This lovely piece is the fourth and final winner from our 2012 guest post blog contest. Enjoy!

One clone, two clones, red clone, blue clone

by Elizabeth Dvorak

I am a coati,

I live in Brazil.

Soon I will be cloned!

 coaties

Just the thought makes me ill! (1)

You think that with two me’s

You’ll have a nice zoo

With pretty coatis for viewers to view

You say I’m endangered, and need to live on

Because all the coatis simply cannot be gone

Our numbers our dropping, much to your dismay.

But why do you think that we’re wasting away?

It’s all thanks to you,

 yes you are the cause

You come with your axes.

 You come with your saws.

You burn and you tear with your land-hungry claws

How can we live when our habitat’s dying,

our homes are cut down and streams are all drying?

The problem can’t be solved with what you are trying

You must understand what I am implying;

Planet first!

Clones later;

that’s all we are crying!

And cloning would decrease bio-di-ver-si-ty,

A variety of genes is more helpful to me.

What if we’re exposed to a new pathogen,

Or our external conditions change again and again?

Some genes can survive, but some simply will not,

The good genes will stay,

the bad ones will be squat.

If we’re all identical, one small attack could wipe us out!

And your exotic zoo will have more reason to pout!

So now you can plainly see,

Clones are not fun like you think they would be!

We can’t have a me that’s exactly like me!

With more genes in our species, we’ll live happily!

And it’s so tough to make cloning successful

Ending poaching would be oh so much less stressful!

With such a teeny tiny chance you will succeed,

Stop working on something we don’t really need!

I once had a friend, mister Gary the gaur.

He was cloned but then lived for just 48 hours!

The danger, the horror, the dreadliest dread!

Oh goodness gracious, me oh my! I could end up deader than dead!!

The biggest misdeeds here,

are your motives I fear.

You aren’t even worried about conservation,

But only your precious and rare reputation!

What’s the point of more us’s if we cant live in our habitat?

 There simply isn’t one, and that’s that!

We want to live, just like you! We don’t want to be made for a zoo!

Created for other people’s entertainment?

Every coati, kept in containment?

And all of us the same, nothing special, nothing new?

We’ll all be DESTROYED

 For the sake of your zoo.


This is the third in the series of four winners from the 2012 guest post blog contest.

by Emma Carline

In recent years, concern has been growing over increased bacterial resistance to antibiotics. An article from The Guardian now asks if we are ready to face the “post-antibiotic apocalypse”. The article comes in reaction to worrying updates on the spread of infectious bacteria containing the NDM1 gene, bacteria’s latest weapon against our most powerful category of antibiotics. Because antibiotics have become integral to medical practices today such as organ transplant, surgery, and chemotherapy, there is certainly reason to panic (Boseley 2010). However, panic is not an excuse for recklessness. Professor Richard James of the centre for healthcare associated infections at the University of Nottingham, proposes that antibiotic resistance be combatted by taxing antibiotic treatments (Boseley 2010). However, merely slapping a tax on antibiotics is both a careless and ethically insensitive method of dealing with the problem. If we want to avert the prophesied antibiotic apocalypse, the first step we should take is to reform doctors’ prescribing practices.

mrsa-cartoon

Since antibiotic overuse has been found to be correlated with antibiotic resistance, most proposed plans of action by specialists like James aim to reduce the amount of antibiotics we use. Taxing antibiotics may accomplish this, but it places an unfair burden on patients. For who ultimately controls how much antibiotics are being used? It’s not the patients. While a patient’s decision to undergo a treatment may be limited by their paycheck, it also depends on how dangerous they believe their condition is, according to their doctor’s diagnosis. If we trust doctors as medical authorities, we generally have confidence in their prescriptions. Thus if a doctor wrongly encourages a patient to take antibiotics, and an antibiotic tax is in place, the patient literally pays the price for their doctor’s diagnosing mistake. Because doctors are so influential in patients’ choices of treatment, it does not make sense to restrict antibiotic use by making patients pay a tax for antibiotic treatments.

It is not only ethically wrong, but inefficient. Taxing antibiotics cuts down on antibiotic use by taking advantage of people’s spending limitations while ignoring antibiotic misuse. This results in people being given antibiotics that don’t actually need them and denying antibiotics from those who do. Taxing antibiotics could demand thousands of dollars from patients while ignoring the issues that caused the pandemic in the first place. If we must reduce antibiotic use, we should first stop prescribing them when they’re not needed. Studies show that overprescribing is commonplace. A 2011 study in Michigan showed that 77.2% of adults diagnosed with bronchitis were prescribed antibiotics by doctors. The vast majority of cases of bronchitis are not caused by bacteria and do not require antibiotics at all. It has been estimated that up to 50% of antibiotic prescriptions are inappropriate. Instead of penalizing people for listening to doctor’s advice, we should aim to make that advice better. Taxing is an inefficient approach to solving the bacterial resistance problem as it does not amend the practices that caused the problem itself.

Not only is regular review of doctors’ prescribing practice needed, but also new medical research. While antibiotics have been developed to fight specialized strains of bacteria they are useless if doctors cannot identify the type of infection a patient has.  As a result, “broad spectrum” antibiotics are used extensively. These antibiotics fight a broad range of bacteria and are used when the exact strain of bacteria is not known. If more research was devoted to developing tests for diagnosing different bacterial infections, we could lessen our dependence on these non-specific mass-produced antibiotics, which are most susceptible to resistance from bacteria. By improving diagnostic tests, we can reduce both antibiotic overuse and misuse – without pinching pennies from patients.


This is the second in the series of four winners from the 2012 guest post blog contest.

by Ayush Ray

What do these four have in common?


2 3

4

1

It was rumored that the North Korean dictator would inject himself with virgin blood to stay young, Pope Innocent VIII on his deathbed was transfused blood of three young boys, and of course we know about the blood drinking habits of Dracula. Fictional or not, Dr. Saul Villeda of Stanford seems to show that these guys were on to something. Can young blood really be the key to the mystery of immortality?

Villeda’s research team shows that it’s partially true… for mice, at least. In the experiments conducted by Villeda and his team, old mice were given transfusions of blood from young mice. The hippocampus of the old mice given young blood showed changes in the expression of 200-300 genes involving synaptic plasticity (the ability of our brain to develop connections between neurons). Also, young blood boosted the strength of neuronal connections where development had previously been stagnant. Essentially, cognitive function of old mice given young blood improved, as shown by conducting a standard memory test.

“Do I think that giving young blood could have an effect on a human? I’m thinking more and more that it might,” said Villeda.

Does Villeda’s quote scare you? Well don’t get your knickers in a knot. It’s unlikely you’re going to have your ol’ grandpa asking for your blood to stay young.  Tony Wyss-Coray, also at Stanford hopes to identify these substances present in young blood that are not present in old geezer blood. What exactly are those substances, and how can this research be applied to humans? Research conducted on telomeres in Harvard in 2010 might give us some clues.

5

Telomeres are essentially ‘caps’ on chromosomes, the natural shortening of which are thought to cause the negative physical consequences of aging. The Harvard team injected an engineered telomerase (enzymes which stop telomeres from shortening)  into genetically modified mice and noticed improvement in many age related complexities including cognitive functions. So the magical substance we’re looking for possibly has something to do with maintaining the telomere sizes in cells.

So what’s the catch? Cancer. It turns out that rejuvenation of dormant telomerase in humans causes a much greater risk of cancer. So, replicating the kind of research at Stanford or Harvard on humans poses two main challenges:

  1. Scientific challenge: We have to recognize the fact that rats are not miniature humans and simply because cancer did not develop after drug injection in the Harvard rats doesn’t mean that humans will not develop cancer either. Also, the price humans pay for greater complexity in physiological functions is a greater challenge is modeling a suitable substance for humans.
  2. Ethical challenge: Let’s assume that this wonder substance has been made. How does one even begin the appeal to review boards to approve testing on humans with such unknown health effects, especially cancer?

Resolving these issues will be a big milestone in our search for immortality. These are the initial speed bump we must over come in order to provide age-related therapies to millions who suffer from cognitive decline and perhaps even other physical degeneration caused by old age. Though it may be too late for the oldest generations among us, for those who are young, we may be on the way to thwarting old age (without having to siphon off the blood of children).




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