Friday, December 14, 2018

Endangered Whales

There was a genetic study done by Andrew DeWoody of the Department of Biological Sciences to see the connection between whales from the East and West coast. There are approximately 27,000 whales on the East and 200 on the West and many think the low number in population was due to commercial whaling, where thousands were killed. However, there were a few that got away and were able to still mate, making the population at approximately 200. When observing the genotypes of both species of whales, it was found that according to their genotypes the two species have diverged genetically. Also found was their was some cases of interbreeding between the few endangered whale species on the West. I found this article interesting because the scientists working on the study were able to determine a lot of information based on comparing the genotypes on the different species of whales.


Humans Vs Chimps

It is known that humans share approximately 90% of their DNA with primary cousins, including your typical chimpanzee. However, it is the other 10% that is found to determine and observe the biology of the species and see what makes them different. Dr. Gilad of the University of Chicago discovered in 2012 that although humans and chimpanzees share similarities in their DNA, their gene regulatory mechanism is indeed different. A gene regulatory mechanism is basically how the way a gene transcribes in the RNA molecule. This just adds to another research tool that scientists can use when looking to study a topic of genetics.

I found this article very interesting because many of us know how similar we are to chimpanzees and those who believe in evolution can easily see this. However, understanding how a gene regulatory mechanism works will help those study the anatomy and development of species. 


Tuesday, December 11, 2018

Blood Platelets with Extra Powers

Blood platelets have a specific job in the body and that is to stop bleeding via clotting. However, these platelets sometimes fail, specifically in times of severe trauma. A bioengineer at the University of British Columbia may have developed a strategy for adding extra powers to these blood platelets so they can arise to these occasions and continue coagulation. Coagulation depends on a series of complex biochemical reactions, which works great for scrapes and paper cuts; however, trauma often overwhelms this process. "Platelets are the first responders to blood vessel ruptures-- they swarm to the edges of an exposed vessel wall, and their shape changes from smooth and round to sticks and star-like, so they can easily clump together". Then to plug the wound, platelets are woven together by fibrin which then hardens and contracts into a clot. The enzyme that winds the fibrin together is called thrombin. Under extreme stress, such as trauma, causes the chain reaction to fizzle out because of "trauma-induced coagulopathy". Dr. Kastrup and student Vivienne Chan inserted thrombin into nano-sized liposomes, and mixed them with thousands of platelets. After the platelets absorbed the nanoparticles, they immersed them in various types of blood samples. The high thrombin platelets clotted blood approximately 30% faster than normal platelets, and formed clots that were 20% stronger.

This is highly interesting research because "Trauma is the leading killer of people under 45 years old and blood loss is the second most common cause of such deaths". If this were to work in clinical trials, this could potentially save millions of lives. If EMT's had access to these kinds of "super platelets" than they could potentially treat trauma victims on the spot leaving the doctors plenty of time to be able to diagnose and treat patients properly when in the hospital. The important thing to understand is that the research is still relatively new, things begin to get tricky once out of the controlled setting. None the less, the possible benefits of these super-platelets are enormous.  

New Tests on Roundworms Using the Antibiotic Minocycline Found to have Increased the Lifespan by Inhibiting Protein Aggregation and Could Lead in to Help the Fight Against Multiple Neurodegenerative Diseases in Humans.

          Many progressive age-related brain disorders are due to impaired proteostasis. Proteostasis is the systematic process of the production of proteins and the disposal of them from the body. Impaired proteostasis could mean a couple different things might be faulty. A well functioning process of proteostasis means that there is a good balance between the production of proteins and the disposal of them. Neurodegenerative symptons begin when there is a disruptance in this balance. Either there is an over/underproduction of proteins or there is an increase/decrease in the disposal of the proteins. Gregory M Solis from the The Scripps Research Institute and colleagues from other research institutes ran tests on Caenorhabditis elegans, a species of roundworms, that are relatively old with deficiency in stress signaling pathways. Stress signaling pathways (SSPs) are the cells way of telling itself that their is stress on the cell. This can include intruding toxins, mechanical damage or extreme temperatures that inhibit reactions that occur in the cell. However, cells that become dependent on this have difficulties responding to stressors later in its life when they lose the ability to activate SSPs. Minocycline, an antiobiotic that is known to have neuroprotective and anti-imflammatory properties in mammals, was used on the worms to suppress cytoplasmic protein synthesis and the production of aggreation-prone proteins. By minimizing the production of these proteins it relieves the demand on the multiple pathways that induce protein synthesis, such as SSPs. Therefore reducing the effects aging has on cellular function.
          Minocycline is used by humans now for medicinal purposes however because of its multitude of side effects which include nausea, vertigo, and mild dizziness just to name a few. The risk for these symptoms has prevented the usage for minocycline for many different neurodegenerative diseases because the harmful effects will have major impacts on the patients who are typically of an older age group, who do not have strong enough metabolic pathways to prevent these symptons. This limits its use in humans right now to its anti-inflammatory effects. As of now Minocycline is a major product used in curing acne vulgaris and sexually transmitted diseases and is soley used for those reasons until methods of reducing the chances of the detrimental symptoms are discovered. 

Bacterial Protein can cause Cancer

Image result for dnak protein

On the 4th of December a new discovery was made about the protein DnaK. This protein is a part of the bacterium mycoplasma, and has been proven to interfere with the mycoplasma infected cell's ability to respond and repair DNA damage. The inability for a cell to repair and respond to DNA damage is a known origin of cancer. The Institute of Human Virology at the University of Maryland School of Medicine are the ones who made this discovery. The study as a whole suggest bacterial infections contribute way more to cancer then thought previously. The study also suggests the DnaK the main protein observed in the study can reduce the efficiency of anti-cancer drugs.

New CRISPR Technology

Image result for crispr

A new study out of the University of Illinois has provided scientists with a new adaptation of how to use CRISPR a new gene-editing technology. The new technology allows the cell's internal machinery to skip over a small portion of the gene when it is transcribed into a template for protein building. This allows scientist to  influence how the a gene is expressed and also eliminate mutated gene sequences. "This new CRISPR-SKIP method alters a single base before the beginning of an exon, causing the cell to read it as a non-coding portion" Since the invention of CRISPR there have been other approaches to skipping exons or eliminating amino acids, like CRISPR-SKIP does. These other methods don't permanently alter the DNA sequence though. The invention of this method can be useful one fay for treating genetic diseases caused by mutations in the genome, such as Huntington's disease.

Scientists direct bacteria with expanded genetic code to evolve extreme heat tolerance

In recent years, scientists have engineered bacteria with expanded genetic codes that produce proteins made from a wider range of molecular building blocks, opening up a promising front in protein engineering.

Thermophiles, or thermophilic bacteria, are a type of extreme bacteria (extremophiles) that thrive in temperatures above 131 degrees Fahrenheit (55 Celsius).

Exposing bacteria with an artificially expanded genetic code to temperatures at which they cannot normally grow, the researchers found that some of the bacteria evolved new heat-resistant proteins that remain stable at temperatures where they would typically inactivate.

The scientists started by tweaking the genome of E. coli so that the bacteria could produce the protein homoserine o-succinyltransferase (metA) using a 21 amino acid code instead of the common 20 amino acid code. Above that temperature, metA begins to inactivate and the bacteria die. At this point, they let natural selection work. Heating the bacteria to 44 degrees Celsius, which is a temperature at which this bacteria cannot survive, the scientists put selective pressure on the bacteria population. As expected, some of the mutant bacteria were able to survive beyond their typical temperature ceiling, thanks to possessing a mutant metA that was more heat stable, all other bacteria died.

The researchers then identified the specific genetic sequence change that resulted in the mutant metA and found it was due to the unique chemical properties of one of their noncanonical amino acids that laboratory evolution exploited in a clever way to stabilize the protein.

Source:  Science Daily  Heat-Resistant Bacteria

Regrowing damaged nerves hinges on shutting down key genes

Quadriplegia is the partial or complete paralysis of both the arms and legs that is usually due to injury or disease of the spinal cord in the region of the neck.

Neurons in the brain and spinal cord don't grow back after injury, unlike those in the rest of the body. Now, researchers have identified some of the key steps taken by nerves in the legs as they regenerate. The findings lay out a path that spinal cord neurons might be able to follow, potentially leading to improved recovery for people paralyzed by spinal cord injuries.

Researchers at Washington University School of Medicine in St. Louis have been working with mice and have identified some of the key steps taken by peripheral nerves, which are those in the arms and legs, as they regenerate. There's no way to reverse a spinal cord injury that has already occurred. The neurons that form the spinal cord do not spontaneously heal themselves.

they have found a set of genes related to sending and receiving chemical and electrical signals, the primary duty of mature neurons , this had to be silenced for the injury to heal, the researchers showed.

The idea that cells must become less mature in order to regenerate is not new, but Cavalli and Oh's study provides evidence in support of that idea. The researchers identified the key molecular and genetic players involved in regressing to a less mature state, and showed that the timing of the regression was crucial to successful recovery.

The scientist are still trying to develop a more detailed understanding of when and for how long specific genes must be shut off.

Source: Science Daily