1. Welcome to Baptist Board, a friendly forum to discuss the Baptist Faith in a friendly surrounding.

    Your voice is missing! You will need to register to get access to all the features that our community has to offer.

    We hope to see you as a part of our community soon and God Bless!

Where are the SuperMutants???

Discussion in '2004 Archive' started by Helen, Dec 31, 2003.

  1. Helen

    Helen <img src =/Helen2.gif>

    Aug 29, 2001
    Likes Received:
    buried in the LA Times back pages, from what I understand, on Dec. 15:

    Waiting for the Supermutants
    How We Know Darwin Got It Wrong
    LA Times Sunday, December 14,2003

    By Paul Gordon, Paul Gordon last wrote for the magazine about the crash of his 1990 Mazda Miata.

    hen the then-nascent Human Genome Project's Traveling Magic Show came trundling through my hometown in the early 1990s, my father, the eminent economist and contrarian H. Scott Gordon, joined the throng at the university auditorium to witness the birth of humanity's brave new world of mapped and conquered genes. He waited for the lecture and the breathless questions to subside, then he stepped to the microphone.

    "It's great that you're hunting down the order of somebody's genes," he said. "What I want to know is: Whose are they?"

    The question hung in the air like a time bomb. With a single thrust, the professor had struck at the best-kept secret of the Human Genome Project: Whose genes were they actually mapping? And his simple query utterly non-plused the council of elevated swamis onstage. He did not get an answer to his question (there were rumors that the "human" the project was mapping was actually a mélange of genes lifted from several workers in the lab), but on that day I recall my father walked out into the sunshine with a rascally grin that stretched from ear to ear.

    Carrying on a rogue's legacy, I have a little interrogatory of my own. As I understand it, Charles Darwin's theory holds that life is pushed forward by a series of advances, or mutations, so powerful that they blow the competition into the weeds. My question is: "Where are they?"

    I've heard that half of the humans who ever lived are alive today. More than 6 billion copies staggering around in an environment seething with toxic waste, car exhaust and cosmic radiation. We're riddled with cancers, tumors, albino bluesmen and twins joined at the hip. But where are the beneficial mutations, the world-beating supermutants potent enough to put the lot of us common, garden-variety humans out to pasture? Six billion rolls of the dice and no one has been born with a brain the size of a basketball? No eyeballs that see in the dark? Nothing?

    I know the lab drawers are brimming with bones and fossils, frozen icemen and piles of petrified droppings from cavemen. There is more physical evidence supporting Darwin's evolution than perhaps any other single scientific theory. Yet a Gallup poll taken at the turn of the millennium revealed that close to half the American public rejects evolution as a theory. I think I know why.

    More than a century after its publication, Darwin's "Origin of Species" is suffering from what I call the "Weapons of Mass Destruction Problem." It's a simple matter of credibility: Show me one fuzzy photo of a bunker lined with missiles, just one underground sarin lab, or mobile anthrax trailer, or glowing chunk of enriched African uranium, and I'll start to reconsider. But until you can find one, I'll stay suspicious about the whole WMD thing.

    Same with evolution. Yes, I know the process of natural selection is long and gradual and mostly invisible, and its complexities are as arcane as a PhD thesis. It has been suggested that human evolution ceased when the social graces of monogamy meant even geeks got to pass along their genes. It may be extremely rare—the fish that grew feet and walked out of the ocean, the monkey that came down from the tree, the ape that picked up the jawbone in "2001: A Space Odyssey"—but natural selection still relies on mutations so wild that they rearrange the order of everything, right? And so I say again: Where are they?

    How do I know those mutations haven't happened yet? Because I watch too much television. The modern entertainment industry is highly efficient at scanning the planet for bizarre creations to flicker across the nightly television screen. So, if there's going to be a paradigm shift involving newer, faster, smarter humans, it's a sure bet that you're going to see it first on television. We've got diet gurus and 12-year-old spelling bee champions and accountants from Montana who can eat car bumpers, but where is the local weatherman with a nose so fine he can nail the forecast just by sniffing the breeze?

    Consider the range of sports on television. Today's athletes define the limits of speed, endurance, agility, strength—every aspect of human physical performance. And talk about a hardball natural selection process: If you can swing a stick, throw a ball, heft a weight or outrun your neighbors, you can be sure there's a talent agent thrashing through the snows of darkest Siberia, checkbook in hand, desperate to deliver your special gift to the gnashing maw of TV sports.

    Given a gene pool of 6 billion-plus, and a television marketplace that supports at least two 24-hour sports networks, why haven't we seen the genetic leaps that are supposed to drive us forward as a species? I'm not talking about pituitary cases such as Shaq and Mike Tyson. I'm talking genuine, hang-it-out mutations—wings, gills, whatever. Where is the athlete with webbed hands who shatters all records for swimming? Where is the six-fingered pitcher who can deliver a knuckleball that loops around third base? Why is there not one, not one, quarterback in the NFL with eyes in the back of his head?

    Conspiracy theorists will say the Olympic Committee is keeping these monsters under wraps: The boxer with an extra joint in his fist; the gymnast who can swing by his tail. But I don't believe it for a moment. The demand for spectacle is too great.

    So, Mr. Darwin: Let's be reasonable. If a fish can grow feet and crawl out of the sea, it doesn't seem that great a stretch to find a two-headed lineman with a lobster claw at each elbow blocking for the Oakland Raiders on Monday Night Football. My advice is forget the cloned farm animals. Maybe it's time to give evolution a little kick in the pants. If you want to rekindle some righteous faith in the power of chromosomes, just snap in a few souped-up genes and pump out a 12-foot Bill Romanowski with cactus spikes and a rack of antlers. Trust me: Just one genuine homegrown supermutant linebacker is all it would take to raise a whole new generation of true believers—even in my family.

    And, baby, think of the endorsements!
  2. Helen

    Helen <img src =/Helen2.gif>

    Aug 29, 2001
    Likes Received:
    Instead, we consistently seem to be going the other way...


    MACHIAS, New York (AP) -- Four-year-old Dalton Eisenhardt and his 2-year-old brother, Wyatt, don't protest or complain about the machines that hold onto them with tubes and cords during every moment of their lives. Despite the tracheotomies, the feeding tubes and ever-present nurses, the boys smile.

    It his harder for those who love them.

    The young brothers are fighting a rare and puzzling chromosome disorder, and doctors in nearby Buffalo have been unable to find anyone anywhere with the same condition. They cannot tell the Eisenhardts what might come next, what toll the disorder ultimately will take.

    So far, dozens of hospital stays, surgeries, doctors' appointments and consultations have produced only more questions. The family hopes that by telling its story, a doctor or other parent will recognize the disorder and tell them what to do.

    "We don't know what to expect," said their mother, Vicki Eisenhardt, in the living room where she spends most of her time caring for her two youngest sons while her husband works as a carpenter. A 10-year-old brother, Tyler, is healthy.

    "What we know we've learned from Dalton," she said.

    The boys have a disorder called unbalanced translocation chromosome 15. Their mother explains the chromosome has an extra piece, a slight defect that affects every organ in the boys' bodies.

    A year ago, doctors gave Dalton six months to live, saying the damage to his lungs was too great.

    "Here we are a year later," his mother said. "Doctors can speculate, but only God knows."

    "We're not giving up," added her sister, Kim Claus, one of several nurses who cares for the boys full-time.

    Mom: Answers needed
    Dalton has been hospitalized 34 times and undergone 19 surgeries. Worrisome episodes where his skin grows gray and clammy have been increasing. Wyatt spent 100 days in intensive care after his birth. His problems have mirrored his brother's.

    Snuggled into his mother's lap one afternoon this week, Wyatt grinned at visitors as his brother slept, blue breathing tubes spilling from both their necks. On this day, Dalton was tired and would spend most of the day in bed. Wyatt was just up from a nap that had been interrupted to have a buildup of saliva suctioned from his tube.

    Dalton has an appointment next week with a specialist in New York City. This week the family was scrambling to secure a flight after learning the small airline that initially offered tickets could not fly the oxygen tanks the boys need to breathe because of federal aviation rules.

    "This is not a trip of luxury. This is a trip of necessity," Eisenhardt said, frustrated at the obstacle.

    The boys' beds and shelves full of supplies and equipment have taken over the living room. Nurses, therapists and medical supply deliveries create a revolving door in the family home, and although insurance pays most costs, unseen expenses like the electricity needed to power the machines add up.

    But the family does not tell its story for pity -- even their neighbors in this Cattaraugus County town of 2,400, have been unaware of their plight.

    The family keeps to itself, Eisenhardt said, but is at the point where answers are needed.

    "When you see your 4-year-old say he hurts, grabbing his chest and so tired he can't walk across the floor, you want to help," Eisenhardt said. "You're going to do anything and everything you can to help him."

    from CNN news this morning

    UTEOTW New Member

    May 8, 2002
    Likes Received:
    Here are a few, among them a mutation that protects against infection by HIV and slows the progress of the disease, a mutation that slows the progress of HIV, a mutation that increases the immune function of cells, a mutation that increases good cholesterol and decreases bad cholesterol, and some protection against heart disease.

    "High blood levels of coagulation factor VII are associated with a risk of ischemic vascular disease. Although factor VII levels may be genetically determined, the relation between genetic polymorphisms of factor VII, factor VII blood levels, and the risk of myocardial infarction has not been established. METHODS: We performed a case-control study of 165 patients with familial myocardial infarction (mean [+/-SD] age, 55+/-9 years) and 225 controls without a personal or family history of cardiovascular disease (mean age, 56+/-8 years). The polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene were studied. Factor VII clotting activity and antigen levels were also measured. RESULTS: Patients with the QQ or H7H7 genotype had a decreased risk of myocardial infarction." from "Polymorphisms in the coagulation factor VII gene and the risk of myocardial infarction" by Iacoviello L, Di Castelnuovo A, De Knijff P, D'Orazio A, Amore C, Arboretti R, Kluft C, Benedetta Donati M in N Engl J Med 1998 Jan 8;338(2):79-85.

    "A 32-base pair inactivating deletion inCCR5 (delta 32) common to Northern European populations has been associated withreduced, but not absolute, HIV-1 transmission risk and delayed diseaseprogression. A more commonly distributed transition causing a valine toisoleucine switch in transmembrane domain I of CCR2B (64I) with unknownfunctional consequences was recently shown to delay disease progression but notreduce infection risk." from "The role of CCR5 and CCR2 polymorphisms in HIV-1 transmission and diseaseprogression." by Michael NL, Louie LG, Rohrbaugh AL, Schultz KA, Dayhoff DE, Wang CE, SheppardHW in Nat Med 1997 Oct;3(10):1160-2.

    "We have recently described a C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins. The 825T allele is associated with a novel splice variant (Gbeta3-s) and enhanced signal transduction via pertussis toxin (PTX)-sensitive G proteins ... Gbeta3-s appears to be associated with enhanced immune cell function in humans." from "Enhanced fMLP-stimulated chemotaxis in human neutrophils from individuals carrying the G protein beta3 subunit 825 T-allele" by Virchow S, Ansorge N, Rubben H, Siffert G, Siffert W in FEBS Lett 1998 Oct 2;436(2):155-8.

    "To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study ... These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD." from "Identification of putative beneficial mutations for lipid transport" by Galton DJ, Mattu R, Needham EW, Cavanna J in Z Gastroenterol 1996 Jun;34 Suppl 3:56-8.

    "Lipoprotein lipase (LPL) is the rate-limiting enzyme in the lipolysis of triglyceride-rich lipoproteins, and the gene coding for LPL is therefore a candidate gene in atherogenesis. ... Conversely, a third frequent mutation in this gene, the Ser447-Stop, is reported by some investigators to underlie higher HDL cholesterol levels and would represent a beneficial genetic variant in lipoprotein metabolism ... Carriers of the Ser447-Stop allele (heterozygotes and homozygotes) had significantly higher postheparin LPL activity (P = .034), normal postheparin HL activity (P = .453), higher HDL cholesterol levels (P = .013), and lower triglyceride levels (P = .044) than noncarriers ... The LPL Ser447-Stop mutation therefore should have a protective effect against the development of atherosclerosis and subsequent CAD." from "Genetic variant showing a positive interaction with beta-blocking agents with a beneficial influence on lipoprotein lipase activity, HDL cholesterol, and triglyceride levels in coronary artery disease patients. The Ser447-stop substitution in the lipoprotein lipase gene" by Groenemeijer BE, Hallman MD, Reymer PW, Gagne E, Kuivenhoven JA, Bruin T, Jansen H, Lie KI, Bruschke AV, Boerwinkle E, Hayden MR, Kastelein JJ.

    "Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels ... Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis" from "PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants," by Margaglione M, Cappucci G, d'Addedda M, Colaizzo D, Giuliani N, Vecchione G, Mascolo G, Grandone E, Di Minno G in Arterioscler Thromb Vasc Biol 1998 Apr;18(4):562-567.
  4. Paul of Eugene

    Paul of Eugene New Member

    Oct 30, 2001
    Likes Received:
    The theory of evolution implies these boys will not leave descendents so that this mutation will be stopped dead in its tracks. We all hope they will be eased in their suffering and even a way found for them to have good health, but . . .

    it would appear that the odds are they will, in fact, not leave descendents.