walker texas ranger tears

As I sat and ate my grilled cheese sandwich on my lunch break not long ago, Walker Texas Ranger played on the TV. Walker’s girlfriend, Alex, has survived being kidnapped and almost killed, and is now lying in a hospital bed while he lovingly comforts her in all his ginger glory. He tells her how much she means to him, and then pulls a ring out of his pocket. And there it is… “Alex, will you marry me?”  It pans to the highlights of their relationship. In typical cheesy 90’s slow-mo style, Alex and Walker stroll through fields hand in hand, laugh together, cry together, and share loving looks into each other’s eyes as their perfectly teased Texas hair blows in the breeze.

And suddenly, I am bawling.

The credits begin to roll and I brush my tears off of my grilled cheese and wipe my eyes. Something isn’t right- I should be laughing hysterically, not crying hysterically. I look at my calendar on my phone and then it makes sense.

Let me tell you folks, hormones are very real. They don’t only control your mood- they control things like sleep, friskiness, stress response, fight or flight response, puberty, hunger, parenting, and in-utero develepment. Pretty much every process or event your body undergoes is driven by hormones in one way or another

But how do they work? Having to direct things from slow-paced things like ovulation to fast-acting processes like adrenaline rushes, how do they make things happen? Where do they come from? Where do they go? How do they get there?

Hormones are little molecules that are manufactured by your body. They can come from individual cells, organs, or more frequently from glands (think thyroid, testes, ovaries, adrenal, etc.). Different glands manufacture different hormones.

Major glands  (wikicommons)

To name a few: Testes and ovaries manufacture sexy hormones that influence puberty, ovulation, parenting, menopause, and male machoism. Your adrenal glands sit on top of your kidneys and produces adrenaline- key in stress response, fight or flight, and cell metabolism. Your thyroid gland in your neck manufactures a variety of hormones, mainly affecting metabolism. The big daddy gland- the pituitary- is buried at the base of your brain and is perhaps our most primitive gland. It regulates just about everything from sleep to sex drive. The pineal gland, also of primitive origin, plays a role in light detection and internal calendar regulation.

From their respective glands, hormones are released into the bloodstream in order to travel to their target tissues. Let’s take adrenaline, for example. Say you’re walking down a dark alley and all the sudden a man steps out in front of you with a knife and says “give me your money!” Time for fight or flight response. Your brain immediately sends signals down to your adrenal glands, which then flood your whole body with adrenaline. But you only need certain tissues to respond, right? Your cardiac muscles need to quicken, your pupils need to widen, your blood vessels need to dilate so you can haul ass. Well, nature has it so that only these target tissues have receptors to recognize these hormones. So while your pinky toe is getting the same dose of adrenaline, it don’t give a $h*t. But the cells of your heart and blood vessels certainly do- and respond to help you get out of this hairy situation. This is how the whole hormone system can be so refined- receptors only exist where their hormones are meant to act.

The guy with a knife is still standing in front of you. You kick him in the balls and run. You make it safely away and stop to catch your breath. That jittery feeling that makes you ready to punch somebody in the face is the adrenaline coursing through your body. Within the next few minutes, you’ll start to feel more normal. This is because the adrenaline is being cycled out of your cells and metabolized to the point of no longer being hormones.

The system is pretty much the same for slow-release events like ovulation and puberty. Your pituitary regulates your internal calendar, activating the right tissues at the right time.

When you break it down like this, it all sounds so scientific and straightforward. But when you’re sitting next to a lady with a baby on an airplane and are desperately hoping she’ll ask you to hold it, or crying at Walker Texas Ranger, it doesn’t feel so scientific or straightforward. Makes you wonder how much of the human experience is just molecules binding to receptors. But then again, maybe that makes it that much more extraordinary.

have you SEEN a dik-dik?

A recent and actual G-chat transcript, between my sister and me.

Alix: Have you SEEN a Dik-dik?

Me: No. What is a Dik-dik?

Alix: A tiny tiny antelope.
             They are monogamous.

They can run 26 mph.

Can you imagine if a Dik-dik ran past you at 26 mph?

It would be amazing.

I wish lap giraffes were real.

Okay got to go. Love you bye.

Of course, I immediately Wikipedia’ed Dik-dik, and was faced with the cutest ungulate I’ve ever seen.

OH MY GOD. (wikicommons)

They are little antelopes that live in Africa. They eat small plants and shrubs, throw it back up, chew it some more, and eat it again. This would be gross, but they’re so tiny that it’s more funny than it is gross.

What really caught my eye in the Wikipedia article was the blurb referring to their monogamy. It reads:

“Monogamy in dik-diks may be an evolutionary response to predation; surrounded by predators, it is dangerous to explore, looking for new partners.”

Monogamy exists all throughout the animal kingdom. Selective pressures vary in each instance of it, but it is safe to make the sweeping statement that monogamy usually evolves as a means to protect highly vulnerable young. Take us, for example. The survival rate of babies (before the present-day civilization) must have been waaaaay higher if Dad stuck around to protect mom and child from saber-toothed tigers and to help provide food. On the other end of the spectrum, consider a housefly. Baby houseflies are ready to buzz off and start life as soon as they hatch. Mom and dad aren’t even around- they’re already off having irresponsible sex with new partners. Monogamy wouldn’t make sense for them.

Dik-dik being sassy. (pbase.com)

Never before had I seen monogamy explained as a response to predatory danger for the parents. No way this could be true, I thought to myself. I researched further, and lo and behold: a whole paper has been published on Dik-dik monogamy. And they found something pretty interesting.

It had been previously assumed that Dik-diks were facultatively monogamous. Facultative monogamy is monogamy that is the result of restrictions on resources. In other words, male Dik-diks could only defend enough territory to accommodate one female, and that’s why they only mated one female. If more resources were available, then the male Dik-diks could afford to pimp two or more females.

Researchers found evidence to the contrary of this model. Male Dik-diks routinely defend territory (and therefore resources) to accommodate several females! Why do they date just one lady, then?

Obviously, because they have the capacity to love. (Alix, you stop reading here. Life will be better if you do.)

No, that’s not true. Rather, it’s because the males are jealous little suckers and don’t want any other guys picking up their girlfriends. It’s formally called mate guarding- and is an evolved behavior that increases the likelihood that their genetic material is passed on to the next generation. If Dik-diks had the equivalent to “The Maury Show,” the audience would be sorely disappointed that Dik-diks rarely question the paternity of their fawns. Daddy Dik-diks keep close enough eyes on their ladies that they’re not too worried about it.

This being said, monogamy rarely occurs in nature without extra-pair copulation, aka “getting some on the side.” In Dik-diks, only males will engage in extra-pair copulation. Mated females are noted to rarely, almost never, engage in extra-pair copulation (go figure).

So, several components contribute to Dik-dik monogamy. It is safer for the tiny, herbivorous animals to stick to their territory instead of going down to the local drinking hole to try to meet new Dik-diks. Also, mated pairs spending almost all of their time together increases paternal fidelity. And even though males have the capacity to mate more females, they don’t- the lingering urge to mate guard has been passed down from earlier times when perhaps the Dik-dik male could only defend territory for one female.

My initial balking reaction to the explanation of Dik-dik monogamy was short-sited. It wouldn’t make sense for the natural world to be as diverse and multifarious if evolution followed a blueprint. Regardless of how many notes I took or outlines I made about monogamy as an evolved reproductive strategy while I was in college, I don’t know diddly squat.

When asking questions about the evolution of life, always remember to keep an open mind. If researchers hadn’t kept open minds about Dik-dik monogamy, we’d still be without the knowledge that males mate one female, even though they can mate more. And I prefer to live in a world where Dik-diks stick by each other's sides in a non-obligatory capacity. Don’t you?

Here's the paper:

Female dispersion and the evolution of monogamy in the dik-dik. Brotherton, PNM, and Manser, MB. Animal Behavior, 1997. Volume 54 (6), 1413-1424.

put your science panties on (part 2)

 Last time, we covered the first part of the journey a neural signal takes on the way to becoming muscular movement.  We started at the brain and made it all the way down the nerve highway to a muscle. And it is here at the neuromuscular junction that you have been waiting with bated breath for the tale to continue.

When an action potential makes it to the end of the nerve road, it must make something happen in your muscles. The electro-chemical energy of the action potential must be somehow translated into kinetic energy. While your muscles are capable of creating large-scale movements like swinging a golf club, the tiny movements of the molecular structures of your muscles is where this kinetic energy is translated. So let’s get up close and personal with muscle structure.

Your muscles are like bundles of cords within bundles of cords- kind of like Russian nesting dolls- bound together by connective tissue. When you get down to the cellular unit, a single muscle cell is called a muscle fiber. A single fiber is made of smaller units called myofibrils. It is in these myofibrils that the basic contractile units of muscles are found. This basic contractile unit is called a sarcomere. Sarcomeres are made up of long proteins that slide past each other to make the muscle contract. These two stringy proteins are actin and myosin.

A relaxed sarcomere

Myosin filaments have these little bulbs hanging off called “myosin heads.” The myosin heads like to link up with the actin filaments. Through a process involving some supplementary energy molecules (holla, ATP!), the myosin heads creep along the actin filaments, bringing them closer together. Think of a little army guys (myosin heads) climbing along a rope (actin). This is muscle contraction on the tiniest level.

Contracted sarcomere

Just watch this. http://www.youtube.com/watch?v=zQocsLRm7_A&feature=fvwp

So, imagine that a whole bunch of sarcomeres are crammed into a muscle fiber. And a whole bunch of fibers are crammed into a single muscle. You’ve got tons of sarcomeres, working simultaneously, causing a whole chunk of muscle to squeeze in on itself.

Well that’s all well and good. But how is it that we’re so coordinated? I wouldn’t call Beyonce’s performance in the video for Single Lady “chunks of muscle squeezing themselves.” I mean, one muscle group is capable of a wide variety of motion, so there must be more nuance to it than  “chunks of muscle squeezing in on themselves,” right?

Right. This is where we go back to part 1- the innervation of the muscle. The complex maze of nerve fibers feeding muscle is responsible for the precise control we have over our movement. Your brain can selectively fire the pathways that feed just part or parts of a muscle. These different combinations are what make a smile different from a frown, from an inquisitive facial expression, from an embarrassed expression, from an amused expression. All use the same muscle groups, but each stimulates them in a different pattern.

The complex neural to motor pathway, to me, is one of the most intricately wired processes in all of Vertebrata, but always funnels down to one of the most basic: the little sarcomere. 

put your science panties on (part 1)

Let me warn you before you embark on this post: it’s a little more technical than usual. We’re going to cover the mechanics of both your nervous system and your muscular system, in our first ever two-part blog post (ooooh, aaaaaah!). So unless you have a solid 20 minutes or so, I suggest saving this one until you are at home with a cup of hot tea with Wheel of Fortune on in the background.

It’s easy to avoid thinking about how your muscles work because it can be an overwhelming thought. How complex they must be to be capable of lifting heavy things and also finite tasks like writing! And even MORE mind-boggling is the system that connects your brain to each and every muscle cell in your body. How in the cornbread hell can a simple thought turn into an intent, and then turn into an action? How can you go from thinking about scratching your head, to intending to scratch your head, to scratching your head? It is confounding.

Your brain has highways reaching out to all of your skeletal muscles. These highways are your nerves. Most of them exit your skull and travel along your spine in that clump called the spinal cord. From there, they branch out to your muscles.  A single one of these nerve cells is called a motor neuron, and is not a blob of a cell like you usually think of.  It has a body and a long skinny “stem” called an axon. They’re long and skinny because- well, they’re highways! In fact, the longest single neuron you have runs from the base of your spine to your toes- up to a meter long. Think of the motor neurons a giraffe has!

Figure 1: A single neuron.

These highway nerve cells are uniquely structured for carrying signals- chemo-electric signals- from your brain to your muscle cells. Your brain tells your muscles what to do via your nerve signals. But these signals are not “encoded” with information- one signal does not vary from the next, nor do they vary in strength. It’s kind of like binary code- it’s either a 1 or a 0. In this case, there’s either a signal, or there’s not. Your neuron fires, or it doesn't. One single signal is called an action potential.

An action potential is basically a change in voltage of the membrane of a nerve cell. It’s like this wave of voltage that travels along one nerve cell, setting off the one after that, and the one after that, and the one after that, and- well, you get the picture. But these nerve cells- their membranes in particular- are specially built for carrying action potentials.

Alright y’all. Time to put your science panties on. It’s about to get real up in here.

The inside of the cell is negatively charged, in respect to the outside of the cell. Positively charged potassium (K) and sodium (Na) ions are floating around, both inside and outside of the cell. There are little pumps in the membrane are constantly pumping these ions against their concentration gradients in and out of the cell to maintain a high concentration of K and low concentration of Na inside the cell- which maintains an internal charge of about -70 millivolts. This is called resting potential.

Figure 2: The basic set up of the axon of a neuron: The movement of Na+ and K+ ions  through channels and a pump
across a the membrane cause depolarization, repolarization, and hyperpolarization of the cell membrane (aka an action potential)

Now, let’s say the neuron’s dendrites become excited enough to set off an action potential. Little voltage-dependent sodium channels will open up, allowing sodium ions to diffuse along their gradient- into the cell. This influx of positively charged ions raises the inside voltage. This part is called depolarization, since the cell is becoming, well, depolarized.

Once the inside of the cell reaches about 40 mV (notice, that number is now positive!), sodium channels close and their neighboring voltage-dependent potassium channels open. Then, the potassium ions have their turn to diffuse along their gradient- out of the cell. This exodus of positively charged ions then causes the intracellular voltage to drop- bringing it back down into the negatives. These potassium channels are a little sluggish, though, and take a while to close. The cell hyperpolarizes a little past the original -70 mV, but is corrected quickly by the trusty Na/K pumps.

This process happens as a wave, traveling down the axon of a neuron. To help the process, a material called myelin wraps around the axon (Fig.1- the white bead looking things). Myelin is white (that’s why the neural tissue of your brain is white… white matter!) and is an insulator. This allows the action potential to skip right through the insulated bits, speeding up transmission to lightening fast speeds. That time you almost dropped your phone in the toilet but caught it right in time? Yeah, those lightening fast reflexes were thanks to myelin.

Once a neuron propogates an action potential all the way down to the terminal buttons, it sends chemical signals (neurotransmitters) out to the next neuron in line and excites its little dendrites- starting the process over. This occurs all the way down to the intended muscle site. And there, the muscle must take this action potential and turn it into kinetic motion. And kinetic motion is WAY more exciting than ion diffusion- so, stay tuned!

Now, I know that if you’re reading this part, you’ve read this entire blog post. And for that, faithful reader, you deserve A TREAT. To claim your treat, simply leave a comment stating your name, and I will write you a poem. And yes, it will hurt my feelings if no one takes me up on my poetry offer. FYI.

cheers to love

You know the moment you meet a special someone and your face flushes when your eyes meet? Or the accidental brush of a hand that makes you jittery and you start to sweat? That hug that makes your heart pound? These are all perfectly normal responses to being smitten.

In the spirit of Valentine’s Day and romance, we’re going to talk about what happens when you get a little frisky. As embarrassing as the topic may be, sexual arousal brings about fascinating responses, born from primal origins long ago in our evolutionary history. Don’t worry; it’s all PG-13.   

Get it girl. (sheknows.com)

Flushing is an especially functional reaction. Increased heart rate forces blood into vascular dermal tissues such as your cheeks. A nice rosy glow communicates to your crush that you are interested, healthy, and sexually operative. (And thanks to the makeup industry, you can now fool people into thinking you are all of these things! Stupid suckers.)

Sweating may seem like a sexual deterrent (after all, pit stains don’t really say “come hither”), but is actually working for you in a romantic setting. You have two types of sweat glands. Eccrine glands are all over your body and really only secrete water and salt. Appocrine glands are found in your armpits and crotchal area and are connected to hair follicles. It is from these appocrine glands that pheromones are emitted. When sweating increases upon sexual arousal, it is your body’s way of dispersing those pheromones into your immediate environment. Though it may be only subconscious, the person of interest will pick up on these smells and (hopefully) react positively to your smell.

When you let your honey into your personal space, you are certainly allowing yourself to be vulnerable. Goosebumps that arise from this sort of closeness are remnants of the ancestral reaction to a potential threat. Think of a porcupine putting up its quills, or a cat’s hair standing on end. You’re on guard and your senses are heightened. Makes sense.

Thank you for setting
unachievable pupil standards,
Belle. Thanks.

My favorite sexual reaction is pupil dilation. Pupil dilation occurs as a means to heighten sight sensitivity, and functions similarly to the goosebumps as a way of being “on guard.” Studies show that men consistently prefer women with big ole’ cartoon pupils. The bigger the pupils, the stronger the attraction. However, this is not mutual. Studies by Tombs and Silverman (2004) show that women prefer men with moderately dilated pupils. They suggest that men with fully dilated pupils are more emotionally charged and pose more of a threat, tending towards violence or forcible acts. It has also been shown that females’ pupil size varies on a monthly cycle- peak size correlating with peak fertility (Caryl et. al).

Our bodily systems are amazingly and elegantly coordinated. Pupil size changing with fertility? That's amazing.

All of this being said, I think the distinction between lust and love must be made. All of these physiological responses are lustful. Love requires some extra ingredients that I’m not sure biology can explain.

Cheers to cool biology and love, friends. Hope you have a wonderful Valentine's Day.

Caryl, Peter G. Jocelyn E. Bean, Eleanor B. Smallwood, Jennifer c. Barron, Laura Tully, Michael Allerhand. Women’s preferene for male pupil-size: Effects of conception risk, sociosexuality and relationship status. Personality and Individual Differences. Volume 46 Issue 4, March 2009. Pg. 503-508.

Tombs, Selina, and Irwin Silverman. Pupillometry, a sexual selection approach. Evolution and Human Behavior 25 (2004), Pg. 221-228.

cwelling

Currently, I am lying on my couch eating King Cake and watching The Two Towers (extended edition, eh hem). Just now, Merry and Pippin escaped the dinner conversation between the quibbling Uruk hai and orcs, and haunting Fangorn Forest towers in the background. Ah, Fangorn Forest- home to that loveable Treebeard. He’s so funny. Mostly, because he is a tree. A walking, talking, poetry-loving tree, who thinks it’s easier to travel south because “somehow, it feels like going downhill.”

A big part of Treebeard’s strength as a character is just this- he is a tree that can move and walk and talk. In the films, his entrance surprises and delights us when Pippin realizes he is clinging onto the face of a conscious tree. It seems contrary to us that a plant should locomote and exhibit behavior of any type. While I am (sadly) unaware of any actual Ents in existence, I am aware of a few plants that are capable of motion.

Sensitive plant, Mimosa
(0364920.netsolhost.com)

Those cute little sensitive plants that grow in the grass, Venus Fly Traps snapping their prey, fields of sunflowers that begin the day facing the east and end it facing west; moonflowers that close up at dawn and reopen at dusk; the world of plants is surprisingly animated.

Without muscles, ligaments, or tendons, how do they do it? When you touch the leaves of a sensitive plant and they close up in a matter of seconds, what do you think is causing the motion?

In most cases, a change in turgor pressure is the mechanism. Turgor pressure is simply the water pressure within a plant cell. By localized swelling in turgor pressure, the shape of a leaf may be altered. For instance, if the cells of just one side of a leaf swells, the whole structure will become bent (Fig. 1). Conversely, if a bunch of cells expel their water, that area of the plant will collapse.

Figure 1: A.) Even turgor pressure B.) Increased turgor
pressure on top layer forces leaf to bend

The stimuli for these pressure changes vary. Sometimes, sunlight exposure will trigger cell swelling (cwelling, new word? I think so). Other times it is a reaction to sensory hairs called trichomes, or simply pressure setting off an ionic message through the cells like dominos. It varies from species to species.

If we could ever get our hands on an Ent, wouldn’t it be something to see if their physiology operates on a turgor pressure differential system? That Isengard and Soromon were defeated basically by the simple act of water diffusion? 

Why yes, Aragorn. We should go get drinks later.

no more flat tires

One weekend when I was sixteen, my family was loading up the car to go visit my grandparents. As I climbed into the backseat, a stabbing pain in my chest hit me. My left shoulder cramped and my left arm was painful to move.  I told my dad about what I was feeling, and we both dismissed it as a random cramp. Five minutes later, the pain was worsening and I wondered if I was having a heart attack at only sixteen years old. We decided to swing by the emergency room just to be sure.

Come to find out, my left lung had spontaneously collapsed. As doctors with x-ray machines and pokey things began to swarm around, I looked at my unshakeable father standing in the corner of the room. He was looking at me and shifting his weight from side to side, with a furrowed brow and crossed arms. This meant he was confused.

It just so happened that my best friend’s father is a pulmonary specialist. As the drugs began to cloud my head, I watched Dad pacing outside of the room with a cell phone to his ear, talking to my friend’s dad, Dr. Liendo. A man with a well-placed sense of humor, he told my dad that I was experiencing a “flat tire,” and after several minutes of conversation, my dad was clear on what was happening.

One of the most misleading physiological comparisons is that of a lung to a balloon. (If I could legally encourage you to deface every balloon/lung demonstration you see at science education centers, I would). A balloon inflates by air being forcefully pushed into the vacant space inside. This is a positive pressure system, since the balloon inflates by air being pushed into it. But lungs do not work like this. They work on a negative pressure system, meaning that air is pulled into the spongy tissue that is the lungs- not an empty cavity like a balloon. What does the pulling, then? Lungs are not muscularized- but your chest cavity is.

Your diaphragm is the muscular floor of your chest cavity. When it is relaxed, it bows upwards. When it contracts, it straightens out and lowers down- making your chest cavity bigger and therefore expanding the lungs, pulling air in. Ahhh, yes. Your lungs are attached to the walls of your chest cavity. At least they’re supposed to be.

They are attached by a thin layer of moisture called the pleura (imagine two sheets of plastic being stuck together when they get wet). Should this adhesive moisture break contact with the lung surface and the chest wall, air will leak from the lung into this pocket, forming what’s called a “bleb” between the lung and chest wall.  Sometimes, the bleb heals and the pleura reseals itself. No harm no foul.

Left: A tiny bleb at the top of the lung
Right: The lung continues to collapse

Other times, the pleural break is large enough that the lung continues to pull away from the chest wall and collapses. Your diaphragm continues to expand the chest cavity, but the lung is a pathetic, shriveled, useless raisin. (This hurts a lot). This can be fixed by inserting a chest tube so that it rests in the chest cavity, allowing the air pocket to escape and the pleura to reseal. If it’s a stubborn one, they might even hook it up to a vacuum and suck it out.

Dr. Liendo likened this system to a tire (the chest cavity) and the innertube within (the lung). To this day, Dr. Liendo tells me that I am allowed “no more flat tires.” I will always be grateful to him for unfurrowing my dad’s brow that day.

And if a rash of vandalism against balloons being used as demonstration lungs breaks out after this, I will not be upset.