Devil be GONE!

In a world of progressive modern technology, where devices are smaller, televisions are bigger and computers are smarter, animal species are becoming extinct.

The Tasmanian Devil, is very close to this dangerous line. A disease discovered in the late 90’s called the “Tasmanian Devil Facial Tumour Disease” has affected 60% of the population. This disease spreads among the isolated species, through fighting, biting and possibly during mating. It is an infectious cancer, incurable at this stage.
The tumour is a contagious cancer cell line, not rejected by the species immune system as they are too similar to there own natural cells. Due to a lack of genetic diversity among the species, the amount of genetic variability among these animals is limited, as is their diminishing ability to survive environmental change.

Numerous animal species in Australia and around the world are facing the loss of genetic diversity. Koala’s, Platypuses, Fish species, Tigers, Monkeys, the list goes on. Scientists are establishing “gene banks” to save the genetic material in a suspended animation, so in the future with the progressing advances in technology they hope to “bring back” or at least return vulnerable species population figures to a sustainable level. We have a responsibility to help, and assist through modern technologies, the animals of the world. The goal ultimately is creating sustainable populations, in which there are enough animals of the species to survive in a healthy, disease free environment.

Primary References:

Tasmanian Devil Facial Tumour Disease: Save the Tasmanian Devil
http://www.tassiedevil.com.au/disease.html
Genetic Times – Breakthrough could save the Tasmanian Devil
http://www.geneticstimes.com.html/

Secondary References:
The Value of Endangered Species: the Importance of Conserving Biological Diversity
http://edis.ifas.ufl.edu/UW064
Endangered Animal of the World
http://www.ypte.org.uk/docs/factsheets/env_facts/end_species.html

Owners resemble their pets more than they think

For centuries our canine companions have been domesticated by humans. They’ve proved invaluable to us in our domestic as well as in our working lives. They’ve been used cross culturally for hunting, protection, transport, even food and fashion; but more recently researchers have been looking at our hairy friends a little more closely. A group of French scientists, for example, have for years provided canine genomic resources to aid in medicine. These genomic resources go towards further understanding the genetic bases of traits and genetic diseases in canines so that they may be used as models to study equivalent human traits. The fact that 75% of human genes have a canine equivalent may make you look at your loving companion a little more closely as she chases her playmates in the dog park, and wonder how many of them share medical conditions with their owners: conditions such as epilepsy, diabetes or cancer. Sharing knowledge on genomics can be used so that both the canine and the human medical discourses may benefit. With mutual information exchange, knowledge of our canine friends and their conditions will help us to live longer and healthier lives as well as assisting us in helping them to live longer and healthier lives alongside us.

Primary resource:
http://apps.isiknowledge.com.ezproxy.library.uq.edu.au/full_record.do?product=WOS&search_mode=GeneralSearch&qid=2&SID=1Dp@E4h@7L4O921O4cA&page=1&doc=7
Guaguere, A. C., Thomas A, et al. 2007. Identification of genes involved in genodermatoses: Example of naso-plantar Keratodermia in the French breed Dogue de Bordeaux. Bulletin de l’académie vétérinaire de France 160 (3) 245-250.

Secondary resources:
http://news.bbc.co.uk/cbbcnews/hi/animals/newsid_3141000/3141812.stm
http://www.broad.mit.edu/mammals/dog/
http://www.funnyphotos.net.au/userimages/user756_1161918531.jpg

Australian Oddities: Help us, Help them.

http://genome.wustl.edu/ancillary/data/whitepapers/Ornithorhynchus_anatinus_WP.pdf

Historically, Australian fauna was considered oddball, misfits from spare parts of evolution. In science this often resulted in Australian native species being overlooked, with costly research deemed unlikely to yield results significant to mankind, as many species disappeared altogether. With the success of recent human gene mapping, however, the differences of Australian fauna may become their saviour as “comparative genetics” rises as a method of understanding the newly mapped Homo Sapiens genome.

P. Temple-Smith et. al. (2003) and J. Graves et. al. (2004) both constructed successful proposals for the sequencing of the Platypus and Tammar Wallaby, by suggesting that monotreme genes may provide explanations of human gene functions. The development of these projects have revealed issues relevant to human medicine such as the lack of a gene in platypus previously believed to control sex differentiation, suggesting a rethink of sex-chromosome related models, and gene expression during different stages of lactation during Tammar Wallaby development, providing possible treatments for premature babies.

Through comparative genetics, and the possible compatible differences between man and marsupial, Australia’s unusual wildlife has shown benefits to scientific research, paving the way for further projects, and thus increasing overall understanding, interest in, and the likelihood of the survival of Australian fauna as a whole.

Ellana S. Hetherington

s41237902

The Chicken and the Rat

The optic nerve is responsible for transmitting the electrical impulses it receives from the photoreceptors of the retina to the brain, enabling us to see. If this nerve becomes damaged, as a result of disease (such as, for example, glaucoma) or from trauma, impairment or loss of vision will result. Damage to this nerve is normally irreversible; however, researchers have recently found a way to regenerate its growth (in a rat) by using embryonic stem cells derived from the neural tube of chickens (NTSCs) at stage 10 of embryological development.

The optic nerve consists of the axons of the ganglion cells of the retina. When the nerve is damaged, these axons cannot pass within its interior because of a lack of myelin or build-up of scar tissue from glial cells. NTSCs have been found to promote the regeneration of these axons by producing neurotrophic factors which stimulate axonal growth. The NTSCs were also found to create a microenvironment which enabled axon elongation. This is thought to be due to the workings of two metallopeptidases (MMP2 and MMP14) – genes involved in the degradation of extracellular matrix (in this case, the glial scar tissue). There was found to be an up-regulation of these genes in the grafting site, possibly directly due to the NTSCs (although this is still under investigation). The time taken for the axons to reach the brain was approximately six to eight weeks after the surgery. These findings have important implications for the future of repairing neural injuries in other species. However, there still exists the ethical problem of using animals for these experiments.

Written by: s4140034

Primary source:
1.) Charalambous, P., Hurst, L.A., Thanos, S., 2008. “Engrafted chicken neural tube derived stem cells support the innate propensity for axonal regeneration within the rat optic nerve”, Investigative Ophthalmology and Visual Science, April 11 [EPub ahead of print], viewed 29 May 2008, <http://www.iovs.org/cgi/rapidpdf/iovs.07-1473v1>.

Secondary sources:
2.) Barnard, S., ‘An introduction to diseases of the optic nerve’, American Academy of Optometry, viewed 29 May, 2008, <http://www.academy.org.uk/lectures/barnard3.htm>.

3.) ‘Neurotrophic factors’, Ceregene, viewed 29 May 2008, <http://www.ceregene.com/neurotrophic.asp>.

4.) Hill, M., 2007. ‘Chicken Development Stages’, University of NSW Embryology, viewed 29 May, 2008, <http://embryology.med.unsw.edu.au/OtherEmb/chick2.htm>.

Image source:
Rural Ramblings <http://www.ruralramblings.com/blog/2007_07_01_archive.html>

Is man's best friend helping us find a cure for blindness?

Progressive Retinal Atrophy (PRA) is the most common type of inherited retinal dystrophies experienced by dogs. PRA is an outer retinal disease affecting the photoreceptors and the pigment epithelium of the eyes, causing a progressive loss of vision, eventuating in blindness.

The retinal condition is recessively inherited through an autosomal gene in all breeds except for the Siberian husky and the Samoyed, in which PRA is a sex-linked trait, due to mutations in the RPGR gene. PRA in dogs is comparative to Retinitis Pigmentosa (RP) in humans, which displays similar clinical characteristics.

At present, there is still no treatment for PRA, however, thanks to the fairly recently assembled canine genome sequence, researchers have been able to identify and locate the mutated genes responsible for retinal degradation. This breakthrough has enabled them to use gene therapy to restore the vision of PRA affected experimental dogs, in which a corrective genetic substance is used to target these mutations/defects. While, gene therapy may sound like a clear winner, it does not actually restore the already damaged parts of the retina, but stops the advancement of PRA, possibly protecting the undamaged photoreceptors.

While this technique of gene therapy is still a work in progress for PRA; clearly alarm bells are ringing as to the immense benefits that would arise from discovering how to cure this condition. It would not only hold benefits for dogs but also across species, namely to the closely related condition in humans.

Rebecca Martens

Primary Resource:

Narstrom, K & Ofri, R 2006, 'Light at the end of the tunnel? Advances in the understanding and treatment of glaucoma and inherited retinal degeneration', The Veterinary Journal, vol. 174, no. 1, pp. 10-22.

http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science?_ob=ArticleURL&_udi=B6WXN-4N3GX66-1&_user=331728&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000016898&_version=1&_urlVersion=0&_userid=331728&md5=181509ac593e61fb9dbef051e9a28d10

Seconday resources:

http://en.wikipedia.org/wiki/Progressive_retinal_atrophy

http://www.cavalierhealth.org/retinal_atrophy.htm

http://www.level1diet.com/1001428_id

Frankenfish: Man’s One-Two Punch in the Gut of Mothernature

Seemingly everyday lifestyle problems that humans encounter have been fixed to please both consumers and producers. Electrical cars made to address petrol prices, genetically selected cows produced for high milk yield and GO cards to reduce bus line ups. It would seem like a revolutionary breakthrough with the introduction of genetically engineered (abbrev. GE) salmon, ‘Frankenfish’ it has been named, that not only grows six times faster than farm-raised salmon but is twice as large and requires only three-quarters as much feed. Naturally, it’d be cheaper and more efficient for farmers and it would mean less wild fish would be killed for produce. The prices on Tasmanian Salmon will then be a pleasant sight for the sore eyes of Australian consumers.

However, the plight of wild salmon populations are at stake with the GE fish threatening their natural habitats and interfering with breeding. The industrial-style fish farming of the GE fish involves converting wild fish into fishmeal as feed. Also, fish from the farms have often escaped from their enclosed pens into the wild, leaving their wild counterparts to compete with the extra few hundred thousand GE fish for food with each escape. Cross-breeding with the GE fish also raises an issue as they are not bred for long term survival. These traits could be inbred into the next few generations of fish, causing a decrease in wild salmon populations instead of reducing the pressure on the wild salmon population.

So before rushing off to the next salmon special at the fish market, consider whether saving those few dollars in our wallets is really worth giving up the wild salmon population.

Written by 41435995

Primary Source:

Labriola, T. 2002. Transgenic Fish: Saviour or Sabateur? Vermont Journal of Environmental Law; April 2003.
http://www.vjel.org/editorials/ED10031.html.
Accessed 27 May 2008.

Secondary Sources:

http://www.greenpeace.org/raw/content/international/press/reports/genetically-engineered-fish.pdf

http://fwcb.cfans.umn.edu/isees/MarineBrief/MBB_1.pdf

Owners resemble their pets more than they think

For centuries our canine companions have been domesticated by humans. They’ve proved invaluable to us in our domestic as well as in our working lives. They’ve been used cross culturally for hunting, protection, transport, even food and fashion; but more recently researchers have been looking at our hairy friends a little more closely. A group of French scientists, for example, have for years provided canine genomic resources to aid in medicine. These genomic resources go towards further understanding the genetic bases of traits and genetic diseases in canines so that they may be used as models to study equivalent human traits. The fact that 75% of human genes have a canine equivalent may make you look at your loving companion a little more closely as she chases her playmates in the dog park, and wonder how many of them share medical conditions with their owners: conditions such as epilepsy, diabetes or cancer. Sharing knowledge on genomics can be used so that both the canine and the human medical discourses may benefit. With mutual information exchange, knowledge of our canine friends and their conditions will help us to live longer and healthier lives as well as assisting us in helping them to live longer and healthier lives alongside us.

Sasha

Primary resource:
http://apps.isiknowledge.com.ezproxy.library.uq.edu.au/full_record.do?product=WOS&search_mode=GeneralSearch&qid=2&SID=1Dp@E4h@7L4O921O4cA&page=1&doc=7
Guaguere, A. C., Thomas A, et al. 2007. Identification of genes involved in genodermatoses: Example of naso-plantar Keratodermia in the French breed Dogue de Bordeaux. Bulletin de l’académie vétérinaire de France 160 (3) 245-250.

Secondary resources:
http://news.bbc.co.uk/cbbcnews/hi/animals/newsid_3141000/3141812.stm
http://www.broad.mit.edu/mammals/dog/
http://www.funnyphotos.net.au/userimages/user756_1161918531.jpg

Population Genetics - what's the best aproach to save frogs?

Batrachochytrium dendrobatidis (frog chytrid fungus) is a parasitic fungus associated with the major decline in amphibian populations in Australia (and the world). First reported in 1998, it’s the only known chytrid to be parasitic to vertebrates. It grows in keratinised cells.
The fungus is thought to be transferred by direct
contact between frogs and tadpoles. Chytrid spread is considered a major environmental disaster for Australian and world frog populations.

Appropriate and effective response requires understanding if the spread of the fungus is due to emergence of pathogenic clones or environmentally determined increase in fungus populations. Determining genetic structure of the fungus and environmental variables will provide direction to the predominant hypothesis and therefore targeted response.

Genetic sequencing provides both framework and answers in international studies that have been struggling with this pathogen, its speed of spread and how it kills frogs. Thirty-five strains of the fungus from 19 species were DNA harvested and a (incomplete) genomic library was established representing 3 continents and including 33 clone sequences.

Low level genetic variation within intercontinental samples was determined where strains evaluated have the genetic signature of a newly emerged pathogen. There is an implication that coalescence time of the entire sample is relatively recent and few mutations have occurred. The study on the affect of the fungus on frogs indicates the recent introduction of the pathogen. Genotypes of frogs are similar in populations where the fungus does and dosen’t spread.

Neither epidemic spread nor endemism explains the problem which means complicated global fungus control problems in the future.



Primary Reference:
Morehouse, E.A., James, T.Y., Ganley, A.R.D., Vilgalys, R., Berger, L., Murphey, P.J. and Longcore, J.E.. (2003) Multilocus sequence typing suggests the chytrid pathogen of amphibians is a recently emerged clone. Molecular Biology 12, 395-403

http://www.blackwell-synergy.com.ezproxy.library.uq.edu.au/doi/pdf/10.1046/j.1365-294X.2003.01732.x
Secondary References:
Laurance, W.F.. (2008) Global warming and amphibian extinctions in eastern Australia. Austral Ecology 33, 1-9
Rachowicz, L.J., Hero, J.M., Alford, R.A., Taylor, J.W., Morgan, J.A.T., Vredenburg, V.T., Collins, J.P. and Briggs, C.. (2005) The Novel and Endemic Pathogen Hypotheses: Competing Explanations for the Origin of Emerging Infectious Diseases of Wildlife. Conservation Biology 19, 5. 1441-1448
Background:
http://en.wikipedia.org/wiki/Population_genetics
http://en.wikipedia.org/wiki/Ecological_genetics
Graphic:
http://www.e-pond.info/green_tree_frog_pictures.html M. Avery

A Touch of Ethics on Chicken Transgenics

Kate Peters - 41406771

Genetic manipulation (GM) is not a new development, with centuries of deliberate cross breeding to produce poultry more suited to human purposes (Almond & Parker 2003). Technology implementations have out-competed previous farm practices; with the ability to achieve traditional breeding goals at a more proficient level (Uzogara 2000).

The goals for transgenic animals are the same as traditional breeding (Campbell et al. 2006); to produce desirable characteristics of improved feed conversion efficiencies, growth rates, lower fat levels, disease and pest resistance, leaner meat, a capacity to utilize low-cost protein diets, and improved egg compositions (Heller 2003).

Although still on an experimental basis; scientists can produce “transgenic animals” by implementing a gene from one animal into the genome of another (Campbell et al. 2006). This process involves the removal of oocytes and in vitro fertilization. The desired gene from another organism is cloned and inserted directly into the nuclei of the fertilized eggs. Some of the cells integrate the foreign DNA, the transgene, into their genomes and express the desired trait/s. Engineered embryos are then surgically implanted into a surrogate mother. Successful development results in a transgenic animal; containing a gene from a third ‘parent’ (which can even be a different species!) (Campbell et al. 2006).

Over the last decade, chickens have become a major target in transgenic research for the mass production of human proteins (Han 2008). Significant technical qualities of chicken genetic and physiological traits give rise to a number of advantages (Han 2008):

• Transgenic line establishment in a 5 month generation time - a fertile rooster is capable of inseminating 10 hens/3 days, recipient hens can produce ten fertile eggs (Han 2008).
• Chickens are relatively easy to maintain (size and traits) (Han 2008).
• Simple composition of egg proteins reduces the cost of protein purification after transgenesis (Han 2008).

Despite the benefits of GM poultry, there is understandable controversy (Uzogara 2000).

• Are humans free to exploit animals for our own purposes, while still implementing humane treatment (Almond & Parker 2003)?
• Does GM of chickens for human benefit push the boundary between humans and non-human animals in a moral and biological sense (Pascalev 2006)?

It is argued that traditional principles of animal welfare, interests and rights are inadequate for evaluating the morality of GM (Pascalev 2006).

References:

• Almond, B & Parker, M 2003, Ethical Issues in the New Genetics, Ashgate Publishing, England.
• Campbell, NA & Reece, JB & Meyers, N 2006, Biology – Seventh Edition – Australian Version, Pearson Education, Australia.
• Han, J.Y 2008, ‘Germ Cells and Transgenesis in Chickens’, Elsevier – CIMID, vol 648, pp. 1-20.
• Heller, K.J (ed.) 2003, Genetically Engineered Food – Methods and Detection, WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim, Germany.
• Pascalev, A.K 2006, ‘We and they: Animal welfare in the era of advance agricultural biotechnology’, Elsevier – Livestock Science, vol. 103, pp. 208-220.
• Uzogara, S.G 2000, ‘The impact of genetic modification on human foods in the 21st century: A review’, Elsevier – Biotechnology Advances, vol. 18, pp. 179-206.

DOGS LEAP FOR JOY - BECAUSE THEY CAN

Vet-stem, based in California, is a company specializing in veterinary regenerative medicine. Animals are injected with stem cells derived from their own tissue, such as fat, in order to treat arthritis, tendon and ligament injuries. Stem cell therapy, using adipose derived stem cells, has been available for horses for the last three years and Vet-stem has recently extended this treatment to dogs.

More than 20% of dogs in the United States are affected with osteoarthritis (OA), a severe debilitating disease causing chronic pain and much suffering. A recent study investigated the effectiveness of a single injection of adipose-derived stem cells into the coxofemoral joints of dogs displaying lameness associated with OA. The results were promising, with patients showing decreased discomfort and increased mobility.

The treatment involves using the dogs’ own adipose-derived stem cells. Two tablespoons of adipose tissue are collected surgically from behind the shoulder blade or from the belly. This sample is then sent away to Vet-stem where the regenerative stem cells are isolated from the adipose tissue. The cells are sent back to the Veterinarian and injected into the injured tissue.

Vet-stem has now treated over 200 dogs with arthritis, tendon and ligament injuries. Dog owners are rejoicing, with a number of clients extremely relieved to find an alternative to euthanasia in order to relieve their pet of chronic pain and suffering. This is an exciting development in the world of stem cell therapy and is leading the way for treatment for a variety of diseases.

Primary References

1. http://vetmedicine.about.com/od/diseasesandconditions/a/Vet_stem.htm
2. http://www.the-scientist.com/pubmed/18183546

Secondary References

1. http://itchmo.com/stem-cell-therapy-for-dogs-and-horses-2841
2. http://abcnews.go.com/Health/Story?id=4109559&page=1

A glimmer of hope for Devil

Tasmanial devils, the world’s largest marsupial carnivore, is threatened with extinction by the Tasmanian Devil Facial Tumor diseases (DFTD). At this moment, DFTD could be confirmed in 59 percents of Tasmania and Tasmanian devils have decreased by 53 percents in sighting since DFTD had appeared in 1996. In fact, some scientists expect that devils would die out in the near future, probably within a decade or two unless some interventions were developed.

However, a glimmer of hope was appeared. Last year, two Tasmanian devil, Cedric and his half-brother Clinky, were injected with dead facial tumor cell by scientists and as a result, Cedric could produce antibodies. This would indicate Cedric has different genetic composition as his brother and it is unaffected by disease or able to respond for a vaccine. This makes scientists find other wild devils which have same genetic make up as Cedric.

And in this year, ABC news reported that scientists found similar DNA as Cedric which seems resistant to diseases in a group of captured devils known as the “special six”. One of the members of the Save the devils Program’s Professor Hamish McCallum also suggests that around 10 to 20 percents of the animals in the west side of Tasmania may have those genes. If those devils and Cedric remain unsusceptible to the disease after the injection of dead facial tumor cell, then those animals would be able to use for some breeding programs to disperse discerning genes to a new generation of devils.

Written by Yuichiro Yoshida

Primary source

Kirkman, J. (2007). Save the Tasmanian devil. Retrieved from Tasmania Devil Program: Viewed 28 May 2008, Available at <>

Mercer, P. (2008) Hope over Tasmanian devil cancer. BBC News 2008 Apr 1. Viewed at 28 May 2008, Available at <>

Australian Broadcasting Corporation, (2008). ‘Special’ DNA could save Tasmania’s devils. Viewed at 28 May 2008, Available at

<>

Secondary sources

Holtcamp, W. Tasmania’s Devil of a problem, viewed at 28 May 2008, Available at

< articleid="1598&issueID="122">

Cataract’s reign of terrier overthrown!

Cataracts are a major cause of blindness for dogs, particularly in purebred breeds. They occur when the transparent lens tissue of the eye becomes opaque, reducing the lens’ ability to focus light onto the retina, which is vital for clear vision. It was recently discovered that HSF4, a gene related to cataracts in humans, is also associated with hereditary cataracts in dogs. A single nucleotide insertion in exon 9 of the canine HSF4 gene alters the transcript reading frame, causing an early stop codon, which results in a shortened, incorrect protein. Thus, a cataract forms.

This discovery arose in a study focussing on Staffordshire Bull Terriers, a breed in which the mutation causes hereditary cataracts. The gene mutation was also found to be autosomal and have recessive inheritance. Another study found the HSF4 mutation causes early-onset hereditary cataract (EHC) in Boston Terriers, but has no association with late-onset hereditary cataract, which also occurs in Boston Terriers. Yet another study discovered the HSF4 mutation is not related to cataracts of the Dachshund or Entlebucher Mountain Dog. Knowledge of HSF4 mutation is continually refined in this fashion.

Discovery of which types of cataract are caused by HSF4 mutation has allowed the development of diagnostic tests to find if a dog is affected, or a carrier of the mutation. Breeders may now use these tests to select against dogs with the mutation and therefore eliminate HSF4 mutation related cataracts from affected dog breeds, freeing terriers from the terror of cataracts.

Lauren Byrne

41724792

Primary References:

Mellersh, C.S., Pettitt, L., Forman, O.P., Vaudin, M., Barnett, K.C., 2006. Identification of mutations in HSF4 in dogs of three different breeds with hereditary cataracts. Veterinary Ophthalmology 9, 369-378.

**Click Here**

Mellersh, C.S., Graves, K.T., McLaughlin, B., Ennis, R.B., Pettitt, L., Vaudin, M., Barnett, K.C., 2007. Mutation in HSF4 associated with early but not late-onset hereditary cataract in the Boston Terrier. Journal of Heredity 98, 531-533.

**Click Here**

Müller, C., Wöhlke, A., Distl, O., 2008. Evaluation of canine heat shock transcription factor 4 (HSF4) as a candidate gene for primary cataracts in the Dachshund and the Entlebucher Mountain Dog. Veterinary Ophthalmology 11, 34-37.

**Click Here**

Secondary Reference:

Wolfer, J.C. Cataract Surgery. Islington Animal Clinic.

http://www.animaleyeclinic.ca/cataracts.htm.

Accessed 26 May 2008.

**Click Here**

We share more than just companionship with our best friend

Researchers discover a genetic cancer link between humans and our best friend

A new report has found that because we share a very similar gene base to dogs, we also share the same genome base for many types of cancers including blood and bone marrow cancers (for example, leukemia) _[1]. Genomes are made up of chromosomes that contain all our genetic material and determine everything from our eye colour to the susceptibility of certain cells to become cancerous.

Researchers in America have long been aware of the fact that genomes of dogs are basically the differential arrangement of our genomes. This is because we diverged from a common ancestor more than 50 million years ago and retained a common basis in regard to genome reorganization associated with cancer _[1]. However, researchers have now recognized the genetic abnormalities that are present in canine tumours that occur naturally. These mutations that occur in nature during these genome reorganizations have very similar consequences in both dogs and humans _[2]. During evolution, these mutations have remained in the genome, being expressed in many generations. This means that some dogs are more likely than others to develop cancer, and the same could be said for humans because we share such a similar genome _[1].

All dogs share a very small gene pool, especially pure-bred dogs. This is why some conditions occur at a higher rate in some pure-bred breeds compared to others. Researchers believe that it will be easier to follow the genetic make-up of dogs, and then apply this knowledge to human DNA in order to recognize the genes that initiate cancer _[1]. What they are looking for is basically cells that continue to replicate to form a tumour and do not die.

This important step in cancer research will path the way for future studies involving the treatment and early identification of cancer in dogs, and eventually humans.

[1] Breen, M, Modiano, J.F (2008) ‘Evolutionarily conserved cytogenetic changes in hematological malignancies of dogs and humans - man and his best friend share more than companionship’, Chromosome Reasearch, vol. 16, pp. 145-154

[2] Buss, S.E (2008) ‘U of Minn researchers discover genetic cancer link between humans and dogs - Studying cancer in dogs may translate into greater insight into cancer risk, diagnosis, and prognosis in humans’, Viewed: 27-05-2008. Available Online: http://www.sciencedaily.com/releases/2008/02/080228112011.htm

Genetics...In the Barnyard?

Cancer is an epic issue throughout the world with millions of people dying from it per year as a cure is yet to be found. It’s so common that if you personally haven’t had cancer, you know someone who has. Yet researchers have developed a new method in an attempt to producing a faster and cheaper way for manufacturing anticancer drugs. By genetically engineering chickens to lay eggs full of cancer-fighting proteins which target and destroy specific tumor cells, researchers will attempt to create a mass production of this anticancer protein.

The foundation for this idea with chicken eggs has been in the grinder for many decades yet has only just become a reality. Researchers at the Roslin Institute in the UK have successfully engineered five generations of chickens who are able to produce these life saving proteins within their eggs. Previous attempts on similar projects with goats resulted in being to expensive yet researchers are hopeful that they wont be stopped by the same problem. Although work is still needed on the project, it is estimated that is will approximately five or more years until drug companies will beginning using chickens to mass produce the anticancer proteins.

More tests will have to be done to ensure the chickens are not under any danger and for the safety of human use. Because it’s dangerous if the proteins are produced anywhere else in the chicken’s body, researchers still have work to do before this product can be made commercial. Only time will tell.

Written by 41534441

Primary Source:
http://news.bbc.co.uk/1/hi/sci/tech/6261427.stm

http://www.medicalnewstoday.com/articles/25623.php

Secondary Source:
http://thedrugnerd.blogspot.com/2007/01/anti-cancer-chicken.html

http://news.softpedia.com/news/Anticancer-Anitviral-Proteins-Produced-in-Transgenic-Chicken-Eggs-44458.shtml

The walking, clucking cancer fighting factory

Researchers at the Roslin Institute have successfully managed to produce three generations of genetically modified chicken, with the amazing ability to lay eggs with relatively high percentage of protein used to make cancer fighting drugs, from a single transgenic cockerel. These genetically modified chickens could be the “drug factories” of the future. It has a huge potential to mass produce not just cancer fighting proteins and drugs but other pharmaceutical proteins at the cost of literally chicken feeds.

Infectious anemia virus was used as the vector, with all of its viral coding sequences deleted and replaced with genes that produce the miR24, which is a type of antibody that has the potential to treat malignant melanoma. The vector used is tissue specific, due to the utilization of regulatory sequences, and is aimed at the oviduct of the laying hens. The cockerel was hatched after the injection of the vector and was mated with numerous hens to produce transgenic progenies. These engineered hens produce eggs with the specified proteins in the egg white, which can be easily extracted, purified and made into cancer fighting drugs. The genetically modified chickens have a relatively high ability to produce transgenic offspring, hence making it commercially viable.

However, there are many ethical issues related with genetically modified animals and their products, which needs to be resolved.

By David Zhang
41765179

Bibliography:
- Primary source: http://www.pnas.org/cgi/reprint/104/6/1771?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=helen+sang&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

- Secondary source:
http://news.bbc.co.uk/2/6261427.stm

Somatic Cell Nuclear Transferring the Technology of Today

Somatic Cell Nuclear Transferring the Technology of Today
Written by: Sophie-Anne Starr

Somatic cell nuclear transfer (SCNT) is quite capable in becoming a very dominant mechanism in genetic management of precious individuals, breeds and species. SCNT has been given a potentially profitable industrial opening in companion animals, which is very distinct from the pharmaceutical and food trade. The role that companion animals play in the emotional lives of humans has allowed SCNT to be used in pet reformation.

In previous studies performed, dogs have been cloned but they have been limited to young large breed dogs. These studies raised the question of: could an aged small breed dog be cloned. So the latest study performed was the cloning of an aged (14years) small breed dog (toy poodle) using a large breed oocyte donor and recipient. The large breeds were used due to the fact that small breeds make it difficult to surgically implant the reconstructed oocyte in their small oviduct. The cloned and somatic cell donor dogs had identical phenotype and genotype, although the mitochondrial DNA was inherited from the oocyte donor dog. In the cloned and donor dog the telomere length did not differ significantly, there are two explanation of why this may have occurred. The cloned offspring did not inherit that telomere lengths from donor dog, they may have been inherited from the oocyte donor dog and could be related to different breeds having specific telomere lengths.

When investigated further somatic cell nuclear transferring could become very beneficially in many aspects of veterinary genetics. For example, increase production of certain animals that carrying desirable or valuable traits, increase endangered species populations, preserve genetic material of animals that have decreased prematurely and the list continues.

Primary Resource:

Jang, G, Hong, S, Oh, H, Kim, M, Park, J, Kim, H, Kim, D, Lee, B 2008, “A cloned toy poodle produced from somatic cells derived from an aged female dog,” Theriogenology, vol. 69, no. 5, pp. 556-563.

Secondary Resource:

Mastromonaco, G & King, W 2007, “Cloning in companion animal, non-domestic and endangered species: can the technology become a practical reality?,” Reproduction, Fertility and Development, vol. 19, no.6, pp. 748-761.

Fido' s Osteoarthritis Vs A Clump of Cells

Stem cells have been the issue surrounding much veterinary research for over 10 years. The latest in investigations is the development of stem cell therapeutics designed to relieve symptoms associated with joint and muscle injuries in canines and other domestic animals. Mesenchymal stem cells (MSCs) are highly adaptable form of somatic cells found in a variety of connective tissues. The most common areas of study are the bone marrow (BM-MSCs) and adipose (AD-MSCs) tissues as possible sources. AD-MSCs have been studied and as of 2003, have been used as a surgical means of treating osteoarthritis, joint and tendon/ ligament injuries. During this treatment, cells are removed from adipose tissue and undergo a series of mincing, washing, collagenase digestion, and centrifugation. The end-product becomes a stromal vascular fraction (SVF) capsule, which is surgically placed near the injury site. Due to their plasticity, these MSCs are able to differentiate into chondrocytes to secrete collagen, glycosaminoglycans, and hyaluronic acid which are all promoters of cartridge formation. This form of treatment has in the past, high success rates and many incurable cases by any other forms of therapy have made full recoveries.

Another area of research is focused on BM-MSCs and their potential in veterinary science. Studies have found that not only do these stem cells differentiate into cartridge, bone and muscle, but may also contribute to neural tissue. Although much study remains ahead, veterinary scientists are focusing on future treatment s for neural, muscular, and osteo-related deficiencies and diseases.

Therefore in terms of canine stem cell research, the world is their oyster.

Primary Source:

• Black, L.L., Gaynor, D., Adams, C., Aron, D., Harman, S., Gingerich, D.A., Harman, R. J. 2007 "Effect of adipose-derived mesenchymal stem and regenerative cells on lameness in dogs with chronic osteoarthritis of the coxofemoral joints: A randomised, double-blinded, multicellular, control trial", Veterinary Therapeutics, Vol: 8, No: 4, Pp: Non specified. http://www.vet-stem.com/, viewed: 28.05.2008.
  
• Secondary Sources:
  
• Barry, F.P., Murphy, J.M. 2004 "Mesenchymal stem cells : Clinical applications and biological characterisation", The International Journal of Biochemistry and Cell Biology, Vol:36, No: 4, Pp: 568-584.


• Bianco, P., Riminucci, M., Grothos, S., Robey, P.G. 2001 "Bone marrow stromal stem cells: Nature, biology and potential applications", Stem Cells, Vol: 19, Pp: 180-192.

Links:

• http://www.en.wikipedia.org/wiki/Mesenchymal_stem_cell-38k-, Viewed: 30.05.2008.


• http://www.en.wikipedia.org/wiki/Adipose_tissue-48k, Viewed: 30.05.2008.

Image:

• Animal and Nature, 2008 "Dog Arthritis", Squidoo, Viewed: 30.05.2008, http://www.squidoo.com/

Why did the chicken cross the road? To get to the other SIGHT!

Although crossing the road is the last thing blind chickens should be doing, scientists at the University of Abertay in Dundee have identified the genetic mutation causing blindness and predisposition to embryonic death in chickens. Retinopathy globe enlarged (RGE) is an inherited condition causing blindness in chickens six to eight weeks after hatching. Biotechnologist Dr Doug Lester and PhD student Hemanth Tummala working with colleagues from Leeds University and Ediburgh’s Roslin Institute have identified mutation of the gene GNB3 to be the cause of RGE. The mutation deletes an essential amino acid, disrupting GNB3’s role in normal eye development. This finding has implications not just for poultry road-safety, but rather is anticipated to assist understanding of a wide range of human disorders including blindness, heart disease, diabetes and even infant mortality.

“Interestingly the human GNB3 gene has not been previously implicated in retinal dystrophy, however a much milder human mutation has been shown to reduce the level of the GNB3 protein by 50% in many tissues of the body and this has been associated with low birth weight, obesity, hypertension, coronary heart disease, type II diabetes and depression,” Dr Lester said. Such finding are expected to play a significant role in discovering the pathogenesis of such diseases, developing gene therapy processes and even restoring sight to sufferers of the inherited human eye disorder cone-rod dystrophy.

Restoring sight to the blind? Now that’s not something to be overlooked.


Primary Resource:

Tummala, H., Ali, M., Getty, P., Hocking, P.M., Burt, D.W., Inglehearn, C.F, Lester, D.H., 2006. Mutation in the Guanine Nucleotide–Binding Protein ß-3 Causes Retinal Degeneration and Embryonic Mortality in Chickens. Investigative Opthamology and Visual Science, 47, 4714-4718.
http://www.iovs.org/cgi/content/full/47/11/4714

Secondary Resources:

Medical News Today, 2006. Chicken Blindness Gene Could Hold Key To Many Human Diseases.
http://www.medicalnewstoday.com/articles/59198.php. Accessed 23 May 2008.

BBC News, 2006. Chicken gene ‘clue to conditions’. http://news.bbc.co.uk/1/hi/scotland/tayside_and_central/6216774.stm. Accessed 23 May 2008.

Saving your pooch with stem cell research

One might ask what is a stem cell. It is an undistinguished cell that divides constantly during the life of the animal and it can create cells that may multiply and can change to specific cell types (Evans et. al 2005).
So say for example a dog has either hip dysplasia (where the ball and socket joint don’t have a snug fit), arthritis, a damaged ligament, a damaged tendon, a fracture or a damaged organ and in order to extend their life the owner is considering hip/joint replacement etc., there is now a another option which is treating the dog with it’s own stem cells to rejuvenate the area and encourage growth (Imber & Rooney 2008).
It works as follows; the stem cells of the dog are collected from the fat cells anywhere on the dog’s body. The stem cells are sent to the lab and then separated and sent back to the veterinary surgery. They are then injected into the affected/painful area in a higher concentration than the dog’s body can achieve. In most cases it reduces pain and makes the dog more comfortable for up to one year.
Stem cells “provide growth factors and chemicals that help the injury heal” and decrease inflammation and prevent scar tissue from forming (Mott 2008).
Nowadays stem cell research is more advanced in animals than humans, perhaps because there is less red tape.

Primary References:
1. Bauer, T.R., Burkholder, T.H., Dunbar, C.E., Ferguson, C., Gu, Y., Hai, M., Hickstein, D.D., Sokolic, R.A., Tuschong, L.M., 2006, Correction of the disease phenotype in canine leukocyte adhesion deficiency using ex vivo hematopoietic stem cell gene therapy, Blood, Vol. 108, pp. 3313-3320

Secondary References:
1. Evans, B, Ladiges, P, Knox, B and Saint, R 2005, Biology: An Australian Focus, McGraw-Hill Australia Pty Limited, 3rd Ed, p 1156
2. Imber, P and Rooney, B 2008, A Dog’s Stem Cell Life, http://www.abcnews.go.com/health/story?id=4109559, Viewed 18/05/08
3. Mott, M 2008, Dogs Get Pricey Stem Cell Therapy, http://www.livescience.com/animals/080123-dog-stemcell.html
Viewed 18/05/08
4. Dunn, S 2007, Police dog back on its paws after stem cell treatment, http://www.katu.com/news/local/10203981.html Viewed 21/05/08

Flipping out: why research is stressing out dolphins

http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-294X.2008.03784.x

Researchers have been telling us for the past decade how human activities such as tuna fishing and dolphin-watching tours put stress on wild dolphins; stress they can ill afford with the existing pressure of our chemical contaminated oceans. Now a new study by researchers from the Marine Genomics Group has identified a new stressor – researchers themselves.

Blood samples from wild bottlenose dolphins (Tursiops truncatus) in a capture-release health survey were subjected to transcriptomic analysis. Transcriptomics involves studying gene expression by examining the RNA or transcripts (messenger molecules which code for proteins) in cells. The number and type of transcripts change over time in response to stimuli. In the bottlenose dolphins it was found that levels of some transcripts significantly increased (they were up-regulated) following veterinary examination, indicating greater stress on the animals than expected.

Genes involved with energy generation and immune function were up-regulated, particularly those concerned with infection response and inflammation. One of these was IL-8, a gene which codes for a chemokine involved in the migration of cells to the site of inflammation. If produced in excess it can lead to the damage of healthy tissue. The up-regulation of these genes corresponds with an acute-phase response, a defense system seen during acute illness or trauma.

So in examining wild dolphins to further conservation efforts, researchers are actually having a negative impact on dolphins’ health and well-being. Maybe this time it’s Flipper who needs rescuing.

By Belinda Cosgrove
41410228

Primary Source - A. Mancia, G. W. Warr, R. W. Chapman (2008) A transcriptomic analysis of the stress induced by capture-release health assessment studies in wild dolphins (Tursiops truncatus), Molecular Ecology 17 (11).

Secondary sources
- http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/acutephase.html
- http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/cytokines_in.html

Getting a Little Too Close and Cuddly

Since European settlement, the population of koalas in southern Australia has been affected by many relocations and population crashes which, has created a history where several populations have been founded by very few animals. This has not caused the koala in these areas to become endangered, but has resulted in a significant reduction in their genetic variability. In Queensland, where the koala populations have not been as greatly affected by humans, there is a much higher variability in their genetics.

Decline of genetic variability can lead to temporary reduction in fitness in the areas such as survival, reproduction, growth rates and the ability to adapt to long-term environmental changes. Inbreeding in koalas from isolated, fragmented populations has shown to cause physical abnormalities. Also, a correlation has been found between increased inbreeding and a rising number of juvenile mortalities.

Studies have been undertaken observing the mitochondrial DNA in koala populations. In a study, 18 different haplotypes were found within selection of certain koala populations but with only one or two haplotypes per population. The nucleotide diversity of koalas was shown to be up to eight times lower when compared to other marsupials.

A significant part conservation plans for the koala should be focused on their genetic management. The koalas today are the sole member of their family and if their genetic variability is allowed to reduce further, this may result in much more adverse consequences in the future.

Written by: Jade Weatherley

Primary Resources
1. Sherwin, W.B., Timms, P., Wilcken, J., Houlden, B., 2000. Analysis and Conservation Implications of Koala Genetics.
http://www.jstor.org/sici?sici=0888-8892(200006)14%3A3%3C639%3AAACIOK%3E2.0.CO%3B2-1

2. Houlden, B.A., Costello, B.H., Sharkey, D., Fowler, E.V., Melzer, A., Ellis, W., Carrick, F., Baverstock, P.R., Elphinstone, M.S., 1999. Phylogeographic differentiation in the mitochondrial control region in the koala, Phascolarctos cinereus (Goldfuss 1817). Molecular Ecology 8. 999-1011.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-294x.1999.00656.x

Secondary Resources
3. Taylor, A.C., Graves, J.M., Murray, N.D., O’Brien, S.J., Sherwin, B., 1996. Conservation genetics of the koala (Phascolarctos cinereus): low mitochondrial DNA variation amongst southern Australian populations. Genetical Research 69. 25-30.
http://www.ncbi.nlm.nih.gov/pubmed/9164173

4. http://en.wikipedia.org/wiki/Mitochondrial_DNA

5. http://en.wikipedia.org/wiki/Haplotype

6. https://www.savethekoala.com/islandkoalas.html

7. http://www.answers.com/topic/koala

Fighting Mastitis.........An Udder Success

Mastitis is a disease of the mammary gland caused by pathogens that find their way into the lumen of the gland through the teat canal. Mastitis is a very efficient disease as it is able to transfer from cow to cow. As antibiotics are only effective in 15% of mastitis cases, scientists have had to develop a new method of fighting this disease. A solution to this antibiotic resistance includes, transgenic cows that produce milk containing an antimicrobial protein called lysostaphin. 30% of all mastitis cases are caused by Staphylococcus aureus.
As milk is used for human consumption and many products are made from it, ongoing research has had to be taken into account. Overall lysostaphin in milk does not appear to be a major concern to human or cow’s health, but is a sensitive issue.

Researchers have found that approximately 71% of cows that were non-transgenic became infected by Staphylococcus aureus, whereas only 14% of transgenic cows became infected. From this research it would soon become relevant to use transgenic cows as they would save money, time and resources. This genetic breakthrough will have a major benefit on the dairy industry, not only on a national scale but on a global scale.

Primary Resource:
Wall, R.J., Powell, A.M., Paape, M.J., Kerr, D.E., Bannerman, D.D., Pursel, V.G., Wells, K.D., Talbot, N. and Hawk, H.W., 2005. ‘Genetically enhanced cows resist intramammary Staphylococcus aureus infection’, Nature Biotechnology 23, pg 445-451.
http://www.nature.com.ezproxy.library.uq.edu.au/nbt/journal/v23/n4/full/nbt1078.html

Donovan, D.M., Kerr, D.E., Wall, R.J., 2005. ‘Engineering disease resistant cattle’, Department of Animal Science, University of Vermont, Burlington

http://www.springerlink.com/content/u1m28j7732815g68/fulltext.pdf
Bliss R.M., 2005. Transgenic Cows Resist Mastitis-Causing Bacteria, U.S. Department of Agriculture.
http://www.ars.usda.gov/IS/pr/2005/050404.htm
Rainard, P., 2005. Transgenic cows expressing an antibacterial endopeptidase in their mammary glands show enhanced resistance to mastitis, Nature Biotechnology 23, pg 430- 432
http://www.nature.com.ezproxy.library.uq.edu.au/nbt/journal/v23/n4/full/nbt0405-430.html
Written by: Callan Cribb

Time to Cluck Bye to Salmonella

Concern for use of antibiotics in animal production soars sky high and once again, scientists are scratching their heads and trying to develop new ways for combating the never ending battle between human & animal health and the air-borne pathogen, salmonella.

The trend against antibiotics is steering scientists down a new and exciting path; a path that has opened new doors for chicken selection producers. This may mean that salmonella will no longer pose such a prominent threat in our food chain and production systems.

The detection of salmonella in chickens is both costly and difficult. Along with being an extreme health hazard, the eradication of salmonella is of a very high priority. The push for breeding of salmonella-resistant chickens is of great importance and many studies are currently underway with the aim of pin-pointing either traits on specific chromosomes or potentially gene expression involved in resistance.

In one particular study, chicken progeny where examined from an inbred population of one line of chickens. It is suggested that the substitution of a nucleotide in the DNA resulted in an amino acid change. This discovery is considered evidence of the fact that chickens inherit the complex trait which inhibits the infection of Salmonella tryhimurium.

Selection for salmonella-resistant chickens will not only increase the health of production populations, but will also reduce the potential entry of disease-causing bacteria in our food chain and production systems. However scientists are still making new discoveries and it will only be a matter of time before we will be able to cluck bye to salmonella.

Written by 41777574

References:Iowa State University Animal Industry Report 2005, Genes for Resistance to Salmonella in Poultry, viewed 27 June 2008, http://www.ans.iastate.edu/report/air/2005pdf/2017.pdf.

INRA press service 2005, Breeding of salmonella-resistant chickens, viewed 27 June 2008, http://www.international.inra.fr/press/salmonella_resistant_chickens.

Genome Research 1997, ‘Resistance to Salmonellosis in the Chicken Is Linked to NRAMP1 and TNC’, Genome Reserch, Cold Spring Harbor Labratory Press, vol. 7, pp. 693-704

Man’s Best Friend Close to our heart.

Can man’s best friend lead the way in cardiac research.

Researchers at the Cardiovascular Research Institute at the NY College of Medicine have shown that dogs injected with stem cells can heal their hearts after the block of one of the arteries that transports blood to the heart. If arteries supplying the heart are blocked they cause a lack of oxygen to the heart muscles and this leads to the tissue damage and death this tissue, this is also known as a myocardial infarct and is one of the leading causes of heart disease.

Using canine stem cells, more specifically cardiac stem cell this study has shown that repair of the damage caused by a myocardial infarct is reversible. By occluding the left coronary artery to induce tissue damage (which seems “slightly” un-ethical) and then injecting cardiac stem cells adjacent to myocardial infarct, the study observed marked improvement of function and repair of the damaged tissue. These stem cells were selected on specific markers that are found in stem cells, after selection these stem cells were grown and then injected.

This is an exciting area of research that can bring about great amounts of insight not only into stem cells but also into the treatment myocardial infarcts after they have occurred.

Primary Source
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1157041&blobtype=pdf

Swab a Scotty

Humans and various dog breeds are victims of von Willebrand’s disease (vWD), which is a hereditary bleeding disorder. The disease is caused by a defect of the clotting factor von Willebrand factor (vWF) and is characterised by serious bleeding episodes that are often fatal. There are three types of vWD, type three is the most severe form, described by the complete absence of vWF in the blood of homozygous affected individuals, and in reduced amounts in heterozygotes. Scottish terrier’s are primarily affected by this type of the disease with the prevalence estimation among the species being 18% to 30%. This type of Von Willebrand’s disease is an autosomal recessive trait and because of genetic investigations can now become a disease of the past for Scottish terrier breeders, with the development of a DNA test to detect both homozygous affected dogs and heterozygous carriers that requires a simple swab of cheek cells. Type three vWD in Scottish terriers is remarkably similar to the type three in human vWD sufferers which plays a key role in this veterinary advancement.

To develop the test, infected vWD tissue was obtained and through polymerase chain reaction (PCR), using primers sequenced from human genes, the complete amino acid sequence of that deoxyribonucleic acid (DNA) was derived. Amplification identified the single base deletion responsible for vWD in the Scottish terrier. Researchers used this concise identification to create a mutation based DNA laboratory test. Apart from the direct benefits to dog breeders, this development is one of significance, as it incorporates human genomics into veterinary treatment.


Key References:

Venta, P.J., Li, J., Yuzbasiyan-Gurkan, V., Brewer, G.J., Schall, W.D., 2000. Mutation causing von Willebrand’s disease in Scottish terriers. Veterinary Internal Medicine Journal 14, 10.

Patterson, D.F., 2000. Companion animal medicine in the age of medical genetics. Veterinary Internal Medicine Journal 14, 1.

Elizabeth Hoffman

Forget about the apple, an egg a day may keep the doctor away!!

There is a brighter future ahead when it comes to cancer treatment and it could be as simple as eating an egg. Researchers at the Roslin Institute in the United Kingdom, you might remember it as the birthplace of Dolly the sheep, have genetically engineered chickens to lay eggs that contain proteins that fight cancer in the egg whites. A number of companies have spent millions of dollars developing the proteins that target and eliminate tumour cells. Bacteria and even goats and rabbits have been used in the attempt to mass produce these therapeutic proteins with little success.
Chickens could be the answer, with their high reproductive rates and egg laying capabilities. The reliability of the chickens producing the anti-cancer proteins has been a difficult obstacle. This problem was overcome by injecting viruses into the embryo through tiny holes in the eggshell. The virus contained genetic sequences which coded for either the protein miR24 which is a cancer-fighting antibody or an antiviral protein human interferon beta-1a. These are used to fight malignant melanoma and multiple sclerosis.
Chicks produced in this way pass on these genes to the next generation after reaching adulthood. The proteins were found in the eggs that were laid by the females. Anticancer antibodies if produced throughout the body can be harmful to the chicken, but the gene expression has been limited to the oviduct at the site of egg white production.
Don’t start cracking eggs just yet. Although the therapeutic protein can be extracted in commercially viable amounts, testing on human effectiveness is still the next step, and eating an anticancer egg could be many years away.

Primary References:
Lillico, S.G., Sherman. A., McGrew, M.J., Robertson, C.D., et al. (2007). Oviduct-specific expression of two therapeutic proteins in transgenic hens. Proceedings of the National Academy of Sciences USA 104, 1771-1776.
Wayman, E (2007). Barnyard Pharmaceuticals. Science NOW Daily News 6 January. http://sciencenow.sciencemag.org/cgi/content/full/2007/116/4

Secondary References:
Lewcock, A (2007). Protein production in chicken eggs cracked. http://www.in-pharmatechnologist.com/news/ng.asp?id=73404-viragen-oxford-biomedica-roslin-institute-protein-transgenic

Would you like diabetes with that dog today?

http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1748-5827.2007.00398.x

An estimated one out of 500 dogs are diagnosed with canine diabetes, a condition caused by a deficiency in insulin. Certain breeds of ‘man’s best friend’, like the Labrador and Beagle, have a greater risk of developing this condition whilst some breeds, such as the German shepherd, have a naturally lower risk of inheriting the disease. Why is this?

Genetics is now explaining why such a separation exists by applying knowledge from human genetics. Canine diabetes is best illustrated as the equivalent of type 1 diabetes in humans. This association allows for a basis for genetic research to further understand the reasons for different susceptibility levels amongst the breeds of dogs in regard to diabetes mellitus.

Genes looked at in humans to determine susceptibility (major histocompatibility complex genes, MHC ) have an equivalent in canines (dog leucocyte antigen genes, DLA). Diabetic dogs and breeds within the diabetes-susceptible category have a strong association with a common haplotype (group of alleles of linked genes) of these genes. Another haplotype has a presence significantly reduced in diabetic dogs compared to non-diabetic dogs which suggests a protective characteristic.

Selective breeding in dogs has lead to a restricted DLA gene pool in many breeds which accounts for the strong distinction between diabetes-susceptible breeds and diabetes-resistant breeds and this predisposed nature should be acknowledged by veterinarians and owners alike.

Primary Reference
Catchpole, B., Kennedy, L.J., Davison, L.J. and Ollier, E.R. 2008.

Canine diabetes mellitus: from phenotype to genotype. Journal of Small Animal Practice. 49, 4-10.

Secondary references

Basic information of canine diabetes mellitus:
Canine Diabetes n.d., Intervet Schering-Plough Animal Health, viewed 23 May 2008, <

http://www.cat-dog-diabetes.com/dogs-diabetes-mellitus.asp

>

Definitions and explanations:

Type 1 Diabetes:
Type 1 Diabetes 2006, International Diabetes Institute, viewed 26 May 2008, <http://www.diabetes.com.au/diabetes.php?regionID=236>

Major Histocompatibility Complex:
Histocompatibility 2008, Medical Microbiology, viewed 26 May 2008, <http://www.cehs.siu.edu/fix/medmicro/mhc.htm>

Haplotype:
Haplotype 2008, Wikipedia, viewed 23 May 2008, <http://en.wikipedia.org/wiki/Haplotype>

Student ID: 41753233

Bite me: Let’s save the dogs!

Currently, 130000 dogs are euthanized in Australia as a result of abandonment in animal shelters (2). Two paramount factors which are of importance are aggression and mass production of litters. Genetics can make a difference to these atrocious statistics.
Lindblad-Toh, K, et al. (2005), have covered nearly 99% of the dog genome. They sampled 10 different dog breeds as well as other canine species resulting in the discovery of 2.5 million individual genetic differences among these breeds. These differences, single nucleotide polymorphisms (SNPs) are utilized in determining ‘signposts’ that can be used to locate the genetic contributions to physical and behavioral traits as well as disease (1).
Additionally the discovery of selective breeding carrying large genomic regions of several million bases of DNA into breeds, called ‘haplotype blocks’, making it much easier to find the genes responsible for behavior (also disease and body size).
SNPs and large genomic regions will help in identifying aggressive and large litter size genomes. Once the genomes are isolated then the genes from that particular genome can be identified and also the protein associated with that gene. This opens multiple avenues of stopping that particular trait from continuing. Additionally, the genes for non aggressive and small litter size must be dominant (3) and a coat colour marker should be used. Once it is, then these genes should be included into the genetic pool so it can be passed to the next generation. Hopefully in time dog abandonment, over population and aggression can be stopped.

References:
Primary:
1. Lindblad-Toh, K, et al. (2005). Genome sequence, comparative analysis and haplotype structure of the domestic dog. Nature 438, 803-819.

Secondary:
2. www.saynotoanimalsinpetshops.com/faq.html
3. www.bowlingsite.mcf.com/GENETICS/colorGen.html
Useful website:
4. www.workingdogs.com/genetics.htm

BY: Candice McKeone- Taylor. 40096559