Wouldn't it be great to be able to stop the bleeding from a cut or wound in as little as six seconds without having to go to extremes? Well, the researchers at Rice University have developed just that (depending on what you consider to be extreme).
They have incorporated the enzyme batroxobin which comes from the venom of a South American pit viper into a hydrogel. This enzyme has been known to help with blood clotting since 1936, but the researchers wanted to find a way to make it useful; especially in the field of medicine. How it works is that the hydrogel is made up of "self-assembling nanofibers" that can be mixed with the enzyme and injected into the site of bleeding. The nanofibers and batroxobin come together and turn into some type of gel which automatically stops the bleeding. This was performed on lab mice in different combinations like the gel without the enzyme or the enzyme without the gel but the only effective combination was having both of them together.
The researchers have named their combination SB50 and hope to have it approved by FDA soon to start incorporating them into the medicine field. They believe this will be a great advantage for patients who need to take anti-coagulants or are using Heparin. Apparently, Heparin is a drug that can block the function of thrombin and this is no Bueno because thrombin is the enzyme that starts all of the reactions that lead to blood clotting. I guess I should add, for those animal lovers, that snakes are not being tortured or forced to donate their venom. The enzyme can be synthesized in a lab without the need of the snake. :)
This seems pretty cool to me and I hope the FDA approves it soon because this can save so many lives!
Article!
Friday, October 30, 2015
Friday, October 23, 2015
Say thank you to your Dad!
Coming from a Mexican family, it is common for the male to
be upset with his wife for not giving him a son. However, we now know that the
sperm is actually whom determines if the child is a boy or girl, so technically
it is the father's fault he didn't get a son. According to this article, there
may be more things fathers may be responsible for.
Researchers at the University of Pennsylvania have
discovered that males who experience a lot of stress through their life can cause
their children to have problems with stress as well. Apparently, the sperm of the
stressed males have an increase in expression on nine microRNAs. They are not
yet sure how these nine miRs have an effect on stress, but they performed three separate
studies on mice to confirm that these nine were the ones responsible.
In their first study in 2013, they stressed mice by changing
them from cage to cage or by having them smell the urine of a fox (which
is their predator). These mice were then allowed to mate, and their offspring
were observed in stressful settings. As they expected, the offspring could not
cope with stress very well. The sperm of the stressed fathers was compared to
the sperm of the mice who were not placed in stressful situations. This is
where the researchers noticed the difference in levels of those nine miRs.
To have a better understanding and further confirm that the
difference in levels was relevant, the researchers performed a second study. They
isolated the nine miRs and microinjected them into mouse zygotes, the control
groups were either injected with only one of those miRNAs or with a random,
irrelevant miRNA. The zygotes were then injected into surrogate female mice for
reproduction. When the offspring became adults, their response to stress was
observed and they had the same results as the mice from the 2013 study. The study
also showed low cortisone levels for the offspring that received the nine miRs
(not sure how this is related).
So how are these nine miRNAs causing stressed mice to pass
their problems with stress to their offspring? From what I understood, the miRNAs
are targeting “stored maternal mRNA” during the short period of time that it
takes the sperm and the egg to fuse and direct zygotic development. In a third
study, they injected the nine miRs into new zygotes and controlled injections
into other zygotes. The zygotes were incubated for 8 hours and the mRNA from
each cell was amplified. The expression of mRNA in the miRs injected mice was
lower than the controlled. The miRNAs seem to decide which mRNAs get translated,
and in this case it relates to chromatin remodeling genes.
Their next step is to figure out if intervening in the stress of adult male mice may have a positive effect on their offspring. They will also look at the genes upstream of the chromatic remodeling genes to maybe find a way of stopping this trait from being passed on to their offspring.Article
Their next step is to figure out if intervening in the stress of adult male mice may have a positive effect on their offspring. They will also look at the genes upstream of the chromatic remodeling genes to maybe find a way of stopping this trait from being passed on to their offspring.
Thursday, October 15, 2015
Born This Way?
As an undergrad I learned there was many research being done on identical twins where one had developed a disease such as cancer while the other was perfectly healthy. Scientists were studying the twins DNA to understand why this happened, their conclusion was epigenetics.
Surprisingly, the scientists in this article are kind of doing the same thing. Researchers at the University of California Los Angeles (UCLA) presented an abstract for one of their current projects at the American Society of Human Genetics 2015 Annual Meeting in Baltimore. According to the article, the researchers have developed an algorithm that can identify the nine regions of the human genome that are most relevant to determining the sexual orientation of males. They are looking specifically at the epigenetics information and how methylation patterns affect these regions. Their study consisted of 37 pairs of twins where one was homosexual while the other was heterosexual, and 10 pairs of twins where both were homosexual (as their control). The algorithm is called FuzzyForest, and it found the 9 regions of the DNA that the researchers are now looking into. Their next step is to understand how methylation patterns play a role in the identified regions to result in differences of sexual orientation. Also, they want to test a general population of males to see how the algorithm works with them. From the twins study, their results were of 70% accuracy which doesn't seem very promising but maybe with more tests and research there may be a way of determining if sexual orientation is actually due to our genes.
The article can be found here Article, and the abstract here https://ep70.eventpilotadmin.com/web/page.php?page=IntHtml&project=ASHG15&id=150123267.
Surprisingly, the scientists in this article are kind of doing the same thing. Researchers at the University of California Los Angeles (UCLA) presented an abstract for one of their current projects at the American Society of Human Genetics 2015 Annual Meeting in Baltimore. According to the article, the researchers have developed an algorithm that can identify the nine regions of the human genome that are most relevant to determining the sexual orientation of males. They are looking specifically at the epigenetics information and how methylation patterns affect these regions. Their study consisted of 37 pairs of twins where one was homosexual while the other was heterosexual, and 10 pairs of twins where both were homosexual (as their control). The algorithm is called FuzzyForest, and it found the 9 regions of the DNA that the researchers are now looking into. Their next step is to understand how methylation patterns play a role in the identified regions to result in differences of sexual orientation. Also, they want to test a general population of males to see how the algorithm works with them. From the twins study, their results were of 70% accuracy which doesn't seem very promising but maybe with more tests and research there may be a way of determining if sexual orientation is actually due to our genes.
The article can be found here Article, and the abstract here https://ep70.eventpilotadmin.com/web/page.php?page=IntHtml&project=ASHG15&id=150123267.
Wednesday, October 7, 2015
I bet you Monsanto doesn't know this... yet!
Some
researchers at the University of Bonn have developed a way to stop roundworms, specifically
the nematode Heterodera schachtii, from producing “tumorous nurse cell systems”
in the roots of beets, potatoes, or soy beans. The article focuses on the loss
in production of sugar from beet plants. The roundworms act as a parasite and
cause the plant to be a lot smaller from its normal size as well as the decrease
in the production of sugar.
First
the researchers thought the roundworm used the plant hormones to grow and nourish
itself. However, after blocking the hormone cytokinin in the plant Arabidopsis
thaliana, they were surprised to see that the roundworm kept growing! Their
next step of course was to block a receptor in the roundworm’s gene that is
crucial for the pathway of synthesizing cytokinin. Without this receptor, the
roundworm wasn't able to produce cytokinin and it “starve[d] the pest”. So it
was the “parasite” itself that was producing the hormone without any help from the
plant; well, except as a source of nutrition.
The
researchers are now trying to apply their findings to other agricultural plants
that experience a similar source of parasitism.
More
genetic modifications for our agricultural plants… what do you think?
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