Friday, October 21, 2016

Music Used to Identify Proteins

            Music for me is something that plays a huge role in my life. I’m always listening, playing, or singing some kind of music. So when I saw this new study it definitely peaked my interest. Structures of proteins can now be studied in a completely new and different way, by listening to music. This technique is theorized to more easily help scientists identify anomalies in proteins.

            By using a process called sonification, the data about the proteins can be turned into musical sounds and melodies. This approach is being used to ask three questions: what can protein data sound like? Are there any analytical benefits to this? In this data can specific elements or anomalies be heard? This technique can be used to help recognize fold structures of proteins by each protein sequence having a melodic shape. The amino acid sequences correlate to musical notes, with their properties being reflected by sound qualities.

            38 people were selected for the test to decide how well the sonification of the three proteins; 1ny9, 1r75, and 1div.pdb, were perceived in relation to data sources. From the 38 people, most of them were students, with 21 of them having more than one year of musical training, 17 having up to or more than one year of protein study, and 10 with no training in either. The subjects were giving four answer choices to choose from in their comparison of the sonifications to visual components: A) similar, B) not similar, C) sometimes similar, D) mostly similar. There were a total of six experiments, with the first two used to establish both positive (similar) and negative (not similar) controls. The results from the experiments showed that a good majority of the subjects were able to discern the correlations between the data related images and sounds. The study is hoping to expand to a more complete fold identification system to identify 3D folds of different proteins. Sonification is also being done on DNA sequences and gene expressions.

Reference:

http://www.heliyon.com/article/e00175

Thursday, October 13, 2016

DNA Analysis of Cats Shows Domestic History

            The first full genome of a cat did not appear until 2007, but in 2014 a higher quality map of an Abyssinian cat named Cinnamon was published. And now since the price for DNA analysis has dropped, further study into a cat’s genome could then be done. An evolutionary geneticist from the Institut Jacques Monod in Paris named Eva-Maria Geigl presented her research on the mitochondrial DNA of 209 domestic cats that were found at 30 different archeological sites in Europe, Africa, and the Middle East. To give you an idea the history of cats span all the way from the dawn of agriculture to the 18th century.

            There were found to be two waves in which the spread of cats occurred. The first was in the eastern Mediterranean and Turkey when agriculture first appeared. It is theorized that there were wild cats that would run off the rodents that tried to eat the farmers’ crop. So the farmers wanted them to stick around to help them out, which eventually lead to domestic breeds. The second wave was found by looking at the mitochondrial DNA lineage from Egypt, showing that the cats began appearing in Bulgaria, Turkey, and sub-Saharan Africa between the times of the fourth century B.C. and the fourth century A.D. The researchers theorize that the cats were kept on ships to help with rodents, and were spread at port cities. This came from the fact that the team found a cat in North Germany that dated back between 700 and 1000 A.D. that had Egyptian mitochondrial DNA.

            It has been believed for years that cats became domesticated in Egypt about 4000 years ago. But based on findings that cat bones had been discovered buried in a 9,500 year old human burial in Cyprus along with Geigl’s findings shows that cats have had a history with humans for a lot longer than first thought. Geigl also discovered by looking at the nuclear DNA of some of the samples that in the Middle Ages the mutation for tabby cats appeared, and that further study could lead to more information. As a cat lover and owner of many cats, I found this article to be very interesting and informative. I had no idea that cats had this kind of history.

http://www.smithsonianmag.com/smart-news/dna-study-details-spread-cats-around-world-180960573/?no-ist

Thursday, October 6, 2016

Is Someone Really Allergic to Penicillin?

            It is being said by the CDC that people who thought they were allergic to penicillin might not actually be. In the US about 10% of patients state that they have an allergy to penicillin, where in actuality less than 1% of the population has a true allergy to the drug. First lets talk about what actually causes a person to have an allergy. A penicillin allergy is actually caused by IgE-mediated reactions to the reactive ingredients in penicillin called antigen determinants. IgE-mediated stands for immunoglobulin E-mediated.  When a person is allergic to penicillin their immune system reacts to the drug as if it is a harmful viral or bacterial infection. When the allergy develops the person’s immune system is then sensitive to penicillin.

            So how could the people who thought they were allergic to penicillin not actually be allergic? One way is that when the person was initially diagnosed as being allergic to penicillin they actually just had similar symptoms as the actual allergy. Or that someone who was allergic simply lost their allergy over time. About 80% of people who had a true penicillin allergy lose their sensitivity to the drug about 10 years after the reaction. So why is this important? This is important because it can reduce the unnecessary use of broad-spectrum antibiotics that people who are allergic to penicillin use. For the people who have thought they were allergic to penicillin they can take a penicillin skin test as well as an oral penicillin-class challenge to test if they are allergic. If both of these are negative then a penicillin allergy can be ruled out.

References


Thursday, September 29, 2016

New Fight Against Skin Cancer

            Alexander Boiko at the University of California Irvine has discovered a new way to fight against melanomas. Melanoma is the most lethal type of skin cancer and can also metastasize very easily. He did this by blocking CD47, which is a cell surface protein on melanin cells, since this will increase the amount the cells were phagocytosed by macrophages. The term phagocytosed is referred to in the paper as “eaten,” and macrophages are a part of the innate immune system and act as phagocytic cells. Another surface protein, CD271, was also found to be important when used with the CD47. CD271 was used in order to target the most aggressive melanoma cells selectively.

            In order for the CD47 to not be eliminated by the immune system, CD47 was overexpressed by metastatic melanomas. To have better results they decided that both proteins needed to be overexpressed in order to trick the immune system so that it could spread to other parts of the body. They found that by blocking of CD47 and targeting of CD271 metastases was stopped in human melanoma tumors that were put in mice. One thing to take note of is that there was major alteration of the microenvironment surrounding the tumors, which helped with the positive results.

            Before this could be done on humans, further research needs to be done in order to see if the combination of CD47 and CD271 can be safely used. But Boiko is hopeful that with the combination of this new therapy as well as other treatments emerging that positive outcomes in the fight against metastatic melanomas will arise.


http://www.cell.com/cell-reports/fulltext/S2211-1247(16)30890-7

Friday, September 23, 2016

Huntington’s Disease

            What exactly is Huntington’s disease? Huntington’s disease (HD) is an inherited neurological condition that affects both the brain and the nervous system. Some of the symptoms people with HD may exhibit are: involuntary muscle movements, slurred speech, depression and anxiety, emotional control issues, and difficultly with thought processes. Once the first symptoms begin normally people live 15 to 20 years with the disease slowly progressing. HD is caused by an inherited change in a huntingtin gene. The huntingtin gene is the gene that is associated with HD. Each parent passes on one of the two huntingtin gene copies they have to their child. If a person has a faulty huntingtin gene copy then they are either affected or pre-symptomatic. This person has a 50% chance that this faulty gene will be passed on to their child.

People can get pre-symptomatic genetic testing done in order to see if they have the faulty huntingtin gene. This means they will test to see how many CAG repeats are in their huntingtin gene. A blood sample is taken from the subject in order to inspect the DNA. The first step of the test is to do polymerase chain reaction (PCR) in order to isolate DNA and make copies. From the millions of copies made from PCR, the DNA fragments need to be separated by Gel Electrophoresis in order to analyze them.

In the huntingtin gene if there are less than 26 repeats of CAG triplet then that is considered the normal range and not faulty, and this person would not have HD. The same goes for the range 27-35 repeats. If a person has 36-39 CAG repeats it is very likely that the person will develop HD. However, it might develop at a later age with less severe conditions, or they might not develop HD at all. Yet if there are more than 40 CAG repeats that person will almost certainly develop HD.

As of right now there is no treatment or cure for HD, but research is ongoing in order to help manage the symptoms. Personally knowing a family that is affected by Huntington’s disease, I feel that more people should be made aware about HD and it’s affects. This is an important cause that people should know about.