It's time to ban experiments on animals!

You can, of course, - if we are satisfied with the prospect not to invent any new medical technology or medicine.

An excerpt from Asi Kazantseva’s book “Someone is wrong on the Internet! Scientific research of disputed issues ”( www.corpus.ru/products/asya-kazanceva-internete-kto-to-neprav.htm ).

It is important to understand that researchers have absolutely no desire to ruin as many innocent animals as possible. Any search for scientific publications for words Animal Testing mainly brings materials on how to minimize the need for such studies. Any experiments on animals are regulated by strict rules and limited to ethical commissions.

In addition, work with animals is a simply expensive, long and laborious process; Everywhere where it is possible to do without it, scientists seek to do this. The number of doctoral degrees in biology awarded in the USA has almost doubled over the past 30 years [1], and the number of animals used has not increased.

Rats and mice (as well as fish, amphibians, reptiles and birds) in the United States are not counted with the accuracy of an individual, but, according to approximate estimates, the total number of vertebrates used in the experiments was about 20 million a year in the mid-1980s [2] and about 17 million a year in the mid-2000s [3]. Much more accurate statistics exist for all mammals in addition to rats and mice (that is, for hamsters, rabbits, pigs, etc.)-in 1984 a little more than 2 million of these animals were used, and in 2014 is exactly 834,453 pieces [4]. These figures seem impressive only until we compare them with the number of animals that are used annually. For example, with 8,666,662,000 chicken eaten in America in 2014 [5].

What are laboratory animals for? Three million mice used in 2013 in the UK are distributed [6] as follows. 59% of animals are involved in obtaining new lines using various methods of genetic modification, 28% move fundamental science, 11.5% are needed for applied medical research. 0.5% of animals are required for veterinary and environmental studies, and the remaining half a percent divide educational projects and the use of mice for diagnosis (for example, if you have a patient with suspicion of one or another infectious disease, but standard tests do not yet detect, you can take a little blood from him, try to infect mice and observe their condition).

If I correctly understood British statistics, then these 59% reflect the intermediate stage of research. These are the animals whose genome was somehow changed, and now they are crossed with each other to obtain genetically homogeneous lines and check whether the changed genes are now working (or, conversely, stopped working) just as it was planned. When this process is completed, they will begin to participate in fundamental or applied research. A significant part of such animals is needed to understand the causes of human diseases [7]. You have some kind of gene that you know for sure (or suppose) that its mutations increase in people the risk of diabetes, or Alzheimer's disease, or atherosclerosis, or some kind of cancer. You find the appropriate gene in the mouse, violate its work, make sure that the animals obtained really get sick more often, and then find out why this is happening and what medicinal substances can compensate for the effect.

This approach is widely used precisely due to the fact that we and we are relatives and many genes are almost identical in our country. But there is another task: the study of those genes that, in the case of humans, on the contrary, noticeably differ not only from the mouse, but even from the genes of chimpanzees. Almost every such gene is naturally suspected that it “makes us people,” and sometimes with the help of genetically modified mice you can get funny confirmations of this hypothesis.

The most famous-and the most important-of these stories began in the late 1980s in one of the primary schools of the city of Brentford (de facto is part of London). Elizabeth Other, who was engaged there with children lagging behind the school curriculum, drew attention to the fact that several students from the same family immediately demonstrate similar speech disorders. They began to speak late, pronounced the words inaudibly (for example, Bu instead of Blue), did not use sentences longer than two or three words, hardly selected words and often pronounced them inaccurately (for example, they said “glass” or “tea”, when they showed a cup and asked what this object is called), and also experienced difficulties with the perception of grammatical constructions (for example, they did not feel the difference between the girls' sentences “ The horse runs ”and“ The girl runs after the horse ”). At the same time, children did not have mental retardation, they normally coped with mathematics, knew how to read and write; Problems were related precisely with oral speech. Elizabeth and her school colleagues turned to the department of clinical genetics of the London children's hospital. Specialists who worked there compiled a genealogy families [8].

It turned out that the child can inherit the disease from his parent with a probability of 50% and in children in the same family the problem can either be pronounced or completely absent. This is a classic picture of the inheritance of one single dominant allele * and this became a sensation: until then it was assumed, and it is not unreasonable that many different genes have contributed to the development of speech. There are really a lot of them, but among them it was possible to identify one particularly important. Later it was identified; called Foxp2; found out that it encodes the transcription factor (protein that activates the reading of some genes) that is important for the development of the brain; that this protein has only two amino acids in a person differs from the protein of chimpanzees and that in Neanderthals he was the same as ours; That FoxP2 is involved in many processes associated with the development of the brain, but most importantly-it is associated with speech not only in people, but, apparently, in general, in all animals that have sound communication between relatives in one form or another. For example, this applies to singing birds: in normal zebrous Amadins quite accurately reproduce the song that they heard in childhood, but when the FOXP2 is suppressed, instead of a single melody, quite fragmented (and all the time are different) sounds [9].

You have already noticed that in most cases, new information about genes receive new information: they find or create a creature in which this gene is broken, and see that it has spoiled. Foxp2 is no exception: mice are created, in which it is simply turned off. In the event that they did not work as a single copy of the gene (in general there are two of them: inherited from mom and dad), animals in principle felt very poorly, but including the mouse was completely absent from the ultrasonic squeak, which they normally use to call their mother. If one normal copy of the gene was still present, the mouse was squealing, but much less than ordinary [10].

But you can not spoil the genes of mice, but on the contrary, sorry for anthropocentricity, improve them. Namely, replace the mouse Foxp2 with the human and see what kind of beast it will turn out. Such mice were first created in 2009 [11]. They differed from ordinary mice in a number of structural and functional features of the brain, but in the context of history about the speech, the most interesting observation was due to the fact that the mouse, which were carried away from the nest of the mouse, really squeaked a little differently, for example, they had more long-length episodes of complex squeak (with sound frequency changes). However, the scientific community was no longer interested in the difference in the squeak, but the differences in learning. In 2014, a large study was published [12], in which mice with the human Foxp2 (animals, which are made for people like people for research purposes, are called: humanized) and ordinary mice wandered through labyrinths in search of food.

There are two ways to determine which of the corridors leads to the feeder. Firstly, you can look at external landmarks. “The food will be on the side where the cross is drawn,” the mouse could say if it were a well -humanized enough for this. Secondly, you can remember your own movements. “Directly and right,” the mouse would explain. During the preliminary tests, scientists noted that humanized mice learn to use external landmarks faster than ordinary mice. However, the researchers were interested in something else: how quickly the animal can abandon the strategy that has lost relevance. After the scientists showed mice for two weeks that to search for food to raise their heads, look at the wall of the laboratory, see the painted cross and go in this direction - they took and turned the maze 180 degrees. If at the same time they began to put the food in another sleeve so that it would be next to the cross again, then ordinary and humanized mice equally quickly understood that only a cross is necessary to believe, and it does not matter that we now turn right to right, but to the left. But if it was still necessary to turn the right, and the cross to ignore, then humanized mice markedly faster switched to the correct behavior.

Why is it important? Because such a learning result shows that mice with the human Foxp2 memorize their own movements. As the authors of the same work showed, a striped body works differently in humanized mice-a section of the brain necessary to form complex and multi-stage motor reactions. This suggests that the human FOXP2, in addition to other functions, can be associated with our complex articulation, the ability to quickly and consistently control lips, tongue, vocal cords to generate many diverse sounds. It is clear that further research is required - and there is clearly no shortage of them ...

1. National Center for Education Statistics - the most valuable storehouse of data on any aspects of American education. Data on biologists - at the link http://nces.ed.gov/programs/digest/d14/tables/dt14_325.22.asp

2. US Congress, Office of Technology Assessment. Alternatives to Animal Use in Research, Testing, and Education. Washington, DC: US ​​Government Printing Office, OTA-BA-273, February 1986. The document is available on the link: http://govinfo.libary.edu/ota/data/1986/8601.pdff

3. Taylor K. et al. Estimates for Worldwide Laboratory Animal Use in 2005 // Alternatives to Laboratory Animals, 2008 July, Vol. 36 (3), 327–342.

4. A schedule that clearly demonstrates a decrease in the number of experimental animals in recent years is available on the link:http://speakingofresearch.com/afacts/statistics/ , and the data on which it is collected by the service of animal and plant health under the US Department of Agriculture: http://www.aphis.usda.gov/wps/portal/aphis/ourfocus/animalwelfare/ (Research Facility Annual Reports).

5. The number of animals clogged in 2014 according to the US Department of Agriculture: at the first link of the bird, according to the second mammals. www.nass.usda.gov/publications/todeys_reports/reports/pslaan15.pdf , www.nass.usda.gov/publications/todays_rePors/lstk0415.pdf

6. Home-office data, units of the British government on public security. Home Office. Annual Statistics of Scientific Procedures on Living Animals. Great Britain, 2013. The publication is available on the link: www.gov.uk/govenment/uploads/system/uPloads/attachment_data/file/327854/spanimals13.pdf

7. Bagle T. et al. Transgenic Animals and Their Application in Medicine // International Journal of Medical Research & Health Sciences, 2013, Vol. 1, Issue 2, 107–116.

8. Hurst J. et al. An Extended Family with A Dominantly Inherited Speech Disorder // Developmental Medicine & Child Neurology, Apr. 1990, Vol. 32, ID. 4, 352–355.

9. Haesler S. et al. Incomplete and Inaccurated Vocal IMITATION KNOCKDown of FOXP2 in Songbird Basal Ganglia Nucleus Area X // Plos Biology, Dec. 2007, vol. 5 (12), E321.

10. Shu W. et al. Alved Ultrasonic Vocalization in Mice with A Disruption in the Foxp2 Gene // Pnas, July 2005; Vol. 102 (27), 9643–9648.

11. Enard W. et al. A Humanized Version of Foxp2 Affects Cortico-Basal Ganglia Circuits in Mice // Cell, May 2009, Vol. 137, Issue 5, 961–971.

12. Schreiweis C. et al. Humanized Foxp2 Acceptions Learning by Enhancing Transitions from Declating to Procedural Performance // Pnas, Sep. 2014, Vol. 111 (39), 14253–14258. 13 Hajar R. Animal Testing and Medicine // Heart Views.

* In Moscow, it is generally accepted that the allele (one of the alternative options for the same gene) is a masculine word, and only Petersburgers use it in a female gender. Nevertheless, Gramota.ru (with reference to the spelling dictionary of the Russian Academy of Sciences) acts on this issue on the side of the northern capital.