Major recent advances in canine genetics, genomics and comparative medicine has resulted in an increased knowledge of canine cardiac disease and treatment. Much of which may prove advantageous in the treatment of human cardiac disease.
Many common congenital and adult onset cardiovascular diseases in the dog are familial, including myxomatous valve disease in the Cavalier King Charles Spaniel and dilated cardiomyopathy in the Doberman Pinscher, Great Dane and Portuguese Water Dog. Additionally, many disease loci have been mapped, which allows for efficient scanning, evaluation and subsequent breeding decisions (Parker et al.).
In one study (Linke et al.), results indicate, that the dog heart contains a stem cell component and that these canine CSCs (cardiac stem cells) are self-renewing, clonogenic and multipotent.
The study also indicates that these resident CSCs-ECCs (cardiac stem cells – early committed cells) can be activated by GFs (growth factors) after infarction to enter the damaged tissue and promote the formation of new myocardium.
The differentiation of these primitive cells (the CSCs-ECCs) into myocytes and coronary vessels repairs the damaged heart by, restoring local wall motion, improving ventricular hemodynamics, and positively interfering with pathologic ventricular remodeling. Hence potentially extremely useful in the treatment of cardiac disease.
These exciting advances in knowledge coupled with the availability of a dense canine genome map signal not only a possible radical change in canine cardiac disease treatment but also possible significant leaps in the understanding and treatment of human cardiac disease.
References
1.Linke A., Mu¨ller P., Nurzynska D., Casarsa C., Torella D., Nascimbene A., Castaldo C., Cascapera S., Bo¨hm M., Quaini M., Urbanek K., Leri A., Hintze T. H., Kajstura J. and Anversa P.
Stem cells in the dog heart are self-renewing,clonogenic, and multipotent and regenerate infarcted myocardium, improving cardiac function.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1157041&blobtype=pdf
2. Grigoropoulos F. N. (a) and Mathur A. (b)
Stem cells in cardiac repair.
(a)Cardiac Research Department, The London Chest Hospital, Bonner Road, London, UK
(b)Department of Clinical Pharmacology, Barts and The London, Charterhouse Square, London, UK
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W7F-4J90W4J-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3470d9dbfec74c6a6d661caf9486434c
3. Parker G. H., Meurs M. K. and Ostrander A. E.
Finding cardiovascular disease genes in the dog.
http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science?_ob=ArticleURL&_udi=B7RN0-4M340NH-2&_user=331728&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000016898&_version=1&_urlVersion=0&_userid=331728&md5=77210f2fa2717681a5e282d33d0a40f9
Sunday, July 13, 2008
Friday, May 30, 2008
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.
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/
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
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.
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.
Thursday, May 29, 2008
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,
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>
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.
Seconday resources:
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