Since
1989
FOUNDER OF MIT - ACADEMY OF FUNCTIONAL MEDICINE & INTEGRATIVE THERAPIES -
Founder of Cryptostain® Microbiology/Microscopy Research
Senior Doctor Spinal Trauma Care Unit USAC Hospital CCHN: 006582/DNA-CCHN Director of M.BS Doctoral Studies USAC University Hospital Saigon VietnamSubsidiary/Affiliate Hospital - Ministry of National Defence Vietnam
COLLEGE OF MEDICAL EVANGELISTS (CME)
LOMA LINDA UNIVERSITY
SCHOOL OF MEDICINE
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WHO Global Report - 2014 - 2023
Alternative Medicine
Strategy - COVID 19
The United Nations Department of
Economic and Social Affairs (DESA)
World Health Organisation
Charter Resolution Decision 115620 20-6-30
The Open University of Complimentary Medicine
(ALMA ALTA) FACULTY OF MEDICAL STUDIES MEDICINA ALTERNATIVA INSTITUTE. (Rhodes)
PhD Lic. 98.4475 c. D.Sc Lic. 2000. 1212 R.
MEDICAL RESEARCH AUSTRALIA
Therapeutic Goods Agency
Schedule 1 defined as Subregulation 4 (2)
regulations of the Therapeutic Goods Act 1989.
Reg No: Y2550431 Item no: 142. Bona Fide Therapeutic Goods (TGA) Schedule 1 Research Association, (RIDDP) Statutory Rules 1990 NO 394
British Council of Complimentary Therapies
Licence Reg; 184/1904/2152/ MITBCCT/ 2000-2021.
Current Member - Directory of Practitioners
Study 1.
We aimed to investigate whether frequency of Ozone Sauna Bathing is associated with the levels of serum C-reactive protein. C-reactive protein is a leading blood marker of systemic inflammation. All medical researchers are complacent and in uni-some that all disease activates through PGe1 and PGe3 endogenous hormone inflammatory biochemistry pathways
The study consisted of 2084 men (42–60 years) without acute or chronic
inflammation.
A total of 533 (25.6%), 1368 (65.6%), and 183 (8.8%) participants
reported having a sauna bath once a week, 2–3 times, and 4–7 times per week; mean
serum C-reactive protein levels were 2.41 (standard deviation 2.91), 2.00 (2.41), 1.65
(1.63) mmol/L, respectively.
In a multivariable analysis adjusted for baseline age, body
mass index, systolic blood pressure, smoking, type 2 diabetes, previous myocardial
infarction, and serum low density lipoprotein cholesterol, alcohol consumption and
physical activity, there was a significant inverse association between the frequency of
sauna bathing and the level of C-reactive protein. Further studies are warranted to
investigate the relationship between sauna bathing and systemic inflammation.
1Department of Medical Biochemistry (Firat Hormones Reseach Group), Firat University, Elazig, Turkey 2Department of Internal Medicine (Endocrine and Metabolic Disease), Firat University, Elazig-Turkey *Corresponding author: Suleyman Aydin, Faculty of Medicine, Department of Medical Biochemistry (Firat Hormones Reseach Group), Firat University, Elazig, Turkey, Tel: 90 5334934643; E-mail: saydin1@hotmail.com Received date: 08 November 2017; Accepted date: 09 November 2017; Published date: 16 November 2017 Copyright: © 2017 Suleyman A, et al.
Ayadin S, Aksoy K, Yardim M. May Heat Releasing Metabolic Hormones (Progesterone) Play Role on the Thermotherapy of Cancer in the Future? Endocrinol Res Metab. 2017, 1:2.
Study 2
Macrophage Polarization in Inflammatory Diseases
Yan-Cun Liu 1*, Xian-Biao Zou 2*, Yan-Fen Chai 1, and Yong-Ming Yao 2,3
1. Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin 300052, P.R.China;
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2. Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing 100048, P.R.China;
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3. State Key Laboratory of Kidney Disease, the Chinese PLA General Hospital, Beijing 100853, P.R.China. * contributed equally to the study.
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Diversity and plasticity are two hallmarks of macrophages. M1 macrophages (classically activated macrophages)are pro-inflammatory and have a central role in host defense against
infection, while M2 macrophages (alternatively activated macrophages)are associated with responses to anti-inflammatory reactions and tissue remodeling,and they represent two terminals of the full spectrum of macrophage activation.
Transformation of different phenotypes of macrophages regulates the initiation, development,and cessation of inflammatory diseases. Here we reviewed the characters and functions of macrophage polarization in infection, atherosclerosis,obesity,tumor,asthma,and sepsis,and proposed that targeting macrophage polarization and skewing their phenotype to adapt to the microenvironment might hold great promise for the treatment of inflammatory diseases.
Macrophages were first identified by Elie Metchnikoff as phagocytic cells which helped to
eliminate pathogens in both invertebrates and vertebrates.
In 1905,his research findings suggested that macrophages from infected animals had elevated ability of killing bacteria, thereby proposing the basis of the concept of macrophage activation [1]. After six decades of efforts, the mechanisms with regard to killing bacteria of macrophages were gradually elucidated,but there were still no definite answers about how macrophages became more efficient bacterial killers. In 1973, North and his colleagues found that independent cellular factors could also promote resistance of infection without involvement of pathogens[2]. Almost at the same time, David indicated that lymphocytes were the major antigen-specific cells responsible for microbicidal activation of macrophages [3]. Soon after that, interferon (IFN)-γ, produced by lymphocytes, was identified as the first factor for interaction between macrophages and lymphocytes [4]. It transforms resting macrophages into active ones which have stronger antigen presenting capacity and complement mediated phagocytosis,and secrete more pro-inflammatory cytokines as well as toxic mediators.
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As the first type of antimicrobial macrophage activation was recognized,it became known as classically activated macrophages(CAM,also known as M1).
In 1989, when the heterogeneity in the helper T-cell compartment was subsequently reported, Mosrnann and Coffman reviewed the different functions and lymphokines secretion between two types of cloned helper Tcells(Th),and proposed the concept of Th1 and Th2[5]. One year later,Abramson and his
Infection by Various Pathogens
Bacteria
When tissues are challenged by pathogens, inflammatory monocytes in circulation are recruited and differentiated into macrophages, which keep a homeostatic status with the resident macrophages in the affected tissues. Generally,macrophages are deliberated to be polarized toward an M1 phenotype in the early stage of bacterial infection. When the pathogen associated molecular patterns (PAMPs) presented in bacteria are recognized by pathogen recognition receptors(such
as Toll-like receptors,TLRs),macrophages are activated and produce a large amount of pro-inflammatory mediators including TNF-α, IL-1, and nitric oxide (NO), which kill the invading organisms and activate the adaptive immunity[11].
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This mechanism has been considered to be involved in infection with Salmonella typhi, Salmonella typhimurium, Listeria monocytogenes [21], and the early phases of infection with Mycobacterium tuberculosis,Mycobacterium ulcerans, and Mycobacterium avium [22]. If macrophage-mediated inflammatory response cannot be quickly controlled, a cytokine storm is formed, thereby contributing to the pathogenesis of severe sepsis [23]. In order to counteract the excessive inflammatory response,macrophages undergo apoptosisor polarize to an M2 phenotype to protect the host from excessive injury and facilitate wound healing[24].For example,microarray analysis and transcriptional profiling of peripheral blood cells showed that typical M1 genes and M1-related genes were replaced by M2 signature during treatment or convalescence in patients with typhoid fever[25].
LPS,large molecules in the outer membrane of gram-negative bbacteria,play a critical pro-inflammatory role in acute infections. As the infection persists,host may present a LPS-tolerant state, and macrophages are polarized to M2 phenotype. A recent study has confirmed that the p50 subunit of NF-κB served as the key regulator of M2-driven LPS-tolerant state in this transformation[26]. As the excessive injury is reduced, however, M2 phenotype macrophages also induce an immunosuppressive state, resulting in a more susceptible situation to re-infection, thus relapse may occur or a carrier state maybe found.
Virus
Macrophage polarization is also involved in virus infection, and M2 phenotype macrophages can suppress inflammation and promote tissue healing. Influenza virus augments the phagocytic function of human macrophages, which is a major feature of M2 phenotype, to clear the apoptotic cells and accelerate the resolution of inflammation [27]. In severe acute respiratory syndrome (SARS)-Cov infection, M2 phenotype macrophages are critical to regulate immune response and protect host from the long term progression to fibrotic lung disease by a STAT dependent pathway[28].In addition,severe respiratory syncytial virus(RSV)induced
bronchiolitis is closely associated with mixed M1 and M2 macrophages[29]. IL-4-STAT6 dependent M2 macrophage polarization can attenuate inflammation and epithelial damage,
