Viruses

mailboxTWiM regularly receives listener email with corrections, comments, suggestions for show topics, requests for clarification, and additional information. A selection of these is archived on this page.

TWiM 24 Letters

Jayne writes:

Thanks so much for your podcasts. I find I am a person who learns best audibly and have just jumped into the science, history, medical and EMS blogs, I Listen to a podcast called SMART EM by a pair of ED docs, and they covered the issue of UTI in Peds. They do journal and study reviews and the found that there isn't any basis for the idea that untreated UTI causing kidney damage for Peds. I know, I know, but they took the time to ferret out all the info. Anyway, I am enjoying your podcasts. I don't think going back to school is something I can do, but about once a week I go to a class on virology, parasitology and microbiology. The tuition is great. No student loans. No sleeping in class.

Thanks,

Al Sacchetti answered: Jayne is correct and not correct depending on who you read. This is one of those topics that will continue to be debated as it is mostly "soft" science.

It is all based on retrospective case studies so you really can't design what would be considered a good scientific study to prove it. Such a study would involve not treating a cohort of children with urinary tract infections and following them and a second subset of treated children to determine if one group develops more hypertension than the other. Not an ethical study to perform.

The other confounder is that there are multiple other causes of hypertension that may overwhelm the cases caused by infant UTI's.

For me the take home message will not become clear for another two decades. That is how long it will take for this generation of treated children to grow old enough to really look at the epidemiology of their hypertension. (As an aside, it is one of those issues that really will not change our practices since we will always treat a UTI in a child.)

On a different note. What would you think Kamagra Online about doing a TWIV on Hepatitis C with a Hepatitis C Virologist, a Transplant Surgeon, a Hepatologist and possibly a hepatitis C patient? From the Bench to the Bedside type of show.

Take care and continue the great work you do with the all the TW's

Al

Jeff writes:

Hi Guys - I was wondering if you had seen the following article in about the lack of acorns being produced in the Northeast this year. In it they mention that the lack of acorns in the past is associated with crashes in the mouse population, then, the author says: "And because the now-overgrown field mouse population will crash, legions of ticks — some infected with Lyme disease — will be aggressively pursuing new hosts, like humans."

Currently here in Atlanta our oak trees are producing massive quantities of acorns. Every few years oaks will begin producing lots and lots of acorns in a season - a phenomenan thought to saturate their predators and try to increase the odds that ssome of their seedlings will germinate and take root. Is there any way that you could do a show (or part of) on some aspect of this Oak-mouse-tick-Borrelia story? It has the parasites (ecto - tick, endo-Borrelia) angle and it has this beautiful tie in to local ecology. I know it isn't typically what you do on the show, but if you can do some aspect of it that would be great. I am going to use this story in my non-science major introductory biology course next semester for some active learning in the classroom, and being able have my students listen to another TWIP/M/V podcast as preparation for those classroom sessions would be too perfect. Does Dr Gwadz have an expertise on the ecology of lyme disease maybe?

Thank you for the great shows, keep up the great work!

Jeff

Georgia Perimeter College

Here is the link:

http://www.nytimes.com/2011/12/03/nyregion/boom-and-bust-in-acorns-will-affect-many-creatures-including-humans.html

Here is an article in American Scientist which passes for a pretty good review on the subject: http://www.americanscientist.org/issues/feature/the-ecology-of-lyme-disease-risk/5

TWiM 23 Letters

Joe writes:

Hello Vincent and Elio

Your recent discussion of mitochondrial interconnections reminded me of a
paper by Dubey and Ben-Yehuda I saw earlier this year describing
intercellular communication utilizing tiny nanotubes that are EM
visualizable and that can transfer DNA, RNA and protein from bacterium to
bacterium.  These structures are able to connect distinct bacterial species
and can confer transient antimicrobial resistance as well as other
phenotypes from one species to another.  I was completely blown away by this
paper and it forced me to think about all of the things that we still don't
really understand about the bacterial world.  The paper is worth looking at
if only for the beautiful microscopy work and elegant experimental details.
I wonder if you'd care to comment on whether this type of mechanism could
explain the origins of the mitochondrial interconnections that you were
discussing on TWIM 21?

I really enjoy the program as it lets me keep up on interesting developments
in areas Ativan Dosage of microbiology outside of my own field.  All the best,

Joe McPhee
----------------------------------------------------------------------------
Joseph McPhee Ph.D.
Michael G. DeGroote Postdoctoral Fellow
Coombes Laboratory
McMaster University

Don writes:

All hail the microbiologists extrordinarie. I look forward to your discussion of the paper on the use of copper to discourage bacterial growth, as you discussed in an early twim.  I was able to convince myself using a copper plated car battery and CuSo4. ie "root killer" and chicken broth for a medium and clarity as an end point. I have since switched to brass, as  it  is more durable, and already "out there" in the market, avoiding the medical vendor or defense contractor  monetary gouge, but the results have not been quite so clear cut. Could you speculate or theorize why this might be so, for an alloy of copper and zinc, vs Cu alone? I delight in your podcasts, and have filled out your questionnaire/survey. Best to you all and please keep going.

DW,MD

TWiM 22 Letters

Jim writes:

I'm greatly concerned about the harmful effects of nanotechnology. I'm old, but have grand kids, who already have to live with all kinds of junk in the environment. I guess it's a topic that fits in the virology category, too, since are not nanotech-sized particles in the viroid category? The scope of nanotechnology is so great that it looks like a wave of change, just like plastics, so perhaps it has to become an obvious and terrible hazard, like DDT or an epidemic before better controls will be considered. Just thought I'd ask what your take is on the topic.

I ran across a nice 3-part series from Marcy of 2010, if you want to use it as Buy Levitra a springboard, or reference for listeners, although plenty of other discussion is easily found on the web.

Part 1: http://www.aolnews.com/2010/03/24/amid-nanotechs-dazzling-promise-health-risks-grow/

Part 2: http://www.aolnews.com/2010/03/24/regulated-or-not-nano-foods-coming-to-a-store-near-you/

Part 3: http://www.aolnews.com/2010/03/24/obsession-with-nanotech-growth-stymies-regulators/


Jim
Smithfield, VA

Richard writes:

Hi Vincent and hosts,

I have a theory, as to why mitochondria would be involved in programmed cell death. It makes sense that, if they are descended from parasitic bacteria, that mitochondria would have had the ability to kill cells. They may well have needed this in order to spread, from cell to cell.

It makes sense that evolution would adopt something already present, in order to kill cells, rather than inventing something new.

I have no proof, but it does seem reasonable.

Thanks as always, for your interesting group of podcasts.

Regards

Richard

TWiM 21 Letters

Casey writes:

Dear TWiM'ers,

Thank you for taking the time to produce these podcasts free of charge.  I hope this style of science podcasting continues to inspire other scientists into creating similar podcasts.

On TWiM #17, you discussed the discovery that mealybugs have symbionts within symbionts, which you guys related to the mitochondria.  Until this year, I was consistently taught that mitochondria are individual sausage-shaped organelles.  Due to their size, shape, and molecular data, they appeared to be a bacterium that was phagocytized.  However, I have now come to learn that mitochondria are truly a reticulum similar to the endoplasmic reticulum.  Interestingly, this information was known as early as 1980 when Ezzatollah Keyhani (from Tehran, Iran) published a paper (Observations on the mitochondrial reticulum in the yeast Candida utilis as revealed by freeze-fracture electron microscopy, Journal of Cell Science, 46, 289-297) describing it as a branched reticulum.  The shape commonly used in textbooks is really just cross sections through the reticulum.

My question is: how did these phagocytized bacteria acquire the reticulum?  Were these started as pili that have since evolved into a reticulum?  In addition, why do textbook authors still present the sausage-shaped mitochondria in textbook diagrams as opposed to the reticulum?  Why has not there been a greater push in academia to present the mitochondria as a reticulum?

This whole idea made complete sense when I viewed the mitochondria as small sausage shaped alpha proteobacteria.  I performed a quick literature search but was not able to find any literature examining this question.

Thank you and keep up the excellent work,

Casey
1st year PhD student

Cindy writes:
Good Morning,

I absolutely love listening to you guys. I have learned so many things from listening to TWiV, I am sure I will have be a step ahead when I take my advanced biology classes. One question though, Once a certain strain of bacteria becomes resistant to antibiotics, how much do these antibiotics need to be modified to combat an illness caused by this bacteria that has grown resistant? I have done Cialis Online research on this question, but so far I have not found an answer. I hope you guys can help me out with informing me about this process.

Thanks in advance,
Cindy

jesper writes:

Dear Vincent,

the other day I was in a discussion about what can get cancer, something that ultimately boiled down to what cancer really is. Our reasoning went along the lines of establishing that there are organisms containing any number of cells, ranging from one and up. If I remember correctly, C. Elegans has 957 cells. Presumably there is some organism with 956, 955 and so on.

It seems it doesn't make any sense to talk about a one celled organism developing cancer - though I am interested to have that confirmed! The nematode just mentioned has cell specialization, so it could presumably develop some form of cancer. What is the lower limit of cells an organism must have to succumb to the decease or should the question really be posed in a completely different way?

Also, some organisms of very few cells occasionally gang up and form a super-organism. This includes some slime moulds and the pre-larvae state of jelly fish. Can such "temporary" organisms develop cancer?

The question is grander than just parasites, and I have a feeling that viruses, living or not, have no propensity to develop cancer. Hence my addressing the question to TWIM.

While I have your attention, allow me to once again thank you and everyone in each of the podcast teams for your effort in sharing your knowledge and doing it in such an enjoyable tone and fashion.

All the best,

Jesper
Software architect
Sweden

Stan Maloy writes:

I was visiting the University of New Mexico last week and ran into a scientist who said that he LOVES TWIM. His only complaint was that he commutes a long distance on his bike and sometimes gets so caught up in the discussion that he has nearly avoided an accident. Not faint praise from a scientist who is known for being extremely critical.

Stanley

TWiM 20 Letters

Atila writes:

Dear TWiMers,

The episode 7, about toxins and antitoxins made me think about the relationship between the bacteria and its plasmids, so I would like to share some speculations I made, without reading more about it (as my graduate project with HIV does not let me read about much else). What I would do if I were the plasmid, or what evolution could do to it:

If I were a plasmid coding for a toxin and an anti-toxin, I would make my toxin small and soluble, so it could diffuse away from the bacterial cell. At the same time, I would code for a large and hydrophobic anti-toxin that would get stuck inside of the cell. So, when a bacteria acquired me, I would make it retain me to live, and at the same time kill all neighbors that didn't have the same idea. They have to acquire me as well or they die. This could explain why TB has so many addiction modules, if it loses some, it may die from the toxin secreted by a neighbor.

Now that all the population has a copy of me inside them, and no other bacteria can grow around them, I can make an anti-toxin that responds to a quorum sensing molecule such as a piece of G6PDH. So, I not only guarantee that only my bacteria survives, I also control  that it grows in a controlled manner. Do you think this may be the case in nature?

Congratulations for the great podcast. I have been listening to fantastic discussions about microbiology coming from you and your guests, it is an unique opportunity for someone at Brazil (and other countries, as I imagine) to listen to these scientific conversations. Keep up the nice work.

Best,
Atila

Alexey writes:

Big thanks for the show, Vincent and co.

I'm 23-year old economist from snowy Russia. About a year ago I got interested in synthetic biology and since than have been learning a lot about genomics, microbiology, biochemistry etc (not without help of your podcasts, which I listen on my way to and from work). But I'm still mostly impressed by the prospects of using biology to create Cialis lifeforms, which can be used to efficiently produce or recycle needed chemical compounds.

Based on stated above i have 2 episode requests/propositions 1. Since I'm 23, I would love to study Biology more in-depth. It would be very helpful (I believe not only for me) to do the survey of existing microbiology related study possibilities and interesting programs in US, Canada or whatever you got detailed information about 2. Since Vincent is virologist, TWiM tends to be disease/infections focused (as TWiP and TWiV). I would really appreciate to hear an episode about non-medical Microbiology application, s.t. Venter's synthetic life creation or current state of affairs in using bacteria to create fuel - in other words something synthetic biology or bioengineering related.

One more time huge thanks for the podcast. It helps people having nothing in common with microbiology except interest not to completely be out of touch.

With respect

Artur writes:

Hi Vincent and Friends,
Great show, always interesting, fantastic speakers, keep up the great work!

I was listening to the #19 podcast, and Michael Schmidt mentioned briefly about the debunking of CC5 mutation and susceptibility to HIV infection in early literature (28 min mark).  I've heard of the CCR5 gene and that having a mutation in it makes a person "resistant to HIV infection", but I"m not sure if that's what Michael was referring to.  I've tried to find more info on what Michael briefly mentioned but searching for CC5 and HIV hasn't resulted in much useful information or answers.  Would you be able to discuss this topic and go more into what was meant by the debunking of the CC5 mutation.

Cordially,
Artur

Peter writes:

Dear Doctors I would like your thoughts on this.
My local doctors surgery has automatic doors so you don't have to touch the door handles, however if you have an appointment booked then you register your arrival by using a touch screen monitor. To me it does not seem to be a particularly good idea get loads of people with ill health to touch the same object. There is no antiseptic hand gel to clean your hands after using the touch screen.

Am I right to be concerned.

TWiM 2 Letters

Barbara Hyde writes:

In the discussion of copper, it should be noted that copper has long been added to marine bottom paints as an anti-fouling agent. Now however there is concern about deleterious environmental effects from its leaching out into the waters.

Barbara Hyde, MBA, CAE
Director, Communications
American Society for Microbiology

Kevin writes:

Vincent:

First of all, thank you so much for providing myself and other microbiologists with this excellent podcast. Your very first episode was extremely fascinating to me, and I will be avidly waiting for all of the future episodes. I hope you and your friends can maintain this caliber for your podcast.

I am an analyst in the microbiology laboratory at a modest-sized pharmaceutical manufacturing company. For those of you that are familiar with pharmaceutical microbiology at a sterile manufacturing site, you would understand why the discussion of the laboratory studies on copper as an actual self-sanitizing material would be interesting. For the most part you talked about possible applications in hospitals, but I would love to hear Michael Schmidt's (and others') opinion on possible manufacturing design changes if the FDA were to ever support them. Currently, Laminar Flow Hoods, Isolators, and most equipment in a sterile facility seems to be made out of 316 stainless steel. You already mentioned that stainless steel can easily harbor bacteria on its surface, but would using copper as an alternative really be that much more effective? Stainless steel can be polished smooth enough to ensure no bacteria hide in cracks or irregularities in the surface when sanitizing agents
are used. Speaking of sanitizing agents, could you even hope to sanitize a copper material with a strong oxidizer like bleach or hydrogen peroxide? Even an autoclave would be brutal on copper utensils such as forceps or hemostats. You would almost be making disposable metal materials. I would love to see what the minimum concentration of copper you would need in an alloy in order to keep a 10^3 or possibly even 10^6 reduction in microorganisms! Also, I'd be very interested in seeing how a spore-forming organism reacts to contact with copper. Is the spore-formation process quick enough to save a Bacillus species organism from certain death? These are the kinds of questions that popped into my mind immediately, and I'd love to hear your take(s) on them.

On an unrelated note:

I'm a 25 year old analyst at this company with slightly over 4 years of industry experience. I would be ecstatic if you could take some time in an episode to describe the differences between industry and academic microbiology, focusing on some of the progression (or hierarchy) in those different fields. In my undergrad my classes were entirely pre-Med focused, and it was only by chance that I ended up in the industry. Now knowing what I do about pharmaceutical manufacturing, I wish that I had known more so I could have prepared a more efficient method of getting further in this field. An MBA would make becoming a manager/supervisor so much easier, and a PhD would make a Senior Scientist level more tangible to me. As it stands now I have no idea how to get further ahead, but a 5 year break from college keeps me reluctant to go back to school and start all over again.

Thank you once again for all you do, and best of luck in your research and with this podcast!

Regards,

Kevin

David writes:

Hi, I'm a new student of microbiolgy at UBC, working in the Redfield lab. I found your podcast very informative and am looking forward to future episodes. If you are looking for interesting people for I'd like to suggest my supervisor Rosie. Among other things, she has a lot of interesting things to say about the recent arsenic bacteria issue.

Please say hello to Prof. Despommier for me, I've never met him but a few years back we talked about an unfruitful venture to get vertical farming going in Vancouver.

David
www.infoenzae.wordpress.com

[Rosie Redfield blogs at http://rrresearch.blogspot.com/]

TWiM 19 Letters

Jim writes:

Hi,

The NPR Science Friday topic recently concerned a discussion and debate amongst several researchers about the Black Plague
( http://www.sciencefriday.com/program/archives/201109023 ).  The discussion seemed pretty complete, but as a lay person I'm  still not sure I understand how the bacterium are identified using old skeletal material, and question that prairie dogs are the major source of Yesinia pestis in the Southwestern US rather than mice, and would like to know if flea excrement is really the material that  transfers the bacteria to people.

Great shows, always.

Regards,

Jim
Smithfield, VA


Jim writes:

Hi guys,

Dr Schmidt, I think, said in TWIM 12, around the 24 minute mark, that bacterial plaques keep growing but viral plaques do not.  It see
ms to me as a person that both would grow to the limits of the dish, or until the nutrient is exhausted, another plaque is encountered, or the environment changed (dried out, chilled, overheated, etc.).  Could you please discuss this a little more.

Thanks.

Jim
Smithfield, VA

[michael was referring to bacterial plaques formed on eukaryotic cells by Burkholderia, and said they continue to grow, in contrast to viral plaques which typically stop]

Michael writes:

Hello Twim and twiv Team.

Wanted to say that i very much enjoyed the Podcast nr 6. Im a Great Fan of Phages myself because they introduced me to Biology in general. I used to have a very poor understanding of biology (our school thought skipping bio and use the time for math instead would be better...) but since i firstly glanced at a Bacteriophage virion of T4 a couple of months back it created a spark in me and i  wanted to know everything about them. Well i had (and still have) to study biology from scratch but i think i made in this short time great advances. Your Podcasts twiv and Twim Viagra are excellent and provide entertainment and Education. Also thanks to the fact that i live in china and here it is very cheap to buy reproductions of Scientific books cheaply (5$ in china compared to +100$ in more "Developed" Parts of the world) i could provide myself with very good learning materials.

Would love to hear more about Phages in the Future, also i would recommend a book. Called "The Bacteriophages" Edited by Richard Calendar. It describes many aspects on Phages and is absolutly perfect for anybody who wants to learn more about them in Detail also describes many aspects of phage therapy. Its not written for the Bio newb like myself but thanks to google i could learn everything i didnt understand along the way.

Greetings from China

thomas

PS i always listen to your Podcasts on my Phone in the kitchen while i cook. So everytime there is a rather long Twiv/Twim my wife knows what im gonna cook will be good since i will spend at least one hour in the kitchen. So i guess thanks from my wife too^^

David  writes:

Is it possible to create a liquid culture that simulates the natural conditions in which Pseudomonoas aeruginosa can survive? I was hoping that one that simulates mammalian lung tissue might work.

Respectfully,
David S. Abuin
Microbiology student from NC State University

BTW, love the podcast.

Don writes:

Could you do a episode on Wolbachia?. It seems to control the reproduction of Drosophila, mosquito etc. Does it's influence extend  to other multicultural {verts? as well.

Two other brief comments,,was there any follow up to using metallic copper in hospitals to control spread of drug resistant microbes>, and although the DRACO protein was undoubtedly made in a Slytherin lab, does not Hogwarts code require a balanced "wait and see" approach. Ill bet you are Ravenclaw/ Don

TWiM 18 Letters

Tim writes:

this recent publication struck me as being interesting and relevant, however I'm not sure I have the background to completely understand it -- as wondering if you would comment on this publication.

thanks!

Here's part of the press release from the University of California at Davis:

///////////////////////////////////////////////////

Lyme disease bacteria take cover in lymph nodes

The bacteria that cause Lyme disease, one of the most important emerging diseases in the United States, appear to hide out in the lymph nodes, triggering a significant immune response, but one that is not strong enough to rout the infection, report researchers at the University of California, Davis.

Results from this groundbreaking study involving mice may explain why some people experience repeated infections of Lyme disease. The study appears online in the journal Public Library of Science Biology at: http://tinyurl.com/3vs8pm9.

"Our findings suggest for the first time that Borrelia burgdorferi, the bacteria that cause Lyme disease in people, dogs and wildlife, have developed a novel strategy for subverting the immune response of the animals they infect," said Professor Nicole Baumgarth, an authority on immune responses at the UC Davis Center for Comparative Medicine.

"At first it seems counter intuitive that an infectious organism would choose to migrate to the lymph nodes where it would automatically trigger an immune response in the host animal," Baumgarth said. "But B. burgdorferi have apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal's immune response."

///////////////////////////////////////////////////////////

here is where I found the press release..

http://www.eurekalert.org/pub_releas...-ldb061611.php

here's a copy of the original article (at PLOS)...

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002066

////////////////////////////////////////////////////////////////////////////////////

thanks again... i'd love to hear your analysis of what is going on here...

Tom writes:

Hello to the Microbiology crew!

While recently reading the *gasp* wikipedia page on "Phytic acid", I found a paragraph of content near the end that threw me for a loop. The claims were cited to an article from the Journal of Biochemistry (http://www.jbc.org/content/early/2010/04/29/jbc.M110.126581.long) stating "Ironically, [phytic acid] is shown to be a required cofactor for YopJ, a toxin from Yersinia pestis.[27] It is also a required cofactor for the related toxin AvrA from Salmonella typhimurium[27]". Perhaps it is only the choice of the word "ironically" that confuses me, but the dynamic seems fascinating.

I'm trying to posit a few plausible sounding explanations, but my biochem is limited, so i'm working from a pop understanding of microbial ecology and evolution.

I kind of get that phosphate (as a key nutrient) is tightly sequestered in phytic acid, much like chelation complexes for metals, but I can't see why it would be advantageous for Y. pestis to have maintained the cofactor dependency to the *toxin* this long. I know E. coli pulls a similar trick by chelating the heck out of free iron (enterobactin, i think), but the fact that the compounds are function labeled "toxin, versus 'iron-aquirer'' skews my intuition.

I guess I'm struggling to understand the genetic logic behind the cofactor. My assumption is that the phytic acid is somehow integrated into Y. pestis' metabolism (maybe the phosphate groups Viagra 100mg are hydrolyzed and absorbed by the Y. pestis?), but from what little i could decipher from the paper, no mechanism for re absorption seems present (only injection).

I suppose it could always be neutral evolution (increasing complexity w/ negligible benefit, see http://skepticwonder.fieldofscience.com/2010/03/in-defense-of-constructive-neutral.html), but the pathways involved seem too tightly regulated to be purely non-advantage yielding for either organism.

If you have the time, I'd love to really take a more rigorous stab at understanding this dynamic (and the paper, of course), both from a biochemical and ecological level.

Thank you very much for your time,
Thomas

David writes:

Episode #11 was an especially interesting one.  I’d like to add to the discussion from Joe’s letter about entropy, from a straight physics perspective.  The 2nd law of thermodynamics (incorrectly referred to as the 3rd law in the letter) has several different but equivalent versions.  The version probably most relevant to this discussion is roughly stated as “In a isolated system, the entropy (disorder) tends to increase in time.”  Note the first part of this version (“In a isolated system”), is often left out when most people state the 2nd law.  The first-part-left-out statement has led some creationists to incorrectly state that the 2nd law prevents evolution from occurring.  People make the mistake of trying to apply the 2nd law to non-isolated systems, which leads to wrong conclusions.

The Earth is an open (non-isolated) system due to the sun.  Because the Earth is open, taking in energy from the sun, matter has energy available to organize itself.  From snowflakes to hurricanes, from viruses to humans, clumps of matter are constantly using energy to decrease or maintain their entropy.  There are many interesting ways that life uses various forms of energy to this, but ultimately it is the availability of energy that gives life the ability to organize.  So life doesn’t “cheat” or “get around” the 2nd law, it obeys the 2nd law (when it finds itself as an isolated system).

-- David

Michael writes:

Greetings TWiM crew!

As someone who spends most of his time on the macroscopic world (animal biomechanics), I have found TWiM to be a wonderful way to get a little foray into the rest (=most) of the biological world each week.  Thank you for making it all happen.

Onto the question: is there any particularly good resource (say, for example, a text or large review manuscript) that has synthesized the current perspectives on biomechanical approaches to microbiology?  I'm familiar with some bits of work in that realm, such as the bacterial fluid mechanics work being done by Kenny Breuer and Tom Powers (mostly because I know Kenny), but I have found it difficult to find any location where this sort of perspective is examined and reviewed at a more general scale.  There have been some nice mentions of microbial biomech in TWiM (such as the discussions of low Reynolds Number flows, where viscous effects dominate), and so I thought perhaps you all knew a good go-to source.

Cheers,

Michael Habib
Assistant Professor of Biology
Chatham University

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