Category Archives: Science Posts


Currently, there is a housefly buzzing around my head. Every single time it lands I attempt this futile clapping motion to destroy it. I fail. I fail time and time again. So, my question is, obviously, WHY CAN’T I HIT YOU!?

After a small amount of Google-sleuthing I found the answer here. It seems Drosophila contain a pair of large aptly named nerves, Giant Fiber. This bundle runs the entire length of the head and down to the thorax. At the endpoint it triggers the thoracic ganglion which then shoots elsewhere. What triggers this giant bundle to begin with? The eyes! It uses visual cues to initiate its escape sequence. I wonder why it would be associated with something like that…

Just an eye... NBDSo if the Giant Fibers end with the thoracic ganglion what happens next? The ganglion shoots the signal to the dorsal longitudinal muscle (DLM) and tergotrochanteral muscle (TTM or “jump muscles”). This moves two thing: the legs and the wings. What do the legs do? JUMP! Thus, the reason they’re called jump muscles. The wings do something a little more complex. Upon receiving a signal  the wings go from the closed position to the open position and slightly elevate. So really the one nerve bundle initiates a double whammy of legs and wings. The strange part is that the TTM does both of these functions. The DLM is only indirectly involved.

So the take away message is that a simple little pathway is why I can’t kill this damn fly.

Sidenote, the paper is a little dated as it was published in 1983 but the general workings are still the same.


Flies didn’t evolve around flyswatters. Gotcha.Owned.

Notch and Delta in a Nutshell

Cell signaling is a very important process within multi-cellular organisms. Yet, many people grossly misunderstand how cells could communicate with one another. During the Answers in Genesis conference that stopped by Morris last year, one individual was under the impression that “cellular e-mail” must exist. “Why? Well, because it must!” *sigh* So, the pathway that I’m going to look at is Notch. Why? Well, because I must!  It’s also pretty cool, I swear.

So here we have the Notch pathway. Notch is a transmembrane protein which means it goes straight through the cell membrane and protrudes on either side. This protein acts as a form of hair-trigger. When activated it cleaves the inside part which heads off to the nucleus to play with gene expression. Notch isn’t activated by just any protein flying into it, and this is where Delta comes into play. Now the specifics vary depending on species (humans don’t actually have Delta but it’s similar and therefore Delta-like) but the purpose remains relatively the same.

**Now, I’m grossly oversimplifying the Notch pathway. I do this not because the areas I’m overlooking are not important (they are!), but this is a neurology post and it’s far too easy to get bogged down in minutia of everything and overlook the cool stuff of one area. **

So Delta and Notch touch, part of Notch breaks off and heads off into the cell to make shenanigans. What does this shenaniganary have to do with cell signaling and the nervous system? These have two functions. One is to adhere the two cells to one another. The other function is in development, in this case neuro-development. Once the cell with Delta contacts the Notch cell the piece inside breaks off and heads for the nucleus. What it does here is stop the cell from differentiating while the Delta cell remains able to do so. Notch inhibits rather than induces. It’s a bit backwards from what you would expect, but the role of Notch in neural development is to say who cannot become neural tissue.  As for the Delta cell, eventually it will move out of the epithelial layer and differentiate into a neuroblast.

If you think about it, this makes sense. If something induces neural differentiation then something should also stop it to avoid something made entirely of nervous system. Now, I can’t emphasize enough that Notch does other things. Those things just reach beyond the scope of this class. This is just a quick look at how two little things poking out of a cell can have a big impact.

The Role of Neuroplasticity in Constraint-Induced Therapy

WOOHOO! I am finally done with my senior paper. As you may surmise from the title I chose to write it on the neuro-mechanics involved with CI therapy. It’s written with a more informal tone but nonetheless it still landed me high marks.  Comments, questions, and retweets (#revfrost) are always welcome. Enjoy!

ABSTRACT: The human brain is capable of extraordinary change. The impact of strokes can be devastating and often times seen as refractory. Constraint Induced (CI) therapy has proved beneficial in alleviating common symptoms caused by strokes. Recent evidence provides an insight in identifying the biological mechanisms exploited by CI-therapy: neurogenesis, gliosis, and synaptogenesis.

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Dynamic Neuroplasticity after Human Prefrontal Cortex Damage. In this article, the authors focused on the effects of a unilateral lesion within the prefrontal cortex. Human vision works upon a rather backwards system. Information from the left side of each eye moves toward the left occipital lobe to be analyzed. The right follows an identical pattern.

So essentially, two sides of the eyeball swap information between hemispheres. From here, the information is sent forward along the current hemisphere to be analyzed by the prefrontal cortex (PFC).Because what else would you expect from the brain? In a nutshell, the left and right fields of vision (of a single eye) are interpreted by different halves of the brain. This is where the problems begin to arise. If the lesion occupies the left PFC, what happens to that information? Does it simply get left unanalyzed and you lose that field in each eye?

In a static environment you could assume that the side affected by the lesion would lose greater processing for that side of the brain. However, if the brain were dynamic and could re-route the circuit, information from that field could have the potential to return. It seems that’s just what occurs but with a small cost. The information destined for the left PFC follows the tradition route back to the prefrontal cortex but stops short, makes a pass through the corpus callosum,  and arrives at the contralateral prefrontal cortex (right side). The right prefrontal cortex actually picks up the slack left from the damaged area. However, as this seems almost too good to be true, this is not the case under all conditions. When an object is detected in the affected field compensation occurs. Yet, when objects are present to both fields simultaneously the right PFC solely analyzes the information from the right field. In other words, the right PFC picks up the slack so long as it has no incoming information itself.

The brain undergoes this change after repeated exposure to left field stimuli on a trial-by-trial basis. While the left PFC never fully recovers, this example shows a rather interesting compensation mechanism that can be achieved plastically. Although the paper never actually discussed this, I can’t help but wonder about the underlying cellular changes associated with this feat. Currently my assumption would just be an increase in synapses (synaptogenesis) favoring the re-wiring across the corpus callosum and to the contralateral cortex. But that’s just my guess. If anyone has any thoughts to the contrary I would certainly be willing to entertain them.

Voytek, B., Davis, M., Yago, E., Barceló, F., Vogel, E., & Knight, R. (2010). Dynamic Neuroplasticity after Human Prefrontal Cortex Damage Neuron, 68 (3), 401-408 DOI: 10.1016/j.neuron.2010.09.018 

*UPDATE*: I figured using ResearchBlogger would be more efficient.

I Think, Therefore I Am

This was a piece written for our Developmental Biology final. I wrote this with the intention of pushing a radical, controversial concept that I had never seen before. This article does not necessarily reflect my own views. This was merely an assignment I had a bit of evil fun with. Enjoy!


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Innate Immunity: So Nice, They Made It Twice

People often use the phrase “do not reinvent the wheel” to describe using an existing method towards a new task rather than creating one anew. Evolution tends to follow a similar philosophy. Many changes utilize genetic toolkits that have long been present, tucked away in the genome of the organism. Sometimes these toolkits have already been used repeatedly for various traits. The common fruit fly (Drosophila melanogaster), a model test subject for over a century, has been scrutinized in remarkable detail to gain an understanding of molecular interactions and evolution. When researchers discovered the NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway in mammals that functioned remarkably similar to the Toll pathway in Drosophila it was assumed that the immunological pathways were homologous (e.g. using the same toolkit).

The NF-kB pathway establishes its importance due to its swift reaction time. Most transcription factors are synthesized as needed. Building a protein from scratch then applying it where

Figure 1: Contrasting transcription pathways between Drosophila and Mammals

needed takes a fair amount of time. Sometimes, like during a pathogenic invasion, the cell cannot survive long enough to produce these proteins. In the immune system these proteins can be constructed preemptively, bound, and inhibited in the cytosol for future use. The NF-kB pathway activates these stored proteins by cleaving the inhibiting molecule and thus allowing the transcription factor, NF-kB, to enter the nucleus. The Toll pathway operates, essentially, in the same fashion as NF-kB (Figure 1). However, Drosophila uses completely different proteins to ultimately provoke a similar immune response with Dorsal-related immunity factor (Dif ).

The Toll pathway plays another, yet significant role only found in Drosophila. After the egg is

Figure 2: The Toll-Dorsal Pathway in Drosophila melanogaster

fertilized it lays the foundation for the rest of development, ventral and dorsal (down and up). Upon fertilization, the ligand Spätzle (SPZ) is distributed across the perivitelline membrane (Figure 2a). From here, SPZ binds to the Toll receptors of cells maternally designated to become ventral. The Toll receptors set in motion a cascade that phosphorylates CACT (the inhibitor) which allows the transcription factor to promote the production of the protein Dorsal (Figure 2b).

These pathways were initially thought to have arisen from a common ancestor to both Drosophila and mammals. However, it seems this is only partially correct. Genomic research opened up new, previously unexplored areas to consider. This pathway did, initially, form in a Eumetazoan ancestor. This pathway was markedly underdeveloped and only contained a few components. When the bilateral lineage diverged into deuterostomes and protostomes the common pathway ended. From here, both NF-kB and Toll evolved independently through gene duplication.

These diverse differences between pathways give great insight to the evolutionary history of the circuit itself. In order to have diverged so far in composition yet retain similar function suggests the ancestral pathway to have been particularly modular. In other words, the ancestral pathway was constructed using multiple pieces (modules). This setup allows individual modules to be modified over time without removing the core process of the system. Drosophila slowly modified this pathway to affect larval development by introducing Dorsal and SPZ into the circuit. As a result, Drosophila is able to use a single genetic circuit for dual regulation.

In Biology, nothing is ever as simple as it appears to be. The subjects could range from immune response pathways and developmental regulation to simple autosomal point mutations, but more research is always needed. The NF-kB pathway was thought to be well known until just recently, yet new information radically altered our understanding of it. With additional research, who knows what we could uncover next?

Belvin, M. P., Anderson, K. V., 1996. A CONSERVED SIGNALING PATHWAY: The Drosophila Toll-Dorsal Pathway. Annual Review Cell Developmental Biology. 12, 396-416.

Lemaitre, B., 2004. The road to Toll. Nature Reviews Immunology. 4, 521-527.

Leulier, F., Lemaitre, B., 2008. Toll-like receptors — taking an evolutionary approach. Nature Reviews Genetics. 9, 165-178.

Waterhouse, R. M., Kriventseva, E. V., Meister, S., Xi, Z., Alvarez, K. S., Bartholomay, L. C., Barillas-Mury, C., Bian, G., Blandin, S., Christensen, B. M., Dong, Y., Jiang, H., Kanost, M. R., Koutsos, A. C., Levashina, E. A., Li, J., Ligoxygakis, P., MacCallum, R. M., Mayhew, G. F., Mendes, A., Michel, K., Osta, M. A., Paskewitz, S., Shin, S. W., Vlachou, D., Wang, L., Wei, W., Zheng, L., Zou, Z., Severson, D. W., Raikhel, A. S., Kafatos, F. C., Dimopoulos, G., Zdobnov, E. M., Christophides, G. K., 2007. Evolutionary Dynamics of Immune-Related Genes and Pathways in Disease-Vector Mosquitoes. Science. 316, 1738-1743.


Many people are familiar with Trisomy 21 in humans. Commonly known as Down Syndrome, Trisomy 21 severely affects human development via complex gene and environmental interactions. Genetically speaking, is this condition novel to humans? Or can this be seen in other primates? Most of the “great apes” contain 24 pairs of chromosomes, humans being the exception with 23. When compared, the two karyotypes  look strikingly similar. The only vast difference occurring on chromosome 2. From the diagram below, the human chromosome 21 and the great ape chromosome 22 look remarkably similar. Documented cases of Trisomy 22 in chimpanzees have been seen as far back as 1969. With the additional #22, symptoms parallel to Down Syndrome appeared. Continue reading

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