Tag Archives: STRIDE

Protecting Hearts

This summer, I received an American Physiological Society Short-Term Research Education Program to Increase Diversity in Health-Related Research (APS STRIDE) fellowship. This fellowship, funded by APS and a grant from the National Heart, Lung and Blood Institute, allowed me to do 10 weeks of research at the University of Missouri. I focused on how aldosterone can decrease adenosine-induced coronary vasodilation, an important cardioprotective mechanism. Aldosterone is a steroid hormone which is associated with activation of the renin-angiotensin-aldosterone system (RAAS) (Klabunde, 2016), and adenosine is an important compound which has numerous roles in the body. This concept becomes important during heart attacks when adenosine would ideally increase dilation (widening) of heart blood vessels to increase blood delivery to damaged areas (Chen et al., 2013). Increased RAAS activation increases levels of aldosterone which ultimately decreases this protective mechanism, and the infarcted areas do not receive the blood they need in order to be protected. I will be exploring how aldosterone performs this action and whether it acts on one of the two main adenosine receptors in question: A2A and A2B. Individuals with high RAAS activation have higher levels of plasma aldosterone as well as a higher risk for heart attack, so understanding this pathway can be beneficial for those individuals. I used mice as an animal model and I am hoping that a better understanding of this mechanism can help humans with heart damage.

We increased plasma aldosterone in the mice by implanting osmotic mini pumps that infused aldosterone over a course of 4 weeks. Afterwards, we dissected coronary artery rings and measured vasodilatory (vessel widening) responses to a few vasodilators and specific agonists of the A2A and A2B receptors. This was done by mounting the rings in a muscle force measuring machine (wire myograph) and collecting data on their isometric tension production. We followed up these experiments with PCR (Polymerase Chain Reaction used to amplify segments of DNA), DHE staining (Dihydroethidium used to detect reactive oxygen species), and western blotting (identification and measurement of proteins).

Spending the summer as a STRIDE fellow was a really amazing experience for me. I’ve always been very passionate and interested in research and this summer was a reaffirmation of that. I enjoyed being involved in the project and working as a part of a team. This fellowship was incredibly helpful because we were able to network with other fellows from all over the country. We also completed regular assignments that strengthened our critical thinking, writing, and communication skills. I express my sincerest thanks to APS and the Bender lab for this opportunity!

References

  1. Chen, J. F., Eltzschig, H. K., & Fredholm, B. B. (2013, April). Adenosine receptors as drug targets–what are the challenges? Retrieved July 28, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/2353593
  2. Klabunde, R. E. (2016, December 8). Renin-Angiotensin-Aldosterone System. Retrieved July 28, 2017, from http://www.cvphysiology.com/Blood%20Pressure/BP015
Maloree Khan is a senior majoring in Biochemistry at the University of Missouri. She is a 2017 APS STRIDE fellow working in Dr. Shawn Bender’s Lab at the University of Missouri Department of Biomedical Sciences. Khan’s fellowship is funded by the APS and a grant from the National Heart, Lung and Blood Institute.
The Life of a Summer Student Researcher

Childhood obesity has become a major health issue in the United States recently. Research studies show that childhood obesity is associated with an increased risk of declined renal function, which is defined as renal injury. Since renal hyperfiltration, which is when the kidneys are working more to than needed, this leads to excessive amounts of protein to be produced in the urine (proteinuria). This condition is typically associated with obesity. The current study will determine if we prevent the renal hyperfiltration, can we decrease proteinuria and/or renal injury?

Working on ground breaking research and being in an environment that is focused and effective was eye-opening for me. I enjoyed being around scientists that had similar mindsets and were able to help me develop a scientific mind of my own. It surprised me that everyone was so open and welcoming to a new unexperienced college student. But it made me more comfortable, especially when some of my experiment’s failed, but they were very helpful and encouraging throughout the entire process. During my time in the lab the initial study I worked on was not successful, so I was give the study I have now and the results that were collected were what my research host expected and it was a successful study that will be continued.

Being a scientists is like riding a roller coaster every day that you enter into the lab. Some days you are so busy with experiments that you forget to eat lunch. But then other days are very slow, because you are waiting on data or results. It is a great environment to learn not only about science but about yourself, how you manage time, how you interact with people, and how well you work alone. I think the best part about being a scientist is that every day is a new challenge because every day you are working on something that could possibly change the world. I think that worst part is that even if you do everything correctly the data can still not turn out how you want it. But overall I really enjoyed the team aspect of working in a lab. Everyone in the lab helps everyone on their projects and vice versa, because everyone wants to see the lab/experiments succeed because it could have a positive impact on the world.

Alyssa Pennington is a senior majoring in Chemistry at Jackson State University. Alyssa is working in Dr. Jan Michael Williams lab at the University of Mississippi Medical Center in Jackson, MS. Alyssa is a second year Short-Term Education Program for Underrepresented Persons (STRIDE) Fellow which is funded by the APS and a grant from the National Heart, Lung and Blood Institute (Grant # 1 R25 Hl115473-01). After graduation Alyssa plans to pursue a career in medicine and research.
My Experience Interpreting Oxidative Stress and Inflammation in Hypoxia Using Lipid Metabolism

This summer I worked on a metabolomics project surrounding the effects that hypoxia, or deficient oxygenation, has on oxidative stress and inflammation. I used metabolomics, or the study of the functional molecules in the body, to interpret the molecular changes that eventually lead to physiological complications. Currently, we know that oxylipins, biological molecules that are metabolized from polyunsaturated fatty acids (PUFAs), are markers of oxidative stress and inflammation in conditions such as hypoxia (1). My lab extracted venous plasma from fetal and newborn sheep that were living at high-altitudes, as hypoxic conditions can be simulated by high-altitude living. By running tests that quantified the oxylipins in fetuses and newborns, I was able to distinguish which metabolites were prominently affected by hypoxic conditions. Later, I was able to find pathways, tracing how certain PUFAs were metabolized and from which PUFAs certain oxylipins were derived. Based on these relationships, I aimed to find possible roots for the oxidative stress and inflammation caused by chronic hypoxia.

These findings highlight our understanding of lipid metabolism as it is affected by high-altitude hypoxia. This study has the potential to help us develop treatments that target inflammatory pathways induced by pre and post-natal hypoxia. For instance, the enzymatic pathway CYP, which metabolizes PUFAs proved to play a large role in the production of oxylipins that were affected by hypoxia. Targeting this pathway early in the womb may help prevent lung dysfunction that may develop just after birth.

An area in my research that I found difficult was the dense literature. At first sight, it was intimidating‒ scientific jargon and compound nomenclature most of all. I realized that as I started connecting terms to function‒ associating oxylipins with potential roles in the body was now feasible. The truth is, it takes time and understanding to grasp the material, but the more I read and the more I searched, the less intimidating it all felt. Around the lab, there are several skills to master‒ several of which consist of success and failure. For instance, I had a hard time developing networks for my metabolites and working with statistical software early on in my research; this is now something I wish to improve. Often, I received results from my data that I did not expect and it reminded me how difficult it was to remain impartial. I ran into a list of questions that, over time, clarified and narrowed what in fact my research would delineate.

I could summarize the life of a scientist in one word: unpredictable. It surprised me how difficult consistency actually was with data. That being said, it is a huge task to filter data and focus on only a few aspects of it; everything seemed important. Moreover, a reliable, cooperative lab team is a vital component to a scientist’s life in the lab. While not everyone is specialized in the same subject or project, a team creates a supportive environment where we feed off of one another’s knowledge and work in collaboration for the interest of science.

References

  1. Gabbs M, Leng S, Devassy JG, Monirujjaman M, Aukema HM. Advances in Our Understanding of Oxylipins Derived from Dietary PUFAs. Adv Nutr 6: 513–540, 2015.
Vanessa Lopez is a junior Biochemistry major at Occidental College in Los Angeles, CA. She is a 2017 Short-Term Research Education Program to Increase Diversity in Health-Related Research (STRIDE) Fellow. She works with Dr. Sean Wilson in his lab at Loma Linda University in Loma Linda, CA. Vanessa’s fellowship is funded by the APS, as well as a grant from the National Heart, Lung and Blood Institute (Grant #1 R25 HL115473-01). Her research is also supported by NIH grants HD083132 [LZ], 1U24DK097154 [OF] through Dr. Wilson’s lab. She is interested in endocrinology and dietetics. Her plan is to go to medical school after graduation.
The Pursuit of the Insulin Signaling Pathway

This summer, I’ve been working full time in the Obesity and Metabolism Lab, within the Human Physiology Department at the University of Oregon. The lab as a whole is pursuing several research objectives related to how human health is impacted by obesity and high fat diet (HFD), which affect more people today than ever before. The objective of my research is to understand how insulin-resistance, the hallmark symptom of type-II diabetes, develops as a result of obesity and HFD.

Insulin is a hormone produced in the pancreas that is delivered throughout the body, signaling cells when they need to take up glucose from the bloodstream for energy. Cells respond to this communication with a so called “signaling cascade.” Insulin binds to a receptor protein at the surface of the cell, sending the signal via more protein interactions inside the cell, toward the nucleus. This eventually leads to new proteins being made from the cell’s DNA, which will help with glucose uptake. These pathways can be very complex, and have “cross-talk” with other pathways for different cellular functions. If the exact mechanisms of the entire insulin signaling pathway where known, then it would be much easier to see exactly where diabetes causes a disruption, and potentially develop better treatments or a cure.

My project looks at just one protein in the insulin signaling pathway, called phosphatidyl inositol-3-kinase and one of its regulatory subunits called p55a. I’m looking to see if fat cells (called adipocytes) behave differently when p55a is upregulated. When there are relatively high amounts of this regulatory subunit, does the cell become more sensitized to insulin, or less? Does it take up glucose better, or worse? These observations will hopefully allow me to infer how p55a modulates PI3K’s role in the insulin signaling pathway.

What did you learn working in the lab?

As my first real research experience, I’ve learned a lot about the process of laboratory work. The biggest thing I’ve noticed so far is that my experiment isn’t moving as quickly as I had anticipated. Much of my time has been spent troubleshooting. I’ll try a procedure, it won’t quite work as it should, and I’ll have to re-trace my steps to determine how I can optimize the process or correct problems. It seems like each week something new arises that needs to be re-done two or three times. For example, I’ve been growing mouse cells in flasks which I will use for my experiment once they have “matured” into adipocytes. This process requires about two weeks of careful cell maintenance, and I’ve had to start over once because they didn’t develop properly. The other researchers in my lab have told me that they, too, still spend a lot of time troubleshooting, and that being able to recognize necessary adjustments is a crucial skill for a scientist to possess.

Life as a Scientist

My day-to-day life as a research scientist is quite different than it was in all my previous jobs. The work is very much self-supervised, and I have a freedom to plan out my daily tasks in an order that I choose. On the other hand, certain time-sensitive procedures dictate my schedule very strictly, such as changing out the growth media for my cells. This needs to be done every three days, or the cells can die. When juggling multiple projects such as this, I’ve found that making a specific schedule is key. I often write out game plans which allocate time to each of my required tasks for the coming days. This keeps me working efficiently, without losing sight of the broader goals for my ten-week fellowship.

Working as part of a lab team is my favorite part. Every day, I’m learning valuable new skills from my co-workers and asking them interesting questions. They’ve all been very accommodating and willing to teach me. We’ve discussed all kinds of topics, ranging from protein function to the application process for graduate school. The lab is an intellectual environment in which I’ve definitely enjoyed spending my summer.

Shawn Melendy is a junior majoring in Biochemistry at the University of Oregon in Eugene, OR. He is a 2017 APS STRIDE Fellow working in Dr. Carrie McCurdy’s Obesity and Metabolism research lab at the U of O. Shawn’s research is funded by the APS and a grant from the National Heart, Lung and Blood Institute (R25 HL115473-01), as well as Dr. McCurdy’s grant from the NIH (R01 DK095926). After finishing his bachelor’s degree at Oregon, Shawn plans to attend graduate school and earn a PhD. in biochemistry, pursuing a career as a research scientist.
In the Lab for the First Time

Throughout the summer, I have been participating in what is my very first research experience. Apart from learning and doing techniques for the first time,  the biggest challenge this summer has been trying to explain what I have been doing for the past month and a half to people that have asked me. My host’s research laboratory works on trying to understand the molecular mechanisms behind heart diseases, specifically working with the mitochondria. This organelle, also known as the “powerhouse of the cell”, is the one responsible for producing energy inside the cell. My project is focused more on mitochondrial dynamics, the fusion and fission processes the mitochondria go through to maintain their relative stability, and the proteins that facilitate them. I have been working to measure and quantify the presence of these proteins in different populations of mitochondria; and recently, I have been checking to see if these proteins become acetylated in samples that have gone through ischemia/reperfusion. Ischemia/reperfusion injury, also known as IR, occurs when the heart tissue is deprived of oxygen and nutrients; then goes through a period of reperfusion, when blood rushes back into the system. This sudden re-oxygenation period causes damage to the heart tissue. If fusion and fission proteins have become acetylated, inactivated due to the addition of an acetyl group, they could be affecting the stability of the mitochondrial population and possibly furthering damage during IR injury.

Life as a Scientist

Being that this is the first time I’ve worked in a research laboratory, it’s been great to finally have the chance to apply some of the knowledge I’ve acquired in my classes to something tangible; or understanding how various subjects I’ve learned from are applied in real life. I’ve spent the last six or seven weeks learning and improving my techniques in order to measure protein expression.  In practices and even in actual runs, we’ve gone over procedures that take pretty much a whole day in order to eliminate possible errors with results. Currently, we’re working with the data we’ve gotten to see if we have to run more experiments in the next few weeks.

I guess the most surprising thing about this summer has been that the life as a scientist runs as a normal nine-to-five workday. Sure, there have been some instances that we stay later than usual or come in earlier to get things done; however, I had imagined something very different I suppose.  Working as part of a lab team has been a great experience, mostly because you learn to have responsibility as a scientist and a coworker. Many of the areas and materials are used by everyone in the lab, so it becomes your responsibility to keep everything organized and stocked. You tend to think about leaving things in the order that you would like someone else to leave them. Apart from that, helping anyone out in the team goes a long way, because at the end of the day, we are all working towards the same goal.

Roberto Guzmán is a sophomore majoring in Cellular Molecular Biology at the University of Puerto Rico, Río Piedras Campus. This summer, he is working in Dr. Sabzali Javadov’s lab at the University of Puerto Rico, Medical Sciences Campus. He is a Short-Term Research Education Program to Increase Diversity in Health-Related Research (STRIDE) Fellow funded by the APS and a grant from the National Heart, Lund and Blood Institute (Grant #1 R25 HL115473-01). After receiving his bachelor’s degree, he plans to obtain a MD and continue into health related research.
Impact of Soybean Oil High Fat Diet on Hypothalamic Feeding Circuits in Mice

It is well known that consuming fatty foods induces obesity, although relatively little attention is given to the effects of different types of fat. The neuroendocrine hormone leptin is known to reduce body weight and fat through inhibition of food intake and increased energy expenditure (Friedman, 2011).  Leptin’s actions are mediated by leptin receptor (OB-r), which is expressed in the arcuate nucleus of the whole hypothalamus (Meyers et al., 2009; Swanson and Sawchenko, 1980).  Leptin may rapidly inhibit food intake by altering the secretion of hypothalamic neuropeptides such as neuropeptide Y (NPY), a stimulator of food intake, and/or corticotropin-releasing hormone (CRH), an inhibitor of food intake. (Jang, et al., 2000). STAT3, a neuronal transcription factor involved in the hypothalamic leptin signaling pathway via OB-r is necessary for the effects of leptin on food intake and hepatic glucose metabolism (Buettner et al., 2006).  In this study, male C57BL/6N mice were fed one of four iso-caloric diets for a duration of 17-27 weeks:  a high fat diet (40%) made up of coconut oil (HFD), a high fat diet containing soybean oil (SO) which is high in polyunsaturated omega-6 fatty acid linoleic acid (LA-HFD), and a vivarium chow control (VC). We hypothesize that transcription levels of OB-r and STAT3 will be down regulated in HFD mice, and that transcription levels of NPY and CRH will increase in the HFD mice. Pre-designed oligonucleotide primers for GOIs will be used and optimized for efficiency and specificity. RNA will be isolated from whole hypothalamus brain samples from each diet using an RNA isolation kit. Gene analysis (qPCR), will be performed to measure transcription levels of each gene. We have been able to cut and section whole hypothalamus brain samples from each diet, and have run efficiencies on the OB-r and STAT3 primer. Our efficiency results so far have shown OB-r and STAT3 primers giving good melt curves and efficiency values that lie within our acceptable range of 90-110%. The next steps will be to run efficiencies on NPY and CRH, and afterwards run qPCR with the isolated RNA samples. This work will give further insight on the regulation of specific genes in different types of diet.

Overcoming Challenges

Going into this project, I had prepared to dedicate a lot of my time to being in lab. I was responsible for my own schedule, which allowed me at times to enjoy some shorter days in lab, while understanding that some days would require me to stay longer to get the required amount of work done. Often, things would not go as planned, as some of the experiments did not yield expected results. When that occurred, I took a step back for a closer look at all the possible sources of error in the experiment. Often, these errors were shown in the experiment’s results, so the source of error was more easily tracked. Sometimes, however, these errors resulted in having to change different aspects of the project. For this current project, we had to change some of the primers that we were using because some of them did not yield good band/efficiency results. Luckily, while this did change what primer was initially going to be explored, it did not change the region or the overarching hypothesis of this project.

Going into lab every day has changed my work ethic greatly. Being able to set my own schedule for experiments has been extremely nice for me, and has allowed me to see personally the progress I am making in my project and the experience I am gaining in lab, which is one of the many pros of being a scientist. This experience has made me more aware of the importance of setting my own schedule, and how flexible it needs to be to account for possible errors in the experiment and setting up various meetings with professors, lab mates, and technicians, which can be considered a con of being a scientist. Experiments will often not give good results, and it may sometimes be frustrating to have to go back and troubleshoot each individual experiment. Having lab mates there, however, was a huge help in overcoming some of the challenges I faced with my experiment. Working as part of a lab team has shown me that each member of the lab collaborates with their peers’ projects and helps each other when necessary. I have learned a lot about each of my lab mates, including their project layout and work ethic. Working together with my lab mates this past summer has allowed to connect with them and gain experience from their guidance and help.

Edward Truong is a junior majoring in Cell, Molecular, Developmental Biology at the University of California in Riverside, CA. He is a Short-Term Research Education Program to Increase Diversity in Health-Related Research (STRIDE) Fellow working in Dr. Margarita Curras-Collazo’s lab at the University of California in Riverside, CA. Edward’s fellowship is funded by the APS and a grant from the National Heart, Lung and Blood Institute (Grant #1 R25 HL115473-01). After graduation, Edward plans to attend medical school and pursue a career as a physician.
Making Networks of Many Kinds

A heart attack, or myocardial infarction, results from blockage of arteries that deliver oxygen-carrying blood to heart tissue (NIH). Once the cells of the affected region die, the heart’s wall may grow so thin that it ruptures, or the heart’s force of contraction can decrease to the point that it is nonfunctional. Heart failure is a major medical problem for both patients and physicians. In the United States alone, approximately 5.7 million people 20 years or older had heart failure, according to data collected between 2009 and 2012. Moreover, there is approximately a fifty percent probability of death within 5 years of diagnosis (Mozaffarian et al., 2016). Angiogenesis, the formation of new blood vessels from preexisting ones (Robich, Chu, Oyamada, Sodha, & Sellke, 2011), is a key process to delaying the progression of heart failure. Angiogenesis helps heal damaged heart tissue by restoring blood flow, and scientists have worked to investigate and stimulate this process because of its beneficial potential. My research project explores angiogenesis throughout the full timeline of heart failure pathology—up to 56 days after myocardial infarction in mice models, or 10 years after myocardial infarction in humans. I also want to determine if there is a relationship between angiogenesis and lipoxygenase 12/15, an enzyme that forms metabolites which can aggravate or inhibit disease, depending on the context (Conrad, 1999). Mice are lipoxygenase 12/15-deficient heal better and have a higher survival rate after myocardial infarction than wild type mice, but the reason for this is unknown. My project is important because previous studies have primarily focused on angiogenesis during a single stage after myocardial infarction, but to fully understand this healing process, we must look at its entire duration. Also, some humans express lipoxygenase 12/15, whereas others do not; if we can understand the role of this enzyme in heart failure pathology, then we can offer more exacting prognostics to patients.

Life in the Lab

To put it simply, my summer research experience has been a continual learning process. Although all of the projects are related, there are so many different types going on simultaneously within the lab. I have gotten the opportunity to observe or help with various types of procedures, such as mice surgeries, exosome measurements, gene expression, and multiple stainings. I have also practiced patience, perseverance, and adaptability, as we have encountered numerous technical difficulties. The histology staining for my slides was not strong enough after my first two attempts, and it was difficult to pinpoint exactly which part of the process or handling was at fault. We had to troubleshoot multiple steps of the protocol and encountered problems with back-ordered supplies before we realized that an antibody used in the staining was getting older and therefore losing its potency. I also tried changing a step of the protocol based on new information, and that seems to have worked better than the original instructions due to the changed circumstances. Because of these issues, we have had to start over multiple times.

There is always work to do in the lab, and I have had to strike a balance between multitasking to get things done, but not taking on too much lest I make a mistake. I like that there are multiple projects going on within the lab, so although they are all related to the cardiovascular system, there is still a decent amount of variety. However, a good many of the protocols require repetitious procedures or long waiting periods, and those are far from my favorite parts. As for working with a lab team, that has been extremely enjoyable. I have made several good friends within my lab, and we learn from and support each other. We are always willing to help each other and therefore work well together, which not only makes for a better working environment, but also makes completing the work itself more efficient.

References

  1. Conrad DJ. The arachidonate 12/15 lipoxygenases: a review of tissue expression and biologic function. Clinical Reviews in Allergy and Immunology 17: 71-89, 1999.
  2. Mozzafarian DM, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, . . .Sandeep RD. Heart disease and stroke statistics—2016 update: a report from the American Heart Association. Circulation: e308-309, 2016.
  3. NIH – National Heart, Lung, and Blood Institute. Myocardial Infarction. (n.d.). In PubMed Health Glossary. Retrieved from https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0021982/.
  4. Robich MP, Chu LM, Oyamada S, Sodha NR, Sellke FW. Myocardial therapeutic angiogenesis: a review of the state of developmental and future obstacles. Expert Rev Cardiovasc Ther. 9(11): 1469-79, 2011.
Carolee (MeMe) Collier is a rising senior majoring in English, pre-med at Auburn University in Auburn, AL. She is a 2017 Short-Term Research Education Program to Increase Diversity in Health-Related Research (STRIDE) Fellow working in Dr. Ganesh Halade’s lab at the University of Alabama at Birmingham in Birmingham, AL. MeMe’s fellowship is funded by the APS and a grant from the National Heart, Lung and Blood Institute (Grant #1 R25 HL115473-01). After graduation, MeMe plans to attend medical school and later use her undergraduate and professional degrees to become both a physician and an author. She also hopes to utilize her research experience by getting involved in clinical research during her career.
A Study into the Effects of Physical Activity and Endothelial Function into Mitigating Preeclampsia

Preeclampsia is a pregnancy-related disease in which complications inflict harm onto the mother and/or baby, and in severe cases may lead to death. These complications are known to affect 2-8% of all pregnancies. My research has two aims focused on uncovering the methodology behind preeclampsia so that it may be diagnosed prior to delivery and successfully combated against. The first relationship I am looking at is one between physical activity levels and the risk of developing preeclampsia. I have theorized that an increase in physical activity levels during pregnancy will cause a decrease in the risk of developing preeclampsia. This will be assessed by the Pregnancy Physical Activity Questionnaire and postpartum medical reports stating if any diagnoses of preeclampsia were present. Preeclampsia is marked by high blood pressure, so the second aim will look at the relationship between the development of preeclampsia and endothelial dysfunction. The endothelium is the layer of cells that line organs, cavities, and especially blood vessels, the heart, and the lymphatic system. I will be looking at how fast blood flows between two points on the body, a measurement called Pulse-Wave Velocity, that will indicate the stiffness of the arteries. Other measurements will also be collected to help assess arterial stiffness, and thus endothelial dysfunction.

I started into this research lab my sophomore year. What I expected was being in a setting similar to my advanced biology lab courses where we ran experiments such as western-blots, PCR reactions, and such. Though my lab does have this component, I chose to be involved in the clinical side of my research, where I would go to see human participants in the hospital. I really enjoyed interacting with human subjects because it made my work feel more personal and translatable to human life. I have learned a lot of new techniques since my first day, such as collecting images of the arterial walls contracting and relaxing as blood flows and also recording blood pressures by listening to the sound of the heart. What surprised me, however, was how difficult it could be to collect clear vascular measurements since a lot of our work required participants to lie still and awake for 2.5 hours, and occasionally not swallow. At times like those, the vascular imaging data would become too distorted or imprecise for the analysis software later. Thus I learned how to help communicate these needs to the participant in a way that still kept them calm and comfortable but help bring clarity and accuracy to the data. Luckily, we have not ran into any major challenges in our study, and so our research question has remained the same.

What have you learned about life as a scientist?

What I’ve learned about the life of a scientist is that your study makes your schedule, in most cases. Though my role in my lab is more flexible than my more experienced peers who tend to be involved in more than one study, my weekly schedule is still created by the availability of the participants. This was sometimes a great thing, such as when your participants come in on time and everything runs smoothly. But it can also have cons, such as participants never showing up, canceling at the last minute, or having scheduled visits at painfully early hours like 7 a.m. What has made it continuously worth it has been getting to learn something new every day not just from my scientific peers, but also from the participants who volunteer their time to helping us hopefully discover more answers and treatments. Being a part of these efforts to understand preeclampsia and mitigate its impact on up to 8% of pregnant women has been one of my most valuable involvements and I hope to continue to grow in this area and as an aspiring scientist.

 

Rumbidzai Majee is a senior majoring in Human Physiology/Pre-med track at the University of Iowa in Iowa City, IA. She is a 2017 STRIDE fellow working in Dr. Gary Pierce’s lab at the University of Iowa in Iowa City, IA. Rumbidzai’s fellowship is funded by the APS and a grant from the National Heart, Lung and Blood institute (Grant #1 R25 HL115473-01). After graduation, Rumbidzai plans to pursue a career as a physician scientist in the area of Obstetrics and Gynecology or Dermatology.
A Glimpse Into My Fight Towards Finding a Safe and Effective Way to Combat Respiratory Dysfunction

My research project this summer focuses on the development of rehabilitative strategies used to combat respiratory dysfunction (the inability to breathe) in patients suffering from spinal cord injuries. Following a spinal cord injury, brainstem projections traveling down the spinal cord are severed, ultimately leading to paralysis of respiratory muscles such as the diaphragm. Consequently, breathing impairments are the primary cause of death for spinally-injured patients. This summer project focuses on a rehabilitative therapy known as intermittent hypoxia (IH) which involves brief and repeated exposures to low oxygen levels over a period of time. When given in low doses (>15 episodes/day), intermittent hypoxia can improve leg strength, walking function, and respiratory function in spinally injured rats and humans. On the other hand, high doses of intermittent hypoxia can elicit spinal inflammation and other pathological consequences. My study seeks to determine whether activation of a certain protein kinase that acts as a marker of inflammation, p38 MAP kinase, is increased in all dose protocols of intermittent hypoxia or just high dose intermittent hypoxia. Assessing the impact of p38 MAP kinase phosphorylation/activation is crucial for the development of safe and effective methods to restore respiratory function in individuals with a spinal cord injury. Currently my research subjects are rats; however, once our lab can ensure that low dose intermittent hypoxia is safe and non-harmful to humans, through my project and many others currently being conducted, we can transition our treatments from animals to humans.

What was it like doing research in a lab?

My research experience this summer was an eye-opening experience that, for the first time in my professional career, allowed me to devote all my time to the research I am passionate about. Conducting research in the lab alongside other undergraduate and graduate students, and post-doctoral fellows, was nerve-wracking yet very rewarding. When I first began my project, part of me was afraid to attempt tasks and techniques that were new to me for fear of ruining valuable data. However, to my surprise everyone in the lab was eager to help me in any way they could even if they were occupied with their own projects. I quickly learned that I would have to develop several techniques for my project to be a more independent and productive researcher. These techniques include immunohistochemistry (IHC) staining and imaging. Thus far, my experiment has been working, with all CTB injections, exposure treatments, perfusions, harvesting, and tissue sectioning going successfully. An unexpected mishap that occurred involved the immunohistochemistry staining. During our first IHC staining trial, we stained only a few of the tissues and had difficulty viewing the markers that were stained for when imaging. This was a result of having used an antibody at a wavelength of light that wasn’t appearing on the microscope. After reviewing literature and past protocols we decided on a different antibody that would produce better images. Although unfortunate, this setback demonstrated that while conducting research several things can go wrong but can just as easily be fixed. As for results, my project is still under the works as I have just reached the imaging phase.

I have found my experience as a scientist this summer to be both rewarding and stimulating. Every day when I come into lab, I am eager to jump into my project and engage in conversation with other researchers about the impact all of our research could one day have. My days consist of running experiments, performing animal care, cutting tissue, and whenever I have down time, reading papers. The best part of my research experience is collaborating with other members in the lab. I enjoy listening to the advice and thoughts of the other researchers because it gives me other perspectives on things. The worst part about being a research scientist is probably accepting mistakes and figuring out how to solve the problems. I found working as part of the team to be an educational experience that helped me improve my communication and leadership skills.

 

Juliet Santiago is a junior majoring in Microbiology and Cell Science at the University of Florida in Gainesville, FL. She is a 2017 Short-Term Research Education Program to Increase Diversity in Health-Related Research (STRIDE) Fellow working in Dr. Gordon Mitchell’s lab at the University of Florida in Gainesville, Florida. Juliet’s fellowship is funded by the APS and a grant from the National Heart, Lung and Blood Institute (Grant #1 R25 HL115473-01). After graduation, Juliet plans to pursue a career as a biomedical scientist in industry or government.