[{"id":225,"title":"Evolution in genetic terms – Is it RNA world or DNA world or is it anything else?","sha":"69b03c4db6269df0798781ef07244e59","user_id":null,"state":"published","body":"\r\nThe RNA world concept that self-replicating ribonucleic acid (RNA) molecules are keys to all current forms of life on Earth and geticists could not go further down might have missed out on how evolution has actually happened in real genetic terms. \r\n\r\nOut of all hypothesis and proposals, one that stands strong in the debate of “RNA before DNA” is \u003cb\u003e “protein synthesis can occur in the absence of DNA but not in the absence of RNA” \u003c/b\u003e. To contest this hypothesis, one should take a close look on life of an RNA molecule and their early degeneration process. \r\n\r\nEarlier RNA-protein interaction systems are highly doubtful because RNA is never a long-time informational molecule and even if they are or they used to be, many such information might got lost. Assuming this kind of unstable molecule being the early days primary replication machinery, information contents might have significantly lost and this will again raise a question on how similar or same species maintains identity?\r\n\r\nTransferring information outside of the nucleus is only required when there is a nucleus.\r\n\r\nTaken together these concepts, \u003cb\u003ewe need to revisit the origin of life in newer genetic terms.\u003c/b\u003e\r\n","created_at":"2015-09-16T17:43:27.824Z","updated_at":"2015-09-18T06:00:54.818Z","zenodo_id":61235,"doi":"http://dx.doi.org/10.5281/zenodo.31054","subject":null,"tags":["evolution","rna","dna","rna world","dna world","genetics"],"vote_count":1,"view_count":1,"score":1.1,"deleted":false,"muted":false,"tweeted":false,"attachment_file_name":null,"attachment_content_type":null,"attachment_file_size":null,"attachment_updated_at":null},{"id":558,"title":"Toward Developing a Comprehensive Theory of Immunology for Guiding Future Immunological Research","sha":"03111b36267c547db30e1cc76aa625cb","user_id":null,"state":"published","body":"Concluding my research in plant and comparative immunology, I theorized that immunity is fundamentally the genetic program’s ability to resist change and maintain homeostasis. All immunological phenomena are governed not by molecular discontinuities mediated by receptor-ligand interactions—known as Continuity Theory—but more specifically by discontinuities that ultimately disrupt the program’s stability. Immunity is the program’s ability to stabilize—to resist natural selection—as replication perpetuates existence. Perceived this way, immunity may be considered the program’s intrinsic predisposition toward adaptation, with evolution originating as the interplay between immunity and natural selection.\r\n\r\nRequisite for biological life is the genetic program’s abilities of replication and stability under environmental forces. Polymerization/replication coexists with the reverse reaction of depolymerization/de-replication. Genetic code strand variants formed through imperfect replication might interfere with the parent molecule’s stability; therefore, parent molecules may—as a form of resistance—catalyze the depolymerization of interfering progeny. Progeny resistant to this degradation could persist and outcompete inferior, less stable replicants. To test this hypothesis and support the aforementioned theory, we must conduct experiments involving competition among identical self-replicating ribozymes occupying finite space and resources, and analyze the resultant spectrum, respective concentration, 3D structure, and catalytic capabilities of ribozyme variants formed over time.","created_at":"2019-01-26T22:43:45.875Z","updated_at":"2019-06-02T06:01:15.447Z","zenodo_id":3236946,"doi":"https://doi.org/10.5281/zenodo.3236946","subject":null,"tags":["evolution","immunity","immunology","adaptation","genetics","homeostasis","natural selection","replication","resistance"],"vote_count":0,"view_count":1,"score":0.1,"deleted":false,"muted":false,"tweeted":false,"attachment_file_name":null,"attachment_content_type":null,"attachment_file_size":null,"attachment_updated_at":null},{"id":23,"title":"Reanimation of Australian Megafauna, Extinct Species and New Zealand Moas","sha":"5d87b73cfbbd112200914f3638f5f3af","user_id":45,"state":"published","body":"After the arrival of the first humans, Indigenous Australians, to the island continent, the previous megafauna became extinct.  As many samples are still extant, deriving DNA samples or fragments and reverse engineering, through multiple generations could allow us to recreate these fauna, or at the very least, increase our understanding of development, evolution and reproductive technology. It will also increase our technical know how for the development of useful synthetic organisms","created_at":"2015-02-11T01:57:22.473Z","updated_at":"2015-05-27T20:43:01.766Z","zenodo_id":21947,"doi":"http://dx.doi.org/10.5281/zenodo.15013","subject":null,"tags":["synthetic","biology","genetics","reanimation","molecularbiology","extinction"],"vote_count":2,"view_count":1,"score":2.1,"deleted":false,"muted":false,"tweeted":false,"attachment_file_name":null,"attachment_content_type":null,"attachment_file_size":null,"attachment_updated_at":null},{"id":152,"title":"Improving our knowledge on the host response to multidrug resistant bacteria.  A key towards combatting superbugs and developing novel host-directed therapies","sha":"ab728b67f16b258841a4a4152f16d62f","user_id":429,"state":"published","body":"Hospital acquired infections, mostly due to multi-drug resistant bacteria or “superbugs” are a growing concern and affects millions of patients every year worldwide. There is an urgent need to find novel treatment to improve the care of the hospitalized patients as bacteria are becoming resistant to all existing antibiotics. Unfortunately, there are limited resources to tackle these bacterial infections as the pharmaceutical industry has stopped developing novel antibiotics. This matter of urgency has been recently recognized from various countries (USA, UK…) and novel strategies are desperately needed. \r\n\r\nIn the general population, there are individual differences between humans that give some people an advantage in their ability to resist severe disease caused by infection. Similar to humans, some mouse strains or mouse mutants are resistant to bacterial infections.  \r\n\r\nThe idea would be to determine the genetic mechanisms of resistance to \"superbugs\" in mice. If we can determine what causes this resistance to multi-drug resistance bacteria, it then we may be able to improve existing treatments. We will also be in a position to develop novel host-directed therapies against superbugs that would target the host rather than the bacteria. This would control the infection and improve the treatment of the diseases. ","created_at":"2015-04-25T07:23:07.529Z","updated_at":"2023-02-07T09:20:56.050Z","zenodo_id":27964,"doi":"http://dx.doi.org/10.5281/zenodo.17159","subject":null,"tags":["superbugs","bacteria infection","antibiotics","host response","genetics","host-pathogens interations","host-directed therapies"],"vote_count":1,"view_count":1,"score":1.1,"deleted":false,"muted":false,"tweeted":true,"attachment_file_name":null,"attachment_content_type":null,"attachment_file_size":null,"attachment_updated_at":null}]