Tips for the New Zebrafish Scientist

Over two years ago, I started a new postdoc using a new model species, zebrafish. Luckily, I was able to collaborate with an established PI with a large, well-maintained zebrafish facility.

I love working with zebrafish- they look beautiful under the microscope and are a great way to expose undergraduates to research. But I’ve learned a few lessons the hard way and wanted to hear what tips and tricks other zebrafish researchers had to share. So of course, I headed to Twitter.

Here are their responses, including a few tips of my own.

1. (Your) Hydration is key

Masai Fish Room
Masai Fish Room, Okinawa Institute of Science and Technology https://flic.kr/p/TCGQ9d

Zebrafish researchers dress very casual, even for scientists. A warm aquatics facility may be great for the zebrafish, but it can be hard on us humans. T-shirts and shorts (if permitted) are common, and I quickly got too warm in my favorite lab coat. Plus, washing fish tanks with bleach is bound to put holes in your clothes.

@ZHAonline also recommends patience when learning how to net. I admit, some days I think the zebrafish are re-enacting a scene from Finding Nemo. “Swim down! Swim down! Swim down!”

2. Mate the most “female” looking females with the most “male” looking males.

The more a fish looks like a female, the better chance it has of laying eggs (bigger belly= more eggs). I like this mating guide.

If you are crossing two different zebrafish strains, this is especially important as sex is typically used to keep track of the source of each fish in a mating pair.

3. Just let them rest

Zebrafish in Research Lab for Animal Testing
Understanding Animal Research, https://flic.kr/p/dwDFuB

You may have been told to only mate fish once a week, but you should also remember that repeatedly mating the same fish is metabolically costly. Make sure to feed your fish a little extra if you plan to mate them frequently. It will also make determining the sex of the fish next week a lot easier when they are nice and chubby!

4. Be careful in-crossing transgenic fluorescent fish

While in-crossing transgenic fluorescent zebrafish is a sure-fire way to get lots of fluorescent embryos, you may discover unexpected phenotypes. If you are not certain whether the transgene in your fluorescent zebrafish impairs the function of any genes, be cautious when generating homozygous transgenic fish. You may unexpectedly reveal a deleterious phenotype normally unobserved in heterozygotes.

5. Mighty morpholinos

With the advent of zinc finger nucleases, TALENs, and CRISPRs, discrepancies between mutants and morpholinos have become apparent. The above article briefly describes the importance of comparing morpholinos with mutants and provides updated guidelines for the use of morpholinos.

6. Sometimes fluorescent protein doesn’t fix.

Never treat GFP transgenic fish with MeOH, trichloroacetic acid, or acetone if you want to retain the fluorescence. Paraformaldehyde is best, and be careful when using various antigen retrieval methods.

I sometimes have trouble observing fluorescence even after fixation in paraformaldehyde, especially with red fluorescent protein. ALWAYS check if your fluorescent protein fixes nicely before starting a big experiment.

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Zebrafish blood vessels. NICHD https://flic.kr/p/s4ukxf

7. Never trust a new transgenic.

You can never assume that a transgenic fluorescent fish has the expression listed on its tank before using it for the first time. On several occasions, I have found fish that do not express their transgene at my time point of interest, or do not express their fluorescent protein strongly enough for proper observation. It is best to check your fish by live imaging or immunohistochemistry when using a new transgenic.

8. It’s a team effort

Zebrafish research runs so much more efficiently when approached from a team perspective. Scheduling feedings over the holidays, monitoring general health of the zebrafish population, time-sensitive mating periods, and identifying stage-specific phenotypes seem unimaginable to me without a team of dedicated students and staff.

8. Look at a larval zebrafish under the microscope.

Just look at it. It is SO cool! Sometimes I take a break from sorting fish just to look at these beautiful creatures. Wonder at the blood cells traveling all around the body in front of your eyes. Check out how the notochord looks like a stack of pennies. If you are using fluorescent fish, look at the fluorescence in a different tissue than you normally focus. You may find a new perspective helpful to your research. At the least, it will remind you of the value of zebrafish in biomedical research and the respect that these animals deserve.

 

9. Get ready for arts and crafts.

Here are some fun things I have seen used or created while working with zebrafish:

  • hand-pulled glass probes for manipulating embryos
  • vacuum grease creates a seal of variable heights between your slide and coverslip
  • 3d-printed food dispensors
  • custom-made embryo troughs
  • tiny beveled needles for cell transplants
  • Scotch-Bright(TM) sponges for holding zebrafish

I think zebrafish lend themselves to creativity since they are harder to contaminate than cells and are big enough to see and handle. I can’t wait to set up my own aquatics facility!

10. Join a zebrafish community.

The Zebrafish Husbandry Association @ZHAonline was quick to offer advise for the creation of this post, and has a number of helpful resources available to new zebrafish scientists.

Other helpful communities include

IMG_20171027_223344329
My cat Rocket is an unwilling member of the fish community.

Do you have any other tips that you wish you knew when starting with zebrafish? Share them in the comments below!

 

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Ketamine’s New Use as an Antidepressant.

It looks like Special K may be more special than we first thought.

Ketamine, the psychedelic drug also known as Special K, has gained attention in recent years from the field of biomedical research for its potential use as an antidepressant. Originally designed as an anesthetic, sedative, and pain killer, sub-anesthetic doses produce a dissociative state in the user, leading to its recreational use. Scientists have found that at even lower doses, ketamine has potent antidepressant effects.

One reason ketamine is being investigated as an antidepressant is its fast action. While most antidepressants take weeks to demonstrate effects, ketamine can provide relief in as little as two hours. How is it that ketamine can achieve similar effects as other antidepressants in such a short time frame? Can we use that knowledge to create better drugs? This is what Dr. Mark Rasenick of the University of Illinois at Chicago is setting out to discover.

Dr. Rasenick studies the mechanisms of antidepressants. Most antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs), work by altering levels of neurotransmitters, the molecules that send signals from cell to cell in the brain. Below is a diagram demonstrating the action of neurotransmitters between two neurons. Antidepressants increase the concentration of neurotransmitters at the synapse by preventing transporters from taking up the molecules into the cell. They can also slow down degradation of neurotransmitters, leading to more at the synapse.

cleft
Source

But what happens next? How do increased levels of neurotransmitters lead to less depression in patients? Does the action of antidepressants have any relationship to increased amounts of neurotransmitter at the synapse?  In fact, researchers still don’t know the answer to those questions. They have found pieces of the puzzle, but it is not yet complete. The next diagram shows one piece of the puzzle that scientists have discovered. Cell signaling is a bit like a relay race, passing the signal like a baton from one protein to the next.

gpcr

  1. Neurotransmitters bind to their receptors on the surface of a cell.
  2. G proteins, a complex of proteins that travel along the inside surface of the cell membrane, couple with the receptor.
  3. G proteins are activated once coupled with the receptor, causing them to travel along the membrane to pass on the signal to another protein, here called the effector.
  4. The G protein activates the effector, carrying on the message to the rest of the cell.

 

Because of this relay, the effector protein is able to amplify the signal to the rest of the cell. It’s kind of like calling your mother with some big news. If you tell her you got a new job or met a new guy, the rest of your extended family and friends will know within 24 hours! This mechanism is an efficient way to pass on signals from one neuron to the next.

Dr. Rasenick found that many antidepressants also increase the movement of the G protein along the cell membrane. The easier the G protein is able to shuttle back and forth between the receptor and the Effector (Adenylyl cyclase, the enzyme that makes cAMP), the greater the signal amplification. Could ketamine do this, too?

Dr. Rasenick and his lab measured the mobility of G proteins in neuronal cell culture before and after treatment with ketamine, and compared it with other antidepressants. Interestingly, they found that ketamine was able to increase G protein mobility just like other antidepressants, but much more quickly. However, the effects of ketamine did not last as long as the slower-acting antidepressants. This suggests that future drugs could be designed to increase G protein movement at the membrane leading to antidepressant effects much more rapidly. Perhaps with the right drug formulation, G protein mobility could be extended to last longer, as well.

There is one mystery to this research: The neurons which Dr. Rasenick used to test ketamine, and other antidepressants, were missing the neurotransmitter transporters, and reinserting those transporters had no effect. That suggests that the antidepressants that we have been using, as well as potential new drugs, likely act through multiple pathways that are yet unknown. Only with the dogged pursuit of pharmacologists, biochemists, and clinicians, will we be able to put the puzzle pieces together to solve mental illness.

Scientists and physicians are excited about the potential of ketamine as an antidepressant. However, the risks associated with abuse of the drug are quite serious. By understanding the mechanism that ketamine uses to create its antidepressant effects, perhaps new, safer treatments can be designed for the treatment of depression.

 

Donati, R.J. and Rasenick, M.M. (2003) G protein signaling and the molecular basis of antidepressant action. Life Sciences 73(1): 1-17.

Czysz, et.al, (2015) Lateral Diffusion of Gαs in the Plasma Membrane Is Decreased after Chronic but not Acute Antidepressant Treatment: Role of Lipid Raft and Non-Raft Membrane Microdomains  Neuropsychopharmacology 40, 766–773.

How Cancer Metastasis Works: EMT and MET

Many of us have heard about metastatic cancer. It is the type of cancer we all fear, as it is difficult to predict where and when a tumor will migrate. Scientists are working to not only cure cancer, but prevent metastasis of cancer to other sites in the body. This is because it is easier to treat tumors when they are at a confined location and it can be impossible to track down and kill every cancer cell.

In order to prevent cancers from spreading, it is important to understand how it occurs. In tissue such as skin or bladder, the cells act as a barrier or lining. They perform this function by being uniform in shape and tightly connected, like bricks in a wall. These cells are called epithelial cells. In cancer, the epithelial cells lose their uniform shape and tight connections, becoming less attached and more motile. In this way, the cells are able to separate and travel away from the tumor to metastasize. When cells behave in this manner, they are described as mesenchymal. This change in cell shape and behavior is called the epithelial to mesenchymal transition, or EMT.

emt
The Epithelial to Mesenchymal Transition, or EMT. Modified from Source 

Dr. Jing Yang at the University of California, San Diego, received the John J. Abel Award in Pharmacology given by ASPET for her pioneering work researching the mechanisms of cancer metastasis. As a postdoctoral fellow, Yang discovered that the protein Twist1 was essential in regulating the epithelial to mesenchymal transition in cancer. This transition actually occurs normally in the body during development as a method for cells to travel to their correct locations in the embryo. “Tumors don’t invent anything new,” says Dr. Yang. “They use what evolution already gave them. They just activate them at the wrong time, in the wrong place and at the wrong dose. If you look at what situation the epithelial cell is able to move, really this is the program that allows stationary epithelial cells to be able to migrate and invade as a single cell.”

At first, it was difficult to prove that epithelial cells became mesenchymal in order to metastasize to a secondary site. When tissue from metastatic sites in human cancers was tested, the cancer cells looked epithelial, not mesenchymal. Dr. Yang proposed that the cells first became mesenchymal in order to gain their migratory capabilities, but reverted to an epithelial type in order to settle at the new tumor site. In other words, the cancer cells underwent the epithelial to mesenchymal transition to metastasize, and then the mesenchymal to epithelial transition (MET) to establish a second tumor. This would make sense, because a cell that is trying to establish itself in a new site would not need migratory capabilities any more.

In order to determine if cancer cells must undergo EMT, followed by MET, in order to metastasize and establish at a secondary site, Yang and her team created a system in which mice were induced to have skin cancer, with the whole body exposed to EMT signals. If the cancer cells did not need to transition from a mesenchymal to epithelial phenotype, they would be able to metastasize anywhere in the body. However, if MET was required, the cancer cells would not be able to establish at distant sites. She also created a model in which EMT was promoted only at the primary tumor site. If cells migrated from this mesenchymal environment and established themselves as epithelial cells at a distant site not receiving EMT signals, it would indicate that EMT is initially required for cancer cells to metastasize, but that it must be reversed for the cells to settle at a secondary site.

In mice with pro-EMT signals throughout the whole body, the cells were unable to metastasize to different sites. Only in the mice with pro-EMT signals restricted to the initial tumor site were the cancer cells able to migrate and found new tumors. This was because the cells were able to undergo first EMT, travel to a different site, and then establish there using MET to revert back to epithelial-like cells. In the other mice, the cells were able to undergo EMT, but not the reverse in order to found new tumors.

Dr. Yang and her team have also been able to capture cancer cells circulating in the blood stream, in a sense getting a snapshot of cancer metastasis. They identified that the cells in the process of metastasis were the mesenchymal type.  This further confirmed their hypothesis that cancer cells must acquire mesenchymal characteristics in order to migrate away from the tumor and travel through the blood stream to a new site.

These findings have direct clinical implications, as anti-EMT drugs have been proposed to prevent cancer metastasis. While the cells at the initial tumor site would not be able to leave and establish secondary tumors, any cells that had already acquired mesenchymal characteristics and were traveling through the body would be encouraged to revert to an epithelial type and settle down at a new site. Until techniques are available to track down all cancer cells, both those established and circulating in the body, drugs that alter EMT should be used with caution.

 

STAT3 as a Multi-organ Target for Tissue Fibrosis

Fibrosis is the formation of excessive fibrous connective tissue, creating scar-like tissue in affected organs. Fibrosis causes a stiffening of tissue, altering the way an organ functions. In dynamic organs such as the lung, fibrosis not only impairs oxygen exchange, but also inhibits the lungs from expanding and contracting during breathing. Fibroblasts are activated in diseases such as pulmonary fibrosis, cirrhosis of the liver, and after myocardial infarction (heart attack). Activated fibroblasts are called myofibroblasts. They become more contractile, migratory, and secrete pro-fibrotic matrix proteins, which form the fibrotic tissue and promote scarring.

IPF
Figure A shows the location of the lungs and airways in the body. The inset image shows a detailed view of the lung’s airways and air sacs in cross-section. Figure B shows fibrosis (scarring) in the lungs. The inset image shows a detailed view of the fibrosis and how it damages the airways and air sacs. Source

Scientists often look for potential drug targets by comparing the entire genome between normal and diseased cells. However, many of the targets identified with this technique are ultimately not suitable for clinical development.  Many genetic targets are correlated, but not causal for pathology.  Even for those that are causal, many do not make it to clinical trials for reasons such as unavailability of drugs that inhibit those targets, insufficient knowledge about the target in order to design an inhibitor, or the target is unreachable by drug molecules.

To speed the transition from the lab to clinical trials, Drs. Andrew Haak and Daniel Tschumperlin of Mayo Clinic experimentally generated a list of druggable targets implicated in fibroblast activation. These are targets for which inhibitors have already been developed, much is known about the target, or the target is easily accessible by drug molecules. Fibroblast activation can be replicated in cell culture by treating fibroblasts with the protein transforming growth factor b, or TGFb. The scientists created a cell culture model of pulmonary fibrosis by activating fibroblasts with TGFb and used molecular biology techniques to inhibit the druggable targets previously identified. After target inhibition, they studied how affected the fibroblasts were by the inhibition of each particular target. They measured cell behavior such as contractility and common markers of activated fibroblasts, such as a smooth muscle actin and collagen. They found that STAT3 was a target that, when inactivated, hindered fibrotic activation, a primary mechanism of pulmonary fibrosis.

Haak tested the inhibition of STAT3 in a cell culture model that closer replicated human pulmonary fibrosis. He received cell samples from patients with the disease and tested the effects of blocking STAT3. He found that their treatment inhibited fibroblast activation, indicating that STAT3 may be a promising target for treatment of pulmonary fibrosis.

While much can be learned from cell culture models, such as the mechanisms behind cell behavior and disease, animal models are critical for pre-clinical testing of potential drugs. The scientists used a mouse model of pulmonary fibrosis, caused by treatment with bleomycin. Following injection with an inactivator of STAT3, the mice demonstrated reduced fibrosis, levels of fibrotic tissue, and markers for activated fibroblasts. This is first step toward the use of STAT3 inhibitors in pulmonary fibrosis.

The protein STAT3 has many previously known functions in the immune system. Because of this, concerns about side effects on the immune system must be addressed. Haak and Tschumperlin are now studying ways in which to selectively inhibit STAT3 function of activated fibroblasts in the lung, but not immune cells. If they are able to create such a selective drug, it could then be tested in clinical trials with patients suffering from pulmonary fibrosis.

The mechanism of action for one currently available drug, nintedanib, is not fully understood. When Haak measured the levels of activated STAT3, he found that it was reduced by nintedanib treatment, suggesting that nintedanib may fight pulmonary fibrosis in part by inactivating STAT3.

Since fibrosis is common to a number of diseases, the scientists decided to test out STAT3 inhibition in liver and heart fibroblasts. They found that common markers of activated fibroblasts were significantly reduced. This implies that STAT3 may not only be a druggable target of pulmonary fibrosis, but other fibrotic diseases, as well. Drugs that can be used in multiple ways are especially valuable, as they lower the expense and increase the speed of drug development and clinical testing. This allows life-changing treatments to be brought more rapidly and affordably to patients suffering from diseases such as pulmonary fibrosis, liver cirrhosis, or cardiac fibrosis.

PKPB-What? Predicting drug levels in pregnant women.

To say many life changes occur during pregnancy would be an understatement. While many women change their behavior for the health of their baby, such as giving up caffeine and alcohol, not all risks to the fetus may be avoided. For example, not all medications a woman takes may be given up when she becomes pregnancy, particularly if not taking the medicine would create greater risks for the baby, such as in the case of HIV. In addition, pregnancy can induce health conditions, requiring medication. In fact, 64% of women continue to take prescribed medications during pregnancy.

As a woman progresses through pregnancy, the changes in her body can have an effect on the medications she takes. In addition to weight gain, the output of the heart increases, as well as blood volume and kidney filtration rates, important factors in drug metabolism. For example, Indinavir is a treatment for HIV whose concentration in the body changes with pregnancy. A dose that was sufficient for a woman before she became pregnant becomes too low during pregnancy to prevent a breakthrough of resistant virus, which could put her and the baby at risk.  For this reason, FDA recommends that Indinavir by itself should not be prescribed to pregnant women.

So how do you determine the correct drug dose for pregnant women? You certainly can’t test out the drug at different doses on a population of pregnant women, as such testing may last longer than pregnancy and may cause damage to the fetus. In addition, you cannot collect multiple blood samples from the fetus during pregnancy. Instead, pharmacologists use mathematical models to predict the levels of drugs in a patient’s system.

Zufei Zhang and Dr. Jashvant Unadkat at the University of Washington believe that PBPK modeling may be the answer. PBPK, or physiologically based pharmacokinetic modeling, is the use of mathematical models to predict the levels of drugs in a patient’s system. Using data from in vitro, pre-clinical and clinical studies, it can estimate drug absorption, distribution, metabolism and excretion. This model breaks down the drug’s path through the body into discrete compartments, often organs and tissues, through which the drug travels at different rates or is chemically modified. This is how a pharmacologist sees a person:

pbpk1
Q: Blood Flow, [X]: Volume Source
Each compartment has its own equation, factoring in blood flow and volume, surface area, drug permeability, and information about drug transformation before elimination. For example, one compartment may have transporters that can specifically transport the drug. A drug may travel very fast through one compartment, but slowly through another. In addition, the drug’s chemical composition may be modified as it moves from one compartment to the next,  on its way to a form that can be excreted from the body.

Previous models of the mother and fetus looked like this:

pbpk2
Source 

However, these models do not account for the growth of the fetus over time. For example, the ability of the fetus to metabolize drugs will change. In addition, the placenta contains transporters which actually efflux, or transport back out, drugs away from the fetus. Throughout the pregnancy, the numbers of these transporters change, affecting the ability of the placenta to protect the fetus from drug exposure. The amniotic compartment is also considered in their model. Drugs that are metabolized by the fetus are excreted into the amniotic fluid, which can then be redistributed in the mother or fetus.

Zhang modified the model to include these parameters:

pbpk3

Solid arrows: Tissue blood flow; dashed arrows: Clearance.  CLPDMP and CLPDFP: bidirectional passive diffusion clearance between mother and placenta and that between fetus and placenta, respectively; CLMP and CLPM: unidirectional transporter-mediated clearances between mother and  placenta.  CLFP and CLPF: unidirectional transporter-mediated clearances between fetus and placenta.  CLMA and CLAM: directional transporter-mediated clearances between mother and amniotic fluid. CLrenal: fetal renal clearance.  CLmet, fetal hepatic metabolic clearance.  CLreabsorp: fetal swallowing.

Zhang used Midazolam, a sedative, as a probe drug in which to test her refined PBPK model. When compared with known data, her model accurately predicted the concentration of the drug in the mother and her fetus at the time of birth. This suggests that this PBPK model could be used to estimate maternal and fetal exposure to Midazolam and drugs that have similar properties.

One advantage of PBPK modeling is its ability to incorporate variables such as different drug formulations, drug compounds, extrapolation across species, and biological changes over time. As previously mentioned, the ability of the placenta to transport drugs changes during pregnancy. Zhang then used the PBPK model to simulate maternal and fetal drug levels of Didanosine, an antiretroviral for HIV, in two different situations. In one, the drug passed through the placenta to the fetus. In the other, placenta included transporters which efflux the drug. This demonstrated the ability of the model to test multiple variables to create custom predictions of drug exposure.

The use of PBPK modeling in pharmacology is on the rise, due to increased computing capabilities and the recent support of the FDA. Recent regulatory attention and successful FDA applications will continue to promote PBPK modeling to inform trial design and dose regimens, improving the chance for success of novel drugs and safer exposures for pregnant mothers.

 

Ke, A.B. et al. (2014) Pharmacometrics in pregnancy: An unmet need. Annu Rev Pharmacol Toxicol. 54: 53-69.

Summer Undergraduate Research Fellowships: Opportunities for Students and Faculty

SURF Logo

Summer research experiences are great opportunities for undergraduates to learn about pharmacology research and gain interest in careers in pharmacology.  Educational studies show that students who have engaged in research experiences report improvements in their technical and personal skills as well as increased confidence in their ability to do research. Students say that research experiences help them learn how to think like scientists, which can include dealing with ambiguity and uncertainty, formulating hypotheses, designing experiments, communicating their findings, and collaborating effectively with both peers and mentors. Further, students from underrepresented groups are much more likely to pursue graduate studies if they have participated in research as undergraduates.

ASPET’s Summer Undergraduate Research Fellowship, or SURF, program began in 1992, and since then over 2,000 students have participated. The goal of the program is to use authentic mentored research experiences in pharmacology to heighten student interest in careers in research and related health care disciplines. There are two award types: institutional awards, which are given to groups of at least five faculty engaged in pharmacology research on a particular campus, and individual awards, which are provided for students who may not have access to institutional programs. The SURF program runs like many other summer research experiences, in which students are paid a stipend to do research over a 10-week period.

Last year, ASPET required that institutions with SURF programs perform assessment of participants using the Survey of Undergraduate Research Experiences (SURE) to measure students’ perceived gains in areas such as self-confidence, clarification of career paths, and understanding of the research process. Data collected from SURF participants can also be compared to other summer research programs across the country that use the survey. The first year of SURE implementation indicated that students perceive gains in many categories, including oral presentation skills, understanding how scientists think, and the ability to analyze scientific literature.

The outcomes of SURF alumni after they graduate from their baccalaureate programs have also been recorded. The top three outcomes observed were matriculation into Ph.D. or MD programs, or direct entrance into the biomedical workforce. Nearly 90% of students who participated in the program are staying in biomedical careers.

 

Initiating a SURF Program

Dr. Lauren Aleksunes, PharmD, PhD, DABT at Rutgers University provided helpful advice for those beginning an ASPET-funded institutional SURF program. To recruit faculty to the program, offering to pay for one year of ASPET membership can be helpful. She also recommended partnering with current programs at your institution that support undergraduates in STEM, your university’s career center, alumni, and industry connections to provide additional opportunities and resources to students. It is also important to measure positive outcomes such as student-authored papers and presentations and graduate school enrollment, as this information may be leveraged to garner additional support for your program.

Dr. Stella Tsirka from Stony Brook University also shared tips for implementing a summer undergraduate research fellowship program at your institution. Identify the needs of your university or department that the SURF program could address, such as student retention in STEM or recruitment of graduate students, in order to find support from within. She also suggested communication and potential collaboration with previously established summer programs on campus to access institutional history and practical advice. Dr. Tsirka also recruited faculty to the program by paying for their first year of ASPET membership, and worked to minimize any regulatory or administrative tasks to make participation more enjoyable for faculty.

Dr. Kevin Murnane had a unique case at Mercer University, which is split among four campuses throughout Georgia. The College of Pharmacy located in Atlanta does not have ready access to undergraduate students, though the College has excellent research capabilities. In order to include undergraduates in his research, Dr. Murnane partnered with Oglethorpe University, a private liberal arts university within Atlanta. By providing opportunities for students at Oglethorpe University, which has limited research facilities, Dr. Murnane was able to recruit a SURF student to his lab through the individual fellowship program.

 

Strategies for Success

While many summer undergraduate research fellowships contain similar characteristics such as visiting speakers and panels throughout the program, there were a few practices of note that were discussed during the ASPET session that were particularly helpful.

The undergraduates in her program desired more interconnected activities among SURF fellows, so Dr. Aleksunes implemented “Science in the News,” an activity in which students worked with each other to report about current research relevant in their field. Activities that bring students together, either social or scientific, encourage a sense of community that is important for promoting self-confidence in science and opportunities for students to learn how to communicate their research and begin to network.

Many SURF program directors advocated the use of LinkedIn as a method for tracking students once they have left the program. One session during the summer program is devoted to the importance of a professional online presence and the development of a LinkedIn account. This mutually beneficial activity for students and educators is now being widely implemented.

 

Undergraduate Tips

SURF participants provided helpful suggestions to students interested in undergraduate research. Natalie Arabian, a junior at California State University, Los Angeles, suggested that students contact faculty who have taught their science courses and ask about research opportunities. She also found graduate student mixers and socials a great way to mingle and learn about research openings. She stressed the importance of speaking to faculty directly rather than through email. It allows the professor to place a face with your name and shows that you are really interested in the research. If a professor says there is not a position available, pay close attention for future opportunities. Perhaps he or she may have more openings in the future. If you are interested in going to graduate school after your bachelor’s degree, look at the professor’s publication record and the number of undergraduates who have been involved.  Once you have joined a lab, never miss an opportunity to learn a new skill. By making yourself as useful as possible, you have a greater chance to perform advanced research techniques and gain a long-term position in the lab.

Chelesa Fearce is an undergraduate student from Spelman College who completed a SURF fellowship at the University of Cincinnati. When choosing a lab in which to perform research, she recommended that undergraduates find an area that is related to their interest. She also said to look at the funding status of the lab in order to know if there are opportunities for continued research. She also commented on how she benefitted from doing research at an institution that was very different from her home campus.

Michael Little, a Ph.D. candidate at the University of North Carolina at Chapel Hill, participated in the SURF program when an undergraduate at Montclair State University.  His summer experience at Rutgers University helped him decide upon a career path, in which he was split between pursuing a PharmD or Ph.D. The opportunity to see the daily life of a Ph.D. or PharmD student helped him finalize his decision, and he said that the SURF program helped him get into graduate school. The additional research experience and personal contacts he gained during the program strengthened his application, and he now is a graduate student in the lab of Dr. Matthew Redinbo, performing pharmacology research. Click here to read more stories from undergraduates in the SURF program.

I had the opportunity for a summer research experience as an undergraduate, and I can concur with the students’ opinions about its benefits. The experience gave me the time to gain expertise in lab techniques and helped to guide my career plans at an early stage. I can still remember when I learned that graduate students do not have to pay for school! Now, I have the chance to mentor undergraduates and pass on the gift that I received. With the support of professional societies like ASPET, we can all contribute to a new generation of biomedical scientists.

To learn more about SURF, visit the website at https://www.aspet.org/awards/surf/.

 

References:

Russell, S. H., M. P. Hancock, and J. McCullough. (2007). Benefits of undergraduate research experiences. Science 316: 548–49.

Eagan, M. K., S. Hurtado, M. J. Chang, G. A. Garcia, F. A. Herrera, and J. C. Garibay. (2013). Making a Difference in Science Education: The Impact of Undergraduate Research Programs. American Educational Research Journal 50(4): 683-713.

Hunter, A., Laursen, S. L., & Seymour, E. (2007). Becoming a scientist : The role of undergraduate research in students’ cognitive, personal, and professional development. Science Education 91(1): 36-74.

 

ASPET Teaching Institute: Developing Mentees Using IDPs

For some graduate students and postdocs in science, entering the job market after graduating can seem a bit like this:

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Entering the job market after graduating. Source

It doesn’t need to be this way! Sure, any life change is scary, but there is a lot that students can do to prepare themselves. However, many trainees approach their future career plans like this:

tumblr_inline_mvkj3kz7hg1rl4543
When my committee asks about my career plans. Source

As mentors, how can we better support our students and help them become more proactive about their future? The ASPET Division for Pharmacology Education held a teaching institute Saturday on developing mentees using individual development plans, or IDPs. Hosted by Dr. Kelly Karpa of the Penn State College of Medicine, the symposium provided suggestions for faculty who are interested in promoting the use of IDPs at their institutions or in their labs.

An individual development plan is a tool for personal and career development that guides employees through the creation and completion of short- and long-term career goals. While the use of IDPs has become increasingly popular in academia in the past few years, individual development plans have long been utilized among government and industry employees. An IDP is created primarily by the employee, informed by discussions with mentors. It is not a one-time exercise but a tool that is used periodically through one’s career to monitor and motivate progress toward long-term goals. Katie Collette has a great post about creating your own IDP on her website, Sickness is Fascinating.

Individual development plans provide a number of benefits to students, both in career development and research. They help trainees…

  • consider the big picture
  • be proactive earlier
  • focus their efforts
  • seek help from mentors
  • clarify expectations
  • minimize conflicts
  • maximize productivity

 

Reporting IDP Use

Dr. Nancy L. Desmond from the Office of Research Training and Career Development at the National Institute of Mental Health spoke on the implementation of IDPs among NIH-funded trainees. In 2012, a Working Group of the Advisory Committee to the NIH Director issued a report on the biomedical workforce, containing the recommendation to require the use of individual development plans for graduate students and postdoctoral fellows on any NIH grant.  Following the recommendation, the NIH posted the Guide Notice NOT-OD-093 encouraging institutions to develop institutional policies and to report on the use of IDPs. In 2014, the policy was updated to require the reporting of whether trainees funded on NIH grants use IDPs. Recipients of any NIH grant supporting trainees are to report how they employed IDPs and whether individual development plans were used for all pre- and/or postdoctoral researchers. Reporting may be submitted via the Research Program Progress Report, Section B. Accomplishments, Q B.4.

The policy strongly encourages implementation of individual development plans, though the NIH does not currently recommend any particular IDP tool. Of the data collected thus far by the NIH, Dr. Desmond stated that reporting has been variable. While some faculty have began using IDPs, others are not enthusiastic partners.

Another speaker at the symposium was Dr. Cynthia Fuhrmann, Assistant Dean of Career & Professional Development in the Graduate School of Biomedical Sciences at the University of Massachusetts Medical School. One of the four creators of myIDP, a tool offered by Science Careers and AAAS, Dr. Furhmann provided advice for faculty to assist trainees in the use of individual development plans.

Trainees need motivation and accountability in order to complete such an exercise, otherwise they will delay its creation in favor of bench work. Faculty advisors can encourage or require their students and postdocs to complete an IDP, and check in on trainees’ progress toward their goals periodically.

 

IDP Tools

A framework on which to create an individual development plan is also very useful to trainees. By providing templates such as those found below, students and postdoctoral fellows are much more likely to form a useful IDP.

In order to set short- and long-term goals using an individual development plan, trainees must be knowledgeable about their career options. As a mentor, you can provide information about careers in science through your network or through online resources such as myIDP and Science Careers articles.

In addition to mentorship from research advisors, thesis committees and career counselors can be helpful when trainees are developing IDPs. Self-assessment tools such as Strengths Finder and the Strong Interest Survey are best done with a counselor rather than interpreting the results alone.

Individual development plans can be implemented on a larger scale through the use of workshops, courses, or peer groups. Dr. Fuhrmann provided an example from the University of Massachusetts Medical School, in which professional development is integrated into the curriculum with opportunities for training, exploration, and mentoring. During Year One and Two, students attend career-related events and receive a broad view of career opportunities in addition to their standard scientific curriculum and thesis research. Third year graduate students are required to take a mini-course called “Career Planning and Creating Your IDP.” Part of a professionalism and research conduct course, students learn to apply a targeted approach to career exploration, how to expand their network, and how to create an IDP action plan with senior student mentors. During Years Four and Five, graduate students select two career plans in which to pursue advanced professional skills. Students revisit their individual development plans each year to check their progress and revise them as needed.

Student perceptions entering the Third Year course were that career planning was not urgent. The students had recently finished their classes and wanted to focus on their research. Other students thought they already knew how to achieve their desired career. At the end of the course, 28 out of 30 students stated they were glad they participated. Survey responses demonstrated that students were glad the course was required and that they will take specific actions toward the preparation of their career, particularly expanding their network. Other comments stated that students would alter their time management habits and meet with mentors more frequently.

A common theme throughout the session was that individual development plans have much more power when mentor feedback is utilized. Dr. Desmond emphasized that the dialog is important, not just completion of the IDP. Several IDP tools provide a summary of the action plan or a timeline of short- and long-term goals, which may be printed off for use in discussion with mentors.

Many faculty value mentorship of their trainees, but are pressed for time and may be untrained in effective mentorship strategies. Individual development plans and their associated tools can be a valuable resource to efficiently and systematically facilitate faculty mentorship of graduate students and postdocs.