Mad Cow Hysteria Nears End

Despite the efforts of animal
rights activists such as Howard Lyman to keep it going, the Mad Cow Disease hysteria continues to recede. The European Commission is currently studying
a proposal to lift its ban on British beef which most observers expect
to occur by the autumn of 1998.

The EC banned British beef in March
1996 after the British government linked bovine spongiform enceophalopathy
(BSE) to a new variant of Creutzfeldt-Jakob Disease (CJD).

Two years later, Great Britain
has gone to extraordinary lengths to remove BSE-infected cattle from its
food supply, and the link between BSE and CJD grows ever more suspect.

There never was much more than
speculation and inference behind the alleged connection between the two
diseases. There hasn’t yet been a single verified case of an individual
eating meat from a BSE-infected animal and subsequently contracting any
form of CJD. In addition, so far there is no evidence that the prion believed
to be the cause of BSE exists in the muscle tissue of cows — so far it
has been found only in the brains of the animals.

In fact the sixth annual report
by the UK’s National CJD Surveillance Unit reported that rates of CJD
in Great Britain are consistent with CJD rates in other countries around
the world, including those that are free of BSE. Unlike some animal rights
extremists, the CJD Surveillance report does not rule out the possibility
that the rise in CJD cases in the UK is due to improvements in diagnoses
techniques, concluding, “It is impossible to say with certainty to
what extent these changes reflect an improvement in case ascertainment
and to what extent, if any, changes in incidence.”

Sources:

“Cretuzfeldt-Jakob Disease Surveillance in the UK, 6th report,” The
National CJD Surveillance Unit, 1997.

David Evans, “Mainland British beef exports ban could be lifted,”
Reuters News Service, June 10, 1998.

Scientists find DNA cure for genetic deafness in mice

Researchers at the University of
Michigan Medical School recently accomplished the first permanent correction
of a deafness-related genetic mutation. The experiment was performed with shaker-2
mice — a strain of mice born that is born deaf due to genetic defects.

Scientists used a Genetic Engineering technology
to first locate the gene responsible for the deafness and then injected
short sections of normal cloned DNA into fertilized mouse eggs. On June
23, 1997 the first shaker-2 mouse without the genetic defects was born.
The results were reported in the May 29, 1998 issue of Science.

The discovery of the defective
gene in mice quickly led researchers to find a nearly identical gene in
human beings that may be responsible for some cases of congenital deafness
in human beings.

“Interaction between scientists
working with the mouse genome and the human genome made it possible to
locate these genes so quickly,” said Sally A. Camper, associate professor
of human genetics at the U-M Medical School. “It’s a perfect
example of how transgenic technology in mice can contribute to research
with the potential to help people.”

Camper noted that there are 12
other related forms of deafness-related mutations in which the responsible
gene remains unknown and that “finding the defective gene is the
first step toward developing new treatments which someday could restore
hearing in children and adults.”

The UM scientist now hope to find
a way to deliver the normal gene into the cells of adult animals. “The
next step is to develop delivery vehicles to introduce the normal gene
into inner ear cells of individuals who carry these deafness genes,”
said Yehoash Raphael, assistant professor of otolaryngology at the UM
Medical school. “Once adequate vectors are available, gene therapy
for genetic-based deafness will become a reality.”

Source:

“DNA cure of genetic deafness in mice helps human research,” UniSci
Science and Research News, May 29, 1998.

Switzerland overwhelmingly rejects ban on genetic engineering of animals, plants

Opponents of Genetic Engineering
of animals and plants had been cautiously optimistic about the chances
of Switzerland becoming the first nation to pass a referendum banning
genetic engineering. Instead more than 65 percent of Swiss citizens voted
no on the proposed constitutional change, sending it down to a huge defeat.

Switzerland is home to close to
200 firms that conduct genetic research, including pharmaceutical giants
Novartis and Roche who aggressively opposed the proposed ban.

Source:

“Swiss oppose ban on genetic research and production,” Nando.net,
June 7, 1998.

“Swiss voters reject curbs on genetic engineering,” CNN, June 7, 1998.

Future promises more genetically engineered animals

As animal rights activists point
out ad nauseum, animal models are not completely analogous to human beings.
Substances which cause cancer in rats sometime fail to cause cancer in
human beings and vice versa. But what if researchers genetically engineered mice and rats to suffer from the same illnesses human beings suffer from?
Well now they can, which is creating an enormous debate about the ethics
of such animal research.

Until recently, scientists relied on
finding mutant strains of mice which suffered from diseases or symptoms
similar to those experienced by human beings. Mice commonly used to test
cancer treatments, for example, are specially bred to be highly prone
to developing cancer.

Advances in biotechnology take
that one step further and allow scientists to alter the genes in mice
embryos so they are born with specific defects such as cystic fibrosis
or arthritis. As National Institutes of Health immunologist Ronald Schwartz
recently told the Washington Post, such animal models should be incredibly
powerful.

John Sharp, superintendent of induced
mutant resource at the Jackson Laboratory, put it bluntly. “More and
more research is moving toward the use of these mice. It’s where
the future of research is headed.”

And it is not just mice. Researchers
at laboratories around the world are genetically altering pigs, goats
and sheep to do everything from produce more easily transplantable organs
to providing delivery mechanisms for medicine in their milk.

As genetic engineering of animals
spreads, so does the opposition movements aimed at limiting or banning it. Those
opposed to such genetic engineering complain it is wrong to design animals
to suffer.

“There really is something
primordially horrible about replicating animals that will suffer endlessly,”
|Bernard Rollin|, a Colorado State University physiologist, told the Washington Post. Other attack genetic engineering as challenging our notions of life
as inherently sacred.

The biggest opposition in recent
years came in Switzerland, where 112,000 Swiss citizens signed a petition
to put a ban on research on genetically altered animals on the ballot.

Failing to use these genetically
engineered animals, however, will mean ignoring an excellent source of
medical information. Genetically engineered mice have already yielded
important information about deadly human illnesses such as |Huntington’s| disease. When scientists removed a gene in mice which corresponds to the
defective human gene that causes Huntington’s, researchers noticed
small protein deposits in the brains of the mice; something that had not
been observed in Huntington’s patients. Upon reexamining the brains
of Huntington’s victims, however, researchers indeed found the protein
deposits, which are now suspected as one of the primary causes of the
diseases’ symptoms.

Source:

Rick Weiss, “Creation of flawed animals raises new ethics issues,”
Washington Post, June 7, 1998.

PETA wants animal hearing experiments stopped

People for the Ethical Treatment of Animals’ Mary Beth Sweetland was up in arms over animal experiments
that researchers at the University of California-San Francisco plan to
carry out on squirrel monkeys.

According to UCSF vice chancellor
for research Zach Hall, researchers Marshal Fong and Stephen Chenung plan
to anesthetize the animals and then expose them to a range of very high
frequency noise. “The animals, when they wake up, will have a hearing
disability, one that’s similar to one that millions of Americans
have [inability to hear high-frequency sounds],” Hall said.

Sweetland wants the experiments
stopped, but Hall said the experiments have already been approved by the
university’s committee on animal research and will have practical
benefits.

“The research seeks to understand
the changes that occur in the brain as the result of sensory deprivation
– in this case, hearing loss – with the hope that we can use what we learn
to relieve the hearing loss caused by loud noise,” Hall said.

As Fong summed it up, “These
people [PETA] are distorting the truth here.”

Source:

“Activists want UC monkeys spared,” Scripps Howard, May 21, 1998.

Animal experiments lead to possible breakthrough in treatment of spinal cord injuries

A study published in the June issue
of Nature Neuroscience reveals just how far scientists have
come in understanding, and possibly someday correcting, |spinal cord| injuries.

Martin Schwab, of the Institute
for Brain Research at the University of Zurich in Sweden, and his colleagues
took rats and cut the nerve fibers in the rats’ brain stem. This
operation effectively removed the ability of the rats to exercise fine
motor control of their front limbs, making it impossible for them to climb
ropes or grasp food pellets.

Then the researchers injected the
rats with a specially engineered antibody called IN-1. Those rats receiving
IN-1 grew new nerve fibers that took over for the damaged fibers. Both
rats and human beings produce growth inhibitors which usually prevent
new fibers from growing. The Zurich researchers hope the things they have
learned in neutralizing these inhibitors in rats will help them to find
a way to neutralize them in human beings.

“This study re-emphasizes
the role of the non-injured nervous system in compensating for the loss
of function after damage,” said Michael Beattie, a neuroscience professor
at Ohio State University who specializes in spinal cord injury. “The
work they’ve done suggests that they’re on the right track to
understanding how to produce therapies that can enhance repair and recovery
of function.”

Source:

Jane E. Allen “New hope for repairing spinal injuries” Associated
Press, May 18, 1998.