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Can't say I see any completely unambiguous evidence of regrowth in either set.
The hairline shots definitely could be shaved hairs (or depilated hairs) rather than new hairs - there is not really a good enough set of before shots to tell.
It appears to have caused a pretty serious chemical burn on the temples which could have damaged the hair in a kind of reaction similar to a depilatory cream.
I don't know anything about the posters concerned but if they do have a history of previously dodgy behaviour, I really don't hold much hope.
More evidence definitely needed. But this stuff is potentially very dangerous, so anybody trying it would need to be very careful. Just take a look at the Wikipedia page for it, and all the warning signs on it - oxidising agent, very toxic, corrosive, and damaging to the environment.Comment
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There's a huge difference between using well-documented, properly researched, legally approved and licenced medications... And sticking a hazardous chemical on your scalp because three people on an Internet forum with no medical training claim it works with no objective proof.Comment
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Anyway, Swiss is a reliable guy; he never scammed mark for that matter either, pretty sure that was just pulled out of your ass m8;
this stuff is dirt cheap and easily accessible, try it if you want, people are using it already, carefully, with no adverse effects; if you want to wait then wait, not much to be discussed, but the fact that its growing hair is indisputableComment
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Yes swiss is varry bad man...does research, presents studies, uses himself as guinea pig, then brings it all to our attention so we can freely make an informed choice. For shame!Comment
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So where to buy, how to mix and apply this stuff? It looks cheap enough and results are to be expected early on so I'm definitely willing to try it out.Comment
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Conpecia, You have some email where you can talk to you and help me build my lotion?
(TRADUCTOR GOOGLE)
ThanksComment
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From another forum poster:
Ok chlorine dioxide got my interest, the anecdotal evidence suggests that it might be doing something (time will tell to what extent!).
While trying to keep an open mind about chlorine dioxide, and trying to accept mr. Liuxuewu's product results (specially those one year results pics in frontal recession) as a possible truth, I tried to identify the pathways on which it might be working. To my surprise a strong oxidizing agent like chlorine dioxide despite the fact that it might destroy most pathogens it may not be regarded as an antibiotic, instead this ability might be regarded as immunomodulation (check Tetrachlorodecaoxide (TCDO) by targeting the macrophage. We're talking about modulating immune responses and inappropriate inflammatory reactions. It's hard to predict to what point this ability could work in our favor (AGA), but the possibilities are tremendous, macrophage is linked directly or indirectly to various pathways/signals of our interest, such as DKK1, NfkB, Wnt, Bcatenin and in this cascade we might even consider down-regulation of androgen receptors expression levels, which is definitely connected to inflammatory pathways.
Be carefull to not misinterpret my words, I'm not saying chlorine dioxide is regulating all these factors to "perfect" levels, because if it did we would definitely be looking into a very very... really really... effective treatment! All I'm saying is that it might be working through these pathways to some extent, and that could justify whatever efficacy it might have on the treatment of AGA.
Although I still believe proteasome inhibition holds much more promise in a safety / efficacy point of view, trying to regulate macrophage with chlorine dioxide might worth the shot...
Please note that I'm not supporting mr. Liuxuewu's treatment, beyond this approach I'm not able to see use for his other ingredients (although I could be wrong), and it's really hard for me to understand the use of propylene glycol in a treatment of this nature, because it's a thick oily substance that sits on the scalp, taking too much time to absorb, forcing prolonged contact with the hair on the skin surface, resulting in breakage/shedding. DMSO sounds definitely like a better approach, although limiting this effect it will increase systemic absorption.
Having this said I might try my own chlorine dioxide solution, much like summersnow and swissTemples (congratulations to both of you for pioneering this experiment), with different dilutions, maybe something like: chlorine dioxide (end result 1000ppm) : deionized water : DMSO (1 : 1 : 1) and variate from this starting point.
For whoever is interested in some reading and I really do recommend to not just take my word on this, below is some interesting literature regarding what I just wrote. Please take in consideration that I'm trying to understand/justify why would chlorine dioxide work for AGA without even knowing if it actually works.
Crosstalk of macrophages and skin stem cells during hair follicle regeneration
31 Jan 2013
. Presentation
Speaker: Mirna Perez-Moreno,
Centro Nacional de Investigaciones Oncológicas (CNIO). Madrid (Spain)
Organizer: IRB Barcelona
Host: Dr.Angel Nebreda, IRB Barcelona
Date: Thursday, 31 January 2013, 16:00h
Place: Aula Fčlix Serratosa, Parc Cičntific de Barcelona, Spain
Abstract: Adult stem cells reside in specialized environments that regulate their behavior. Over last decade a number of studies have been instrumental for defining regulatory pathways controlling their proliferation and/or differentiation. Although, the current challenge in the stem cell field is the identification of factors that mobilize endogenous stem cell pools in tissues to promote regeneration.
Using mouse skin, a well-characterized model to study stem cell behavior, we have identified that the spatiotemporal secretion of signals arising from macrophages are able to orchestrate stem cell regenerative capabilities, allowing them to differentiate and integrate properly in the regenerating hair follicles. These signals involve the release of Wnt ligands from a fraction of skin resident macrophages that are able to control hair follicle stem cells activation, hair grow and tissue regeneration. Our results indicate that macrophages contribute to the activation of skin epithelial stem cells, adding new insight to the cues underlying their regenerative potential, which may have future implications in skin repair, inflammatory skin diseases, aging and cancer.
WF10 is a solution of OXO-K993 containing stabilized chlorite ions that focuses on supporting the immune system by targeting the macrophage, a type of white blood cell that coordinates much of the immune system to regulate normal immune function. Normally functioning macrophages can alternate between one of two basic states: phagocytic and inflammatory. Phagocytic macrophages digest invading organisms, such as viruses, and initiate a biological defense pathway. Inflammatory macrophages, in turn, induce a variety of reactions, including fever, sweating, swollen glands, malaise and appetite loss, the common, uncomfortable signs of illness. Such responses, while entirely normal, must be turned on and off in a controlled manner. If left unchecked pathogens can overdrive the system toward the inflammatory state creating an imbalance that may lead to such medical disorders as chronic inflammation, immune deficiency, organ damage and tumour proliferation.
WF10's mode of activity is believed to be based on how macrophages regulate the immune system. Research suggests that, in some cases, WF10 may rebalance improperly functioning immune systems. The drug has potential applications in adjuvant cancer therapy, diseases related to immune deficiencies and the management of chronic viral infections.
Oxoferin, a topical wound healing agent, is a diluted form of WF10, a chlorite-based, immunomodulating drug. The Company believes that research to-date suggests Oxoferin has a positive impact on wound healing leading to contraction, closure and faster healing of wounds.
Chronic, hard-to-heal wounds are a serious problem with an increasing incidence. Chronic wounds can be caused by such conditions as burns, pressure sores and poor circulation in the lower extremities. Co-morbid conditions, such as diabetes and atherosclerosis, reduce blood flow to the extremities and also increase the likelihood of developing chronic wounds such as diabetic foot ulcers and venous ulcers.
WF10, which contains chlorite as the active principle, causes profound changes in macrophage function and activation of gene expression, and appears to downregulate inappropriate immunological activation. The loss of T-cell function observed in HIV-infected patients likely requires the involvement of chronically activated macrophages. Therefore, the persistently activated macrophage represents a therapeutic target that is, unlike HIV, not highly mutable. With this target as a focus, WF10 is being developed for use in advanced HIV disease. WF10 is currently being studied in the US, Europe and Asia for treatment of late-stage HIV disease, as well as recurrent prostate cancer, late post-radiation cystitis, autoimmune disease and chronic active hepatitis C disease.
Due to its oxidizing properties, TCDO can destroy most pathogens although it is not regarded asantibiotic. But the main reason for its use for dressing of wounds is not its bactericidal activity. This drug is regarded asimmunomodulating, that is, it acts by stimulating the immune system of the body. Tetrachlorodecaoxide combines with the haem part of hemoglobin, myoglobin and peroxidase, forming a TCDO-haemo complex. This in turn activates the macrophages and accelerates the process of phagocytosis which engulfs most of the pathogens and cell debris present on the surface of the wound, thus cleaning the wound surface and helping in the regenerative process. Tetrachlorodecaoxide is also mitogenic and chemotactic. The mitogenic impulse gives rise to two factors, MDGF(Macrophage derived growth factor) and WAF (Wound angiogenesis factor). The MDGF deposits fibroblasts and synthesizescollagen fibers which fills the gap in the wounds, the WAF helps in the formation of new capillaries which further enhances the healing process. The chemotactic impulse acts on the myocyte (muscle cell) and causes it to contract, thereby bringing the wound edges closer and reducing the wound surface. Simultaneous influence of all these factors accelerate the wound healing with minimal scarring
Treatment of macrophage-related disorders
US 20120134929 A1
ABSTRACT
The present invention provides a method of treating a macrophage related disease comprising administering to a subject in need thereof an effective amount of an oxidative agent or an immunosuppressive agent. The present invention also provides a method of modulating macrophage accumulation or activation comprising administering to a subject in need thereof an effective amount of an oxidative agent or an immunosuppressive agent. The oxidative agent can be chlorite or a chlorite containing compound.
Macrophages are white blood cells produced by the division of monocytes. Monocytes and macrophages are phagocytes, and play a role in innate immunity (non-specific immune defenses) as well as helping to initiate adaptive immunity (specific defense mechanisms). These cells phagocytose (engulf and then digest) cellular debris and pathogens either as stationary or as mobile cells. When activated by pathogens or by other mechanisms, macrophages stimulate and recruit lymphocytes and other immune cells to respond to the insult.
Although macrophages play a vital role in host immune defenses, activated macrophages are also involved in the progression of a number of diseases and disorders. Activated macrophages elicit massive leukocyte infiltration and flood the surrounding tissue with inflammatory mediators, pro-apoptotic factors, and matrix degrading proteases. These actions can result in inflammation that can dismantle tissues to the point of inflicting serious injury. Tissue destruction perpetrated by macrophage-induced inflammation has been associated with the development of tumors, autoimmune disorders, and other conditions.
Oxidative agents such as chlorite can return macrophages to their inactivated state. Immunosuppressant agents can mitigate macrophage activation. The present invention provides methods for the treatment of macrophage-related diseases and related conditions with oxidative agents or immunosuppressant agents.
Targeting androgen receptor to suppress macrophage-induced EMT and benign prostatic hyperplasia (BPH) development.
Lu T1, Lin WJ, Izumi K, Wang X, Xu D, Fang LY, Li L, Jiang Q, Jin J, Chang C.
Author information
Abstract
Early studies suggested macrophages might play roles in inflammation-associated benign prostatic hyperplasia (BPH) development, yet the underlying mechanisms remain unclear. Here we first showed that CD68(+) macrophages were identified in both epithelium and the stromal area of human BPH tissues. We then established an in vitro co-culture model with prostate epithelial and macrophage cell lines to study the potential impacts of infiltrating macrophages in the BPH development and found that co-culturing prostate epithelial cells with macrophages promoted migration of macrophages. In a three-dimensional culture system, the sphere diameter of BPH-1 prostate cells was significantly increased during coculture with THP-1 macrophage cells. Mechanism dissection suggested that expression levels of epithelial-mesenchymal transition (EMT) markers, such as N-cadherin, Snail, and TGF-?2, were increased, and administration of anti-TGF-?2 neutralizing antibody during co-culture suppressed the EMT and THP-1-mediated growth of BPH-1 cells, suggesting THP-1 might go through EMT to influence the BPH development and progression. Importantly, we found that modulation of androgen receptor (AR) in BPH-1 and mPrE cells significantly increased THP-1 and RAW264.7 cell migration, respectively, and enhanced expression levels of EMT markers, suggesting that AR in prostate epithelial cells might play a role in promoting macrophage-mediated EMT in prostate epithelial cells. Silencing AR function via an AR degradation enhancer, ASC-J9, decreased the macrophage migration to BPH-1 cells and suppressed EMT marker expression. Together, these results provide the first evidence to demonstrate that prostate epithelial AR function is important for macrophage-mediated EMT and proliferation of prostate epithelial cells, which represents a previously unrecognized role of AR in the cross-talk between macrophages and prostate epithelial cells. These results may provide new insights for a new therapeutic approach to battle BPH via targeting AR and AR-mediated inflammatory signaling pathways.
Macrophages in inflammation.
Fujiwara N1, Kobayashi K.
Author information
Abstract
The inflammatory process is usually tightly regulated, involving both signals that initiate and maintain inflammation and signals that shut the process down. An imbalance between the two signals leaves inflammation unchecked, resulting in cellular and tissue damage. Macrophages are a major component of the mononuclear phagocyte system that consists of closely related cells of bone marrow origin, including blood monocytes, and tissue macrophages. From the blood, monocytes migrate into various tissues and transform macrophages. In inflammation, macrophages have three major function; antigen presentation, phagocytosis, and immunomodulation through production of various cytokines and growth factors. Macrophages play a critical role in the initiation, maintenance, and resolution of inflammation. They are activated and deactivated in the inflammatory process. Activation signals include cytokines (interferon gamma, granulocyte-monocyte colony stimulating factor, and tumor necrosis factor alpha), bacterial lipopolysaccharide, extracellular matrix proteins, and other chemical mediators. Inhibition of inflammation by removal or deactivation of mediators and inflammatory effector cells permits the host to repair damages tissues. Activated macrophages are deactivated by anti-inflammatory cytokines (interleukin 10 and transforming growth factor beta) and cytokine antagonists that are mainly produced by macrophages. Macrophages participate in the autoregulatory loop in the inflammatory process. Because macrophages produce a wide range of biologically active molecules participated in both beneficial and detrimental outcomes in inflammation, therapeutic interventions targeted macrophages and their products may open new avenues for controlling inflammatory diseases.
Monocyte/macrophage androgen receptor suppresses cutaneous wound healing in mice by enhancing local TNF-? expression
Jiann-Jyh Lai, Kuo-Pao Lai, Kuang-Hsiang Chuang, Philip Chang, I-Chen Yu,Wen-Jye Lin and Chawnshang Chang
George Whipple Lab for Cancer Research, Department of Pathology, Department of Urology, Department of Radiation Oncology, and Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA.
Address correspondence to: Chawnshang Chang, Box 626, 601 Elmwood Avenue, Rochester, New York 14642, USA. Phone: (585) 273-4500; Fax: (585) 756-4133; E-mail: chang@URMC.rochester.edu.
First published November 9, 2009
Submitted: March 26, 2009; Accepted: September 16, 2009.
Cutaneous wounds heal more slowly in elderly males than in elderly females, suggesting a role for sex hormones in the healing process. Indeed, androgen/androgen receptor (AR) signaling has been shown to inhibit cutaneous wound healing. AR is expressed in several cell types in healing skin, including keratinocytes, dermal fibroblasts, and infiltrating macrophages, but the exact role of androgen/AR signaling in these different cell types remains unclear. To address this question, we generated and studied cutaneous wound healing in cell-specific AR knockout (ARKO) mice. General and myeloid-specific ARKO mice exhibited accelerated wound healing compared with WT mice, whereas keratinocyte- and fibroblast-specific ARKO mice did not. Importantly, the rate of wound healing in the general ARKO mice was dependent on AR and not serum androgen levels. Interestingly, although dispensable for wound closure, keratinocyte AR promoted re-epithelialization, while fibroblast AR suppressed it. Further analysis indicated that AR suppressed wound healing by enhancing the inflammatory response through a localized increase in TNF-? expression. Furthermore, AR enhanced local TNF-? expression via multiple mechanisms, including increasing the inflammatory monocyte population, enhancing monocyte chemotaxis by upregulating CCR2 expression, and enhancing TNF-? expression in macrophages. Finally, targeting AR by topical application of a compound (ASC-J9) that degrades AR protein resulted in accelerated healing, suggesting a potential new therapeutic approach that may lead to better treatment of wound healing.
Macrophages (Greek: big eaters, from makros "large" + phagein "eat"; abbr. M?), are a type of white blood cell that engulf and digest cellular debris, foreign substances, microbes, and cancer cells in a process called phagocytosis. Macrophages were first discovered by Élie Metchnikoff, a Russian bacteriologist, in 1884.[1] They are found in essentially all tissues[2] where they patrol for potential pathogens by amoeboid movement. They play a critical role in non-specific defense (innate immunity), and also help initiate specific defense mechanisms (adaptive immunity) by recruiting other immune cells such as lymphocytes. In humans, dysfunctional macrophages cause severe diseases such as chronic granulomatous disease that result in frequent infections.
Beyond increasing inflammation and stimulating the immune system, macrophages also play an important anti-inflammatory role and can decrease immune reactions through the release of cytokines. Macrophages that encourage inflammation are called M1 macrophages, whereas those that decrease inflammation and encourage tissue repair are called M2 macrophages.[3] This difference is reflected in their metabolism, where macrophages have the unique ability to metabolize one amino acid, arginine, to either a "killer" molecule (nitric oxide) or a "repair" molecule (ornithine).
Macrophages and angiogenesis: a role for Wnt signaling
Andrew C Newman1 and Christopher C W Hughes123*
Macrophages regulate many developmental and pathological processes in both embryonic and adult tissues, and recent studies have shown a significant role in angiogenesis. Similarly, Wnt signaling is fundamental to tissue morphogenesis and also has a role in vascular development. In this review, we summarize recent advances in the field of macrophage-regulated angiogenesis, with a focus on the role of macrophage-derived Wnt ligands. We review data that provide both direct and indirect evidence for macrophage-derived Wnt regulation of physiologic and pathologic angiogenesis. Finally, we propose that Wnt signaling plays a central role in differentiation of tumor associated and wound infiltrating macrophages to a proangiogenic phenotype.
NF-kappaB regulates androgen receptor expression and prostate cancer growth.
Zhang L1, Altuwaijri S, Deng F, Chen L, Lal P, Bhanot UK, Korets R, Wenske S, Lilja HG, Chang C, Scher HI, Gerald WL.
Author information
Abstract
Prostate cancers that progress during androgen-deprivation therapy often overexpress the androgen receptor (AR) and depend on AR signaling for growth. In most cases, increased AR expression occurs without gene amplification and may be due to altered transcriptional regulation. The transcription factor nuclear factor (NF)-kappaB, which is implicated in tumorigenesis, functions as an important downstream substrate of mitogen-activated protein kinase, phosphatidylinositol 3-kinase, AKT, and protein kinase C and plays a role in other cancer-associated signaling pathways. NF-kappaB is an important determinant of prostate cancer clinical biology, and therefore we investigated its role in the regulation of AR expression. We found that NF-kappaB expression in prostate cancer cells significantly increased AR mRNA and protein levels, AR transactivation activity, serum prostate-specific antigen levels, and cell proliferation. NF-kappaB inhibitors decrease AR expression levels, prostate-specific antigen secretion, and proliferation of prostate cancer cells in vitro. Furthermore, inhibitors of NF-kappaB demonstrated anti-tumor activity in androgen deprivation-resistant prostate cancer xenografts. In addition, levels of both NF-kappaB and AR were strongly correlated in human prostate cancer. Our data suggest that NF-kappaB can regulate AR expression in prostate cancer and that NF-kappaB inhibitors may have therapeutic potential.Comment
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Hello I am swissTemples and the guy whose pictures Conpecia posted here.
I will be replying to questions on here since my stuff got posted and some people accused me of things. Let's go:
It's been around way longer than that but never made a big impact because people shied away from the initial shock loss it causes to most people.
I would never ever ever shave my temples and neither am I making any profit off of this. So how is it snake oil? I made pictures of my progress on a private forum (phg) and when conpecia asked me if he could post them publicly I agreed.
I have dumped several thousand dollars into experimental hairloss, used stuff on my head people like you wouldn't even dream about using and yet this is the response some people give me. Typical. Have some humility and appreciate the sacrifices others make in your benefit.
Please do tell me how I scammed anyone, especially since I never owned a store or otherwise sold or advertised anything? In fact the only thing I ever did was give away stuff for free out of my own pocket if my scalp was already overloaded with other test substances. Just last month I gave away 3g of Tofacitinib worth 600$ to thomson adams to test it in my stead. Baseless smear campaign cause I'm the guy calling out *real* scamming when I see it.
Yes it did burn my temple. I might have to reduce the chlorine dioxide percentage. Personally I can live with it.
The problem with the growth is that the new hairs shed again if chlorine dioxide application is continued. Hence making it difficult to see progress. I've now started spacing out the application further and it seems to stick now, so hopefully I can make better photos in the future.
And there's a huge difference between a bitter hairloss forum user who tries to smear people's reputation and a guy taking the risk of using a potentially dangerous substance on his head and sharing the results. What's that old saying again? Oh right, beggars can't be choosers.Comment
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