Dr Simon Raymond,
Consultant, Alumnus, Melbourne University, Parkville, VIC, 3010, Australia
© 2019 Sift Desk Journals. All Rights Reserved
VOLUME: 1 ISSUE: 2
Page No: 86-89
Dr Simon Raymond,
Consultant, Alumnus, Melbourne University, Parkville, VIC, 3010, Australia
Dr Simon Raymond MD
Alumnus of Melbourne University, Australia
Dr Simon Raymond, Site Attachment Inhibition Therapeutics: A New Mode of Action Pathway for Antimicrobial Therapy (2017)SDRP Journal of Computational Chemistry & Molecular Modelling 1(2)
The concern with respect to antimicrobial resistance and the associated health threat has gained increasing attention and there has been difficulty in gaining traction globally. Given the lack of success by the two pathways established to date which have focused on: 1) “replication of infective agent” and, 2) “immune system enhancement," the current researcher has conceptualized and developed the new, or third, mode of action pathway represented by “site attachment inhibition (or, negation of cellular attachment by infective agents).” The current author anticipates site attachment inhibition therapeutics to include drug (medication) based therapies, stem cell based treatment (including prenatal and earlier) incorporating new generation immunization methods, and waveform (E.g. electromagnetic radiation) based treatment. With respect to viruses, support for the likely success of the new mode of action pathway: A) the known CCR5-?32 mutation achieves resistance (immunity) against HIV through negation of cellular attachment; B) other areas of medicine use analogous receptor antagonism (E.g. beta blocker therapy); C) advanced IT uses analogous site attachment inhibition to remove viruses. With respect to bacteria, support for the likely success of the new mode of action pathway: A) advanced IT uses analogous site attachment inhibition to remove IT infections; B) glycoproteins are key receptors for attachment and, analogous to glycoprotein IIb/IIIa medications which inhibit (negate) platelet aggregation and thrombus formation, it seems reasonable to pursue antagonism or blockade of other glycoprotein receptors in order to prevent bacterial attachment to human cells (note: this is also relevant to viral infections); C) the human immune system coats infective agents in an attempt to negate cellular attachment, therefore this mode of action represented by site attachment inhibition makes scientific sense.
Attention must be directed toward correctly identifying the target receptors and appreciating the difference between association and causation. Looking at mutations noticed in the human population and connecting this to the innate resistance they possess to certain infections is not enough as this may simply represent association as opposed to causation. Even the known CCR5-?32 mutation has not been completely confirmed as direct/causative of the inhibition of attachment observed in research analyses.
There is direct relevance to cancer, including breast cancer. Examples include: (A) the vaccine (immunization) against HPV used for prevention of cervical cancer; (B) tamoxifen used, through antagonism (or, blockade), of estrogen in preventing further issues relating to breast cancer development (or, metastatic spread).
Future research by the current author will likely include delineation of the application of quantum physics to medicine and surgery, starting with neurology and immunology, and in what circumstances this is appropriate. In addition, the merger between fields including immunology, neurology, IT, and advanced physics (quantum physics) that appears likely to commence. Furthermore, detailed delineation of new generation immunization methods to be developed based on site attachment inhibition, briefly detailed by the author in previous reports, including by way of stem cell therapy at the prenatal stage or earlier, of which evidence in support of the likely potential for success being that of the above mentioned CCR5-?32 mutation (with association and causation issues being taken into account). In addition, the details regarding the unique new mode of action pathway - site attachment inhibition - with the only previous related research (or, minority research) more focused on aspects such as masking foreign entity identification and related methods.
It is also likely that the current researcher will further explore and delineate the relationship between memes, mind viruses, IT viruses and biological viruses.
Ethics committee and community consideration remain important.
In conclusion, this paper presents the new, or third, mode of action pathway in antimicrobial therapy represented by site attachment inhibition therapeutics.
Biographical Notes
Simon Raymond is a graduate of medical school who shifted into high level medical and scientific research. The above stated researcher is a consultant specialising in Medical and Scientific Research and an Alumnus of Melbourne University (Rank of Number 1 in Australia and Number 33 in the World). The above stated Researcher has acted as a Reviewer for the respected Medical Journal of Australia, has received invitations internationally to review from prestigious medical journals including Journal of American Medical Association Network. He has received award in recognition of his research by Royal Australasian College of Surgeons (PSC, 2006) and invited to conferences internationally as an official Delegate and Researcher, including that in USA and China. He has worked as the Principle Researcher in the highest-powered form of medical trial—Randomised Controlled Trial (RCT). The above stated Researcher is also a Member of the Golden Key International Society for Honoured and outstanding Academics. The above stated researcher has research indexed by well respected universities including Harvard university.
The concern with respect to antimicrobial resistance and the associated health threat has gained increasing attention and there has been difficulty in gaining traction globally. Given the lack of success by the two pathways established to date which have focused on: 1) “replication of infective agent” and, 2) “immune system enhancement," the current researcher has conceptualized and developed the new, or third, mode of action pathway represented by “site attachment inhibition (or, negation of cellular attachment by infective agents).” The current author anticipates site attachment inhibition therapeutics to include drug (medication) based therapies, stem cell based treatment (including prenatal and earlier) incorporating new generation immunization methods, and waveform (E.g. electromagnetic radiation) based treatment. With respect to viruses, support for the likely success of the new mode of action pathway: A) the known CCR5-Δ32 mutation achieves resistance (immunity) against HIV through negation of cellular attachment; B) other areas of medicine use analogous receptor antagonism (E.g. beta blocker therapy); C) advanced IT uses analogous site attachment inhibition to remove viruses. With respect to bacteria, support for the likely success of the new mode of action pathway: A) advanced IT uses analogous site attachment inhibition to remove IT infections; B) glycoproteins (or, glycoprotein receptors) represent key sites for attachment and, analogous to glycoprotein IIb/IIIa medications which inhibit (negate) platelet aggregation and thrombus formation, it seems reasonable to pursue antagonism or blockade of other glycoprotein receptors in order to prevent bacterial attachment to human cells (note: this is also relevant to viral infections); C) the human immune system coats infective agents in an attempt to negate cellular attachment, therefore this mode of action represented by site attachment inhibition makes scientific sense.
Attention must be directed toward correctly identifying the target receptors and appreciating the difference between association and causation. Looking at mutations noticed in the human population and connecting this to the innate resistance they possess to certain infections is not enough as this may simply represent association as opposed to causation. Even the known CCR5-Δ32 mutation has not been completely confirmed as direct/causative of the inhibition of attachment observed in research analyses.
There is direct relevance to cancer: Examples include: (A) the vaccine (immunization) against HPV used for prevention of cervical cancer; (B) tamoxifen used, through antagonism (or, blockade), of estrogen in preventing further issues relating to breast cancer development (or, metastatic spread).
FUTURE RESEARCH
NB: Microorganisms may be also be utilizing complex communication methods, including that based on quantum physics, in addition to voltage gated ion channel activity based communications.
(1) Microorganisms in the CNS performing voltage gated ion channel communications, possibly demonstrating consciousness or at least a level of awareness.
(2) An Axis that appear potentially to have been formed (at least in part) by microorganisms from the
intestine(s) through to the pituitary gland (gut-brain axis), and notably the pituitary gland is an area
around which used to be termed historically as the seat of the soul, or mind.
Based on the above, it could be viewed that these two signs (indications) demonstrate the attempted invasion of the mind of the person by another entity, for instance that of the infective microorganisms. The implication of microorganisms in mental illness has been delineated previously by the current author (researcher) in reports listed below in the section titled References.
It is worth considering whether a level of total (or, near total) control could be gained by the microorganisms, causing mental illness at the level of psychosis or insanity. The above is worth further investigating.
In conclusion, this paper presents the new, or third, mode of action pathway in antimicrobial therapy represented by site attachment inhibition therapeutics. This is intended to be applicable to all infective agents including viruses and bacteria. Indications supporting the likely success of site attachment inhibition therapeutics:
With respect to viruses, support for the likely success of the new mode of action pathway: A) the known CCR5-Δ32 mutation achieves resistance (immunity) against HIV through negation of cellular attachment; B) other areas of medicine use analogous receptor antagonism (E.g. beta blocker therapy); C) advanced IT uses analogous site attachment inhibition to remove viruses. With respect to bacteria, support for the likely success of the new mode of action pathway: A) advanced IT uses analogous site attachment inhibition to remove IT infections; B) glycoproteins (or, glycoprotein receptors) represent key sites for attachment and, analogous to glycoprotein IIb/IIIa medications which inhibit (negate) platelet aggregation and thrombus formation, it seems reasonable to pursue antagonism or blockade of other glycoprotein receptors in order to prevent bacterial attachment to human cells (note: this is also relevant to viral infections); C) the human immune system coats infective agents in an attempt to negate cellular attachment, therefore this mode of action represented by site attachment inhibition makes scientific sense.
Attention must be directed toward correctly identifying the target receptors and appreciating the difference between association and causation. Looking at mutations noticed in the human population and connecting this to the innate resistance they possess to certain infections is not enough as this may simply represent association as opposed to causation. Even the known CCR5-Δ32 mutation has not been completely confirmed as direct/causative of the inhibition of attachment observed in research analyses.
The relevance to future cancer treatments is also discussed. In addition, further areas for research by the current author are delineated.
New generation immunization methods based on site attachment inhibition are discussed and have been detailed briefly by the current researcher in previous reports.
Ethics committee and community consideration remain important, especially when dealing with consciousness, awareness, and biological materials.
In conclusion, this manuscript presents the new, or third, mode of action pathway in antimicrobial therapy represented by site attachment inhibition therapeutics.
Raymond, S. (2016) Development of New Strategic Pathways for Antiviral Therapy. J Clin Cell Immunol, 7:5(Suppl),
View ArticleRaymond, S. (2016) Consciousness and the Development of New Strategic Pathways for Antiviral Therapy: A Focused Analysis on HIV. International Journal of Sciences: Basic and Applied Research (IJSBAR), 29(3):146-154.
Raymond, S. (2016) The Development of New Antimicrobial Pathways: Combatting the Threat of Antimicrobial Resistance, International Journal of Sciences: Basic and Applied Research (IJSBAR), 30(2):22-28.
Raymond, S. (2016) Combatting the global threat of antimicrobial resistance and antiviral deficiencies. Imperial Journal of Interdisciplinary Research (IJIR), 3(1):676-680.
Raymond, S. (2016) The role of infectious disease and inflammation in psychiatric illness. Imperial Journal of Interdisciplinary Research (IJIR), 3(1):510-513.