Influenza is a viral infection that is constantly changing. It has not been discovered yet the exact way that viral infections like these are becoming drug resistant without waiting for new and untreatable strains arise. Using a novel genetic screen, researchers at the University of California have mapped out the resistance options of influenza's M2 channel against its anti-viral medication inhibitors. This allows the clinically known resistant mutations to be identified without contamination from outside sources. This led to novel mutations that were known to exist in viruses but not to be drug resistant. The same methods were used against a drug that has not been put out on the market yet for clinical use. This enabled the researchers to identify more new resistance mutations. This research will allow new antiviral agents to be tested to predict the resistance options before clinical use.
Read more at: http://www.sciencedirect.com/science/article/pii/S0022283616303023
Sunday, November 27, 2016
Monday, November 14, 2016
Construction and Rescue of a Molecular Clone of Deformed Wing Virus (DWV)
The problem of honey bees being endangered has been brought to light a lot more in social media and the news lately. Honey bees are extremely important in the agriculture business and human nutrition. Deformed wing virus (DWV) is playing a major role in the colony mortality but not much is known about this virus. This virus comes from Varroa jacobsoni mite infestations which has been spread to every continent but Australia due to colony trade. The University of Vienna is trying to close the gap between field research and lab findings to complete an in-vitro model. At this point, colony survival depends on close supervision and help. Once a colony shows DWV symptoms, the colony is more than likely going to fail. DWV can lead to crippled wings and discoloration. A genomic sequence of DWV has been known since 2006 but there are a limited number of tools that are available for studying bee viruses in the lab. The researchers took infectious DWV from a molecular clone that produces DWV symptoms. Through newly made anti-AWV monoclonal antibodies, expression of DWV proteins, producing the virus' progeny, and host cell tropism could be confirmed. Koch's postulates were fulfilled so the virus did not need to be isolated and purified. From this research, a reverse genetics system was developed and applied for DWV pathogenesis. This provides a new basis to study the unknown aspects of DWV along with the molecular mechanisms behind transmission. This study covered the preliminary background needed to continue research to hopefully find a way to minimize the transmission of DWV before honey bees become extinct.
Wednesday, November 9, 2016
Scientists Find Key Protein For Spinal Cord Repair
Zebrafish have the ability to heal their own spinal cord after it has been severed which is definitely not something humans are capable of. Researchers at Duke found the specific protein that plays a major role in this process. This discovery can be a major one towards applying it to people. When the fish's spinal cord is severed, a bridge is formed. First wells extend and connect the gap then nerve cells follow. By 8 weeks the injury is completely healed and the fish has its normal capabilities again. To determine which genes were changed, the scientists monitored the activity of the genes that had large changes once damage was done to the spinal cord. CTGF or connective tissue growth factor is a gene coded for proteins that is secreted from cells. The levels of this rose in the cells that formed the bridge. When CTGF was deleted, the fish were not able to regenerate. The human CTGF protein is extremely similar (almost 90%) in the amino acid make up to the zebra fish. When human CTGF was added to the fish, regeneration was faster. Since healing is more complex in mammals due to the scar tissue, the scientists do not think CTGF alone is sufficient enough to regenerate in people. The next step mice and when the CTGF levels are the highest. At this point, the scientists are believing that it is how the protein is controlled and not the actual make up.
Read more at: https://today.duke.edu/2016/11/scientists-find-key-protein-spinal-cord-repair
Read more at: https://today.duke.edu/2016/11/scientists-find-key-protein-spinal-cord-repair
Saturday, October 29, 2016
Therapeutic reversal of food allergen sensitivity by mature retinoic acid–differentiated dendritic cell induction of LAG3+CD49b−Foxp3− regulatory T cells
As someone who has a food allergy to the most random things, I found this research to be super exciting. Anaphylaxis can be life threatening and there isn't really a cure found yet. Regulatory dendritic cell therapy has been effective in mice with allergic disease and has worked with cells from atopic asthmatic patients. So far, it has been found that DC immunotherapy can be effective in reversing food allergies through the operative mechanism.
More can be read at: http://www.jacionline.org/article/S0091-6749(16)30969-1/abstract
More can be read at: http://www.jacionline.org/article/S0091-6749(16)30969-1/abstract
Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice
If it were possible to live a much longer life, would you take the opportunity? Researchers at Washington University School of Medicine are working on a way to do this. NAD+ availability decreases as a person ages or when they get certain diseases. Nicotinamide mononucleotide or NMN is a NAD+ intermediate that can enhance NAD+ biosynthesis in mice. When mice were administered NMN over a 12 month period, NAD+ was quickly synthesized which reduces age-associated physiological decline. The age-associated gene expression changes in certain organs was also prevented. Instead of the mice just keeping what appears to be a steady age, the mice were actually doing the opposite of aging. This research would have to be tested much further until it was applied to humans but it showed no toxicity in the mice tested. This could be a really good thing for people with life threatening disease but can also be abused.
To read more: http://www.cell.com/cell-metabolism/pdf/S1550-4131(16)30495-8.pdf
To read more: http://www.cell.com/cell-metabolism/pdf/S1550-4131(16)30495-8.pdf
Monday, October 17, 2016
New Molecular Biology Technique Could Help Identify Virus-Fighting Potential of Existing Drugs
According to a study reported in PLOS Computational Biology, a new molecular biology technique can be used to identify the virus-fighting potential of existing drugs designed to treat other conditions. Researches at Vanderbilt have developed a strategy to identify drugs with the potential to fight other deadly viral infections. Gene-trap insertional mutagenesis is being used to identify genes that allow viruses to take over human cells but are not necessary for cell survival. Next, a computational framework was used to screen existing drugs that effect these genes. There were 110 genes that produce proteins that could serve as targets for existing drugs. Many of these genes were involved in HIV-1 and Ebola. So far, it was found that the anti-arrhythmia drug ajmaline as a potential Ebola treatment. This method still has a lot of research to be done and many trials to go through before it can actually be used but I believe that it is a good start. By using drugs that have known effects, known side effects, and are already approved for treatment for other conditions could be a very big advancement in the medical field. Instead of having to do massive amounts on research for a new treatment and for the treatment to be specifically designed for one virus such as Ebola, it would be a time saver to just use known drugs.
Read more at: http://www.news-medical.net/news/20161003/New-molecular-biology-technique-could-help-identify-virus-fighting-potential-of-existing-drugs.aspx
Read more at: http://www.news-medical.net/news/20161003/New-molecular-biology-technique-could-help-identify-virus-fighting-potential-of-existing-drugs.aspx
Saturday, October 8, 2016
Newborn Gut Microbiome Predicts Later Allergy and Asthma, Study Finds
Allergy season is here unfortunately but what if the microbes in your gut during the first month of life determine your risk of having allergies or asthma later in life? Researchers at the University of California in San Francisco and the Henry Ford Health System in Detroit have studied this and the results show that certain gut microbes in infants increase the risk of allergies and asthma later in childhood. It was found that a molecule that reduce the abundance of a certain immune cell that prevents allergies were present in at-risk babies. The only other strong links found between allergies and asthma were males were more likely to be affected and having a dog in the household actually lowered the risk of allergies and asthma. Could the microbes in these baby's gut be altered so that they will not have such a high risk of having allergies or asthma later in life?
Read more at: https://www.ucsf.edu/news/2016/09/404071/newborn-gut-microbiome-predicts-later-allergy-and-asthma-study-finds
Read more at: https://www.ucsf.edu/news/2016/09/404071/newborn-gut-microbiome-predicts-later-allergy-and-asthma-study-finds
Monday, October 3, 2016
News from the Primordial World
How the life began on Earth is a question that might not ever be answered during our lifetime for certain. However, there is a new theory being looked at. Instead of assuming RNA was evolved into DNA and proteins, the new theory assumes that RNA and DNA evolved simultaneously. Researchers at The Scripps Research Institute discovered that there is a significant loss of stability when RNA and DNA share the same backbone which they would have if it was a RNA world. The instability would cause difficulties in the ability to hold information and replicate correctly. There showed to be a loss of function when RNA and DNA were mixed. The researchers have come to the conclusion that RNA in the beginning would have been altered like they are today if RNA nucleobases accidentally join a DNA strand; enzymes will come and fix this mistake. The researchers have assumed that the sophisticated enzymes were probably not around at this time. If DNA and RNA arose at the same time, DNA would have had its own homogeneous system early on. RNA would have still produced DNA but DNA would have had its own raw material first.
To read more: http://www.scripps.edu/newsandviews/e_20161003/krishnamurthy.html
To read more: http://www.scripps.edu/newsandviews/e_20161003/krishnamurthy.html
Monday, September 26, 2016
New 'Trojan Horse' Antibody Strategy Shows Promise Against All Ebola Viruses
Ebola is a virus that the general public tends to freak out about as soon as a case pops up. A lot of this stems from not being educated on the topic but a lot of it also comes from there not being a highly effective or approved vaccine yet. Ebola has killed thousands in Africa so far in about two dozen different outbreaks. Researchers at Albert Einstein College of Medicine have found a strategy to target an Achilles' heel that all known viruses of Ebola have. So far, two antibodies have been able to stop the invasion of Ebola into human cells. Up until this research, the most promising antibodies were monoclonal antibodies but these only neutralize a specific virus. Ebola virus Zaire has monoclonal antibodies that can neutralize the virus but Sudan and Bundibugyo do not have any antibodies known to neutralize them yet. The goal is to find a monoclonal antibody that protects against all five ebolaviruses. In 2011, a group of researchers were able to expose the Achilles' heel of all of the ebolaviruses. They must all bind to a specific host-cell protein to infect and multiply. This also holds true to the Marburg virus. They realized that if the specific protein was neutralized or if the viral protein that binds was neutralized, Ebola would not be able to multiply. However, these targets lay deep in cells so that the immune system does not see them and antibodies cannot protect them. This is where the "Trojan horse" strategy comes into play. This strategy tricks the virus into carrying the antibody with them into the host cell which would neutralize the virus before it is able to bind and multiply. So far, when tested in the lab when harmless viruses are genetically altered to have all of the glycoproteins from all five ebolaviruses, all five viruses were neutralized. Next, mice were injected with the two most lethal ebolaviruses. The mice did not live due to the fact that the antibodies were specifically designed to bind to the human protein. The researchers plan to test the antibodies on nonhuman primates next. This research could be a huge breakthrough with many viruses. If researchers can continue to find the Achilles' heel for more and more viruses, antibodies could be made more diverse since there is a better understanding. This could protect people from many viruses as a whole.
See more at: http://www.einstein.yu.edu/news/releases/1196/new-trojan-horse-antibody-strategy-shows-promise-against-all-ebola-viruses/#sthash.eZ4rfMru.dpuf
See more at: http://www.einstein.yu.edu/news/releases/1196/new-trojan-horse-antibody-strategy-shows-promise-against-all-ebola-viruses/#sthash.eZ4rfMru.dpuf
Wednesday, September 21, 2016
Extremotolerant tardigrade genome and improved radiotolerance of human cultured cells by tardigrade-unique protein
Tardigrades or water bears are extremely small aquatic animals that can tolerate extreme dehydration and once dehydrated can tolerate a variety of extremes. The most tolerant species is Ramazzottius varieornatus. This species has lost the gene pathways that promote stress and have a high expression of species unique proteins. Tardigrade unique proteins were used to test X-ray induced DNA damage on cultured human cells and the damage was suppressed by 40%. These unique proteins are the start of understanding how tardigrades are able to withstand so many physical stressors and environments once they become dehydrated. This can enable the study of new genes and mechanisms that can be used to stand high stress and be used for protection.
More can be read about this at: http://www.nature.com/ncomms/2016/160920/ncomms12808/full/ncomms12808.html
More can be read about this at: http://www.nature.com/ncomms/2016/160920/ncomms12808/full/ncomms12808.html
Wednesday, September 14, 2016
Snail venom holds key to better diabetes treatments
Diebetes is a huge problem millions of Americans deal with on a daily basis but what if human insulins were not the best insulins? Researchers in Australia and the U.S. have teamed up and studies have shown that the insulin found in the venom of cone snails can bind to human insulin receptors. Human insulins have to be be structurally altered before they are able to function correctly where the snail insulin is already structurally correct and can immediately bind to the receptors. Without the structural change happening, the snail insulin can bind and speed up the cell signaling process. The researchers are now trying to use this information to design new treatments. I personally do not have to ever deal with diabetes but I know many people that do. Research like this can definitely help many people get the immediate shot of insulin they need and it can start helping faster and more effectively. Hopefully this will be able to be a long term fix and will be something that is not too cost effective or hard to come by.
To read more information: http://www.wehi.edu.au/news/snail-venom-holds-key-better-diabetes-treatments
To read more information: http://www.wehi.edu.au/news/snail-venom-holds-key-better-diabetes-treatments
Tuesday, September 6, 2016
Molecular Biology Post 1
Lately in the news we have heard about the flesh-eating bacteria of group A streptococcus. Due to many studies at the Houston Methodist Research Institute and the U.S. National Institute of Allergy and Infectious Diseases, the mechanism of the bacterial disease has been identified based off of sequencing of almost 5,000 group A streptococcus genomes. The severity of the cases caused by group A streptococcus vary in severity. The most common case is strep throat but can be as sever as necrotizing fasciitis. Once sequencing the genome, the original hypothesis was failed to be rejected, changes in the genetic makeup have caused new epidemics. The alterations were in genes that encode two dominant toxins. The genetic changes result in production of single nucleotide polymorphisims, two of which highly increased the production of two toxins that are harmful to humans.
I believe that this method could pave the road for many other discoveries when it comes to unknown mechanisms. This bacteria just so happened to be a very good model organism so sequencing was easier than a bacteria with a massive genome or one that lacks scientists' knowledge. By sequencing, the cause of many diseases was able to be pinpointed down to the exact genes that were being altered.
This article was found at https://www.sciencedaily.com/releases/2015/08/150810172453.htm
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