Proteins are probably the most important class of material in the body. Proteins are not just building blocks for muscles, connective tissues, skin, and other structures. They also are needed to make enzymes. Enzymes are complex proteins that control and carry out nearly all chemical processes and reactions within the body. The body produces thousands of different enzymes. Thus, the entire structure and function of the body is governed by the types and amounts of proteins the body synthesizes. Protein synthesis is controlled by genes, which are contained on chromosomes. View or Download The Human Genome Landmarks Poster
Genes are contained in chromosomes.
A chromosome contains hundreds to thousands of genes. Although most chromosomes are found in the nucleus of a cell, some are also found in the cell's mitochondria. These organelles are responsible for changing energy into a form the cell can use. Chromosomes are structures that carry an organism's DNA, which contains all of its genetic information. Every human cell contains 23 pairs of chromosomes, for a total of 46 chromosomes.
A chromosome contains hundreds to thousands of genes. Although most chromosomes are found in the nucleus of a cell, some are also found in the cell's mitochondria. These organelles are responsible for changing energy into a form the cell can use. Chromosomes are structures that carry an organism's DNA, which contains all of its genetic information. Every human cell contains 23 pairs of chromosomes, for a total of 46 chromosomes.
Certain HLA-DRB1 *01 (HLA-DR1) and HLA-DRB1*04 (HLA-DR4) alleles, also known as “shared epitopes”, have been associated with susceptibility to RA [56]. Shared epitopes are probably the primary risk factor for increased ACPA production in RA [57]. A high risk for the development of ACPA-positive RA was observed in patients carrying one or two shared epitope alleles [58]. In shared epitope positive patients, smoking was not only associated with positive ACPA, but also with absolute serum anti-CCP levels (2). Reference: (1), (2), (3), Effects of tobacco smoke on immunity, inflammation and autoimmunity Yoav Arnson, et al., Journal of Autoimmunity 34 (2010) J258eJ265 View More
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Chromosomal location 9q13
Approved name: lncRNA negative regulator of fibroblast-like synoviocyte migration, SYNCRIP interacting Fibroblast-like synoviocytes represent a specialized cell type located inside joints in the synovium. These cells play a crucial role in the pathogenesis of chronic inflammatory diseases, such as rheumatoid arthritis. Chromosome Number 6 DR1 are associated with rheumatoid arthritis, and while not the strongest association with the highest risk for early onset arthritis is within the DR4 bearing native American population. There frequency of DR4-DQ8 haplotypes reach extreme nodal levels. Arthritis has been identified in a precolumbian remains from Italy, the affected individual bearing the DRB1*0101 allele.[25] DRB1*0101 and most DR4 have in common a 'shared epitope'.[26][27] In this hypothesis a common region of the beta chain, positions 67 to 74, are common and may be integral to presenting auto-immunological peptides. By serotype - chromosome 6 other measurement DR4 is associated with extraarticular[2] rheumatoid arthritis[3] hydralazine-induced female systemic lupus erythematosus[4] pemphigoid gestationis[5] phemphigus foliaceus[6] obstructive hypertrophic cardiomyopathy[7] IgA nephropathy[8] 'shared syndrome'-systemic sclerosis/rheumatoid arthritis[9] and polymyalgia rheumatica.[10] By allele DRB1*04 is associated with increased risk for alopecia areata.[11] DRB1*04:01 is associated with multiple sclerosis,[12] rheumatoid arthritis,[13] type 1 diabetes,[14][15] lyme disease induced arthritis[16] DRB1*04:02: drug-triggered[17]/idiopathic pemphigus vulgaris,[18][19] type 1 diabetes,[15] SLE associated anti-cardiolipin and anti-ß2 glycoprotein I[20] DRB1*04:03: polycystic ovary syndrome,[21] SLE associated anti-cardiolipin and anti-ß2 glycoprotein I[22] DRB1*04:04: anti-citrullinated fibrinogen[23] in rheumatoid arthritis,[13] autoimmune hepatitis[24] DRB1*04:05: rheumatoid arthritis,[25] Autoimmune hepatitis,[26] type 1 diabetes[14][15] DRB1*04:06: caspase-8 autoantibodies silicosis-systemic sclerosis (SSc)-systemic lupus erythematosus (SLE)[27] DRB1*04:09: T. cruzi infection with cardiomyopathy[28] By haplotype DR4-DQ8 is a risk factor for papillary thyroid carcinoma,[29] juvenile diabetes, coeliac disease and rheumatoid arthritis.[30] DRB1*04:DQA1*03:03-DQB1*04:01 haplotype: type III autoimmune polyglandular syndrome,[31] autoimmune hepatitis,[32] autoimmune pancreatitis[33] DRB1*04:DQA1*03-DQB1*03:02 haplotype: Type 1 diabetes[34][35] with DRB1*04:01, *04:05, *04:02 increasing risk when DQ8 is present.[36] By genotype DRB1*01:01/*04:04 and *01:01/*04:01 increases risk of mortality in rheumatoid arthritis, with eschemic heart disease and smoking.[37] these same genotypes are associated with rheumatoid vasculitis.[38] |
A trait is any gene-determined characteristic and is often determined by more than one gene. Some traits are caused by abnormal genes that are inherited or that are the result of a new mutation.
Genes make up less than 2% of human DNA; the remaining DNA (mostly Bacterial DNA) has important but still largely unknown functions.
Of the 2%, Genetic Birth Defect may account for less than 5%, if you weren't born with RA than you can not owe it to genetics solely; and behavior may have contributed to it but again it is not the root cause. |
Infection in Rheumatoid Arthritis and Antigen-Specific Immunotherapy (Chris Chalk, 2017)
There is no single gene which is the cause of RA. There have been major advances in the last years in terms of understanding the genetic factors which predispose to RA. Many of these have come from whole genome scans in large cohorts of people with RA.
More than 10 genes have now been identified and work is currently in progress to establish exactly what these genes do and how they interact with one another and environmental factors. Similarly, there is no single environmental factor which is sufficient, by itself, to cause RA.
There are three stages in the course of RA in which genetic or environmental factors may play a part. The first is the time leading up to the onset of RA. Factors which act during this time are called susceptibility genes or environmental risk factors. It is only these factors which can be thought of as truly contributing to the cause of RA. The next phase, which takes three to twelve months is termed the persistence phase. Many people who develop joint inflammation after, for example a viral infection, get better within a few weeks. In other people the arthritis persists and develops into RA. Various genetic and environmental factors influence whether arthritis becomes persistent. Finally there is the chronic phase of RA. In this stage genetic or environmental factors (including treatment) may influence the severity of the disease. It is very important to distinguish in which of the three phases of RA any particular gene or environmental factor plays a part. Only then can we know what the likely outcome would be of removing or modifying this particular factor. For example, if eating plums was a risk factor for developing RA (it isn't as far as we know!) but had no effect on the severity of the disease once RA had developed, then there would be no point in advising people who had RA to stop eating plums. There might, however, be some merit in advising the non-affected member of an identical twin pair to stop eating plums in order to try and prevent the development of RA.
Genome editing (also called gene editing) is a group of technologies that give scientists the ability to change an organism's DNA. These technologies allow genetic material to be added, removed, or altered at particular locations in the genome. Several approaches to genome editing have been developed. A recent one is known as CRISPR-Cas9, which is short for clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. The CRISPR-Cas9 system has generated a lot of excitement in the scientific community because it is faster, cheaper, more accurate, and more efficient than other existing genome editing methods. Scientists are still working to determine whether this approach is safe and effective for use in people.(1)
There is no single gene which is the cause of RA. There have been major advances in the last years in terms of understanding the genetic factors which predispose to RA. Many of these have come from whole genome scans in large cohorts of people with RA.
More than 10 genes have now been identified and work is currently in progress to establish exactly what these genes do and how they interact with one another and environmental factors. Similarly, there is no single environmental factor which is sufficient, by itself, to cause RA.
There are three stages in the course of RA in which genetic or environmental factors may play a part. The first is the time leading up to the onset of RA. Factors which act during this time are called susceptibility genes or environmental risk factors. It is only these factors which can be thought of as truly contributing to the cause of RA. The next phase, which takes three to twelve months is termed the persistence phase. Many people who develop joint inflammation after, for example a viral infection, get better within a few weeks. In other people the arthritis persists and develops into RA. Various genetic and environmental factors influence whether arthritis becomes persistent. Finally there is the chronic phase of RA. In this stage genetic or environmental factors (including treatment) may influence the severity of the disease. It is very important to distinguish in which of the three phases of RA any particular gene or environmental factor plays a part. Only then can we know what the likely outcome would be of removing or modifying this particular factor. For example, if eating plums was a risk factor for developing RA (it isn't as far as we know!) but had no effect on the severity of the disease once RA had developed, then there would be no point in advising people who had RA to stop eating plums. There might, however, be some merit in advising the non-affected member of an identical twin pair to stop eating plums in order to try and prevent the development of RA.
Genome editing (also called gene editing) is a group of technologies that give scientists the ability to change an organism's DNA. These technologies allow genetic material to be added, removed, or altered at particular locations in the genome. Several approaches to genome editing have been developed. A recent one is known as CRISPR-Cas9, which is short for clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. The CRISPR-Cas9 system has generated a lot of excitement in the scientific community because it is faster, cheaper, more accurate, and more efficient than other existing genome editing methods. Scientists are still working to determine whether this approach is safe and effective for use in people.(1)
Dirty Genes
https://www.amazon.ca/dp/0062698141/ref=as_li_ss_tl... Dirty Genes: A Breakthrough Program to Treat the Root Cause of Illness and Optimize Your Health After suffering for years with unexplainable health issues, Dr. Ben Lynch discovered the root cause—“dirty” genes. Genes can be “born dirty” or merely “act dirty” in response to your environment, diet, or lifestyle—causing lifelong, life-threatening, and chronic health problems, including cardiovascular disease, autoimmune disorders, anxiety, depression, digestive issues, obesity, cancer, and diabetes. |
CRISPR in Context: The New World of Human Genetic Engineering
In 2012,
Emmanuelle Charpentier and Jennifer Doudna discovered they could hijack a mechanism that bacteria use to protect themselves from viruses with a piece of RNA acting as a guide and a protein called Cas9 acting as the scissors. Scientists can now target, remove, and replace any stretch of the double-stranded DNA molecule in any living thing, easy, quick, inexpensive, and so precise, scientists can switch out a single base pair in the more than three billion base pairs that make up the human genome. They received the 2020 Nobel Prize in Chemistry.
CRISPR in Context: The New World of Human Genetic Engineering
https://www.youtube.com/watch?v=RNRZchHaKgw
Emmanuelle Charpentier and Jennifer Doudna discovered they could hijack a mechanism that bacteria use to protect themselves from viruses with a piece of RNA acting as a guide and a protein called Cas9 acting as the scissors. Scientists can now target, remove, and replace any stretch of the double-stranded DNA molecule in any living thing, easy, quick, inexpensive, and so precise, scientists can switch out a single base pair in the more than three billion base pairs that make up the human genome. They received the 2020 Nobel Prize in Chemistry.
CRISPR in Context: The New World of Human Genetic Engineering
https://www.youtube.com/watch?v=RNRZchHaKgw
NOTES:
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The pathogenesis of
rheumatoid arthritis IB McInnes, G Schett - New England Journal of Medicine, 2011 - Mass Medical Soc Conclusions Severe disease manifestations, such as vasculitis, nodule formation, scleritis, and amyloidosis, that are associated with persistent, uncontrolled inflammation have become rare. A rich pipeline of biologic and small-molecule agents, and of potential clinical biomarkers, exists that will add to our therapeutic armamentarium. In time, this should render remission achievable in increasing numbers of patients. However, much remains to be resolved. We need to understand the factors that lead to loss of tolerance and that cause localization of inflammation in the joint. We need to find ways to promote immunologic resolution or homeostasis and repair of damaged joints. We must elucidate the mechanisms driving the various systemic disorders that contribute substantially to reductions in the quality and length of life. Ultimately, we must strive to develop curative and preventive therapeutics that will transform the notion of rheumatoid arthritis as a chronic disease. |
The pathogenesis of rheumatoid arthritis - IB McInnes, G Schett - New England Journal of Medicine, 2011 - Mass Medical Soc [PDF] wustl.edu
A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis. Nat Immunol. 2019 Feb;20(2):141-151.
Association of the PD‐1.3A allele of the PDCD1 gene in patients with rheumatoid arthritis negative for rheumatoid factor and the shared epitope The main finding in the present study is that the functionally important polymorphism in the PDCD1 gene is associated with a subset of RA. Because the polymorphism in this gene has previously been shown to be associated with SLE (8), these new data provide some of the first evidence at the gene level of common genetically defined mechanisms being involved in RA and SLE. https://onlinelibrary.wiley.com/doi/full/10.1002/art.20280
Americans have sequenced human DNA to discover they have twenty six thousand genes . A few years later they sequenced the genome of rice to discover it has fifty thousand genes. The more a living creature evolves more genes it has this simply proves that rice is more evolved than humans.
PTPN22 |
Association between the PTPN22 gene and rheumatoid arthritis and juvenile idiopathic arthritis in a UK population: further support that PTPN22 is an autoimmunity gene (1).
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IL
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Interleukins (ILs) are a group of cytokines (secreted proteins and signal molecules) that were first seen to be expressed by white blood cells (leukocytes). ILs can be divided into four major groups based on distinguishing structural features. However, their amino acid sequence similarity is rather weak (typically 15–25% identity). The human genome encodes more than 50 interleukins and related proteins.[1]
The function of the immune system depends in a large part on interleukins, and rare deficiencies of a number of them have been described, all featuring autoimmune diseases or immune deficiency. The majority of interleukins are synthesized by helper CD4 T lymphocytes, as well as through monocytes, macrophages, and endothelial cells. They promote the development and differentiation of T and B lymphocytes, and hematopoietic cells. Interleukin receptors on astrocytes in the hippocampus are also known to be involved in the development of spatial memories in mice.[2] |
IL (Interleukin Factors) |
IL-1a/b: Macrophages and B cells [TH1]:
Lymphocyte activation Macrophage stimulation Leukocyte adhesion Acute Phase Protein IL-2: T: Cells T Cell proliferation and differentiation IL-3: T Cell: Multi-lineage colony stimulation factor IL-4: TH2: B- Cell Growth Isotype Switching IgE (Basophils-Anaphylaxis) IgG IL-5: TH2: B-Cell Growth, IgA, Eosinophils (Allergic Diseases) Il-6: T and B Cells: B Cell differentiation, Acute Phase Protein IL-7: Bone Marrow: B and T Cell Proliferation from pre- B and T Cells IL-8: Monocytes: to Neutrophil, basophil, and T cell NEUTROPHIL RECRUITMENT chemotaxis angiogenensis Superoxide release Granule Release IL-9: T Cells: Enhance T cell survival, Mast cell activation, Synergy with erythropoietin IL-10: TH2 and Treg: Inhibition of cytokine synthesis in TH1, IL-11: Osteoclast formation, Colony stimulation, Pro-inflammatory cytokine production IL-13: TH2: Isotype Switching, Fibrosis, M2 activation, Mucus production IL-12: APC [Macrophages]: ACTIVATE TH1 Cells IL-14: TH1: Stimulation of B cells, Inhibit Ig secretion, IL-15: Monocytes: T Cell proliferation IL-17: TH17 Promote IL-8 (Neutrophil recruitment) IL-21: TH17 and THfh: B CELL ACTIVATION IL-23: Macrophages: TH17 cells IL-22: TH17 proliferation TGFa: Increase T cell response TGFb: TH2 and Treg: Inhibition of T and B Cells, Increase collagen synthesis TF: NFkB TH1 proliferation IFNy: APC: ACTIVATION OF TH1 FROM NK CELLS Product of TH1 (Intracellular) Activation of Macrophages IgG TNF IL-1 IL-12 (Positive FB) TNF: Product of TH1 |
What induces TH1 Development?
IL-12 from DC IFNy from NK Cells T-bet What induces TH2 Development? From CD4: IL-4 GATA-3 What induces TH17 Development? From DC: IL-1 IL-6 IL-23 TGF-B |
P-coumaric acid
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P-coumaric acid controls your detoxification pathways.
We use it. Bees use it. All animals use it. But bees only have 56 genes, or 47 genes for coding for p-coumaric acid -- for cytochrome p450s that are controlled by p-coumaric acid. So basically without the fungi, you don't have p-coumaric acid, the genes are turned off. So the bees are dependent upon these fungal compounds that are in decomposing wood for their detoxification pathways. When you remove the wood, their detoxification pathways are turned off, there is a hyper-accumulation of toxins -- fungicides, herbicides, insecticides, etc. The bees develop malaise, they are not able to take care of themselves as well. Mites carry viruses 14:16 sec., Paul Stamets - Report from the Underground | Bioneers https://www.youtube.com/watch?v=DAw_Zzge49c |
Sequencing of Chloroplast Genomes from Wheat, Barley, Rye and Their Relatives Provides a Detailed Insight into the Evolution of the Triticeae Tribe
Christopher P. Middleton, et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3948623/
Christopher P. Middleton, et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3948623/
We estimate that barley diverged from rye and wheat approximately 8–9 million years ago (MYA). The genome donors of hexaploid wheat diverged between 2.1–2.9 MYA, while rye diverged from Triticum aestivum approximately 3–4 MYA, more recently than previously estimated. Interestingly, the A genome taxa T. boeoticum and T. urartu were estimated to have diverged approximately 570,000 years ago.
Blood Type Biochemistry and Human Disease by D Rose Ewald and Susan CJ Sumner, 2017
Associations between blood type and disease have been studied since the early 1900s when researchers determined that antibodies and antigens are inherited. In the 1950s, the chemical identification of the carbohydrate structure of surface antigens led to the understanding of biosynthetic pathways. The blood type is defined by oligosaccharide structures, which are specific to the antigens, thus, blood group antigens are secondary gene products, while the primary gene products are various glycosyltransferase enzymes that attach the sugar molecules to the oligosaccharide chain. Blood group antigens are found on red blood cells, platelets, leukocytes, plasma proteins, certain tissues, and various cell surface enzymes, and also exist in soluble form in body secretions such as breast milk, seminal fluid, saliva, sweat, gastric secretions, urine, and amniotic fluid. Recent advances in technology, biochemistry, and genetics have clarified the functional classifications of human blood group antigens, the structure of the A, B, H, and Lewis determinants and the enzymes that produce them, and the association of blood group antigens with disease risks. Further research to identify differences in the biochemical composition of blood group antigens, and the relationship to risks for disease, can be important for the identification of targets for the development of nutritional intervention strategies, or the identification of druggable targets.
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Theory of a possible link between testosterone and Autism
28:35
autism we looked at the relationship between typical sex differences in autism because what is amiss more common in boys so we were trying to understand why why why why does being a boy lead you to a higher likelihood that you'll develop autism and the answer we're getting is that one factor may be prenatal testosterone 32:15 today testosterone replacement therapy has become popular among older men in some advertisements it's touted as a miracle cure much as Braun Sekhar claimed more than a century ago pharmacies doctors and drug companies make a lot of money selling testosterone preparations sales have increased sharply since 2007 |
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LOSS of EYE Sight (Genetics, Luxturna)
IRDs: Progressive deterioration of Rod or Cones depending upon the disease
RPE65 is one of more than 260 genes that could be responsible for a patients IRD
RPE cells are essential for the critical process that converts light into electrical impulses sent to the brain to create sight
Mutations in the RPE gene lead to vision loss due to the "loss of function" or "death" of the RPE cells and eventual degeneration of the photo receptors
AMD: Age Related Macular Degeneration -
IDYOURIRD program is not for the diagnosis of patients with, or suspected of having, AMD. There appears to be both a genetic component (people with a family history are at higher risk) and environmental component (smoking may double the risk) to AMD
RPE65 is one of more than 260 genes that could be responsible for a patients IRD
RPE cells are essential for the critical process that converts light into electrical impulses sent to the brain to create sight
Mutations in the RPE gene lead to vision loss due to the "loss of function" or "death" of the RPE cells and eventual degeneration of the photo receptors
AMD: Age Related Macular Degeneration -
IDYOURIRD program is not for the diagnosis of patients with, or suspected of having, AMD. There appears to be both a genetic component (people with a family history are at higher risk) and environmental component (smoking may double the risk) to AMD
SAN FRANCISCO, June 12, 2019 /PRNewswire/ -- Invitae (NYSE: NVTA), a leading medical genetics company, today announced the launch of ID YOUR IRD, an initiative with Spark Therapeutics to offer genetic testing at no charge to patients suspected by their healthcare providers of having an inherited retinal disease (IRD), a group of rare, progressive eye disorders that may result in vision loss or blindness and are caused by inherited genetic changes."
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DNA Ancestry Test
Twins get 'mystifying' DNA ancestry test results (Marketplace)
https://www.youtube.com/watch?v=Isa5c1p6aC0 The most certain thing they can tell you is which continent you're from, the rest is an estimate although MyHeritage gave the closest results; Ancestry DNA and Family Tree are pretty consistent too. What did you think of your results? Take our Marketplace poll on Facebook. |
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Technology Futurist, Geopolitics Expert, Sci-Fi Novelist (jamiemetzl.com)
WHO calls for global gene editing research registry as ...https://newatlas.com › gene-editing-moratorium-who-global-registry › 58993
Following on from a recent call for a global moratorium on human germline gene editing, several scientists have pushed back against the idea, suggesting blanket prohibition is both redundant and ...Global Gene Editing Regulation Tracker and Indexhttps://crispr-gene-editing-regs-tracker.geneticliteracyproject.org
Gene editing of the human embryo or germline that results in genetic changes that are passed down to the next generation. This type of gene editing is the most controversial because changes are inherited and because it could theoretically be used to create "designer babies".
Following on from a recent call for a global moratorium on human germline gene editing, several scientists have pushed back against the idea, suggesting blanket prohibition is both redundant and ...Global Gene Editing Regulation Tracker and Indexhttps://crispr-gene-editing-regs-tracker.geneticliteracyproject.org
Gene editing of the human embryo or germline that results in genetic changes that are passed down to the next generation. This type of gene editing is the most controversial because changes are inherited and because it could theoretically be used to create "designer babies".
Genetic Engineering
- The ability to move genetic material (genes) from one organism to another
- Transgenic pigs produce human Factor VIII, a blood-clotting agent needed by hemophiliacs
- Transgenic_pigs_produce_functional_human20160224-10644-1kq56lz.
- pdf (d1wqtxts1xzle7.cloudfront.net)The-Generation-of-Transgenic-Pigs-as-Potential-Organ-Donors-for-Humans.pdf (researchgate.net)
Science says to legalize transgenic human embryos worldwidetechnology24.blogspot.com/2015/09/science-says-to-legalize-transgenic.html
A group of British biomedical organizations including the Medical Research Council and the Wellcome Trust (the largest philanthropic group in the UK) has issued a joint statement calling for the legalization of genetically modifying human embryos. The aim is the use of a technique of genetic edition (known as CRISPR-Cas9) that could eliminate certain inherited diseases.
Currently it is not legal altered germ cell genes as eggs, sperm and embryos for ethical reasons, although their potential clinical benefits could reverse this situation, starting a path that could lead to the introduction of the first genetically modified embryo in a womb.
The undersigned organizations argue that it is possible to see that the CRISPR-Cas9 technique is safe enough for use in human embryos and stem cells; in this way it would ensure that inherited diseases are not transmitted from generation to generation.
"We believe that genome editing techniques can have a significant potential for clinical application in the future, and would be open to support the development of new therapeutic approaches if enough research evidence to justify moving," says the joint statement. The CRISPR-Cas9 is a simple and effective technique to edit genomes eliminating germline mutations and hereditary defects that are behind 6,000 single-gene diseases; biomedical organizations have put on the agenda the debate on the relevance and need for its use, which would open unexpected paths in the history of medicine.
Currently it is not legal altered germ cell genes as eggs, sperm and embryos for ethical reasons, although their potential clinical benefits could reverse this situation, starting a path that could lead to the introduction of the first genetically modified embryo in a womb.
The undersigned organizations argue that it is possible to see that the CRISPR-Cas9 technique is safe enough for use in human embryos and stem cells; in this way it would ensure that inherited diseases are not transmitted from generation to generation.
"We believe that genome editing techniques can have a significant potential for clinical application in the future, and would be open to support the development of new therapeutic approaches if enough research evidence to justify moving," says the joint statement. The CRISPR-Cas9 is a simple and effective technique to edit genomes eliminating germline mutations and hereditary defects that are behind 6,000 single-gene diseases; biomedical organizations have put on the agenda the debate on the relevance and need for its use, which would open unexpected paths in the history of medicine.
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It's Alive, But Is It Life: Synthetic Biology and the Future of Creation https://www.youtube.com/watch?v=rU_pfCtSWF4 For decades, biologists have read and edited DNA, the code of life. Revolutionary developments are giving scientists the power to write it. Instead of tinkering with existing life forms, synthetic biologists may be on the verge of writing the DNA of a living organism from scratch. In the next decade, according to some, we may even see the first synthetic human genome. Join a distinguished group of synthetic biologists, geneticists and bioengineers who are edging closer to breathing life into matter. This program is part of the Big Ideas Series, made possible with support from the John Templeton Foundation. Original Program Date: June 4, 2016
106:56 into video "Making a virus with pandemic potential and releasing it into the environment...THEY ACTUALLY DID MAKE A POLIO VIRUS AND PUBLISHED IT..." |
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How They Caught, The Golden State Killer
https://www.youtube.com/watch?v=KT18KJouHWg Your genetic code is probably already in a database, without you ever giving a sample or permission. References: 1. Phillips, C. (2018). The Golden State Killer investigation and the nascent field of forensic genealogy. Forensic Science International: Genetics, 36, 186-188. -- https://ve42.co/Phillips2018 2. Guerrini, C. J., Robinson, J. O., Petersen, D., & McGuire, A. L. (2018). Should police have access to genetic genealogy databases? Capturing the Golden State Killer and other criminals using a controversial new forensic technique. PLoS biology, 16(10), e2006906. -- https://ve42.co/Guerrini 3. Ram, N., Guerrini, C. J., & McGuire, A. L. (2018). Genealogy databases and the future of criminal investigation. Science, 360(6393), 1078-1079. -- https://ve42.co/Ram2019 |
AntiTourette's
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