Mother Knows Best: Breast Milk Affects Cognitive Function

 

 

By Celine Cammarata

Bacteria, parents’ experiences, poverty – the list of environmental factors that affect cognition continues to grow, and now there’s a new one: breast milk.  The composition of a mother’s milk can confer cognitive advantages to her offspring.

 

It’s known that the cytokine TNF (tumor necrosis factor), which works primarily in the immune system, is also found in the central nervous system, and past evidence has even suggested that TNF knockout mice may have some cognitive gains.  Now, researchers have revealed that spatial learning and memory are improved in mice whose mothers lack one or both TNF alleles.

 

Mice born to mothers with little or no TNF outperformed their peers on the Morris Water Maze, a widely used test of spatial memory that depends on the hippocampus.  These animals also demonstrated a transient elevation of neural proliferation in the dentate gyrus region of the hippocampus during development, which may underly their increased cognitive skills; inhibiting this increased proliferation eliminated the behavioral differences.  Furthermore, gene expression and dendrite morphology of dentate gyrus neurons were also altered in these offspring.

 

Why?  The answer could not be genetic: mice whose biological mothers were genetically normal, but who were raised by TNF-deficient foster mothers, had the same advanced skills.  So did offspring of genetically normal mothers, when the mother’s TNF levels were inhibited directly by administering antibodies for the protein postpartum.  It turns out that reducing TNF leads to lower levels of several chemokines in the mother’s milk.  Because newborn mice can’t fully break down such proteins, when these chemokines are present in milk they can reach the pup’s digestive tract in concentrations high enough to effect the immune and nervous systems from the gut.  Thus, the lack of these proteins can have an effect as well.  Although the precise mechanism of how milk composition alters hippocampal development is not yet clear, it may act in part by altering the number of white blood cells present in circulation.

 

TNF levels in the body can decrease as a downstream effect of mild stress and physical activity, as might occur when animals live in a challenging environment.  Perhaps this system of using low TNF to trigger increased cognitive capacity in offspring evolved as a way for parents to better “prepare” their young for the world.

Cutting out HIV: One Step Closer to the Cure

 

 

Elaine To

Currently, individuals who test positive for HIV are put on highly active antiretroviral therapy (HAART), a cocktail of multiple drugs that inhibit different aspects of the viral life cycle. While there are drugs that prevent the integration of the viral genome into the host cell genome, there is no known mechanism to remove the viral genome post-integration. This is also the reason we cannot completely eradicate HIV from infected individuals—even after HAART treatment, the viral genome persists in inactive memory T cells. In order to address this, Hauber et al. re-engineered the commonly known Cre recombinase enzyme, directing the novel Tre recombinase to target sequences in the HIV long terminal repeat regions. These regions flank the viral genome, allowing Tre recombinase to cut the targeted sequences within these regions and excise the viral genome from the host cell’s genome.

Lentiviral transduction was used to deliver the Tre recombinase vector into cells. The vector was designed to place Tre under the control of a Tat dependent promoter, ensuring only the infected cells that express the HIV protein Tat will express Tre. Flow cytometry was used to analyze HeLa cells infected with HIV that contained blue fluorescent protein. Cells transduced with the Tre vector had fewer blue fluorescing cells while the blue fluorescing population remained stable in cells transduced with a control vector. Immunoblots confirmed the protein expression of Tre in the Tre transduced cells. Additionally, the time course of Tre expression matched the time course of the decreasing blue fluorescence seen in the flow cytometry experiment. PCR and DNA sequencing checked that the exact DNA sequence intended to be cut out was removed in the Tre transduced cells.

Viral gene delivery comes with a fear of deleterious effects on the host cells. The researchers first examined this possibility in Jurkat cells using a re-designed vector that constitutively expresses Tre. Between the Tre and control transduced cells, there were no differences in tubulin expression, growth rate, apoptosis, or cell cycle progression. When this constitutive Tre vector was transduced into CD4+ T cells isolated from a human donor, the cells displayed similar activation and cytokine secretion profiles as compared to the control vector. The Tat dependent and constitutive Tre vectors were both transduced into hematopoietic stem cells (HSCs) without any change on the abilities of the HSCs to differentiate into the expected cell lineages. Karyotyping and comparative genomic hybridization revealed that CD4+ T cells have no Tre dependent genomic aberrations. Lastly, Tre was shown to be incapable of cutting DNA sequences within the host genome that are similar to the targeted HIV LTR sequences.

The core experiments behind this paper are the in vivo studies done in Rag knockout mice, which can be transplanted with human immune cells and used as a humanized animal model. CD4+ T cells were isolated from human donors, transduced with the Tat dependent vector, and transplanted into the mice, which were then exposed to HIV. The mice displayed lower viral counts and higher frequencies of human T cells versus the control transduction vector. Similar results were obtained when mice were given Tre transduced HSCs. Thus, the researchers elegantly show that their engineered Tre recombinase can alleviate the symptoms of HIV infection. However, reliable methods of gene delivery are yet in development, and the inactive memory T cells harboring the latent HIV reservoir do not express Tat, precluding Tre expression. If combined with methods that activate viral protein expression in the presence of HAART, Tre recombinase therapy may yet play an important role in the cure of HIV.

Feeling overworked? You’re not alone.

 

 

Celine Cammarata

Regardless of beliefs or traditions, many of us would probably like to be at home with our families right now.  But cells need tending, data points need collecting, and science halts for no man – or at least so it seems.  I recently got to wondering, are the hours of a scientist as crazy as they feel?

In a nutshell yes, we do work a lot – but not that much more than other professions.

You’ve probably already seen this info graphic, showing that science is the most coffee-consuming profession, and it’s no surprise when you consider our hours.  A paper posted to arXiv in 2012 examined the times at which papers are downloaded from Springer to gain insight into when scientists are working.  The U.S., Germany, and mainland China top the list in paper downloading.  Based on this metric, scientists tend to work late into the night as well as on weekends.  Trends in specific time distribution vary by country, with American scientists favoring long evenings over working on weekends; Chinese scientists closing shop overnight, but taking little rest over the weekend; and German scientists splitting the difference.  Interestingly, American scientists seem to be particularly bad at taking a lunch break – while China and Germany showed appreciable dips in paper downloading around early afternoon, no such trend is seen in the U.S.

All those nights and weekends add up.  In 2005 the NSF reported that scientists and engineers working in education (which included those doing research and teaching at universities as well as K-12 teachers) work an average of 50.6 hours a week overall, or over 52 hours a week for those in biology or engineering.  Scientists seeking tenure work a bit more, averaging 52.51 hours per week overall. Interestingly, those with children tend to work only slightly fewer hours per week than their childless counterparts, although the effect of children on working hours is more pronounced for women than for men.  Finally, it’s worth noting these figures do not include graduate students.

However, this workload is not as uncommon as one might think.  According to a Telegraph article earlier this year, over 80% of white collar professionals now clock more than 40 hours a week, with 28% working 50 hours a week or more – up from 19% in 2011. Of course, this is for UK workers, whereas the above numbers refer to the United States.

Nonetheless, the increasing commonality of long working hours doesn’t indicate that there is no problem.  The authors of the arXiv paper conclude that “scientists today are spending much more time working than initially intended. They are deprioritizing their hobbies, leisure activities, and regular exercises, which negatively influenced their mental and physical health.”  What are your thoughts?  Leave a comment and join the discussion!

The Gut-Brain Connection

 

Robert Thorn

In my last post, I talked about some interesting developments in the study of the gut microbiome and the effects changes in the gut environment can have on human health and development. As more work is done in the field of gut microbiomes more links are found between human disease and the types of bacteria that are present in the gut. A recent paper in Cell has found a new link between the neurodevelopment disorder, autism spectrum disorder (ASD) and a change in the microbiome. In addition to the cognitive impairments that are associated with ASD, many of those affected by ASD also have gastrointestinal problems. This correlation between ASD and gastrointestinal problems prompted the researchers to see if there was any link between the gut microbiome and ASD.

The researchers decided to focus on one specific type of ASD, called maternal immune activation (MIA)-associated ASD. There is a correlation between activation of a mother’s immune system by an infection at some point during pregnancy and an increased risk of ASD in the child. The researchers in this study take advantage of the ability to mimic MIA-associated ASD using a mouse model where they activate a pregnant mouse’s immune system. They go on to show that the offspring of the immune activated mice show similar gastrointestinal defects to those correlated with human ASD. The researchers investigate the type of bacteria that are colonizing the gut of the MIA offspring and they found that the MIA-associated ASD mice have a similar imbalance in the gut microbiome as those seen in humans with ASD. This result shows that the MIA offspring closely resemble ASD not only neurologically and behaviorally, but also gastrointestinally.

After characterizing this imbalance, they aimed to correct it by introducing good bacteria into the mice. They treated MIA offspring mice with human commensal bacteria, B. Fragilis, to fix the imbalance. They find that the treatment with B. Fragilis was able to rescue much of the gastrointestinal problems. Surprisingly, they also find that many of the ASD associated behaviors were ameliorated by the treatment with B. Fragilis, showing improvements in behaviors associated with anxiety, repetition, and communication. Although the treatment ameliorated some of the behaviors, the mice still show some hallmarks of ASD such as sociability and social preference defects. Upon further investigation, the researchers are able to link this rescue to serum levels of metabolites. They find that increases in serum levels of metabolites from the gut are associated with an increase in anxiety like behavior and that these serum levels are normalized by B. Fragilis treatment. This finding is important in linking the mechanisms of both gastrointestinal problems with some of the autism-related behavioral abnormalities.

With the prevalence of ASD rising to about 1 in every 88 live births in the US, this research is making important steps towards finding ways to alleviate some of the symptoms of ASD. In addition to helping further the treatment of ASD, they were also able to show a link between the gut microbiome, serum metabolites and distinctive behavioral defects.

The Most Scizzling Papers of 2013

 

The Scizzle Team

Bacteriophage/animal symbiosis at mucosal surfaces

The mucosal surfaces of animals, which are the major entry points for pathogenic bacteria, are also known to contain bacteriophages. In this study, Barr et al. characterized the role of these mucus associated phages. Phages were more commonly found on mucosal surfaces than other environments and adhere to mucin glycoproteins via hypervariable immunoglobulin like domains. Bacteriophage pre-treatment of mucus producing cells provided protection from bacterial induced death, but this was not the case for cells that did not produce mucus. These studies show that there may be a symbiotic relationship between bacteriophages and multicellular organisms which provides bacterial prey for the phages and antimicrobial protection for the animals.

[hr]

Interlocking gear system discovered in jumping insects

Champion jumping insects need to move their powerful hind legs in synchrony to prevent spinning. Burrows and Sutton studied the mechanism of high speed jumping in Issus coleoptratus juveniles and found the first ever example in nature of an interlocking gear system. The gears are located on the trochantera (leg segments close to the body’s midline) and ensure both hind legs move together when Issus is preparing and jumping. As the insect matures, the gear system is lost, leaving the adults to rely on friction between trochantera for leg synchronization.

[hr]

HIV-1 capsid hides virus from immune system

Of the two strains of HIV, HIV-1 is the more virulent and can avoid the human immune response, whereas HIV-2 is susceptible. This may be due to the fact that HIV-2 infects dendritic cells, which detect the virus and induce an innate immune response. HIV-1 cannot infect dendritic cells unless it is complexed with the HIV-2 protein Vpx, and even then the immune response isn’t induced until late in the viral life cycle, after integration into the host genome. Lahaye et al. found that only viral cDNA synthesis is required for viral detection by dendritic cells, not genome integration. Mutating the capsid proteins of HIV-1 showed that the capsid prevents sensing of HIV-1 cDNA until after the integration step. This new insight into how HIV-1 escapes immune detection may help HIV vaccine development.

[hr]

Transcription factor binding in exons affects protein evolution

Many amino acids are specified by multiple codons that are not present in equal frequencies in nature. Organisms display biases towards particular codons, and in this study Stamatoyannopoulos et al. reveal one explanation. They find that transcription factors bind within exonic coding sequences, providing a selective pressure determining which codon is used for that particular amino acid. These codons are called duons for their function as both an amino acid code and a transcription factor binding site.

[hr]

Chromosome silencing

Down syndrome is caused by the most common chromosomal abnormality in live-born humans: Trisomy 21. The association of the syndrome with an extra (or partial extra) copy of chromosome 21 was established in 1959. In the subsequent fifty years a number of advances have been made using mouse models, but there are still many unanswered questions about exactly why the presence of this extra chromosome should lead to the observed defects. An ideal experimental strategy would be to turn off the extra chromosome in human trisomy 21 cells and compare the “corrected” version of these cells with the original trisomic cells. This is exactly what a team led by Jeanne Lawrence at the University of Massachusetts Medical School has done. Down syndrome is not the only human trisomy disorder: trisomy 13 (Patau syndrome) and trisomy 18 (Edward’s syndrome), for example, produce even more severe effects, with life expectancy usually under one to two years. Inducible chromosome silencing of cells from affected individuals could therefore also provide insights into the molecular and cellular etiology of these diseases.

[hr]

Grow your own brain

By growing organs in a dish researchers can easily monitor and manipulate the organs’ development, gaining valuable insights into how they normally develop and which genes are involved. Now, however, a team of scientists from Vienna and Edinburgh have found a way to grow embryonic “brains” in culture, opening up a whole world of research possibilities. Their technique, published in Nature, has also already provided a new insight into the etiology of microcephaly, a severe brain defect.

[box style=”rounded”]Scizzling extra: In general, 2013 was a great year for growing your own kidneyspotentially a limb and liver. What organ will be next? [/box]

[hr]

Sparking metastatic cell growth

A somewhat controversial paper published in Nature Cell Biology this year showed that the perivescular niche regulates breast tumor cells dormancy. The paper showed how disseminated breast tumor cells (DTC) are kept dormant and how they can be activated and aggressively metastasize. Based on the paper, this is due to the interaction of interaction with the microvascularate, where thrombospondin-1 (TSP-1) induces quiescence in DTC and TGF-beta1 and periosstin induces DTC growth. This work opens the door for potential therapeutic against tumor relapse.

[hr]

Fear memories inherited epigenetically

Scientists showed that behavioral experiences can shape mice epigenetically in a way that is transmittable to offspring.  Male mice conditioned to fear an odor showed hypomethylation for the respective odor receptor in their sperm; offspring of these mice showed both increased expression of this receptor, and increased sensitivity to the odor that their fathers had been conditioned on.  Does this suggest that memories can be inherited?

[hr]

Grid cells found in humans

Scientists have long studied rats in a maze, but what about humans?  An exciting paper last August demonstrated that we, like out rodent counterparts, navigate in part using hippocampal grid cells.  Initially identified in the entorhinal cortex of rats back in 2005, grid cells have the interesting activity pattern of firing in a hexagonal grid in the spatial environment and as such are thought to underlie the activity of place cells. Since then grid cells have been found in mice, rats, and monkeys, and fMRI data has suggested grid cells in humans.  This paper used electrophysiological recordings to document grid cell activity in humans.

[hr]

Sleep facilitates metabolic clearance

Sleep is vital to our health, but researchers have never been entirely sure why.  It turns out part of the function of sleep may be washing waste products from the brain, leaving it clean and refreshed for a new day of use.  Exchange of cerebral spinal fluid (CSF), which is the primary means of washing waste products from the brain, was shown to be significantly higher when animals were asleep compared to waking.  This improved flow was traced back to increased interstitial space during sleep, and resulted in much more efficient clearance of waste products.  Thus, sleep may be crucial to flushing metabolites from the brain, leaving it fresh and ready for another day’s work.

[box style = “rounded”] Robert adds: As a college student my friends and I always had discussions about sleep and it was also this mysterious black box of why we actually need to sleep. Studies could show the effects of lack of sleep such as poor cognition and worse memory but this paper linked it to an actual mechanism by which this happens. First of all I found it very impressive that the researchers trained mice to sleep under the microscope. On top of that showing the shrinkage of the neurons and the flow of cerebrospinal fluid which cleans out metabolites finally linked the cognitive aspects of sleep deprivation to the physical brain. [/box]

[hr]

Poverty impedes cognitive function

People who are struggling financially often find it difficult to escape poverty, in part due to apparently poor decision making.  Investigators demonstrated that part of this vicious cycle may arise from cognitive impairment as a direct result of financial pressures.  The researchers found that thinking about finances reduced performance on cognitive tasks in participants who were struggling, but not in those who were financially comfortable.  Furthermore, farmers demonstrated poorer cognitive performance before harvest, at a time of relative poverty, compared to after harvest when money was more abundant.

[hr]

Gut Behavior

2013 has definitely been the year of the gut microbiome! Studies have shown that diet affects the composition of trillions of microorganisms in the human gut, and there is also a great deal of evidence pointing towards the gut microbiome affecting an individual’s susceptibility to a number of diseases. Recently published in Cell, Hsiao and colleagues report that gut microbiota also affect behavior, specifically in autism spectrum disorder (ASD). Using a mouse model displaying ASD behavioral features, the researchers saw that probiotic treatment not only altered microbial composition, but also corrected gastrointestinal epithelial barrier defects and reduced leakage of metabolites, as demonstrated by an altered serum metabolomic profile. Additionally, a number of ASD behaviors were improved, including communication, anxiety, and sensorimotor behaviors. The researchers further showed that a particular metabolite abundant in ASD mice but lowered with probiotic treatment is the cause of certain behavioral abnormalities, indicating that gut bacteria-specific effects on the mammalian metabolome influence host behavior.
[hr]

Your skin – their home

A paper published in Nature examined the diversity of the fungal and bacterial communities that call our skin home. The analysis done in this study revealed that the physiologic attributes and topography of skin differentially shape these two microbial communities. The study opens the door for studying how the pathogenic and commensal fungal and bacterial communities interact with each other and how it affects the maintenance of human health.

[hr]

Discovery of new male-female interaction can help control malaria

A study published in PLOS Biology provided the first demonstration of an interaction between a male allohormone and a female protein in insects.  The identification of a previously uncharacterized reproductive pathway in A. Gambiae has promise for the development of tools to control malaria-transmitting mosquito populations and interfere with the mating-induced pathway of oogenesis, which may have an effect on the development of Plasmodium malaria parasites.

[box style = “rounded”]Chris adds: “My friend chose this paper to present at journal club one week, because he thought it was well written, interesting etc etc. Unbeknownst to him, one of the paper’s authors was visiting us at the time. We sit down for journal club and one of the PIs comes in, sees the guy and exclaims (with mock exasperation) “you can’t be here!” Me and the presenter look at one another, confused. He presents journal club, and luckily enough, the paper is so well written, that he can’t really criticize it!” [/box]

[hr]

Using grapefruit to deliver chemotherapy

Published in Nature Communications, this paper describes how nanoparticles can be made from edible grapefruit lipids and used to deliver different types of therapeutic agents, including medicinal compounds, short interfering RNA, DNA expression vectors, and proteins to different types of cells. Grapefruit-derived nanovectors demonstrated the ability to inhibit tumor growth in two tumor animal models. Moreover, the grapefruit nanoparticles used in this study had no detectable toxic effects, could be manipulated or modified to target specific cells/ tissues, and were economical to create. Grapefruits may have a bad reputation for interfering with drugs, but perhaps in the future we will be using grapefruit products to deliver drugs more effectively!

[hr]

Getting CLARITY

In May, a new technique called CLARITY to effectively make tissue transparent through a new fixation technique was published in Nature. This new process has allowed them to clearly see neuron connection networks not possible before because they can now view the networks in thicker tissue sections. This new advancement will help researchers be able to better map the brain, but this new technology can also be to create 3-D images of other tissues such as cancer. This new ability allows us to gain better insight into the macroscopic networks within a specific tissue type.

[hr]

Crispier genome-editing

This year, the CRISPR technique was developed as an efficient gene-targeting method. The benefit of this method over the use of TALENS or a zinc-finger knockout is it allows for the rapid generation of mice that have multiple genetic mutations in just one step. The following review gives even more information on this new technique and compares its usefulness to that of TALENS and zinc-finger knockouts. Further, just couple of weeks ago, two back-to-back studies in Cell Stem Cell using the CRISPR-Cas9 system to cure diseases in mice and human stem cells.  In the first study the system was used in mice to correct the Crygc gene that causes cataracts; in the second study the CRSPR-Cas9 system was used to correct the CFTR locus in cultured intestinal stem cells of CF patients. These findings serve as a proof-of-concept that diseases caused by a single mutation can be “fixed” with genome editing using the CRISPR-Cas9 system.

What was your favorite paper this year? Let us know! And of course – use Scizzle to stay on top of your favorite topics and authors.

So What Is It You Do, Exactly?

Tips and anecdotes on how to explain your science over the holiday dinner.

 

The Scizzle Team

 

Pick your project carefully

Chris works on a malaria vector and how it survives by blood-feeding, so he usually just says he’s trying to kill all the malaria mosquitoes. After that people rarely have follow up questions, since it’s a goal people can easily get behind!

[box style=”rounded”]Scizzle tip: Work on a disease everyone knows[/box]

Be prepared

Stephanie says that everyone should have an elevator pitch ready to pull out of their back pocket at a moment’s notice! Start working on your 3 minute miracle as soon as you’ve picked up a pipette and learned which way to point it.

[box style=”rounded”]Scizzle tip: This doubles as a great networking tool![/box]

Try once (and you might never get asked again)

Robert’s first lab experience was during a summer internship, and he shares: for the first month I was working there I was commuting from the suburbs to NYC to work. Since my dad was retired at the time he usually drove me in and would pick me up when I was done. When he picked me up he would always ask me about what I had done that day. In the beginning it was simple stuff to explain like sectioning kidneys, doing dissections, etc. One day I had done PCR for the first time and when my dad asked me what I did that day I went on the spiel about PCR. How you have DNA and primers and taq polymerase and dNTPs. I explained it as simply as I could think going one step at a time and slowly and ended with “basically, its like photocopying DNA and we use it to see what genes the mice have”. After a pause my dad said to me “I have no idea what you were just talking about.” I offered to try to explain again but he politely declined and that was the last time he asked me about what I did in lab.

[box style=”rounded”]Scizzle tip: Don’t use fancy words[/box]

Tell them what you do

Celine suggests to focus on what she does rather than what she studies: if I tell my people that I work on cortical interneuron circuits their eyes glaze over, but if I say that I use a tiny electrode to listen to neurons and observe their behavior, people are actually quite interested.  A good visual helps a lot too; for a long time I had a picture on my phone from my electrophysiology rig monitor showing neurons and a blood vessel, and even people who don’t care about science at all thought it was pretty neat.

[box style=”rounded”]Scizzle tip: Have good visuals! (Just make sure it’s not gross)[/box]

What’s your model organism?

Thalyana’s words of wisdom for those studying model organisms: be careful how you explain what organism you are studying. For example, I study the nematode C. elegans, and I made the mistake of saying “I study worms” at a family get-together. I spent the rest of the party explaining that I do not spend my day digging in the soil for earthworms! Also, if you study yeast, make sure to point out that you are not brewing beer in the lab (…unless you are!).

[box style=”rounded”]Scizzle tip: Choose your words! C.Elegans sounds way more sophisticated than worms[/box]

Start with something they know

Joseph tells us the importance of a few key words: I recently tried to explain my research on the evolution of developmental mechanisms in moss, and found myself seeing an increasingly confused face in front of me.  I was then helpfully notified that, while delving into details about making mutant lines and tracking cell divisions, I had left the word “evolution” out of my explanation!  This was a great learning experience; there are words that your mother/father/aunt/cousin has probably heard in the news that relate to what it is you do, so make sure to use them!

[box style=”rounded”]Scizzle tip: Use those buzzwords![/box]

Keep it Real

Zach tries to relate his work to human problems and interactions: as a computer scientist, my work often has broad applications, so I look for the human element – an analogy to a common problem or familiar pain often helps people to understand how my work is useful. It helps to anthropomorphize as well – presenting my work as teaching a silly, ignorant computer how to complete a useful task is often easier than trying to convey the set of abstractions and mechanical and electrical processes that are the true nature of my work.

[box style=”rounded”]Scizzle tip: Find the human element[/box]

 

Do you have a tip on how to deal with the question or a funny story? Please share!

Marathon + grad school ≠ impossible!

 

Elaine To

Graduate students are expected to spend a significant amount of time in lab running experiments and reading literature. Marathon training is a large time commitment, and very necessary to ensure a strong finish and avoid injury. It seems impossible that someone who isn’t already an elite runner would attempt to train for a full marathon (26.2 miles or 42.2 km) while working towards a PhD. And yet, that is my current goal!

It all started approximately one year ago when my new year resolution was to push myself into shape. Previously, working out and staying fit had not been priorities in my life. The marathon team at my university had just added a half marathon (13.1 miles or 21.1 km) training plan and I wanted to set a long term goal for myself that I wasn’t sure I would accomplish and then accomplish it (hopefully). During group runs I figured it wouldn’t matter that I ran slower than the rest of them since they’d be running more miles anyway. The first 4 mile training run very nearly discouraged me from the entire thing until I realized it wasn’t about running fast: it’s about running at a comfortable pace that allows you to finish. In that way, distance running became a metaphor for graduate school for me.

Since then I’ve run two half marathons, but after the second one I realized I needed to aim for the next challenge. Hence, I’m now training for my first full marathon! I run slightly faster now than when I first started, but it’s still slower than the rest of the running team, so my training time commitment sometimes feels greater. We’ll have a short series here on Scizzle’s blog following me as I progress over the next couple months and providing tips on how to juggle training, lab, and life! How is this different from the rest of the marathon blogs out there? 1) I am far from an elite runner and 2) I’m a graduate student!

So if your new year resolutions include taking on running then here are 3 tips for starting on the path to accomplish your goal:

[ordered_list style=”upper-roman”]

  1. Find a running group to run with. Not only do they help hold you to the training plan when experiments get in the way, but they can also show you a variety of nice running trails in the area. If there isn’t a group associated with your academic institution, local running stores can often make recommendations.
  2. Buy a good pair of running shoes from a runner’s specialty store. Yes, it will be expensive, but the store will analyze your running gait and recommend the best shoe to help you avoid injuries. It’s a worthwhile investment especially since you can also wear the shoes into lab.
  3. Make sure you have clothing appropriate for the weather you’ll be training in. Many races take place in the spring and autumn, which means training occurs in the winter or summer. Depending where you live, this can range from comfortable to downright painful.

[/ordered_list]

As for me? I’m currently running one long run every weekend and supplementing with 1-2 shorter runs during the week when I get out of lab early enough or during long incubations. This past Saturday we did 11 miles and we’ll soon be running distances greater than I’ve ever run before. Stay tuned!

Too Young for Cancer?

 

Neeley Remmers

Officially, cancer awareness month is over, but honestly where this disease is concerned, we should constantly strive to increase cancer awareness amongst the general public. For this post, I have decided to highlight one area of cancer that gets very little attention, cancer in adolescents and young adults (persons ranging between the ages of 15-39 years) or AYAs for short. Like most, initially I had the bias that cancer in persons under the age of 50 and older than 12 rarely occurred. However, more than 72,000 AYAs learn they have cancer each year in the United States, a number up to seven times larger than the number of children under the age of 15 that are diagnosed with cancer (taken from American Cancer Society’s Facts and Figures). Cancers that are common in AYAs often are rare in the traditional adult oncology clinic—germ cell tumors, leukemias and lymphomas, melanoma, thyroid cancer, and sarcomas, but we are seeing more and more AYAs diagnosed with the more common adult cancers such as breast, colon, ovarian and prostate cancer as well. Unfortunately, AYAs face a number of unique medical issues that adults do not when seeking treatment for cancer. First and foremost, diagnosis often comes late because many physicians rarely think that an AYA displaying the signs and symptoms of cancer could actually have cancer. This alone makes treatment more difficult as cancers typically become more resistant to therapies as they advance.

In addition to receiving late diagnosis, it is becoming evident that cancers in AYAs are genetically different from those seen in either children or adults. This leads to AYA patients receiving treatments that may not be the most effective for their cancer. This is has become most evident in acute lymphoblastic leukemia (ALL) where recent clinical trials indicate that in some cases, AYA patients with ALL may have better outcomes when treated with pediatric regimens versus adult regimens. Work done by Dr. Christine Harrison of Newcastle University in the United Kingdom has shown that some AYAs with ALL have genetic changes that are typical of younger patients, whereas others have previously unknown alterations (Moorman et al., J Clinical Oncology. 2012). Another current, ongoing study done by a team lead by Dr. Cheryl Willman, director of the University of New Mexico Cancer Center, where tumor samples from 500 ALL tumors taken from children, teens, and AYAs has provided some indication that genetic differences do in fact occur in ALL based on patient age. For instance, some AYA tumors have genetic alterations that are often seen in older children with ALL who are at high risk of relapse. (AYAs and high-risk older pediatric patients tend to have worse outcomes than the vast majority of younger children with ALL.)

A similar comparative study has begun for AYAs with colorectal cancer by Dr. Anna Franklin at MD Anderson and her team of colleagues at MD Anderson and Colorado, and preliminary results from this study also indicate that genetic differences occur between tumors from AYAs versus tumors from adults. However, this phenomenon is not seen in all types of tumors affecting AYAs. For example, genetic differences were not seen in breast cancer cases even though AYAs are diagnosed with more aggressive subtype than older patients; however, the reasoning for this discrepancy is not yet fully understood. More research is needed to gain a better understanding of AYA tumor biology. These biological differences may require different treatment strategies in AYAs as compared to children or adults to achieve the best possible outcomes.

Finally, AYAs have more long-term health effects that arise from either latent cancer cells or are a side-effect of their treatment. Some of these health effects include being put at a higher risk for developing cataracts, hearing loss, chronic pain, limb amputation, hypopituitarism, loss of bone mass, and cardiac problems to name a few. Survivors of AYA cancers, like their pediatric counterparts, are also at increased risk for life-threatening problems such as second primary cancers and psychiatric issues such as post-traumatic stress disorder and depression. Unfortunately, many AYA survivors are often unaware of or underestimate their heightened risk for these late health effects; the same is true of many of the doctors and health care providers these survivors see after leaving the confines of active cancer treatment and follow-up.

The reality of AYA cancer is that this is a highly understudied field that is in need of more researchers and clinicians help fill the knowledge gaps to improve treatments for this patient group. Additionally, greater awareness amongst AYAs and physicians alike is needed so we can begin to diagnose their cancers while they are still at an early stage and the importance of realizing that AYA survivors are at a much higher risk for additional health complications later in life.

The information for this post was taken from the NCI website www.cancer.gov under their page dedicated to cancers in adolescents and young adults.