Auto-Immune disorders

This forum is to discuss general things concerning TSOI.
Gnikmj97
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Joined: Sun Jun 28, 2020 4:44 am

Auto-Immune disorders

Post by Gnikmj97 »

Good Afternoon, I'm curious if your Quadramune would be beneficial for use in helping with Psoriasis or Psoriatic Arthritis. My wife takes medication I don't like due to potentially long lasting effects and I would feel much better if I could find an all natural solution. Has TSOI looked into application in this area for Quadramune as an immune regulator?
Gnikmj97
Posts: 5
Joined: Sun Jun 28, 2020 4:44 am

Re: Auto-Immune disorders

Post by Gnikmj97 »

I read in an earlier PR that Quadramune ingredients had some TNF inhibition effects is why I asking about it in regards to Psoriasis. The drug I was equating too in Humira a TNF Blocker. I believe it was the May 5, 2020 Press release.
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TimGDixon
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Re: Auto-Immune disorders

Post by TimGDixon »

Our focus has been the inflammation due to Sars/CoV2 infection (covid-19) and you are correct about not only TNF-a, but IL-6 too. IL-6 is a inflammatory cytokine that is elevated in serum and skin lesions of patients with psoriasis. If you have not, please see this prepublication paper on the inhibition of IL-6, TNF-a. https://therapeuticsolutionsint.com/CV/ ... -01274.pdf

I have an experimental cream that may help. The original development work was done for concrete workers in Mexico. They have dirty cement that contains a compound known as hexavalent chromium that causes the skin barrier disruption. That work has been delayed due to covid-19.

In the meantime a dear friend of mine had been telling me about his son who had retired from the Air Force as a jet aircraft mechanic. He suffers from skin barrier disruption due to prolonged and chronic exposure to jet fuel. I made him this cream and his hands are healing where before they constantly cracked, bled, and never healed. His hands are healing for the first time in several years. Now, he is also on another product we developed called NanoPSA which is a potent activator of Phase II enzymes - my friend's son has free circulating benzenes and aromatic hydrocarbons in his blood stream - the NanoPSA will eliminate it over time. I don't think NanoPSA is indicated here.

I share with you my original research and if you think your wife would be interested in trying it I am willing to prepre a batch custom for her. This is not a product we are currently offering so i would not charge you except for feedback - no promises - but i'm willing if she is.

JP-5, JP-8 Military Jet Fuel

Affected Organ Systems:
Developmental (effects while organs are developing), Hepatic (Liver), Immunological (Immune System), Neurological (Nervous System)

Cancer Classification: EPA: Not evaluated. IARC: Not classifiable as to carcinogenicity to humans. NTP: Not evaluated

Chemical Classification: Hydrocarbons (contain hydrogen and carbon atoms)

Summary: Jet fuels JP-5 and JP-8 are substances used as aircraft fuels by the military. JP-5 and JP-8 is shorthand for jet propellants 5 and 8. JP-5 is the U.S. Navy's primary jet fuel, and JP-8 is one of the jet fuels used by the U.S. Air Force. Both of the substances are composed of a large number of chemicals, and both are colorless liquids that may change into gas vapor. They smell like kerosene, since kerosene is the primary component of both JP-5 and JP-8. They are made by refining either crude petroleum oil deposits found underground or shale oil found in rock.

Applying jet fuel (JP-8) to the skin of mice has been shown to induce immune suppression. JP-8–treated keratinocytes secrete prostaglandin E2, which is essential for activating immune suppressive pathways. The molecular pathway leading to the upregulation of the enzyme that controls prostaglandin synthesis, cyclooxygenase (COX)-2, is unclear. Because JP-8 activates oxidative stress and because reactive oxygen species (ROS) turn on nuclear factor kappa B (NF-κβ), which regulates the activity of COX-2, we investigate here whether JP-8–induced ROS and NF-κβ contributes to COX-2 upregulation and immune suppression.

JP-8 has been shown to induce the production of ROS in keratinocytes as measured with the ROS indicator dye, aminophenyl fluorescein. Fluorescence was diminished in JP-8–treated keratinocytes overexpressing catalase or superoxide dismutase (SOD) genes. JP-8–induced COX-2 expression was also reduced to background in the catalase and SOD transfected cells, or in cultures treated with N-acetylcysteine (NAC).

When NAC was injected into JP-8–treated mice, dermal COX-2 expression, and JP-8–induced immune suppression was inhibited. Because ROS activates NF-κβ, we wondered if this transcriptional activator played a role in the enhanced COX-2 expression and JP-8–induced immune suppression.

When JP-8–treated mice, or JP-8–treated keratinocytes were treated with a selective NF-κβ inhibitor, parthenolide, COX-2 expression, and immune suppression were abrogated. Similarly, when JP-8–treated keratinocytes were treated with small interfering RNA specific for the p65 subunit of NF-κβ, COX-2 upregulation was blocked. These data indicate that ROS and NF-κβ are activated by JP-8, and these pathways are involved in COX-2 expression and the induction of immune suppression by jet fuel.

We propose here to show that the phytoalexin pterostilbene (PTER) is a potent inhibitor of NF-κβ and ROS. The NF-κB pathway is often recognized as a critical link between inflammatory processes and cancer development [1]. Although the mechanisms mediating the protective role of PTER included several signaling pathways such as the regulation of Sirt1, extracellular regulated kinase (ERK) and NF-ĸB pathways [2], the activation of Nrf2 pathway is a promising approach to skin barrier disruption caused by long term exposure to JP-8.

The nuclear-cytoplasmic distribution of Nrf2 protein altered by the PTER was found in vitro and in vivo, demonstrating the stimulatory role of PTER on the nuclear translocation. As a self-adaptive mechanism in cells, Nrf2 expression was changed in numerous diseases with inflammation and oxidative stress. A significant decrease in nuclear Nrf2 expression was observed in the affected brain regions of Alzheimer disease (AD) and liver of SAMP8 mice with a systemic accumulation of oxidative stress [3, 4].

Under physiological conditions, Nrf2 binds to Kelch-like ECH-associated protein-1 (Keap1), therefore, the dissociation of Nrf2 from Keap1 is the first step of Nrf2 nuclear translocation [5]. Ramkumar et al. [5] found that PTE could disturb the Nrf-Keap1 interaction and promote the nuclear translocation of Nrf2 in the human embryonic kidney cells.

Abstract:
The Department of Defense (DoD) has identified that one of the main complaints of personnel exposed to JP-8 jet fuel is irritant dermatitis. The purpose of this investigation is to describe the JP-8-induced inflammatory cytokine response in skin. JP-8 jet fuel or acetone control (300 microl) was applied to the denuded skin of rats once a day for 7 days. Skin samples from the exposed area were collected 2 and 24 h after the final exposure. Histological examination of skin biopsies showed neutrophilic inflammatory infiltrate. Reverse transcription-polymerase chain reaction (RT-PCR) was performed utilizing skin total RNA to examine the expression of various inflammatory cytokines. The CXC chemokine GROalpha was significantly upregulated at both time points, whereas GRObeta was only increased 2 h post final exposure. The CC chemokines MCP-1, Mip-1alpha, and eotaxin were induced at both time points, whereas Mip-1beta was induced only 24 h post exposure. Interleukins-1beta and -6 (IL-1beta and IL-6) mRNAs were significantly induced at both time points, while TNFalpha was not significantly different from control. Enzyme-linked immunosorbent assay (ELISA) of skin protein confirmed that MCP-1, TNFalpha, and IL-1beta were modulated as indicated by PCR analysis. However, skin IL-6 protein content was not increased 2 h post exposure, whereas it was significantly upregulated by jet fuel after 24 h. Data from the present study indicate that repeated (7 days) JP-8 exposure induces numerous proinflammatory cytokines in skin. The increased expression of these cytokines and chemokines may lead to increased inflammatory infiltrate in exposed skin, resulting in JP-8-induced irritant dermatitis [6].

Methods of Action of PTER: ↓ = downregulation ↑ = upregulation
• ↓IL-6 & TNF-α secretion ↓COX-2, ↓iNOS, ↓IL-6, ↓TNF-α, ↓PAI-1, ↓CRP, ↓MCP-1, ↓resistin, ↓leptin, ↓Migration of macrophages toward adipocytes [7].

• ↓Cell viability, ↓cyclin D1, ↓c-Myc, ↑PARP, ↓TNF -α, ↓IL-1β, ↓IFN-γ, ↓iNOS, ↓COX-2 [8].

• ↑Nuclear Nrf2, ↑HO-1, ↑CAT, ↑SOD, ↑GPx, ↑Bcl-2, ↓Bax, ↓caspase-3 [9].

One of the first steps in the cascade of events leading to immune suppression is the binding of the lipid mediator of inflammation, platelet-activating factor (PAF) to its receptor which induces the production of immune regulatory factors such as prostaglandin E2 (PGE2) and interleukin (IL)-10 [10]. Blocking PAF receptor binding with a series of PAF receptor antagonists, or blocking PGE2 production with a selective cyclooxygenase-2 inhibitor blocked JP-8-induced immune suppression [10]. Similarly, neutralizing IL-10 function in vivo abrogated JP-8-induced immune suppression [11]. Although JP-8 is a complex mixture of over 260 different organic chemicals, there is abundant evidence indicating that the aromatic hydrocarbons found in JP-8 induce immune suppression [12].

The skin is the largest organ of the body and its main purpose is to provide barrier function for the preservation of body homeostasis. However, contained within the skin are specialized elements that provide immunological function. Langerhans cells and dermal dendritic cells serve as antigen presenting cells that can initiate and/or regulate immune reactions [13, 14, 15].

Epidermal keratinocytes secrete a wide variety of immune regulatory cytokines that have diverse effects on immune reactivity [16]. Dermal mast cells also contribute to the immunological function of the skin. Due to the abundant expression of high-affinity Fcϵ receptors on their surface, and their ability to secrete histamine following IgE cross-linking, mast cells have been traditionally associated with allergic-type immune reactions [17].

However, newer findings indicate that mast cells influence a wide variety of nonallergic immune responses [18] and participate in inducing immune regulation and tolerance [19]. In the skin, IL-10–secreting mast cells have been shown to limit pathology during a contact dermatitis reaction [20] and play an essential role in the induction of immune suppression following exposure to the environmental carcinogen ultraviolet (UV) radiation [21, 22). In addition, mast cell density in human skin correlates with susceptibility to both nonmelanoma [23] and melanoma skin cancers [24] suggesting that the immunomodulatory function of mast cells is likely to be important for the development of skin cancer.

It is abundantly clear that over exposure or long-term exposure to JP-8 (and JP-5) results in a severe cytokine cascade that is immune system driven. Pterostilbene is a potent regulator of inflammatory immune responses. The rationale for using NanoStilbene Cream in hexavalent chromium exposure leading to contact dermatitis is very similar in that it also activates the same pathways as JP-8 does in causing severe immune reaction.

NanoStilbene Cream

This unscented body cream offers carefully selected plant-based ingredients. It spreads easily and absorbs fast, providing nourishment in abundance. It soothes dry skin, sensitive skin, and adds plenty of moisture to keep the skin supple, healthy, and youthful. A unique formulation of Soy, Jojoba, Coconut and Palm extracts that restores skin's natural balance for radiant health. In addition, this cream contains Patented NanoStilbene, a potent antioxidant and anti-inflammatory made with Nanoparticle Pterostilbene.

Pterostilbene (PTER) is a natural compound predominantly found in blueberries. Studies show that PTER is an effective anti-oxidative and anti-inflammatory agent.

Allergic contact dermatitis (ACD) is an important occupational disease caused mainly by topical exposure to hexavalent chromium (Cr(VI)), an impurity of cement manufacture. In Europe, the prevalence of ACD is approximately 4–5% in cement workers [1]. In some Asian countries the prevalence is even higher, such as 40% in Singapore and 13% in Taiwan [2,3]. Due to its high prevalence, ACD exerts an important occupational health impact on those workers. The pathologic process of ACD has been well defined as a cell-mediated type IV hypersensitivity reaction in which many cell types are involved, including keratinocytes, dendritic cells, T-lymphocytes and leucocytes [4]. Reactive oxygen species (ROS) activation was proposed as the initial event, as it leads to the activation of transcriptional factors and signaling pathways, including NF-κB and p38 mitogen-activated protein kinase (MAPK) pathway, which leads to the release of pro-inflammatory cytokines such as TNF-α and IL-1β [5,6,7]. Interestingly, the p38-downstream kinase MAPK-activated protein kinase 2 (MK2) has recently been explored in inflammatory disorders of the skin, such as psoriasis and has become a therapeutic strategy for anti-inflammatory disease. Disruption of MK2 signaling leads to a significant reduction in the level of several pro-inflammatory cytokine production [8]. ROS are also involved in the activation of the NLRP3 inflammasome, which is required to direct the proteolytic maturation of inflammatory cytokines, such as IL-1β and IL-18. Recent studies have indicated that the NLRP3 inflammasome is often wrongly activated by environmental irritants, thus resulting in cutaneous inflammatory diseases [9]. Moreover, ROS can facilitate the process of ACD by changing the extracellular microenvironment [10]. When skin is exposed to Cr(VI), it can penetrate and bind to keratinocytes and immune cells. The intracellular reduction of Cr(VI) is associated with the production of ROS, leading to dermal toxicity, cytokine excretion and skin hypersensitivity [1].

Contains: Water, Vegetable Glycerin, Stearic Acid, Myristyl Myristate, Cetearyl Alcohol, Ceteareth-20, Glycerol Stearate, Simmondsia Chinensis, (Jojoba) Seed Oil, Glycerin Soja (Soybean) Oil, Cetyl Alcohol, Acrylates/C10-30 Alkyl Acrylate Crosspolymer, Butyrospermum Parkii (Shea) Butter, Calendula Officials Flower Oil, Passiflora Edulis (Passion Fruit) Seed Oil, Oryza Sativa (Rice) Bran Oil, Euterpe Oleracea (Acai Palm) Fruit Oil, Phenoxethanol, Ethylhexylglycerin, NanoStilbene.

NanoStilbene Cream References:
1. Shelnutt, S.R.; Goad, P.; Belsito, D.V. Dermatological toxicity of hexavalent chromium. Crit. Rev. Toxicol. 2007, 37, 375–387.
2. Goh, C.L.; Gan, S.L.; Ngui, S.J. Occupational dermatitis in a prefabrication construction factory. Contact Dermat. 1986, 15, 235–240.
3. Guo, Y.L.; Wang, B.J.; Yeh, K.C.; Wang, J.C.; Kao, H.H.; Wang, M.T.; Shih, H.C.; Chen, C.J. Dermatoses in cement workers in southern Taiwan. Contact Dermat. 1999, 40, 1–7.
4. Toncic, R.J.; Lipozencic, J.; Martinac, I.; Greguric, S. Immunology of allergic contact dermatitis. Acta Dermatovenerol. Croat. 2011, 19, 51–68.
5. Fuchs, J.; Zollner, T.M.; Kaufmann, R.; Podda, M. Redox-modulated pathways in inflammatory skin diseases. Free Radic. Biol. Med. 2001, 30, 337–353.
6. Matos, T.J.; Duarte, C.B.; Goncalo,M.; Lopes,M.C. Role of oxidative stress in ERK and p38MAPK activation induced by the chemical sensitizer DNFB in a fetal skin dendritic cell line. Immunol. Cell Biol. 2005, 83, 607–614.
7. Chao, W.; Deng, J.-S.; Huang, S.-S.; Li, P.-Y.; Liang, Y.-C.; Huang, G.-J. 3,4-dihydroxybenzalacetone attenuates lipopolysaccharide-induced inflammation in acute lung injury via down-regulation of MMP-2 and MMP-9 activities through suppressing ROS-mediated MAPK and PI3K/AKT signaling pathways. Int. Immunopharmacol. 2017, 50, 77–86.
8. Singh, R.K.; Najmi, A.K.; Dastidar, S.G. Biological functions and role of mitogen-activated protein kinase activated protein kinase 2 (MK2) in inflammatory diseases. Pharmacol. Rep. 2017, 69, 746–756.
9. Chen, R.J.; Lee, Y.H.; Yeh, Y.L.; Wang, Y.J.; Wang, B.J. The Roles of Autophagy and the Inflammasome during Environmental Stress-Triggered Skin Inflammation. Int. J. Mol. Sci. 2016.
10. Corsini, E.; Galbiati, V.; Nikitovic, D.; Tsatsakis, A.M. Role of oxidative stress in chemical allergens induced skin cells activation. Food Chem. Toxicol. 2013, 61, 74–81.

Definitions:
ACO=acetyl-coA carboxylase; AMACR=a-methylacyl-CoA recemase; Bcl-2=B-cell leukemia/lymphoma 2; CAT=catalase; CDNK1A=cyclin-dependent kinase inhibitor 1A; CDNK1B=cyclin-dependent kinase inhibitor 1B; COX-2=cyclooxygenase-2; CPT-1a=carnitine palmitoyl-transferase 1a; CRP=C-reactive protein; FAS=fatty acid synthase; G6PDH=glucose-6-phosphate dehydrogenase; GLUT4=glucose transporter4; GPx=glutathione peroxidase; HDL-C=high density lipoprotein cholesterol; HO-1=heme oxygenase-1; HOMA-IR=homeostatic modelassessment-insulin resistance; IFN-g=interferon gamma; IkBa=inhibitor of kappa B; IL-1b=interleukin 1 beta; IL-4=interleukin 4; IL-6=interleukin 6; IL-8=interleukin 8; iNOS=inducible nitric oxide synthase; LC3 II=autophagy-related protein light chain 3 II; LDL-C=low densitylipoprotein cholesterol; MAPKs=mitogen-activated protein kinases; MCP-1=monocyte chemoattractant protein-1; ME=malic enzyme; MMP=matrix metallopeptidase; mTOR=mammalian target of rapamycin; Nrf2=NF-E2-related factor 2; p70S6K=70 kDa ribosomal protein S6kinase; PAI-1=plasminogen activator inhibitor-1; p-AMPK=phosphorylated adenosine monophosphate activated protein kinase; PARP=polyADP-ribose polymerase; PCNA=proliferating cell nuclear antigen; p-eIF2a=phospho-eIF2a; p-ERK1/2=phosphorylated-extracellular signal-regulated kinase 1/2; PHF=paired helical filaments; PI3K=phosphatidylinositol 3-kinase; p-JNK1/2=phospho-JNK1/2; sICAM1=solubleintercellular adhesion molecule-1; PPARa=peroxisome proliferator activated receptor alpha; ROS=reactive oxygen species; SOD=superoxidedismutase; TNF-a=tumor necrosis factor-a; VEGF=vascular endothelial growth factor; VLDL-C=very low density lipoprotein cholesterol.

References:

[1] Regulation and Function of NF-kappaB Transcription Factors in the Immune System https://pubmed.ncbi.nlm.nih.gov/19302050/
[2] A Review of Pterostilbene Antioxidant Activity and Disease Modification https://pubmed.ncbi.nlm.nih.gov/23691264/
[3] Age-related Changes of Nrf2 and Phosphorylated GSK-3β in a Mouse Model of Accelerated Aging (SAMP8)https://pubmed.ncbi.nlm.nih.gov/21784539/
[4] Expression of Nrf2 in Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/17204939/
[5] Reporter Protein Complementation Imaging Assay to Screen and Study Nrf2 Activators in Cells and Living Animals https://pubmed.ncbi.nlm.nih.gov/23826874/
[6] JP-8 Jet Fuel Exposure Induces Inflammatory Cytokines in Rat Skin https://pubmed.ncbi.nlm.nih.gov/15251112/
[7] Hsu CL, Lin YJ, Ho CT, Yen GC. The inhibitory effect of pterostilbene on inflammatory responses during the interaction of 3T3-L1 adipocytes and RAW 264.7macrophages. J Agric Food Chem 2013;61:602e10.
[8] Paul S, Rimando AM, Lee HJ, Ji Y, Reddy BS, Suh N. Anti-inflammatory action of pterostilbene is mediated through the p38 mitogen-activated protein kinase pathway in colon cancer cells. Cancer Prev Res 2009;2:650e7.
[9] Bhakkiyalakshmi E, Shalini D, Sekar TV, Rajaguru P, Paulmurugan R, Ramkumar KM. Therapeutic potential of pterostilbene against pancreatic beta-cell apoptosis mediated through Nrf2. Br J Pharmacol 2014;171:1747e57.
[10] Platelet Activating Factor Receptor Binding Plays a Critical Role in Jet Fuel-Induced Immune Suppression https://pubmed.ncbi.nlm.nih.gov/15020195/
[11] Mechanisms involved in the immunotoxicity induced by dermal application of JP-8 jet fuel. Ullrich SE, Lyons HJ Toxicol Sci. 2000 Dec; 58(2):290-8.
[12] Dermal Exposure to Jet Fuel Suppresses Delayed-Type Hypersensitivity: A Critical Role for Aromatic Hydrocarbons https://pubmed.ncbi.nlm.nih.gov/17890764/
[13] Epidermal langerhans cell-deficient mice develop enhanced contact hypersensitivity. Kaplan DH, Jenison MC, Saeland S, Shlomchik WD, Shlomchik MJ Immunity. 2005 Dec; 23(6):611-20.
[14] Dynamics and function of Langerhans cells in vivo: dermal dendritic cells colonize lymph node areas distinct from slower migrating Langerhans cells.
Kissenpfennig A, Henri S, Dubois B, Laplace-Builhé C, Perrin P, Romani N, Tripp CH, Douillard P, Leserman L, Kaiserlian D, Saeland S, Davoust J, Malissen B Immunity. 2005 May; 22(5):643-54.
[15] Dermal dendritic cells, and not Langerhans cells, play an essential role in inducing an immune response. Fukunaga A, Khaskhely NM, Sreevidya CS, Byrne SN, Ullrich SE J Immunol. 2008 Mar 1; 180(5):3057-64.
[16] The role of epidermal cytokines in the generation of cutaneous immune reactions and ultraviolet radiation-induced immune suppression. Ullrich SE
Photochem Photobiol. 1995 Sep; 62(3):389-401.
[17] Signalling through the high-affinity IgE receptor Fc epsilonRI. Turner H, Kinet JP Nature. 1999 Nov 25; 402(6760 Suppl):B24-30.
[18] Role of mast cells in allergic and non-allergic immune responses: comparison of human and murine data. Bischoff SC Nat Rev Immunol. 2007 Feb; 7(2):93-104.
[19] Mast cells are essential intermediaries in regulatory T-cell tolerance.
Lu LF, Lind EF, Gondek DC, Bennett KA, Gleeson MW, Pino-Lagos K, Scott ZA, Coyle AJ, Reed JL, Van Snick J, Strom TB, Zheng XX, Noelle RJ
Nature. 2006 Aug 31; 442(7106):997-1002.
[20] Mast cell-derived interleukin 10 limits skin pathology in contact dermatitis and chronic irradiation with ultraviolet B. Grimbaldeston MA, Nakae S, Kalesnikoff J, Tsai M, Galli SJ Nat Immunol. 2007 Oct; 8(10):1095-104.
[21] Mast cell migration from the skin to the draining lymph nodes upon ultraviolet irradiation represents a key step in the induction of immune suppression. Byrne SN, Limón-Flores AY, Ullrich SE J Immunol. 2008 Apr 1; 180(7):4648-55.
[22] Dermal mast cells determine susceptibility to ultraviolet B-induced systemic suppression of contact hypersensitivity responses in mice. Hart PH, Grimbaldeston MA, Swift GJ, Jaksic A, Noonan FP, Finlay-Jones JJ
J Exp Med. 1998 Jun 15; 187(12):2045-53.
[23] Susceptibility to basal cell carcinoma is associated with high dermal mast cell prevalence in non-sun-exposed skin for an Australian populations.
Grimbaldeston MA, Green A, Darlington S, Robertson BO, Marshman G, Finlay-Jones JJ, Hart PH Photochem Photobiol. 2003 Dec; 78(6):633-9.
[24] Association between melanoma and dermal mast cell prevalence in sun-unexposed skin. Grimbaldeston MA, Pearce AL, Robertson BO, Coventry BJ, Marshman G, Finlay-Jones JJ, Hart PH Br J Dermatol. 2004 May; 150(5):895-903.

/Timothy G. Dixon/
June 23, 2020
EhrTSOI
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Re: Auto-Immune disorders

Post by EhrTSOI »

Hi Tim

Your offer to custom batch the experimental cream that's working for your friends son to Gnikmj97 wife is huge in my books. This is a great company, with a hard working CEO that cares for his shareholders.

EHReyes
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TimGDixon
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Re: Auto-Immune disorders

Post by TimGDixon »

Thats very kind of you, thank you. Nothing in the blend will cause her harm or discomfort so there is nothing to lose in trying and i am happy to try.

He has since named it Tim's Excellent Remedy so i print it on the label for him that way (i cut his name/address). I don't know if my stuffy old board of directors will let me call it that if we ever release it hahahahah
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trader32176
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Re: Auto-Immune disorders

Post by trader32176 »

I'm good with Tim's Remedy any day of the week . Flintstones hasn't branched out into making creams yet. :lol:
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TimGDixon
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Re: Auto-Immune disorders

Post by TimGDixon »

But are you good with "Tim's Excellent Remedy" LOL.

I was only joking about my "stuffy" old board - the Board is Dr. Ichim and I and we are far from stuffy LOL...

Recent photo taken of the BOD.
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trader32176
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Re: Auto-Immune disorders

Post by trader32176 »

Hahaha Tim,

Loved that pic of the BOD :) :D :lol:
rrao11
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Re: Auto-Immune disorders

Post by rrao11 »

Tim - curious! Which one is you?

The other would be Tom.

:D :D
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TimGDixon
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Re: Auto-Immune disorders

Post by TimGDixon »

hahahahah :lol: we're dual personalities.
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