Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotron in Canada: Professor, Department of Biochemistry, McGill University

Publisher: In-Sight Publishing

Publisher Founding: March 1, 2014

Web Domain: http://www.in-sightpublishing.com

Location: Fort Langley, Township of Langley, British Columbia, Canada

Journal: In-Sight: Independent Interview-Based Journal

Journal Founding: August 2, 2012

Frequency: Three (3) Times Per Year

Review Status: Non-Peer-Reviewed

Access: Electronic/Digital & Open Access

Fees: None (Free)

Volume Numbering: 12

Issue Numbering: 1

Section: A

Theme Type: Idea

Theme Premise: “Outliers and Outsiders”

Theme Part: 29

Formal Sub-Theme: None

Individual Publication Date: November 1, 2023

Issue Publication Date: January 1, 2024

Author(s): Scott Douglas Jacobsen

Word Count: 5,006

Image Credit: None.

International Standard Serial Number (ISSN): 2369-6885

*Interview conducted July 11, 2021.* 

*Please see the footnotes, bibliography, and citations, after the publication.*

Abstract

Professor Albert Berghuis is a Professor in the Department of Biochemistry at McGill University. Berghuis discusses: Canadian Light Source; X-ray diffraction; 3D modelling through X-rays; evolution of this resistance to various antibiotics; other research institutes; break through a scientific barrier; plazomicin; “emerging bacterial pathogens”; threshold; and Synchrotron.

Keywords: Albert Berghuis, antibiotics, antibiotic resistance, Canadian Light Source, McGill University, Synchrotron, X-ray diffraction, University of Saskatchewan.

Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University

Scott Douglas Jacobsen: So, let’s start with the Canadian Light Source at the University of Saskatchewan. What is this like? Is this a research facility or institute?

Professor Albert Berghuis: Yes, what is that thing? The Canadian Light Source is a research facility, and practically speaking; it is a bunch of magnets put in a giant circle with lots of sophisticated instrumentation attached to it to accelerate electrons at high velocities through this ring that is going to – I don’t know how fast you think, but they go incredibly fast. These instruments scientific instruments look a little bit like CERN, right? In Switzerland/France, where they use it, they use electrons and positrons, then bounce them onto each other. That’s not what’s happening here. They spin them around. Every time you make an electron want to go around a curve; it emits radiation depending on how fast it goes the kind of radiation that is generated at the synchrotron is X-rays. It is these X-rays that we are interested in.

So, you can take X-rays at your dentist or your doctor for an X-ray. That’s just, a puny amount of X-rays we can have. We have instruments in our lab that are 1000 times more intense, and they are still puny compared to what a synchrotron can do so we use these X-rays to illuminate our samples. You put a sample in front of the X-ray beam. The X-rays go partly through there. Partly, they get bounced off through the samples, and the way they bounce off gives us information on what is in our sample. This is what is known as X-ray diffraction.

Jacobsen: And so, the main point of the research is always based around X-ray diffraction in terms of using that as the methodology.

Berghuis: Yes, or in a sense, a step further is that the main objective: we make these samples. These are biological samples as you saw in the article. We put the ribosome in a crystalline form in front of it to figure out the exact three-dimensional structure of the ribosome.

Jacobsen: Basically, you’re doing 3D modelling through X-rays or structural analysis.

Berghuis: It is more that. We’re using X-rays to see an object, right? Remember that to see an object; you have to use a wavelength that corresponds to the size of the object. We want to see atoms and how far atoms are apart. So, we have to use a wavelength in that range, about one to two angstroms, so light wavelength with one to two angstroms is X-rays. That’s the kind of wavelength you have at that point. So we can see those atoms and molecules. So it is not modelling. We can see it.

Jacobsen: That’s very cool.

Berghuis: It takes a lot of computational stuff because there is a little tiny problem in that this is well-known in X-rays. It is where the fundamental part we have a little bit problem of to see things,. Yu need a lens, right? Your eye has lenses, and there are no x-ray lenses. But that is a computational problem. Thankfully, nowadays, there is mostly some complex math involved in that. But in the end, we can still see those molecules.

Jacobsen: So, are you working with the math department?

Berghuis: No, no, not anymore. But the theory of how the scattering of X-rays can allow you to see things was all developed around 1900 and 1910. Very clever physicists were involved in figuring that out. Now that theory is firmly established, we don’t need that anymore. Although, yes, clever programmers, because you can think they started with seeing the structure of salt. Now, moving that to the structure of the ribosome, that we solved with these 300,000 atoms. It is exponentially much more complex so computers come in, and indeed, some knowledge of computer programming can prove helpful once in a while.

Jacobsen: So, ok, you resist new antibiotics for some bacteria. So, how can you look at it, in some ways? It is quite a big jump. The evolution of this resistance to various antibiotics.

Berghuis: So, yes, it is good that we have some time here. So, we don’t see evolution, right? We are in a time point here, right? We cannot turn the clock back and see how things were so much in the past. We can see, based on indices in general, when you think about molecular evolution or gene evolution, we see the current state and the diversity. We can rationalize that they started at a similar point and, therefore, pretend to turn the clock back of what that was like previously. But in the end, we see how resistance is now. I think another misconception. I’m sure this right. People think antibiotic resistance started when we started using antibiotics.

Jacobsen: That’s right. Or a common phrase, my daddy ain’t a monkey, this sort of thing. This standard objections to evolution. It is a similar idea.

Berghuis: Yes, but antibiotic resistance. Evolution works. Evolution, as most people think about it, does not work as fast; you don’t see evolution at our time scales of human life. They know that that’s not how things go, except for viruses. That’s how we can see the evolution to the Delta variant, for instance, of COVID-19 or if under extreme pressure. But the kind of resistance out there for antibiotics is almost exclusively ancient, with ancient resistance that has been out there for thousands and thousands and thousands of years. They have been optimized over those thousands and thousands of year. What has happened since Fleming developed penicillin, and we started using them at quantities that are, from a biological point of view, like insane, where we’re making kilograms, especially where you are in farmland. They’re using an insane amount of antibiotics in husbandry, for instance, right? And that has resulted not so much in evolution as in selection that they entered the bacteria that don’t have the resistance are disappearing, and the ones that do have the resistance are multiplying. So it is not evolution, but it is a selection we have been seeing since 1940, so that’s the last 80 years. Does that answer a little bit of your question?

Jacobsen: It does answer a little bit of it.

Berghuis: Yes. Of course, with that is this nasty thing of bacteria that are very friendly with their neighbours and can give them all kinds of DNA presence, so, the genes encoding resistance have been spread around. This is not evolution, but it is spreading helpful stuff to your friendly neighbours; hence, these things have spread across the globe.

Jacobsen: And so, this project you started five years ago?

Berghuis: Yes, well, in many ways, the grant idea started in 1995 when I became an assistant professor as all research is correct, you evolve and accumulate and build on previous results. But indeed, about five years ago, we made the decision. We’ve been studying this specific class of antibiotics. We knew that a new member of this one was about to be put on the market. The company had been developing that. We knew the company, we knew the compound, we knew the various clinical studies that have been done so, at that point, we say we like to see how this thing works at an atomic-molecular level already it was out, it was known from all those clinical studies. What kind of resistance exists for this, even this newest antibiotic? And so we said we also want to see how that clinical resistance works so that started putting that in place and making that all happen. That took about five years to get to the final result.

Jacobsen: Wow, what was the feeling when you finally got those results?

Berghuis: Oh, like I said, I started this, when I became an assistant professor; I had dreams about it. I said we could see both aspects and do the resistance as clearly as these molecules are not as big as the ribosome I was like, Yes, forget the ribosome. That’s not going to happen now we made that happen. So, seeing the first results of that and especially how much we could see, I was beyond excited. Yes.

Jacobsen: So functionally, why must you know the three hundred thousand atoms to get the 40 atoms?

Berghuis: So the 40 atoms? But how do those 40 atoms sit in the ribosome? And to do that. I guess the analogy would be, what a steering wheel looks like. But if you want to know how the steering wheel sits in the car and how the whole car works, knowing the steering wheel and maybe the shaft is not going to quite cut it, you need to know the entire car.

Jacobsen: Yes, that makes sense.

Berghuis: So, unfortunately, and especially when the steering wheel is inside the car if you want to take a picture of that, it does not work. You take a picture of the entire car.

Jacobsen: Yes. Were there any other research institutes that were deep collaborators for the long term on this particular project?

Berghuis: Yes. So the reason why we could do the ribosome structure is this built up very much on Nobel Prize-winning research of groups that solved for the first time the ribosome structure. So it is not that for the first time I’ve seen the ribosome. This was Nobel Prize-winning research. We see this whole giant structure with a brand new antibiotic bound to it, and it explains how this particular antibiotic works. But building on this ribosome structure of my colleague Martin Schwing, who is at McGill; it was a massive help with this, and he’s also a co-author on the paper because he was a grad student and a postdoc in the two labs that got the Nobel Prize for this. So, having him in the lab made me think I could do this. Duplicating it is not really duplicating somebody else’s work, but still, you’re building on all that information; this was somebody who had been in that lab and done that kind of research, so it was finally possible for us to build on that research because we had the person in-house who could help us with it.

Jacobsen: When you break through a scientific barrier, something that was quite interesting that was noted in the information that was sent to me was that you have this research taking five years once that barrier is broken. With a new generation of antibiotics or a new antibiotic, it would take a tenth the time to get that same kind of result. So how does this have an entire order of magnitude reduction in the amount of time taken into the future by your estimates as an expert?

Berghuis: So, why? Right? Think of it it is really like studying these ribosomes. If I go into the lab of the groups that do these structures and study ribosomes daily, the expertise will be available. The right equipment is all out there. If you read a paper, there are all kinds of little issues that you’ll have to struggle with and figure out yourself. Tiny things of organization. If you use this instrument, the optimal settings are slightly different than if somebody else in their setting with a slightly different version has that show. it is an awful lot of optimization so it took us five years to figure out all these optimizations. Remember, the ribosome is two parts. There are the 30s and the 50s. It also has a piece of mRNA in it. It has tRNA in it. We have to purify each of these tRNAs. We had the mRNA to synthesize which mRNAs to use. It takes a lot of optimization to pure those parts, then trying to get the right conditions in putting this all together into a form that can be used at the synchrotron.

You saw the equator, like, we sent so many samples over there, and only a few of those were of the right quality. We’ve done it in our lab. We know how to do this with our setup. We have the persons who are doing this in our lab. So that’s why this will now be an awful lot easier. Also, taking the data from the synchrotron, typically 99.999 percent of the labs work on things that are, 100 times 1000 times smaller. All the software in the default values of how you deal with the data have been set up for that. We had to throw that out the door and come up with it. So we had to re-paramatize our programs to deal with things that are everything. When you make a structure ten times bigger, your probs become ten times bigger. This thing was several scales more significant, and I saw all our problems were several scales more significant. But we figured that out. We jumped the hoops. As I said, we went through there. Now we know what to do. Does that make sense?

Jacobsen: Yes. One hundred percent does. 

Berghuis: So that’s right. But trust me, if another lab in Canada wants to try to do this, even though we’ve described everything and you think I can follow the recipe, I guess it is the same right as your mother’s recipe for a dish, if you try to make it, does it taste the same? Never quit. Right?

Jacobsen: Yes, that’s right. As the particular drug was a plazomicin, is that correct pronunciation?

Berghuis: Yes. 

Jacobsen: As I said, so when the phrase is used, emerging bacterial pathogens within the paper, what is the classification there that you’re looking at in terms of these “emerging bacterial pathogens” that would prompt the need to use plazomicin or things similar in the future?

Berghuis: So, pathogens are, of course, by definition, bacteria that are harmful to us. There are lots of bacteria that are very nice to us, and we need them like in all our microbiota. Things like that. The emerging ones are the conventional ones. Antibiotics are not helpful because they do acquire more resistance mechanisms so those are the emerging bacterial pathogens that we aim for. I’m guessing I’m trying to think where we said this precisely in the paper, but that’s the issue, right?

What’s more, the ability to treat bacteria with current antibiotics is declining, and those are the ones that plazomicin has been geared to you to be used for. Partly, it was explicitly developed to circumvent a lot of the resistance tricks that are out there. So that’s what made this one, in many ways; it is a potent antibiotic.

Jacobsen: Could a similar set of experiments be done to examine this kind of resistance when you don’t use one antibiotic but use two? So you have this kind of overlap of effects to see, how did these interactions work on this particular structure?

Berghuis: So, yes and no, I’ll give a complicated answer here. So, for aminoglycosides, this is not the case. There is what you’re talking about: this combination therapy using two drugs to treat something. So, there are various versions of that idea out there. The most effective one, and this is even with aminoglycosides very often used. So, think of a bacteria, right? It is a complex living machine with a couple of machines inside that make this bacterium duplicate and survive, and a number of them are essential. One of the essential ones is the ribosome because it makes proteins, and other essential machinery is the making of the bacterial cell wall. So what now? If you attack the bacterial cell wall and the ribosome simultaneously, you might be able to reason this out, like because you want to generally keep drug doses low. Maybe I don’t need as much of either one of them if I use them both in combination. They might synergize. Lo and behold that is true. That is a very standard treatment with aminoglycosides. They use great aminoglycosides that attack the ribosome and beta-lactam antibiotics like penicillin and cephalosporin that attack the bacterial cell wall , they work together in synergy. You must use less of each to get more than double the effect.

So, that is one way of thinking of synergies because if you use two drugs together, you want to see the synergy that they work together in concert, that the effect is greater than the sum of the individual parts .On top of that is, of course, lowering drug concentrations [] toxicity, which is always a concern that works best. You would think of reasoning if the two targets were different. Yes. In this case, a cell wall and the ribosome. But there are also examples of within the ribosome that you can, because it is such a complex machine, you can target one part and another that will have a more significant effect and that, indeed, there is a relatively new drug. Although it was ancient in France. We have been studying that drug as well, and it has indeed two ingredients. Two drugs that work in concert on the ribosome and thereby cause the bacteria to die. But to your question, can you study simultaneously if it is different machinery? Do you do a different set of experiments to look at those parts again?

Jacobsen: And for practical applications of some of these areas of research. I mean, about antibiotic resistance globally, many populations can be at risk here. So how does this increase the efficiency of this technique or recipe, as you called it, reduce this problem? Is it a possibility, potentially into the 2020s? Not the far future.

Berghuis: So the far future, the 20 years. So, antibiotic resistance is a complex problem, which, the WHO has already identified. It is giving information out for people, so they use it properly, giving out to doctors reduced use. All of these measures are ultimately aimed at using antibiotics as little as possible and only to the most beneficial effect that means misused, avoid misuse, proper use so that you don’t create more antibiotic resistance. That’s a whole public health aspect, especially when you think of places like India, which is notorious for the massive spread of antibiotic resistance because there you can buy antibiotics over the counter. You don’t need the prescription drug; you go to your pharmacy. I feel I have a cold. I will take penicillin for this, even though it is a virus. It is pointless, right? Or I feel I am in this. One of my colleagues at McGill talked to me about this,. That it is widespread. That the production of antibiotics there is substandard therefore, even if you go, you take this drug three weeks or a whole week, seven doses, right? And you really should stick to that prescription. If you do that in India, it might well be that the doses only contain half of your antibiotic. So, there are all levels of complication in this, the global fight against antibiotic resistance that go well beyond… 

We aim to facilitate the development of next-generation antibiotics, right? Provide the critical information to make that industry go faster. Of course, we’re not in a position to do the vast clinical trials in all of this kind of stuff. So, the current modus operandi in antibiotic research, in general, is that. Research universities push the discovery and the development further and further as the industry is increasingly reluctant to pick up on these projects, and we’ll see how far we have to push this forward before the industry picks this up. It used to be 10 or 15 years ago. We wouldn’t have to push as far as we do now because the industry has become far more reluctant. A case in point is plus or minus in itself the drug. So this was the original idea of plazomicin does come out of Montreal, out of the University of Montreal, by a guy who studies these antibiotics. He started this 15 years ago, if not more. Through these compounds, we interacted at that time as well, so he finally got a company spun off. A company that was based in California to take this antibiotic, get investors to do all the clinical trials it took, in the end, so close to 10 years to pass through all of the things that. This is the way these things go.

You can’t rush clinical trials. You have to do that properly. In 2018, they got this approved. But beforehand, they had two clinical trials, hoping to market this drug for urinary tract infections and skin infections. If I got the facts completely straight in my head, but this is, hopefully, it is correct. The skin infection part was a raving success. The clinical trials, the urinary tract infections. The FDA wanted to see some more data, so it was not harmful. But they said we need some more data. However, all of the investors finally pulled out. The CEO put all his money stock back into the company to keep things afloat. But that only worked for so long. They had a couple of other drug development projects. They put that on hold, and despite all of his efforts, the company went bankrupt, at which point they sold the patents for plazomicin to two companies to pay off all their debts and things like that. 

And so these are patent-holder companies that are producing it, one for China and one for the rest of the world, if I recall. But this is now a company that holds a patent and license for companies to produce it. But no more research and development is going on, and all the investors that invested feel burned; they will not invest in any antibiotic research and development whatsoever anymore. So this is another story of how, from the economic point of view, it is very, very difficult to bring a new antibiotic to market. Which means while we know everybody knows that, we need newer antibiotics, right? The resistance will only spread, so we need to come up with newer ones that have less resistance. Will that resistance be permanent? You can be optimistic or pessimistic about that.

Nonetheless, you will need some newer ones, regardless of how optimistic or pessimistic you are. But the industry is not investing in it. So that means places like my lab and all kinds of other labs have to push the research further and further, so that the risk level of a company gets smaller and smaller and smaller.

Jacobsen: When is that threshold usually?

Berghuis: Oh, it depends, where you are or what the disease is. I don’t know if you’ve read it. I think this is a big issue at the moment in the States for a drug that’s supposed to help with Alzheimer’s. I don’t know if you’ve heard that story.

Jacobsen: What particular drug is this?

Berghuis: Forget the name, but the drug for a year of treatment, I think it was $56 million or so per treatment. The efficacy of that drug is in severe question. They don’t even really know if it does anything, and a whole pile of people at the FDA review board stepped down because they were not happy that it received FDA approval anyway. So, here’s a drug that will make if it is approved. If people are taking it, it will bring the company vast amounts of cash, and it is not even clear if it will ever work. So there’s a very different threshold over there compared to antibiotics. The same goes for a lot of cancer research. We have an elite compound that shows some efficacy in animal models that will already get you very far in the industry and will start to pick it up. This is economics, right? The problem with antibiotics is if you take them for a week or so, whatever the prescription is, you’re done. You don’t have to take it. Any different than with high blood pressure medication, cholesterol-lowering medication, or cancer medication. All of those are long-term treatments. As soon as they are approved, they are also approved for minimal things because the FDA wants to protect all agencies, and the WHO wants to protect them for as severe cases as possible, which means for a company, your market goes from this big to suddenly this big.

Jacobsen: When using the Synchrotron and trying to see the actual structure of what is happening with the ribosome with antibiotics. What are some of the difficulties that come along with having this happen? I did look it up. The Synchrotron was built in 2004. Yes, so, you have a 17-year-old machine that is still widely used and probably will be used well into the future based on its applicability and the size of the staff attached. So, what are the difficulties when trying to get an accurate picture of this structure?

Berghuis: So, yes, problems are difficult steps along the way. So the first part is, getting the samples in the right, and I mentioned right, producing these ribosomes, producing all of the elements, that can be used at a synchrotron, which means we have to grow crystals of the ribosome and then find the right conditions that they can be irradiated there. We’re doing this at cryogenic temperatures to lower the damage of X-rays. Once the sample is at the synchrotron, not all samples are equally good. We know we sent a whole pile of them, and each one has to be tested to figure out which one is good. I know it is hard to come up with a good analogy for that one. But from some samples, the image will be fuzzy. From some samples, the image will be much sharper.

So, what we would call resolution is that the resolution we can get from an experiment differs depending on the sample and the intensity of the x-rays that come up from the Synchrotron. So, at the moment, I think the Synchrotron is about to come up again. They have some issues because that machine does not run 24 hours, seven days a week, 52 weeks a year. They have their fair share of problems with that thing, keeping it operational as well. But you try it multiple times. One of the things we did a lot of experimenting with is we knew how to make the ribosomes and the whole thing around there. But how much plazomicin did we add to our mixture to see it? Like, think of it, if you have samples containing a million ribosomes in there, and this is the number is far more significant than that, do we have to add a million of the plazomicin or two million or three million or four million to make sure that it sits in there to see it all the time? Because if we only see it once in every hundred, we don’t see it. Hmm. So that was an experiment. We had to try it. Get the data processed, all the data. Look at it, and finally, in the end, can we see it or not? No, we can’t see it. OK, let’s try again. Change that parameter so it is a lot of iterative steps until you finally get to see what you were hoping, that it is finally there when that finally worked, as I mentioned to you before, we saw it more clearly than I thought was possible.

Jacobsen: That’s great. I mean, it is science. It is fascinating. You’ll know people have this stereotype of a very dry endeavour. I think it is that it is a very long-term endeavour. So it is a slow-boiled excitement.

Berghuis: It is, yes. I do think my students go through the same thing. I try to explain it like think of being a discoverer. Right? Most people are like Columbus. What must have felt, although there’s the story, is far different in natural history, but the fake story, right? He sailed across, and he didn’t know if there was another side to the north, to the Atlantic suddenly, he did see land like, whoa! Right? That was a fake story, but I still realized, like at that point in this fake version of history, I saw something that nobody had ever seen before,. People didn’t believe I could see. That is very much what we do. We see things that have not been seen before, and we see them for the first time. That is… And, when we started, suddenly, a whole pile of things made sense. The same, maybe with a steering wheel like, “Oh,” and then connect. “So that’s how it turns the wheels. Oh, how?” Right? And you are when you see that you go like, “I’m probably the first person in the universe who understands how these wheels work because nobody has ever looked at them.” Right? Chances are, on other planets in other galaxies, they don’t have ribosomes, right? So, that kind of realization is somewhat intoxicating. That’s why we keep on doing this.

Jacobsen: Are there any areas of the research, the questions that I have not asked that should be addressed as we close today?

Berghuis: Let me think, I think. It is always important to talk about research. That’s a team effort, and I am incredibly proud of the students in my lab who worked on this right. I’m the guy sitting behind the desk. I come up with some of these ideas, right? It feels a bit like designing or writing a piece of music, but with amazing musicians that can make your stuff come alive.

Jacobsen: Professor, thank you very much for your time today.

Berghuis: Okey doke. Hopefully, you can synthesize out of all of this rambling. 

Bibliography

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Footnotes

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Citations

American Medical Association (AMA 11th Edition): Jacobsen S. Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University. November 2023; 12(1). http://www.in-sightpublishing.com/berghuis

American Psychological Association (APA 7th Edition): Jacobsen, S. (2023, November 1). Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University. In-Sight Publishing. 12(1).

Brazilian National Standards (ABNT): JACOBSEN, S. Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University. In-Sight: Independent Interview-Based Journal, Fort Langley, v. 12, n. 1, 2023.

Chicago/Turabian, Author-Date (17th Edition): Jacobsen, Scott. 2023. “Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University.” In-Sight: Independent Interview-Based Journal 12, no. 1 (Winter). http://www.in-sightpublishing.com/berghuis.

Chicago/Turabian, Notes & Bibliography (17th Edition): Jacobsen, S “Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University.” In-Sight: Independent Interview-Based Journal 12, no. 1 (November 2023).http://www.in-sightpublishing.com/berghuis.

Harvard: Jacobsen, S. (2023) ‘Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University’, In-Sight: Independent Interview-Based Journal, 12(1). <http://www.in-sightpublishing.com/berghuis>.

Harvard (Australian): Jacobsen, S 2023, ‘Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University’, In-Sight: Independent Interview-Based Journal, vol. 12, no. 1, <http://www.in-sightpublishing.com/berghuis&gt;.

Modern Language Association (MLA, 9th Edition): Jacobsen, Scott. “Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University.” In-Sight: Independent Interview-Based Journal, vo.12, no. 1, 2023, http://www.in-sightpublishing.com/berghuis.

Vancouver/ICMJE: Scott J. Conversation with Professor Albert Berghuis on Antiobiotics and the Only Synchrotronin Canada: Professor, Department of Biochemistry, McGill University [Internet]. 2023 Nov; 12(1). Available from: http://www.in-sightpublishing.com/berghuis.

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