-Caveat Lector-

hi,

the following article looks and sounds like white coated scientists
making some easily forgettable progress .... but whoa there ....

If governments can demonstrate that all neurological and psychological
behaviour is controlled by genes,
then when undesirable genes and behaviour become socially unacceptable
eg. statements like most of americans are mentally unwell - then it becomes
very easy to prescribe corrective pharmaceuticals.... and disregard any
other social implications of this unease.

There are two great divides in behavioural biology -
1. one that behaviour and aggression is INNATE/GENETICALLY INBORN
2. the other that it is socially  learned
[3. some combination of the above - most likely imo]

If science proves that there is no such thing as a tabla rasa - that the
dice are loaded by genetics, then they don't have to answer for the poor
lifestyles of many victims, their starvation and poverty, rather they can
say that
all disease of the mind is genetic rather than influenced by society.

Although people have for many years tried to make racial/eugenics arguments
against the races/skin colours most trapped by poverty eg. in the states,
and tried to infer genetic inferiority .... these ideas have lacked
researched biochemical proof. [proofs that are published in public]

It is a LONG LONG way from the common earthworm to human neurobiology, but
the implications of this type of research should not be lost on us.


Research team creates mutant worms

Discovery shows direct link between gene and behavior
Associated Press

      A study by Utah and Texas researchers has shown how a genetic mutation
may change a worm's feeding behavior.

      The researchers created mutant worms that were unable to eat and
swallow properly.

      "We've shown it's possible to draw a direct line between a specific
gene and a specific aspect of behavior," said University of Utah geneticist
M. Wayne Davis, principal author of the study published this week in the
journal Science.

      "If we can take what we learn in the worm . . . we can move up to
understanding how more complicated behaviors in more complicated animals
like people are made up of smaller behaviors, each controlled by separate
genes," Davis said.

      Science's editors said the study "demonstrated, with unprecedented
thoroughness, the ripple effect of a specific genetic mutation all the way
out to the change in behavior it causes."

      The study "is really terrific," said Cori Bargmann, an anatomy and
biochemistry professor at the University of California, San Francisco.

      She said it is one of a few cases where scientists traced a single
gene to its effect on the transfer of electrical signals in muscles and,
ultimately, to a visible behavior.

      Davis, a postdoctoral fellow in biology, was hired by the University
of Utah last summer. He conducted the research for his Ph.D. thesis at the
University of Texas Southwestern Medical Center in Dallas.

      The study involved Caenorhabditis elegans, a nonparasitic nematode
that has only 1,000 cells and is as long as a dime is thick, Davis said.

      Davis and his colleagues studied a gene named exp-2. When the gene is
mutated a certain way, the worms cannot defecate properly and become
constipated. The same mutation prevents the worm from laying eggs or eating
properly.

      Davis' research team discovered the gene by pinpointing its location
and linking its mutant forms to various abnormalities.

      Exp-2 orders production of a protein. Four of the proteins form a
tube-like potassium channel. Each of the worm's muscle cells has hundreds of
such potassium channels.

      When similar calcium channels open, electrically charged calcium ions
flow into muscle cells, increasing the voltage so the muscles contract.
Then, when exp-2 potassium channels open, potassium flows out, quickly
reducing the voltage so the muscles relax.

      When a normal worm eats, the contraction and relaxation of muscle
cells in its mouth and throat allow it to suck in water and bacteria from
surrounding soil, then spit out the water while swallowing the bacteria,
Davis said.

      Davis compared normal worms with two kinds of mutant worms, which were
created by soaking parent worms in a toxic chemical.

      In one kind of mutant, the exp-2 gene became hyperactive. As a result,
potassium flowed out of muscle cells prematurely, so the worms' throat
muscles began to relax before fully contracting. Worms with two of these
mutant genes could not eat at all and died. Worms with one mutant gene had
trouble sucking in water and bacteria so they ate poorly, Davis said.

      The scientists created a second mutation in which the exp-2 gene did
not work at all. Such worms could contract their throat muscles, but could
not relax them. Those worms sucked in bacteria and water, but could not spit
out the water.

      "They eat very inefficiently," Davis said. "They are partly starved
all the time."

      By comparing how normal and mutant worms ate, "we've shown you can
make specific changes in a single gene that lead to specific changes in the
voltage of muscle cells, which in turn lead to specific changes in the way
those muscle cells act, thereby changing the feeding behavior," Davis said.

      Davis' Texas co-authors of the study were geneticist Leon Avery,
postdoctoral fellows Richard Fleischhauer and Joseph Dent, and
neuroscientist Rolf Joho.

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