Rogaine, better known in medical circles as Minoxidil, was discovered as part of the search for better anti-hypertensives. A vasodilator, Rogaine causes your blood vessels to loosen up, inducing a drop in your blood pressure. Coincidentally, it also makes hair grow. Some lucky biochemist noted this, instantly transforming the humdrum vasodilatory results of Minoxidil into the volcanic eruption of cash that is Rogaine. This is the bizarre magic of pharmacology, a world in which side effects and desired effects often switch roles, and transforms a drug from a middling vasodilator to the salvation for those wishing for a more hirsute image.
The world of drugs is astonishingly replete with these stories. Viagra was an attempt at combating high blood pressure, Dramamine was (and still is) an anti-histamine. Bimatoprost was designed to combat glaucoma, but is better known today as "Latisse," as a mechanism to grow longer and stronger eyelashes. These are the good surprises, the marketable variations that keep pharmacological research into orphan diseases and concepts viable.
But this doesn't explain some of the strange products. The substances where you know someone, somewhere, just decided to start playing with it on a whim. A classic example of this is Protamine sulfate, a counter-agent to Heparin which we use to address the bleeding that can be a side effect of administration. Protamine sulfate is an interesting little molecule, small, positively charged, and derived from fish sperm. Yes, I said fish sperm. The swimmer's swimmers.
Someone somewhere decided to see what fish sperm could do in the context of anti-coagulative poisoning. Someone somewhere cut out the testes of a fish, isolated chemicals, and derived a use. Someone somewhere STILL does this, in order to provide us with a source of Protamine Sulfate.
And this, my friends, is science.
Saturday, February 27, 2010
Thursday, February 25, 2010
Post Mortem
There are four of them, cold on their metal carts. They await our inspection like a receiving line, welcoming us to their one last public appearance. They are a palette of unpleasant shades, skin ranging from sickly bronze to dark black, with mottled variations in between. Four bodies, four men clad as they were in their final moments of life. We hear each of their stories, a grand rounds of thanatophelia. A portly white man in a tracksuit, inflated further by bacteria, was found in a rooming house. A black man, naked and covered in cuts and blood, found sprawled outside a bathroom. A middle aged caucasian, colored a sickening shade of tan by what can only have been long-running liver failure, brought in from the streets. An elderly widower, rope still around his neck, a victim of his own hand.
We are here in the medical examiner's lab to find the rest of their story, to explain the nature of their passing. We are here to make sure these men left us on their own terms, that no plot twist of assault or poison embellished lives their unassuming lives. We wheel the portly man to a station, and the examiner's strip his clothes. He has been dead at least four days, and in that time his natural bacterial fauna has energetically gone to work, decaying and fermenting his tissues and fluids. Even without this assistance, failures of self-repair have already started a process that, for lack of a better term, can only be described as melting.
We remove his clothes, taking with them swathes of sliding skin. The windbreaker is lined with a thick layer of dermis, slimy with the products of decay. Bubbles of blood ooze out of his mouth. Each movement brings more, a slow cascade of filth marring an already distended face. We cut him open, slicing him like a ripe fruit, a rapid parturition of a material between flesh and fluid. We listen to the examiner's mouth running, a non-stop series of puns and humor oddly fitted to the fetid sickly sweet alcoholic stink of decay pouring out of the deceased abdomen. "The report on this one wont be long" he says, shifting intestines out of the way, "but there will be an appendix." With this he pulls out the small vestigial organ, brandishing it at the room. We attempt to smile obligingly.
We drain aqueous humor from his eye for toxicology (it being the most representative body fluid after death). We remove his organs, and weigh them, trying in vain not to lose any bits of the molten instruments of life. We cut out his heart, and at first glance, it is tremendously large. It is the cause of his death, this hypertrophy, a growth of muscle leading to irregular electrical transmission. We cut out the rest of him, opening his skull and draining out the erstwhile center of his being. We find nothing else of interest, bag up his relevant bits, and mark the chart natural causes. We close the last chapter of his sad and lonely life, and consign the body to public burial. We write a report no one will read. We walk out of the lab, and back into the regular world, with it's animate people, it's fresh air.
I drive home, windows down in the cold winter air. The smell is still in my nostrils, coloring everything with sweet reek that is indescribably wrong. I drive home, waiting for the world to stop smelling of death.
We are here in the medical examiner's lab to find the rest of their story, to explain the nature of their passing. We are here to make sure these men left us on their own terms, that no plot twist of assault or poison embellished lives their unassuming lives. We wheel the portly man to a station, and the examiner's strip his clothes. He has been dead at least four days, and in that time his natural bacterial fauna has energetically gone to work, decaying and fermenting his tissues and fluids. Even without this assistance, failures of self-repair have already started a process that, for lack of a better term, can only be described as melting.
We remove his clothes, taking with them swathes of sliding skin. The windbreaker is lined with a thick layer of dermis, slimy with the products of decay. Bubbles of blood ooze out of his mouth. Each movement brings more, a slow cascade of filth marring an already distended face. We cut him open, slicing him like a ripe fruit, a rapid parturition of a material between flesh and fluid. We listen to the examiner's mouth running, a non-stop series of puns and humor oddly fitted to the fetid sickly sweet alcoholic stink of decay pouring out of the deceased abdomen. "The report on this one wont be long" he says, shifting intestines out of the way, "but there will be an appendix." With this he pulls out the small vestigial organ, brandishing it at the room. We attempt to smile obligingly.
We drain aqueous humor from his eye for toxicology (it being the most representative body fluid after death). We remove his organs, and weigh them, trying in vain not to lose any bits of the molten instruments of life. We cut out his heart, and at first glance, it is tremendously large. It is the cause of his death, this hypertrophy, a growth of muscle leading to irregular electrical transmission. We cut out the rest of him, opening his skull and draining out the erstwhile center of his being. We find nothing else of interest, bag up his relevant bits, and mark the chart natural causes. We close the last chapter of his sad and lonely life, and consign the body to public burial. We write a report no one will read. We walk out of the lab, and back into the regular world, with it's animate people, it's fresh air.
I drive home, windows down in the cold winter air. The smell is still in my nostrils, coloring everything with sweet reek that is indescribably wrong. I drive home, waiting for the world to stop smelling of death.
Wednesday, February 24, 2010
City of Bronze
A year ago, scientists working tirelessly in the field of sunless tanning stumbled upon something that is considered, in the world of pharmacological research, the holy grail. Bremelanotide, a melatonin based chemical trigger, does more than impart a subtle bronze glow. It activates the hypothalamus, triggering a chemical cascade of inevitable arousal. Thirty minutes later, your internal Barry White soundtrack turns on, and like young men in springtime, your thoughts inevitably turn to love.
More importantly (at least to these fortunate researchers), is the fact this magic pill has an equal effect on the fairer sex. Despite all the popular legends about tiger horn, oysters, and spanish fly, science has yet to conclusively find a pill to trigger amorous intent in the fairer sex. This is the great untapped marketplace of sexual pharmacology. Female arousal disorder is ubiquitous, affecting more women then erectile dysfunction does men. A pill that induces a mental state of arousal, as well as a physical one, is literally the magic bullet of psychogenic sexual dysfunction.
Plus, it gives you a tan!
More importantly (at least to these fortunate researchers), is the fact this magic pill has an equal effect on the fairer sex. Despite all the popular legends about tiger horn, oysters, and spanish fly, science has yet to conclusively find a pill to trigger amorous intent in the fairer sex. This is the great untapped marketplace of sexual pharmacology. Female arousal disorder is ubiquitous, affecting more women then erectile dysfunction does men. A pill that induces a mental state of arousal, as well as a physical one, is literally the magic bullet of psychogenic sexual dysfunction.
Plus, it gives you a tan!
Friday, February 19, 2010
Fidelity Booster
Prairie Voles mate for life. Montane Voles screw around.
Two almost identical species, with two almost identical evolutionary niches, and two fundamentally different behaviors. Of course, Scientists being scientists, this contradiction has recently been studied, and the difference comes down to the presence or absence of one single, solitary gene.
Prairie Voles, like Humans, have a specific promotor gene for the proteins oxytocin and vasopressin. Montane voles, like our promiscuous cousin the Chimpanzee, do not. The relevance of this theoretically revolves around the fact that oxytocin is the hormonal equivalent of love, the chemical we secrete when around those we care about, from family to romantic partners. It is the substance that cements bonds varying from the love between mother and child to the mild affection for an erstwhile fling. In the case of the Montane vole, its relevance revolves around the fact that voles modified to express this promoter show monogamous tendencies. To put it simply, we seem to have found the gene for romantic love.
The practical implication of this for human therapy is as a treatment for those unfortunates afflicted with Nymphomania or Don Juan syndrome, two clinically valid syndromes in which lasting affection is an unattainable goal, an illness in which deeper human contact is only a vaguely understood concept. The impractical implication is the possibility of behavioral modification, an inoculation against temptation. Imagine a world where marriage vows came with genetic checks, with shots created to redesign your brain and your heart. Would we be happier, stripped of the evil of temptation and mistrust, but simultaneously robbed of the validation our relationships receive from these tests?
We learn more about the brain every day, the bizarre interplay of electricity and chemistry that reduces somehow into our individual selves. Each day we reduce what was once magical and spiritual down to chemistry. It might be depressing, if it wasn't so fascinating.
Thursday, November 19, 2009
Myxamatosis
In their interminable effort to eradicate the rabbit infestation, the Australians at one point stooped to biowarfare. The rabbits had caused incalculable damage to the ecosystem, and at a population that may number in the billions, the Aussies were running out of bullets, and were markedly tired of rabbit stew.
Their attempt at a solution was to translocate a recent species jumping virus, the myxovirus of a Brazilian rabbit-like creature, to their own outback. Myxovirus had symbiotically adapted to its rainforest host, causing no symptoms, and no mortality. But in european rabbits, the adorable bunnies we know and love, the disease is one of the most infectious, invasive, and destructive diseases we have ever seen. In virology and infectious disease terms, the virus is hotter than hot.
At first glance, the effort was incredibly successful. A massive area of Australia was virtually depopulated of bunnies. But soon enough, nature ran its course, and the .1% of immune rabbits soon exploded again. But the effort had born some fruit. The research into myxovirus, a poxvirus variant, had shown quite a bit about the virus, which had intrigued researchers worldwide with its recent species jump.
We don't understand much of why viruses infect the species they infect. They pick and chose in live animals, infecting some and not others. When they jump species, it is almost always an extremely potent infection. But while studying the virus, a remarkable lab happenstance led to a researcher noting that myxovirus's selectivity was based less on animal type, and more on the presence or absence of a single immunoresponse pathway. A pathway coincidentally absent in virtually all human cancer.
One day, this accidental discovery could be on par with the discovery of penicillin. These viruses preferentially attack solely cancer cells. Mouse studies have shown 90% efficacy in eliminating gangliomas, some of the most resilient and cantankerous brain cancers we generate. This virus, this rabbit plague, kills cancer cells, and only cancer cells.
Myxamatosis. fantastic.
Their attempt at a solution was to translocate a recent species jumping virus, the myxovirus of a Brazilian rabbit-like creature, to their own outback. Myxovirus had symbiotically adapted to its rainforest host, causing no symptoms, and no mortality. But in european rabbits, the adorable bunnies we know and love, the disease is one of the most infectious, invasive, and destructive diseases we have ever seen. In virology and infectious disease terms, the virus is hotter than hot.
At first glance, the effort was incredibly successful. A massive area of Australia was virtually depopulated of bunnies. But soon enough, nature ran its course, and the .1% of immune rabbits soon exploded again. But the effort had born some fruit. The research into myxovirus, a poxvirus variant, had shown quite a bit about the virus, which had intrigued researchers worldwide with its recent species jump.
We don't understand much of why viruses infect the species they infect. They pick and chose in live animals, infecting some and not others. When they jump species, it is almost always an extremely potent infection. But while studying the virus, a remarkable lab happenstance led to a researcher noting that myxovirus's selectivity was based less on animal type, and more on the presence or absence of a single immunoresponse pathway. A pathway coincidentally absent in virtually all human cancer.
One day, this accidental discovery could be on par with the discovery of penicillin. These viruses preferentially attack solely cancer cells. Mouse studies have shown 90% efficacy in eliminating gangliomas, some of the most resilient and cantankerous brain cancers we generate. This virus, this rabbit plague, kills cancer cells, and only cancer cells.
Myxamatosis. fantastic.
Wednesday, November 18, 2009
The Egg Lobby Wins Again
The unlikely culprit behind H1N1 shortages is out there, hiding in a chicken coop. Oddly enough, the reason behind the production bottleneck of vaccine has been a shortage in fresh fertilized eggs. This bizarre happenstance occurs due to the bizarre nature of the orthomyxidae (flu) virus that is the source of pandemic flu. Influenza A, the culprit behind the spanish flu epidemic of 1918, is the only human flu variant with the capability to cross-infect multiple species. This cross infection is the root culprit behind the potential of flu to break out of the normal seasonal infectious boundaries, and run rampant.
Viruses aren't like other organisms. In fact, its debatable if they are even alive. Once a virus infects your cells, it rips itself apart, reproducing its component pieces. Reassembly is random, just components bouncing into each other, making up for inefficiency with copious volume. These fractions include the RNA that makes up the flu's genetic blueprint. The problem is that if two viruses infect the same cell, say a pig cell, there is nothing stopping genetic fragments from pig-only flu from integrating into the genome of a human-infectious flu. This is where the danger arises. Humanity has seen just about every variant of flu that is human-infectious. Our bodies know how to fight these. They make us sick, but we beat them, and a good fraction of us are just immune to each variant. When a pig or bird virus integrates into one that can attack us, it become a type that we have never seen before. (a phenomenon known as antigenic shift)
This cross-species infectious pattern is why we are facing a shortage. The vaccine you receive, whether nasally or intramuscularly, was brewed up fresh by infecting the membrane of an unborn chicken. We do this in order to generate the same swapping effect that generates pandemic flu, but with the opposite effect. Growing the virus in the egg allows for less infective genomic fragments to integrate in, creating a flu virus with the same immune system ID as the pandemic variety, but with none of the infectious capabilities. This inactivated virus serves as our vaccine, driving an immune response without a risk of infection.
This process is arduous and difficult. Not only that, but the recombination is random, and ineffective. Imagine trying to produce the volume of vaccine necessary by farming eggs that may not even make the product you need. Now imagine doing this with a shortage of eggs.
Incredible Edible Infected Eggs. I suppose they ARE good for us.
Viruses aren't like other organisms. In fact, its debatable if they are even alive. Once a virus infects your cells, it rips itself apart, reproducing its component pieces. Reassembly is random, just components bouncing into each other, making up for inefficiency with copious volume. These fractions include the RNA that makes up the flu's genetic blueprint. The problem is that if two viruses infect the same cell, say a pig cell, there is nothing stopping genetic fragments from pig-only flu from integrating into the genome of a human-infectious flu. This is where the danger arises. Humanity has seen just about every variant of flu that is human-infectious. Our bodies know how to fight these. They make us sick, but we beat them, and a good fraction of us are just immune to each variant. When a pig or bird virus integrates into one that can attack us, it become a type that we have never seen before. (a phenomenon known as antigenic shift)
This cross-species infectious pattern is why we are facing a shortage. The vaccine you receive, whether nasally or intramuscularly, was brewed up fresh by infecting the membrane of an unborn chicken. We do this in order to generate the same swapping effect that generates pandemic flu, but with the opposite effect. Growing the virus in the egg allows for less infective genomic fragments to integrate in, creating a flu virus with the same immune system ID as the pandemic variety, but with none of the infectious capabilities. This inactivated virus serves as our vaccine, driving an immune response without a risk of infection.
This process is arduous and difficult. Not only that, but the recombination is random, and ineffective. Imagine trying to produce the volume of vaccine necessary by farming eggs that may not even make the product you need. Now imagine doing this with a shortage of eggs.
Incredible Edible Infected Eggs. I suppose they ARE good for us.
Tuesday, November 17, 2009
Conduction
His face a mask of confusion, the older man sat down, easing his bulky upper torso carefully into the seat. He had walked in tentatively, shuffling in sandals, his feet and lower legs marked with accidental scuffs. Intimidated and alone, he looked around at us, apprehensive and not entirely sure what to do in this new situation.
The interview began slowly, the questions non-specific and general. He was in the hospital for memory loss, he self-reports, and we nod encouragingly. He told us he had trouble thinking. He would lose his thoughts. Each question came back with its own short answer, or merely a quiet request to hear it again, because he had forgotten.
We all looked at him, assessing his frame for signs of what had caused his problem. His barrel chest indicated potential emphysema. His swollen abdomen told us liver failure. It could be alcoholic damage, either direct or from hepatic emphysema. It could be alpha-1-anti-trypsin deficiency liver disease. We all sat there, thinking the mechanics through in our fact-sodden minds. Until someone asked him his children's age. For five long minutes he couldn't remember. For five long minutes we held our breath. He finally answered, his mind able to dig out the autobiographical information that should have resided right on the surface of his thoughts.
His dementia is conductive, the information of his life not gone, but inaccessible, blocked off behind a decaying network. He knows this, he can sense the absence of thought, the lack of interplay between his current situation and his wealth of acquired experience. He terrifies me, his condition a mirror to my worst fears. He lives in my nightmare, lost in his mind and completely aware of it. We have seen so many things, so much pain, and so much triumph. But this slow degeneration, this quicksand of conductive impotence, it cuts through the defenses. It makes me scared.
The interview began slowly, the questions non-specific and general. He was in the hospital for memory loss, he self-reports, and we nod encouragingly. He told us he had trouble thinking. He would lose his thoughts. Each question came back with its own short answer, or merely a quiet request to hear it again, because he had forgotten.
We all looked at him, assessing his frame for signs of what had caused his problem. His barrel chest indicated potential emphysema. His swollen abdomen told us liver failure. It could be alcoholic damage, either direct or from hepatic emphysema. It could be alpha-1-anti-trypsin deficiency liver disease. We all sat there, thinking the mechanics through in our fact-sodden minds. Until someone asked him his children's age. For five long minutes he couldn't remember. For five long minutes we held our breath. He finally answered, his mind able to dig out the autobiographical information that should have resided right on the surface of his thoughts.
His dementia is conductive, the information of his life not gone, but inaccessible, blocked off behind a decaying network. He knows this, he can sense the absence of thought, the lack of interplay between his current situation and his wealth of acquired experience. He terrifies me, his condition a mirror to my worst fears. He lives in my nightmare, lost in his mind and completely aware of it. We have seen so many things, so much pain, and so much triumph. But this slow degeneration, this quicksand of conductive impotence, it cuts through the defenses. It makes me scared.
Subscribe to:
Posts (Atom)