Sleep Your Way to Enhanced Learning Skills

 

In the background is an entorhinal cortex neuron that was studied. The blue-green trace shows neocortical slow oscillation while the yellow trace shows the persistent activity of entorhinal corticalneuron, even when the inputs from neocortex were silent. (Credit: Mayank Mehta)

Pulling and “all-nighter” before a test may become the preferred method of learning – if your all-nighter consists of actually sleeping.  Studies have found that your brain processes information while you sleep, enhancing your memory when awake.

Scientists at UCLA studied the activity of the brain region involved with learning by examining three connected brain regions in mice – the neocortex (new brain), the hippocampus (old brain), and the entorhinal cortex (intermediate brain that connects the new and old). Previous studies have shown that dialogue between the new and old brain is critical for memory formation. This research team measured the activity of single neurons from each of these areas of the brain to determine which region was activating the other areas and how the activation spread. They were surprised to discover that the entorhinal cortex showed persistent activity at all times – during waking hours and during sleep. The entorhinal neurons were “behaving as if they were remembering something even under anesthesia.”

People spend one-third of their lives sleeping, and studies have shown that interrupted sleep or lack of sleep can result in adverse effects on one’s health. Just as sleep plays a vital role in promoting physical health, the results of this study show that good sleeping habits can have beneficial effects on memory and learning capability as well.

Northwestern University researchers studied how memories can be reactivated and strengthened during sleep through external stimulation. The participants in this study were taught to play two different musical tunes with key presses. The participants then took a 90-minute nap, at which time only one of the two tunes was played throughout the sleep period. The participants’ electrical brain activity was recorded by electroencephalography (EEG). This method ensured that the music was presented during the slow-wave sleep, a stage linked to strengthening memories. The results showed the participants made fewer errors when playing back the tune that was presented while they slept. This study showed that memory is strengthened for something you’ve already learned by reactivating the information while sleeping. Senior author of this study, Ken Paller, stated, “External stimulation during sleep can influence a complex skill.” 

Researchers from Michigan State University have been investigating how people may be learning while they sleep due to an unconscious form of memory that is not yet well understood. They suspect this is a separate form of memory that processes information without one’s awareness. Kimberly Fenn, lead researcher, stated, “Simply improving your sleep could potentially improve your performance in the classroom.” A research study from the University of Notre Dame shows that going to sleep shortly after learning something new is most effective for processing and recalling that material.

Scientists have studied the effects of sleep through countless research studies and have discovered that good sleeping habits provide many health benefits. More recently researchers have been studying the relationship between sleep and brain function. These studies have also shown a positive connection between sleep and the ability to process information and enhance your memory when awake.

http://www.sciencedaily.com/releases/2012/10/121007134729.htm 

 

The Contagious Yawn

Is yawning really contagious? When you see someone yawn, do you yawn too? Have you ever thought about the conditions in which you yawn? For example, do you tend to yawn more when you’re tired, when you’re around those who are close to you, or do you yawn any time you see someone else yawn no matter what? Contagious yawning is an interesting thing to think about. For most people, they think if they see someone yawning, they will yawn too within seconds later. However, behaviors show that we can’t catch a yawn from just anyone. Yawning happens more commonly between people who are close to us. We tend to catch the yawns of family members and friends, and the yawns of strangers don’t always phase us.

The reason that we may yawn after someone we are close to yawns, is because yawning and empathy have been shown to be linked together. Empathy is having the ability to being able to relate to another’s feelings and emotions. Studies have shown this in humans and other animals such as the chimpanzee. Researchers have presented videos of yawning chimpanzees and also chimpanzees who aren’t yawning to humans. After the videos, they focused on the humans’ yawning responses, the context of relationships, and compared the responses of males and females. Researchers had found that the gender of the yawning individual in the video played a big role in its responsive yawners. The studies show that high amounts of males had yawned when they saw other males yawning, and there were low amounts of males yawning when females yawned as well as low amounts of females yawning when they saw either gender yawning.

Another study has found that dogs were able to catch yawns from their owners, which also shows that yawning is in fact an empathy-based response. Research in the study shows that when dogs heard the sound of a human yawn instead of actually seeing the yawn, it made yawning seem more contagious in the dogs. The study used family and friends that the dogs recognized as well as including strangers in the experiment. Findings had shown that the dogs were prone to yawn more when they heard familiar yawns than when they heard unfamiliar yawns, which is a good study that proves that yawning can be contagious between those who are close to us.

However, not all yawns are contagious ones, but those that are contagious usually are started from seeing or hearing a yawn first. Just like many have probably heard before, research has indicated that yawning may be caused due to a temperature change of the brain. For example, when our body temperature begins to fall, we start to feel tired, which causes us to yawn. While I was researching this topic of “contagious yawning” and writing this blog, I must say that I myself couldn't stop yawning after reading about it and thinking about the concept of yawning. I believe that is proof to show that yawning is contagious. I bet if you aren’t yawning yet, you might be very shortly after thinking about whether or not yawning is contagious.

http://www.sciencedaily.com/releases/2011/12/111212092649.htm

http://sciencefriday.com/blogs/07/17/2012/the-contagious-nature-of-yawning.html?audience=2&series=2

 

 

 

 

 

Dysfunction of Memory B Cells in HIV Infected Persons

Dysfunction of Memory B Cells in HIV Infected Persons

Written by Lisa M Roberts

              The working definition of the lymphatic system as provided by the website Patients Against Lymphoma (2004) is as follows,

                         “The lymphatic system consists of organs, ducts and nodes. It transports a watery clear fluid called lymph.  This fluid distributes immune cells and other factors throughout the body.  It also interacts with the blood circulatory system to drain fluid from cells and tissues.  The lymphatic system contains immune cells called lymphocytes, which protect the body against antigens (viruses, bacteria, etc.) that invade the body “(Lymphoma.org, 2004).

     More specifically the lymphatic system is composed of several bodily organs.  The bone marrow, spleen, thymus gland, and lymph nodes are all a part of this system.  The Text book The Language of Medicine describes the lymphatic system as an immune system of the Body (Saunders, 2007. P.531).   It is a specialized system which defends against invasive antigens.  The lymphatic system includes lymphoid organs, their products (lymphocytes and antibodies) and macrophages (phagocytes) which are used to resist foreign organisms and toxins, to keep tissues and organs undamaged by hostile agents or invaders (Saunders, 2007. P.531).  

     The breakdown of the lymphatic system is a precursor to immune deficiency and the many diseases that prey on the body.  Immune reaction is vital to an organism’s survival. Millions of simple bacterial and fungal antigens would wreak havoc in our bodies without the intervention of the lymphatic reaction of phagocytes and macrophages which fight the infection in the first place and then sweep up the debris.  There are also other disease fighting cells such as natural killer T cells and memory B cells with specialized functions within the lymphatic system. These cells go after hostile antigens killing and destroying tumor and viraly affected cells.

            Current research confirms that persons infected with the HIV-1 virus are subject to lymphatic system damage within 14 – 27 days of the initial infection (Levesque, 2009).  The HIV-1 virus extensively damages the immune system by targeting B cells.  Lymphatic B cells are phenotypically damaged and their levels reduced in the host organism. Once compromised  T lymphocytes such as Helper T cells and B cells are unable to respond properly to antigenic substances.  This leaves the organism open to systemic damage and disease.

            The B cell lymphocyte originates within the bone marrow.  It’s major function is to produce antibodies for an healthy immune response to pathogenic invaders.  The B cell is a precursor to the plasma cell. The Plasma cell generates the B memory cells which incite a rapid response to an antigen that has been encountered at least once before.  The patients with HIV-1 infection have damaged memory B cells which have been primed for apoptosis (De Milito, 2004).  The memory cells are not only reduced in number they are phenotypically altered, damaged and permanently impaired.  They no longer maintain the ability to recognize antigens that have been dormant in the body or that have been previously encountered.  This gives rise to invasion of the organism by secondary and opportunistic infection and disease that the organism would normally fight off with a rapid immune response.  In an article for the Journal of Current HIV Research, A. De Milito states that the cellular and humoral arms of the immune system are no longer able to control infection and that this results in the inability for lymphocytes to function thus creating the avenue of pathogenic opportunistic invasion.  De Milito further states that,

     “ a pathological feature induced by the persistent viral replication is the aberrant activation of cells of the immune system.  Among these cells, B lymphocytes are severly damaged and show signs of functional alterations.” (De Milito, 2004).

     After researching  peer reviewed medical journal articles from Pubmed it was discovered that the researched data confirmed the information reported in the De Militos research for  Duke University.  Research has shown that within human patients which are infected with HIV-1 the memory B cells are quickly damaged, altered and permanently impaired in the host organism due to HIV-1 virus related pathogenic mechanisms (De Milito, 2004).  Research data also confirms that this gives rise to increased infection by secondary and opportunistic antigens and disease causing agents which continue to weaken the comprimised human organism.  The research data further confirmed that the altering of the memory B cell function and structure somehow enabled the HIV-1 virus to replicate freely without evoking a response from the antibodies circulating within the hosts immune response system. The data also pointed to the inability to regenerate the B cell once it is damaged by the interactions with the HIV-1 virus despite treatment with antiretroviral therapy (Titanji et al, 2006).  Though early treatment with antiretroviral therapy did restore T cell counts in the infected patients, the B cells and their memory B cell counterparts were never regenerated to normal phenotypic or functional levels within the infected individual  (Titanji et al , 2006).

     Researchers are still looking for further data to aid in the understanding of the process of the HIV-1 virus and it’s replication processes within the human organism.  A furthering of scientific research may one day bring about a cure for the incredibly complex process of organism destruction and ultimately death brought about by HIV-1 infection.

De Milito, A. (2004). B lymphocyte dysfunctions in HIV infection. Current HIV Research, Jan;2910: 11-21. Retrieved on October 13, 2012 from Pubmed.

Levesque MC, Moody MA, Hwang KK, Marshall DJ, Whitesides JF, Amos JD, et. AL. (2009). Polyclonal B cell differentiation and loss of gastrointestinal tract germinal centers in the earliest stages of HIV-1 infection. Procedings of the National Academy of Science. Jul 7;6(7):e1000107. Retrieved on September 13, 2012 from Pubmed.

Lymphatic System (2004) Patients Against Lymphoma, retrieved October 30, 2012 from Lymphoma.org.

Titanji K, De milito, A, Cagigi A, Thorstensson R, Grutzmeier S, Atlas A, et. Al. (2006). Loss of memory B cells impairs maintenance of long-term serologic memory during HIV-1 infection. Blood, Sep 1; 108(5): 1580-7. Retrieved on October 13, 2012 from Pubmed.

Why We Age.

            The concept of why we age has never occurred to me. I always knew aging was natural, but I have never wondered why it is natural. After doing some research, i have found that there are quite a few scientific and psychological theories on this topic. On a biological stand point, there are still quite a few, so i am going to sum up a few of them.
            There is the “DNA and Genetics theory” which explains aging based on the programming of our DNA. Based on many external factors, we can either speed up or slow down DNA damage. A theory called “Telomerase Theory of Aging” by scientists at Geron Corporation, and it explains how, every time our cells divide, the telomeres shorten and it is believed that it causes DNA damage because it causes the cells to duplicate incorrectly. Dr. Don Kleinsek, a researcher trying to determine the reasoning for aging, believes that we may be able to inject the correct hormone, in order to help repair our genes. In order to do that, researchers would need to know what each of the telomeres are responsible for. 
            Another theory, first introduces by Professor Vladimir Dilman and Ward Dean, called “ The neuroendoctrine Theory”, which claims wear and tear on the neuroendocrine system is what causes aging.  According to this theory, the hypothalamus and it’s function is what ages us.  The hypothalamus is a small part of our brain that controls the releasing of hormones in our glands and organs. After time, though, the hypothalamus losses its precision and regulatory abilities. Also, the receptors in our body that take in hormones, become less sensitive to the individual hormones, after time.
             There are theories as to why the hypothalamus’s function declines after time. One theory is that the hypothalamus is damaged by Cortisol, a hormone made from our adrenalin glands in the kidneys. Cortisol is a hormone that increases with age, and if it is damaging to the hypothalamus, it becomes a cycle of damage being done to the hypothalamus. Dr. Dean believes that hormone replacement for the hormones in the hypothalamus could open up many doors for improving , controlling, and balancing our endocrine system.
               The next theory is the "Free Radical Theory" and it was started by Denham Herman MD. The name "free radical" refers to a molecule that has an extra electron, and an extra negative charge. Because of the extra electron, the molecule sticks to another molecule and tries to steal its electrons. when this happens, the molecule that had an exctron taken from it, becomes a free radical, and the process starts over. Free radicals often times damage cell membranes and from that comes metabolic waste which, when accumulated, can cause damage to our cells communication, it can disrupt the synthesis of our DNA, RNA, and protein, it can lower our energy levels and it can negatively affect other chemicals and their processes in our bodies. On the other hand, Free radicals can be transformed by free-radical-scavengers. Free radical scavengers are, what we call, anti-oxidants. They can bind to  free radicals, and stabilize them. Though there are many more sources and much more information on this topic, this is a brief summary of a few of the theories as to why we age.


All of my information was found at:  http://www.antiaging-systems.com/articles/160-theories-of-aging


-Renee Gulick. 

The Genetics of Addiction

When scientists are looking for "addiction genes," they are looking for the biological and environmental differences that make a person more or less susceptible to addiction.  It might be harder for certain people with certain genes to quit something once they have already started. The question is why are some people so easily addicted to drugs and/or alcohol, while other people can party and never do it again?  Some people may experience more severe withdrawal symptoms if they try to quit a drug, then others, and some have no withdrawal systems at all. We sometimes think it's a simple matter of willpower or your train of thought, but the fact is, it has more to do with the roll of the genetics. Also the factors that make it harder to become addicted also may be genetic.

            Scientists and researchers will never find just one single addiction gene.  Addiction has been proven as the result of many interacting genes.  Of course, personal experience, including childhood experiences, environmental and social influences matter in the role of addiction. Researchers have been constructing pedigrees of large families with addiction problems as a first step to understanding the roles and factors of addiction.  A pedigree can reveal whether or not a certain trait has a genetic component.  That means, whether or not the trait is passed down from parent to child by way of genes. But because addiction is influenced by multiple genes as well as many other risk factors, this can be a complicated process. Using this pedigree data, researchers and scientists can begin to track down genes. Researchers begin by comparing certain DNA sequences of individuals who are addicted with those individuals who are not. They can then narrow down the possibilities to identify a small number of so-called "candidate genes" for addiction. But not every addict will carry the same gene, and not every person who carries an addiction gene will exhibit the same trait or get addicted to the same thing, or even get addicted to anything at all. For example, the A1 allele of the dopamine receptor DRD2 gene is much more common in people addicted to alcohol.  Most of these genes wouldn't even have been discovered without the use of animal studies, mice preferably. These studies on done on mice shows that the increased expression of the Mpdz gene experience less withdrawal symptoms from barbiturates then mice without this gene. Also, certain studies show that people that are non-smokers are more likely to carry a protective gene, CYP2A6, which causes them to feel more nausea and dizziness from smoking cigarettes. In alcoholism, it is rare for people with two copies of the ALDH*2 gene to even become alcoholics, and people without this gene seem to be more susceptible to this disease. In both animals and humans, individuals who are less sensitive to these unpleasant effects have a higher rate of addiction. Regions on chromosomes 4 and 5 that govern the neurotransmitter GABA appear to play a key role in determining alcohol tolerance (http://money.cnn.com/2009/10/16/news/genes_addiction.fortune/index.htm).

This study has taught me that addiction happens because of many factors, whether its genetics, environmental or situational. The fact or the matter is that addiction is a disease.  Your surroundings, genetics and experiences and maybe just a little will power, affect your susceptibility to become addicted.

(http://money.cnn.com/2009/10/16/news/genes_addiction.fortune/index.htm)

Man Made Cows

http://www.nature.com/news/animals-engineered-with-pinpoint-accuracy-1.11506

 

Animals engineered with pinpoint accuracy

More accurate genetic modification has created allergen-free cow's milk and pigs that could serve as a model for atherosclerosis. Amy Maxmen 02 October 2012

                I found a very interesting article that I think you will all like and find intriguing as I did. I also found it especially exciting to be able to read a biology article and be able to make sense of all the terms they used.  Anyways there are scientists that have worked on creating animals which is called animal biotechnology.  Which to me sounds a lot like a Frankenstein reproduction of animals, but the reasoning behind it is quite interesting. Researchers have been working toward blocking a secretion found in cow’s milk that produces an allergy-inducing protein. Successfully these researchers accurately blocked its allergy- inducing protein production using the technique of RNA interference. Although they had attempted other methods such as,” replacing the gene encoding beta-lactoglobulin with a defective form, but this proved nearly impossible because the techniques available to introduce foreign genes into animal genomes were not precise, and misplaced genes failed to express themselves correctly,”(Maxmen). However, this did lead them to experimenting with RNA interference. “RNA interference (RNAi) and TALENs are more accurate at targeting the gene in question than are earlier genetic engineering techniques,” (Maxmen).  Whereas RNA interference was useful in helping eliminate the protein. It could not get rid of the protein entirely without the help from TALENs which speed up the process and are used to eliminate beta-lactoglobulin.  “RNAi cannot eliminate the protein completely because some messenger RNA slips past the blockade, but each TALEN targets a specific DNA sequence in the genome and cuts it. As the body repairs the break, mutations are often introduced that render the targeted gene non-functional,” (Maxmen).

                So much enthusiasm has been behind this type of research. I myself find myself stuck on the fence feeling nervous debating if this is good thing or not.  The whole reason behind animal biotechnology was to produce healthier and safer food that would be available in large quantities to the public that would support healthy human development. So many people worry about what they are getting at their local grocery store, and they should. It wasn’t too long ago that there was an outbreak of mad cow disease which killed countless people. Never the less there have been plenty of support and investment that have gone into this type of research to help prevent cases like mad cow disease. And besides,” despite years of investment, almost no animal has been approved by regulatory agencies around the world,” (Maxmen). So how safe are these genetically made animals really? One of the researchers from this article even admits that he hasn’t even tried one of his cow’s milk because he isn’t allowed or permitted by New Zealand law. Furthermore this leads me to believe that this type of animal’s development is not safe for a reason. And if a researcher won’t even test his own product regardless of laws or permits it indicates that this gentlemen doesn’t really back and support his research a hundred percent.

Crossing Over to Blue Eyes

            When we were discussing crossing over, and genetics I was thinking about a question that I had when my daughter was born in 2010. I know that my daughter is a combination of mine and her father’s chromosomes and also our ancestor’s genes, generations and generations of science and biology combining to make up our family. I remember in high school learning that the brown eye gene was dominant over the blue eye gene, which made my question even more baffling. The question that I was going to bring up in class but I decided against is how is it that I am able to have a bi-racial daughter who is African-American and Caucasian and her father and I both have brown eyes, but she was given the most amazing blue eyes that I have seen on a bi-racial person. Now I know that there are blue eyes on both my mothers and fathers side, but not on her fathers’ side…when I was researching articles for this assignment, I came across this article that gave me a little bit better of an understanding. http://news.sciencemag.org/sciencenow/2008/02/01-01.html?ref=hp  “Don’t it Make Your Brown Eyes Blue?”  by Elizabeth Quill February 1, 2008.      

            I know that even though brown eyes dominate over blue eyes there is still a possibility that the offspring of two brown eyed parents can win the crossover and get the blue eyed gene. I was very shocked to get a chance to see the slight probability of this amazing gift unfold in my own daughter that I brought into this world. The HERC2 gene is what I have to thank for this incredible work of beauty, it turns out that this gene that all blue eyed individuals hold can all be traced back to 

a “single common ancestor that was born some 6,000 to 10,000 years ago.”
I know that is not common for infant babies to have blue eyes for the first few months of their lives, which is what I believed was the case in this situation, but a little over two years after the day I was blessed with my angel her eyes are still as gorgeous if not more so than the day she was put into my world. It amazes me that these pretty blue eyes are not only meant for people of European decent, but also that they would not be possible without a mutation of a gene. This mutation that I am speaking of took place somewhere in my family history, made me a part of but somehow managed to dodge my chemical make-up and hit my daughter, this is one of the many miracles of biology and science in general. I know that crossing over was the main function of this whole ordeal and I think that it is really cool to get a first-hand experience to back up this example and give me a reference to relate this terminology to. Desiree Everson