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C60oo Open Scientific Discussion

c60 baati mitochondrial antioxidant

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#61 bixbyte

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Posted 28 April 2015 - 10:32 PM

Table 1 in this study shows how much C60 is absorbed into different types of rodent tissues over time:

http://www.docdroid....cology.pdf.html

 

They inject a single dose of radiologically tagged C60 into rats and then measure at different intervals.   What is really strange here is that Table 1 shows gradually increasing saturation in muscle over time up to 14 days.   At the 30 day point the saturation begins to come down.    This alone seems strange because the blood levels are near zero at day 7.   How can the tissue saturation continue to grow so dramatically between days 7 and 14?   Does someone have a hypothesis about why that happens?

 

The final column in Table 1 shows an alternative experiment where they dose the rats five consecutive days and then wait 14 days.   The measurement they have in muscle for this alternative experiment is much lower than the 14 day measurement in muscle for a single dose of C60.   How is that possible?    Does someone have a theory to explain that?   I did not read most of the study and there may be an explanation there.

 

It's worth noting that the measurement in muscle is less at 30 days than 14 days, but at 30 days is still higher than seven days.    It really looks like the saturation from one dose takes a long time to work its way through mitochondrial membranes, and it is a shame in this study that they did not do measurements at two months, three months, etc, to establish how rapidly the C60 comes out of tissues.

 

OK therefore your muscles are a place to store Fullerenes and that is all I see. SO FAR.... 



#62 HighDesertWizard

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Posted 29 April 2015 - 01:00 PM

A couple things...

 

A New York Times Magazine article about the Cholinergic Anti-Inflammatory Pathway and leveraging it in treating Arthritis...
Can the Nervous System be Hacked?
The Mechanism of the treatment described is the same as one shown in one of the experiments in that graphic figure I've posted with multiple mice on it above, i.e., electrically stimulate the Vagus Nerve... It's on Slide 8 of that Slide Set...
The point relevant to this C60-OO discussion.... Practical evidence that CAIP-Spleen related healthful functions work both in mice and in In Humans...

 

 

 

Hypothesis: Parabiotic rejuvenation takes place in the older mouse because it has access to more youthful Vagus-CAIP Signaling via acess to the younger mouse’s spleen.

 

I reference evidence, here, that I take to be strong, that supports that Hypothesis Statement... There is something like comparable evidence vis-a-vis C60-OO that I'm working up into an argument for a post in this thread...


Edited by HighDesertWizard, 29 April 2015 - 01:08 PM.


Click HERE to rent this advertising spot for C60 HEALTH to support Longecity (this will replace the google ad above).

#63 Kalliste

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Posted 29 April 2015 - 06:20 PM

I think you are a bit obsessed with the whole Vagus things. Not saying it's all wrong or anything, but you should start your own thread on that topic, I think it's derailing this topic.


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#64 Kalliste

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Posted 03 May 2015 - 11:43 AM

 

Biomaterials. 2015 Mar;45:115-23. doi: 10.1016/j.biomaterials.2014.12.032. Epub 2015 Jan 20.
Preparation of hydrophilic C60(OH)10/2-hydroxypropyl-β-cyclodextrin nanoparticles for the treatment of a liver injury induced by an overdose of acetaminophen. Abstract

Stable hydrophilic C60(OH)10 nanoparticles were prepared from 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) and applied to the treatment of an acetaminophen overdose induced liver Injury. C60(OH)10 nanoparticles were produced by cogrinding α-CD, β-CD, γ-CD and HP-β-CD and characterized in terms of solubility, mean particle diameter, ζ-potential and long term dispersibility in water. Hydrophilic C60(OH)10 nanoparticles with particle sizes less than 50 nm were effectively produced by cogrinding HP-β-CD with C60(OH)10 at a molar ratio of 1:3 (C60(OH)10:CD). The resulting C60(OH)10/HP-β-CD nanoparticles were stable in water and showed no aggregation over a 1 month period. The C60(OH)10/CDs nanoparticles scavenged not only free radicals (DPPH and ABTS radicals) but also reactive oxygen species (O2(•-) and •OH). When C60(OH)10/HP-β-CD nanoparticles were intraperitoneally administered to mice with a liver injury induced by an overdose of acetaminophen (APAP), the ALT and AST levels were markedly reduced to almost the same level as that for normal mice. Furthermore, the administration of the nanoparticles prolonged the survival rate of liver injured mice, while all of the mice that were treated with APAP died within 40 h. To reveal the mechanism responsible for liver protection by C60(OH)10 nanoparticles, GSH level, CYP2E1 expression and peroxynitrite formation in the liver were assessed. C60(OH)10/HP-β-CD nanoparticles had no effect on CYP2E1 expression and GSH depletion, but suppressed the generation of peroxynitrite in the liver. The findings indicate that the protective effect of C60(OH)10/HP-β-CD nanoparticles was due to the suppression of oxidative stress in mitochondria, as the result of scavenging ROS such as O2(•-), NO and peroxynitrite, which act as critical mediators in the liver injuries.

 

Anthony Loera posted this in a separate topic, posted it here "for the records". There are quite the number of C60 studies using different delivery systems coming to the same conclusion. That is nice. I wonder if C60 would protect against cigarette smoke, that has all kinds of crazy radicals in it.


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#65 Kalliste

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Posted 03 May 2015 - 12:42 PM

This is a study that I found on PEG-C60 and LED therapy. I'm a bit interested in phototherapy and LLLT so I'm browsing papers on the subject. Anyway this is perhaps reason to be cautious about combining light and C60? Can't get fulltext right now.

 
Abstract

The purpose of this study was to evaluate Fullerene as a therapeutic photosensitizer in the treatment of atherosclerosis. An atherosclerotic experimental rabbit model was prepared by causing intimal injury to bilateral external iliac arteries using balloon expansion. In four atherosclerotic rabbits and one normal rabbit, polyethylene glycol-modified Fullerene (Fullerene-PEG) was infused into the left external iliac artery and illuminated by light emitting diode (LED), while the right external iliac artery was only illuminated by LED. Two weeks later, the histological findings for each iliac artery were evaluated quantitatively and comparisons were made among atherosclerotic Fullerene+LED artery (= 4), atherosclerotic light artery (= 4), normal Fullerene+LED artery (= 1), and normal light artery (= 1). An additional two atherosclerotic rabbits were studied by fluorescence microscopy, after Fullerene-PEG-Cy5 complex infusion into the left external iliac artery, for evaluation of Fullerene-PEG incorporated within the atherosclerotic lesions. The degree of atherosclerosis in the atherosclerotic Fullerene+LED artery was significantly (< 0.05) more severe than that in the atherosclerotic LED artery. No pathological change was observed in normal Fullerene+LED and LED arteries. In addition, strong accumulation of Fullerene-PEG-Cy5 complex within the plaque of the left iliac artery of the two rabbits was demonstrated, in contrast to no accumulation in the right iliac artery. We conclude that infusion of a high concentration of Fullerene-PEG followed by photo-illumination resulted not in a suppression of atherosclerosis but in a progression of atherosclerosis in experimental rabbit models. However, this intervention showed no adverse effects on the normal iliac artery.

 

 

http://link.springer...0270-007-9238-8



#66 niner

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Posted 03 May 2015 - 01:11 PM

Anyway this is perhaps reason to be cautious about combining light and C60?


It would depend on the frequency of the light, and to a lesser extent on the intensity.



#67 Kalliste

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Posted 03 May 2015 - 02:08 PM

Pity so little is known, I hope I have not given myself increased artherosclerotic plaques by shining lights at my head. Time will tell.



#68 Kalliste

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Posted 05 May 2015 - 09:57 AM

Here is a Review on fullerens from 2007. No news for oldtimers but a good summary of what was known at that time. Helps to explain why there is an interest in fullerenes.

 

 

Results published in 1999 have shown that fullerenes have a potential as biological antioxidants. The antioxidant property is based on the fact that fullerenes possess large amount of conjugated double bonds and low lying lowest unoccupied molecular orbital (LUMO) which can easily take up an electron, making an attack of radical species highly possible. It has been reported that up to 34 methyl radicals have been added onto a single C60 molecule. This quenching process appears to be catalytic. In other words the fullerene can react with many superoxides without being consumed. Due to this feature fullerenes are considered to be the world’s most efficient radical scavenger and are described as radical sponges (Krusic et al 1991). The major advantage of using fullerenes as medical antioxidant is their ability to localize within the cell to mitochondria and other cell compartment sites, where in diseased states, the production of free radicals takes place.

Experiments on rats done by Najla Gharbi and coworkers proved this remarkable trait. They showed that aqueous C60 suspensions prepared without using any polar organic solvent, not only have no acute or sub acute toxicity in rodents, but also protect their livers against free-radical damage (Gharbi et al 2005). Rats are intoxicated with CCl4, which led to the formation of trichloromethyl radical CCl3, causing severe damage to the liver on reaction with oxygen. Trichloromethylperoxy radicals CCl3OO•, a highly reactive species which rapidly initiates the chain reaction of lipid peroxidation (Slater et al 1985), is formed. C60 is able to scavenge a large number of these radicals per molecule leading to the result that rats pre-treated with C60 and intoxicated with CCl4 showed no liver damage. Considering the histopathological examinations and biological tests, pristine C60 can be considered as a powerful liver-protective agent when used in a dose-dependent manner.

When fullerene is derivatized with polar groups, as in case of polyhydroxylated fullerenes (fullerenol) and C60 tris(malonic)acid, they become water soluble enabling them to cross the cell membrane and localize preferentially to mitochondria (Foley et al 2002; Youle and Karbowski 2005), which generate great masses of cellular oxygen free radicals. This phenomenon makes them useful for a variety of medical applications (Tsai et al 1997; Lotharius et al 1999; Bisaglia et al 2000). These radical scavengers have shown to protect cell growth from various toxins that can induce apoptotic injuries in vitro (Lin et al 1999; Lin et al 2002; Chen et al 2004) in different cell types such as neuronal cells (Dugan et al 1997; Bisaglia et al 2000), hepatoma cells (Huang et al 1998), or epithelial cells (Straface et al 1999).

Apoptosis is of critical importance for variety of physiological and pathological phenomenon which led numerous scientists to design experiments in this regard. Daniela Monti et al investigated the protective activity of this drug against oxidative stress-induced apoptosis. 2-deoxy-D-ribose (dRib) or TNF-αplus cycloheximide were used as agents to trigger apoptosis in human peripheral blood mononuclear cells (PBMCs) by interfering with the redox status of cell and mitochondrial membrane potential. It was found that carboxyfullerenes, also known as C60 tris(malonic)acid, was able to protect quiescent PBMCs against apoptosis by preserving the mitochondrial membrane potential integrity, which is the early stage of apoptosis (Monti et al 2000). Other interesting results showing that fullerenes have potential as biological antioxidants were also published by Dugan et al The authors treated transgenic mice carrying a defective copy of the gene encoding for human superoxide dismutase (SOD1), which led to amyotrophic lateral sclerosis (ALS), with C60 tris(malonic)acid. SOD1 knock out mice treated with C60 developed symptoms of disease 10 days later and lived 8 days longer than untreated control mice (Dugan et al 1997).

Fullerenes are also used for cytoprotective action against UVA irradiation (Xiao et al 2006). The ultraviolet A radiation (320–400nm) generates reactive oxygen species, which have a biological effect on human skin cells, leading to cell damage or cell death. Once again the radical scavenging nature of water soluble fullerene derivative namely Radical Sponge® (C60 with poly(vinylpyrrolidone)) was utilised to protect human ore mammalian cells against oxidative stress, through catalytic dismutation of superoxide. The ability of Radical Sponge® to enter into depth of human skin epidermis due to its stability towards oxidative decomposition makes it more reliable than Vitamin C and enables the prevention of both UV skin-injuries and skin aging, without photosensitization and cytotoxicity.

Water soluble fullerenes namely fullerenols and malonic acid derivatives of C60 have attracted great attention in the field of neurosciences. The brain contains a number of different unsaturated fatty acids, and underlies aerobic metabolism, and has limited ability to regenerate damaged tissues, making it a very sensitive organ towards oxidative damage caused by free radicals. These reactive oxygen species being O2- (superoxide), •OH (hydroxyl) radicals and closed shell H2O2 molecules (Halliwell 1992). Fullerene derivatives have the ability to inhibit the chain reaction of lipid peroxidation by scavenging intermediate peroxyl radicals, stopping them from attacking adjacent fatty acid chains ore membrane proteins, which would lead to glutamate-receptor-mediated excitotoxicity and apoptotic cell death. In cell culture experiments, C60 tris(malonic)acid rescued cortical neurons from a broad range of insults and was furthermore found to show robust neuroprotection in a number of other cell culture models of neurological disease including Parkinson’s disease (Dugan et al 1997).

http://www.ncbi.nlm....les/PMC2676811/


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#69 Kalliste

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Posted 05 May 2015 - 10:39 AM

Using nano-antioxidants to treat Parkinson :)

 

 

Exosomes are naturally occurring nanosized vesicles that have attracted considerable attention as drug delivery vehicles in the past few years. Exosomes are comprised of natural lipid bilayers with the abundance of adhesive proteins that readily interact with cellular membranes. We posit that exosomes secreted by monocytes and macrophages can provide an unprecedented opportunity to avoid entrapment in mononuclear phagocytes (as a part of the host immune system), and at the same time enhance delivery of incorporated drugs to target cells ultimately increasing drug therapeutic efficacy. In light of this, we developed a new exosomal-based delivery system for a potent antioxidant, catalase, to treat Parkinson's disease (PD). Catalase was loaded into exosomes ex vivo using different methods: the incubation at room temperature, permeabilization with saponin, freeze–thaw cycles, sonication, or extrusion. The size of the obtained catalase-loaded exosomes (exoCAT) was in the range of 100–200 nm. A reformation of exosomes upon sonication and extrusion, or permeabilization with saponin resulted in high loading efficiency, sustained release, and catalase preservation against proteases degradation. Exosomes were readily taken up by neuronal cells in vitro. A considerable amount of exosomes was detected in PD mouse brain following intranasal administration. ExoCAT provided significant neuroprotective effects in in vitro and in vivo models of PD. Overall, exosome-based catalase formulations have a potential to be a versatile strategy to treat inflammatory and neurodegenerative disorders.

http://www.sciencedi...168365915002138



#70 Kalliste

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Posted 12 May 2015 - 11:16 AM

Here is a neat-o up to date over-view on Mitochondrial dysfunction, seems relevant with regards to c60 although the substance is not mentioned. I hope this is not too far off-topic.

 

 

Abstract
Background

Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Examples of such illnesses include bipolar disorder, multiple sclerosis, Parkinson’s disease, schizophrenia, depression, autism, and chronic fatigue syndrome.

Discussion

While the majority of patients with multiple sclerosis appear to have widespread mitochondrial dysfunction and impaired ATP production, the findings in patients diagnosed with Parkinson’s disease, autism, depression, bipolar disorder schizophrenia and chronic fatigue syndrome are less consistent, likely reflecting the fact that these diagnoses do not represent a disease with a unitary pathogenesis and pathophysiology. However, investigations have revealed the presence of chronic oxidative stress to be an almost invariant finding in study cohorts of patients afforded each diagnosis. This state is characterized by elevated reactive oxygen and nitrogen species and/or reduced levels of glutathione, and goes hand in hand with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines.

Summary

This paper details mechanisms by which elevated levels of reactive oxygen and nitrogen species together with elevated pro-inflammatory cytokines could conspire to pave a major road to the development of mitochondrial dysfunction and impaired oxidative metabolism seen in many patients diagnosed with these disorders.

 

http://www.biomedcen...1741-7015/13/68


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#71 Kalliste

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Posted 18 May 2015 - 01:47 PM

I must have missed out on the issue of MitoFlashes.

Seems kind of related to c60 I guess.

 

 

Scientists have a crystal ball on their hands: bursts of activity in the energy-producing mitochondria in a worm’s cells accurately predict how long it will live.

The findings, published today in Nature1, suggest that an organism’s lifespan is, for the most part, predictable in early adulthood. Unlike other biomarkers for ageing, which work under limited conditions, these mitochondrial bursts are a stable predictor for a variety of genetic, environmental and developmental histories. “Mitochondrial flashes have an amazing power to predict the remaining lifespan in animals,” says study lead Meng-Qiu Dong, a geneticist who studies ageing in the Caenorhabditis elegans worm at the National Institute of Biological Sciences in Beijing. “There is truth in the mitochondrial theory of ageing.”

The mitochondria are organelles that power the cells of plants, animals and other eukaryotic organisms. During energy production, they produce reactive oxygen molecules, such as free radicals, that can cause stress and damage the mitochondria. Although mitochondria break down over time, the mitochondrial theory of ageing, first proposed2 in 1972, remains controversial and unproven. For instance, some long-lived organisms, such as naked mole rats, endure with high levels of oxidative damage. Nevertheless, many scientists think that mitochondria remain the primary drivers of ageing.

Swan song

Dong became interested in the 2008 discovery3 that mitochondria produce reactive oxygen molecules in 10-second pulses — ‘mitoflashes’ — every couple minutes. For the first time, scientists could observe individual mitochondria and their rates of activty through the course of an animal’s life. In this study, Dong initially compared mitoflash rates in short-lived C. elegans worms, which live an average of 21 days, to long-lived worms that live an average of 30 days or more. She found that, in all of the animals, there were two moments in life when mitoflashes bunched closely together: one burst during early adulthood and another during senescence.

At first, she expected that the burst later in life would be the important one. “It was a total failure,” she says. Instead, it was the early burst that revealed a correlation between flash frequency and lifespan: worms with an average lifespan of 21 days had more frequent flashes during this burst than their longer-lived brethren. The correlation held across 29 genetic mutants with various lifespans.

Mitoflashes also proved to be a powerful record of a worm’s early life experiences. For instance, worms exposed to heat shock or starvation tend to have longer lives, and predictably, their mitoflashes occurred at longer intervals. Even genetically identical worms that had different lifespans due to chance events alone showed the same correlation between mitoflash frequency and longevity. The most striking finding came when Dong treated a long-lived worm to increase its production of reactive oxygen molecules. This shortened the worm’s life and increased the rate of mitoflashes.

“It’s a great paper,” says Jan Gruber, a biogerontologist at the Yale-National University of Singapore College. He had expected to see a gradual decline in mitoflashes over time, and was particularly surprised by the burst that comes towards the end of life, a kind of swan song. “We know that the mitochondria shut down with ageing,” he says. “Why do they shut down in a dramatic fashion?”

 



#72 Kalliste

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Posted 18 May 2015 - 03:26 PM

More work on using larger structures (I think) of C60 and others to treat tumors.

 

Comparative analysis of the secondary electron yield from carbon nanoparticles and pure water medium Abstract

The production of secondary electrons generated by carbon nanoparticles and pure water medium irradiated by fast protons is studied by means of model approaches and Monte Carlo simulations. It is demonstrated that due to a prominent collective response to an external field, the nanoparticles embedded in the medium enhance the yield of low-energy electrons. The maximal enhancement is observed for electrons in the energy range where plasmons, which are excited in the nanoparticles, play the dominant role. Electron yield from a solid carbon nanoparticle composed of fullerite, a crystalline form of C60 fullerene, is demonstrated to be several times higher than that from liquid water. Decay of plasmon excitations in carbon-based nanosystems thus represents a mechanism of increase of the low-energy electron yield, similar to the case of sensitizing metal nanoparticles. This observation gives a hint for investigation of novel types of sensitizers to be composed of metallic and organic parts.

10053_2015_1194_Fig1_HTML.gif

http://link.springer...d/e2015-50908-y



#73 Kalliste

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Posted 26 May 2015 - 07:02 PM

I have been pondering this article for a few days and the logic in my mind sounds like this "Hmm Mitoflashes of ROS seems to influence lifespan somehow, and when the ROS production is dialed up with a chemical modulator the lifespan decreased, what would happen if you introduced a substance that quenches ROS effectively near the mitochondria...? Do we know of a substance that do just that? A weird little substance that has been found to increase lifespan in some trials......" :ph34r:

 

 

 

I must have missed out on the issue of MitoFlashes.

Seems kind of related to c60 I guess.

 

 

Scientists have a crystal ball on their hands: bursts of activity in the energy-producing mitochondria in a worm’s cells accurately predict how long it will live.

The findings, published today in Nature1, suggest that an organism’s lifespan is, for the most part, predictable in early adulthood. Unlike other biomarkers for ageing, which work under limited conditions, these mitochondrial bursts are a stable predictor for a variety of genetic, environmental and developmental histories. “Mitochondrial flashes have an amazing power to predict the remaining lifespan in animals,” says study lead Meng-Qiu Dong, a geneticist who studies ageing in the Caenorhabditis elegans worm at the National Institute of Biological Sciences in Beijing. “There is truth in the mitochondrial theory of ageing.”

The mitochondria are organelles that power the cells of plants, animals and other eukaryotic organisms. During energy production, they produce reactive oxygen molecules, such as free radicals, that can cause stress and damage the mitochondria. Although mitochondria break down over time, the mitochondrial theory of ageing, first proposed2 in 1972, remains controversial and unproven. For instance, some long-lived organisms, such as naked mole rats, endure with high levels of oxidative damage. Nevertheless, many scientists think that mitochondria remain the primary drivers of ageing.

Swan song

Dong became interested in the 2008 discovery3 that mitochondria produce reactive oxygen molecules in 10-second pulses — ‘mitoflashes’ — every couple minutes. For the first time, scientists could observe individual mitochondria and their rates of activty through the course of an animal’s life. In this study, Dong initially compared mitoflash rates in short-lived C. elegans worms, which live an average of 21 days, to long-lived worms that live an average of 30 days or more. She found that, in all of the animals, there were two moments in life when mitoflashes bunched closely together: one burst during early adulthood and another during senescence.

At first, she expected that the burst later in life would be the important one. “It was a total failure,” she says. Instead, it was the early burst that revealed a correlation between flash frequency and lifespan: worms with an average lifespan of 21 days had more frequent flashes during this burst than their longer-lived brethren. The correlation held across 29 genetic mutants with various lifespans.

Mitoflashes also proved to be a powerful record of a worm’s early life experiences. For instance, worms exposed to heat shock or starvation tend to have longer lives, and predictably, their mitoflashes occurred at longer intervals. Even genetically identical worms that had different lifespans due to chance events alone showed the same correlation between mitoflash frequency and longevity. The most striking finding came when Dong treated a long-lived worm to increase its production of reactive oxygen molecules. This shortened the worm’s life and increased the rate of mitoflashes.

“It’s a great paper,” says Jan Gruber, a biogerontologist at the Yale-National University of Singapore College. He had expected to see a gradual decline in mitoflashes over time, and was particularly surprised by the burst that comes towards the end of life, a kind of swan song. “We know that the mitochondria shut down with ageing,” he says. “Why do they shut down in a dramatic fashion?”

 

 



#74 bixbyte

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Posted 26 May 2015 - 08:28 PM

More work on using larger structures (I think) of C60 and others to treat tumors.

 

Comparative analysis of the secondary electron yield from carbon nanoparticles and pure water medium Abstract

The production of secondary electrons generated by carbon nanoparticles and pure water medium irradiated by fast protons is studied by means of model approaches and Monte Carlo simulations. It is demonstrated that due to a prominent collective response to an external field, the nanoparticles embedded in the medium enhance the yield of low-energy electrons. The maximal enhancement is observed for electrons in the energy range where plasmons, which are excited in the nanoparticles, play the dominant role. Electron yield from a solid carbon nanoparticle composed of fullerite, a crystalline form of C60 fullerene, is demonstrated to be several times higher than that from liquid water. Decay of plasmon excitations in carbon-based nanosystems thus represents a mechanism of increase of the low-energy electron yield, similar to the case of sensitizing metal nanoparticles. This observation gives a hint for investigation of novel types of sensitizers to be composed of metallic and organic parts.

10053_2015_1194_Fig1_HTML.gif

http://link.springer...d/e2015-50908-y

 

This study does not appear to be valid.

If one needs radiation treatment to kill cancer

and the C60 absorb the radiation to prevent cellular damage

then how does the radiation kill the cancer?

And the study is about C60 in water not C60 in oil.



#75 Kalliste

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Posted 27 May 2015 - 04:23 AM

It is a study on nanoclusters of C60 which have different characteristics. I posted it mainly because I'm starved for news on "our" c60.

 

 

More work on using larger structures (I think) of C60 and others to treat tumors.

 

Comparative analysis of the secondary electron yield from carbon nanoparticles and pure water medium Abstract

The production of secondary electrons generated by carbon nanoparticles and pure water medium irradiated by fast protons is studied by means of model approaches and Monte Carlo simulations. It is demonstrated that due to a prominent collective response to an external field, the nanoparticles embedded in the medium enhance the yield of low-energy electrons. The maximal enhancement is observed for electrons in the energy range where plasmons, which are excited in the nanoparticles, play the dominant role. Electron yield from a solid carbon nanoparticle composed of fullerite, a crystalline form of C60 fullerene, is demonstrated to be several times higher than that from liquid water. Decay of plasmon excitations in carbon-based nanosystems thus represents a mechanism of increase of the low-energy electron yield, similar to the case of sensitizing metal nanoparticles. This observation gives a hint for investigation of novel types of sensitizers to be composed of metallic and organic parts.

10053_2015_1194_Fig1_HTML.gif

http://link.springer...d/e2015-50908-y

 

This study does not appear to be valid.

If one needs radiation treatment to kill cancer

and the C60 absorb the radiation to prevent cellular damage

then how does the radiation kill the cancer?

And the study is about C60 in water not C60 in oil.

 

 



#76 Kalliste

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Posted 05 June 2015 - 11:36 AM

 

Lifestyle
Nova C60 Announces Introduction of Active Acne Cream and Clarifying Cleanser to Product Line

Nova C60 announces the addition of its new Acne Cream and Clarifying Cleanser to its product line.

nova_gplusicon-1.jpgStouffville, Canada - June 5, 2015 /MarketersMedia/ — Nova C60 (www.NovaC60.com), the leading provider of unique health and beauty products, is proud to announce the introduction of its new active Acne Cream and Clarifying Cleanser to its list of available products.

Nova C60's new acne cream and cleanser work together to clean and revitalize the skin, while also treating and eliminating acne and breakouts. The acne cream is approved by Health Canada and delivers time-released acne-fighting salicylic acid to reduce blemishes, re-invigorate the skin, and help to make it look more beautiful.

"Nova C60's acne cream and skin revitalizer also contain the Nobel Prize-winning Fullerene and Lipo Fullerene from Mitsubishi Corporation Japan," says Brad Lawson, owner of Nova C60. "In addition to controlling acne, these products also provide the skin with increased hydration and its anti-oxidants inhibit sebum production and neutrophil infiltration for superior acne-fighting skin care.”

Nova C60’s Acne Cream also has wound-healing and anti-inflammatory properties. This helps to control and heal acne, which is an inflammatory response of the skin. Essentially, these properties counteract the swelling and redness of pimples.

“The Clarifying Cleanser, in particular, neutralizes skin-damaging free radicals thanks to its controlled delivery of salicylic acid, which not only reduces existing blemishes, but also invigorates, revitalizes, and beautifies the skin,” explains Lawson. “Because the cleanser maintains a healthy pH level to improve the skin, it won’t irritate your skin or cause inflammation; it will just leave your face feeling refreshed, beautiful, and acne-free.”

“With our mission to offer the best high-quality products to our customers, it's little wonder that we decided to add these two products to our offerings," concludes Lawson.

Nova C60 offers a variety of unique products to customers around the world. For more information about the Nova C60 skin care line, visit http://www.novac60.com/.

For more information about us, please visit http://www.novac60.com

Contact Info:
Name: Brad Lawson
Organization: Revolutionary Brands Inc

Source: http://marketersmedi...duct-line/83699

 



#77 Kalliste

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Posted 05 June 2015 - 02:47 PM

 

Beyond Mitochondria, What Would be the Energy Source of the Cell? Author(s): Arturo S. Herrera, Maria del C.A. Esparza, Ghulam Md. Ashraf, Andrey A. Zamyatnin and Gjumrakch Aliev Pages 32-41 (10) Abstract: Currently, cell biology is based on glucose as the main source of energy. Cellular bioenergetic pathways have become unnecessarily complex in their eagerness to explain that how the cell is able to generate and use energy from the oxidation of glucose, where mitochondria play an important role through oxidative phosphorylation. During a descriptive study about the three leading causes of blindness in the world, the ability of melanin to transform light energy into chemical energy through the dissociation of water molecule was unraveled. Initially, during 2 or 3 years; we tried to link together our findings with the widely accepted metabolic pathways already described in metabolic pathway databases, which have been developed to collect and organize the current knowledge on metabolism scattered across a multitude of scientific articles. However, firstly, the literature on metabolism is extensive but rarely conclusive evidence is available, and secondly, one would expect these databases to contain largely the same information, but the contrary is true. For the apparently well studied metabolic process Krebs cycle, which was described as early as 1937 and is found in nearly every biology and chemistry curriculum, there is a considerable disagreement between at least five databases. Of the nearly 7000 reactions contained jointly by these five databases, only 199 are described in the same way in all the five databases. Thus to try to integrate chemical energy from melanin with the supposedly well-known bioenergetic pathways is easier said than done; and the lack of consensus about metabolic network constitutes an insurmountable barrier. After years of unsuccessful results, we finally realized that the chemical energy released through the dissociation of water molecule by melanin represents over 90% of cell energy requirements. These findings reveal a new aspect of cell biology, as glucose and ATP have biological functions related mainly to biomass and not so much with energy. Our finding about the unexpected intrinsic property of melanin to transform photon energy into chemical energy through the dissociation of water molecule, a role performed supposedly only by chlorophyll in plants, seriously questions the sacrosanct role of glucose and thereby mitochondria as the primary source of energy and power for the cells. - See more at: http://www.eurekasel...h.NvGRa8yq.dpuf

 

Interesting paper on energyproduction in the cell, posted in one of the LLLT threads. Semi related to C60 (mitochondrial stuff)


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#78 niner

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Posted 05 June 2015 - 07:38 PM

 

Our finding about the unexpected intrinsic property of melanin to transform photon energy into chemical energy through the dissociation of water molecule, a role performed supposedly only by chlorophyll in plants, seriously questions the sacrosanct role of glucose and thereby mitochondria as the primary source of energy and power for the cells. - See more at: http://www.eurekasel...h.NvGRa8yq.dpuf

 

Interesting paper on energyproduction in the cell, posted in one of the LLLT threads. Semi related to C60 (mitochondrial stuff)

 

So these guys think we are photosynthesizing?  "seriously questions the sacrosanct role of ... mitochondria"?  Wow, how does stuff like this get published?



#79 Turnbuckle

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Posted 06 June 2015 - 12:55 AM

 

 

Our finding about the unexpected intrinsic property of melanin to transform photon energy into chemical energy through the dissociation of water molecule, a role performed supposedly only by chlorophyll in plants, seriously questions the sacrosanct role of glucose and thereby mitochondria as the primary source of energy and power for the cells. - See more at: http://www.eurekasel...h.NvGRa8yq.dpuf

 

Interesting paper on energyproduction in the cell, posted in one of the LLLT threads. Semi related to C60 (mitochondrial stuff)

 

So these guys think we are photosynthesizing?  "seriously questions the sacrosanct role of ... mitochondria"?  Wow, how does stuff like this get published?

 

 

 

Look up the publisher and you will see how such crazy stuff get published--

 

Bentham Open journals claim to employ peer review; however, the fact that a fake paper generated with SCIgen had been accepted for publication, has cast doubt on this. Furthermore, the publisher is known for spamming scientists with invitations to become a member of the editorial boards of its journals.

 


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#80 Kalliste

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Posted 06 June 2015 - 04:55 AM

If it was a bunk-paper please delete it from this thread.


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#81 Turnbuckle

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Posted 06 June 2015 - 11:35 AM

If it was a bunk-paper please delete it from this thread.

 

Not necessarily bunk. It's just not clear that it has been peer reviewed. Certainly the journal you linked to has a problem. But this work also appeared in Central Nervous System Agents in Medicinal Chemistry, and the lead researcher seems legit--at least from his group's write up. On the other hand, the writing is vague and over the top, and thus slightly suspicious.

 

 

The excellence of Dr. Aliev's professional service deserves special attention. He serves as an editor or an editorial board member for many prestigious journals. He has served and is currently serving as a grant review board member and reviewer for international granting agencies and foundations. In addition, Dr. Aliev possesses prodigious administrative skills, including logical decision-making, high efficiency, and his excellent rapport with colleagues, friends, employers and subordinates. Dr. Aliev is an outstanding scientist and administrator with a unique and distinguished ability in cell and molecular biology, neurodegeneration and ultrastructural pathology as well as neurology and cardiology.

 



#82 ceridwen

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Posted 06 June 2015 - 01:12 PM

Mitochondria lurking about in people's bodies waiting to revert to their bacterial form when they will take people over and kill them. Please tell me it's not like that. I've been reading how the cells power houses turn deadly
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#83 Allen Walters

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Posted 08 June 2015 - 04:39 PM

 

Is there any known issue with interacting with pharmaceuticals?  For instance and particularly, would c60 blunt the effects or increase the rate at which the body excretes a pharmaceutical?  Say, such as an Angiotensin II receptor antagonist? 

 

Based on the number of consistent reports -- it is fair to say that C60 at a sufficient dose significantly blocks the effect of ethanol intoxication -- almost completely depending on dose -- and no hangover.

 

I can personally attest that a 45mg dose of C60 caused a significant drop in the efficacy of diazepam (valium) needing 14 mg to get the same effect as the normal 4 mg dose.

 

 

I have had the same effect with alcohol. before I used c60/oo I could only drink about three beers and I would have a hangover from that. I had even stopped drinking for several years because of it. Some months after beginning c60/oo administration I got divorced, so I started going to the bars and drinking. To my surprise I didn't get hangovers. I found that I could drink till I couldn't even crawl and no hangover. I didn't connect this to the c60/oo, I just thought I didn't get them anymore. Then I stopped c60/oo and about 6 months after, I started getting hangovers. That's when I made the connection. I started taking it again and the hangovers stopped. Seems the effects last awhile.
 


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#84 niner

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Posted 08 June 2015 - 05:01 PM

Then I stopped c60/oo and about 6 months after, I started getting hangovers. That's when I made the connection. I started taking it again and the hangovers stopped. Seems the effects last awhile.

 

This could tell us something about how long c60oo sticks around in the body, but we'd need to know how much you were taking and for how long.  If you remember, what was your dosing history?   (There's one other variable; the level of c60oo needed for hangover protection.  From those of us noticing anti-hangover effects, maybe we could figure out who's taking the least c60oo.  That would give us a vague lower bound, but it's still kind of an underdetermined problem.)



#85 sensei

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Posted 08 June 2015 - 05:26 PM

 

 

This could tell us something about how long c60oo sticks around in the body, but we'd need to know how much you were taking and for how long.  If you remember, what was your dosing history?   (There's one other variable; the level of c60oo needed for hangover protection.  From those of us noticing anti-hangover effects, maybe we could figure out who's taking the least c60oo.  That would give us a vague lower bound, but it's still kind of an underdetermined problem.)

 

 

Regarding the effect on diazepam action:

 

I only experienced it after a 45 mg dose ( 50 ml bottle made by V ) - day of

 

I'm off diazepam as of 6/1/2015  (tapered from 15 mg /day to 1 mg/day over 8 months)

 

30 ml of my homemade C60OO (maybe 20-25 mg) every other day MAY be responsible for lack of night sweats and sleeping through the night without awakening.

 

Multiple awakenings have been a hallmark of the taper, and I expected they would continue after complete cessation, but my sleep is actually better.


Edited by sensei, 08 June 2015 - 05:27 PM.

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#86 Turnbuckle

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Posted 08 June 2015 - 06:27 PM

 

Then I stopped c60/oo and about 6 months after, I started getting hangovers. That's when I made the connection. I started taking it again and the hangovers stopped. Seems the effects last awhile.

 

This could tell us something about how long c60oo sticks around in the body...

 

 

Not necessarily, as C60 could be repairing the liver, in which case its effects would last much longer than its physical presence.


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#87 niner

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Posted 09 June 2015 - 12:25 AM

 

 

Then I stopped c60/oo and about 6 months after, I started getting hangovers. That's when I made the connection. I started taking it again and the hangovers stopped. Seems the effects last awhile.

 

This could tell us something about how long c60oo sticks around in the body...

 

Not necessarily, as C60 could be repairing the liver, in which case its effects would last much longer than its physical presence.

 

I dunno.  People with very healthy livers still get very horrible hangovers if they drink too much.  I think that c60oo has to be interfering in the hangover process itself.   The effect is immediate upon starting c60oo, so that also argues against a repair process, which would need to take at least some amount of time.


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#88 HighDesertWizard

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Posted 09 June 2015 - 03:22 AM

It turns out that Alcohol impacts Cytokine expression...

 

Ethanol (alcohol) is known to alter cytokine levels in a variety of tissues including plasma, lung, liver, and brain. Studies on human monocyte responses to pathogens reveal ethanol disruption of cytokine production depending upon the pathogen and duration of alcohol consumption, with multiple pathogens and chronic ethanol promoting inflammatory cytokine production... Cytokines affect the brain and likely contribute to changes in the central nervous system that contribute to long-term changes in behavior and neurodegeneration. Together these studies suggest that ethanol disruption of cytokines and inflammation contribute in multiple ways to a diversity of alcoholic pathologies.

 

In his LongeCity profile, Turnbuckle notes a 30 year alcohol tolerance improvement. We're about the same age and I've noticed comparable effect. So is there a study that confirms the age variance response to alcohol in terms of variance in Cytokine Expression between young and old?

 

Male adolescent rats display blunted cytokine responses in the CNS after acute ethanol or lipopolysaccharide exposure, published 2015

 

...assessment of plasma endotoxin concentrations revealed (i) whereas robust increases in plasma endotoxin were observed in adults injected with LPS, no corresponding elevations were seen in adolescents after LPS; and (ii) neither adolescents nor adults demonstrated increases in plasma endotoxin concentrations following i.p. or i.g. ethanol administration. Analysis of BECs indicated that, for both routes of exposure, adolescents exhibited lower BECs than adults. Taken together, these data suggest that categorically different mechanisms are involved in the central cytokine response to antigen exposure versus ethanol administration. Furthermore, these findings confirm once again that acute ethanol intoxication is a potent activator of brain cytokines, and calls for future studies to identify the mechanisms underlying age-related differences in the cytokine response observed during ethanol intoxication.


Edited by HighDesertWizard, 09 June 2015 - 03:24 AM.

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#89 Allen Walters

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Posted 09 June 2015 - 05:42 PM

 

Then I stopped c60/oo and about 6 months after, I started getting hangovers. That's when I made the connection. I started taking it again and the hangovers stopped. Seems the effects last awhile.

 

This could tell us something about how long c60oo sticks around in the body, but we'd need to know how much you were taking and for how long.  If you remember, what was your dosing history?   (There's one other variable; the level of c60oo needed for hangover protection.  From those of us noticing anti-hangover effects, maybe we could figure out who's taking the least c60oo.  That would give us a vague lower bound, but it's still kind of an underdetermined problem.)

 

 

I was and am taking 1Tbs per day.



#90 niner

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Posted 09 June 2015 - 06:57 PM

I was and am taking 1Tbs per day.

 

Thanks Allen.  That's a pretty big dose--  15 ml.  Commercial c60oo is 0.8 to 0.9mg/ml, depending on source, so you're getting 12-13.5mg/day.  The next question is what's the minimum amount of c60oo that provides an anti-hangover effect?  I've been using 7.5mg/week for a while, and haven't had a hangover in a long time.  I don't know if I've really had enough alcohol to generate a hangover, though.







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