*Red Numbered footnotes (1) are links that will take you to the sites that were quoted/referred to. They are sited in MLA format below.
Open Itunes. Play your favorite song. Close your eyes and just listen. Soak up every single component the music offers to you. Are the lyrics what makes this song your favorite? The rhythm? The tune? Or is it the melody that sews these notes as a favorite? Without all that, what would be left?
The beats of any given song in music are very much like the long intergenic non-coding RNAs (lincRNAs) that have been pushed aside in the field genetics - necessary for the whole but rarely noticed. The term intergenic refers to a sequence of DNA that do not hold genes but are found between clusters of DNA that do. Non-coding RNA (ncRNA) is defined as a RNA molecule that is not translated to proteins. Because of this, until recent studies and researches, scientists have overseen the full potential, importance and function of these non-coding genes. One of these ncRNAs that scientists have classified as "junk" are the lincRNAs. Recent researches contradict this classification as lincRNA's have now been proven to carry out essential functions for organisms such as guiding proteins to their attachment sites on specific RNAs/DNAs , as well as organizing the pluripotency of embryonic stem cells.(1) But even with these functions necessary for life, primitive discoveries a relationship between this particular ncRNA and the causation of cancer due to another one of it's functions of regulating the process of rapid cell growth, or cell profileration.
Why I refer to this discovery as primitive is because scientists have only recently decided that these lincRNA's are not worthless. Currently studying lincRNA, assistant professor of Stem Cell and Regerative Biology
at Harvard University, John L. Rinn stated through his research, the Rinn Lab(2), that any misregulation of lincRNAs can result in tumor. This misregulation of lincRNAs can occur due to factors due to in malfunctions in the organism's status of epigenetics, cell division and cell cycle. How Rinn and his crew sought out to clarify between this fatal disease and this particular non-coding RNA by profiling lincRNAs to different types of cancer in order to specify which lincRNA plays a role in the actual formation and growth of cancer. Why this is such an extreme and crucial contribution to the field of genetics is because retracing cancer back to it's origin may lead to further discoveries of how to cure it and even further, how to prevent it.
Howard Hughes, from the Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, is also conducting researches/studies between lincRNA's and the progression of cancer. The first point he makes in his publication, Long Intergenic Noncoding RNAs: New Links in Cancer Progression (3), is that the lincRNA's ability to control transcriptional alteration leading to the differences between normal cells and cancerous cells indicate there is a direct link between lincRNAs and cancer progression. Another point Hughes discusses is the fact that several types of lincRNAs have the ability to control gene expressions. It does so with a process called chromatin modification where the lincRNA attaches specific histone-modifying enzymes to chromatin. Chromatin modification is an epigenitc process when disturbed, can lead to uncontrolled cell division that will result into a tumor. Traits of these epigentic changes such as it being long-lasting/stable and being heritable provide the same traits to cancer. For example, cancer is divided into stages that measure the degree of seriousness, the potential harm it can cause to the patient, how far it has spread/size of the cancerous tumor and whether it can be removed. (4) Because the epigentic changes that can lead to the formation of tumors are long-lasting and stable, once the cancer reaches a certain stage, it becomes too late for a cure or method to remove it. It is also a common practice for doctors to ask their patients whether there they have had relatives with cancer during their diagnosis. This is because of the heritable traits of epigentic alterations made during chromatin modification. The chances of these alterations being passed down are still unknown because only 1% of the 3,000+ lincRNA's identified (scientists say there are bound to be more) have been characterized. It is also uncertain which type of lincRNA's have the ability to control gene expression and chromatin modification. And even if scientists did eventually uncover every lincRNA there is to be uncovered, identify each one and come to a conclusion as to which type of lincRNA controls gene expression, the concept of randomness and mutation would still affect the probability of a person getting cancer instead of their two younger siblings because their grandmother had suffered from it. (5)
The new found information of lincRNAs and the relationship it has to cancers is extremely beneficial to not only understand our biological make up and functions, but also for a possible cure for cancer as well. For example, Stephen Baylin from Johns Hopkins University School of Medicine is trying to nurture the epigentic alterations begin tumors to form using drugs such as azacitidine and entinostat. (6) Baylin and his team combined the two drugs in order to prevent tumor growth on patients who have gone through treatments that showed no signs of success. As a result, 28 of the 62 patients were given the drug combination
and other chemotherapies. 8 of those patients responded successfully to the treatment. His conclusion also claims that the epigenetic
treatment also stimulated the patients' immune systems to attack tumors. As you can see, scientists are constantly finding new contributions, theories, and information through researches and experiments to uncover the potential change a mere noncodingRNA can bring to human life and the topic of genetics. So next time you tune out the world with your iPOD, make sure you're keeping up with the beat of the music - it could be in sync with the very heartbeat your DNA works for.
MLA Citations:
1) Saey, Tina Hesman. "Missing Lincs - Science News." Science News. 11 Dec. 2011. Web. 1 Apr. 2012. <http://www.sciencenews.org/view/feature/id/336570/title/Missing_Lincs>.
2) Rinn Lab 2009. "Large Intergenic Non-Coding RNAs (lincRNAs)." Rinnlab.com. Broad Institute, 2009. Web. 11 Apr. 2012. <http://www.rinnlab.com/research.html>.
3) Hughes, Howard. "Long Intergenic Noncoding RNAs: New Links in Cancer Progression." Cancer Research.
American Association for Cancer Research, 1 Jan. 2011. Web. 16 Apr.
2012. <http://cancerres.aacrjournals.org/content/71/1/3.full>.
4) "Staging." American Cancer Society. Cancer.org, 2010. Web. 29 Apr. 2012. <http://www.cancer.org/Treatment/UnderstandingYourDiagnosis/staging>.
5) Klitzman, Robert. "Am I My Genes?" Genetics as Rorschachs: Pondering Our Genes and Our Fate.
Psychology Today, 29 Mar. 2012. Web. 1 Apr. 2012.
<http://www.psychologytoday.com/blog/am-i-my-genes/201203/genetics-rorschachs-pondering-our-genes-and-our-fate>.
6) Saey, Tina Hesman. "Old Cancer Drugs Offer New Tricks." Science News.
2 Apr. 2012. Web. 17 Apr. 2012.
<http://www.sciencenews.org/index/generic/activity/view/id/339613/title/Old_cancer_drugs_offer_new_tricks>.
Biology can be tough. But when facing a challenge, you just gotta brace yourself and say: Bring It On. Welcome to my biology blog (:
Sunday, April 29, 2012
Tuesday, April 17, 2012
How to Train A Dragon? No. How to Train Your DNA.
"Tired of your look? Want to change your body? Get off your lazy butt and EXERCISE!" Everyone has been called lazy at least once in their lifetime and who can we blame? Life does get tiring sometimes, but for those athletes, fitness freaks and jocks, working out is an everyday goes-without-saying activity. They aspire to change their body for the better. Little do they know that as they work to change their body, they are actually changing their DNA methylation for the better as well.
DNA methylation is when certain expressions of the gene are turned 'on' or 'off' in accordance to improving the organisms bodily functions. It has bee hypothesized that exercise changed your genetic code entirely, but this hypothesis was ruled out by scientists such as Professor Juleen Zierath. Zierath proved that the alteration in DNA methylation caused by exercise led to better protection of cells from oxidative damage along with improved transport of fats, sugars and other nutrients throughout the body. Her study involved observing the muscle tissues of a group of people that just carried out a 20 minute workout session and comparing their muscle tissues to a group of people who did not participate in the workout. She also compared the workout group's skeletal muscles 3hours before and after the workout to further identify the alterations. It became evident from this comparison that he alterations made in DNA methylation were to improve and make better the body's performance.
It was also stated by another researcher who contributed to Zierath's study, Dr. Donal O'Gorman, that regular exercise and workout activities were essential for metabolic health and prevention of diseases. Regular exercises are needed because the alterations in methylation are not permanent, they are, in simplest terms, our body's response to exercise. To get this response, we must workout regularly and even daily, as though to 'remind' our DNA to turn certain expressions 'off' while leaving others 'on'. By exercising, it is as though we teach our DNA to transport nutrients more efficiently, build muscle, and improve our bodily functions to be healthy.
http://www.naturalnews.com/035259_daily_exercise_DNA_disease_prevention.html
DNA methylation is when certain expressions of the gene are turned 'on' or 'off' in accordance to improving the organisms bodily functions. It has bee hypothesized that exercise changed your genetic code entirely, but this hypothesis was ruled out by scientists such as Professor Juleen Zierath. Zierath proved that the alteration in DNA methylation caused by exercise led to better protection of cells from oxidative damage along with improved transport of fats, sugars and other nutrients throughout the body. Her study involved observing the muscle tissues of a group of people that just carried out a 20 minute workout session and comparing their muscle tissues to a group of people who did not participate in the workout. She also compared the workout group's skeletal muscles 3hours before and after the workout to further identify the alterations. It became evident from this comparison that he alterations made in DNA methylation were to improve and make better the body's performance.
It was also stated by another researcher who contributed to Zierath's study, Dr. Donal O'Gorman, that regular exercise and workout activities were essential for metabolic health and prevention of diseases. Regular exercises are needed because the alterations in methylation are not permanent, they are, in simplest terms, our body's response to exercise. To get this response, we must workout regularly and even daily, as though to 'remind' our DNA to turn certain expressions 'off' while leaving others 'on'. By exercising, it is as though we teach our DNA to transport nutrients more efficiently, build muscle, and improve our bodily functions to be healthy.
http://www.naturalnews.com/035259_daily_exercise_DNA_disease_prevention.html
Brain: Playground Swing or Rocking Chair?
Being young at heart can be a little problem for those who've lived more years than they'd like to admit. And of course, solutions involve people dying a few strands, having a lift here and there or shaving off a few years to seem, look and appear young. But is appearing young the real issue? What if your brain aged faster than other people's? What if you're young at heart, high on the swing when your brain is already resting on a rocking chair?
Reported by Tina Hesman Saey in ScienceNews, Ahmad Salehi's study with pilots show that a specific version of a gene may impact the aging of a person's brain. The specific version of a gene is called BDNF. Specifically, Salehi's research involved the performances of pilot's distinguished into two groups - one group made up of pilots with the BDNF gene and the other group with those who don't - on a flight simulator test. The study carried out for over two years and the results proved that pilots who had the BDNF gene showed a drop about three times more in their flight stimulator test compared to the pilots who didn't. Differences in scores were seen in areas such as reaction time, navigational skills, positioning of planes and performance/decision making in emergency situations.
There was also an obvious decrease in areas associated to learning and memory in the brain for those who had the BDNF gene. For example, those who had this particular gene had lost more volume of their hippocampus (part of the brain used for navigation and spatial memory) in comparison to those who have the normal version of the gene. This contributes to the possibility that the BDNF gene impacts the brain to age faster as all of the pilots that had the volume of their hippocampus measured were 65. Although they were all the same age, their hippocampus volume differed due to the presence of this gene.
But having this gene does not cause a person to be at a disadvantage at all. "The drop in scores was not so dramatic that pilots should be removed from the cockpit", as Tina Hesman Saey quotes Salehi. None of the pilots were more or less capable than the others at a drastic measure. It is also important to keep in mind that the degree of impact this BDNF gene has on the brain aging is not clear entirely as it is still an ongoing research topic and is fairly recent. A neurologist and neuroscientist from University of California, William Mobley, states that "It could be one of a thousand factors that play a role (in the brain aging)". With this statement, other scientists are trying to figure out how to counteract this gene and possibly slow the brain aging. But until further research is done, for now, whether you have this brain aging gene or not, it seems as though being young at heart is the best young you can be.
Reported by Tina Hesman Saey in ScienceNews, Ahmad Salehi's study with pilots show that a specific version of a gene may impact the aging of a person's brain. The specific version of a gene is called BDNF. Specifically, Salehi's research involved the performances of pilot's distinguished into two groups - one group made up of pilots with the BDNF gene and the other group with those who don't - on a flight simulator test. The study carried out for over two years and the results proved that pilots who had the BDNF gene showed a drop about three times more in their flight stimulator test compared to the pilots who didn't. Differences in scores were seen in areas such as reaction time, navigational skills, positioning of planes and performance/decision making in emergency situations.
There was also an obvious decrease in areas associated to learning and memory in the brain for those who had the BDNF gene. For example, those who had this particular gene had lost more volume of their hippocampus (part of the brain used for navigation and spatial memory) in comparison to those who have the normal version of the gene. This contributes to the possibility that the BDNF gene impacts the brain to age faster as all of the pilots that had the volume of their hippocampus measured were 65. Although they were all the same age, their hippocampus volume differed due to the presence of this gene.
But having this gene does not cause a person to be at a disadvantage at all. "The drop in scores was not so dramatic that pilots should be removed from the cockpit", as Tina Hesman Saey quotes Salehi. None of the pilots were more or less capable than the others at a drastic measure. It is also important to keep in mind that the degree of impact this BDNF gene has on the brain aging is not clear entirely as it is still an ongoing research topic and is fairly recent. A neurologist and neuroscientist from University of California, William Mobley, states that "It could be one of a thousand factors that play a role (in the brain aging)". With this statement, other scientists are trying to figure out how to counteract this gene and possibly slow the brain aging. But until further research is done, for now, whether you have this brain aging gene or not, it seems as though being young at heart is the best young you can be.
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