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Getting into the psyche of a virus

3/31/2016

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Virus DNA replication
A few questions have sprung to my mind regarding our last post:
1) Why are viruses so destructive and even deadly?
2) What then, does get rid of a virus?
3) Viral infections, once begun, often progress to bacterial infections, but why?

I’m NOT going to get to those questions just yet, because a suggestion was made by a loyal fan (can I call you that, Don?) to cover what an antiviral is, as opposed to an antibiotic. This makes sense given that antiviral drugs for the flu are available, and you may have been prescribed that in lieu of an antibiotic. So, let’s see what the difference is between an antibiotic and an antiviral, before we get onto our other questions.

In this graphic, we go back to the basics to find a strategy to undermine a virus. A virus is nothing more than a capsule or vehicle for its DNA/RNA. And we learned from our antibiotic post that antibiotics target specific molecules within a cell that disrupt its normal cellular functioning. Well, with a virus, there’s no molecule to disrupt, so antibiotics are actually useless against it.
So what do scientists target against a virus? 1) the capsule, and 2) the DNA/RNA.

A virus’ one and only mission is to make more copies of itself. But since it doesn’t have the infrastructure to do so, it takes over a cell in order to use all the special enzymes and building materials to for its own goal: to copy its DNA/RNA and make new virus capsules to house those new copies. If this is the case, can you guess what the antiviral might target in order to stop viruses from making copies of itself?

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Virus versus bacterium

3/25/2016

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Flu versus bacterium
We left off with the question: why don’t antibiotics work on viruses? But then I proceeded to "answer" that it was because bacteria are alive and viruses are not. So you were probably thinking, why is she asking that question again? Because I wanted to show this graphic, that’s why!

This chart depicts the main outside and inside components of a virus versus a bacterium. A virus is merely a capsule that carries nuclear information stored in the form of DNA or RNA. A bacterium also carries nuclear information. But here’s the big difference: A bacterium is by definition a cell; it contains all the components to process fuel to support its functions, like getting around to find food or mates, and to make repairs to malfunctioning equipment. It is a self-contained organism that is capable of surviving on its own and “providing” for itself, and therefore has structures (organelles) within to perform these basic functions. Antibiotics disable these critical functions, like the Gyrase enzyme that unwinds the DNA from the previous post. So if the antibiotic can disable that function, the bacterium cannot perform the tasks dictated by that DNA, and it will die.

In contrast, a virus is merely a container for its DNA or RNA. There’s no infrastructure to fix itself, to process fuel, etc. It is NOT a cell, and therefore, not ALIVE. So, knowing that antibiotics mainly cripple a vital function of a cell, how do you go about doing that when that particular function doesn’t exist in your target? And how do you kill something that’s not alive anyway? THAT, is the fundamental reason why antibiotics don’t work on viruses.

Three more questions to follow up from this discussion: 1) Why are viruses so destructive and even deadly, 2) What then, does “inactivate” or get rid of a virus? And 3) I said in the previous post that viral infections once begun often progress to bacterial infections, but why? We’ll cover these topics next!
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What really tames a virus?

3/18/2016

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Cipro, antibiotics, gyrase, Scientific American
When you’re sick and have been diagnosed by your doctor as having symptoms consistent with the flu, sometimes you’ll get prescribed an antibiotic. But antibiotics don’t work on viruses, and Influenza is a virus. So, what’s the deal?

The answer to why antibiotics do not work on viruses is very simple: it’s because viruses are not alive, and antibiotics target alive things. The reason why some docs prescribes antibiotics anyway lies in the fact that viral infections can progress to bacterial infections. The antibiotic is meant to head off or fight the bacterial infection. So, let’s talk about how exactly antibiotics work.
Antibiotics do one of two things: 1) they kill the bacteria (Bactericidal), or 2) they stop the bacteria from functioning normally (Bacteriostatic), as they are cells after all. This graphic which I did a LONG time ago for Scientific American shows the particular mechanism for the antibiotic Cipro, and furthermore, how the bacteria evolves to render Cipro ineffective. Basically, the mechanism of action for Cipro is that it cripples an enzyme called Gyrase, an enzyme that unwinds the DNA to allow replication to occur. If its DNA can’t be unwound, then the bacterium can’t replicate.
Now that you know the basics of why antibiotics work on bacteria, why do you think that antibiotics don’t work on viruses?
Answers and exploration, in next post.
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The flu season

3/17/2016

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Influenza infection, influenza infection versus common cold
We’re starting a new topic that is dear to my heart, only because I have a personal connection in having participated in research in this field 20 years ago as a lab tech in the Laboratory of Infectious Diseases at the NIH.

But before we even really dig in, let's start with a very basic question: what is the difference between the common cold and the flu? The answer can be found in the above image.

Look at the temperature labeling! Both the common cold and the flu are caused by viral infections, and both start out as head colds. The fundamental difference is that in flu, virus may reach the lungs and cause widespread infection. In a common cold, this does not occur.
Here's a 52-sec. video showing a simplified process of how you get the flu.

Now, the next question I want to ask has to do with treatment of the flu. Has anyone ever been prescribed an antibiotic for the flu?

https://vimeo.com/148268843


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Meal planning is essential

3/12/2016

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Meal planning, dietary planning, meat substitutes, changing eating habits
One of the most frustrating things about science is that, as information is gathered and then disseminated, sometimes the data then proves contradictory to a prior statement. To a scientist, this is a normal occurrence and is all in the pursuit to contribute to the “What we know” category.
However, when this becomes a matter impacting upon daily life, like what CAN we eat, what do we consumers do with this contradictory evidence?
I’m a meat-eater. I cook a lot of ground turkey, chicken and fish, but I enjoy so many different kinds of meat. Steak? Nom nom. Lamb? Bring it. Ham and bacon? Must be brunch time! And hot dogs? YES, a Hebrew National, reduced-fat, all-beef, slathered with Harris Teeter brand chicken chili and shredded cheddar...oh YEAH.
Our scientific history, when it comes to healthy eating, is peppered with over-rulings, from fats to sugar substitutes to carbs to sugars. But instead of completely demonizing the current food “enemy,” what if we try to moderate, and control/reduce our portions? I am not sure I can completely give up animal proteins, but, I can at least try to reduce my intake!
I cook 5-6 nights a week. Depicted are the most common meals I tend to prepare, and the thoughts I’ve come up with thus far on my modified strategy. I know alot of the portion sizes are because I have been doing this a LONG time, and so for example, I portion out a 12-16 oz bag of frozen veggies to ensure that I have enough for two meals for 2 people. Likewise, a 16-oz bag of fresh spinach is 4 servings. With meat, like salmon, I buy a big slab that I immediately cut into 5-ish oz portions, wrap up and freeze. I have a food scale, which is probably the most valuable kitchen tool I own.
SO, when this IARC announcement came out, I decided that there were some things I had wanted to get back to, that I had been too lazy to do before. For one, I have always LOVED tofu. I grew up in a household where we always had 3-4 kinds of tofu in our fridge: the plain kind, the “fried” kind, the fermented kind, and the stinky kind. I have wanted to cook more with it, but the prices in regular grocery stores makes it hard for me to buy when I know I could buy 4X the amount at a Chinese grocery store, but which is a good 45’ drive for me. So, this is a great reason to simply swallow the cost and perhaps treat it like a veggie.
I would love suggestions and to hear how you might be trying to reduce your animal protein intake!

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The verdict on meat...?

3/11/2016

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NDMA, meat, IARC on processed meats, N-nitrosodimethylamine
In late October, 2015, the International Agency for Research on Cancer (IARC), an independent entity established by the World Health Organization 50 years ago, put forth a statement classifying red meat as “probably carcinogenic,” and processed meats as “carcinogenic.” For a full reading of the press release (it’s only 1.5 pages), go to:
http://www.iarc.fr/en/media-centre/pr/2015/pdfs/pr240_E.pdf
Now, if you’re a meat-eater like me, you may be alarmed. So, I wanted to dive into this further to give it some context.
A Harvard University health publication from 2004 (updated in 2008) gave me a good start on the history into the study of red meat and what we already knew about its influence on cancer risk (colon cancer, more specifically). There are two major studies they point out, one from Europe with nearly 500,000 participants, and one from the US of nearly 150,000 participants. Regarding the European group, to quote directly from this publication:
“The people who ate the most red meat (about 5 ounces a day or more) were about a third more likely to develop colon cancer than those who ate the least red meat (less than an ounce a day on average).”
The IARC’s job is to examine all current data produced around the world and interpret the findings of the data. So the pronouncement does NOT specify amounts of red meat and processed meat that might be safe to eat.
What is key is frankly something that the science world has been advocating for a while now–based on past research–to limit your intake of red meat, and definitely to limit your intake of processed meats.
The 64,000-dollar question is: if I do not plan to cut out red meat completely, how much do I limit my red/processed meat intake?
This is one reason I am highlighting the Harvard article, because it does give us some type of gauge, based on data, of the amount of red meat that significantly increased colon cancer risk. This is ONLY meant to allow us to understand what parameter was in place that led to the outcome, but by no means does that mean that if you eat say, 4 ounces of red meat a day, you’re in the clear.
The other piece of this is to understand why there’s a connection between red or processed meats and cancer incidence. It all goes back to chemistry, of course, whereby these particular types of meat produce chemical compounds that can damage the DNA in our cells. This class of chemicals are the N-nitroso compounds; specifically, NMDA, and has been listed as a known probable carcinogen according to the IARC, the Environmental Protection Agency (EPA), and the National Toxicology Program (NTP). We know from basic biology that cells have repair mechanisms in place, HOWEVER, when the damaging substance overwhelms the cells, repair mechanisms can’t keep up and a damaged cell is left behind.
With respect to processed meats which includes anything cured, smoked, pickled, and amalgamated (like hot dogs) from animal body parts, I kind of think we ALWAYS knew they were bad for us. So, although I do still eat bacon, ham, and hot dogs, it is a rare “treat” and not a weekly staple.
In the end what are we to do?
Next post, I’ll at least share MY strategy with you.

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We conclude on family...of the transitive nature

3/4/2016

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Periodic table organization, elemental families, transition metals
In life, there are always exceptions to a rule. And though we have these rather elegant patterns that dictate the organization of our periodic table, we also have a gigantic asterisk to denote an exception to these patterns. This exception is the transition metals, as their reactive electrons are mercurial!
We‘ve been stressing the importance of valence electrons, those in the outermost shells of the atom, because these are the ones that are most prone to being snatched, to snatching, or, to share, all in the pursuit of obtaining the full valence shell “octet” status.
Transition metals, however, are curious in that the general rule for filling up shells one by one doesn’t really apply. In fact, the second to the last shell tends to get filled before the valence shell. Look at copper. One would think the filling order would be: 1s2, 2s2, 2p6, 3s2, 3p6, 4s2, 3d9, according to the rule. Actually the last shells as filled this way: 3d10, 4s1!
Each shell level (n=1, 2, 3, 4 etc) can hold a maximum of 32 electrons, but often due to optimizing spread as a result of electron-electron repulsive forces, proton attraction pulling them closer to the center, and electron spin, the electrons don’t often max out that 32....Unless it’s a transition metal! In this case, often this second to last outer shell gets “over-stuffed,” and sometimes these inner-shell electrons are involved in reactions! This is why these elements end up with a “B” designation in their groups, because frankly, they do NOT fit into the patterns that the “A” groups do.

Thanks for sticking with this journey. I hope it gave you more appreciation for the Periodic Table and the evolution through which it has gone!

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Between family members, traits are uncanny

3/3/2016

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Periodic table organization, elemental families, valence electrons, elements and their reaction characteristics
We’re now going to cover the elemental families that comprise the table. You can easily find the family descriptions online, so I’ll try to look at this from a different angle.
The chemical properties of an element are determined mainly by how many valence electrons it has. This factor also greatly dictates the organization within the table of the elements because it dictates how that element will react in the presence of other elements. So let’s look at the elements of the left-most column, IA: these elements have one electron in their outermost shell. This lone electron occupies the outermost orbital by itself, and is therefore highly susceptible to being taken away by elements that are one electron away from having a completely full outermost shell of 8 electrons (Ionic bonding; octet rule). What about the fact that more and more protons are present as we go down the group? We’ve learned that that collective proton force prevents electrons from being snatched. But remember, these electrons get farther away from the proton forces as more shells are added, so physically, they’re not influenced so much by the protons.
The fact that these elements very easily lose their lone valence electron means that they REACT similarly to each other when interacting with other elements. That’s what gives them SIMILAR chemical properties and hence what makes them logically part of the same group.
Why would elements in group IA allow this, for as a result it now has an unbalanced charge of +1? Here’s the beautiful part: once that lonely electron is gone, that original, outermost shell is now empty. For all elements but Hydrogen, “underneath” that now-empty shell is a full, and therefore stable, shell! It’s happy to lose that one electron in order to reveal the full shell underneath! Now it effectively has a full valence shell.
SO, did anyone catch the “A” designation after the group “I” part? Next post!

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