The Biology Blogger

When we hear a story about a gene variation that makes a person immune to malaria, people get excited. But, how excited would people be if that same gene that makes people immune to one disease left them more susceptible to another disease? I don’t know how excited we’d be. Unfortunately, that’s happened. According to an article I read at the New York Times, those in Africa that developed a gene that allowed for an immunity against an ancestor to the modern day malaria are more prone to get HIV.  Alone, this gene could be the cause of 11% of the cases of HIV.

The question people are asking is: why is it when one disease is protected against, the other becomes more likely to infect the person?  The answer to that lays on the receptors of the red blood cells and the white blood cells.  Malaria attaches to a receptor that is found on red blood cells.  This receptor is meant to attach to a hormone called CCL5.  About 10,000 years ago, humans in Africa stopped having those receptors and they suddenly stopped getting malaria.

Now that HIV is around, though, one scientist suddenly had a realization.  Robin Weiss is a biologist at University College of London.  He found that HIV was using red blood cells to get around the body in particular patients.  Instead of the malaria attaching to the receptor, the HIV attaches to the receptor.  And what you get is a case of increased HIV infections.  It sounds confusing?  It is.  Scientists realized that if there is a lack of this one receptor on the red blood cells, HIV increases.  If there is a lack of the receptor on the white blood cells, HIV goes away.  It’s confusing.

What does this all mean, though?  It explains why HIV is so dangerous in Africa.  More importantly, though, it gives more information into understanding about the biology behind HIV.  We don’t know much about HIV.  It’s relatively new so we can’t do genetic research.  That’s irritating for scientists because if we knew about the genome, we might be able to target it better.  This research, although very upsetting, could lead to more information on potentially finding a vaccine.  On an aside, a trial for a vaccine against HIV was just cancelled.

Hopefully we can find a cure for this virus.  But, right now, we just have more knowledge.  We are starting to understand more and more on how this virus works.  It’s not a lot, but it’s something.  Now all we need is to get a vaccine out, huh?

Alright, this is a topic that is a bit of a passion for me because I used to have ferrets as a kid.  I can remember when I was around the age of eight, I saved up my twenty five dollars and I adopted one of the few ferrets that were left.  The Black-Footed Ferret is quickly moving towards extinction.  Scientists say that a colony that currently has half of America’s population of Black-Footed Ferrets was recently hit back the Plague (the same as the Black plague) and a third of these 300 ferrets have died already from it.  This is scary, especially because of this…

In the 1970s, there were only 18 left in this area.  However, with the careful work of scientists and the contributions from different people, they were able to increase that population.  Three hundred might not seem like a lot, but when you only have eighteen to create that population, it’s a really great number.

The problem comes in, though, when the Plague hits again.  We can fight the Plague off like its no big deal.  A little antibiotics and we’re done.  For ferrets, if they get the Plague, they’re dead.  Simple as that, bada bing, bada boom, they’re gone.  No sickness, just death.  Because of this, if an outbreak happens in a ferret colony, a lot of them can die.

So, why should we care?  The ferrets are another species on this planet.  Although we have little interaction with them, they are an important part of the ecosystem.  If the ferret population was high, ranchers in the area would not need to worry about prairie dogs eating all the grass that their herds need for grazing.  A single ferret can eat 150 prairie dogs in one year.  Sure, that’s not an overly abundant amount.  But, 300 ferrets eating 150 prairie dogs is a bit more.

Scientists are finding ways to try and help the ferrets.  They have developed a vaccine to really fight against it, but the truth is, it’s a very time costly job.  Travis Livieri is doing everything in his power to try and save them.  He wants the colony to grow again because they’ve been using the offspring from this colony to start other colonies.  There aren’t many ferrets left.  It’s unfortunate and there’s little people can do.  But…There is something you can.  Stop by the Black-Footed Ferret Conservation Program.  Learn about it and if you can, donate.  The population is dying because of this Plague and if we can help, I say we do it.

When one species dies, it can have catastrophic consequences for the overall ecosystem.  Prairie dogs need their predator.  The Black-Footed Ferret can be saved; however, it does take some work.  This is just another example of how species are dying out and an example of the need for human intervention.

When I heard (or read) that there was suggestion of farms in Manhattan, I had to question it.  Is there room?  Of course not.  Unless you want to use Central Park, there’s no place to put farms and even then, being a New York myself, I love Central Park the way it is.  So, I naturally had to dwell deeper.  How the heck could we put farms in Manhattan?  Or any other city for that?  Then I saw it…Vertical Farms.  Now, this has been discussed for quite some time, but I had to write about it.

In theory, what they are hoping is that they can do the one thing that is expected in Manhattan: build up.  Skyscrapers can be built and people feel that some of these could be used for farms.  It’s a nice idea in theory, but there are issues to it.  Before I talk about the issues, though, let’s look at some of the really great things that could come from this.  First, take a look at this picture that I have provided and tell me what you think about.

As you can see, the building would be used with many floors to grow food.  According to an article in the New York Times, one thirty story skyscraper with pure farms on it could make enough food to feed 50,000 people.  That’s a lot of people and that could definitely do some good in lowering the cost of food if there were numerous of them.  But, then we need to look at some issues that come along with it.

It will cost hundreds of millions to make one of these towers.  How much money can the food that is made here make a year?  If it can make a lot, then perhaps the investment would be a good move.  But, the issue that I think a lot of people have (including me) is this: is this the most effective way to increase food production?  And more so than that…Why would someone with a skyscraper want to do this over renting it out to someone?  Which will pay more?

I propose something to those that want to do this.  I am all for the skyscrapers, but why does an entire building need to be a farm?  What if only a certain number of floors on numerous skyscrapers were converted into farms?  It’s not uncommon to see the roof of a building housing a garden.  What if you used this technique, but on a smaller scale?  Why does it need to be 30 stories and a new building?  Can’t it just be an addition to an already built skyscraper and fewer floors?

Until we know just how successful this is going to be, we need to keep in perspective that this is very expensive.  If this is the best way to increase our production for food, then great.  But, there are other ways.  I like the idea, but I wonder if it will work.  What about all you?  Think it’ll work?

Hey everyone…I just wanted to apologize for the long absence.  Had some computer issues and then had some issues with some other things around the house that I got sidetracked from this blog.  I wanted to really apologize to you all for that.  I know you were looking forward to a continuous stream of biological news.  I know I was looking forward to posting it.  Anyways, I am sure you’re asking yourself: alright, so you were gone for a week, did you think up anything new to talk about?  As a matter of fact, I did…Here are some ideas I have for the future of the blog.  Feel free to throw any input you have if you think an idea is absolutely crazy!

• Start a forum for the blog.  As traffic starts to increase, I began to think that something interesting for the blog would be its own special forum for people interested in biology.
• Start a new section on the blog called My Hypotheses.  Although I cannot actually run the experiments myself, they are just different things I think are going to happen and my outtake on it.
• Bring on some other writers.  Because I want to try and make this as much of a community as I can, I want to bring on other writers who would want to post the news or post their own hypotheses about different things.  If you’re interested, please leave a comment and I’ll get back to you.

So as you can see, these are some of the plans that I have for the blog.  I intend on doing some of these updates every once in a while so you know what’s going on.  I really want to create a community around this niche, so if you have any suggestions, feel free to leave some words.  I look forward to hearing from you.

-Jacob

What do you get when you use antibiotics far too much for any old sickness?  Antibiotic resistant bacteria is what you get.  Why?  It’s very simple.  The bacteria learn how to defend against whatever that antibacteria is.  It’s the same for anything.  If you cough on me, I’m going to get sick.  When I get better, if someone with that exact same strand of sickness coughs on me, I won’t get sick.  I’ve grown immune to it.  The same happens for bacteria.  They get immune to what we use against them and then continue to wreck havoc.

For instance, methicillin-resistant Staphylococcus aureus (MRSA) is a super bug.  No longer can it be treated with beta-lactam antibiotics.  Sure, there are antibiotics to counter MRSA, but as bacteria get used to different treatments, they become more and more resistant.  Add the fact that bacteria reproduce like crazy and you get a very simple understanding on why we need to be worried about these resistances.  Fortunately, there is hope.

Rockefeller University scientists have found a way to target the gene in the bacteria that creates this resistance.  In essence, they made a drug that removed the gene’s ability to make the bacteria resistant.  By doing that, the bacteria can be destroyed.  Called Ceftobiprole, this drug was tesed against MRSA which kills more people in and out of hospitals than any of the other drug-resistant bacteria.  The results from this were phenomenal.  100% knock out of the bacteria.  Not 50%.  Not 99.9%.  All bacteria were knocked out.

But, this wouldn’t be an effective treatment if they didn’t try other bacteria as well.  So, the scientists tesed Ceftobiprole on VRSA which is another S. aureus strain that is resistant to vancomycin.  What they found was incredible.  Ceftobiprole knocked them out as well.  By knocking out the gene that allows the bacteria to adapt and become resistant, the antibiotic was able to do its job in destroying the bacteria.

This research is interesting…For so long, the way the game worked was we created an antibiotic, used it for a while, and then stopped using it because the bacteria had grown resistant.  In this case, the bacteria can’t grow resistant.  Therefore, we can see the scientists had played a different game than normal.  Instead of trying to find a way to destroy the bacteria, they found a way to stop its resistance.  Get rid of its defenses and it becomes even easier to destroy.

I think this can prove incredibly useful in a lot of bacterial infections.  I can’t think of any way that the bacteria can best this.  However, science shows that anything is possible and I know that these scientists will have to continue working to ensure that they stay one up on the bacteria.  In this game, scientists won.  Scientists 1 - Bacteria 0.

Source: Science Daily.

When certain signals in a cell start to alter and change, the cells undergo unusual levels of growth which result in tumors.  That’s all cancer really is…an unusual level of cell growth which results in a growth that can kill a person.  There are treatments for cancer, such as radiation and chemotherapy which targets and tries to destroy the cells that are growing in an unusual level.  However, that doesn’t always do it and it doesn’t get to the root of the problem: getting control of that signal that alters the growth of the cells.

Using rats, scientists have started to experiment and find a way in which they can find the ideal level of Myc (a signaling molecule that had a direct connection in the growth of cells).  Basically, if Myc is too low, the cells start to die out and if Myc is too high, the cells start to grow larger with no control and they become tumors.  In the past, scientists had experimented with just turning the Myc molecule off; however, they found that cells actually needed this to survive, so it was proven that turning it off just wouldn’t be a good idea.

What they did realize, though, was that when they tweaked the Myc molecule and just lowered the levels below the threshold that caused tumor growth, the cells actually returned to normal size.  For any scientist, this was probably a very exciting thing.  The importance of finding this threshold was pivotal because Myc exists in both healthy and unhealthy cells.  By figuring out what level was suitable for normal cells and what levels would trigger tumor growth, scientists are now able to figure out a medication that could be used for cancer treatment.

The way I see it, this is a really great way to try and cure cancer.  High levels of Myc is the cause of 50% of cancers.  If a drug were introduced that somehow lowered these levels below the threshold, the cells would naturally return to normal and start dying normally.  However, the thing that scientists need to be careful of is lowering it too much.  If the Myc is turned off completely, the cells will die.  It’ll be a bit of trial and error I am sure to try and find a way to lower the Myc effectively without lowering it too much.

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In the 80s, when HIV first started to appear, no one knew what to do about it.  As time went on, drugs started appearing that would help the patient with it, but would never get rid of it.  As more time went on, other drugs started appearing.  However, the fundamental cause of it and the ability for it to spread was never touched on.  There was nothing scientists could do.  If an infected person transmitted the virus to another person, chances are that person is going to get it.  However, scientists seem to have made a breakthrough that could lead to a new type of therapy for treating HIV patients.  Could it work?  Let’s first take a look at what they do.

As everyone knows, HIV targets the T-cells in our immune system.  It destroys them which is why if someone has it, they are more susceptible to other illnesses.  A person with HIV could die from a disease that would normally not cause any harm.  The thing about HIV is that it requires two receptors on the surface of the T-cell to get into that cell.  One of those is CCR5 which allows things to bind to it.  HIV uses this receptor to bind to the cell and then inject its genetic code to take over the cell.  Without this CCR5 receptor, though, HIV could not spread.  Science has found a way to disable that receptor.

By using a zinc finger protein, scientists are trying to promote mutations in the genetic code of this CCR5 receptor.  But, what is a zinc finger protein?  It is a type of protein that, specifically in this experiment, carries an enzyme to the receptor and breaks the genetic code.  When the repair process occurs for the genetic code, it repairs different than normal.  By doing this, the receptor effectively becomes disabled.  Without it, the HIV can’t transfer.  In essence, this is doing the same thing that a very rare number of people naturally have.  Basically, there are some people that are immune to HIV because their receptor is mutated.  Scientists are hoping that they can take these T-cells from the body and then alter them before putting them back in.  This ultimately creates an immunity to HIV.

Now comes the big question: can it really work?  When testing it out on mice that had AIDS, they used actual human cells.  What they found was after they had disabled the CCR5 receptor and followed the cells for some time, the viral load in that mouse reduced tremendously.  This group of researchers is now hoping to do a human trial in which they will take the T-cells from an HIV patient and then alter the CCR5 receptor before putting it back into them.  Their hopes?  To reduce that patient’s viral load.

I have doubts about this…First and foremost, what will happen if the HIV is removed from the patient?  The CCR5 receptor will still be disabled.  Will that patient then never have use of that receptor again?  Furthermore, on a more ethical stand point, who gets the treatment?  If you find a cure for HIV, you can charge as much as you want.  With Africa having such a high rate of HIV and AIDS, will they get any treatment?  I hope that this therapy does work, I really do.  I just wonder if there will be side effects.  I suppose the human trials will prove what side effects are.  Regardless, this is really a break through in HIV therapy and could prove life saving for so many millions.  Great work.

Earlier, I wrote about how the rise in temperature has caused a change in the type of fish in the Rhode Island Sound.  And I said in the article that the rise in the temperature on the Earth could impact us.  Well, it does.  West Nile Virus first appeared in 1999 as we all remember.  It was spread by mosquitoes and we were told to ensure that we didn’t keep damp environments around because of the fear of mosquitoes multiplying and then spreading West Nile.  That was a common fear, but it only spread even more when, in 2002, a new strand of West Nile Virus appeared.  By 2005, it had replaced the old strand and had caused numerous deaths.  Now, over 100 people a year die from this strand.

So, what happened?  How did this strand of West Nile Virus do so much damage while the other one didn’t?  And more importantly: how did it spread so fast?  Two scientists, Kilpatrick and Kramer, conducted an experiment to try and determine what effects temperature had on the spread of the virus and to try and determine when the virus can be transmitted by mosquitoes.  What the studies showed was that this new strand was much easier passed from mosquitoe to human than the old strand.  What they also found was that this new strand had a better advantage when the temperature increased.

Both strands were able to increase its spread when the temperature was higher.  What this means is that as the heat on the planet increases, the increased replicating of the virus will continue to rise and the spread of the virus will continue quickly.  This new strand is better at replicating in the mosquitoe because of the increased temperature, scientists suggest.  Now what they are looking to prove is whether or not the temperature had a connection in the new strain’s ability to invade so effectively.

A lot of people know about West Nile Virus…The increase in its ability to spread should be a warning call to people about the threat of global warming.  We’re told that global warming might melt the ice caps and that the water might rise.  Okay, that’s sort of a bothersome image.  But, because of global warming, we can suddenly see an increase in a disease.  This has a direct connection to us.  It’s not about fish this time…It’s about a disease that can kill humans.  And, if the virus continues to spread and replicate as fast as it is, it could start to kill more people.  Global warming is an issue…One that we, as a people, need to figure out a solution for.

With the general election going on now and Barack Obama going head on against John McCain, one of the big issues that will continue to pop up is global warming. Both candidates will try and say that they have the best plan to fix the global warming problems. Unfortunately, regardless of what either candidate says about the global warming issue, one thing is for certain: it most definitely is occurring. Despite what some critics might say about how it’s not happening and that we need to focus on other things, studies suggest that global warming is very real and that we need to do something to correct it.

When looking at the fish communities in Narragansett Bay and the Rhode Island Sound, scientists found something that was incredibly troubling. Normally living in these bodies of water are vertebrae species (fish), but scientists are noticing that more invertebrates (lobsters, etc) are starting to appear. And, rather than species that feed on the bottom (benthic), there are species that are now feeding higher up in the water column (pelagic). So, the big question that people ask is: why does this matter?

It matters because of the domino effect. Consider this food chain…Phytoplankton normally sink to the bottom of the ocean to the bottom fish. However, more and more, it is being found that the phytoplankton are being consumed by the zooplankton by fish that prey on plankton. This has led scientists to a conclusion about the increase in the number of lobster and crab: because there are less bottom feeders to eat the phytoplankton, the invertebrates are eating them instead which is resulting in an over population of the species.

When looking at this, we can see that the food web has altered. Sure, it might not matter much to you and I, but the food web leads up to us one way or another. Fish is a big market in that area and normally, they would catch cold water fish which are bigger. Fishers are finding that they are catching more fish, but they are smaller. Warm water fish are naturally smaller, but more abundant. The waters are getting warmer and that is, scientists argue, only possible because of global warming.

The big fear that scientists have now is that this area of water (in Rhode Island) will begin to change and turn into estuaries to the south. They have similar problems where animals that would not usually appear in the area are suddenly popping up. And, there is only enough space for so many animals. So, these new, dominant animals are beating the other ones out. So, I think you can see where this is leading…Sooner or later, where do the cold water fish go when there is only warm water? No where. Global warming is an issue that we need to worry about because as much as this article only talks about the fish, it will harm us as well.

For those that know, a B-cell is a cell that is a part of the immune system that creates antibodies to give the body a sign when that antigen enters the body again. Basically, once you’re sick for a first time, it never happens again because your body has developed an immunity. That immunity comes from the antibody. Unfortunately, the B-cell isn’t all good. Research suggests that the receptor on the surface of the B cells actually cooperates with the MYC oncogene (a gene that regulates other genes and, when mutated, often causes cancer). This cooperation speeds up the development of lymphomas.

Cancer grows fast enough as we all know. However, the issue at hand is that with the increased speed of these lymphoma developments, it gives less time for doctors to essentially treat it. Studies show that Non-hodgkins lymphomas have become 85% more prevalent in the past twenty years. The unfortunate fact is that 90% of those are B-cell lymphomas. But, scientists do have hope. According to the lead research, Yosef Refaeli, PhD:

“Our findings have pointed to the B-cell receptor and its signaling pathways as very promising therapeutic targets for B-cell lymphomas.”

What does that mean? It means that they are looking to see if there is a way to treat lymphoma by working with the B-cell receptor. The study showed that with the B-cell receptor working, in essence, it was creating a autoimmune response with the tumor. So, the body began to destroy itself, but not the tumor. What they did was blocked the B-cell receptor with immunosuppressants. If the immune system is not beating itself up, then there’s nothing to worry about. The tumors were effectively destroyed.

Dr. Refaeli was thrilled and rightfully so. If this treatment does work then they can use this understanding to try and combat other cancers, lymphomas, but also autoimmune diseases. By understanding how the B-cell interacts with the MYC oncogene, scientists can find a way to hopefully limit its uses for the tumor. Survivability can increase tremendously with this research.

What does that mean for all of us though? I mean…How many people possibly die from autoimmune diseases alone? Here’s a number…Autoimmune disease death is the number eight cause of death among women aged 15-64. There are a lot of ways people can die and to be ranked number eight is definitely reason enough to be excited about this research. For more numbers, here’s this: 19,160 people have died from Non-hodgkins Lymphoma this year. So, when we look at these numbers and realize what this research could do, I have to say one thing: Hats off to Dr. Refaeli and his team.