Friday, April 29, 2011

What Does Systolic And Diastolic Me

Adverse events are more frequent than

recently published in the journal Health Affairs, an article which demonstrated that adverse events are ten times more frequent than previous estimates.


In this study, researchers used a proprietary application called Global Trigger Tool , compared with commonly used systems of voluntary reporting of errors or coding systems used by records of patient records, and recognized methods recommended by the Agency for Healthcare Research and Quality in Health USA (AHRQ). This will focus in 3 hospitals in implementing security measures the patient, and showed that among the records of 795 patients, the methods recommended by the AHRQ identified 35 adverse events, while the Global Trigger Tool detected 354 events, which means that up to 90% of hospital adverse events are passed high.


Dr. David C. Classen, principal investigator of the study, said: "The more mistakes seek more they will come "

Tuesday, April 26, 2011

Woman Breastfeeding A Man



English democracy is a system in which the two dominant parties can outlaw parties at will, leaving the field clear for Franco or imputed political corruption.
PP government and agree to challenge all Bildu lists. In a case like this I wonder: Why are the judges?

Euskadi has a population of 2 million inhabitants, and as anti-terrorist services 50,000 people are "polluted." It is curious to observe how those accused of corruption are freely in elections, but those who advocate particular ideologies are set aside for "democracy."


50,000 citizens

unable to participate as candidates even though they have no conviction. The parties law is unjust, since independence political conviction but not ideologies like Franco, comes to cases as fanciful as this one, towns where nobody can occur, and DB is the only election bid.

Suppose that once the person J. was a member of an outlawed list A. Subsequent inclusion in another list B does not affect only him, but his status of "contaminated" automatically extends to all the list B, which is the person F. If C is a third list that person F is contaminated the whole list because it is a person against whom the only thing you can say is that agreed on a list with the person J.



The voice of the "contaminated

" It's simple. I, a decade ago, was financial controller at a table for Euskal Herritarrok. There was a crime, and my work was being control the voting and counting process was legitimate. It's been a lot of years and I can not attend the election. My only crime was serious and be in a table representing a legal political choice. The fact of getting into an application contaminate the rest. And not only that! You could be right now contaminated belong to a forum where I am. "




No more manipulated electoral processes throughout Europe and misleading than those made in Euskadi. Then those same people who manipulate elections describe themselves" true democrats " .





course if the English democracy!




Monday, April 25, 2011

Spam Error In Sending Mail Through Outlook

LAUTARO GÓMEZ RAMOS ... I met him ...

Lautaro Dr Ramos Gomez 1923 - 1996

The January 14, 1996 died in Santiago a great veterinarian, Dr. Lautaro Gómez Ramos, upright, kind, optimistic and supportive, who distinguished himself by his great spirit of public service that led him to assume major responsibilities for state agencies and the profession.

The news of his departure was unexpected, sudden and painful for all those who were his disciples and friends at the School of Veterinary and Animal Sciences, University of Chile, where he served as an academic for 30 years. Some talked to him two days before he died, when down the halls of our school and gave us his last word smiles and optimistic and hopeful in the future. On this occasion, visited the school and library in search of new information, as it did regularly, to feed the database of scientific information that had been created in the Society of Veterinary Medicine.

His career began in 1948 at the Dairy Cooperative of Santiago and later in the Milk Producers Association of O'Higgins. In 1958 he joined the Ministry of Agriculture, where he held several positions, culminating in his public career served as director of the Animal Health Division of the SAG and Head of National Control Plan of Foot in 1970.

His academic career began in 1959 at the University of Chile, a professor of the departments of Dairy and Animal Farm. He was also Professor of Animal Physiology and in his later years as a professor at the University of Inspection and Food Hygiene.

Generations of veterinarians who were his students attracted affection and respect.

The distinguished scientific publishing numerous works, also participating as an active member in scientific sociedads, becoming President of the Society of Veterinary Medicine, Chile, a position he held from 1993 until his death. His deep sense

guild and his love for the profession led him to turn his effort into the Veterinary Medical College of Chile, where he served as Director, Secretary General and President of the Order from 1980 to 1982.

The disappearance of Dr. Lautaro Gómez Ramos is a painful and irreparable loss to his distinguished family, to whom we extend our special sincesar condolences. For those permanecermos a while longer in this world, his life is an example of solidarity, fairness and humanity, qualities that make us think that God is with him (Techno Vet 2 (1), 1996).


I met him! Don

Lautaro was my professor in veterinary medicine U de Chile. Tatarita we called it the talk got caught a little by the quickness of his ideas. I played in my exam grade where I asked about the economy agopecuaria of Chiloé, knowing that he had been on the island a year before! I traveled with him to Buenos Aires and Montevideo. Ever traveled together around the center of Chile, reaching Calbuco.

I became more a friend of his in the Society of Veterinary Medicine. He was very active, optimistic, visionary and lover of his profession. Way back in the 90's I always visit when I was in school. I remember being told repeatedly his arguments with a Minister of Agriculture, of which he was very proud because the Apparently it had somehow turned the hand ... I also remember when there was a cabezaso on a shelf in my office, and apparently complained that it hurt a little ...

All I can say finally that I would have liked many of us, his friends and colleagues, we would have been something like him!

Thursday, April 21, 2011

Female Bmi Great Britain

Libya: the key to understanding the conflict

"With energy, water and enough credit for infrastructure development, a nation can be free the grip of foreign creditors. That may be the real threat of Libya: can show the world what is possible. "




ELLEN BROWN and Chair of the Public Advocate Banking Institute


OIL" OR CENTRAL BANKS?

Several authors have noted the curious fact that the Libyan rebels took time out of his rebellion in March to create its own central bank, that before they had a government. Robert Wenzel wrote in the Journal of Political Economy:


"I've never heard speak of a central bank created in a matter of weeks a popular uprising. This suggests that the rebels are more than a lot of poor people in rags and that there are some pretty sophisticated influences behind his movement. "
.

Alex Newman wrote in The New American:
"In a statement issued last week, the rebels reported the results of a meeting held on 19 March. Among other things, these so-called revolutionaries ragged announced the "appointment of Central Bank of Benghazi as the monetary authority responsible monetary policies in Libya and the appointment of a governor of the Central Bank of Libya, with temporary headquarters in Benghazi."
. Newman cited

the Senior Editor of CNBC John Carney, who asked
"Is this the first time a revolutionary group has created a central bank, while still in the midst of the struggle against the entrenched political power? certainly seems to indicate the extraordinarily powerful bankers have become central to our time. "
.

Another anomaly is the official justification for taking up arms against Libya. They are supposed violations of human rights, but the evidence is contradictory. According to an article published on the website of Fox News on February 28: United Nations
While working feverishly to condemn Libyan leader Muammar al-Gaddafi to crack down on demonstrators, Human Rights Council is about to adopt a report full of praise on performance on human rights in Libya.


This document praises Libya for improving educational opportunities for making human rights a "priority" and to improve its framework "constitutional." Several countries, including Iran, Venezuela, North Korea, Saudi Arabia and even Canada to Libya have given positive marks for the legal protection offered to its citizens - now rebel against the regime and face bloody reprisals.

Say what you say about personal crimes Gaddafi, the Libyan people seem to be thriving. A delegation of doctors from Russia, Ukraine and Belarus, wrote in an appeal to Russian President Dmitri Medvedev and Prime Minister Putin, who after having become familiar with life in Libya, in his opinion in a few nations people lived in the same comfort:
"They [the Libyans] are entitled to free treatment, and their hospitals are equipped with the best medical equipment. Education in Libya is free and capable young people have the opportunity to study abroad at government expense. On marriage, young couples receive 60.000 dinars (about 50.000 U.S. dollars) of financial aid. The state provides loans without interest, and apparently, no date. Due to government subsidies the price of cars is much lower than in Europe, that are affordable for everyone. Gasoline and bread cost a dime, and agriculture is not taxed. The Libyan people are calm and peaceful, not Lebanese, and is very religious. "

note that the international community has been misinformed about the struggle against the regime.
"Who would not like such a regime?"
.

Even if it's just propaganda, there is no denying at least a popular achievement Libya's government to pipe water to the desert by construction of the irrigation project's largest and most expensive in history , the GMMR of 33 billion U.S. dollars (Great Man-Made River). Even more than oil, water is crucial for life in Libya.
.

The GMMR provides 70 percent of the population with drinking water and irrigation, pumping from the Nubian aquifer system in southern coastal areas populated 4,000 miles north. The Libyan government has made at least some things right.



Another explanation for the assault on Libya is that it is "all about oil", but here theory is also problematic. As noted in the National Journal, the country produces only about 2 percent of world oil . Saudi Arabia alone has enough spare capacity to offset any loss of Libyan oil production if the market disappeared. And if it comes to oil, why the rush to create a new central bank?
.


Another provocative information circulating on the Net is an interview with "Democracy Now" Gen. Wesley Clark (R), 2007. In it, the general said that about 10 days after September 11, 2001, another general told him that he had taken the decision to attack Iraq. Clark was surprised and asked why. "I do not know" was the reply. "I guess they do not know what else to do!"
Later the same general said the plan was to attack to seven countries in five years: Iraq, Syria, Lebanon, Libya, Somalia, Sudan and Iran.


What do these seven countries have in common?
In the context of banking, one that stands out is that none of these countries is one of 56 members Bank for International Settlements - BIS (Bank of International Settlements - Internationaux Banque des Règlaments). That obviously puts beyond the reach of long arm of the central bank of central bankers in Switzerland.
. Most renegades

batch were Libya and Iraq, both of which have been attacked. Schortgen Kenneth Jr., writing on Examiner.com, said "six months before the U.S. to attack Iraq to topple Saddam Hussein, the country had begun to accept euros instead of dollars as payment for its oil, and that made him a threat to the global dominance of the dollar as reserve currency, and its dominance as the petrodollar . " According


Russian an article entitled "The bombing of Libya - Gaddafi's punishment for his attempt to reject the Dollar", Gaddafi tried the same thing: it began a movement to reject the dollar and the euro , and called on Arab and African nations use a new currency, the gold dinar. Gaddafi suggested the establishment of a united African continent, with 200 million people using the single currency. .
Last year, the idea was adopted by many Arab countries and most African countries. The only opponents were the Republic of South Africa and head of the League of Arab States. The initiative was viewed negatively by the U.S. and the European Union, French President Nicolas Sarkozy , calling Libya "a threat to the financial security of mankind" , but Gadhafi did not swayed and continued to push for the creation of a united Africa.

And that brings us back to the puzzle of the Central Bank of Libya. In an article published in the Market Oracle, Eric Encina observed:
"A fact rarely mentioned is that the Central Bank of Libya is 100% owned. Currently, the Libyan government creates its own money, the Libyan dinar, by means of its own central bank. Few can argue Libya is a sovereign country with its vast resources of their own, capable of sustaining their own economic destiny.
A major problem for the global banking cartels is that doing business with Libya must pass through the Central Bank of Libya and use their national currency, a place where they have absolutely zero control or power.
therefore, overthrow the Central Bank of Libya (CBL) may not appear in the speeches of Obama, Cameron and Sarkozy, but this is definitely the priority of the globalist agenda to absorb Libya into the hive of nations obedient. "
.

not only Libya has oil. According to the IMF, the central bank has about 144 tonnes of gold in their vaults. With such reservations, who needs to BPI (BSI), the IMF and its rules?
All of which leads to a closer look at the rules of the BPI and its effects on local economies. An article in the BIS website indicates that central banks are part of the Central Bank Governance Network * (1) should have sole or principal objective "to preserve price stability." They remain independent of governments to ensure that political considerations do not interfere with this mandate. "Price stability" means the maintenance of a stable money supply, even if it means creating more debt. Central banks are discouraged to increase the money supply by printing money and using it to benefit the State, either directly or as loans.
.

In a 2002 article in Asia Times, "The BIS versus National Banks", Henry Liu Jianchao stated:
"BIS legislation only serves the sole purpose of strengthening the international banking system, even at the risk of national economies. The BIS does to the national banking system that the IMF did to the national monetary regimes.
national economies under financial globalization no longer serve the national interest ... FDI [foreign direct investment] called foreign currency, mainly dollars, has been sentenced to many national economies to an unbalanced development for export, just to make interest payments in dollars, with little net benefit to national economies. "
He added: " according to the State Theory of Money, no government can fund its own national currency with all their development needs to maintain full employment without inflation."
This theory of state money refers to money created by governments rather than private banks.
.

The presumption of the rule prohibiting loans from the central bank itself del gobierno es que éstos son inflacionarios, mientras que los préstamos existentes en dinero de bancos extranjeros o del FMI no lo son. Pero en realidad todos los bancos, ya sean públicos o privados, crean en sus libros el dinero que prestan. La mayor parte del dinero nuevo hoy proviene de préstamos bancarios. Y tomar préstamos del propio banco central estatal tiene la ventaja de que el préstamo es sin intereses. Y está demostrado que la eliminación de intereses reduce el costo de los proyectos públicos en un promedio de 50% .
Y así parece ser cómo funciona el sistema libio. Según Wikipedia, las funciones del Banco Central de Libia son “la emisión y regulación de los billetes y Currency in Libya "and" the management and issuance of all government loans. " Libya's state bank issues the national currency and lends money for state purposes.
.

That would explain where Libya gets the money to provide free education and medical care and interest free loans of $ 50.000 for the newlyweds. Also explain the country where it got the $ 33 billion to build the Great Man Made River project. The Libyans are concerned that NATO bombing is perilously close to work, creating another threat of humanitarian disaster.
So is this new war for oil or by banks? Perhaps both - and water, too.

With energy, water and enough credit for infrastructure development, a nation can be free from the clutches of foreign creditors. That may be the real threat of Libya: can show the world what is possible.

Most countries have no oil, but new technologies could make oil-producing countries are not energy independent, especially if infrastructure costs are reduced to half of the bank loans of public property the nation. Energy independence would free governments the web of international bankers, and the need to move the production to foreign markets to pay debts.


If Gadhafi's government falls, it will be interesting to see if the new central bank joined the BIS, the national oil industry if it is sold to investors, and if education and health care are still free.
.
www.sinpermiso.info Translation: Antonio Zighelboim


Incorporated
The Matrix Project. EPM

NOTE:
* (1) Central Bank Governance Network: The group is chaired by Mr. Stanley Fischer (Bank of Israel). Its members are Mr. Stefan Ingves (Sveriges Riksbank), Mr Mervyn King (Bank of England), Mr Henrique Meirelles (Central Bank of Brazil), Mr. Duvvuri Subbarao (Reserve Bank of India), Mr. Axel Weber (Deutsche Bundesbank), Ms. Janet Yellen (Board of Governors of the Federal Reserve System), Ms. Zetia Akhtar Aziz (Bank Negara Malaysia) and Zhou Xiaochuan (People's Bank of China).

Melbourne Short Lease

Seroprevalence of feline leukemia virus present in populations of wild and captive CATS. Patricia Gutierrez Gallardo

Seroprevalence of feline leukemia virus present in populations of wild and captive felines. 2011

Patricia Gutierrez Gallardo


veterinarian Feline Leukemia Virus (FeLV) is one of the retrovirus of importance in domestic cats (Felis catus) was discovered in 1964 from a domestic cat that had lymphoma, although it is unclear origin, is described that is closely associated with species that are phylogenetically related to the domestic cat. There are two variants of this virus an exogenous, which is usually detected in infected domestic cats, and a variant endogenous, which is presented as provirus inserted in the cells of domestic cats. It is known that endogenous variant has an origin from ancestors of domestic cats which ate a mouse infected with murine leukemia virus, which was able to infect germ cells, and may well perpetuate the species to date. However, this presents no greater risk because they have not been associated pathological changes to their presence, but if there is infection with a variant exogenous recombination can be generated and eventually produce a more lethal disease. Within

related species is the domestic cat and the wildcat (Felis silvestris silvestris), which is the ancestor of the domestic cat. In a study in Scotland, this species has been detected a seroprevalence of 10% by direct ELISA in a population of 50 individuals during the years 1992 and 1997 (Daniels et al, 1999). Additionally in 1996 and 1997 in populations from France, Switzerland and Germany from a total sample of 51 individuals revealed a seroprevalence of 49% (Leutenegger et al, 1999). In turn, we used commercial kits for the detection of FeLV, where the 38 individuals captured in France, he obtained a seroprevalence of 27% (Fromont et al, 2000).

most recent data from a study of Ostrowski et al (2003), which captured 55 individuals of wild cat in Saudi Arabia between 1998 and 2000, where seroprevalence was 3%. Additionally we analyzed other gender-related species Felis in the same region, the sand cat (Felis margarita), which showed that the prevalence of FeLV was 8% of a total of 17 individuals captured.

Another species which has been investigated prevalence of FeLV is the Iberian lynx (Lynx pardinus) where the publication of Luaces et al (2008), sampled in the years 1993 to 2003 obtained 25 samples were analyzed by ELISA kit, which yielded no positive results yet The virus was detected by PCR in 6 of 21 samples, corresponding to 16.7%. One explanation may be that the virus generated in lynx not cross-react with standardized commercial kits for cats not being detected. Additionally, the source of infection may be due to the proximity of human settlement bobcat, and feral domestic cats (Felis catus) and European wild cat (Felis silvestris), which may even share the lynx territories and thus be the focus of infection transmission.
One of the cases recorded in captivity corresponds to a bobcat (Lynx rufus), which reached the Zoological Medicine Service at Colorado State University (USA), with clear nasal mucus FeLV, was confirmed by indirect immunofluorescence direct ELISA, unfortunately the animal did not survive. It was confirmed that the animal was removed after 48 hours of birth, his mother's side and was powered by a domestic cat, which transmitted the infection to a fatal outcome (Sleeman et al, 2001).

In Namibia, conservation foundation cheetah (Cheetah Conservation Fund - CCF) has analyzed over 100 samples for FeLV in cheetahs (Acinonyx jubatus) Namibia wild and no positive animals were detected. However, in one of the cheetahs brought by seizure, there was nasal mucus associated with FeLV, which was confirmed by ELISA, further positive cheetahs were 3, which had some contact with the first cheetah infected, these individuals include infected died of various situations related to infection with FeLV. This is the first confirmed case of FeLV associated with lymphoma in a domestic cat. It is assumed that the source of infection with FeLV exposure had been for a domestic cat cheetah in its previous location at CCF, these data indicate that FeLV is endemic in wildlife populations of cheetahs in Namibia, but the cheetahs are susceptible to infection with FeLV and its consequences (Marker et al, 2003). In a study by Munson et al. (2004), 81 cheetahs sampled between 1992 and 1998 population of Namibia, tested for FeLV antigen by ELISA, there were no antibodies or antigens for FeLV.

The puma (Puma concolor) in Florida are conducted routine testing for FeLV and FIV, in the case of FeLV have been negative since 1978 and 2002, however between 2002 and 2003 there was an outbreak with 28 positive individuals 143 samples for the 19.5%. We conducted a monitoring plan and vaccination against FeLV negative patients younger than 4 months old. With regard to the monitoring plan was established that the 28 individuals, 18 presented a regressive state, 5 were latent and 5 had persistent viremia, of which 2 died from sepsis, 2 and 1 by interspecific aggression by anemia / dehydration. The vaccination plan began in November 2003 to April 2007, where wild cougars FeLV negative 52 received at least one inoculation of these pumas only 26 received a "booster." During vaccination no adverse effects and most of the Cougars developed antibody response. After this outbreak, no positive animals was detected again and allowed to vaccinate, it is believed that infection was not able to replicate in individuals given the number of recessive disease in individuals and not generated latent virus nasal mucus. The source of infection in cougars is unknown, it is speculated that the source of infection was from domestic cats, as consumption of these other FeLV-infected cats may be an effective means of transmission, also found remains of domestic cats the stomachs of necropsied cougars in California and two Florida pumas (Cunningham et al, 2008). Additionally

studies have been conducted in lions (Panthera leo), between 1984 and 1991, 255 individuals were sampled residents of the Serengeti National Park in Tanzania, 51 from the Ngorongoro Crater and Lake Manyara 5 from the analysis by ELISA for p27 antigen of FeLV. The results indicate that the prevalence for FeLV was negative in all samples (Hofmann-Lehmann et al, 1996). In conclusion


infection with the Feline Leukemia Virus is rare in wild species, would only be linked to related species with the domestic cat, as in the case of the wild cat (Felis silvestris silvestris) and the sand cat (Felis margarita .) In other reported cases has been in contact with domestic cats as reported the bobcat, which was nursed by a mother cat, in the case of the cheetah can not be said that there was direct contact, but the possibility is present since it was seized from a human settlement, which probably existed or had pets the presence of feral cats. In the case of cougar has not been reported another outbreak, but is essential to continue monitoring populations and protect habitat for this species, preventing the establishment of urban areas close to populations of cougars. It is important to establish the infective status of the species and that through this we learn that pathogens can dramatically affect population size and take action respect, more so in the case of FeLV and wildlife that this disease has been fatal in all cases reported with persistent viremia. Bibliography



Cunningham M, Brown M, Shindle D, Terrell S, Hayes K, Ferree B, McBride R, Blankenship E, Jansen D, Cittinus S, Roelke M, Kiltie R, Troyer J and O'Brien S (2008 .) Epizootiology and management of feline leukemia virus in the Florida puma. Journal of wildlife disease 44 (3), 2008, pp.537-552.

Daniels M, Golder M, Jarrett O and MacDonald D (1999). Feline Viruses in Wildcats from Scotland. Journal of Wildlife Diseases, 35 (1), 1999, pp. 121-124

Fromont E, Sager A, Leger F, Bourguemestre F, Jouquelet E, Stahl R, Pontier D and Artois M (2000). Prevalence and pathogenicity of retroviruses in wildcats in France. Veterinary Record (2000). 146, pp.317-319

Hofmann-Lehmann R, Fehr D, Grob M, Elgizoli M, Packer C, Martenson J, O´Brien S and Lutz H (1996). Prevalence of antibodies to feline parvovirus, calicivirus, herpesvirus, coronavirus, and immunodeficiency virus and of feline leukemia virus antigen and the interrelationship of these viral infections in free-ranging lions in east Africa. Clinical and Diagnostic Laboratory immunology, sept. 1996. Vol. 3, N°5 p. 554-562

Leutenegger C, Hofmann-Lehmann R, Riols C, Liberek M, Worel G, Lups P, Fehr D, Hartmann M, Weilenmann P and Lutz H (1999). Viral infections in free-living populations of the European wildcat. Journal of wildlife disease, 35 (4), 1999, pp. 678-686

Luaces I, Doménech A, García-Montijano M, Collado V, Sánchez C, Tejerizo G, Galka M, Fernández P and Gómez-Lucía E (2008). Detection of Feline leukemia virus in the endangered Iberian lynx (Lynx pardinus). J Vet Diagn Invest 20:381–385 (2008).

Marker L, Munson L, Basson P and Quackenbush S (2003). Multicentric T-cell Lymphoma Associated with Feline Leukemia Virus infection in a Captive Namibian Cheetah (Acinonyx jubatus). Journal of Wildlife Diseases, 39(3), 2003, VOL. 39, NO. 3, pp. 690–695.

Munson L, Marker L, Dubovi E, Spencer J, Evermann J and O’Brien S (2004). Serosurvey of viral infections in free-ranging Namibian Cheetas. Journal of Wildlife Diseases, 40(1), 2004, pp. 23–31

Ostrowski S, Van Vuuren M, Lenair D and Durand A (2003). A serologic survey of wild felids from central west Saudi Arabia. Journal ofnwlidlife disease, 39(3), 2003, pp. 696-701

Sleeman J, Keane J, Johnson J, Brown R and VandeWoude S (2001). Feline Leukemia Virus in a Captive Bobcat. Journal of Wildlife Diseases, 37(1), 2001, VOL. 37, NO. 1, January 2001. pp. 194–200.

Tuesday, April 19, 2011

How Much Does A Chest Wax Cost?

Interview with Daniel Castro "Illusion"

Q: Hi, Daniel, how's the filming?

R: Hello, thank you very much for making me this interview Bloguionistas . I still much your site and for me is an honor to interview her. Filming is going well, a discontinuous rate as expected.

Q: Is it true that you are financing all with your own money?

A: Yes, indeed. I'm paying for, but unfortunately I can not afford to pay the team. I wish I could, but yes that boosts the costs and it would be impossible to finance. If profits for the movie, some would go to them, of course.

Q: Have you tried to get some kind of grant for this project? Have you inquired into some production?

A: Well, this issue is interesting. Yes, I presented an initial version of the script to aid in script writing. No luck in the ICAA, not in the Comunidad de Madrid and in Navarra. And that in some cases would have the backing of a producer more or less known. Being rejected aid to writing the script made me think that either would be easy to win grants for film production. I think that is partly because it is a script, and a project that does not fit exactly into the usual parameters of the film "eligible."

Q: What movie do you mean by "eligible"?

A: Well, I can speak from my experience, and just say that the more serious (in the sense of non-comic) is a project, how much social relevance has, the more expensive, ambitious and "conventional" is the production proposal, the easier it is to obtain a grant. If, however, that show is a cheap project, comic production "guerrilla" and without any social message, it is very difficult to get aid.

P: It is also possible that you have been denied such aid because the script was just bad.

A: Well, it's a possibility, yes.


Q: But do you think, right?

A: No, I think it is a project that falls outside of the grants schemes. So even tried to get aid to production.

Q: You could have tried, right? The "no" and you had ...

A: Introduce a subsidies is a subordinate effort and some time, waiting until they get concessions, submission to a delivery date and running, make contracts to all workers in a call ... I read, called the hiring of at least two meritorious from some autonomous region. We are working on my shooting four or five people. Really I have to recruit and bring me two young (to 40 percent more equipment) of a certain community in order to collect a grant? Might try to distort this, ask people to be enrolled in that community, distort the contracts with these young people but .... I do not want do such things. I want to make a movie not a master in creative accounting.

P: Well, it is clear but ... why not "crowdfunding? Those of " Cosmonaut" is they are riding very well.

A: Well, yes, "The Cosmonaut" have a complex project that requires more funding than mine. Also, from what I have worked in advertising and are very adept at creating events and merchandising for his movie ... in my case, I prefer not doing so much to this stage and, instead, focus on making the movie, that on script is relatively simple and better as soon as possible. I do not rule, much less resort to the specific phases crowdfunding for post-shoot: financing post-production, festivals, distribution, payment of copies ... That, I think that everyone who contributes to the production of this film should get something in return , after a certain amount, at least, a DVD copy and a kiss from the director in place of your body you choose.


Q: Did you ever see "Illusion" in theaters in Spain?

A: No, I think. In much of Spain there are no cinemas. Even there in a few provincial capitals. If you have no chance or see "Torrente 4", imagine what ours. If films produced by solvent companies can not be released, if large small film festivals are just as much as possible is "Illusion" will not be released in cinemas, at least not extensively. But make no mistake, there are very few small films that make money with their film premieres. What we are doing this movie know. But we also know is that we want to make a good movie. A movie of us proud. For now we are getting there. But much remains to be done.

Q: It's nice ... but impractical, "the film will stay in the can, on the hard disk or wherever?

A: No. The ship, without going to 35mm (ie, in digital format) to all distributors, all producers, all the festivals, all neighboring communities, all video platforms on the Internet, so that the movie can be bought and seen by everyone as possible.

Q: How much pasta you are leaving this?

A: I can let myself between fifteen and twenty thousand euros. I have nothing.

Q: Where do we get?

A: In a couple of accounts I have in different banks.

P: Yeah, but ... how it got there?

A: I have nearly fifteen years working as a scriptwriter, I have saved. I also sold a screenplay option last year.

Q: Do you get the money?

A: I hope so. But it is not easy. If not recovered, I will consider it well spent: a master's degree in management, production and interpretation would have paid more.

Q: That is another, you're the protagonist. Not a professional actor. Are not you afraid? Have you no shame?

A: Well ... sometimes I do gives a bit of fear and shame. Other times I think, why not? I wrote the role for a character I know who've played several times already, in short, in a movie. I will technically worse than a professional actor, but ... I know exactly what the director wants him, why the writer wrote that sentence as well ... and just because I save time explaining things to an actor, I think it may be worthwhile.


Q: Do you know that all this can be seen as a monument to your ego?

A: Yes, it is possible ... you mean the movie?

P: Sure. But ... also this interview.

R: Why?

P: Interview yourself is pretty crazy.

R: Ya. Maybe ... but hey, I think I did ... I remember Truman Capote also

Almodóvar ... P: Yeah, but they were already important people. Compared with them is pretty crazy too.

R: ...

Q: Some people in the asylum by less serious than this ...

R: What? Why it's autoentrevistarse?

P: Yes

R: So serious you see?

Q: I would say it is a pathological narcissism.

R: Well, you and I are the same, right? Why do you treat me so harshly? Huh? Why? Did not we agree that this was promoting? Why insist on boycotting, forever? Huh? Why am I doing this?

Monday, April 18, 2011

Bonefish Grill, Carmel

VIRAL DISEASES OF DOMESTIC ANIMALS. 2011. Patrick E. Berrios

ENFERMEDADES VIRALES DE LOS ANIMALES DOMÉSTICOS. SITUACIÓN EN CHILE. 2011
Berrios Patricio Etchegaray


304 pages Price: $ 12,500 plus shipping.
ISBN: 978-956-345-247-1
Intellectual Prop. Reg No. 202497


I. About the author:


Dr. Patricio Berrios is a senior veterinarian with great dedication to research and university teaching, activities in which over a lifetime of work has given vocation and a great generosity contribution to the formation of countless generations of veterinarians. He received his veterinary degree in Animal Science, Faculty of Veterinary Medicine, University of Chile in 1963. Subsequently, several studies had top-level professional development, emphasizing that allowed him to obtain the degrees of Master of Science and Dr. Of Philosophy (Ph.D.), University of California, Davis, study stays well in Venezuela, Switzerland and Spain.

Berrios Patricio Etchegaray has been a pioneer in the study of animal viruses in Chile. His research projects have focused mainly on the study of herpes virus in cattle, horses and goats; rotavirus in cattle, sheep, goats, horses and pigs, parainfluenza type 3 virus in cattle, sheep and horses, and equine influenza.

For 10 years he was director of the journal scientific "Advances in Veterinary Science, Faculty of Veterinary Medicine, University of Chile.

In 2007, the Veterinary Medical Association of Chile AG awarded the National Award for Scientific Activity, in recognition of his outstanding contribution in this field.


Dr. Berrios has participated as author or editor in the following books:

Veterinary Virology. 1983. Berrios P. and Celedon MO. Text 175 pages. Serimpres printing. 2 edition 1988. 3 rd edition 1990. 4 th edition 1993.

Veterinary Immunology. 1984. Editor and co-author. Text 184 pages. Serimpres printing. Registration N º 59675/24/4/1984.

Immunoprophylaxis in Veterinary Medicine. Main Vaccines used in pets. P. Berrios, J. López. Text 192 pages. Development Project 93 to 140. Department of Pathology and Preventive Medicine. Faculty of Veterinary Medicine. Universidad de Concepción. 1999.

Veterinary vaccinology. " Susan E. Elvira Mendoza, Patricio Etchegaray Berrios, Jose Abel Ciprian Carrasco and Eliseo Hernández Baumgarten. Text 256 pages. National Autonomous University of Mexico. Ciudad Universitaria, 04510, Mexico City Graduate School of Cuautitlan. Cuautitlán Izcalli, Estado de Mexico. 1 st December 2005 edition.

delivery Book now has 3 chapters: 1. Veterinary Virology, 2. Viral diseases, and 3. Viral zoonoses. It has 304 pages and has a value of $ 10,000. The direction of Dr. Berrios is: pbetch19@gmail.com


II. About the book: Foreword




This collection of class notes viral disease of domestic animals, do not pretend to be anything more than that. In fact correspond to my notes from classes conducted at the University of Chile, Universidad de Concepcion, Universidad Iberoamericana of Science and Technology, and Andrés Bello University, between 1977 and 2010. During 33 years of university teaching in veterinary medicine, the matters discussed have been gradually improved through consultations with various specialists and complemented by reading scientific papers related to the topics.

The issue of Virology, an introductory to the viral disease, focusing primarily a veterinary virology in which the various chapters tend to be a database of viral diseases that are generally taught in a course the following semester.

viral diseases for the main virus diseases of domestic animals, emphasizing their presentation in Chile endorsed by research carried out in universities and other state services. Each disease addresses the etiology, symptomatology, pathology, diagnosis, prevention and situation in the country. It delivers all the papers published by Chilean specialists in this area.

As viral zoonoses, as a supplement in addition to rabies and hantavirus presented Chile, added the most important zoonoses in the Americas described as indicated by the Pan American Health Organization.

With regard to bibliographic records have prioritized national benchmarks which must be covered in approximately 99%. I

comment my original idea was to write a book on microbiology and infectious diseases of importance in veterinary medicine. It was not possible. Even I would have liked to extend the theme infectious diseases specialist birds and fish that are not my specialty, but it was not possible.

would be very satisfactory if this little book contains teachings that would be useful to students of veterinary medicine and veterinary medical colleagues need to remember knowledge of this type. If so I would feel very gratified.

A second issue that I realize before I retire from the university classroom, I promise to substantially improve the content so that it is up to date infectious diseases specialist this issue continues to affect that. Like Pandora's box is open most likely have to address new issues, both in emerging viruses in the prevention and control through modern vaccines.

I can only thank the many students and colleagues who have made me reflect on the validity of some concepts that I have allowed to issue openly in teaching and in some cases several conferences and meetings. And they are subsequently discharged into each chapter.

My thanks to the veterinarians, Miguel Norambuena G. Bacteriological Institute of Chile, Ramón Rodríguez T., and V. Pinochet Lautaro University Chile and Delbert G. McKercher, University of California for introducing me to the viral infectious disease of domestic animals.

The context of these notes is based on my professional definition: I MédicoVeterinario graduated from the University of Chile, I am a virologist with a Ph.D. from the University of California, and I am a teacher educator simply by calling.





TABLE OF CONTENTS Part I. FOREWORD

PRINCIPLES OF VIROLOGY

1.

INTRODUCTION 1. 1. Historical
1. 2. Definition
virus 1. 3. Location of the virus in nature

2. THE VIRUS AS PHYSICAL ENTITIES

2. 1. Size
virus 2. 2. Viral morphology

3. CHEMICAL ENTITIES AS VIRUSES

3. 1. Chemical composition of the virus
3. 2. Viral inactivation
3. 3. Preservation of viral infectivity
3. 4.
viral purification
4. VIRUSES AS BIOLOGICAL ENTITIES

4. 1. Bases viral taxonomic classification
4. 1. 1. Viral classification
4. 2. Viral replication
4. 2. 1.
viral growth curve 4. 2. 2. Stages viral replication.
4. 2. 3. Examples of viral replication
4. 3. Antiviral chemotherapy
4. 3. 1. Antiviral drugs
4. 4. Cultivation of the virus
4. 4. 1. Multiplication of virus in laboratory animals
4. 4. 2. Multiplication of virus in eggs
4. 4. 3. Multiplication of virus in cell cultures
4. 5. Viral quantification
4. 5. 1. Quantitative measurement of viral infectivity
4. 5. 2. Quantal measurement of viral infectivity
4. 5. 3. Measurement of viral hemagglutinating capacity
4. 6. Viral genetic
4. 6. 1. Mutations
4. 6. 2. Genetic recombination between

virus 5. THE VIRUS AS ENTITIES IMMUNOGENIC

5. 1. Antiviral immunity
5. 2. Viral antigens
5. 3. Viral serological diagnosis
5. 4. Antiviral vaccines

6. THE VIRUS AS pathogenic entities

6. 1. Input, output and dissemination of the virus in the body
6. 2. Production mechanisms of viral disease
6. 2. 1. Acute
6. 2. 2. Persistent infection: latent, chronic and slow
6. 3. Viral oncogenesis

7. VIRAL DIAGNOSIS

7. 1. Diagnostic techniques
7. 2. Sampling.
diagnostic chain


Part II. VIRAL DISEASES OF DOMESTIC ANIMALS

1. INTRODUCTION TO THE INFECTOLOGY

1. 1. Infective General
1. 2. New viruses that affect humans and animals
1. 3. Situation in Chile. Past, present and future of major viral diseases
pets.
1. 4. Viruses such as infectious diseases specialist and epidemiological entities. Virus, host and a half
environment. Viral traffic. Emerging
1. 5. Infective Glossary
1. 6. Acronyms health-related agencies


2. VIRAL DISEASES OF HORSES

2. 1. Equine influenza
2. 2. Equine rhinopneumonitis
2. 3.
EVA 2. 4. Equine encephalitis
2. 5. Equine infectious anemia
2. 6. Equine rotavirus
2. 7.
equine rhinovirus 2. 8. Equine Reovirus
2. 9.
equine adenovirus 2. 10, Parainfluenza type 3
2. 11. Other equine viruses
2. 12. Health requirements for the importation of horses under a temporary regulation admission


3. VIRAL DISEASES OF CATTLE

3. 1. FMD
3. 2. IBR
3. 3. Parainfluenza Type 3
3. 4. Bovine viral diarrhea / mucosal disease
3. 5. Enzootic bovine enzooótica
3. 6. Other viral diseases of cattle
3. 7. Bovine viral abortion
3. 8. Some vaccines used in cattle in Chile


4. VIRAL DISEASES OF SHEEP AND GOATS

4. 1. Slow Virus
4. 2. Rotavirus and coronavirus sheep
4. 3. Parainfluenza type 3 in sheep
4. 4. Bluetongue
4. 5. Contagious ecthyma
4. 6. Other viral diseases of sheep and goats


5. VIRAL DISEASES OF SWINE

5. 1. Porcine circovirus
5. 2. Porcine reproductive and respiratory syndrome
5. 3. Parvovirus
5. 4. CSF
5. 5. Swine encephalomyocarditis
5. 6. Aujeszky's disease or pseudorabies
5. 7. TGE
5. 8. Porcine enteroviruses
5. 9. Porcine rotavirus
5. 10. Other viral diseases of pigs
5. 11. Swine Influenza
5. 12. Porcine viral abortion


6. VIRAL DISEASES OF DOGS

6. 1. Canine Distemper
6. 2. Canine parvovirus
6. 3. Canine infectious tracheobronchitis
6. 4. Canine Infectious Hepatitis
6. 5. Canine Coronavirus
6. 6. Canine oral papillomatosis
6. 7. Canine Influenza
6. 8.
canine rabies
7. VIRAL DISEASES OF

cats 7. 1. Feline panleukopenia
7. 2. Feline rhinotracheitis
7. 3. Feline Calicivirus
7. 4. Feline Leukemia
7. 5. Immunodeficiency syndrome in cats
7. 6. Rabies in cats
7. 7. Feline infectious peritonitis
7. 8. H1 N1 virus in cats

8. OTHER VIRAL DISEASES

8. 1. Avian influenza in Chile
8. 2. Rabbit Myxomatosis
8. 2. 1. Rabbit control using the myxomatosis virus
8. 3. Emerging Viral Diseases
8. 4. Brain transmissible spongiform
8. 4. 1. Prions
8. 4. 2. BSE or mad cow disease.


Part III.
viral zoonoses
1. Viral zoonoses in Latin
1. 1. Dengue
1. 2. West Nile fever
1. 3. American hemorrhagic fevers
1. 4. Lymphocytic choriomeningitis
1. 5. Equine encephalitis
1. 6. Other encephalitis
1. 7. Bunyavirus fever caused by group C
1. 8. Encephalomyocarditis
1. 9. Contagious ecthyma
1. 10. Ilheus Fever
1. 11. Mayaro fever
1. 12. Disease Oropouche
1. 13. Yellow fever
1. 14. Other viral zoonoses
1. 15. Hantavirus
1. 16. Asian bird flu. Highly pathogenic avian influenza
EPILOGUE


The eradication of smallpox worldwide has been a milestone for health. The virtually eradicated rinderpest next in importance, but this time with a purely veterinary connotation. It is expected that the next disease to be controlled and eliminated polio are human and FMD.

Asian bird flu and swine flu have sparked warnings in international health agencies, creating a series of measures to early detection of dissemination throughout the world. In Chile, the Ministry of Health (2006) developed a manual on prevention of avian influenza to poultry workers who would be the first contact with the new virus. An example is that preventive measures have been implemented globally by the threat of avian and swine influenza.

Stopping the spread of bovine spongiform encephalopathy through measures that control the food chain, has been successful, and we have been away from this serious disease, prion.

The emergence of ISA in Chilean salmon farming and the consequent economic and social disaster that resulted, made wise lessons being implemented in 2010 aimed at forcing the report outbreaks quickly and to take measures such as epidemiological greater separation between units salmon, and the recruitment of veterinarians for each unit. In 2004, exports of salmon in Chile and Norway were similar, with the introduction of ISA virus Chilean exports fell by about 66% compared to Norway. This situation should never happen if they had taken the relevant sanitary measures.

To conclude I can only express my satisfaction with the actions of the Agricultural and Livestock Service of Chile in effective health action that Chile has allowed to stay free of FMD, classical swine fever, equine infectious anemia and Newcastle, while emerging diseases are being controlled pig.

No doubt that the mere fact of not having FMD for more than two decades, is a source of pride for our profession.

Friday, April 15, 2011

Sample Letter Provisional Letter

feline immunodeficiency virus IN CAPTIVE AND WILD CATS. Patricia Gutierrez Gallardo. HISTORICAL OUTLINE

Feline Immunodeficiency Virus in wild and captive felines
Patricia Gutierrez Gallardo


veterinarian Feline Immunodeficiency Virus is of great importance in domestic cats, the first isolated from Feline Immunodeficiency Virus (FIV) was performed in UC Davis, California, in 1986 for veterinary immunologist Niels Pedersen, who discovered the virus in a domestic cat (Felis catus). You confirmed that this virus belongs to the genus Lentivirus like the human immunodeficiency virus, therefore, based on the similarities it shares with the human immunodeficiency virus, began to investigate more about the origin of these, starting studies Prevalence, characterization and sequencing of the same, using as a model of human viruses.

In studies, most published wild cat is the lion (Panthera leo), which presents a wide range of studies regarding the prevalence of many viruses, including the Feline Immunodeficiency Virus (FIV). In this case, in many African populations has been determined prevalence and reaches 100% of animals tested, for example, in the Serengeti (Roelke et al, 2009), however, there are publications which states that in Namibia and Asiatic lion populations no evidence of FIV (Troyer et al, 2008). Additionally it was established that the virus was not carrying any signs of illness in them due to an ancient virus-host coevolution.

10.8 million years ago in Eurasia were born the first modern cats of the genus Panthera, which later expanded into Africa where one hypothesis is that acquired the virus here, which was then dispersed through the great migrations in Europe and Asia across the Bering Strait to North America and then to South America, expanding infection worldwide. However, Roelke et al. (2009), showed that in populations of African lions in Botswana, no signs of lymphadenopathy, gingivitis, papillomas, decreased muscle mass, among other signs. Also worth mentioning that although there are signs of disease there are no records to indicate reproductive dysfunction that impairs the population. On the other hand, captive lions have also been found individuals infected in zoos in Europe, however, these individuals are African lions, in the case of Asiatic lions, there was no presence of FIV (Lutz et al, 1992). Additionally most commonly used diagnostic techniques in all publications are Western blot for the detection of antibodies and ELISA, while this work used some method of direct diagnosis and viral isolation or PCR.

Another cat has been widely studied case of Puma (Puma concolor), where, many researchers have put their interest on the species, are considered a population at risk, as the Florida subspecies of puma, establishing a first step in studies prevalence. Most American publications on this species are in North America, reflecting prevalences in different populations. In the case of South America, there are few studies that address the issue as an example, Olmsted et al (1992) and Carpenter et al (1996) briefly mention Chilean populations of wild and captive, resulting in both publications with seronegative patients, unfortunately not discussed specifically the sampling site.

should not be unusual to find evidence in the bobcat (Lynx rufus), and living in sympatry with the Cougar and found for example in California populations of seroprevalence of 40% (VandeWounde and Apetrei C, 2006).

In South America the Ocelot (Leopardus pardalis) is one of the cats that have shown seroprevalence of 50% on Barro Colorado, Panama (Franklin et al, 2008). However, no evidence has been found in Brazil or Bolivia.

Similarly, in Leopards (Panthera pardus), African populations have a prevalence greater than 75%, while in Asia there is no evidence of infection with FIV. As in Cheetahs (Acinonyx jubatus), Serengeti where populations have reported a prevalence of 22% (Olmsted et al, 1992). While people in western and southern Africa, there is no evidence of infection (Hofmann-Lehmann et al, 1996). Additionally in Namibia have not been found positive individuals (Munson et al, 2004).

Europe have been tested in wild cats (Felis silvestris silvestris), where until 1999, it was not shown the presence of infection (Leutenegger et al, 1999), however, a year after specimens were found positive for the 7.9% of the total assessed in France (Fromont et al, 2000). Additionally, we found a prevalence of 6% in populations of Saudi Arabia (Ostrowski et al, 2003).

In captive animals have been found in Tiger (Panthera tigris) and Jaguars (Panthera onca), with HIV infection than 5% and 25% respectively, in zoos Europe (Lutz et al, 1992).

the case of cats present in Asia, Pallas's cat (Otocolobus manul) is the only species to date that has tested positive for FIV in the wild. This supports the hypothesis that IVF is not African and Asian origin. Further studies support the phylogenetic relationship of the FIV-Oma strain for the Pallas cat with FIV-Aju strain, corresponding to the cheetah, which had some kind of closeness in the Caspian Sea (Brown et al, 2010) which could have caused the infection. Studies have shown a prevalence of 50% among Pallas Cat (VandeWounde and Apetrei, 2006).

In conclusion the importance of Feline Immunodeficiency Virus in wildlife species is not clear because the world is widespread but does not seem to greatly affect the infected individuals, however, although it has been associated with the presence of some nasal mucus these do not involve to a population decline, which is environmentally beneficial. It is necessary to establish surveillance plans in seronegative populations as it is not easy to predict that they are resistant to infection and can be fatal in them the presence of the disease, as it is very likely to be susceptible. In Chile there are five species of wild cats, of which exist only in the Puma seroprevalence studies published. Reflecting a lack of information for cat populations
colo-colo (Leopardus colocolo), cat wink (Leopardus guigna), the Andean cat (Leopardus Jacobite) and Geoffroy's cat (Leopardus geoffroyi). Bibliography




Brown M, Munkhtsog B, Troyer J, Ross S, Sellers R, Fine A, Swanson W, Roelke M and O'Brien S (2010) Feline immunodeficiency virus (FIV) in wild Pallas' cats. Veterinary Immunology and immunopathology 134 (2010) 90-95.

Carpenter M, Brown E, Culver M, Johnson W, Pecon-Slattery J, O'Brien S and Brousset D (1996). Genetic and phylogenetic divergence of feline immunodeficiency virus in the puma (Puma concolor). Journal of virology Oct.1996. Vol. 70 n°10. p. 6682-6693.

Franklin S, Kays R, Moreno R, TerWee J, Troye J and VandeWoude S (2008). Ocelots on Barro Colorado Island Are Infected with Feline Immunodeficiency Virus but Not Other Common Feline and Canine Viruses. Journal of Wildlife Diseases, 44(3), 2008, pp. 760–765.

Fromont E, Sager A, Leger F, Bourguemestre F, Jouquelet E, Stahl R, Pontier D and Artois M (2000). Prevalence and pathogenicity of retroviruses in wildcats in France. Veterinary Record (2000). 146, pp.317-319

Hofmann-Lehmann R, Fehr D, Grob M, Elgizoli M, Packer C, Martenson J, O´Brien S and Lutz H (1996). Prevalence of antibodies to feline parvovirus, calicivirus, herpesvirus, coronavirus, and immunodeficiency virus and of feline leukemiavirus antigen and the interrelationship of these viral infections in free-ranging lions in east Africa. Clinical and Diagnostic Laboratory immunology, sept. 1996. Vol. 3, N°5 p. 554-562

Leutenegger C, Hofmann-Lehmann R, Riols C, Liberek M, Worel G, Lups P, Fehr D, Hartmann M, Weilenmann P and Lutz H (1999). Viral infections in free-living populations of the European wildcat. Journal of wildlife disease, 35 (4), 1999, pp. 678-686

Lutz H, Isenbügel E, Lehmann R, Sabapara R and Wolfensberger C (1992). Retrovirus infection in non-domestic felids: serological studies and attempts to isolate a lentivirus. Veterinary Immunology and Immunopathology, 35 (1992) 215-224.


Munson L, Marker L, Dubovi E, Spencer J, Evermann J and O’Brien S (2004). Serosurvey of viral infections in free-ranging Namibian Cheetas. Journal of Wildlife Diseases, 40(1), 2004, pp. 23–31

Olmsted R, Langley R, Roelke M, Goeken R, Adger-Johnson D, Goff J, Albert J, Packer C, Laurenson K, Caro T, Scheepers L, Wildt D, Bush M, Martenson J and O´Brien S (1992). Woldwide prevalence of lentivirus infection in wild feline species: epidemiologic and phylogenetic aspect. Journal of virology, Oct.1992, vol. 66, N° 10. P. 6008-6018.

Ostrowski S, Van Vuuren M, Lenair D and Durand A (2003). A serologic survey of wild felids from central west Saudi Arabia. Journal ofnwlidlife disease, 39(3), 2003, pp. 696-701

Roelke M, Brown M, Troyer J, Winterbach H, Winterbach C, Hemson G, Smith D, Johnson R, Pecon-Slattery J, Roca A, Alexander K, Klein L, Martelli P, Krishnasamy K and O'Brien S (2009). Pathological manifestations of feline immunodeficiency virus (FIV) infection in wild African lions. Virology 390 (2009) 1–12.

Troyer J, Vandewounde S, Pecon-Slattery J, McIntosh C, Franklin S, Antunes A, Johnson W and O´Brien S (2008). FIV cross-species transmission: an evolutionary prospective. Veterinary immunology an immunopathology 123 (2008) 159-166.

VandeWounde S and Apetrei C (2006) Going wild: lessons from Naturally Occurring T-lymphotropic lentiviruses. Clinical microbiology reviews. Oct. 2006. Vol 19, No. 4 p.728-762.

Twins Birthday Party Invitation Wording

ALLEGED HEALTH WORLD GRAND PRIX MOTORCYCLE




On April 7 was held World Health Day. Each year the Organization World Health Organization (WHO) chooses a theme important to promote measures that improve health. This year is the issue of antimicrobial resistance with the slogan " unless we act now, there is no cure morning."

WHO calls on the population and patients, policy makers and planners, clinicians and prescribers, pharmacists and providers and the pharmaceutical industry, the adoption of six policy measures to help stop the spread antimicrobial resistance.

Tuesday, April 12, 2011

Where To Get Hair Extensions In Fredericton

2011 VETERINARY Berrios Chilean Patricio Etchegaray

HISTORICAL OUTLINE VETERINARY Berrios Chilean Patricio Etchegaray


1 .- VETERINARY MEDICAL EDUCATION SCHOOL

18/4/1898
VETERINARY MILITARY SCHOOL OF VETERINARY MEDICINE SCHOOL CIVIL

10/11/1916 OF AGRONOMY AND VETERINARY UNIVERSITY OF CHILE
12/4/1928

SCHOOL OF VETERINARY MEDICINE UNIVERSITY OF CHILE
20/4/1938

SCHOOL OF VETERINARY MEDICINE UNIVERSITY OF SOUTHERN
VALDIVIA

07/09/1954 UNIVERSITY SCHOOL OF VETERINARY
CONCEPTION (CHILLÁN CAMPUS) 3/10/1972


1989: THREE SCHOOLS OF MEDICINE VETERINARY
2002: ONCE "" "
2003: FIFTEEN" ""
2004: TWENTY-NINE ""
2011: ...

2 .- RELEVANT INSTITUTIONS: National Stud


1912 DEPARTMENT OF GENERAL SERVICES
1912 QUINTA NORMAL FOR AGRICULTURE
1915 1916 VETERINARY RESEARCH SERVICES
VETERINARY SOCIETY OF CHILE 26/8/1926
NSTITUTE OF VETERINARY RESEARCH VETERINARY MEDICAL ASSOCIATION 1935
OF CHILE 16/9/1955

3 .- VETERINARY MEDICAL RELEVANT

Dr. Hugo K. W. Sievers Dr. Ramon Rodriguez
Dr. Eduardo Fuenzalida Toro
Dr. Enrique Loyola
Amion L. Dr. Gustavo Hoecker
Dr. Danko Brncic

Dr. Francesco di Castri

Dr. Hugo Diaz Oyarzun Dr. Julio San Miguel

Dr. Luis Schmidt Hermann Dr. Alfredo V. Schuler Dr. Adolfo Hube
W. Dr. Teresa Marín
Acchiardo
Among many others! 4 .-

JOURNAL OF VETERINARY MEDICINE

Journal of Veterinary Medicine
Chile
Zooiatría
Monographs of Veterinary Medicine Animal Pathology
Advances in Veterinary Science Veterinary Medicine
Files
Tecno Vet
MEVEPA

5. - OUTSTANDING SHARES OF VETERINARY MEDICINE UNIVERSITY RESEARCH

CHILENA.
Public Health: Zoonoses. FOOD HYGIENE. ENVIRONMENT. POLLUTANTS. EMERGING DISEASES

ANIMAL HEALTH:
ERADICATION OF FOOT
DISEASE ERADICATION OF CLASSICAL SWINE FEVER ERADICATION
NEWCASTLE DISEASE CONTROL
equine infectious anemia
CONTROL OF AVIAN INFLUENZA CONTROL ALTERNATIVE
Ag 1 rabies virus

Fuenzalida-Palacios RABIES VACCINE CENTER
ARTIFICIAL INSEMINATION VALDIVIA


6 .- Background bibliographic


BERRIOS, P. Loyola Eduardo Fuenzalida. A paradigmatic veterinarian. Vet tech 9 (3): 5 - 6, 2001.

ANONYMOUS. Veterinary Medicine in Chile. Class notes. UNICIT. 2002. 15 p.

DIAZ, I. A look at veterinary medical education in Chile: fact or fantasy. Vet tech. 9 (3): 3 - 5, 2003.

Rosendo, S. Brief history of 100 years of teaching veterinary medicine in Chile and its future projection. Av Cs. Vet. 13 (2): 41 - 49, 1998.

Army Drunk On Duty Counseling

genetic factors that influence infectious disease resistance in salmonids and their application in breeding programs EDUARDO FUENZALIDA

Genetic factors that influence infectious disease resistance in salmonids and their application in breeding programs

Arch Med Vet 42, 1-13 (2010)


JM Yáñez, V Martínez *

Genomics Unit and Animal Breeding, Research Laboratory of Animal Biotechnology and Genomics (FAVET-INBIOGEN), Faculty of Science Veterinarias y Pecuarias, Universidad de Chile, Santiago, Chile.
# Programa de Becas de Postgrado de CONICYT (21060530)
* Casilla 2 correo 15, La Granja, Santiago, Chile; vmartine@uchile.cl.


SUMMARY

The control of infectious diseases is essential in the success of salmon aquaculture. Genetic improvement of disease resistance may provide a feasible and sustainable option for the management of these diseases. Marker-assisted selection (MAS) or Gene-assisted selection (GAS), represent a valuable alternative to the conventional schemes for improving disease resistance using pedigree. Nevertheless a previous knowledge of the genetic factors involved in the trait is necessary to implement this methodology. In this review, the most important aspects of genetic resistance to infectious diseases in salmonids and their suitability for breeding programmes are both reviewed and discussed. Firstly, we briefly mention the most important infectious diseases in Chile. Furthermore, we include aspects related with conventional breeding for this quantitative trait, such as selection criteria, genetic variation of resistance and genetic correlations with other traits. We also review three approaches used in molecular identification of genetic factors involved in resistance: candidate genes, with particular emphasis on the major histocompatibility complex (MHC) or MH genes, detection of quantitative trait loci (QTL) and gene expression studies. Finally, we discuss the use of this information in the Implementation of Schemes That include breeding disease resistance in Their breeding goal.

Key words: salmon, disease resistance, breeding Programmes, QTL. SUMMARY




The control of infectious diseases is critical to the success of salmon farming. Genetic improvement of disease resistance may provide a feasible and sustainable option for controlling them. The Molecular Marker Assisted Selection (MAS) or Genes (GAS) is projected as a valuable alternative to conventional breeding for resistance. However, to implement this methodology is required prior knowledge of the genetic factors involved in character. In this paper we review and discuss the most important aspects of genetic resistance to infectious diseases in salmonids and their applicability to breeding programs. First, it briefly presents the most important infectious diseases nationwide. In addition, aspects related to conventional breeding for this quantitative trait, such as selection criteria, genetic variation of resistance and genetic correlations with other production traits of interest. Moreover, we review three molecular approaches used in identifying genetic factors involved in resistance: genes, candidate emphasis on the major histocompatibility complex (MHC) or MH genes, detection of quantitative effect loci (QTL) and gene expression studies. Finally, we reviewed and discussed in relation to the use of this information in implementing molecular breeding programs that include resistance to infectious diseases within its target selection.

Keywords: salmon, disease resistance, breeding programs, QTL. INTRODUCTION





The salmon farming is a major aquaculture activities at national level and one that generates products aquaculture more economic value worldwide (FAO 2006). As with other intensive animal production systems success of this activity depends largely on the control of infectious diseases. A clear example of the impact that can cause certain diseases in salmon farming is the crisis that has hit in recent years the domestic salmon industry as a result of outbreaks of infectious salmon anemia (ISA).

breeding programs have increased the economic return to the farms. The breeding objective should be defined for each species and each population. In general, all those traits of economic importance should be included in the breeding objective. Therefore, in salmon include traits related to body growth, color and texture of meat, as well as genetic resistance to viral diseases and bacterial type (Gjedrem 2000). So far, breeding programs have included only disease resistance based on information from relatives, which affects the degree of genetic progress achievable in each generation. This is because the accuracy with which breeding values \u200b\u200bare predicted using family information is lower compared with that obtained when using information from the candidates themselves breeders (Falconer and Mackay 1996). Furthermore, kin selection can not use Mendelian sampling variation and at the same time, it is difficult to manage inbreeding rates to acceptable levels when the number of families is relatively low (Martinez 2007).

DNA markers are variations in the sequence of this molecule, which allow genotype identification by laboratory tests. These markers have been used in identifying quantitative effect loci (QTL) in different species, ie the search for genomic regions that explain a relatively high proportion of variation for a particular genetic characteristic. The information of molecular markers linked to these QTL and genes of major effect can be included in breeding programs, in what has been called marker-assisted selection (MAS) or genes (GAS). These methodologies can be useful in programs that include characters complicated to measure in the candidate selection, as is the case of infectious disease resistance (Meuwissen 2003). In order to implement programs involving MAS or GAS disease resistance within the breeding objective, we first must understand the genetic factors that explain the quantitative variation for this feature. In recent years there has been progress in dissecting the genetic component involved in the host response against certain pathogens, mainly using animal models such as chicken and mouse (Qureshi et al 1999). In salmonids there is scant information about the genetic architecture of disease resistance, but it is hoped that with the current development and availability of genomic resources in these species and the most knowledge about the biology of the immune response in teleosts, is available in future more background on QTL or genes involved in the change of character.

This review briefly discusses the health aspects more relevant to national salmon farming today. In addition, we review aspects of conventional breeding to increase resistance to disease and the molecular tools used in identifying genetic factors involved in these characters. Finally, we discuss the utility of molecular information on the implementation of programs for genetic improvement in salmon, including resistance within the breeding objective. INFECTIOUS DISEASES

salmon

CHILE In Chile, salmon farming has produced a remarkable and sustained development over the past twenty years, reaching a volume Approximate total harvest of 628 thousand tons during the year 2006.1 The health status of farmed fish is one of the main factors affecting the economic return of the salmon industry. Despite the scientific, professional and technical expertise aimed at improving aspects of health management, new pathological conditions have emerged gradually in the different species of salmonid fish. From the economic point of view, infectious diseases (viral and bacterial) are the most relevant diseases (Smith et al 2001).

Among the main bacterial disease affecting salmonid fish farming in Chile can be Piscirickettsiosis mention or salmon rickettsial syndrome (SRS), bacterial kidney disease (BKD), the syndrome of juvenile rainbow trout (sTfR) and enteric disease of red mouth (ERM). Among the most important viral diseases are infectious pancreatic necrosis (IPN), viral erythrocytic necrosis (VEN) (Smith et al 2001) and recently the ISA virus. A detailed description of each of these diseases largely outweigh the purpose of this review. However, three of them deserve to be highlighted because of its current impact on the national salmon. First, it is noteworthy that he has been responsible Piscirickettsiosis of the biggest losses in the growing stage in the Chilean salmon industry. For example, according to the Technological Institute of Salmon (INTESAL), an institution that monitors illness among producers, in January 2007 caused piscirickettsiosis more than half (55.6%) of total monthly mortality in terms of biomass, taking into account information obtained for Atlantic salmon (Salmo salar), coho salmon (Oncorhynchus kisutch) and rainbow trout (Oncorhynchus mykiss) (Leal and Woywood 2007). Moreover, despite the fact that in Chile the IPN virus caused smaller losses in terms of tonnes of dead fish, because it is a disease that primarily affects juveniles, according to the Fisheries Research Fund (FIP) IPN virus outbreaks in the country affected 48% of total farms, 61% of the centers of smoltification and 49% of centers finished in 1999 (FIP 2003), causing huge losses to the industry. Finally, in mid-2007 there was an outbreak of ISA causing high mortalities in Atlantic salmon in a fish farm located in Chiloé. Since that date there have been consecutively numerous outbreaks, which has been considered the ISA as a disease prevalent in areas X and XI of the southern regions of the country, causing major economic losses to the industry (SERNAPESCA 2008).

whereas these diseases are of great importance to the salmon industry in Chile and that the measures used for the prevention and treatment of them (vaccinations, antibiotics, etc..) Showed no significant results to date, it is imperative to develop new strategies to establish an effective and sustainable control of these diseases. Genetic improvement of disease resistance is a feasible solution to the problem (Stear et al 2001). However, in the national research so far has been low and there are no published studies aimed at identifying genetic factors that influence resistance. Nonetheless, at present carried out several research projects using quantitative genetic tools, molecular and functional genomics to identify genetic factors associated with resistance to the three most economically important diseases for the national industry Piscirickettsiosis , IPN and ISA.2

CONVENTIONAL BREEDING RESISTANCE TO INFECTIOUS DISEASES

resistance to infectious diseases can be defined as the ability to initiate and maintain host responses aimed at preventing the establishment of an infectious agent and / or remove the body. Select animals to increase disease resistance is a feasible method to improve productivity and animal welfare, which also offers certain advantages over other methods of control against infections (Stear et al 2001). In Norway, since 1993 has included the resistance to viral and bacterial diseases in conventional breeding programs in salmon (Gjøen and Bentsen, 1996). However, this methodology presents some difficulties mainly related to the selection criteria used to measure the resistance. Here, we review the main aspects of conventional breeding for resistance to infectious diseases in salmon.

CRITERIA SELECTION IN THE IMPROVEMENT OF RESISTANCE
CONVENTIONAL
Different selection criteria that could potentially be used to measure disease resistance in fish breeding programs. While in some schemes and the selection is used by experimental challenges against pathogens, remains an open question what the most appropriate selection criteria, ie which measurement should be performed in candidates for measuring resistance. Here we review some aspects studied so far in this field.

Challenge against pathogens. Disease resistance can be measured in terms practical and survival (or mortality) of individuals against infection. You can use epidemiological data from field outbreaks to make inferences about the genetic resistance to infectious diseases. For this purpose it is necessary that the pedigree of the population can be determined and that the records are structured survival as family information (Guy et al 2006). However, using information from field outbreaks has some disadvantages such as the difficulty to recognize the exact cause of death, because the factors that influence survival under these conditions are different. Furthermore, the availability of information depends on the occurrence of outbreaks, which are usually controlled to reduce economic losses. Moreover, the inference of the pedigree by using molecular markers can increase costs. However, survival data can be obtained from experimental challenges, which can be standardized, facilitating evaluation of the results. Also, the challenges are more advantageous presmolts in terms of costs, compared with postsmolts used in field studies. Notwithstanding the foregoing, it is required that there is a high correlation between the results obtained from pre and postsmolts challenges. To date, we have reported a high correlation genetics (up to 0.95) between field trials and experimental challenges to furunculosis in Atlantic salmon (Gjøen et al 1997, Ødegård et al 2006). Therefore, for selection schemes that include resistance to a particular disease within its goal of improvement, challenge tests are more accurate and appropriate field outbreaks, since they reduce the variability caused by environmental factors and are more feasible to implement in practice. Indeed, in this way is as determined resistance to viral and bacterial diseases in the conventional breeding program for Atlantic salmon, done in by Aquagen Norway (Gjøen and Bentsen 1996, Aquagen 2005).

immunological and physiological variables. Direct selection to improve the genetic resistance to diseases based on evidence challenges can be costly and time consuming. Furthermore, in conventional breeding programs can only be compiled using information from relatives. Indirect selection based on the measurement of other characteristics that are genetically correlated with disease resistance, could simplify data collection and at the same time could allow the incorporation of individual information. Some studies have aimed to determine the variation genetic physiological and immunological variables, and the correlation between them and the survival of the salmon challenge tests. Examples of variables that have been studied to date are: hemolytic activity of serum and serum lysozyme activity (Røed et al 1993, Lund et al 1995), plasma cortisol (Fevolden et al 1993), and IgM antibody titers (Lund et al 1995), α2-antiplasmin serum (Jump et al 1993), bactericidal activity and complement activity (Hollebecq et al 1995). However, even though some studies show significant correlations between resistance and immune parameters, the proportion of variation overall survival can be explained by the immunological variables has been considered too low to be useful as selection criteria. Thus the prediction of breeding values \u200b\u200bfor survival based on these variables may not be adequate (and Bentsen Gjøen 1996). The latter is reasonable considering the complexity of the mechanisms involved in immune response and the large number of factors may be involved in disease resistance, which causes a great difficulty when attempting to use the information in a single parameter in the determination of the resistance. On the other hand, the use of all related physiological variables survival with a methodology would be costly and less feasible to implement in practice.

GENETIC VARIATION OF RESISTANCE TO INFECTIOUS DISEASES

A prerequisite for improving a property by artificial selection it is this genetic variation. Heritability (h2) is the proportion of total phenotypic variance that is attributable to additive genetic variance (Falconer and Mackay 1996). It is important to note that this property is not only a character but also of the population, environmental conditions and how they evaluated the phenotype (Falconer and Mackay 1996). Depending on how you measure disease resistance, heritability may have different values \u200b\u200band incomparable, due to differences in defining the character and the model used in the analysis (Ødegård et al 2006, Ødegård et al 2007). To date, there are a large number of papers which described additive genetic variation and to estimate the heritability values \u200b\u200bfor resistance to various viral and bacterial diseases in salmonids (Table 1). This shows that the genetic improvement of these characteristics will be satisfactory and is a viable alternative for the control of these diseases in salmonids. However, given the specific case of the absence of such studies for resistance to Piscirickettsiosis, one of the most important diseases for the national salmon.



Table 1. Values \u200b\u200bof heritability (h2) and standard error (±), estimated for resistance to various infectious diseases in salmon.
heritability values \u200b\u200b(h2) and Their standard error (±) for resistance to infectious diseases in salmonids Different.




genetic correlation between resistance to infectious diseases INTEREST AND OTHER CHARACTERISTICS OF PRODUCTIVE

The potential to simultaneously improve the genetic resistance to different diseases and other economically important characteristics depend on the genetic correlations among these traits. Few studies have aimed to identify genetic correlations for disease resistance in salmon. Some work on Atlantic salmon have shown a positive genetic correlation between resistance to various bacterial diseases such as furunculosis, BKD, vibriosis and cold water vibriosis (Gjedrem and Gjøen 1995, Gjøen et al 1997). However, there is a weak negative genetic correlation between resistance to viral disease ISA and other bacterial diseases such as furunculosis, vibriosis and cold water vibriosis (Gjøen et al 1997). In rainbow trout analyzed the genetic correlation between the disease viral hemorrhagic septicemia (VHS) and bacterial diseases and sTfR ERM. Contrary to what was observed in Atlantic salmon, the genetic correlation between resistance to bacterial diseases was weakly negative, whereas resistance to viral disease was positively correlated with sTfR and negatively correlated with ERM (Henryon et al 2005). However, all these correlations were estimated with some degree of uncertainty due to the low number of families used in the study (Henryon et al 2005).

Moreover, it is important to understand the genetic correlation between disease resistance and other characteristics in salmon production. To date, we have determined genetic correlations between disease resistance and traits related to growth (weight and body length, growth rate and food conversion efficiency). The results range from negative genetic correlations moderate to low (Henryon et al 2002), through inconsistent correlations (Beacham and Evelyn 1992, Henryon et al 2002), to moderate and low positive correlations (Standal and Gjerde 1987, Gjedrem et al 1991, Perry et al 2004). INTERFACE

-MOLECULAR AND GENETIC IMPROVEMENT OF RESISTANCE TO DISEASES

Large advances in the generation and use of molecular markers, automated sequencing methods and new techniques available to the transcriptomics data analysis, have helped to identify QTL and genes associated with complex traits in various species of vertebrates. Salmonids, are not out of this boom in the development of new techniques for genomic analysis. This fact is reflected in the considerable increase of genomic resources for salmonid species during the past five years and the consolidation of an international collaborative group aimed at establishing priorities and maintenance of these resources (Consortium for Genomic Research on All salmonids Program, cGRASP, Canada). Currently, these tools are starting to be used in identifying genetic factors involved in resistance to infectious diseases in salmonids. The strategies used in the study of the genetic architecture of resistance are based mainly on the analysis of candidate genes, QTL mapping and gene expression studies. CANDIDATE GENES



candidate gene theory says that a significant proportion of the phenotypic variation of a feature in a population is determined by the presence of polymorphisms in major effect genes involved in the expression of that character, allowing the identification of these genes (Rothschild and Soller 1997). This approach requires knowledge of the biology of the species, biochemical pathways and, especially, gene sequences, to study the variation of specific candidates. In aquaculture, the availability of gene sequences is limited, but it is expected that a greater number of genes to be incorporated into public databases in the short term.

In vertebrates, the major histocompatibility complex or MHC has attracted much attention in studies of association between genetic variants and disease resistance. However, have been proposed and studied other genes may also play an important role in the mechanism of resistance in productive species, model organisms and humans (Hill 1999, Qureshi et al 1999). To date, no studies that aim to define the association between other candidate genes, other than the MHC, and resistance to infectious diseases in salmon.

major histocompatibility complex (MHC). The MHC is a multigene family that acts at the interface between the immune system and infectious diseases. The MHC gene family comprises two subfamilies: class I genes and class II (Bernatchez and Landry 2003). Both classes are for membrane glycoproteins involved processing and elimination of pathogens (Thorgaard et al 2002). MHC class I genes are expressed on the surface of all nucleated somatic cells. Play an important role in immune defense against intracellular pathogens by binding peptides, mainly viral, in the cytoplasm and presenting them to lymphocytes TCD8 + (Bernatchez and Landry 2003, Grimholt et al 2003).

In vertebrates, two types of MHC class I: classical (Ia) and non-classical (Ib) (Klein and O'Huigin 1994). MHC class Ia genes are highly polymorphic, expressed in most tissues during infection and its transcription is modulated by specific promoter elements (Interferon-mediated response). By contrast, MHC class Ib genes show less polymorphism, restricted expression and are not modulated at the transcriptional level during infection (Thorgaard et al 2002).

On the other hand, class II MHC genes have a more restricted expression pattern, as expressed in antigen presenting cells (B lymphocytes and macrophages). Basically, they are involved in maintaining the extracellular environment by presenting antigens, particularly bacterial cells to CD4 + (Bernatchez and Landry 2003, Grimholt et al 2003).

MHC genes have been identified, cloned and characterized in salmon Atlantic rainbow trout and other salmonids (Grimholt et al 1993, Hordvik et al 1993, Hansen et al 1996, Shum et al 1999, Shum et al 2002). In addition, it has been shown that these genes are highly polymorphic in these species (Grimholt et al 1994, Miller and Withler 1996, Hansen et al 1999, Garrigan and Hedrick 2001, Aoyagi et al 2002, Grimholt et al 2002). As in other vertebrates, two types of class I genes, the UAA that are highly divergent, non-polymorphic and expressed at low levels, and the UBA are polymorphic, expressed at high levels in spleen and structural features similar to those of class Ia molecules (classical), which present antigens to T lymphocytes (Shum et al 1999). The class II genes are divided into class II A (SAA) and II B or (DAB), depending on whether coding for α or β chain of the molecule, respectively (Grimholt et al 2000, Stet et al 2002). Both loci (DAA and DAB) cosegregated as haplotypes, suggesting a close physical linkage between them in Atlantic salmon (Stet et al 2002). This, coupled with the expression of a single locus of MH class I genes (Grimholt et al 2002), could allow more easily associate MH alleles and disease resistance in this species (Stet et al 2002).

In teleosts, unlike what happens in other vertebrates, genes class I and II MH segregate independently (Hansen et al 1996, Bingulac-Popovic et al 1997, Sato et al 2000), therefore, instead of speaking of a 'complex' major histocompatibility complex (MHC) is more appropriate to speak of 'genes MH 'in these species (Grimholt et al 2003). The absence of linkage between genes class I and class II has potential implications in the natural selection of polymorphisms in both classes. If these two types of genes were linked, the selection of a particular class II allele inevitably change the frequency of an allele linked class I and vice versa (Shum et al 2001). Furthermore, the absence of linkage allows independent segregation of immunological traits in fish genes associated with class I (cytotoxicity in response to viral infection) and class II genes (humoral response against bacteria).

have investigated the association between a polymorphism linked to MH class II genes and resistance against the virus of infectious hematopoietic necrosis (IHN) in backcrosses of rainbow trout and cutthroat trout (Oncorhynchus clarki). The effect of polymorphism on survival was small and significant in one of the two families studied, suggesting that this mutation may be linked to a gene that influences resistance to IHN. However, environmental effects and the involvement of other genes involved in the property may mitigate the effect of this locus (Palti et al 2001). In Atlantic salmon have demonstrated the association between MH class IIB alleles and resistance specific Aeromonas salmonicida (Langefors et al 2001, Lohman et al 2002). In this same species have been associated with gene variants MH class I and class II in susceptibility to IHN (Miller et al 2004). Moreover, we have determined the association between specific alleles of genes MH class I and II and the resistance to ISA and furunculosis independently (Grimholt et al 2003). Based on the results of this study, we selected resistant and susceptible genotypes, which were subsequently crossed to generate progeny with genotypes for high and low mortality expected. The study partially confirmed the expectations in terms of resistance and susceptibility of individual alleles MH class I and IIA against ISA, previously set by Grimholt et al (2003). This is because some variants that showed to be associated with resistance in the previous study did not establish a better survival in this second trial, however, variants previously associated with susceptibility repeated their performance (Kjøglum et al 2006).

Although associations have been established between MH gene variants and disease resistance has been shown that it is not the only factor influencing genetic variation of this feature in salmon. In Salmon Atlantic has been found that there is an effect that is not related to the MH genes in terms of resistance to IPN, furunculosis and ISA (Kjøglum et al 2005). This effect, nearly 10% on average for the three diseases produce significant genetic variation in the survival of challenged families (alleles identical in MH), which can be explained on the basis of a difference in polygenic effects associated with feature. Additionally, this study found an effect associated with the tank, which significantly influence the observed variation for resistance to IPN. Therefore, this technical factor should be considered when analyzing genetic resistance to infectious diseases by challenge tests (Kjøglum et al 2005). Due to the polygenic nature of disease resistance is important to consider the background genome and the interactions that can occur between genes (epistasis), which makes further analysis of individual candidate genes involved in resistance variation. DETECTION OF QTL



QTL mapping is a strategy that can provide information about the location and effect of genes that are influencing a complex quantitative trait, such as resistance to infectious diseases. Detection methodologies QTL is based on the use of DNA markers to identify genomic regions involved in genetic variation of a given character of productive interest.

DNA markers. The development of markers based on DNA variations have generated a great impact on studies of genetic variation in animals and fish. Within the DNA markers are widely used RFLPs (polymorphism restriction fragment length), RAPDs (random amplified polymorphic DNA), AFLP (amplified fragment length polymorphism), microsatellites and SNPs (single nucleotide polymorphisms .) These vary each other in their mode of inheritance, identification and detection methods, number of locus ranging and polymorphic information content (Liu and Cordes 2004).

The AFLPs have the advantage that they can be generated more easily and more cheaply than SNPs and microsatellites, because it is not needed for generation of genomic information. However, its mode of inheritance, as is codominant RAPDs, ie can not distinguish heterozygous from homozygous dominant genotypes without using special equipment and software (Piepho and Koch 2000). This reduces the amount of information provided by these markers.

Microsatellites are nucleotide sequences, between 1 to 6 base pairs repeated in tandem. The different alleles are generated due to variation in the number of repetitions. Key features found to be highly variable, codominant inheritance file and found to be abundant and widely distributed throughout the genome. The great advantage of microsatellites is their high degree of polymorphism. Moreover, his analysis is based on the amplification of DNA using chain reaction (PCR) is performed so quickly, at low cost and the amount of DNA required is minimal (in the order of nanograms). In salmonids there are many microsatellites available for use in genetic studies (Phillips et al 2009).

Furthermore, the SNPs may be present in both coding and noncoding regions. They are usually biallelic, are evenly distributed on the genome and are more abundant than microsatellites. Therefore, are ideal for the construction of dense genetic maps, which can be used in fine mapping of QTL and genes help identify causal genetic variation for specific characters. Recently, based on the alignment of sequences over 100,000 ESTs (expressed sequence tags) have been detected more than 2,500 Putative SNPs in Salmo salar, with a higher validation rate to 70% (Hayes et al 2007).

QTL detection for disease resistance in salmonids. The development of a genetic map is the first step toward identifying QTL. To date, we have built linkage maps for rainbow trout (Young et al 1998, Sakamoto et al 2000, Nichols et al 2003, Guyomard et al 2006), Atlantic salmon (Moen et al 2004b, Gilbey et al 2004 ), brown trout (Salmo trutta) (Gharbi et al 2006) and arctic char (Salvelinus alpinus) (Woram et al 2004). Studies with microsatellites

aimed to detect QTL for disease resistance in salmonids have QTL identified two medium and large effect for resistance to IPN in rainbow trout. These loci explained a large proportion (27% and 34%) of the phenotypic variation in a family from a backcross of a strain susceptible to IPN (YK-RT101) and one resistant (YN-RT201) (Ozaki et al 2001).

In this same species using AFLP and microsatellite markers were found associated with resistance to IHN in three different linkage groups (Rodriguez et al 2004). For the same disease have been detected RFLP markers associated with resistant and susceptible families in backcrosses of rainbow trout and cutthroat trout (Palti et al 1999).

In Atlantic salmon, with a multifaceted strategy that combines the Transmission Disequilibrium Test (TDT), the identification of Mendelian segregation of markers and survival analysis, we were able to detect two QTL associated with resistance to ISA, using AFLP markers in two families own brothers (Moen et al 2004a). In a more recent study, it has managed to validate the presence of one of the QTL detected by Moen et al (2004a), this time using microsatellite markers in a larger number of fish. This QTL explained 6% of the phenotypic variation for resistance to ISA and has been located in linkage group 8 of Atlantic salmon (following the notation SALMAP) (Moen et al 2007).

In this same species using differential recombination rates between sexes have detected three QTL for resistance to IPN through a methodology based on two stages. First, analysis was performed using only the recombination of the males to determine linkage groups with significant effects, using two to three microsatellite loci per chromosome. Next, using the recombination of the females and a greater number of markers per linkage group were confirmed and positioned the QTL detected previously (Houston et al 2008b). The most significant QTL, mapped on linkage group 21, was subsequently confirmed through analysis of nine additional families and a greater saturation of markers (Houston et al 2008a).

Overall confidence intervals for QTL are extensive. This has two consequences. First, wide intervals may contain a large number of genes (thousands) and, therefore, identify the causal polymorphism of the variation is very complex. Secondly, the use of these QTL in MAS programs is complicated because the linkage phase between marker and QTL throughout the population may be different from that given in families, subject to study. An alternative to reduce the confidence intervals in QTL mapping is to use information from linkage analysis in conjunction with information from the LD population (Meuwissen et al 2002). Through simulation studies, methodologies that use this information together have been tested successfully in the fine mapping of QTL in commercial populations of salmon (Hayes et al 2006). This, together with the availability of dense genetic maps, help to reduce the confidence intervals on identification of QTL in these species. The information in these QTL, together with the sequencing and physical mapping of the genome, will facilitate the identification of mutations causing resistance through positional studies. These mutations may be used directly in breeding programs. FUNCTIONAL GENOMICS



Functional genomics, defined as the application of experimental methods of genomic coverage or system for assessing gene function from data and background from structural genomics (mapping and sequencing), is becoming a primary area of \u200b\u200binterest (Hiendleder et al 2005). The basic idea of \u200b\u200bthe methodologies used in this area is to broaden the spectrum of biological research at a holistic level where they study, simultaneously, a large amount of transcribed genes and proteins. Currently, resources Available in salmon genomics have allowed some approaches to the study of infectious diseases response using functional genomics tools.

gene expression. Genes whose expression levels are changed in response to infection can be identified by high throughput techniques (High-throughput). For example, using a technique called subtractive hybridization under conditions of suppression (SSH), using liver samples from individuals injected with a bacterin of V. anguillarum and normal individuals, we detected more than 25 genes involved in immune response in rainbow trout, including protein sequences acute phase of inflammation, coagulation and complement system (Bayne et al 2001). By the same technique, genes involved in signal transduction, innate immunity and other processes have been identified as relevant to the challenge with A. salmonicida in Atlantic salmon (Tsoi et al 2004).

On the other hand, the availability of libraries of ESTs and cDNAs has allowed the development of DNA microarrays that can be used to study the differential expression of a large number of genes simultaneously in salmonids (Rise et al 2004b, Ewart et al 2005, von Schalburg et al 2005). Using a microarray of human cDNAs were identified transcripts Atlantic salmon differentially expressed against challenge with A. salmonicida. However, due to the divergence of species, only 6% of the sequences of DNA microarray hybridization showed detectable anti-liver cDNA salmon (Tsoi et al 2003). Rise et al (2004a) conducted the first study based on a microarray constructed from cDNAs libraries of salmon. Thus, in Atlantic salmon genes have been identified that show differential expression, depending on whether macrophages from infected and uninfected Piscirickettsia salmonis and hematopoietic kidney challenged or challenged individuals from the same pathogen. These genes are characterized by immune relevant functional annotations could be used as molecular biomarkers of infection with P. salmonis (Rise et al 2004a). Furthermore, using a cDNA microarray of Atlantic salmon with more than 4,000 genes extracted from liver, spleen and anterior kidney, have discovered several genes differentially expressed in response to infection by A. salmonicida (Ewart et al 2005). Moreover, we analyzed the transcriptomic response compared to vaccination with a bacterin of A. salmonicida in Atlantic salmon, revealing temporal and tissue differences in expression levels, which can have relevance in the establishment of protection (Martin et al 2006). Moreover, we have studied the gene expression profile in response to a DNA vaccine IHN virus in rainbow trout, detected 910 genes modulated in the injection site and also identified the overexpression of genes related to type I interferon system (IFN-1) in other tissues, suggesting that this system is the basis of early antiviral immunity (Purcell et al 2006). In the above studies, some transcripts that showed variation in expression levels compared to infection had no homologs in GenBank, so their functions remain still unknown (Rise et al 2004a, Ewart et al 2005, Martin et al 2006, Purcell et al 2006). Therefore, it should work based on the encoded protein sequences and their role in the immune response to decipher its role against infection.

To date no studies designed to analyze the differential expression between resistant and susceptible fish for a particular infection. The information provided by this type of analysis can be used in the discovery of new groups of genes, with or without an assigned function, which could be related to disease resistance (Walsh and Henderson 2004). However, it should be noted that differentially expressed genes may be, probably acting in trans, ie, whose expression is regulated by other genes (Martinez 2007), which will have implications when these polymorphisms associated with resistance. Another possibility is to consider the differential expression levels as a quantitative trait. This may allow the identification of QTL associated with differences in gene expression patterns between resistant and susceptible individuals (eQTL) (Pomp et al 2004, Koning et al 2005). However, it is still unclear how the information provided by analysis of expression can be used in breeding programs (Walsh and Henderson 2004).

MOLECULAR MARKER ASSISTED SELECTION (MAS) AND GENE-ASSISTED SELECTION (GAS)

A crucial parameter in the detection of QTL and the subsequent application of MAS programs is the level of linkage disequilibrium (LD) that exists between markers and causal mutations of the variation in population-level character. Linkage Disequilibrium



whereas 2 loci, A and B, each with two alleles, A / and B / b, the LD is defined as: P (A Otherwise, the probability of A given B is different from the probability of A given b. The linkage equilibrium (LE), therefore, is the opposite situation: P (A marker exists only within families and not throughout the population, rates of recombination can break the association between marker alleles and QTL between families. Therefore, the linkage phase between marker and QTL should be determined in each generation and each family separately. To determine if the marker and QTL are in LD within each family is required phenotypic records and genotypes in each generation. This makes the implementation of MAS using markers in LD with the QTL only within families is very attractive (Dekkers and van der Werf 2007). In the case of disease resistance, all available within the program families must be challenged in each generation, as in conventional schemes.

MORE IN STOCKS IN LD

Using dense map information can make use of LD between markers and the causative mutation of character variation across the population (LD between families). There are two possibilities to exploit the LD population in MAS schemes. You can use the information on the effect of a particular haplotype in LD with the polymorphism beneficial across the population or can predict the genetic value of individual maps from dense genomic coverage (Selection genomic) (Lande and Thompson 1990 , Meuwissen et al 2001). The effectiveness of these strategies depends on the magnitude of the effects associated with or polymorphisms. When estimating the effects of haplotypes across the entire genome, it is possible to use these effects to select from generations after the initial estimate, without having the phenotypes (Meuwissen et al 2001). Recombination LD will decay in each generation and the magnitude of this decrease will depend on various population parameters (Meuwissen et al 2001). In practice, it is necessary to verify the response to selection in each generation and this can re-estimate the effects using a random sample of individuals in the population. GAS



have been identified as GAS using populations in LE you get a higher genetic progress in relation to that achievable by using MAS. This is because in MAS schemes are selected markers associated with QTL and in the case of GAS, is selected directly favorable polymorphism (Villanueva et al 2002). However, in practice it is likely that MAS programs are carried out using information from a large number of markers to predict the allelic effects of QTL over the same time while GAS programs, probably only a limited number of polymorphisms available. Therefore, MAS schemes can generate greater genetic progress because they use a higher proportion of genetic variance. However, it is necessary to take into account the cost associated with genotype a larger number of markers (Martinez 2007).

factors influencing the profitability of GAS include: the amount of variation explained by the available genes, the frequency of favorable alleles and the availability of a test for the study population, potential pleiotropic effects and costs related to the implementation of genotyping. Therefore, it is necessary to assess these factors from a financial standpoint and determine its benefit compared with other methods described.

USE OF MAS IN IMPROVING THE RESISTANCE

Best Linear Unbiased Predictor (BLUP) uses aggregate information from the pedigree and phenotypes to predict the genetic values \u200b\u200bof individuals. Molecular markers give a new source of information whose impact will be given greater precision when predicting breeding values. Thus, the response to selection will be substantially better in character in which the accuracy is low, ie, characters with low heritability or characters that can not be measured in their own candidates for selection, as is the case of disease resistance (Meuwissen 2003). The relative increase in accuracy depends on the amount of variation explained by markers, which depends on the number of QTL identified and used in breeding schemes (Lande and Thompson 1990). In

productive species has shown that the effects of QTL have a leptokurtic distribution, with a small number of loci of large effect and a larger number of loci of small effect (Hayes and Goddard 2001), which is probably the case aquaculture species (Martínez et al 2005). Therefore, it is expected that more than one marker is necessary for MAS programs are efficient (Martinez 2007). Also, consider the pleiotropic effects of the different polymorphisms and possible negative effects on other features. For example, negative genetic correlations detected between resistance to viral and bacterial diseases can be a problem if the goal is to select for resistance against a wide range of pathogens. On the other hand, failure to consider non-additive genetic effects in the analysis model could decrease the precision with which estimates the effects-additive genetic.

is likely that future SNP genotyping on a large scale allows the use of these markers in the selection of players in a cost-effective. Therefore, we can expect MAS programs using LD markers through of the population are implemented at the whole genome. However, it is necessary to determine the economic benefits of the use of a single haplotype versus the use of multiple haplotypes and determine which of the two methods is best for the population under selection.

also practice other factors should be considered when using QTL information to improve disease resistance in salmonids, for example, the epidemiology of various diseases and economic considerations relating to program implementation. CONCLUSIONS



There is limited and scattered information regarding the genetic factors involved in resistance to infectious diseases in salmon. However, the early development of genomic resources in these species will provide new tools for genetic dissection of these characteristics. The use of these tools is very helpful to identify loci or genes that significantly influence the variation of these characters. This information will be essential to implement programs involving MAS or GAS resistance within the breeding objective. These methods increase the accuracy in the selection of candidates for breeding, thereby improving the response to selection. However, each case must study the economic feasibility of implementing these new strategies and the benefit compared to conventional breeding schemes. NOTES



1 Salmonchile 2007, http://www.salmonchile.cl/files/T4-Mundial% 201996-2006.pdf [Consultation: 12/02/2007].

2 Maldonado, personal communication. REFERENCES



Aoyagi K, Dijkstra JM, Xia C, Denda R, M Ototake, K Hashimoto, T Nakanishi. 2002. Classical MHC class I genes Composed of Highly divergent sequence lineages share a single locus in rainbow trout (Oncorhynchus mykiss). J Immunol 168, 260-273. [ Links ]

Aquagen. 2005. Selection for increased disease resistance gives results. Information letter Nº 5. Norway. [ Links ]

Bayne CJ, L Gerwick, K Fujiki, M Nakao, T Yano. 2001. Immune relevant (including acute phase) genes identified in the livers of rainbow trout, Oncorhynchus mykiss, by means of suppression subtractive hybridization. Dev Comp Immunol 25, 205-217. [ Links ]

Beacham TD, TPT Evelyn. 1992. Genetic variation in disease resistance and growth of chinook, coho, and chum salmon with respect to vibriosis, furunculosis, and bacterial kidney disease. Trans Am Fish Soc 121, 456-485. [ Links ]

Bernatchez L, C Landry. 2003. MHC studies in nonmodel vertebrates: what have we learned about natural selection in 15 years? J Evol Biol 16, 363-377. [ Links ]

Bingulac-Popovic J, F Figueroa, A Sato, WS Talbot, SL Johnson, M Gates, JH Postlethwait, J Klein. 1997. Mapping of mhc class I and class II regions to different linkage groups in the zebrafish, Danio rerio. Immunogenetics 46, 129-134. [ Links ]

De Koning DJ, Ö Carlborg, C Haley. 2005. The genetic dissection of immune response using gene-expression studies and genome mapping. Vet Immunol Immunopathol 105, 343-352. [ Links ]

Dekkers J, J Van der Werf. 2007. Strategies, limitations and opportunities for marker-assisted selection in livestock. In: Marker-Assisted selection - Current status and future perspectives in crops, livestock, forestry and fish. FAO, Rome, Italy, Pp 167-184. [ Links ]

Dorson M, E Quillet, MG Hollebecq, C Torhy, B Chevassus. 1995. Selection of rainbow trout resistance to viral haemorrhagic septicaemia virus and transmission of resistance by gynogenesis. Vet Res 26, 361-368. [ Links ]

Ewart K, J Belanger, J Williams, T Karakach, S Penny, S Tsoi, R Richards, S Douglas. 2005. Identification of genes differentially expressed in Atlantic salmon (S. salar) in response to infection by Aeromonas salmonicida using cDNA microarray technology. Dev Comp Immunol 29, 333-347. [ Links ]

Falconer DS, TFC Mackay. 1996. Introduction to Quantitative Genetics. 4th ed. Essex, UK. [Links]

FAO, Food and Agriculture Organization of the United Nations. 2006. State of world aquaculture. FAO Fisheries Technical Paper. No. 500. Rome, Italy. [Links]

Fevolden SE, R Nordman, Refstie T, Røed KH. 1993. Disease resistance in Atlantic salmon (Salmo salar) selected for high or low response to stress. Aquaculture 109, 215-224. [Links]

FIP, Fisheries Research Fund, Chile. 2003. Risk of introducing infectious diseases in salmon. Final Report Project FIP \u200b\u200b2001-08. [Links]

Garrigan D, Hedrick PW. 2001. Class I MHC polymorphism and evolution in endangered California Chinook and other Pacific salmon. Immunogenetics 53, 483-489. [ Links ]

Gharbi K, A Gautier, RG Danzmann, S Gharbi, T Sakamoto, B Hoyheim, JB Taggart, M Cairney, R Powell, F Kreig, N Okamoto, MM Ferguson, LE Holm, R Guyomard. 2006. A linkage map for brown trout (Salmo trutta): chromosome homeologies and comparative genome organization with other salmonid fish. Genetics 172, 2405-2419. [ Links ]

Gilbey J, E Verspoor, A McLay, D Houlihan. 2004. A microsatellite linkage map for Atlantic salmon (Salmo salar). Anim Genet 35, 98-105. [ Links ]

Gjedrem T, R Salte, HM Gjøen. 1991. Genetic variation in susceptibility of Atlantic salmon to furunculosis. Aquaculture 97, 1-6. [ Links ]

Gjedrem T, HM Gjøen. 1995. Genetic variation in susceptibility of Atlantic salmon (Salmo salar L.) to furunculosis, BKD, and cold-water vibriosis. Aquac Res 26, 129-134. [ Links ]

Gjedrem T. 2000. Genetic improvement of cold-water fish species. Aquac Res 31, 25-33. [ Links ]

Gjøen HM, HB Bentsen. 1997. Past, present and future of genetic improvement in salmon aquaculture. ICES J Mar Sci 54, 1009-10014. [ Links ]

Gjøen HM, T Refstie, O Ulla, B Gjerde. 1997. Genetic correlations between survival of Atlantic salmon in challenge and field tests. Aquaculture 158, 277-288. [ Links ]

Goddard, ME, THE Meuwissen. 2005. The use of linkage disequilibrium to map quantitative trait loci. Aust J Exp Agr 45, 837-845. [ Links ]

Grimholt U, I Hordvik, VM Fosse, I Olsaker, C Endresen, O Lie. 1993. Molecular cloning of major histocompatibility complex class I cDNAs from Atlantic salmon, Salmo salar L. Immunogenetics 37, 469-473. [ Links ]

Grimholt U, I Olsaker, C de Vries Lindstrom, O Lie. 1994. A study of variability in the MHC class II beta-1 and class I alpha-2 domain exons of Atlantic salmon, Salmo salar L. Anim Genet 25, 147-153. [ Links ]

Grimholt U, A Getahun, T Hermsen, RJ Stet. 2000. The major histocompatibility class II alpha chain in salmonid fishes. Dev Comp Immunol 24, 751-763. [ Links ]

Grimholt U, F Drablos, SM Jorgensen, B Hoyheim, RJ Stet. 2002. The major histocompatibility class I locus in Atlantic salmon (Salmo salar L.): polymorphism, linkage analysis and protein modelling. Immunogenetics 54, 570-581. [ Links ]

Grimholt U, S Larsen, R Nordmo, P Midtlyng, S Kjoeglum, A Storset, S Saebø, RJ Stet. 2003. MHC polymorphism and disease resistance in Atlantic salmon (Salmo salar); facing pathogens with single expressed major histocompatibility class I and class II loci. Immunogenetics 55, 210-219. [ Links ]

Guy DR, SC Bishop, S Brotherstone, A Hamilton, RJ Roberts, BJ McAndrew, JA Woolliams. 2006. Analysis of the incidence of infectious pancreatic necrosis mortality in pedigreed Atlantic salmon, Salmo salar L., populations. J Fish Dis 29, 637-647. [ Links ]

Guyomard R, S Mauger, K Tabet-Canale, S Martineau, C Genet, F Krieg, E Quillet. 2006. A type I and type II microsatellite linkage map of rainbow trout (Oncorhynchus mykiss) with presumptive coverage of all chromosome arms. BMC Genomics 7, 302. [ Links ]

Hansen JD, P Strassburger, L Du Pasquier. 1996. Conservation of an alpha 2 domain within the teleostean world, MHC class I from the rainbow trout Oncorhynchus mykiss. Dev Comp Immunol 20, 417-425. [ Links ]

Hansen JD, P Strassburger, GH Thorgaard, WP Young, L Du Pasquier. 1999. Expression, linkage, and polymorphism of MHC-related genes in rainbow trout, Oncorhynchus mykiss. J Immunol 163, 774-786. [ Links ]

Hayes B, ME Goddard. 2001. The distribution of the effects of genes affecting quantitative traits in livestock. Genet Sel Evol 33, 209-229. [ Links ]

Hayes B, A Gjuvsland, S Omholt. 2006. Power of QTL mapping experiments in commercial Atlantic salmon populations, exploiting linkage and linkage disequilibrium and effect of limited recombination in males. Heredity 97, 19-26. [ Links ]

Hayes B, JK Laerdahl, S Lien, T Moen, P Berg, K Hindar, WS Davidson, BF Koop, A Adzhubei, B Høyheim. 2007. An extensive resource of single nucleotide polymorphism markers associated with Atlantic salmon (Salmo salar) expressed sequences. Aquaculture 265, 82-90. [ Links ]

Henryon M, A Jokumsen, P Berg, I Lund, PB Pedersen, NJ Olesen, WJ Slierendrecht. 2002. Genetic variation for growth rate, feed conversion efficiency, and disease resistance exists within a farmed population of rainbow trout. Aquaculture 209, 59-76. Erratum: Aquaculture 216, 387-388. [ Links ]

Henryon M, P Berg, NJ Olesen, TE Kjær, WJ Slierendrecht, A Jokumsen, I Lund. 2005. Selective breeding provides an approach to increase resistance of rainbow trout (Onchorhynchus mykiss) to the diseases, enteric redmouth disease, rainbow trout fry syndrome, and viral heamorrhagic septicaemia. Aquaculture 250, 621-636. [ Links ]

Hiendleder S, S Bauersachs, A Boulesteix, H Blum, GJ Arnold, T Fröhlich, E Wolf. 2005. Functional genomics: tools for improving farm animal health and welfare. Rev Sci Tech Off Int Epiz 24, 354-377. [ Links ]

Hill AV. 1999. Genetics and genomics of infectious disease susceptibility. Br Med Bull 55, 401-213. [ Links ]

Hollebecq MG, B Faivre, C Bourmaud, C Michel. 1995. Spontaneous bactericidal and complement activities in serum of rainbow trout (Oncorhynchus mykiss) genetically selected for resistance or susceptibility to furunculosis. Fish Shellfish Immunol 5, 407-426. [ Links ]

Hordvik I, U Grimholt, VM Fosse, O Lie, C Endresen. 1993. Cloning and sequence analysis of cDNAs encoding the MHC class II beta chain in Atlantic salmon Salmo salar. Immunogenetics 37, 437-441. [ Links ]

Houston RD, A Gheyas, A Hamilton, DR Guy, AE Tinch, JB Taggart, BJ McAndrew, CS Haley, SC Bishop. 2008a. Detection and confirmation of a major QTL affecting resistance to infectious pancreatic necrosis (IPN) in Atlantic salmon (Salmo salar). Dev Biol (Basel) 132, 199-204. [ Links ]

Houston RD, CS Haley, A Hamilton, DR Guy, AE Tinch, JB Taggart, BJ McAndrew, SC Bishop. 2008b. Major quantitative trait loci affect resistance to infectious pancreatic necrosis in Atlantic salmon (Salmo salar). Genetics 178, 1109-1115. [ Links ]

Kjøglum S, U Grimholt, S Larsen. 2005. Non-MHC genetic and tank effects influence disease challenge tests in Atlantic salmon (Salmo salar). Aquaculture 250, 102-109. [ Links ]

Kjøglum S, S Larsen, HG Bakke, U Grimholt. 2006. How specific MHC class I and class II combinations affect disease resistance against infectious salmon anaemia in Atlantic salmon (Salmo salar). Fish Shellfish Immunol 21, 431-441. [ Links ]

Klein J, C O'Huigin. 1994. The conundrum of nonclassical major histocompatibility complex genes. Proc Natl Acad Sci USA 91, 6251-6252. [ Links ]

Lande R, R Thompson. 1990. Efficiency of marker-assisted selection in the improvement of quantitative traits. Genetics 124, 743-756. [Links]

Langefors A Lohm J, Grahn M, Andersen O, T von Schantz. 2001. Association Between major histocompatibility complex class IIB alleles and resistance to Aeromonas salmonicida in Atlantic salmon. Proc R Soc Lond B Biol Sci 268, 479-485. [Links]

J Leal, D Woywood. 2007. Piscirickettsiosis in Chile: Progress and prospects for control. SalmoCiencia 2, 34-42. [Links]

Liu ZJ, Cordes JF. 2004. DNA marker technologies and Their Applications in aquaculture genetics. Aquaculture 238, 1-37. [Links]

Lohm J, M Grahn, Å Langefors, Andersen Ø, A Storset, T von Schantz. 2002. Experimental evidence for major histocompatibility complex-allele-specific resistance to a bacterial infection. Proc R Soc Lond B Biol Sci 269, 2029-2033. [ Links ]

Lund T, T Gjedrem, H Bentsen, D Eide, HJS Larsen, KH Roed. 1995. Genetic variation in immune parameters and associations to survival in Atlantic salmon. J Fish Biol 46, 748-758. [ Links ]

Martin S, S Blaney, D Houlihan, CJ Secombes. 2006. Transcriptome response following administration of a live bacterial vaccine in Atlantic salmon (Salmo salar). Mol Immunol 43, 1900-1911. [ Links ]

Martínez V, G Thorgaard, B Robison, M Sillanpää. 2005. Simultaneous consideration of environmental and genetic effects in QTL mapping: an application to early development in double haploid lines of rainbow trout. Genet Res 86, 209-221. [ Links ]

Martínez V. 2007. Marker-assisted selection in fish and shellfish breeding schemes. In: Marker-Assisted selection - Current status and future perspectives in crops, livestock, forestry and fish. FAO, Rome, Italy, Pp 329-362. [ Links ]

Meuwissen THE, B Hayes, M Goddard. 2001. Prediction of total genetic value using genomewide dense marker maps. Genetics 157, 1819-1829. [ Links ]

Meuwissen THE, A Karlsen, S Lien, I Olsaker, ME Goddard. 2002. Fine mapping of a quantitative trait locus for twinning rate using combined linkage and linkage disequilibrium mapping. Genetics 161, 373-9. [ Links ]

Meuwissen THE. 2003. Genomic selection the future of marker-assisted selection and animal breeding. In: Marker-assisted selection: a fast track to increase genetic gain in plant and animal breeding? FAO, Rome, Italy. [ Links ]

Miller KM, RE Withler. 1996. Sequence analysis of a polymorphic MHC class II gene in Pacific salmon. Immunogenetics 43, 337-351. [ Links ]

Miller KM, JR Winton, AD Schulze, MK Purcell, TJ Ming. 2004. Major histocompatibility complex loci are associated with susceptibility of Atlantic salmon to infectious hematopoietic necrosis virus. Environ Biol Fishes 69, 307-316. [ Links ]

Moen T, KT Fjalestad, H Munck, L Gomez-Raya. 2004a. A multistage testing strategy for detection of quantitative trait loci affecting disease resistance in Atlantic salmon. Genetics 167, 851-858. [ Links ]

Moen T, B Hoyheim, H Munck, L Gomez-Raya. 2004b. A linkage map of Atlantic salmon (Salmo salar) reveals an uncommonly large difference in recombination rate between the sexes. Anim Genet 35, 81-92. [ Links ]

Moen T, AK Sonesson, B Hayes, S Lien, H Munck, THE Meuwissen. 2007. Mapping of a quantitative trait locus for resistance against infectious salmon anaemia in Atlantic salmon (Salmo salar): comparing survival analysis with analysis on affected/resistant data. BMC Genetics 8, 53. [ Links ]

Nichols KM, WP Young, RG Danzmann, BD Robison, C Rexroad, M Noakes, RB Phillips, P Bentzen, I Spies, K Knudsen, FW Allendorf, BM Cunningham, J Brunelli, H Zhang, S Ristow, R Drew, KH Brown, PA Wheeler, GH Thorgaard. 2003. A consolidated linkage map for rainbow trout (Oncorhynchus mykiss). Anim Genet 34, 102-115. [ Links ]

Ødegård J, I Olesen, B Gjerde, G Klemetsdal. 2006. Evaluation of statistical models for genetic analysis of challenge test data on furunculosis resistance in Atlantic salmon (Salmo salar): prediction of field survival. Aquaculture 259, 116-123. [ Links ]

Ødegård J, I Olesen, B Gjerde, G Klemetsdal. 2007. Evaluation of statistical models for genetic analysis of challenge-test data on ISA resistance in Atlantic salmon (Salmo salar): Prediction of progeny survival. Aquaculture 266, 70-76. [ Links ]

Ozaki A, T Sakamoto, S Khoo, K Nakamura, MRM Coimbra, T Akutsu, N Okamoto. 2001. Quantitative trait loci (QTLs) associated with resistance/susceptibility to infectious pancreatic necrosis virus (IPNV) in rainbow trout (Oncorhynchus mykiss). Mol Genet Genomics 265, 23-31. [ Links ]

Palti Y, JE Parsons, GH Thogaard. 1999. Identification of candidate DNA markers associated with IHN virus resistance in backcrosses of rainbow (Oncorhynchus mykiss) and cutthroat trout (O. clarki). Aquaculture 173, 81-94. [ Links ]

Palti Y, KM Nichols, KI Waller, JE Parsons, GH Thorgaard. 2001. Association between DNA polymorphisms tightly linked to MHC class II genes and IHN virus resistance in backcrosses of rainbow and cutthroat trout. Aquaculture 194, 283-289. [ Links ]

Perry GML, P Tarte, S Croisetière, P Belhumeur, L Bernatchez. 2004. Genetic variance and covariance for 0+ brook charr (Salvelinus fontinalis) weight and survival time of furunculosis (Aeromonas salmonicida) exposure. Aquaculture 235, 263-271. [ Links ]

Phillips RB, KA Keatley, MR Morasch, AB Ventura, KP Lubieniecki, BF Koop, RG Danzmann, WS Davidson. 2009. Assignment of Atlantic salmon (Salmo salar) linkage groups to specific chromosomes: conservation of large syntenic blocks corresponding to whole chromosome arms in rainbow trout (Oncorhynchus mykiss). BMC Genet 10, 46. [ Links ]

Piepho HP, G Koch. 2000. Codominant analysis of banding data from a dominant marker system by normal mixtures. Genetics 155,1459-1468. [ Links ]

Pomp D, MF Allan, SR Wesolowski. 2004. Quantitative genomics: exploring the genetic architecture of complex trait predisposition. J Anim Sci 82, 300-312. [ Links ]

Purcell MK, KM Nichols, JR Winton, G Kurath, GH Thorgaard, P Wheeler, JD Hansen, RP Herwig, LK Park. 2006. Comprehensive gene expression profiling following DNA vaccination of rainbow trout against infectious hematopoietic virus. Mol Immunol 43, 2089-2106. [ Links ]

Qureshi ST, E Skamene, D Malo. 1999. Comparative genomics and host resistance against infectious diseases. Emerging Infect Dis 5, 36-47. [ Links ]

Rise ML, SRM Jones, GD Brown, KR von Schalburg, WS Davidson, BF Koop. 2004a. Microarray analyses identify molecular biomarkers of Atlantic salmon macrophage and hematopoietic kidney response to Piscirickettsia salmonis infection. Physiol Genomics 20, 21-35. [ Links ]

Rise ML, KR von Schalburg, GD Brown, RH Devlin, MA Mawer, N Kuipers, M Busby, M Beetz-Sargent, R Alberto, AR Gibbs, P Hunt, R Shukin, JA Zeznik, C Nelson, SRM Jones, DE Smailus, SJM Jones, JE Schein, MA Marra, YSN Butterfield, JM Stott, SH Ng, WS Davidson, BF Koop. 2004b. Development and application of a salmonid EST database and cDNA microarray: data mining and interspecific hybridization characteristics. Genome Res 14, 478-490. [ Links ]

Rodriguez MF, S LaPatra, S Williams, T Famula, B May. 2004. Genetic markers associated with resistance to infectious hematopoietic necrosis in rainbow and steelhead trout (Oncorhynchus mykiss) backcrosses. Aquaculture 241, 93-115. [ Links ]

Røed KH, KT Fjalestad, A Strømsheim. 1993. Genetic variation in lysozyme activity and spontaneous haemolytic activity in Atlantic salmon (Salmo salar). Aquaculture 114, 19-31. [ Links ]

Rothschild MF, M Soller. 1997. Candidate gene analysis to detect genes controlling traits of economic importance in domestic livestock. Probe 8, 13-20. [ Links ]

Sakamoto T, RG Danzmann, K Gharbi, P Howard, A Ozaki, SK Khoo, RA Woram, N Okamoto, MM Ferguson, L Holm, R Guyomard, B Hoyheim. 2000. A microsatellite-based map for rainbow trout (Oncorhynchus mykiss) characterized by large sex-specific differences in recombination rates. Genetics 155, 1331-1345. [ Links ]

Salte R, HM Gjøen, K Nordberg, T Gjedrem. 1993. Plasma protein levels as potential marker traits for resistance to furunculosis. J Fish Dis 16, 561-568. [ Links ]

Sato A, F Figueroa, Murray BW, Malaga-Trillo E, Zaleska-Rutczynska Z, H Sultmann, Toyosawa S, Wedekind C, Steck N, Klein J. 2000. Nonlinkage of major histocompatibility complex class I and class II loci in bony fishes. Immunogenetics 51, 108-116. [Links]

SERNAPESCA, National Marine Fisheries Service, Chile. 2007. Balance on the health status of infectious salmon anemia in Chile in July 2007 to July 2008. [Links]

Shum BP, Rajalingam R, Magor KE, Azumi K, Carr WH, Dixon B, Stet RJ, Adkison MA, Hedrick RP, Parham P. 1999. A divergent non-classical class I gene in salmonids preserved. Immunogenetics 49, 479-490. [Links]

Shum BP, L Guethlein, LR Flodin, MA Adkison, RP Hedrick, RB Nehring, RJ Stet, C. Secombes, P Parham. 2001. Modes of salmon MHC class I and II Evolution Differ from the primate paradigm. J Immunol 166, 3297-3308. [Links]

Shum BP, PM Mason, KE Magor, LR Flodin, Stet RJ, Parham P. 2002. Structures of two major histocompatibility complex class I genes of the rainbow trout (Oncorhynchus mykiss). Immunogenetics 54, 193-199. [Links]

P Smith, J Larenas, P Vera, J Contreras, C Venegas, Rojas ME, Guajardo A. 2001. Main diseases of salmonid fish cultured in Chile. Veterinary Medicine Monographs 21, 3-19. [Links]

Standal M, B Gjerde. 1987. Genetic variation in survival of Atlantic salmon during searearing period. Aquaculture 66, 197-207. [ Links ]

Stear MJ, SC Bishop, BA Mallard, H Raadsma. 2001. The sustain-ability, feasibility and desirability of breeding livestock for disease resistance. Res Vet Sci 71, 1-7. [ Links ]

Stet RJM, B de Vries, K Mudde, T Hermsen, J van Heerwaarden, BP Shum, U Grimholt. 2002. Unique haplotypes of co-segregating major histocompatibility class II A and class II B alleles in Atlantic salmon (Salmo salar) give rise to diverse class II genotypes. Immunogenetics 54, 320-331. [ Links ]

Thorgaard GH, GS Bailey, D Williams, DR Buhler, SL Kaattari, SS Ristow, JD Hansen, JR Winton, JL Bartholomew, JJ Nagler, PJ Walsh, MM Vijayan, RH Devlin, RW Hardy, KE Overturf, WP Young, BD Robison, C Rexroad, Y Palti. 2002. Status and opportunities for genomics research with rainbow trout. Comp Biochem Physiol B Biochem Mol Biol 133, 609-646. [ Links ]

Tsoi SC, JM Cale, IM Bird, KV Ewart, LL Brown, SE Douglas. 2003. Use of human cDNA microarrays for identification of differentially expressed genes in Atlantic salmon liver during Aeromonas salmonicida infection. Mar Biotechnol 5, 545-554. [ Links ]

Tsoi SC, KV Ewart, S Penny, K Melville, RS Liebscher, LL Brown, SE Douglas. 2004. Identification of immune-relevant genes from Atlantic salmon using suppression subtractive hybridization. Mar Biotechnol 6, 199-214. [ Links ]

Villanueva B, R Pong-Wong, JA Woolliams. 2002. Marker assisted selection with optimised contributions of the candidates to selection. Genet Sel Evol 34, 679-703. [ Links ]

von Schalburg KR, ML Rise, GA Cooper, GD Brown, RA Gibbs, CC Nelson, WS Davidson, BF Koop. 2005. Fish and Chips: Various methodologies demonstrate utility of a 16,006-gene salmonid microarray. BMC Genomics 56, 126. [ Links ]

Walsh B, D Henderson. 2004. Microarrays and beyond: what potential do current and future genomics tools have for breeders? J Anim Sci 82, 292-299. [ Links ]

Withler RE, PT Evelyn. 1990. Genetic variation in resistance to bacterial kidney disease within and between two strains of coho salmon from British Columbia. Trans Am Fish Soc 119, 1003-1009. [ Links ]

Woram RA, C McGowan, JA Stout, K Gharbi, MM Ferguson, B Hoyheim, EA Davidson, WS Davidson, CE Rexroad, RG Danzmann. 2004. A genetic linkage map for Arctic char (Salvelinus alpinus): evidence for higher recombination rates and segregation distortion in hybrid versus pure strain mapping parents. Genome 47, 304-315. [ Links ]

Young WP, PA Wheeler, VH Coryell, P Keim, GH Thorgaard. 1998. A detailed linkage map of rainbow trout produced using doubled haploids. Genetics 148, 839-850. [ Links )