TWN have now made available the final and correct version of the 
paper by Traavik and Heinemann that was circulated last week.

301kb  pdf: 
http://www.biosafety-info.net/file_dir/719762120455431f1a3942.pdf



>The paper below is a draft version, the full version with refs will
>be available at TWN "in due course". - Keith
>
>
>GM WATCH daily
>http://www.gmwatch.org
>---
>---
>1.Introduction from GM Watch
>2.Genetic Engineering (GE) and Omitted Health Research: Still No
>Answers to Ageing Questions
>---
>---
>1.Introduction from GM Watch
>
>The following paper, 'Genetic Engineering and Omitted Health
>Research: Still No Answers to Ageing Questions' is highly recommended.
>
>The paper points out that many scientific questions concerning health
>effects of GMOs that were raised 20 years ago still remain unanswered.
>
>The paper discusses - in remarkably clear and readable terms - the
>health hazards related to genetically engineered (GE) plants used as
>food or feed, with mention of GE vaccines including si RNA- and
>nanobio-technologies.
>
>Amongst the many points the authors note:
>
>*very few studies on the possible effects of GE  food/feed on
>potential animal or human consumers have been published in
>peer-reviewed journals
>
>*a consensus has emerged that the effects observed in some published
>studies must be experimentally followed up but THIS HAS NOT BEEN DONE.
>
>*most of the animal feeding studies performed so far have been
>designed exclusively to reveal only husbandry production differences
>[eg do animals gain weight satisfactorily on a GE feed compared to a
>non-GE feed?]
>
>*studies designed to reveal physiological or pathological effects are
>extremely few
>
>*these studies demonstrate a quite worrisome trend - studies
>performed by the industry find no problems, while studies from
>independent research groups often reveal effects that should merit
>immediate follow-up, confirmation and extension
>
>*such follow-up studies have not been performed
>
>*studies are inhibited by lack of funds for independent research
>
>*studies are also inhibited by the reluctance of producers to deliver
>their GE materials for analysis
>
>*the transgenic DNA sequences provided by GE food/feed producers
>can't be relied on
>
>*the transgenic DNA sequences provided can differ from the inserted
>sequences found in the actual genetically engineered plants
>
>*transgenic modification techniques can result in either degradation
>of the incoming DNA, or insertion of rearranged copies into the plant
>DNA
>
>*some genetic elements in the introduced genetic constructs may act
>as "hotspots" for recombination
>
>*among other rearrangments, rearranged transgenic fragments may be
>found scattered through the genome
>
>*the diffferences between the transgenic DNA sequences given by
>producers and the actual inserted sequences found in their products
>means that risk assessments made prior to approval do not necessarily
>cover the potential risks associated with the products
>
>*if transgenic DNA and proteins are taken up from mammalian
>gastro-intestinal tracts, instead of being degraded during digestion,
>this could lead to chronic diseases
>
>*only two published reports have investigated the fate of
>foreign/transgenic DNA in humans
>
>*the consequences of DNA persistence and uptake represent yet another
>area of omitted research
>
>*some recent publications have demonstrated that foreign DNA and also
>proteins may escape degradation, to persist in the gastro-intestinal
>tracts and even to be taken up from the intestines and transported by
>the blood to internal organs in biologically meaningful versions
>
>*allergenicity is a major concern with genetically engineered foods
>
>*tests for allergenicity are usually carried out with bacteria and
>not with the versions of the transgenic protein which people are
>exposed to, ie the actual protein produced in genetically engineered
>plants
>
>*the Bt-toxins expressed in genetically engineered plants have never
>been carefully analysed, and accordingly, their characteristics and
>properties are not known
>
>The authors conclude, "We are left with a high number of risk issues
>lacking answers, adding up to a vast area of omitted research, and
>this falls together in time with a strong tendency towards corporate
>take-over of publicly funded research institutions and scientists."
>
>2.MAIN TEXT ONLY - REFERENCES OMITTED
>
>Genetic Engineering (GE) and Omitted Health Research: Still No
>Answers to Ageing Questions
>
>Terje Traavik, PhD, DVM
>Scientific Director, GENOK-Norwegian Institute of Gene Ecology
>Professsor of Gene Ecology, School of Medicine, University of Tromso, Norway
>
>And
>
>Jack Heinemann, PhD
>Director, NZIGE-New Zealand Institute of Gene Ecology
>Ass. Professor, School of Biological Sciences, University of
>Canterbury, Christchurch, New Zealand
>
>Introduction.
>
>Some of the most crucial scientific questions concerning health
>effects of GE and GEOs (genetically engineered organisms) were raised
>up to twenty years ago. Most of them have still not been answered at
>all, or have found unsatisfactory answers.  We believe, as Mayer and
>Stirling  said, "in the end it is often the case that those who
>choose the questions determine the answers". Will another twenty
>years pass before societies realize the urgent need for public
>funding of genuinely independent risk- and hazard-related research?
>The time for such investment is now so that a new scientific culture
>with working hypotheses rooted in the Precautionary principle (PP)
>can discover other, possibly even more important questions of safety.
>
>In the present article we will mainly confine ourselves to putative
>health hazards related to GE plants (GEPs) used as food or feed, with
>some brief notes on GE vaccines as well as the novel si RNA- and
>nanobio-technologies. This does not mean that we do not recognize the
>paramount, indirect threats to public health posed by social,
>cultural, ethical, economic and legal issues.
>
>In the specific context of food or feed safety assessment "hazard"
>may be defined as a biological, chemical or physical agent in, or
>condition of, food with the potential to cause an adverse health
>effect. The hypothetical hazards of whole GM foods, i.e. those
>hazards that have been realized so far, fall into a few broad
>categories. They are either related to the random and inaccurate
>integration of transgenes into recipient plant genomes, uncertainty
>with regard to direct or indirect effects of the polypeptide product
>of the transgene, or uncertainty with regard to DNA types and
>circumstances promoting uptake and organ establishment of foreign DNA
>from mammalian gastro-intestinal tracts .
>
>A number of scientific concerns have been raised in connection with
>public and animal health. In the following we will discuss, in some
>detail, a few of these. Some of them have been thoroughly discussed
>in excellent, very recent reviews .
>
>Our contribution is based on "gene ecology"; a new,
>cross-disciplinary scientific field intended to provide holistic
>knowledge based on the precautionary principle .
>
>Some of the concerns we raise will also be relevant for environmental
>risk assessments of GEOs due to the fact that the processes discussed
>can take place in an ecosystem at large as well as in the ecosystems
>represented by mammalian organisms.
>
>Do we know that any GE food/feed is safe for consumption?
>
>For a composite material like food/feed, reductionistic approaches
>testing single components in vitro are highly unsatisfactory and
>cannot by definition clarify important safety issues. In spite of the
>obvious need, very few studies designed to investigate putative
>effects of GE nucleic acids or food/feed on potential animal or human
>consumers have been published in peer-reviewed journals. A consensus
>has emerged that the effects observed in some published studies must
>be experimentally followed up. To this day, this has not been done.
>
>Most of the animal feeding studies performed so far have been
>designed exclusively to reveal husbandry production differences
>between GEOs and their unmodified counterparts. Studies designed to
>reveal physiological or pathological effects are extremely few, and
>they demonstrate a quite worrisome trend : Studies performed by the
>industry find no problems, while studies from independent research
>groups often reveal effects that should have merited immediate
>follow-up, confirmation and extension.
>
>Such follow-up studies have not been performed. There are two main
>factors accounting for this situation: The lack of funds for
>independent research, and the reluctance of producers to deliver GE
>materials for analysis.
>
>Can we rely on the transgenic DNA sequences given by GE food/feed producers?
>
>If the transgenic DNA sequences given in the notifications differ
>from the inserted sequences found in the GEPs, the risk assessments
>made prior to approval of the GEPs for marketing do not necessarily
>cover the potential risks associated with the GEPs.
>
>The most thoroughly studied transgenic events are:
>
>Bt-transgenic maize Mon810
>Bt- and glufosinate-transgenic maize Bt176
>Glyphosate-transgenic maize GA21
>Glufosinate-transgenic maize T25 (Liberty Link)
>Glyphosate-transgenic soybean GTS 40-3-2
>
>Even amongst the most thoroughly studied and some of the oldest
>commercial GEPs, recent independent work has revealed that the nature
>of the rearrangements vary, and deletions (Mon810, GA21, Bt176),
>recombinations (T25, GTS 40-3-2, Bt176), tandem or inverted repeats
>(T25, GA21, Bt176) as well as rearranged transgenic fragments
>scattered through the genome (Mon810) have been reported.
>
>The transgenic modification techniques are prone to introduce such
>rearrangements because exogenous DNA transfer in plants elicits a
>"wound" response, which activates nucleases and DNA repair enzymes.
>This may result in either degradation of the incoming DNA, or
>insertion of rearranged copies into the plant DNA .  In addition, the
>nature of the DNA constructs used to make transgenic plants may
>influence the rearrangement tendencies for a given transgenic event.
>Some genetic elements in the constructs may act as "hotspots" and
>elicit recombinations at high frequencies.
>
>While it was earlier assumed that integration of transgenic
>constructs took place at random locations in the recipient plant
>genome, it has now become apparent that integration sites are
>concentrated in or near elements such as retrotransposons (T25,
>Mon810, GA21) and repeated sequences (Bt11 maize) , and this poses
>additional risks. Firstly, by introducing a new promoter or new
>enhancer motifs, transgenic insertions into, or close to, such
>elements may lead to altered spatial and temporal expression patterns
>of plant genes located close to and even far from, the insert.
>Secondly, a strong retrotransposon LTR promoter may upregulate the
>transgene expression level. Thirdly, defective retrotransposons may
>start "jumping" under the influence of transacting factors recruited
>by the insert . All these events may have unpredictable effects on
>the long-term genetic stability of the GEOs, as well as on their
>nutritional value, allergenicity and toxicant contents. These
>putative processes represent areas of omitted research with regard to
>health effects of GEOs.
>
>Are transgenic DNA and proteins taken up from mammalian GIT
>(gastro-intestinal tracts)?
>
>If DNA and proteins from GEOs persist in, and are taken up from
>mammalian GIT, this could theoretically, as will be further explained
>below, ultimately lead to development of chronic disease conditions.
>The fate and consequences of DNA persistence and uptake is, however,
>not extensively studied, and therefore represents yet another area of
>uncertainties connected to GEPs.
>
>It has generally been claimed that DNA and proteins are effectively
>degraded in mammalian GITs. This has been based on assumptions that
>have never been systematically examined. A restricted number of
>recent publications have demonstrated that foreign DNA and also
>proteins may escape degradation, to persist in the GIT and even to be
>taken up from the intestines and transported by the blood to internal
>organs in biologically meaningful versions. These findings should not
>have come as such a surprise, since scientific articles from the
>1990s  strongly indicated that this was an area of omitted research,
>as stated by a number of reports .
>
>Briefly summarised, the present conception of DNA persistence and
>uptake includes long fragments of ingested DNA. DNA may be detected
>in the faeces, the intestinal wall, peripheral white blood cells,
>liver, spleen and kidney, and the foreign DNA may be found integrated
>in the recipient genome. When pregnant animals are fed foreign DNA,
>fragments may be traced to small cell clusters in foetuses and
>newborns. The state of GIT filling, and the feed composition may
>influence DNA persistence and uptake. Complexing of DNA with proteins
>or other macromolecules may protect against degradation.
>
>So far only two published reports have investigated the fate of
>foreign/transgenic DNA in humans.   The consequences of DNA
>persistence and uptake thus represent yet another area of omitted
>research. Extrapolating from a number of experiments in mammalian
>cell cultures and in experimental animals, it is conceivable that in
>some instances insertion of foreign DNA may lead to alterations in
>the methylation and transcription patterns of the recipient cell
>genome, resulting in unpredictable levels of gene expression levels
>and products.  Furthermore, even small inserts may result in a
>so-called "destabilisation" process, the end-point of which may be
>malignant cancer cells .
>
>The BSE/new variant Creutzfeld-Jacob's Disease epidemics caused by
>the prion proteins painfully illustrated the phenomenon of protein
>persistence, uptake and biological effects.
>
>Two recent publications indicate that this phenomenon may be more
>general that realized. A hallmark of prion diseases and a number of
>other debilitating, degenerative diseases, i.e. Alzheimer's and
>Huntington's diseases, is deposition of "amyloid fibrils". Recent
>studies indicate that any protein can adopt a confirmation known as
>"amyloid"  upon exposure to appropriate environmental conditions.
>Whether that is the case for GE food/feed that is already in the
>marketplace is unknown.
>
>The consequences of protein persistence and uptake will vary with the
>given situation. Generally spoken there is a possibility that toxic,
>immunogenic/allergenic or carcinogenic molecules may gain entry to
>the organism via cells in the gastrointestinal walls. The persistence
>of the Bt-toxin Cry1Ab in faeces means a potential for spread on the
>fields through manure. The ecological effects, e.g. on insect larvae
>and earthworms, are at the moment an issue of shear speculation.
>
>Have the protein contents of GE food been altered in unpredictable ways?
>
>Transgenes or upregulated plant genes may give rise to toxicants,
>anti-nutritients, allergens and, putatively, also carcinogenic or
>co-carcinogenic substances. The concentration of a given transgenic
>protein may vary according to the location(s) in the recipient host
>cell genome of inserted GE construct DNA, and to environmental
>factors influencing the activity of the transgenic regulatory
>elements, e.g. the 35S CaMV promoter. The biological effects of a
>given transgenic protein, e.g. the Cry1Ab Bt-toxin, may be
>unpredictably influenced by posttranslational modifications,
>alternative splicings, alternative start codons for transcription,
>chimeric reading frames resulting from integration into the reading
>frame of a plant gene, and complex formation with endogenous plant
>proteins.
>
>The influence of foreign DNA insertion on endogenous plant gene
>expression patterns may vary with local environmental factors, the
>actual insertion site(s), the number and stability of the inserts,
>transgenic promoter effects, methylation patterns of the insert(s),
>and post-transformational mutations in the transgenic protein coding
>as well as in regulatory sequences. Even a single nucleotide change
>may affect the properties of a protein, or it may create a new
>transcription factor-binding motif. Detailed studies of these
>phenomena under authentic conditions are lacking, and hence we are
>confronted with yet another area of omitted research.
>
>May GE food/feed give allergies?
>
>One of the major health concerns related to GEPs is that the
>transgenic product itself, e.g. a Bt toxin, or changed expression of
>endogenous plant genes may result in allergenic compounds. The risk
>assessment of allergens often follows an allergenicity decision tree
>. These "trees" are based on in vitro tests comparing a limited
>number of structures, usually only one, of the transgenic protein
>with known allergens. Hence, these comparisons are hopeful that the
>protein isolated for the test matches all proteins produced from the
>same gene in the GEP. But in fact this is unlikely because
>allergenicity tests are usually carried out with bacteria-, not in
>planta-produced versions of the transgenic protein. Glycosylation
>invariably takes place in plants, but not in bacteria, so this form
>of post-translational modification of both the transgenic protein and
>endogenous proteins would not be tested. Allergenic characteristics
>of proteins, and also their resistance to degradation in the
>organism, can be affected by glycosylation. Other protein
>modifications may also take place, adding to the unpredictability of
>transgenic products .
>
>Another important question related to allergenicity is whether post
>marketing surveillance can provide useful information about allergens
>in GE foods. For a number of reasons this is not likely to happen .
>Treatment of allergy is symptomatic, whatever the cause may be. The
>allergic case is often isolated, and the potential allergen is rarely
>identified. The number of allergy-related medical visits is not
>tabulated. Even repeated visits due to well-known allergens are not
>counted as part of any established surveillance system. Thus, during
>the October 2000 Starlink episode, it proved very difficult to
>evaluate Starlink (containing Bt-toxin Cry9C) as a human allergen .
>An additional reason for this was that the ELISA tests, used by FDA,
>that found no anti-Cry9C antibodies in suspected human cases were
>dubious because bacterial, recombinant antigens were used instead of
>the Cry9C maize versions that the individuals had been exposed to.
>
>Case: Bt toxins in Bt-transgenic GEPs
>
>It is very important to be aware of the fact that the Bt-toxins
>expressed in GEPs have never been carefully analysed, and
>accordingly, their characteristics and properties are not known. What
>is clear from the starting point, however, is that they are vastly
>different from the bacterial Bacillus thuringiensis protoxins, used
>in organic and traditional farming and forestry for decennia . The
>difference is evident already at the gene level, since the versions
>found in GEOs are engineered to produce active Bt toxins. By
>extrapolation these have a number of potentially unwanted biological
>characteristics, ranging from solubilization of the protein under
>natural conditions and effects on insect and mammalian cells, to
>persistence and non-target effects in the environment. In addition,
>the posttranslational modifications that may influence conformations,
>cellular targets and biological effects of GEP-expressed Bt-toxins
>are unknown, and hence we once more identify an area of omitted
>research.
>
>During the last few years a number of observations that may be
>conceived of as "early warnings" of potential health and
>environmental risks, have appeared in the literature. Most of them
>have, however, not been followed up by extended studies.
>
>Case: Transgenic, glyphosate-tolerant (Roundup Ready) GEPs
>
>These GEPs have an inserted transgene, cp4 epsps, coding for an
>enzyme that degrades the herbicide glyphosate. The whole idea is of
>course the combined use of the GEP and the herbicide. Recent studies
>indicate that in some cases such GEPs are associated with greater
>usage of glyphosate than the conventional counterparts . A very
>restricted number of experimental studies have been devoted to health
>or environmental effects of the GEPs or the herbicide itself. Some of
>these may be considered "early warnings" of potential health and
>environmental risks, and they should be rapidly followed up to
>confirm and extend the findings . Consequently: yet another area of
>omitted research.
>
>Is the 35S CaMV promoter inactive in mammalian cells?
>
>Cauliflower mosaic virus (CaMV) is a DNA-containing para-retrovirus
>replicating by means of reverse transcription (Poogin et al., 2001).
>One of the viral promoters, called 35S is a general, strong plant
>promoter. It has been used to secure expression of the transgenes in
>most of the GEOs commercialized so far.
>
>Industry proponents have claimed unconditionally that the 35S is an
>exclusive plant promoter, and hence cannot, even theoretically,
>represent a food/feed safety issue .
>
>In addition to studies in yeast  and in Schizosaccharomyces pombe ,
>there are published studies indicating that the 35S CaMV promoter
>might have potential for transcriptional activation in mammalian
>systems . And the final proofs have been made available during the
>last couple of years. First, 35S promoter activity was demonstrated
>in human fibroblast cell cultures , thereafter in hamster cells , and
>very recently one of us (TT) has demonstrated substantial 35S
>promoter activity in human enterocyte-like cell cultures. Such cells
>are lining up the surface of human intestines. However, no published
>studies have investigated 35S CaMV activity in vivo, and this is
>hence an obvious area of omitted research.
>
>May the use of antibiotic resistance marker genes (e.g. nptII)
>present health hazards?
>
>The antibiotic kanamycin is used extensively in crop genetic
>engineering as a selectable marker, inter alia in GE oilseed rape
>event lines like MS1Bn x RF1Bn and Topas 19/2.
>
>A selectable marker is a gene inserted into a cell or organism to
>allow the modified form to be selectively amplified while unmodified
>organisms are eliminated. In crop genetic engineering the selectable
>marker is used in the laboratory to identify cells or embryos that
>carry the genetic modifications that the engineer wishes to
>commercialize. The selection gene is used once briefly in the
>laboratory, but thereafter the genetically modified (GM) crop has the
>unused marker gene in each and every one of its cells.
>
>There are multiple well-known mechanisms for cross-resistance to
>antibiotics of a particular type . Kanamycin is a member of the
>family aminoglycoside antibiotics. There are approximately 17
>different classes of aminoglycoside-modifying enzymes. Some of these
>inactivate up to four different aminoglycosides. Cross-resistance
>between kanamycin and other aminoglycosides, e.g. gentamycin and
>tobramycin, was found to vary markedly between isolates.  All of the
>antibiotics mentioned are used to treat human diseases.
>
>Along with cross-resistance to aminoglycoside antibiotics, pathogenic
>bacteria frequently develop multiple drug resistance transmitted on a
>single plasmid . Pathogenic bacteria do acquire plasmids with
>multiple antibiotic resistance genes in areas where the antibiotics
>are used extensively. Such incidents illustrate the potential health
>effects of HGT. Multiple resistance genes on a single plasmid can
>simultaneously adapt a bacterium to several unrelated antibiotics.
>One antibiotic at a time is all that is necessary to maintain the
>plasmid.
>
>In spite of the belief of many genetic engineers that kanamycin is no
>longer employed in medical applications, there is evidence that the
>antibiotic is used extensively for some applications.
>
>Concluding remarks: Where do we go from here?
>
>We have discussed in some detail a handful of selected, unanswered
>risk questions related to the first generation of transgenic GEOs.
>There are many more risk issues. Among them are issues of Horizontal
>Gene Transfer (HGT), the new generations of multitransgenic GEOs for
>pharmaceutical and industrial purposes, safety questions related to
>GE vaccines, the new nanobiotechnology approaches and the
>applications of small inhibitory (si) RNAs for a number of medical
>purposes. Furthermore, we have the "questions not yet asked", and we
>have the problem of whether available methods and regulatory
>frameworks will be able to pick up and manage the conceived risks
>once they become reality.
>
>In recent publications it has been demonstrated that the presently
>used sampling and detection methods may fail to detect GE materials
>in food and feed. In another article it was demonstrated that HGT
>events, that potentially carry very serious public health
>consequences, would not be detected in time for any meaningful
>preventive actions. And it has been illustrated that the siRNA
>techniques are not as "surgically targeted" as initially indicated.
>
>We are left with a high number of risk issues lacking answers, adding
>up to a vast area of omitted research, and this falls together in
>time with a strong tendency towards corporate take-over of publicly
>funded research institutions and scientists.
>
>We must as citizens and professionals join together to reverse the
>present situation. Publicly funded, independent research grants must
>become a hot political issue. That would be the most efficient remedy
>for lacking answers and corporate take-over of science. And finishing
>off, we once more quote Mayer and Stirling : "Deciding on the
>questions to be asked and the comparisons to be made has to be an
>inclusive process and not the provenance of experts alone". But then
>again, whom should the society rely on for answers and advice when
>the time comes that all science resource persons work directly or
>indirectly for the GE producers?
>
>
>Dr. Terje Traavik is the author of more than 180 scientific articles
>and book chapters. He founded and was the professor of virology at
>the University of Tromsö, Norway from 1983-2003. He has had a high
>number of national and international assignments. At the present he
>serves as the Executive Committee Chairman for the GE/GMO Biosafety
>Capacity Building Program covered by a MoU (Memorandum of
>Understanding) between GENOK-Norwegian Institute of Gene Ecology and
>and UNEP (United Nations Environment Program). Being originally a
>medical and molecular virologist, Traavik later crossed into
>molecular and cellular cancer research. In 1992 he received the Erna
>and Olav Aakre Foundation Prize for Excellent Cancer Research. In the
>early 1990s he was the Board Chairman of the national research
>program "Environmental effects of biotechnology", which was funded by
>the Research Council of Norway. In 1997 he initiated and became the
>first Director of GENOK-Norwegian Institute of Gene Ecology, and
>since 2003 he is professor of gene ecology at the University of
>Tromso.
>
>Dr. Jack Heinemann is at the present an Assoc. Professor at the
>School of Biological Sciences, University of Canterbury,
>Christchurch. He is the Director of the NZIGE-New Zealand Institute
>of Gene Ecology, and an adjunct professor at GENOK-Norwegian
>Institute of Gene Ecology. He serves on the United Nations
>Environment Programme-GENOK Biosafety Capacity Building Executive
>Committee. Dr. Heinemann was the 2002 recipient of the New Zealand
>Association of Scientists Research Medal. He is the author of a high
>number of scientific articles, reviews and book chapters. He was one
>of the real pioneers within HGT (horizontal gene transfer) research,
>and has given major contributions to this area as well as related
>fields within bacterial genetics and molecular biology.
>
>
>
> >Hi Ken ;
> >
> > > > If someone developed a genetically modified plant
> > > > that would grow well in marginal areas and
> > > produced
> > > > high quality vegetable oil, that could be easily
> > > > extracted, would that be a good thing or a bad
> > > > thing? Or for that matter, if someone developed a
> > > > plant that grew well in marginal areas and
> > > contained
> > > > high-quality protein, low glycemic carbohydrates,
> > > > and many needed trace nutrients, would that be a
> > > > good thing or a bad thing?
> > >
> > > This is the cruel hoax and seduction.  Taken in
> > > isolation of course it is a good thing, but the
> > > problem is it is never in isolation.  How many tests
> > > and failures were needed to make this one success?
> > > What was the total cost to the earth?  How many
> > > crops
> > > needed to be destroyed?  How many small farmers put
> > > out of business or committed suicide?  How many
> > > other
> > > life forms (birds, animals, fish, people, viruses,
> > > bacteria, etc) were affected or decimated (or made
> > > more dangerous)?  And your case is only hypothetical
> > > wishful thinking for the future.  The failures are
> > > here already.
> >
> >I should have added the failures and suicides are
> >already here.  Furthermore, the question is not
> >whether this is a good thing or not, the question is
> >whether it should receive patent protection or not.
> >
> >What if I add to this fantastic oil and protein plant
> >the fact that is has very small seeds which can be
> >carried everywhere by wind, water, train, ship, and
> >combine.  Then we add that it is a strong growing
> >plant which tends to overgrow the existing vegetation.
> > Then the developers of this plant ride around the
> >country and spread seeds everywhere.  Seed is spread
> >worldwide even against the wishes of many nations.
> >Private household farm crops are overtaken by this
> >plant and destroyed worldwide.  Commercial farm crops
> >are overgrown by this plant and on top of that need to
> >pay patent licensing fees (as well as lawyer and court
> >costs if they choose to fight).  Then we add that the
> >developers of this plant expect very high patent fees,
> >and the courts agree (in other words farms are forced
> >to pay or close).
> >
> >Still think it should have patent protection?
> >
> >BR
> >Peter G.
> >Thailand
>
>
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