AP Biology class blog for discussing current research in Biology

Author: palindromeprincess

Low Iron, Sticky Blood, and Strokes

Photo taken by BruceBlaus

Photo taken by BruceBlaus

Scientists at Imperial College London discovered that low iron levels make blood “stickier” and thus, result in a higher risk of having a stroke.  The most common type of stroke, ischaemic stroke, is a result of a lack of blood supply to the brain caused by small clots.  These researchers found that iron deficiency increases stickiness of platelets, which cause clotting when stuck together (original article).  This connection between iron deficiency and stickier blood was made previously, but its implications are just now being identified.

In this recent study, about 500 patients with a disease called hereditary haemorrhagic telangiectasia (HHT) were studied because their condition allows small blood clots to travel to the brain more often than clots in people without the condition.  The patients with low iron were more likely to have a stroke, and their platelets stuck together to form a clot more quickly than those of patients with higher iron levels.  More specifically, having a moderately low iron level (about 6 micromoles/liter) about doubled the risk of stroke when compared to the risk with a normal iron level.  This is a strong start to proving the link between iron levels and strokes, but more research must be done to fully prove the connection because there are more steps that occur between the clot forming and the stroke occurring.

Scientists are hoping that the newly discovered implications of this research could help lower the risk of stroke in high-risk patients through the monitoring and regulation of iron levels.  Could simply raising a person’s iron level help prevent strokes? I believe that further research will reveal a more complex solution involving a process that occurs between the clotting and the actual stroke.

Sleeping: Switch off the Lights, Switch on the Neurons


Photo taken by André Karwath

Photo taken by André Karwath

Scientists at Oxford University’s Centre for Neural Circuits and Behaviour “identified the switch in the brain that sends us off to sleep”  (see original article) by doing a study on fruit flies (Drosophilia).  This part of the brain had been discovered in 2011 (see this article about the discovery), but the new research identifies more specifically the molecules and sleep-causing cells involved. 

The switch (which is made of several molecules) in the fly brain is likely similar to the switch in the human brain because both species have a similar group of sleep neurons.  This switch regulates the neurons that cause organisms to sleep (the neurons that are targets of anesthetics).   The sleep neurons are active when the organism is tired and needs sleep (it is the result of these neurons being activated that causes sleep), and less active when it is well rested.  The switch or “homeostat” is one of two devices that regulate sleep (the other is the body clock that distinguishes night from day in humans). It records the hours a person is awake and then signals the neurons that cause sleep when the person needs to rest.    

In the study, flies were kept awake all night.  Regular flies slept more the next day, while the mutants could not do this.  The mutants were found to “nod off” (determined by the fact that flies stop moving when they sleep) and were found to have learning and memory issues.  In these mutants, researchers found a key molecular piece of the “sleep switch” and determined that it was broken.  This resulted in the neurons that cause sleep not being activated; this led to insomnia.

Now that the sleep switch has been “pinpointed”, what new drugs will be created to treat insomnia and other sleep disorders?  People are also wondering if this more specific discovery will help answer the larger question of why animals need sleep at all.  As someone who does not get much sleep, I find this new identification very interesting and relevant in the busy lives of people today.

The Perfect “Enzyme Cocktail”



Photo taken by Vincecate

There is currently a great desire worldwide to create fuels from plants (that are abundant and not eaten).  For background on this topic, click here.  This process is possible, but making the fuel is expensive, time consuming, and difficult.  However, chemists at the Department of Energy’s Pacific Northwest National Laboratory have done research to develop a new, highly improved method for procuring economical, more realistic biofuels.

The most crucial step in the biofuel production process (making fuel from plants such as corn stalks and switchgrass) is the break down of sugar polymers into monomers, which can then be made into fuel compounds.  Plants contain energy, which they store in their carbon bonds.  This energy can be converted to fuel if these bonds are broken.  However, lignocellulose, which holds the plants together structurally, is difficult to break apart.

Finding a more efficient way to break down the sugars in plants would greatly lower the cost of biofuel production.  Trichoderma reesei is a fungus that can “churn out enzymes that chew through molecules like complex sugars”.  Thus, the fungus produces many enzymes that can help to procure fuel from plants.  New research is being done to find which of these enzymes (called glycoside hydrolase) work most efficiently together and individually at different temperatures, pressures, and pH levels in an effort to reach maximum efficiency in the process.  Chemist Aaron Wright said, “Identifying exactly which enzymes are doing most of the work you need done is crucial for making this an economical process.”

This procedure of tracking each enzyme through each stage of a complicated process would normally take months to complete with regular enzyme testing (perhaps like the testing we did in class, but much more complex!).  However, Wright’s team created a chemical probe that allows intense testing to be accomplished in only a few days.

As the price and sources of gas are such common concerns today, I am curious to see if this experiment will come to fruition to produce an environmentally friendly, sustainable, efficient, and economical source of fuel.

Original Article

Regular Cell Activity Could Help Heal Wounds


Photo taken by EMW

Photo taken by EMW

Biologists already know that flaws in metabolic processes in mitochondria (such as cell respiration) cause aging in many cells and tissues.  Now, they are exploring the converse situation.  Scientists from the Stem Cell Program and Boston Children’s Hospital are doing research to see if the trait that allows young animals to easily repair and regenerate their tissues can be produced in adult animals.  A protein called Lin28a (shown in image) is active in embryonic stem cells, and when scientists reactivated this protein (by reactivating the Lin28 gene) in older animals, the animals were able toregrow soft tissues (cartilage, bone, skin).  Lin28a promotes this regrowth partially by improving metabolism in mitochondria as it increases the production of enzymes involved in the making of energy.  As we learned in class, we need free energy to grow and create new cells. In this way, “Lin28a helps generate the energy needed to stimulate and grow new tissues”.  Essentially, the enhancing of the regular energy making process that the mitochondria perform could lead to advanced “regenerative treatments”.  (Click here for a graphical abstract of this study that helps to better understand the ideas behind the research.)

Additionally, experiments have been done that show that activity in the mitochondria can be enhanced without the stimulation of Lin28a.  This implies that a “healing cocktail” could be created pharmacologically.  I find it fascinating to see how cell processes, such as those that we learned about in class, can have such major implications for the future of regenerative medication.  Will they create new, more efficient drugs to help heal wounds?

Original Article


New Information on DNA Repair Could Mean Better Cancer Treatments

Photo Taken by EMW

Photo Taken by EMW


It has been accepted that DNA repairs itself.  However, a discovery concerning how this process occurs could lead to more efficient, and thus less damaging, cancer treatments.  Medical researchers at the University of Alberta have expanded the knowledge that scientists have regarding two proteins: BRCA1 (shown in the image) and TopBP1.  These proteins were previously thought to play identical roles in the DNA repair process.  However, this team of researchers recently showed that BCRA1 searches for any damaged DNA and then signals for help, while TopBP1 searches for DNA damaged specifically due to a problem with the DNA replication process and then signals for help.

Cancer Treatment Improvements?

When DNA becomes too damaged, cancer results.  The new cancer DNA can then copy itself and spread.  New ideas concerning radiation therapy making the cancer DNA unable to repair itself and unable to replicate are arising with this new discovery about the DNA-repairing proteins’ roles.  For instance, once cancer cells are damaged, proteins try to fix them, renewing the cancer cells.  Treatment could potentially be targeted at these proteins to stop them from fixing the cancer DNA and allowing the replication process to continue, now that we more fully understand their functions.

I find it fascinating to see how a rather basic discovery can have such major outcomes, and I am curious to see if further research will determine if certain medication can affect these powerful proteins.  Are there any other potential benefits to this protein-related discovery?


Original Article

For more information about DNA damage and repair and the role of the TopBP1 protein, click here. (Section 4 on this link talks about the similarities between BRCA1 and TopBP1.)




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