Monday, December 1, 2014
Thursday, March 20, 2014
Will Alzheimer's Soon be Cured?
I was recently watching the movie Rise of the Planet of
the Apes and in that a scientist is trying to cure Alzheimer’s since his
dad is being attacked by that illness and he is trying to prevent it. Long story short he tests it on apes
and they get incredibly intelligent and attack the humans. But besides that I
was interested on the topic of Alzheimer’s and I wanted to find out if there
actually is going to be a cure for it. I decided to look the topic up and found
the article “Cure for Alzheimer’s” that was on Mail Online and looked the topic
up on Wikipedia for additional information.
The article talks about how in about five years we may have
a cure for Alzheimer’s or at least something that will decrease the effects of Alzheimer’s.
Harry Cayton the chief executive of the Alzheimer’s society said “This really
does make us optimistic”.
From Wikipedia and this online post they both said that
Alzheimer’s is increasing exponentially. On the Mail online website it said
that in Britain 500,00 people suffer from AD or Alzheimer’s disease. On
Wikipedia it said that there are about 26.6 million people with AD all over the
world and in 2050, 1 in 85 people will have AD. But luckily they have found a
cure.
 |
| On the right you see a normal brain and on the left you see a brain of someone with the Alzheimer's Disease |
In class we were learning about how they may soon find a
cure for HIV by attacking the receptors on the cells that the HIV virus
attaches to. This is kind of similar but a little different. The scientist have made a vaccine that
attacks a protein called beta-amyloid which damages brain cells.
Trials are being done in the United Kingdom and the
results show that it is safe and there are no side effects. I thought how did
these people do this and they said that the made mice genetically engineered to
have something close to AD. They tested it on them and soon found it worked. Before this Professor Richard Morris, of Edinburgh's
department of neuroscience said that there was o way to look at animal’s short-term
memory.
But with the use of mazes that changed they could use this vaccine and
find out if it worked since with Alzheimer’s the people struggling with the
disease can usually remember things that happened a long time ago but not
things that happened recently. With this vaccine the plaque on the brain is
removed and the person can remember and learn things easier.
Within about five years after testing the vaccine on larger groups it
will be open to the public and the rates of Alzheimer’s will hopefully decrease.
The future is looking a hole lot
brighter now that scientists are discovery these things.
Pictography:
Rise of the Planet of the Apes:
Brain Comparison:
Wikipedia:
Cure for Alzheimer’s:
Wednesday, March 19, 2014
Genetic Editing Fights HIV
The HIV virus is one
of the leading causes of death in our world today, with 50,000 new cases developing
per year. As HIV is much more common in poverty-stricken countries, my knowledge
of its existence only began in middle school, through television programs and
news articles. I’d assume that the case is the same for many Americans, as less
than 1% of our population is infected by the HIV virus.
Upon first learning of the virus a few years ago, I was
shocked to hear that there was no vaccine or treatment to rid a person of HIV.
I had erroneously thought that with the technology we have today, scientists
would have surely found a way to cure such a widespread disease. If the human
race has the ability to send a man to the moon and back, shouldn’t we be able
to mix up a concoction that kills a predator a million times smaller than the
tip of a needle?
As we learned in biology class this past week, creating a
vaccine or successful treatment for HIV is definitely not as simple as “mixing
up a concoction”. The contraction of diseases is different in every case, so HIV
is sadly not as preventable as diseases like the flu. The HIV virus is spread
when certain bodily fluids of an infected person, such as blood, enter the
body. When the virus enters the blood stream it attaches to two white blood
cell receptors, first the CD4 and then the CCR5. The virus membrane then fuses
with the cell membrane, and attacks the white blood cell, eventually rendering
it useless to fight off diseases.
As we learned in our blood typing unit, everyone’s blood
cells are different, and the receptors and markers they have greatly contrast
with those of others’. When investigating the blood cells of those that are
unaffected by HIV, it has been found that they lack CCR5 receptors, preventing
the virus from attaching to the red blood cells. The first thing that comes to
mind when thinking about a way to treat and prevent HIV after hearing this is
to eliminate the receptors. If some people can survive without them shouldn’t
that be the case for everyone else? This is true, but removing eliminating a
receptor certainly isn’t an easy job.
How can the receptors be removed? This long-asked question
is finally being answered by Carl
June and Pablo Tebas, immunologists at the University of Pennsylvania in
Philadelphia. Their answer: Gene editing by way of enzymes. I learned of
this discovery by reading an article titled “Gene-editing Method Tackles HIV in
First Clinical Test” in the news section of the Nature Publishing Group
website, (URL “Nature.com”). The article was published on the 5th of
March 2014, written by Sara Reardon. The
article can be accessed by following this
link: http://www.nature.com/news/gene-editing-method-tackles-hiv-in-first-clinical-test-1.14813
Researchers
working with June and Tebas are using enzymes called zinc-finger nucleases
(what a name!) to find and destroy the genes in the cultured immune cells of 12
people infected with HIV. The enzymes target genes responsible for the CCR5
receptor in a search and destroy mission, killing off the problem from the root.
The treatment was
successful in “about 25% of each participant’s cultured cells” writes Reardon, which were then transfused back into the blood
of the patient from which they came. Half of the patients stopped their normal
antiretroviral drug therapy, and their levels of virus and T cells, T cells
being the type of white blood cells infected.
An image of a healthy T cell from a scanning electron microscope
The HIV levels rose more slowly
than they typically would without drug therapy, while the T cell count went up
and remained high for weeks.
This led
researchers to conclude that the presence of the virus drove the genetically modified
T cells to multiply and spread throughout the body in response.
“In short, the
presence of HIV seemed to drive the modified immune cells, which lacked a
functional CCR5 gene, to proliferate in the body.” says Reardon.
Researchers suspect that the virus was unable
to infect and destroy the altered cells.
In one of the
patients, the virus did not return at all over the twelve week period off of
antireviral drug therapy. Upon examination, the man was found to have already
had one non-working copy of CCR5. Quoting
Tebas, Reardon says that “Nature had done half of the job”.
This finding
suggests that others with one mutated copy of CCR5 would be perfect recipients
for the gene editing treatment. The team is currently enrolling people with
this trait in a new study, and are working on increasing the percentage of
modifiable cells and the rate at which the cells multiply in the body.
June, one of
immunologists responsible, says that he expects there to be even better enzymes
on the market in the near future, capable of targeting genes better than the zinc-finger
nucleases now are. He also thinks that enzyme based gene altering will be
available clinically in the not so far off future. These enzyme treatments are
not solely beneficial to curing HIV, but also certain other diseases.
“He expects researchers to start to look at
their potential for altering cells in people with disorders that result from
mutations in a single gene, such as sickle cell anaemia, certain types of
cancer and even metabolic diseases in the brain.”, Reardon writes of June.
This news is very
exciting to me, as June and Tebas’ discovery seems to be one of the most
genuine breakthroughs in HIV treatment that I have recently heard of. However,
it does seem like a very complicated treatment plan. Considering that the
countries with the highest percentages of HIV per population are those in Southern
Africa, a region known for its low income, I can’t help but think that the
treatment won’t be accessible to those who need it most if it is ever used
clinically. These transfusions and alterations aren’t the type of things that
can be done outside of sate of the art hospitals and laboratories, and they don’t
sound very cheap either.
I hope that the
gene alteration treatment of HIV is successful in years to come, but I still
worry about those who cannot access and afford it. Will healthcare cover the
costs? Do most of these people even have health care? I hope that when the time
comes for this treatment to be revealed, the cost of saving a life from the
slow death of HIV won’t be too much for those who need it.
Article Citation:
Reardon, Sara.
"Gene-editing Method Tackles HIV in First Clinical Test." Nature.com.
Nature Publishing Group, 5 Mar. 2014. Web. 20 Mar. 2014.
Picture Location:
"Type 2 Breakthrough?"
The article: “Major Step in Preventing Type 2 Diabetes” written by Haley Bridger, Broad Institute Communications, on March 2, 2014 talks about a huge breakthrough in preventing type 2 diabetes. Researchers at the Broad Institute and Massachusetts General Hospital basically found mutations in a gene that is believed to reduce the risk of type 2 diabetes in people including people with risk factors such as obesity and old age.
(http://www.webmd.com/diabetes/ss/slideshow-type-2-diabetes-overview):
They basically discovered that rare mutations of the gene “SLC30A8” can reduce the risk of type 2 diabetes by 65%. This drug was tested on people of different ethnic groups, and the drug worked, proving that it may work on people world-wide.
What makes the mutation of this gene so important in fighting type 2 diabetes? Well, the protein that is encoded by “SLC30A8” is shown to play an important role in insulin-secreting in the pancreas, and also somewhat influence the risk of type 2 diabetes. If this protein is activated, it may just be the best possible way to reduce risk. The research group found that the mutation terminates the function of the gene “SLC30A8”. This mutation affects the function of the protein ZnT8 which transports zinc into insulin producing beta cells. Zinc is very important in the steps of creating insulin. Researchers, currently, are looking into why this can reduce the risk of type 2 diabetes.
This is a huge breakthrough and, in my opinion, a very important one. Type 2 diabetes effects the lives of more than 300 million people world-wide. While you can change your lifestyle habits by what you eat, exercising and taking medicine, there is no real cure. I think that it’s great that they are conducting research on something that can really reduce your chances of getting type 2 diabetes. If type 2 diabetes isn't managed correctly, it can be fatal. It’s so common that I almost truly believe that we should really thrive to find a definite cure for it.
I chose type 2 diabetes for my blog because it has a lot to do with what we were recently learning about in class. We basically learned that you have insulin receptors on your cells which receive insulin. This then allows the receptors to send a signal to GluT transporters, telling them to open. With type 2, this whole communication system is fried so when the receptors receive insulin, they don’t send signals and the GluT transporters remain closed. We didn't spend a lot of time on type 2 diabetes so I was still curious on why it’s so hard to find a common cure, and I also wanted to learn more about it. This article was very interesting to me because there at a breakthrough in finding a cure for type 2. I’m curious to see what will come of this breakthrough in the future. Will it be confirmed as a solution for greatly lowering your risk of type 2 or not?
Post by Connor Mulligan
The article: “Major Step in Preventing Type 2 Diabetes” written by Haley Bridger, Broad Institute Communications, on March 2, 2014 talks about a huge breakthrough in preventing type 2 diabetes. Researchers at the Broad Institute and Massachusetts General Hospital basically found mutations in a gene that is believed to reduce the risk of type 2 diabetes in people including people with risk factors such as obesity and old age.
(http://www.webmd.com/diabetes/ss/slideshow-type-2-diabetes-overview):
They basically discovered that rare mutations of the gene “SLC30A8” can reduce the risk of type 2 diabetes by 65%. This drug was tested on people of different ethnic groups, and the drug worked, proving that it may work on people world-wide.
What makes the mutation of this gene so important in fighting type 2 diabetes? Well, the protein that is encoded by “SLC30A8” is shown to play an important role in insulin-secreting in the pancreas, and also somewhat influence the risk of type 2 diabetes. If this protein is activated, it may just be the best possible way to reduce risk. The research group found that the mutation terminates the function of the gene “SLC30A8”. This mutation affects the function of the protein ZnT8 which transports zinc into insulin producing beta cells. Zinc is very important in the steps of creating insulin. Researchers, currently, are looking into why this can reduce the risk of type 2 diabetes.
This is a huge breakthrough and, in my opinion, a very important one. Type 2 diabetes effects the lives of more than 300 million people world-wide. While you can change your lifestyle habits by what you eat, exercising and taking medicine, there is no real cure. I think that it’s great that they are conducting research on something that can really reduce your chances of getting type 2 diabetes. If type 2 diabetes isn't managed correctly, it can be fatal. It’s so common that I almost truly believe that we should really thrive to find a definite cure for it.
I chose type 2 diabetes for my blog because it has a lot to do with what we were recently learning about in class. We basically learned that you have insulin receptors on your cells which receive insulin. This then allows the receptors to send a signal to GluT transporters, telling them to open. With type 2, this whole communication system is fried so when the receptors receive insulin, they don’t send signals and the GluT transporters remain closed. We didn't spend a lot of time on type 2 diabetes so I was still curious on why it’s so hard to find a common cure, and I also wanted to learn more about it. This article was very interesting to me because there at a breakthrough in finding a cure for type 2. I’m curious to see what will come of this breakthrough in the future. Will it be confirmed as a solution for greatly lowering your risk of type 2 or not?
Post by Connor Mulligan
Tuesday, March 18, 2014
Change Your Microbes and Change Your Weight
The article “Bacteria in the Intestines May Help Tip the
Bathroom Scale, Studies Show” written by Denise Grady on March 27, 2013 from
the New York Times, talks about new research that has revealed that bacteria in
your gut helps to determine whether you gain or lose weight.
Gastric bypass surgery is a very common weight loss surgery,
however scientists have not fully understood why this surgery works until now. New
studies show that this surgery works mainly because the microbe levels, or bacteria
in your intestines, are altered when you have this surgery.
Gastric bypass surgery is a surgery to make your stomach smaller. Your stomach is divided
into a small upper section and a larger bottom section. The top section of your
stomach is where your food will now go, and it holds only about 1 ounce of
food. A small part of your jejunum is then connected to a small hole in your new,
smaller stomach. The food you eat will now travel from the stomach into this
new opening into your small intestine. The duodenum and a small part of the
jejunum are now bypassed, or skipped, so there is less absorption of calories.
However, besides less absorption of calories, another major
reason why this bypass surgery works is the change in microbe levels, or microbiota,
which account for a reasonable percentage of a person’s weight loss after this
surgery. Usually after this surgery, patients lose about 65% to 75% of their
excess weight, and 20% of that weight loss has been found is due to the microbiota
in your intestines.
Researchers at Massachusetts General Hospital including Dr.
Lee M. Kaplan, director of the obesity, metabolism and nutrition institute, say
that this new information could gradually lead to treatment that could alter
the microbiota in the intestines to help people lose weight without having the
bypass surgery. But for now, the gastric bypass surgery is the most effective
weight loss procedure. Dr. Kaplan says, “In
no way is manipulating the microbiota going to mimic all the myriad effects of
gastric bypass. But if this could produce 20 percent of the effects of surgery,
it will still be valuable.” He means that the bypass surgery has other beneficial
results that don’t have to do with the microbiota so the surgery is still the
best way to lose weight, however if they could come up with a treatment to lose
20% of the effects, it would still be worth it.
The exact way that the
intestinal microbiota can cause weight loss is still being researched.
Scientists do know that people who tend to gain more weight have certain
microbes to make them gain weight that trim people might not have.
A study in which scientists took
the breath tests of 792 patients to figure out what microbes they had in their
intestines, revealed that the microbe Methanobrevibacter smithii is present in
these people who tend to gain weight. It is most likely partially responsible
for their obesity because this microbe is designed to absorb as many calories
as possible from food. Thousands of years ago, humans might have needed this microbe
when they needed every calorie they could get out of their food because they
didn’t know when their next meal would be, but with a modern day diet, these microbes
are not needed. It is believed that other microbes might be similar to this
microbe and might be somewhat responsible for a person’s obesity, so by
changing or removing these microbes, it could help a person lose weight.
This article relates to our
biology class because we have talked about bypass surgeries. When we were on
our Circulatory System unit, we talked about coronary bypass surgery. This
surgery occurs when a coronary artery is clogged, and oxygen-rich blood can’t
get to your heart’s muscles to keep it pumping. So, you need to have a bypass
surgery which takes a vein from your leg to go around, or skip, the blocked coronary
artery. The gastric bypass surgery is just like this surgery, but instead, it
is going around, or skipping, the duodenum.
It also relates to our class
because we have talked about the bacteria that is in our intestines when we
read “The Bacteria inside My Gut” by George Liles during the digestive system
unit. We read about how once your food reached your intestines, there are more
than 5,000 species of microbes that live there. They contain enzymes that are
needed to break down foods that our bodies can’t digest. They then convert the
nutrients to energy, and create gaseous waste as a byproduct of this process.
I think these new findings could
be very beneficial because scientists might be able to find a treatment to help
a person lose weight without having to have a surgery. A medicine that could
change the microbe levels in your body would help you avoid the money, effort,
pain, and recovery time of a bypass surgery. This new information could be a crucial
step in understanding weight gain and weight loss.
Picture citation: http://www.nlm.nih.gov/medlineplus/ency/imagepages/19268.htm
Ancient Amoeba-Killing Virus Resurrected
Recently, I came across a very interesting article on the
New York Times website; “Out of Siberian Ice, a Virus Revived,” by Carl Zimmer (http://www.nytimes.com/2014/03/04/science/out-of-siberian-ice-a-virus-revived.html?ref=science&_r=0).
This article is about the revival of a virus that has been
frozen in the permafrost of a Siberian riverbank for over 30,000 years. Discovered
by a team of researchers led by Chantal Abergel and Jean-Michel Claverie from Aix-Marseille
University in France, this virus is completely new to the world of science.
Scott O. Rogers of Bowling Green State University believes that being able to
retrieve a virus that is so old, and being able to actually grow it “goes
beyond what anyone else has done.” Nothing like this has been possible before,
and is an amazing feat for these scientists.
The researchers found that when they added pits of the
permafrost to amoebae, they amoebae began to die. They discovered that giant
viruses were multiplying inside the amoebae and killing them.
During their research and experiments, they found that the
virus is much different from the common ones we know today. This new virus,
that they called pithovirus, is 1.5
micrometers long and 25 percent bigger that viruses found before. According to Dr. Arbergel, “Sixty percent of
its gene content doesn’t resemble anything on earth.” They believe that these
viruses must have been parasitic life forms that were common very early in the
history of life.
Although these viruses are different from anything any
scientists have seen before, they pose no threat to humans. This particular
virus only infects amoebae, but some scientists are concerned that some other
disease-causing viruses could still be undiscovered in the permafrost. They
believe that even though it is possible that some viruses could infect humans,
the risk of an outbreak is extremely low.
This year in biology class we have been learning about
cells, bacteria, and viruses. We have learned that, in humans, viruses infect the
host cell and use it to infect the rest of the body. When the viruses are
infecting single-celled organisms, like amoebae, they don’t have anything else
to attack, and they end up just killing the organism.
I think it’s amazing that the scientists were able to grow a
virus back to its normal activity after 30,000 years of being frozen in
permafrost. I never thought that anything like that could be possible. Who
knows, maybe next they’ll be able to bring animals back from extinction!
Picture Citation:
Bartoli,
Julia. Pithovirus. 2012. Science, France. The New York Times. Web. 8
Mar. 2014.
Friday, March 14, 2014
The Fight Against HIV
I read an article titled"Gel Protects Monkeys From HIV After Sex" It was written by Donald G. McNeil Jr. on March 12, 2014 on http://www.nytimes.com/2014/03/13/health/gel-protects-monkeys-from-hiv-after-sex-study-finds.html?ref=science
In this article they talk about possible protection from HIV in a gel applied after sex with an infected mate. The gel would only be used in females however. This gel doesn't have a complete 100% success rate though with one of six macaques given it still contracting HIV. The gel contains raltegravir which prevents the virus from integrating with the cells DNA.
HIV is a virus caused by the virus connecting with the CCR-5 protein receptor on your cells. It connects to these receptors causing the cell to open allowing it to enter the cell and infect it. Once it gets in it bursts open the cell causing it to go to other cells in the body.
However the human testing on this gel does cause moral conflict. Because the gel is combating what could be a deadly disease they can't really justify giving someone a placebo. The other possible option is instead of a placebo they give the person another drug already approved for human use.
This connects to our biology class because we were talking about cell receptors and mutations allowing people to be immune to HIV. This immunity comes from not having the CCR-5 receptor. Without this receptor the cell will not open so the virus can not get in.
"Macaque" http://www.theguardian.com/science/2008/oct/16/neuroscience-medicalresearch
In this article they talk about possible protection from HIV in a gel applied after sex with an infected mate. The gel would only be used in females however. This gel doesn't have a complete 100% success rate though with one of six macaques given it still contracting HIV. The gel contains raltegravir which prevents the virus from integrating with the cells DNA.
HIV is a virus caused by the virus connecting with the CCR-5 protein receptor on your cells. It connects to these receptors causing the cell to open allowing it to enter the cell and infect it. Once it gets in it bursts open the cell causing it to go to other cells in the body.
However the human testing on this gel does cause moral conflict. Because the gel is combating what could be a deadly disease they can't really justify giving someone a placebo. The other possible option is instead of a placebo they give the person another drug already approved for human use.
This connects to our biology class because we were talking about cell receptors and mutations allowing people to be immune to HIV. This immunity comes from not having the CCR-5 receptor. Without this receptor the cell will not open so the virus can not get in.
"Macaque" http://www.theguardian.com/science/2008/oct/16/neuroscience-medicalresearch
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