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How Poop is Fighting COVID-19
By Laura Gardner, Biochemistry and Molecular Biology ‘22
Author’s Note: With so much information in the media and online about COVID-19, I find many people get lost in, and fall victim to, false information. I want to reassure the Davis community with factual information on how Davis is fighting COVID-19. With UC Davis’ strong scientific community, I was curious what tools were being used to mitigate the spread of COVID-19. In January 2021, I attended a virtual COVID-19 symposium called Questions about Tests and Vaccines led by Walter S Leal, distinguished Professor of the Department of Molecular and Cellular Biology at University of California-Davis (UC Davis). In this symposium, I learned about Dr. Heather Bischel’s work testing the sewer system. This testing is another source for early detection of COVID-19. In combination with biweekly testing, I have no doubt that UC Davis is being proactive in their precautions throughout the pandemic, which made me personally feel more safe. I hope that this article will shed light on wastewater epidemiology as a tool that can be implemented elsewhere.
Dr. Heather Bischel is an assistant professor in the Department of Civil and Environmental Engineering at the University of California, Davis. Bischel has teamed up with the city of Davis through the Healthy Davis Together initiative to use wastewater epidemiology, a technique for measuring chemicals in wastewater, to monitor the presence of SARS-CoV-2, the virus that causes COVID-19 [6]. When a person defecates, their waste travels through the pipes and is collected in the sewer system. In both pre-symptomatic and asymptomatic individuals, their feces will carry the genetic material that indicates the virus is present. This is because SARS-CoV-2 uses angiotensin-converting enzyme 2, also known as ACE2, as a cellular receptor, which is abundantly expressed in the small intestine allowing viral replication in the gastrointestinal tract [1]. This serves as an early indicator of a possible COVID-19 outbreak and leads to quick treatment and isolation, which are important to stop the spread of the disease.
Samples are taken periodically from manholes around campus using a mechanical device called an autosampler. These autosamplers are lowered into manholes to collect wastewater flow samples every 15 minutes for 24 hours. Next, the samples are taken to the lab where they are able to extract genetic material and use Polymerase Chain Reaction (PCR) to detect the virus. Chemical markers that attach to the specific genetic sequence of the virus are added to the sample, which reacts to the COVID-19 virus by fluorescing visible light. This light is the signal that indicates positive test results.
The samples are collected throughout campus, with a focus on residential halls. An infected person will excrete the virus through their bowel movements before showing symptoms. The samples are so sensitive that if even just one person among thousands is sick, they are still able to detect the presence of COVID-19 genetic material. When a PCR test provides a positive signal, the program works closely with the UC Davis campus to identify if there has been someone who has reported a positive COVID-19 test. If no one from the building is known to be positive, they send out a communication email asking all the students of the building to get tested as soon as possible. That way the infected person can be identified and isolated as soon as possible, eliminating exposure from unidentified cases [4].
In collaboration with the UC Davis campus as well as the city of Davis, Dr. Bische has implemented wastewater epidemiology throughout the community. Since summer 2020, Dr. Bische’s team of researchers have collected data which is available online through the Healthy Davis Together initiative [4].
In addition to being an early indicator, this data has also been used to determine trends, which can indicate if existing efforts to combat the virus are working or not [2]. Existing efforts include vaccinations, mask wearing, washing hands, maintaining proper social distancing, and staying home when one feels ill. UC Davis has implemented protocols including biweekly testing and a daily symptom survey that must be completed and approved in order to be on campus.
Wastewater epidemiology has been implemented all over the world, at more than 233 Universities and in 50 different countries, according to monitoring efforts from UC Merced [3]. This testing has been used in the past to detect polio, but has never before been implemented on the scale of a global pandemic. Lacking infrastructure, such as ineffective waste disposal systems, open defecation, and poor sanitation pose global challenges, especially in developing countries [2]. Without tools for early detection, these communities are in danger of having an exponential rise in cases.
“Our work enables data-driven decision-making using wastewater infrastructure at city, neighborhood, and building scales,” Dr. Bische stated proudly in her latest blog post [2]. These decisions are crucial in confining COVID-19 as we continue to push through the pandemic.
Summary of how wastewater epidemiology is used to fight COVID-19
References:
- Aguiar-Oliveira, Maria de Lourdes et al. “Wastewater-Based Epidemiology (WBE) and Viral Detection in Polluted Surface Water: A Valuable Tool for COVID-19 Surveillance-A Brief Review.” International journal of environmental research and public health vol. 17,24 9251. 10 Dec. 2020, doi:10.3390/ijerph17249251
- Bischel, Heather. Catching up with our public-facing COVID-19 wastewater research. Accessed August 15, 2021.Available from H.Bischel.faculty.ucdavis
- Deepshikha Pandey, Shelly Verma, Priyanka Verma,et al. SARS-CoV-2 in wastewater: Challenges for developing countries, International Journal of Hygiene and Environmental Health,Volume 231,2021,113634, ISSN 1438-4639, https://doi.org/10.1016/j.ijheh.2020.113634.
- Healthy Davis Together. Accessed February 2, 2021. Available from Healthy Davis Together – Working to prevent COVID-19 in Davis
- UCMerced Researchers. Covid Poops Summary of Global SARS-CoV-2 Wastewater Monitoring Efforts. Accessed February 2, 2021. Available from COVIDPoops19 (arcgis.com)
- Walter S Leal. January 13, 2021. COVID symposium Questions about Tests and Vaccines. Live stream online on zoom.
A Dive into a Key Player of Learning and Memory: An Interview with Dr. Karen Zito
Image by MethoxyRoxy – Own work, CC BY-SA 2.5
By: Neha Madugala, Neurology, Physiology, and Behavior, ‘21
Author’s Note: After writing a paper for the Aggie Transcript on the basics of dendritic spines, I wanted to take a more in-depth look at current research in this field by interviewing the UC Davis professor Karen Zito, who is actively involved in dendritic spine research. While there are still a lot of questions that remain unanswered within this field, I was interested in learning more about current theories and hypotheses that address some of these questions. Special thanks to Professor Zito for talking to us about her research. It was an honor to talk to her about her passion and knowledge for this exciting and complex field.
Preface: This interview is a follow-up to an original literature review on dendritic spines. For a more in-depth look at general information on dendritic spines, check out this article.
Neha Madugala (NM): Can you briefly describe some of the research that your lab does?
Dr. Karen Zito (KZ): My lab is interested in learning and memory. Specifically, we want to understand the molecular and cellular changes that occur in the brain as we learn. Our brain consists of circuits, connecting groups of neurons, and the function of these circuits allows us to learn new skills and form new memories. Notably, the strength of connections between specific neurons in these circuits can change during learning, or neurons can form new connections with other neurons to support learning. We have been mainly focusing on structural changes in the brain. This includes questions such as the following: How do neurons change in structure during learning? How do new circuit connections get made? What are the molecular signaling pathways that are activated to allow these changes to happen while learning? How is the plasticity of neural circuits altered with age or due to disease?
NM: What are dendritic spines?
KZ: Dendritic spines are microscopic protrusions from dendrites of neurons and are often the site of change associated with learning. Axons of one neuron will synapse onto the dendritic spine of another neuron. Spines will grow and retract during development and synapses between a spine and axon will form during learning, forming complex circuits that allow us to do intricate tasks such as playing the piano.
NM: Transient spines only last a couple of days. What role do they play in learning?
KZ: One hypothesis for the function of transient spines is that they exist to sample the environment, allowing the brain to speed up its ability to find the right connections required for learning. Thus, the rapid growth and retraction of transient spines in the brain helps our neurons find the right connections required to form the new neural circuits by sampling many more connections and narrowing in on the right ones. For instance, in a past study on songbirds, researchers found that baby songbirds with faster moving transient spines were able to learn songs quicker than baby songbirds with slower moving transient spines. Once these transient spines find the right connection, they will transition from transient to a permanent spine to partake in a circuit that supports a new behavior, such as the songbird learning a new song.
NM: Can presynaptic neurons directly synapse onto a dendrite or only a dendritic spine?
KZ: Many neurons do not have spines at all. Spines are predominantly present on neurons in the higher order areas of the brain involved in learning, memory, perception and cognition. Spiny neurons are present in areas of the brain where neural connections are changing over time, or plastic — allowing the brain to learn, adjust, and change. Certain areas of the brain do not require a lot of change and, in some cases, circuit change may be detrimental to function. For example, we may not want to change connections established for movement of specific muscles.
NM: What is the difference between synapses that occur directly on a dendrite versus onto a dendritic spine?
KZ: Importantly, the molecular composition at synapses can vary widely between synapses, regardless of whether this connection occurs at a shaft or a spine. Therefore, it is difficult to name specific compositional elements always found at a spine versus a shaft. Inhibitory synapses, formed by GABAergic neurons, tend to be found directly on the shaft of dendrites. Glutamatergic neurons, which are excitatory, in the cerebral cortex tend to synapse on dendritic spines, but can also connect directly with the dendrite.
NM: All dendritic spines have excitatory synapses that require NMDA and AMPA receptors [1]. Are these receptors necessary for these spines to exist?
KZ: To my knowledge, we do not know the answer to this question. It is possible to remove these receptors a few at a time, and spines do not disappear. However, it is really hard to remove a receptor from a single spine and, if the receptors are removed from the entire neuron, it is often replaced with another receptor in a process called compensation. In order to test if this is possible, someone would have to knock out all genes encoding AMPA receptors and NMDA receptors, which is over seven genes, to see if spines still formed. Notably, if AMPA receptors are internalized, the spine typically shrinks, and if more AMPA receptors are brought to the surface, the spine typically grows. Indeed, the number of AMPA receptors at the synapse is directly proportional to the size of the spine.
NM: What drives spine formation and elimination when creating and refining neural circuits?
KZ: There really is no definitive answer to this question currently, and many of those performing dendritic spine research are interested in answering these questions. Let’s first look at formation. One theory suggests that there are factors coming from neighboring neurons, such as glutamate or BDNF [2], which promote spine formation. However, it is unclear which of these are acting in vivo, in the animal. Also, spine formation is much greater in younger animals compared to older animals. That can suggest that the cells are in a different state when younger versus older. The cell can be a less plastic state where all the spines are moving slowly, seen in older animals, or more plastic states where all the spines are moving more quickly, seen in younger animals. Thus, there appears to be a combination of intrinsic state, or how plastic the cell is, and extracellular factors such as the presence of glutamate that dictates spine formation. Elimination is similar in that we do not really know the entire molecular signaling sequence that is driving it. It is a fascinating question for so many reasons. For example, when we are young we overproduce spines, and as we grow the spine density declines as our nervous system selectively chooses which connections to keep. Then, as adults, our spine density remains relatively stable. However, we obviously keep learning as adults, even though our spine density remains constant. One hypothesis is that, as a spine grows while learning, a nearby spine with no activity shrinks and eventually becomes eliminated. In fact, we have observed this phenomenon in our studies. Therefore, there may be some local competition between these spines for space. This keeps the density the same across most of the adult life span.
NM: Does learning drive the formation of synaptic spines or does synaptic spine formation drive learning?
KZ: This may depend on the type of learning. Both have been observed. Studies have been done imaging the brain during learning. Some people have found an increase in new spine growth suggesting that learning drives new spine formation. Other people say they found the same number of new spine growth, but a greater amount of new spine stabilization, suggesting that learning drives new spine stabilization.
NM: It has been observed that some intellectual disabilities and neuropsychiatric disorders are associated with an abnormal number of dendritic spines when compared to a neurotypical individual. Is this related to the insufficient production of dendritic spines at birth or deficits in pruning?
KZ: Indeed autism spectrum disorders have been associated with an increase in spines. This could potentially be associated with an overproduction of spines or reduced spine elimination. Notably, the majority of neurological disorders resulting in cognitive deficits, such as Alzheimer’s disease, are associated with decreased spine densities. It is unclear if the spine numbers or brain function diminishes first, but much of the current research seems to suggest that the spines go away first, leading to the cognitive problems observed. In many disorders with too few spines, there is a normal formation of spines but excessive elimination. This is seen as Alzheimer and schizophrenic patients’ spine density is relatively normal prior to disease onset. For Alzheimer’s specifically, some researchers suggest that the molecular release of the pathogenic amyloid beta peptide binds to molecules on the surface of the dendritic spine that drive spine loss.
NM: How might dendritic spine research help in treating neuropsychiatric and neurodegenerative disorders?
KZ: Current research is looking at how to stabilize and destabilize dendritic spines. If we were able to manipulate the stability of these spines, we could potentially help rescue the stability of spines in patients with neuropsychiatric disorders, which could potentially lead to better therapies and outcomes. Understanding the pathways that control the stability of these spines will allow researchers to find targets for future therapeutic treatments.
Footnotes
- Receptors that are permeable to cations. They are usually associated with the depolarization of neurons.
- Brain-derived neurotrophic factor (BDNF): Plays a role in the growth and development of neurons.
Cryogenic Electron Microscopy: A Leap Forward for UC Davis
Photo originally published in Structural Studies of the Giant Mimivirus. PLoS Biol 7(4): e1000092. doi:10.1371/journal.pbio.1000092. License: CC BY 2.5.
By Nathan Levinzon, Neurobiology, Physiology, and Behavior ‘23
Author’s Note: The purpose of this article is to inform the UC Davis community about the arrival and use of a groundbreaking technology to campus. I hope to have provided a comprehensive introduction to Cryo-EM, information on Cryo-EM at UC Davis, and an example of how the technology is already being used to solve problems in biology on campus. I also aim to share my excitement regarding this technology in the hope that I inspire others to pursue this interesting and advancing field of study.
Cryo-electron microscopy, often abbreviated as “Cryo-EM,” is a version of microscopy that uses beams of electrons instead of light to illuminate cryogenically frozen samples. Because the wavelength of an electron is much shorter than the wavelength of light, samples can be imaged at mind-boggling resolutions. After the sample is captured in many orientations, the images are compiled in software to finally resolve a three-dimensional image. “If you want to imagine what it’s like to use this technology,” UC Davis Professor Jawdat Al-Bassam explains in an interview for the College of Biological Sciences, “think about walking into a museum, looking at a statue, taking pictures of it, and figuring out how to put those pictures together to get a three-dimensional picture. In essence, that’s what we do with molecules. They are like small molecular statues, and we take images of them at a variety of angles and orientations. We combine these images to get a design plan for how these molecules are put together ” [1].
As a result of recent advances in technology and software, the progress in the resolution of Cryo-EM seems limitless. New microscopes on the market have brought the lowest resolution down to about two angstroms—twice the diameter of a hydrogen atom—with even higher resolutions yet to come. Before 2010, scientists could achieve maximum resolutions of about four angstroms. This incredible and exciting variant of microscopy stands to shape the future of biological sciences. Dean of Biological Sciences Mark Winey says that “Cryo-EM is certainly part of the portfolio of technology that any campus like UC Davis should have,” and it’s easy to see why [1].
One of the most advanced Cryo-EM microscopes on the market today is the newly released Glacios Cryo-Transmission Electron Microscope (TEM) by Thermo-Fisher. On the surface, the Glacios functions like any other TEM: A cryogenically frozen sample is prepared and shot with electrons that hit a camera in order to resolve a high-resolution, black and white image. What makes this microscope different, however, is its groundbreaking camera. The camera has a pixel size slightly smaller than the area that electrons interact with, which enables a high-speed electron detector to find the center of electron events with sub-pixel precision. The end result is a fourfold increase in resolution from older TEMs while simultaneously reducing aliasing, a sampling error caused by electron interference.
With this microscope, researchers can examine life at the molecular level better than ever before. The closed-system design of the microscope ensures a safe and robust pathway through every step of microscopy, from sample preparation and optimization to image acquisition and data processing of up to twelve samples [2]. Its massive throughput is as impressive as its small footprint, allowing for it to be installed in labs with pre-existing infrastructure. Autonomous sample loading and lense alignment have made Cryo-EM faster and easier for both the budding and seasoned scientist.
UC Davis has recently made a large investment of its own in Cryo-EM. On January 31, 2020, the College of Biological Sciences celebrated the ribbon-cutting for their own ThermoFisher Scientific Glacios Cryo-Transmission Electron Microscope, outfitted with a Gatan K3 direct detector camera. Festivities were short-lived, however, because labs were already in line to use this new machine. Researchers at Professor Al-Bassam’s lab were some of the first to use this microscope while studying kinesin, a motor protein found in eukaryotic cells. By utilizing Cryo-EM to resolve the structure of kinesin, they concluded that kinesin’s tails open a part of the motor that encapsulates ATP, slowing the movement of these motors and allowing kinesin to cluster and work together. With this new microscope in hand, these researchers are now able to unravel the functions of kinesin and how it interacts with other kinesin to move and group. The complete paper discussing the binding between kinesin tail and motor domains and its function in microtubule sliding can be found in the January 2020 edition of eLife [3].
Cryo-EM has never been easier, safer, and more accessible to use UC Davis. With the purchase of the Glacios, UC Davis has made itself ready to introduce a new generation of researchers to the field of modern biology. Resolutions that were thought impossible ten years ago are now a reality, and new advancements continue to push the bounds at which samples can be imaged at. With the quickening pace of advancements in Cryo-EM, there is no telling what mysteries researchers at UC Davis will uncover next.
References
- Slipher, David, et al. “CRYO EM: Unleashing the Future of Biology at UC Davis.” UC Davis College of Biological Sciences, 31 Jan. 2020, biology.ucdavis.edu/cryo-em. Accessed 23 Mar. 2020.
- “Cryo TEM: Cryo-EM.” Thermo Fisher Scientific – US, www.thermofisher.com/us/en/home/electron-microscopy/products/transmission-electron-microscopes/glacios-cryo-tem.html.
- Bodrug, Tatyana, et al. “The Kinesin-5 Tail Domain Directly Modulates the Mechanochemical Cycle of the Motor Domain for Anti-Parallel Microtubule Sliding.” ELife, vol. 9, 2020, doi:10.7554/elife.51131.
You might have to use more than a microscope, there’s more to genetics than what meets the eye: An interview with Dr. Gerald Quon
By Tannavee Kumar, Genetics & Genomics 20’
Author’s Note: As an undergraduate studying genetics and genomics and computer science, I wanted to interview a former professor to find out the steps he took in order to do computational research in the biological sciences. I was interested in finding out more about the growing field of computational biology and wanted to help shed light on a field to students that may be similarly interested.
Background
You received a Bachelors in Math, then a masters in Biochemistry, then a PhD in Computer Science; did you always know that you wanted to do research in biology? If so, what made you want to start off with a technical education rather than something traditional like biology or chemistry? If not, how did you come to discover applications of computer science in Biology even 15 years ago?
No, I did not start off wanting to do anything related to biology. I started my undergrad thinking I would make computer games. How I kind of got into this was a week before my undergrad, I got an email from my university asking if I wanted to be a part of the first cohort of a bioinformatics program. I initially declined.
As I was looking for my third internship in my co-op program, I had a friend who found a job for a professor in Toronto, and my friend asked if I wanted to work on this cool project about predicting how proteins fold into these 3D structures. I told him I don’t know anything about protein structures, but sure! It was a lot of fun.
Is that what inspired you to pursue Biochemistry for further education?
I think that first internship was very pivotal, because it really nurtured my interest in protein structures. When I finished my undergrad, I was kind of bored of computer science, which is why I thought I would do a PhD studying protein structures.
How do you see life sciences research evolving and progressing in the coming years, given the inclusion of this new field?
In my opinion, we will see more and more blurring of boundaries. In 25 years, there is going to be more undergraduate programs less defined by walls like “life sciences,” “chemistry,” and better recognition that everybody borrows knowledge and skills from many fields. It will be very difficult to do a life sciences degree without learning anything about math or statistics. Similarly, more people in traditional quantitative disciplines will want to take those classes in the life sciences. Essentially there will be fewer walls.
How would undergraduates studying quantitative subjects, like mathematics, statistics, or computer science be made aware of the growing demand for such skills in the Life Sciences?
The classic way to become introduced to such areas would be through coursework, internship with a company, or research with a professor. The last two ways are not very optimal. At the end of the day, in a standard undergraduate program, you have summers, and if you are ambitious you can try to do research during the school year. However, you can only do so many different kinds of internships before you graduate. If you did one every summer of college, and even two before hand, even that would not be sufficient for getting a nice, representative sample for all the things you can work on.
That is where universities need to do a better job of creating opportunities for students to engage with people from industry and research so that they don’t need 4-5 months to figure many essential things out.
Research and Beyond
Can you briefly describe some of the research that your lab does?
We are currently working towards a few different directions. A large project at the moment is studying the genetics of mental disorders and neurodegeneration, for example we look at the genetics of Alzheimer’s disease, schizophrenia, autism, etc. Our main goal is to mechanistically understand how genetic variants associated with these mental conditions modify disease risk. Much of those mechanistic studies currently look at events that happen at the molecular level. This is great and very useful; however, since the majority of the research is geared at the molecular level we don’t have a good understanding of what variants do functionally at the level of the cell. How does it affect the functional properties of the cell, such as neuron electrophysiology? Or, how is the organization of the tissue affected?
Other areas we work on are on building better models to understand how cells are spatially organized in the brain, as well as building models that quantitatively describe cell population behavior. We know that cells behave differently when put into different contexts. It’s of interest to build a model to predict what happens when you put together different kinds of cells in different combinations, orientations, or conditions.
Lastly, a third project being worked on is on the therapeutic end. We are essentially trying to identify the druggable region of the genome. There are a lot of computational problems in trying to determine what is druggable.
How do you think the integration of the computational sciences has shed light on how biological processes are interconnected, and what do they make clear that a molecular approach may not be able to?
In human genetics, computational models play a huge role in hypothesis generation. They do a good job leveraging big data, such as genomics, to prioritize which variants should be tested using molecular approaches, for example, when molecular approaches are costly or too slow to systematically test many variants across a genome. The role of computation is parsing through the many possibilities that you can’t explore molecularly.
For example, a study we worked on four years ago was to try and find a causal variant for obesity. Most human genetic studies only point to a region of the genome where causal variants might hide, but don’t tell you exactly which one is the true causal one. When these regions are big, like hundreds of kilobases long, you need computational tools to identify the precise causal one to test experimentally. In that study, computational tools played the pivotal role of identifying the causal variant that was ultimately tested and shown to drive large changes in obesity risk.
How does computational research like your own lead to the progression of curated care in the health industry?
At a superficial level, in some ways it accelerates some of the biomedical discoveries that are being done today. The obesity study is one example. If you didn’t have the computational resources, you would spend years and years trying to find the right variant. However, we found it relatively quickly with computation.
For healthcare specifically, fields such as machine learning are revolutionizing care today. People from statistics, computer science, and math are working directly with clinicians and hospitals to develop highly accurate ‘digital pathology’ software, they help predict when patients will need to come into the hospital or whether they are high risk for a disease.
Oftentimes, conditions and diseases are misdiagnosed, which leads to inappropriate treatments. How would research in this area begin to remedy this common problem in the healthcare industry?
Most diseases are heterogeneous, which means that a group of people who are diagnosed with the same condition might actually have different underlying conditions, and need different treatments. Many computational approaches based on molecular and clinical data are being developed to identify more homogeneous groups of patients, to help achieve precision medicine. This allows for the most accurate prescription of medication and treatments. This is because these homogenous groups help identify the underlying disease phenotype which means access to better directed medication.
During your time as a PhD student, you also “explored the application of models built from deconvolving gene expression profiles, for personalized medicine.” Can you go more in depth to how these models were built and how it can advance our ability to provide a more accurate prognosis to patients?
During my PhD, we were trying to predict the prognosis of early stage lung cancer patients. If you are diagnosed with early stage lung cancer say stage 1B, clinicians have to make important decisions, such as how much e.g. chemotherapy to give you. If they give you too much, it will get rid of the primary tumor, but you will increase your risk of recurrence. But if you don’t give enough, you don’t get rid of the primary tumor.
Back then, fourteen year ago or so, genome expression profiling was just becoming popular. People were thinking maybe we can predict whether these stage 1B patients were going to be at high risk of recurrence or not. Our motivation for that problem was essentially to build a computational model to predict based on molecular signatures if they should be given extra therapy or not. That in itself is a hard problem. Additionally, before single cell sequencing was available, it was hard to take a sample of a tumor and only sequence the tumor cells. Often times you would have contamination of normal cells that would mess up the signatures you would get. We had to develop a computational method to extract out only the signatures due to tumor cells, and show that once you do that it is much easier to predict prognosis.
Where do you think research will be in the next 10-20 years?
We are going to see a lot more connections across more previously isolated fields. For example, with respect to human psychiatric genetics, a lot of focus right now is at the molecular impact of genetic variants, but in the near future I’d expect there to be much closer integration with clinicians to also study the impact on behavior, and with the experimental biologists to study the impact on brain development and organization.
***Special thanks to Dr. Gerald Quon for this interview
Aggie Transcript Interview: Dr. Janine LaSalle
By Mari Hoffman, Genetics and Genomics ‘21
Author’s Note: I chose to interview Dr.LaSalle because of my interest in epigenetics and the relationship that our genes have with environmental interactions. Dr. LaSalle’s lab focuses on the role of epigenetics in the human autism-spectrum and many other neurodegenerative disorders. Her research group looks at the pathogenesis of the disorders by focusing on heritable changes that are not encoded in the DNA, such as DNA methylation and imprinted genes. It was an honor to get to talk to Dr. LaSalle about her research, as she is extremely passionate about this very complex and exciting topic.
A Conversation with Dr. Kate Scow: “I just totally lost my heart to soil”
By Sara Ludwick, Environmental Science and Management, 2019
Author’s note: I read about Dr. Scow’s research while looking for a faculty member to interview for a class assignment. She is a professor of Soil Science and Microbial Ecology at UC Davis, and her research emphasizes microorganisms’ roles in providing ecosystems services. Dr. Scow was featured in an article on a UC Davis website about carbon sequestration as a tactic to address climate change, and from there I discovered Russell Ranch, where she serves as Director (1). I immediately became interested in the variety of experiments conducted on the experimental farm, and began to learn more about Dr. Scow’s work. Her work is extensive; in addition to directing Russell Ranch, she actively works with Ugandan smallholder farms on irrigation. I sat down with Dr. Scow to discuss her passion for soil, what her research has taught her, how her relationship with soil has evolved, and what other people can learn from the powerful ecosystem that lives underground. (more…)
Aggie Transcript Interview—Dr. Walter Leal
By Bukre Coskun, Cell Biology, ‘18
Author’s Note:
“As a student in Professor Walter Leal’s biochemistry class, I was inspired by his dedication to motivating students and obvious enthusiasm for his field of research. Professor Walter Leal has achieved international recognition for his research on the molecular basis of insect communication and insect olfaction. Leal, a professor in the UC Davis Department of Molecular and Cellular Biology and former chair of the UC Davis Department of Entomology, has made significant strides towards understanding how chemicals deter mosquitos. He has identified key mosquito receptors that can guide the development of better mosquito repellents to prevent the spread of deadly diseases. He is a past president of the International Society of Chemical Ecology, an elected fellow of the American Association for the Advancement of Science (AAAS), and the first non-Japanese scientist to earn tenure in the Japan Ministry of Agriculture. I had a conversation with Professor Leal about his path to research, his philosophy on teaching, and the significance of his work with insects.”
Aggie Transcript Interview—Dr. Daniel Starr
By Lauren Uchiyama, Biochemistry and Molecular Biology, ’17
Author’s Note:
“I chose to write this piece because I felt Dr. Dan Starr is unique in that he is equally passionate about teaching and research. As an undergraduate in his BIS 104 cell biology class, I feel he highlights research well by teaching us from an experimental and historical perspective, which makes learning even more fun and interesting. His reputation as a difficult, yet acclaimed educator has made him one of the most prominent biology professors at UC Davis. I hope you enjoy getting to know him as much as I did!”
UC Davis Hosts DataRescue Event To Archive Climate Research
By N. J. Griffen, English, ‘17
Author’s Note:
“I chose to write about this topic as a response to one of the many uncertainties that exists under our newly elected president, Donald Trump. More specifically, this article is meant to encompass the nationwide effort by scientists, professors, researchers and archivists to safeguard, backup and protect work conducted in the realm of climate science. This topic, I believe, should be integrally important to most residents of this planet; due to the fact that we have no choice but to live the entirety of our lives here on earth. Therefore, my interview of the archivists at UC Davis seeks to uncover the motives and connotations that the DataRescue Davis event assumes.”
“Let’s Take a Deep Breath”: Managing Hypertension by Bridging the Clinic-Home Healthcare Gap
Independent Project Findings
By Harsh Sharma, Neurobiology, Physiology, and Behavior, ’13
Author’s Note:
“I wrote this paper to share my independent project takeaways with everyone who is interested in, or a part of, the healthcare field. This project taught me a lot about what we can do to help our patients get the most out of the clinic they go to. As you gain experiences in the medical field, think about the services your organization offers and how you can use your skills to enhance those services to the next level!”