Film, Media & TV0 min ago
Do You Agree That Vivisection For The Development Of New Drugs, Stem Cell Organs, Etc Can Be Regarded As Equivalent To Utilising Animals For Human Needs?
47 Answers
It is submitted that vivisection for the development of new drugs, stem cell organs, etc is equivalent to slaughtering animals for food & for other animal products, using them to do certain tasks and/or as pets, etc.
Specifically bred (or kept alive) animals are kept to achieve specific purposes – like for vivisection, livestock in farming, for sport, working animals. Animals bred for specially for the sole purpose of experimentation, food or work are often kept in less cruel conditions than if those animals were living wild, fending a living for themselves. Animals living wild usually suffer death by disease, hunger, predation, etc. That’s life. Sometimes human civilisation needs are also urgent.
The efficacy of drugs should be grounded on sound biochemical, pharmacological & medical principles, logic, objectivity; tested by controlled drug trails, not on haunches & flawed scientific theories, principles & understanding. Scientific knowledge demands concrete proof & evidence, as well as open to exhaustive learned peer reviews in Scientific Journals, conferences, etc.
Drugs often have side-effects & should not be prescribed indiscriminately on a long-term basis for non-life threatening or innocuous conditions. One of main principles of pharmacology is that drugs can be agonists (enhancers) or antagonists (inhibitors).
Animal farming for food is essential. Likewise, animal vivisection is essential in pharmacological R&D for new drug agonists (enhancers) or antagonist (inhibitors) of specific biochemical metabolic pathways & processes.
Drugs (as analogues & agonists) attached (lock & key fashion) to biological substrates (in cell receptors in membranes, DNA, enzymes, precursor macromolecules, etc) can switch on or off certain biochemical pathways hence providing the desired chemotherapeutic interventions.
Specifically bred (or kept alive) animals are kept to achieve specific purposes – like for vivisection, livestock in farming, for sport, working animals. Animals bred for specially for the sole purpose of experimentation, food or work are often kept in less cruel conditions than if those animals were living wild, fending a living for themselves. Animals living wild usually suffer death by disease, hunger, predation, etc. That’s life. Sometimes human civilisation needs are also urgent.
The efficacy of drugs should be grounded on sound biochemical, pharmacological & medical principles, logic, objectivity; tested by controlled drug trails, not on haunches & flawed scientific theories, principles & understanding. Scientific knowledge demands concrete proof & evidence, as well as open to exhaustive learned peer reviews in Scientific Journals, conferences, etc.
Drugs often have side-effects & should not be prescribed indiscriminately on a long-term basis for non-life threatening or innocuous conditions. One of main principles of pharmacology is that drugs can be agonists (enhancers) or antagonists (inhibitors).
Animal farming for food is essential. Likewise, animal vivisection is essential in pharmacological R&D for new drug agonists (enhancers) or antagonist (inhibitors) of specific biochemical metabolic pathways & processes.
Drugs (as analogues & agonists) attached (lock & key fashion) to biological substrates (in cell receptors in membranes, DNA, enzymes, precursor macromolecules, etc) can switch on or off certain biochemical pathways hence providing the desired chemotherapeutic interventions.
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Peter Pedant stated, “Drugs ... attached ....to biological substrates (in cell receptors in membranes, ...) can switch on or off certain biochemical pathways. OK - care to name one? “
I wrote: 'Drugs (as analogues & agonists) attached (lock & key fashion) to biological substrates (in cell receptors in membranes, DNA, enzymes, precursor macromolecules, etc) can switch on or off certain biochemical pathways hence providing the desired chemotherapeutic interventions'.
Let me explain in more detail from a biochemist’s hat: Cell membranes have receptors that transport metabolites and other macromolecules in and out of cells. Likewise, DNA have sections that act as switches to turn expression of sections (i.e., genes) of DNA ‘on’ or ‘off’.
A CELL HAS ALL THE DNA BUT NOT ALL ARE EXPRESSED (OR SWITCHED ON) ALL THE TIME.
Enzymes are proteins that act as biological catalysts. Protein have binding sites to interact with metabolites/macromolecules, including medicine. Enzymes are involved in biochemical pathways that use precursor metabolites & macromolecules to form further precursors until the resulting products are formed.
All I wrote are in my own words. I take great exception to your rude unfounded speculation that I plagiarise. I do not cull stuff & plagiarise from the net. I write using my own knowledge, perceptions, understanding, take, opinions, sentence of my own. Like most graduates, I do not do plagiarism. Unlike you, I am capable of writing my own articles/dissertations.
I wrote: 'Drugs (as analogues & agonists) attached (lock & key fashion) to biological substrates (in cell receptors in membranes, DNA, enzymes, precursor macromolecules, etc) can switch on or off certain biochemical pathways hence providing the desired chemotherapeutic interventions'.
Let me explain in more detail from a biochemist’s hat: Cell membranes have receptors that transport metabolites and other macromolecules in and out of cells. Likewise, DNA have sections that act as switches to turn expression of sections (i.e., genes) of DNA ‘on’ or ‘off’.
A CELL HAS ALL THE DNA BUT NOT ALL ARE EXPRESSED (OR SWITCHED ON) ALL THE TIME.
Enzymes are proteins that act as biological catalysts. Protein have binding sites to interact with metabolites/macromolecules, including medicine. Enzymes are involved in biochemical pathways that use precursor metabolites & macromolecules to form further precursors until the resulting products are formed.
All I wrote are in my own words. I take great exception to your rude unfounded speculation that I plagiarise. I do not cull stuff & plagiarise from the net. I write using my own knowledge, perceptions, understanding, take, opinions, sentence of my own. Like most graduates, I do not do plagiarism. Unlike you, I am capable of writing my own articles/dissertations.
As to thalidomide - I was working in medical information when this case was at last fully explained. It turned out that when the producers of thalidomide said it had been tested on animals, that wasn't true. When the tests were in fact done - very simple tests on hen's eggs, the teratogenicity was discovered. If these and other ( e.g. mice ) tests had been done before the product was released, the malformations would never have happened. None of them.
Old_Geezer stated, “I'd rather vivisection didn't exist, but when researchers who are clearly more knowledgeable of the issue than I am tell us that for some things there is no substitute then one feels it isn't easy to condemn it”
Suitable animal models (like primates for Alzheimer’s research) are invaluable.
An example of the biochemical complexity involved is the research in finding a treatment/cure for Alzheimer’s disease(AD).
The physiological changes of AD are the deposition in the brain of extracellular spherical amyloid (Aβ) plaques & surrounded by intracellular tau tangles. Aβ plaques & tau tangles are notably found in the cerebral cortex, hippocampus, limbic system & subcortical nuclei of the brains of AD sufferers.
Recently monoclonal antibodies for amyloid plaques or vaccine have been found to clear away amyloid plaques by a third within 6 months in the brains of Alzheimer’s Disease (AD) sufferers in clinical trials.
Such treatment can delay onset of AD by 5 years. Neuroimaging techniques involving positron emission tomography (PET), single photon emission computed tomography (SPECT), structural MRI gamma scanning can detect AD process around 3 years before the clinical onset of cognitive impairment.
Other possible treatment include:
:: Inhibiting Aβ release from parent protein by using compounds like protease inhibitors, estrogen, nerve growth factors, cholesterol lowering drugs, etc.
:: Inhibiting Aβ aggregation by using vaccination, decoy peptides, etc. Decoy peptides (5 to 9 AA chain) had been synthesised that can bind with Aβ plaques, changing β-amyloid into a non-toxic form.
:: Inhibiting the effects of the AD by, for example, using antioxidants and copper/zinc chelators to reduce oxidative stress, anti-inflammatory drug to reduce brain inflammation, and NGF to maintain neurons.
:: Replacing deficient enzymes and other proteins by, for example, using gene therapy or by direct administration.
Suitable animal models (like primates for Alzheimer’s research) are invaluable.
An example of the biochemical complexity involved is the research in finding a treatment/cure for Alzheimer’s disease(AD).
The physiological changes of AD are the deposition in the brain of extracellular spherical amyloid (Aβ) plaques & surrounded by intracellular tau tangles. Aβ plaques & tau tangles are notably found in the cerebral cortex, hippocampus, limbic system & subcortical nuclei of the brains of AD sufferers.
Recently monoclonal antibodies for amyloid plaques or vaccine have been found to clear away amyloid plaques by a third within 6 months in the brains of Alzheimer’s Disease (AD) sufferers in clinical trials.
Such treatment can delay onset of AD by 5 years. Neuroimaging techniques involving positron emission tomography (PET), single photon emission computed tomography (SPECT), structural MRI gamma scanning can detect AD process around 3 years before the clinical onset of cognitive impairment.
Other possible treatment include:
:: Inhibiting Aβ release from parent protein by using compounds like protease inhibitors, estrogen, nerve growth factors, cholesterol lowering drugs, etc.
:: Inhibiting Aβ aggregation by using vaccination, decoy peptides, etc. Decoy peptides (5 to 9 AA chain) had been synthesised that can bind with Aβ plaques, changing β-amyloid into a non-toxic form.
:: Inhibiting the effects of the AD by, for example, using antioxidants and copper/zinc chelators to reduce oxidative stress, anti-inflammatory drug to reduce brain inflammation, and NGF to maintain neurons.
:: Replacing deficient enzymes and other proteins by, for example, using gene therapy or by direct administration.
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