Q1: So I understand that both the control and miR-24 overexpressed cells were isolated from the cancerous epithelial cell lines. Is there a reason why you guys sampled from the cancerous lining? In addition, were the miR-24 overexpressed cells naturally found from the cancerous epithelial cell lines or were normal cells induced/ engineered in someway to overexpress the miR-24?

Q2: I am aware that there is currently no cure for IBD. Do you think the findings from this research can be used to explore possible treatments for this disease?

Thank you!

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This is honestly the best composed poster I have seen on this padlet, specifically your experimental design graphic. Well done! I'd love it if you could answer a few questions I had after reading/watching your presentation and poster

Do you think there is any merit to testing a control group fed a normal diet but also administered Asp and Flu to see the effect on body weight and fat mass the drug alone has? Or is this unnecessary and can be forgone like in your study?

Do you believe there is a way to have your tool PharmOmics determine whether the drug predicted to target the disease will be preventative or simply treat the disease? Was there any initial indication between Aspirin and Fluvastatin before the experiment that would have let you predict their different efficacies?

Thank you for your research and again excellent work!

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Hi Andres! Great job on your presentation, I really liked your poster! I have a couple questions regarding your project:

1. Regarding the identified transcription factors using Metascape, would it be possible to perform CO-IP experiments using those transcription factors and different HPV proteins such as E5?

2. In the future directions you mention short-term vs. long-term HPV infection, would there be a way to model the different longevities of infection in vitro? What are some distinctive phenotypic differences between the two?

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Hi Ami, great work on your presentation!

1) I'm curious about how lower expressions of mir-24 affects AKT activity and the rest of the pathway. Were you able to obtain any results on that and would that be relevant to your research?

2) Standard research data question: but what does the fold change in Figure 2B represent?

Thank you for your presentation! :)

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Hey Jennifer! I found your presentation to be highly informative on a topic that I have never studied before. I have a few questions for you.
1. In order to achieve the proliferation of the dental epithelium, the mice were genetically engineered to lack either the YAP inhibitor or to constitutively express the active form of YAP. Initially, you had suggested that this pathway has hope to reconstruct and regenerate lost teeth in humans, but genetic engineering is not feasible in this sense. How would you expect you can apply this research outcome to a new model that can be applied to humans. Since you were able to find that this does in fact increase proliferation, is there a way that we could apply this to in vitro stem cells from humans in order to culture new teeth?

2. You mentioned that the overexpression of YAP seemingly caused the dedifferentiation of the ameloblasts back into a progenitor state, which warranted you to conduct further experiments to determine the causality of YAP expression and ameloblast dedifferentiation. If YAP overexpression does in fact cause the dedifferentiation of these cells, will this impact the already existing structures that are present, and will there be a method to prevent this from happening in vivo? For the potential applications of this research, the dedifferentiation of the cells could suggest potential impacts in other tissues that could be beneficial, so will you continue to focus on dental tissues, or will you attempt to achieve this dedifferentiation in other tissues?

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Thank you for the project! I think the research was well done. Here are some questions I have.

1) How would the results have differed if there was a male population in the samples for the research?

2) Why did the group decide to choose otherwise healthy patients for this research when type-2 diabetes can arise in patients with different forms of diseases?

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Hi Ryan!
I really enjoyed hearing about this project! I have a few follow-up questions:

1) What other diseases, if any, could targeting this mechanism prevent?

2) Also, how would your results have changed if the patient samples did have a good amount of muscle mass?

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Hi Xihui

Awesome presentation, it was great to hear about your work on CIDP. I did not know a lot about this topic going in, but your poster and video abstract definitely broke down your research succinctly. I had a couple of questions:

1)About what age were the mice used in the study? Were they male or female? Does the age of the mice affect the immune cell population, and if so, could that affect the quantity of TNF observed throughout the in vivo experiments?

2) What role, if any, does TNFR2 play in the TNF/TNFR1 pathway? It was listed as one of the knockout genes in the Fig. 6B legend, so I was curious as to why it was targeted as a gene of interest.

Thanks in advance for any response, and I hope to learn more about your work in the future!

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Hello Yash! Very interesting research; I though the effects of cholesterol on immune system is a very relevant to today’s medical research.

I have a few questions regarding your figures:

1. In the confocal microscopy figure, what is happening in the stimulated + added cholesterol images? What is the purpose of showing the different fluorescent colors? I ask this because i do not see a difference between the green and blue fluorescents.

2. In the Statins qPCR* expected results, what does the result tell us if there is an increase in Fluvastatin and Atorvastatin?

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Thank you all for composing such an interesting and easy to follow research project. Here are some questions that I have:
1. I know you explained that PharmOmics was a software to look for overlap, but how does it specifically work in terms of sequencing? Do you take a specific sample of the tissue and then sequence the desired DNA in those cells? Or is it based on an already known gene library?

2. Since these drugs worked to prevent the NAFLD stage of steatosis, do you by any chance know that reason why it may not be effective on the later stages of NALFD?

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Thank you for the excellent presentation! Your team's poster is wonderful and has a great organizational structure that draws attention to the data specifically.

Upon reading through your poster, I had a few questions about the continued scope of this study.

I am curious about this tool's applications to other types of phages, beyond just mycobacteriophages. Do you believe that there would be any factors that would prevent this tool from working across a broad-spectrum of phages?

Additionally, do you believe that this method of identifying HGT events could be combined with previous sequence based techniques such as gene synteny (order) to more accurately identify instances of HGT or is this method alone sufficient?

Again, excellent work on the project! Especially you Raneesh ;)

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Absolutely great presentation and poster. I thoroughly enjoyed reading through all of this and seeing the research but I have a few question.
1) What other factors could have lead to ischemia which were not accounted for, especially when coronary artery diseases can have a multitude of underlying causes.

2) How did you set up the experiment to have it set where the mice would be in hypoxic conditions for an hour. Was this based on human results that showed significant ischemia?

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Hey Jennifer, you did a great job in choosing your topic and doing the poster. I cannot wait to see the results of your future experiments. I  have a few questions regarding your research about this experiment.
1) I understand that you did the experiment with insertion and deletion and used controls to figure out the results. For example figure 2, shows deletion of Lats1/2 results in increased  nuclear YAP and figure 4 shows that overactivation of YAP results in irregular morphology of the cervical loop. My question is that in designing this experiment what methods did you use and how did you go about choosing these controls used in fig 2,3,4 and 5.
2) What challenges did you face while doing the research and designing this experiment and for future what would you want to change or do you think going the same route is a better option for you? What kind of experiments and methods are you planning in doing for testing the dedifferentiation of ameloblast.
Good luck for future studies

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Hi there ! I think your research is so so interesting! I learned about nonalcoholic fatty liver in my nutrition class, so I was immediately drawn to your research. In my class, I learned that you could prevent fatty liver by living a clean lifestyle filled with nutritious food and healthy activities. I must have missed it, but was there a control mouse that was used and not given any drugs and instead just given a clean diet and exercise? Also, did you try other painkillers such as acetametaphin or ibprophen before coming to a settlement on aspirin?

Again, great work !!

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Hi, I found your research on heart defects to be extremely interesting and relevant. I had no ideas that the disease was so common in births. I had some questions about the work.
Is the alteration in flow consistent with other types of congenital heart defects (i.e. do all defects produce the same flow)?

Are there potential inherent differences in the tissues of the umbilical cord and heart which may affect the experiment's results?

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Hi Ivan,
This was a very interesting research and I enjoyed reading it!!
I have a few questions,
while the adult free-living nematode is attracted to numerous bacteria why do you think it's not attracted to P.flourecense, and the larvae are specifically attracted to this bacteria?

what changes in gene expressions can lead to this behavior, and how do you think this change in behavior can benefit the Strongyloidiasis?

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Hello Ivan! First of all, I want to say that you did a very great job of presenting your research project. It's very easy to follow and understand the information. I have some quick questions after watching your presentation.
1. Is there any specific reason to choose "older, gravid, adult females" to observe for tracking assay? Is it just because they are bigger so easier for the camera to follow or there are any other biological reasons?
2. Could you explain more your b and c graph in the tracking assay since I did not really understand it? Why in the short-term, nematodes move away from the bacteria, and why it's similar to the result you got in figures b, c?
3. In what way do you think the study helps to contribute to reducing human diseases from parasites?
Thank you, and again, you did excellent job!

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Hi there ! I really enjoyed your presentation! I think the work that you are doing is very relevant to real life and has a great future in the field of medicine! I just had a couple of questions for you- How did you know to take cells from the umbilical chord and not other parts of the body? Why did you specifically wait 72 hours after harvesting the cells?

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I wanted to start off by thanking you for your presentation! Here were a couple questions I had while looking at your poster.

1. How can gaining a better understanding of microbial interactions help to inform health measures for nematode control (especially in impoverished regions previously mentioned in your presentation)?

2. Also, you mentioned that S. ratti in adults were more likely to grow on most bacteria, whereas iL3s were subject to mostly soil bacteria. Do we know why this might be different despite the similar conserved behavioral responses? How can we use the information about its widespread growth pattern in further research?

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Hello, Jessica! Your research was very well presented and I enjoyed learning about the treatment and prevention of non-alcoholic fatty liver.

I have a few questions regarding your results:

1. Fluvastatin resulted controlling weigh gain after treatment. However, it controls the weight better than in the control. What may have cause the stable weight compared to the control group? (referring to Fig. 4)

2. In conclusion, Fluvastatin and Aspirin treat NAFLD with Aspirin having a slightly greater effect. Fluvastatin is different because it also has an effect in regulating weight gain. Which treatment based on your research will be best suitable to treat NAFLD?

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I really enjoy reading your poster and watching the abstract video.
Here are some questions I have:
1) Is there a reason why you decided to conduct your study on GC content instead of AT content?

2) You mention that this study can be used for phage therapy to treat diseases such as skin acne and C. difficile infections, could you explain how it could be done?

Thank you.

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Hi Christopher. thank you for sharing your research with us!! I really enjoyed reading your poster.
My question are:
how did you come up with the idea to test the effect of intracellular PH in the MM cell?

As we can see in this study the MM cells use the CAIX and NHE-1 to regulate their internal ph. my question is, now that they have this mechanism, why do the cells that were incubated in normal in PH 6.7 have a higher rate of apoptosis than those that were incubated in PH 7.2?

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Hi Jessica! Fantastic job on your presentation, it was very easy to follow and also very informative. I was wondering whether you had any thoughts on why there have been no FDA-approved drugs that are prescribed for NAFLD? Is it an uncommon diagnosis? I was also wondering what your possible explanation is as to why aspirin could only prevent and not reverse steatosis. Thank you so much!

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Hi LeAnn! Great job on your presentation, your research project is super interesting! I have a couple questions regarding pre-fusion gb:

1. Once you have purified pre-fusion gb, because it is less energetically favorable, how can you confirm that the structure won't fold into a more favorable position? In other words, how can you confirm that the purified structure of pre-fusion gb matches the structure of pre-fusion gb in vivo?

2. In terms of a potential treatment, what aspects of the structure would you hypothesize could be targeted by a drug? Is there a hypothesized mechanism by which a potential drug can interact with the pre-fusion gb?

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Excellent presentation, Joshua!

Just a few questions from me:
Why was the distinction made between recovery of ipsilateral versus contralateral axonal sprouting? Is there a significant functional difference between these types of axons that are relevant to white matter strokes?

What differentiates the lines of the iPSC-GEPs? Even though in these specific findings there was found not to be significant difference between the lines used, in what circumstances would one line of stem cells lead to more favorable outcomes than another line?

Thanks so much!

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Hi Roxanne! Thank you so much for this presentation--it was really interesting. I had a few follow up questions!

1) How did you get to the hypothesis that it was mitochondrial fission that leads to these protective effects?

2) What other diseases, if any, do you see this research potentially being beneficial to combat other than coronary artery disease?

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Hi LeAnn! Thank you for sharing your work with us. I was really impressed by how many techniques are incorporated in your research. Your abstract and poster are also very clear and easy to follow. I have some questions about what is to come for your research:
1. What are some specific steps to prevent triggering the transition from the pre-fusion GB state to the post-fusion GB state?

2. What are some methods that can be used to ensure that the unknown structure is the pre-fusion GB structure of interest?
Thanks again for sharing about your research, and I look forward to hearing more from your team!

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Hi Ivan! This presentation is very interesting since I have never really thought a lot about the interactions between parasites and bacteria. So, I do have a couple of questions:

I was wondering a little more about what you mean by the neural mechanisms that mediate stage-specific behavior? Would you study this with the same experimental set-up and methods as your current experiment?

How did you determine which bacteria impacts the parasite? Was this in the context of just human skin or just in general? Do you think the environment in which the parasite interacts with the bacteria impacts the outcome?

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Hi Ruchal, great presentation! I appreciated the graphics within your video presentation as well as in your poster since it made it easier to follow along. I had a couple questions as well:

1) Were there significant variations between PD-L1-expressing exosomes amongst the different cell lines? For example, did the 2F7 cells express more PD-L1 in the exosomes following a particular treatment more so than Raji cell line after it underwent the same treatment? If there were variations, why would the exosomal PD-L1 expression be different?

2) Are there any other immune checkpoint molecules which are overexpressed in AIDS-NHL tumor microenvironments that are of interest in your research? I know other cancers also evade tumors by overexpressing CTLA-4 or PD-1, so are there other proteins or cytokines which also lead to inhibition of the immune system?

Thanks again for the wonderful talk!

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Hi Jessica! This is really cool, I really enjoyed your video.
Here are a couple questions I have:
1. Do you think a combination therapy of both fluvastatin and aspirin would have a better outcome in preventing steatosis?

2.  What were the other drugs that were predicted for NAFLD and why weren't they used?

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Hi Ryan! Thanks for sharing your research with us and for providing a clear and informative video abstract. I was fascinated by the conclusions that your team has already reached and look forward to hearing more about it. I have some questions after reading through the poster:
1. Why was the adipose tissue specifically obtained from an abdominoplasty, and would the results of the experiment change if it was taken from another source?
2. Would there be a way to apply these techniques on patients who are predisposed to diabetes
Thanks again!

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I had a couple of questions.
How can inflammation caused by the immune system affect other health diseases and are they contributing to the cause of diabetes via obesity?

Can mutations in the proteins and/or receptors involved in the immune system or in the adipose tissue allow rescue of function in those proteins, gaining back normal and healthy functioning of the human body, either to alleviate the symptoms of diabetes or to prevent the occurrence of it?

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Hi Roxanne! I just wanted to say that was great presentation and  very interesting! I'm excited to see the possible therapeutic applications that will stem from your research. Unfortunately, I was unable to make the live zoom poster session, but I had just two questions:

1. Why is it that when looking at the results, cell survival decreased when cells were treated with dobutamine and P110 compared to the other forms of stimulated exercise (ISO and AICAR) with P110?

2. How was it determined that ischemia should be induced for an 1hr in the experiment?

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We would also like to thank Dr. Yirong Peng from the Jules Stein Eye Institute for her support in the application of Seurat

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Hi Christopher, really interesting research you've done here. I had some questions regarding the project.
When the project is brought to the next stage with in vivo testing, how would you induce hypoxic or lower pH conditions to sensitize the myeloma to the proton pump inhibitors?

What concentrations of proton pump inhibitors were used, and have you tested different concentrations to find the most effective?

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Hi Jennifer! This is a really cool project! I have never really been exposed to this area of study before so this is a cool place to start! I do have a couple of questions:

I was wondering if you could further elaborate on how you were able to induce YAP overactivation in the mice? Also, how does the drug you inject activate conditional insertions or deletions? Was this process done in already adult mice? Was the staining and imaging used to confirm that the mice did induce YAP overactivation?

What do you think are some limitations to your findings, especially in terms of how it can be utilized clinically? What complications do you suspect to come when trying to test this in humans? Do you think that this finding can actually help individuals who lose their teeth, referring to money and accessibility?

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quick questions!
how do you see new guidelines being made in the future and how would these affect the clusters and those identified in each?

Since certain tests were used to determine their similarities, do you predict that other tests can possibly contradict current findings? If so, what would that entail for the categorization of the clusters?

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Hi Ryan! This was such an interesting topic and I really like the figures you have in your poster.
Here are my questions for you:
1. Did you purposely only have women in your experiment because women have more adipose tissue than men?
2. How did you categorize overweight versus obese? Was there a cutoff weight or BMI?

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Hello Ivan, just wanted to start off by saying really great presentation, and really interesting research topic. Just a few questions that arose while watching your presentation video was what would be the most effective health condition that you believe in understanding these microbial interactions would help in preventing? Also, your presentation was very concise and easy to follow that is why I am intrigued to see if you will be open to exploring how you can figure out how neural mechanisms mediate behavior in nematodes?

Thank you again for your effort in presenting this novel research on microbial interactions.

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Hi Christopher! Your research is Very interesting. I have a few questions for you,
If the intracellular pH of MM cells were decreased, could it harm the non MM cells that are in the bone marrow?

How where the two proteins, HHE-1 and CIAX identified and could there be other targets that you identified that could help in treating MM?

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I wanted to start by thanking you for your presentation- you were very organized and your study was very interesting to read about! I have a few questions relating to your experiment!
1. I was wondering could you briefly describe how you went from the skin fibroblast to the induced pluripotent stem cell?

2. Can you describe the mechanism that explains how the resulting GEPs are mostly biased towards astrocytes?

3. I'm curious as to what the next steps might be as to how to get this into a clinical study after your findings were presented?

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I love genetics and stem cells, and I love this idea! Although, I do have some questions.

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I love genetics and stem cells, and I love this idea! Although, I do have some questions.

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1. Can you think of methods for studying the stem cells via microscopy or another analysis, that would allow us to understand the timing of the replication cycle of these cells? Then we could appropriately time our injection the CRISPR system with the DNA repair factors. This would dramatically increase the efficiency of the gene editing if this technique is possible.

2. For someone who has not taken an MIMG lab (me) what is the significance of the molar ratios of what was put into the sample for this experiment?

3. How will using equimolar amounts on K562BFP cells help make the analysis better?

Thank you for your research and this presentation! I hope to see more research from you in the future, and I look forward to your answers!

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Great job! I really enjoyed learning about this topic especially because it is so prevalent in the US! I have a few questions for you. When collecting data for your research, why did you choose you subjects to be predominantly female between the ages of 30 and 50? Do you think you would have different results if you chose males or a different age group?
Also, why did you use flow cytometry analysis for observing your data? Would a different method allow you to view all of your different factors that were present?