Reply To: Scripts 2015

[EKKeymaster]

[F1]This would inclue Genetics-Nano-Glyphosates-Chemtrails—Pesticides-Industrial Pollutants-Endocrine Disrupting Chemicals-Processed Foods-Sugars-Sweetners-XenoEstrogens-Flouride-Metals—Toxic chemicals in tobacco-Mercury from Fish and Vaccines- —etc
[F2]Today this could be a cause due to NANO spraying and Glyphosate contamination which would include the organics since they use this on those foods as well
[F3]Now that is what I call a success—the determining factor here is that the medical people have no idea what to do and when only 20-25% are successful what is not indicated in this study is if they are debilitated as a result of either treatment —or the use of mainstream solutions
[F4]Incredible eh—they won’t go near it and yet they advocate this
[F5]Does this sound like the Mark of the Beast mentioned biblically—without the mark one cannot buy or sell anything—just a thought
[F6]Stats Like this can be fabricated—and most times are unreliable as facts or truth
[F7]Interesting thing here for a democratic country they are being un democratic offering no freedom of choice and yet these are the very ones who would critize different cultures and religions for also being draconian –what hypocracy
[F8]This also can be true with any form of exercise—when one utilizes a simple means of calculating weight X movement and for a period of time you will see results—take for example time your self for 10 20 minutes and do one exercice for that time frame—and then measure the weight times the amount of times –you moved it in some fashion—that will equal poundage or tonnage depending on the weight and the amount it was moved —the same principle will apply with movement
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Show of the Month May 9 2015
 
NanoParticles in the Bloodstream
 
Scientists resolve debate over how many bacteria fight off invaders
 
Researchers follow zinc to uncover pathway that fine-tunes brain signaling
Targeting cancer therapy with phosphoproteomics
USDA Gives $3.8 Million in Grants to Develop and Promote Nanotech in Food
 
Soft robot- Shaping itself and moving with own internally generated power
Scientists resolve debate over how many bacteria fight off invaders
 
 
 
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NanoParticles in the Bloodstream
10.28.04
 
Molecule-size sensors inside astronauts’ cells could warn of health impacts from space radiation.
 
 
Wouldn’t it be nice if the cells in your body would simply tell you when you’re starting to get sick, long before symptoms appear? Or alert you when a tumor is growing, while it’s still microscopic and harmless? –The ability to detect changes inside of individual cells while those cells are still inside your body would be a boon to medicine. NASA-supported scientists are developing a technology right now that could, if it works, do exactly that.–The scientists don’t actually coax the cells into talking, of course. The idea is to place “nanoparticles” inside the cells to function as molecule-size sensors. Whenever these sensors encounter certain signs of trouble — a fragment of an invading virus perhaps — they would begin to glow, signaling the outside world that something is wrong.[F1]–It’s an elegant technology, and because it can be customized to target many combinations of specific cell types and specific problems[F2], it’s also a very potent one. Research on nanoparticles has blossomed in recent years, with scientists exploring how they can be used to treat everything from cancer to genetic diseases such as cystic fibrosis. NASA is interested in how this technology might help tackle another health issue– radiation exposure.-One of the main hurdles for a mission to Mars is the radiation dose that astronauts would receive during their 6-month journey there. The spaceship would be shielded, but the best radiation shields NASA has now might not fully protect the astronauts. So scientists are looking for medical ways to monitor, prevent, and repair the ill effects of radiation. To make the challenge even harder, these solutions must work well in space, where astronauts must be able to treat themselves, and where there’s little spare room for bulky medical equipment.-James Baker, director of the Center for Biologic Nanotechnology at the University of Michigan, believes that nanoparticles can help. His research group has received a grant from NASA to look into it. “Nanoparticles let us monitor the actual biological impact of radiation on the astronauts’ bodies, which is more meaningful than simply measuring the radiation itself,” Baker explains. [F3]
 
Above: Nanoparticles are larger than typical molecules but smaller than viruses. (They’re labeled ‘nanoscopic’ in this diagram). They’re similar in size to many proteins, which is part of the reason the can operate well inside of cells. Image courtesy University of Michigan-Ann Arbor.—Picture this: Before a space mission, an astronaut uses a hypodermic needle to inject a clear fluid, laced with nanoparticles, into his bloodstream. During flight, he puts a small device in his ear. This device, shaped like a hearing aide, uses a tiny laser to count glowing cells as they flow through capillaries in the eardrum. A wireless link relays those data to the spaceship’s main computer for processing.–This sci-fi scenario is still at least 5 to 10 years away, but a lot of the necessary pieces are already taking shape in the laboratory[F4].–That clear fluid injected into the astronaut’s bloodstream would contain millions of microscopic nanoparticles. The nanoparticles themselves are nothing new: Scientists have been using them in the laboratory for at least 5 years, and they have employed them safely in lab animals.–The particular kind of nanoparticle that Baker uses resembles tumbleweed: a little ball-shaped bundle of branching “twigs” growing out from a central point. –
nanoparticles called dendrimers
By itself, this tumbleweed is inert. (That’s good: it means it’s not toxic.) It only serves as a generic platform upon which to build. All the useful functions of the nanoparticle — seeking out the right kind of cells, detecting signs of radiation damage, offering up a fluorescent “red flag” — come from molecules attached onto this scaffolding. The free ends of the twigs provide lots of binding points where these molecules can be attached (128 locations with the nanoparticles Baker’s group uses)[F5].
Right: The nanoparticles that Baker’s group uses are called ‘dendrimers,’ and are built up by adding branching segments around a central core. Image courtesy University of Michigan-Ann Arbor. [More]–Choosing which molecules to attach is how scientists customize the nanoparticle to do their bidding. For example, Baker’s group wants to tweak their nanoparticles to enter a kind of white blood cell called a lymphocyte, which is especially sensitive to radiation.–“How do we specifically target lymphocytes?” asks Thommey Thomas, a research assistant professor on Baker’s team. “Because once you inject nanoparticles into the bloodstream they can go anywhere, right?”–“We had to find some specific targeting molecules on the surface of these lymphocytes,” he explains.–All of the body’s cells naturally have “receptor” molecules embedded on their outer surfaces. These receptors control which chemicals can enter the cell: for example, a kidney hormone in the bloodstream only enters kidney cells. By attaching a molecule to their nanoparticles that matches up with a specific receptor on lymphocytes, the researchers assure that these roaming nanoparticles wind up inside only the right cells[F6].–Left: James Baker, director of the Center for Biologic Nanotechnology at the University of Michigan. [More]–Once inside the lymphocytes, nanoparticles need a way to detect radiation damage. One way is to watch for signs that the cell is about to self-destruct. Lymphocytes commit cellular suicide (called “apoptosis”) when they’ve been damaged by radiation. This is a genetically programmed behavior carried out by special “suicide” enzymes. Baker’s group has discovered how to attach to the nanoparticles a fluorescent dye molecule that reacts to these suicide enzymes. [F7]Lymphocytes beginning to self-destruct due to radiation damage would glow.–The research group has also developed a laser system to count the glowing cells. They’ve already shown that it can count cells in a mouse’s bloodstream as those cells pass through the capillaries in its ear, but Baker says it’s still too early to know what form this laser system would take for a space mission–maybe a micro-laser integrated into a hearing-aide-like device, he speculates.–The net result: continuous, real-time monitoring of radiation damage to the cells in an astronaut’s bloodstream — no bulky medical equipment required.
More Information
Center for Biologic Nanotechnology — home page for the group at the University of Michigan performing the research discussed in this article
Voyage of the Nano-surgeons — ([email protected]) NASA-funded scientists are crafting microscopic vessels that can venture into the human body and repair problems — one cell at a time.
Can People Go to Mars? — ([email protected]) Space radiation between Earth and Mars poses a hazard to astronauts. How dangerous is it out there? NASA scientists are working to find out.
Dr. James Baker — biographical sketch for the director of the Center for Biologic Nanotechnology
 
 
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Scientists resolve debate over how many bacteria fight off invaders
Date:May 7, 2015
Source:Rockefeller University
Every inch of our body, inside and out, is oozing with bacteria. In fact, the human body carries 10 times the number of bacterial cells as human cells. Many are our friends, helping us digest food and fight off infections, for instance. But much about these abundant organisms, upon which our life depends, remains mysterious. In research reported May 7 in Cell, scientists at Rockefeller finally crack the code of a fundamental process bacteria use to defend themselves against invaders.–For years, researchers have puzzled over conflicting results about the workings of a type of immune system found in many species of bacteria. Some data showed that, when a virus invaded a bacterial cell, this mechanism — known as type III CRISPR-Cas — would target the virus’s DNA, preventing it from adopting the bacteria’s machinery in order to copy itself and infect more bacteria. But other experiments suggested type III CRISPR-Cas could only disable a virus by cleaving the viral RNA.–Luciano Marraffini and Poulami Samai, both at Rockefeller, wanted to get to the bottom of this puzzle. In their experiments, Samai, a postdoctoral fellow, tested the cleavage of DNA and RNA by the type III CRISPR-Cas system. But she added a key ingredient no one else had before, a protein known as RNA polymerase, which the cell uses to transcribe DNA to RNA. She and Marraffini, head of the Laboratory of Bacteriology, saw that CRISPR-Cas did, indeed, cleave the RNA produced from a virus’s DNA — but it would also cleave the virus’s DNA.–There are advantages to such a two-pronged system, says Marraffini. Many viruses integrate into the genomes of the cells they infect and remain dormant, he says, causing no harm. In fact, these viruses can be beneficial to bacteria, by carrying toxins that help bacteria promote their own survival, for instance. The diphtheria toxin, for instance, is secreted by a species of bacteria, but the gene encoding the toxin comes from a virus. “By requiring viruses to begin transcribing their DNA into RNA before disabling them, the type III CRISPR-Cas system leaves dormant viruses intact, allowing them to continue benefiting the bacteria that host them,” he notes.-Learning the details of how microbes carry out their functions can have important implications for health and science, Marraffini says. Besides being an incredibly abundant form of life on the planet, fueling the health and disease of every species and ecosystem, microbes have been the source of a number of technological tools that have revolutionized science and medicine.–“More than forty years ago, scientists discovered enzymes that cut DNA from studying the viruses that infect bacteria, inspiring a new class of tools that created a revolution in biomedicine,” says Marraffini. Now, new technology based on another type of CRISPR-Cas is leading another wave in that revolution, allowing scientists to quickly and easily manipulate genomes in ways they never could before. “This is a testament to how the basic biology of microbes can be very useful. Microbes are a crucial part of biology on the planet, and it’s important to understand how they work.”–Story Source-The above story is based on materials provided by Rockefeller University. -Journal Reference-Luciano Marraffini et al. Co-transcriptional DNA and RNA Cleavage during Type III CRISPR-Cas Immunity. Cell, May 2015 DOI: 10.1016/j.cell.2015.04.027 show
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Researchers follow zinc to uncover pathway that fine-tunes brain signaling
A study team led by researchers at the University of Pittsburgh School of Medicine who used specially developed technologies to “follow the zinc” have uncovered a previously unknown pathway the brain uses to fine-tune neural signaling — and that may play a role in Alzheimer’s and other diseases. Their findings appear online this week in the Proceedings of the National Academy of Sciences.–Scientists have long observed the presence of bubble-like vesicles that contain the neurotransmitter glutamate and zinc at the synapses, specialized contacts among neurons where neurotransmitters are released to propagate electrical signals through the brain. Glutamate is the major excitatory neurotransmitter in the brain, but the need for synaptic zinc, an essential element that acts as a co-factor for many enzyme and regulatory proteins, has not been understood, said Thanos Tzounopoulos, Ph.D., associate professor in the Auditory Research Group, Department of Otolaryngology, Pitt School of Medicine.–“Until now, we haven’t had the ability to quantify or follow zinc when it is released into the synaptic cleft,” he said. “In this study, we employed new tools to do that and found a pathway that could be important for conditions such as Huntington’s disease and Alzheimer’s.”Co-investigator Stephen Lippard, Ph.D., and his team at the Massachusetts Institute of Technology (MIT) developed an agent that fluoresces when it binds zinc, making it possible for the first time to measure zinc levels accurately and track the element’s movements. They also created an agent that blocks zinc activity, thus allowing them to disrupt the metal’s actions to determine its function.–The researchers learned that, indeed, zinc was released from vesicles and diffused from the release site. Surprisingly, it could bind to so-called extrasynaptic glutamate NMDA-type receptors, just like the neurotransmitter glutamate. Whereas glutamate activates these receptors, zinc inhibits them.”Glutamate acts like an accelerator of neuronal activity, while zinc behaves like a brake that fine tunes that signal,” Dr. Tzounopoulos said. “The receptors that zinc influences are thought to play a role in neurodegenerative diseases, so these findings could open new research avenues in the field.”–Story Source-The above story is based on materials provided by University of Pittsburgh Schools of The Health Sciences. Note: Materials may be edited for content and length.-Journal Reference-Charles T. Anderson, Robert J. Radford, Melissa L. Zastrow, Daniel Y. Zhang, Ulf-Peter Apfel, Stephen J. Lippard, Thanos Tzounopoulos. Modulation of extrasynaptic NMDA receptors by synaptic and tonic zinc. Proceedings of the National Academy of Sciences, 2015; 201503348 DOI: 10.1073/pnas.1503348112 –University of Pittsburgh Schools of the Health Sciences. “Researchers follow zinc to uncover pathway that fine-tunes brain signaling.” ScienceDaily. ScienceDaily, 4 May 2015. <www.sciencedaily.com/releases/2015/05/150504154950.htm>.
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Targeting cancer therapy with phosphoproteomics
Medulloblastomas (MB), the most common malignant pediatric brain tumor, originate from dysregulation of developmental signaling pathways. To discover important drug targets within these pathways, researchers have undertaken the first quantitative mass spectrometry-based phosphoproteomic approach to identify important phosphorylation events, using the Hh signaling pathway as the model.- Quantitative phosphoproteomic analysis was performed using SILAC (Stable Isotope Labeling with Amino acids in Cell culture), combined with strong cation exchange fractionation and phosphopeptide enrichment by immobilized metal affinity chromatography (IMAC), followed by multiplexed quantitative mass spectrometry- The study revealed changes in phosphorylation of 94 proteins only 25 minutes after Shh exposure. Motif analysis revealed a novel and critical role for the kinase, CK2, in mediating 45 percent of all early phosphorylation events. Importantly, CK2 affects terminal Hh signaling components, circumventing challenges of emergence of resistance and a priori resistance commonly encountered with existing small molecule inhibitors developed for medulloblastoma. CK2 inhibitors demonstrated early and sustained inhibition of Hh signaling across several mammalian cell types, including MB cells. In vivo, mice harboring flank MB allografts derived from Ptch+/−;Tpr53−/− tumor harbouring a point mutation in Smo that renders them resistant to other Hh pathway inhibitors, showed near-complete cessation of tumor growth in response to TBB, a highly potent and selective inhibitor of CK2.– This quantitative phosphoproteomic approach to Hh signaling has provided a perspective that was unattainable with previous transcription and genome-based efforts. This success using one pathway will set the foundation for others to apply a similar approach in different tumor initiating pathways.–Story Source-The above story is based on materials provided by American Association of Neurological Surgeons (AANS). Note: Materials may be edited for content and length.–American Association of Neurological Surgeons (AANS). “Targeting cancer therapy with phosphoproteomics.” ScienceDaily. ScienceDaily, 6 May 2015. <www.sciencedaily.com/releases/2015/05/150506182709.htm>. This quantitative phosphoproteomic approach to Hh signaling has provided a perspective that was unattainable with previous transcription and genome-based efforts. This success using one pathway will set the foundation for others to apply a similar approach in different tumor initiating pathways.–Story Source-The above story is based on materials provided by American Association of Neurological Surgeons (AANS). Note: Materials may be edited for content and length.–American Association of Neurological Surgeons (AANS). “Targeting
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USDA Gives $3.8 Million in Grants to Develop and Promote Nanotech in Food
The US Department of Agriculture (USDA) is giving millions of dollars to universities across America for the development and study of nanotechnology to be used in food.–Despite research existing on the potential concerns over health and safety of nanotech in food, the USDA wants to push forward with nanotech in full force. This agency of the government is known for its revolving door relationship with Big Food.–A statement from the Center for Food Safety sums up the health concerns well–“The subject of nanotechnology and our food supply offers an alarming view of the potential for human health issues. Amazingly, the U.S. government currently does not regulate the use of nanotechnology in food products, despite its widespread use and serious public health concerns. Europe and the Canadian government have taken the first steps to limit the use of nanotechnology in food, but the U.S. has so far only issued draft guidelines to companies.”–So what is this nanotechnology exactly? That’s a complicated question. According to the USDA, “Nanomaterials can occur naturally, for example in volcanic ash and ocean spray, and may also be incidental byproducts of human activity, such as homogenization or milling. They can also be produced intentionally with specific properties through certain chemical or physical processes.”–These intentionally created nanomaterials have been in use in the US food supply for over ten years — mostly in packaging and processing. According to UnderstandingNano.com,-“Clay nanocomposites are being used to provide an impermeable barrier to gasses such as oxygen or carbon dioxide in lightweight bottles, cartons and packaging films. Storage bins are being produced with silver nanoparticles embedded in the plastic. The silver nanoparticles kill bacteria[F1] from any material that was previously stored in the bins, minimizing health risks from harmful bacteria.”–Nanotech is increasingly being pursued for use directly in the food we eat, rather than just in the packaging. According to Popular Mechanics:“The most commonly used nanoparticle in foods is titanium dioxide. It’s used to make foods such as yogurt and coconut flakes look as white as possible, provide opacity to other food colorings, and prevent ingredients from caking up. Nanotech isn’t just about aesthetics, however. The biggest potential use for this method involves improving the nutritional value of foods.-“Nano additives can enhance or prevent the absorption of certain nutrients. In an email interview with Popular Mechanics, Jonathan Brown, a research fellow at the University of Minnesota, says this method could be used to make mayonnaise less fattening by replacing fat molecules with water droplets.”-There has been a 1000% increase in nanotech used for food since 2008 and is now being deployed by major companies including Kraft, General Mills, Hershey, Nestle, Mars, Unilever, Smucker’s and Albertsons.-This is where the $3.8 million in USDA grants come in. According to the PDF released by the USDA, the grants entail; “University of Wisconsin, Madison, WI $450,100 | Tailor polyanhydride nanoparticles to encapsulate and release antibiotics to protect shrimp against bacterial pathogens.”
“Pennsylvania State University, University Park, PA $447,788 | Obtain a basic understanding of starch-nanoclay interactions in dispersion; evaluate the disintegration, release, and antimicrobial properties of cross-linked, crystallized, and iodine-loaded starch fibers; determine the effect of alignment and drawing on thermomechanical properties of starch fibers; and assess the feasibility of using a multi-jet electrospinning setup to scale the electrospinning process for starch fiber production.”
“Rutgers University, New Brunswick, NJ $450,000 | Complete a national survey that will examine the acceptance of food nanotechnology; assess consumers’ beliefs about the relationship of nanotechnology to healthfulness; evaluate acceptability of nanomaterials in functional foods and pet food applications; examine the acceptable characteristics of nano-enabled smart food packaging; assess use value of visuals communicating the potential for nanotechnology; and examine how consumers use visuals to interpret nanotechnology concepts.”
The Rutgers University grant reveals that the USDA will be funding market research to directly benefit the businesses seeking to manufacture and market nanotechnology for food.-What are the real implications of this? There’s one thing for sure; the element of power is a very necessary thing to consider. With all technology like this, monopolization and hierarchical structures are a potential problem. The USDA and other health oversight agencies have a long track record of approving controversial practices used in our food that later turn out to have deadly health and environmental impacts. Understanding the current players in the agro-tech business including Monsanto and Syngenta, you can see how this could end badly.-The implications of this are significant for the future of Agorism, sustainable food, independent agricultural business, monopolization of food, the health of the people consuming this food, and much more.-No one is saying that nanotech in food is inherently bad, but with the history of the organizations funding this technology, people are naturally suspicious. More research is needed and concerns must be addressed before nanotech in our food becomes our next big mistake.-Please share this with as many people as possible. It is relevant to everyone.-This article is free and open source. You have permission to republish this article under a Creative Commons license with attribution to the author and TheAntiMedia.org. Tune in! The Anti-Media radio show airs Monday through Friday @ 11pm Eastern/8pm Pacific. Image credit: National Cancer Institute. Help us fix our typos: [email protected].
 
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Soft robot- Shaping itself and moving with own internally generated power
Date: May 5, 2015
Source: University of Pittsburgh
Summary:What if a new material would allow for development of a ‘soft robot’ that could reconfigure its own shape and move using its own internally generated power?
 
 
 
Time evolution of a rectangular SP-BZ gel in non-uniform light; time increases from (a) to (d). Both ends of the sample are exposed to light; the central circular region is not illuminated.
For decades, robots have advanced the efficiency of human activity. Typically, however, robots are formed from bulky, stiff materials and require connections to external power sources; these features limit their dexterity and mobility. But what if a new material would allow for development of a “soft robot” that could reconfigure its own shape and move using its own internally generated power?–By developing a new computational model, researchers at the University of Pittsburgh’s Swanson School of Engineering have designed a synthetic polymer gel that can utilize internally generated chemical energy to undergo shape-shifting and self-sustained propulsion. Their research was published April 30th in the journal Scientific Reports, published by Nature.–The authors are Anna C. Balazs, PhD, the Swanson School’s Distinguished Professor of Chemical and Petroleum Engineering and the Robert v. d. Luft Professor; and Olga Kuksenok, PhD, –Research Associate Professor.–“Movement is a fundamental biological behavior, exhibited by the simplest cell to human beings. It allows organisms to forage for food or flee from predators. But synthetic materials typically don’t have the capability for spontaneous mechanical action or the ability to store and use their own energy, factors that enable directed motion” Dr. Balazs said. “Moreover in biology, directed movement involves some form of shape changes, such as the expansion and contraction of muscles. So we asked whether we could mimic these basic interconnected functions in a synthetic system so that it could simultaneously change its shape and move.”-As a simple example in nature, Drs. Balazs and Kuksenok use the single-celled organism euglena mutabilis, which processes energy to expand and contract its shape in order to move. To mimic the euglena’s mobility, Drs. Balazs and Kuksenok looked to polymer gels containing spirobenzopyran (SP) since these materials can be morphed into different shapes with the use of light, and to Belousov-Zhabotinsky (BZ) gels, a material first fabricated in the late 1990s that not only undergoes periodic pulsations, but also can be driven to move in the presence of light.-“The BZ gel encompasses an internalized chemical reaction so that when you supply reagents, this gel can undergo self-sustained motion,” Dr. Kuksenok explains. “Although researchers have previously created polymer chains with both the SP and BZ functionality, this is the first time they were combined to explore the ability of “SP-BZ” gels to change shape and move in response to light.”-As Balazs and Kuksenok noted, these systems are distinctive because they not only undergo self-bending or folding, but also self-propelled motion. Namely, the material integrates the powerful attributes of each of the components-the ability of SP-functionalized gels to be “molded” with light and the autonomous mechanical actions of the BZ gels.-According to Dr. Balazs, there were unexpected results during their research. “Uniform light exposure won’t work. We had to place the light at the right place in order for the gel to move. And if we change the pattern of the light, the gel displays a tumbling motion.-“We also found that if we placed the SP in certain regions of the BZ gel and exposed this material to light, we could create new types of self-folding behavior.” The next phase of the research will be to combine the patterning of the SP and BZ functionality in the gels with the patterning of the light to expand the polymer’s repertoire of motion.–Dr. Balazs adds that these SP-BZ gels could enable the creation of small-scale soft robotics for microfluidic devices that can help carry out multi-stage chemical reactions.–“Scientists are interested in designing biomimetic systems that are dissipative — they use energy to perform a function, much like our metabolism allows us to carry out different functions,” she explained. “The next push in materials science is to mimic these internal metabolic processes in synthetic materials, and thereby, create human-made materials that take in energy, transform this energy and autonomously perform work, just as in biological systems.”–The benefit of using polymer gels instead of metals and alloys to build a robot is that it greatly reduces its mass, improves its potential range of motion and allows for a more “graceful” device.–“To put it simply, in order for a robot to be able to move more autonomously in a more biomimetic way, it’s better if it’s soft and squishy,” Dr. Kuksenok says. “It’s ability to grab and carry something isn’t impeded by non-flexible, hard edges. You’d also like its energy source incorporated into the design so that it’s not carrying that as extra baggage. The SP-BZ gel is pointing us in that direction.”–Story Source-The above story is based on materials provided by University of Pittsburgh. Note: Materials may be edited for content and length.-Journal Reference-Olga Kuksenok, Anna C. Balazs. Designing Dual-functionalized Gels for Self-reconfiguration and Autonomous Motion. Scientific Reports, 2015; 5: 9569 DOI: 10.1038/srep09569
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[F1]Including yours—brain damage—liver damage—skeletal damage-spleen damage and the oxidation of healthy cells throughout the body and the use with nanobots inside the body
[F2]NanoParticles—are a billionth in size—and with the intro on nano becoming incorporated in everything today the discarding and waste management of these particulates are becoming more prevalent
[F3]They are talking micron levels which is a millionth in size
[F4]In other words they had the social network they had in there homeland and that was transferred with them—so environmental factors then would have been minimized stress wise due to the network of the cultural connection—which the ones who have been assimilated would not have that type of support
And immigrants usually will stick together even if they are from differing countries—due to the social aspect
[F5]Studies done on what could get effected in the Body
[F6]So this will imply strongly we will need something more effective to reduce or remove these out of the body
[F7]Best to avoid any and all products made with any nano compostions—since there is no way to prevent the harmful effects—that so far can be determined
[F8]Interesting —a explosion and the reactor is in safe stable –hmm I am reall y impressed with this fantasy
[F9]I am again impressed
[F10]Seems to me it was not exactly ready—potential sabotage??just a thought
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Show of the Month May 16 2015
 
Link between vitamin E, exposure to air pollution
Saffron and retina- neuroprotection and pharmacokinetics
Study shows where damaged DNA goes for repair
Scientists Find Alarming Deterioration In DNA Of The Urban Poor
Is the toxic potential of nanosilver dependent on its size?
Nanoparticles can damage DNA, increase cancer risk
Explosion rocks nuclear power plant in New York
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Link between vitamin E, exposure to air pollution
­ A new study from King’s College London and the University of Nottingham has found an association between the amount of vitamin E in the body, exposure to particulate pollution and lung function. The paper adds to growing evidence from previous studies suggesting that some vitamins may play a role in helping to protect the lungs from air pollution. Although the new study did not specifically demonstrate a protective effect, it is the first to show a clear link between vitamin E concentrations in the blood and exposure to fine particulate pollution in the general population.– Particulate matter (PM) [F2]is one of the main air pollutants thought to be damaging to human health. Previous studies have reported an inverse association between exposure to PM and lung function. However, the underlying mechanisms linking ambient air pollution to lung function are not yet fully understood–The new data, published in the American Journal of Respiratory and Critical Care Medicine, looked at the association between lung function and a set of metabolites — chemical signatures circulating in the blood — and between these metabolites and exposure to PM10 and PM2.5 (particles smaller than 10 and 2.5 microns, respectively)[F3] determined as the concentrations of these pollutants at the participants’ residence-Two-hundred and eighty metabolites were measured in the blood of over 5,500 fasting volunteers from the Twins UK study who had also undergone a spirometry or lung test. This test determines the lung’s forced vital capacity (FVC), a measure of the amount of air you can exhale with force after you inhale as deeply as possible, and forced expiratory volume (FEV), a measure of the amount of air you can exhale with force in one breath–. A subset of this group of twins — around 500 participants — living in the Greater London area also had their long-term exposure to PM estimated from their postcode using computer modelling of air pollution across London. Participants completed a medical history and lifestyle questionnaire, including questions on whether they took vitamin supplements– The profiling revealed 13 metabolites significantly associated with FVC, 10 of which were also identified for FEV. Of the metabolites associated with lung function, eight were also significantly associated with exposure to both PM2.5 and PM10. In all eight instances, a higher exposure to PM was found to correlate with lower levels of the metabolite and a lower FEV.– Among the eight metabolites identified were two well-known antioxidants, alpha tocopherol or a-tocopherol (biologically active form of Vitamin E) and a metabolite of ascorbic acid (Vitamin C) known as threonate. Both compounds have previously been linked to lung function as well as exposure to PM-The strongest association both with PM2.5 and FEV was seen with vitamin E. Individuals with a higher exposure to PM2.5 had significantly lower levels of alpha-tocopherol and also had lower lung function. These findings provide further evidence supporting the theory that PM damages lungs through oxidative attack while alpha-tocopherol acts to minimise oxidative injury.-Dr Ana Valdes, Reader at the University of Nottingham and co-author of the study, explained: ‘Our work builds on a number studies exploring whether some vitamins can counteract the negative effect on lungs caused by air pollution. More work is needed to establish whether antioxidant supplements do indeed provide protection to the lungs in the general population.’-Professor Frank Kelly, Head of the Environmental Research Group at King’s College London and co-author of the study, said: ‘These new findings are consistent with previous reports which observed lower levels of vitamin E in people with lung conditions such as asthma. However, we do not yet fully understand which types of particulate pollution specifically damage the lungs or which vitamins best interfere with this pathway to reduce the level of damage– Story Source–The above story is based on materials provided by King’s College London.
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Saffron and retina- neuroprotection and pharmacokinetics.
Vis Neurosci. 2014 Sep;31(4-5):355-61
Authors: Bisti S, Maccarone R, Falsini B
Abstract
Age-related macular degeneration (AMD) is a retinal neurodegenerative disease whose development and progression are the results of a complex interaction between genetic and environmental risk factors. Both oxidative stress and chronic inflammation play a significant role in the pathogenesis of AMD. Experimental studies in rats with light-induced photoreceptors degeneration demonstrated that saffron may protect photoreceptor from retinal stress, preserving both morphology and function and probably acting as a regulator of programmed cell death, in addition to its antioxidant and anti-inflammatory properties. Recently, a randomized clinical trial showed that in patients with early AMD, dietary supplementation with saffron was able to improve significantly the retinal flicker sensitivity suggesting neuroprotective effect of the compound. Here, we examine the progress of saffron dietary supplementation both in animal model and AMD patients, and discuss the potential and safety for using dietary saffron to treat retinal degeneration. –PMID: 24819927 [PubMed – indexed for MEDLINE]
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Study shows where damaged DNA goes for repair
Date:May 3, 2015
Source:Tufts University
 
Summary-New research sheds light on the process of DNA repair in the cell. Expanded repeats of the CAG/CTG trinucleotide in yeast shift to the periphery of the cell nucleus for repair. This shift is important for preventing repeat instability and genetic disease. Going out to the ‘repair shop’ at the nuclear periphery is a previously unrecognized yet important step to maintain repetitive DNA and to prevent damage to chromosomes, researchers report–A Tufts University study sheds new light on the process by which DNA repair occurs within the cell. In research published in the May 15 edition of the journal Genes & Development and available May 4 online in advance of print, Tufts University biologist Catherine Freudenreich and her co-authors show that expanded repeats of the CAG/CTG trinucleotide (CAG) in yeast shift to the periphery of the cell nucleus for repair. This shift is important for preventing repeat instability and genetic disease.–CAG expansions are significant because they are at the root of several neurodegenerative and neuromuscular diseases such as Huntington’s disease, myotonic dystrophy and multiple subtypes of spinal cerebella ataxia.–Short triplet repeats do not always cause problems. However, sometimes short triplet repeats expand and become longer than normal. The expanded repeat sequences change the shape of the DNA molecule from a double helix into a hairpin-like structure that is difficult for the cellular machinery to replicate and repair and can cause breakage of the DNA molecule.–Disease occurs when the numbers of expanded CAG trinucleotide repeats exceed a stability threshold. For Huntington’s disease, the threshold is 38 to 40 repeats. Myotonic dystrophy results when there are close to 200 repeats.–“Appropriate repair of DNA damage at CAG repeats is vital to the cell as proper repair can prevent further expansion and aggravation of the disease,” says Freudenreich.–In their study, “Regulation of Recombination at Yeast Nuclear Pores Controls Repair and Triplet Repeat Stability,” the researchers introduced CAG repeats of different sizes into budding yeast chromosomes. The repeat-containing chromosomes were tagged with a fluorescent molecule, so that their location in the cell nucleus could be followed visually.–“We found that the chromosomes containing the expanded CAG repeats moved from the interior of the nucleus to the nuclear periphery to be repaired,” says Freudenreich. “Our research shows that the DNA with expanded repeats makes this ‘trip’ for repairs. Proximity to the nuclear envelope helps the repair of the repeat to occur without mistakes.”-“When the movement of the DNA molecule was prevented, the chromosomes broke more frequently, and the repeat was more likely to be mutated,” says Freudenreich. “Thus, going out to the ‘repair shop’ at the nuclear periphery is a previously unrecognized yet important step for repetitive DNA to be maintained and to prevent damage to chromosomes.”–“The longer the repeat, the greater the frequency of relocation,” Freudenreich notes. “For example, CAG-130 relocates more often than CAG-70, and an unexpanded CAG-15 does not relocate more than a non-repeat control. We think if the replication machinery stalls at the repeat it triggers relocation.”–Normally, each single strand of DNA serves as a template for remaking the other strand. The enzymes involved in DNA replication rebuild each strand to make two chromosomes out of one. One section of the double-stranded DNA molecule is separated into two single strands. The resulting Y-shaped structure is called the replication fork. This process stalls when there is a problem with the DNA.–At the periphery, the damaged DNA interacts with the nuclear pore complexes (NPCs), a complex of proteins that serves as gatekeeper between the cell’s nucleus and the surrounding cytoplasm. One of these gatekeepers is the Nup84 complex and the associated Slx5/8 complex. They are present at every NPC.–The research team showed that both of these complexes are needed for repeat DNA to be repaired properly. The Slx5/8 complex plays a vital role: it is required for tethering the repeat DNA to the NPC, and it appears to regulate a known repair protein (Rad52) in order to facilitate appropriate repair, thereby preventing repeat expansions and chromosome breakage.–“The nuclear pore complex plays a role in preventing chromosome breaks as well as preventing instability of the CAG repeat, so it has a role in DNA repair,” says Freudenreich. Story Source-The above story is based on materials provided by Tufts University. Note: Materials may be edited for content and length. Journal Reference-Xiaofeng A. Su, Vincent Dion, Susan M. Gasser, Catherine H. Freudenreich. Regulation of recombination at yeast nuclear pores controls repair and triplet repeat stability. Genes & Development, 2015; DOI: 10.1101/gad.256404.114
 
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Scientists Find Alarming Deterioration In DNA Of The Urban Poor
The urban poor in the United States are experiencing accelerated aging at the cellular level, and chronic stress linked both to income level and racial-ethnic identity is driving this physiological deterioration.–These are among the findings published this week by a group of prominent biologists and social researchers, including a Nobel laureate. Dr. Arline Geronimus, a visiting scholar at the Stanford Center for Advanced Study and the lead author of the study, described it as the most rigorous research of its kind examining how “structurally rooted social processes work through biological mechanisms to impact health.”
What They Found
Researchers analyzed telomeres of poor and lower middle-class black, white, and Mexican residents of Detroit. Telomeres are tiny caps at the ends of DNA strands, akin to the plastic caps at the end of shoelaces, that protect cells from aging prematurely. Telomeres naturally shorten as people age. But various types of intense chronic stress are believed to cause telomeres to shorten, and short telomeres are associated with an array of serious ailments including cancer, diabetes, and heart disease. Evidence increasingly points to telomere length being highly predictive of healthy life expectancy. Put simply, “the shorter your telomeres, the greater your chance of dying.”-The new study found that low-income residents of Detroit, regardless of race, have significantly shorter telomeres than the national average. “There are effects of living in high-poverty, racially segregated neighborhoods — the life experiences people have, the physical exposures, a whole range of things — that are just not good for your health,” Geronimus said in an interview with The Huffington Post.–But within this group of Detroit residents, the ways in which race-ethnicity and income were associated with telomere length were strikingly varied. -White Detroit residents who were lower-middle-class had the longest telomeres in the study. But the shortest telomeres belonged to poor whites. Black residents had about the same telomere lengths regardless of whether they were poor or lower-middle-class. And poor Mexicans actually had longer telomeres than Mexicans with higher incomes.-Geronimus said these findings demonstrated the limitations of standard measures — like race, income and education level — typically used to examine health disparities. “We’ve relied on them too much to be the signifiers of everything that varies in the life experiences of difference racial or ethnic groups in different geographic locations and circumstances,” she said. –According to Geronimus, it’s important to consider not just racial-ethnic identity, but also “the extent to which it is validated, or discriminated against, or even understood within your everyday life experience” can affect an individual’s health dramatically, Geronimus said. “Race is not race is not race. Poverty is not poverty is not poverty. Early health deterioration is sensitive to a broad range of life experiences.”
When Ethnic Identity Impacts Health
So why did poor Mexicans in this study have longer (i.e., generally healthier) telomeres than the nonpoor Mexicans? Geronimus first noted that most poor Mexicans in Detroit were either first-generation immigrants to the United States or part of close-knit ethnic enclaves[F4]. In contrast, nonpoor Mexicans were more often born in the U.S. and were more integrated into American culture through work or school.–“If they’re immigrants, then they come with a different cultural background and upbringing that didn’t stress that as Mexicans they were somehow ‘other’ or ‘lesser’ than other Americans,” said Geronimus. “They come with a set of support systems and with a cultural orientation that doesn’t undermine their sense of self-worth. They then often live in these ethnic enclaves, many of them don’t speak anything other than Spanish, and so they’re not interacting with Americans who view them as ‘other’ or who treat them badly. It’s not that they’re immune to that treatment but they’re not as sensitive to it and they also just don’t experience it as often.”–On the other hand, nonpoor Mexicans are more likely to be “exposed to some of the negative views of Mexicans held by some Americans, the conflation of anyone of Mexican origin as being an immigrant or possibly an undocumented immigrant, or even more neutral assumptions like ‘they must speak Spanish,’ or ‘they don’t understand English.'” Ironically, in seeking to become socially mobile and avoid the stress of poverty, these lower-middle-class Mexicans may face even more pronounced stressors tied to their ethnic identity.–Geronimus said the findings of the new study, based on quantitative physiological research, “line up perfectly” with previous ethnographic studies of Mexicans in Detroit done by another researcher, Dr. Edna Viruell-Fuentes of the University of Illinois at Urbana-Champaign. A health site summarized the conclusions of Viruell-Fuentes’s work–In 2007, Viruell-Fuentes interviewed 40 first- and second-generation Mexican immigrant women in the Detroit area. Though she points out that racial dynamics are hard to measure, based on her interviews Viruell-Fuentes believes that “identifying experiences that are discriminatory may be a learned process.” Often first-generation women characterized certain interactions as simply rude, while second-generation women labeled similar experiences as discriminatory. […]–In a 2012 review paper, Viruell-Fuentes pointed out that the first generation tends to stay within ethnic enclaves that may buffer some of the social disadvantages that immigrants face. “For the second generation, what I think is different, is that they have a lifelong exposure to an environment that stigmatizes their identity, which in turn can affect their health negatively,” she said.–“Often the question is raised, what is it about immigrants that makes them more resilient?” Viruell-Fuentes said. “But the other piece of the question for me is, what is it about the United States that is damaging to people’s health?–Other health effects tied to race-ethnicity identified in the new study could be viewed as counterintuitive. Income level seemed to have no effect on the telomere lengths of black Detroit residents, while the telomeres of poor whites were significantly shorter than those of nonpoor whites. Why? -The study’s authors noted—Much research suggests the separation between poor and nonpoor blacks in everyday life is less marked than between poor and nonpoor whites. Not only do blacks tend to have greater residential proximity owing to residential segregation, but often poor and the nonpoor blacks are members of the same families and social networks, practice reciprocal obligations, or have similar experiences of cycling between low and moderate incomes. –Income instability among middle-class blacks reflects job insecurity, a relative lack of conventional assets or wealth to tide them over in rough times, or a network-level division of labor whereby some are expected to contribute to family economies through income generating work, others contribute by seeing to the family caretaking needs that facilitate the employment of others, and still others provide important services and skills as barter exchange.–Researchers also highlighted the hypersegregation in the Detroit area. “Most blacks in our sample live almost exclusively with other blacks (97% of Eastside Detroit residents are black) or are the majority group in integrated neighborhoods (e.g., 70% of Northwest Detroit residents are black), [and] whites are a clear minority in all of our Detroit areas (ranging from 2% to 21% of residents).”–They found that associations between telomere length and perceptions of neighborhood physical environment and neighborhood satisfaction were strongest for blacks, and questioned whether “safety stress, physical environment, and neighborhood satisfaction tap into a more global construct of how black participants experience Detroit neighborhoods, which on balance may be more positively than for white or Mexican participants.”–In contrast, regarding white Detroit residents, the researchers wrote, “Perhaps with the exodus of most whites and many jobs from Detroit, the shrinking benefits of labor union membership and public pensions, and the overall reduction in taxation-based city services, the poor whites who remain are particularly adversely affected by the social and ecological consequences of austerity urbanism. Lacking the financial resources, social networks, and identity affirmation of the past, remaining Detroit whites may have less to protect them from the health effects of poverty, stigma, anxiety, or hopelessness in this setting.”–Geronimus summarized, “I think a lot of people just don’t understand how bad it is for some Americans. It’s disproportionately people of color given our history of residential segregation and racism, but it’s also anyone who gets caught. It’s like the dolphins who get caught in the fishing nets, it’s anyone who gets caught there. If anything, some of our evidence suggests that whether it’s the poor Mexican immigrant or the African-Americans who have been discriminated against and dealt with hardship for generation after generation, they’ve developed systems to cope somewhat that perhaps white Detroiters haven’t. So there’s great strength in these populations. But it’s not enough to solve these problems without the help of policymakers and more emphatic fellow citizens.”
Telomeres, Health, And Social Justice
One co-author of this new study is Dr. Elizabeth Blackburn. She helped to discover telomeres, an achievement that won her the Nobel Prize in physiology in 2009.
When her research began in the mid-1970s, Blackburn worked on identifying telomeres in one-celled organisms she laughingly calls “pond scum.” But over the years, as she and other scientists discovered the far-reaching human health implications of telomeres, her focus shifted.–“So much of what makes people either well-being or not is not coming from within themselves, it’s coming from their circumstances. It makes me think much more about social justice and the bigger issues that go beyond individuals,” she said in an interview from her office at the University of California San Francisco.–Blackburn believes that vital questions relevant to social policy have remained unanswered because the issues were highly complex and it was easy to question data from qualitative research methods, like people’s questionnaire answers about their personal experiences and perceptions. “When something’s really hard to assess, the easy thing is to dismiss it. They say it’s soft science, it’s not really hard-based science.”–But now telomere data is providing a new way to quantitatively analyze some of these complex topics. Blackburn ticked off a list of studies in which people’s experiences and perceptions directly correlated with their telomere lengths: whether people say they feel stressed or pessimistic; whether they feel racial discrimination towards others or feel discriminated against; whether they have experienced severely negative experiences in childhood, and so on. –“These are all really adding up in this quantitative way,” she said. “Once you get a quantitative relationship, then this is science, right?”
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Is the toxic potential of nanosilver dependent on its size?
Anna Huk12, Emilia Izak-Nau23, Bogumila Reidy4, Matthew Boyles2, Albert Duschl2, Iseult Lynch5 and Maria Dušinska1*
· * Corresponding author: Maria Dušinska [email protected]
Author Affiliations
Particle and Fibre Toxicology 2014, 11:65 doi:10.1186/s12989-014-0065-1
Published: 3 December 2014
Abstract
Background
Nanosilver is one of the most commonly used engineered nanomaterials (ENMs). In our study we focused on assessing the size-dependence of the toxicity of nanosilver (Ag ENMs), utilising materials of three sizes (50, 80 and 200 nm) synthesized by the same method, with the same chemical composition, charge and coating.
Methods
Uptake and localisation (by Transmission Electron Microscopy), cell proliferation [F5](Relative growth activity) and cytotoxic effects (Plating efficiency), inflammatory response (induction of IL-8 and MCP-1 by Enzyme linked immune sorbent assay), DNA damage (strand breaks and oxidised DNA lesions by the Comet assay) were all assessed in human lung carcinoma epithelial cells (A549), and the mutagenic potential of ENMs (Mammalian hprt gene mutation test) was assessed in V79-4 cells as per the OECD protocol. Detailed physico-chemical characterization of the ENMs was performed in water and in biological media as a prerequisite to assessment of their impacts on cells. To study the relationship between the surface area of the ENMs and the number of ENMs with the biological response observed, Ag ENMs concentrations were recalculated from μg/cm2 to ENMs cm2/cm2 and ENMs/cm2.
Results
Studied Ag ENMs are cytotoxic and cytostatic, and induced strand breaks, DNA oxidation, inflammation and gene mutations. Results expressed in mass unit [μg/cm2] suggested that the toxicity of Ag ENMs is size dependent with 50 nm being most toxic. However, re-calculation of Ag ENMs concentrations from mass unit to surface area and number of ENMs per cm2 highlighted that 200 nm Ag ENMs, are the most toxic. Results from hprt gene mutation assay showed that Ag ENMs 200 nm are the most mutagenic irrespective of the concentration unit expressed.
Conclusion
We found that the toxicity of Ag ENMs is not always size dependent. Strong cytotoxic and genotoxic effects were observed in cells exposed to Ag ENMs 50 nm, but Ag ENMs 200 nm had the most mutagenic potential. Additionally, we showed that expression of concentrations of ENMs in mass units is not representative. Number of ENMs or surface area of ENMs (per cm2) seem more precise units with which to compare the toxicity of different ENMs.
 
 
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Nanoparticles can damage DNA, increase cancer risk
April 17th, 2007 in Nanotechnology / Bio & Medicine
Tissue studies indicate that nanoparticles, engineered materials about a billionth of a meter in size, could damage DNA and lead to cancer, according to research presented at the 2007 Annual Meeting of the American Association for Cancer Research.– Nanoparticles are small enough to penetrate cell membranes and defenses, yet they are large enough to cause trouble by interfering with normal cell processes, researchers at the University of Massachusetts say. –Such nanoparticles are currently in use in electronics, cosmetics, and chemical manufacturing, among others industries. Because of their extremely small size, they can be difficult to isolate from the larger environment, as they are much too small for removal by conventional filtering techniques[F6].–When nanoparticles find their way into cancer cells, they can wreak havoc, according to Sara Pacheco, an undergraduate researcher at the University of Massachusetts. Yet very little is known about how they behave in the environment or how they interact with and affect humans-“Unfortunately, only a very small portion of research on nanoparticles is focused on health and safety risks, or on threats to the environment,” Pacheco said. “I am concerned because so many new nanoparticles are being developed and there is little regulation on their manufacture, use and disposal.”- Pacheco and her colleagues looked at how two different types of nanoparticles could cause DNA damage in the MCF-7 line of breast cancer cells– She and her team examined the genotoxicity of silica and C60 fullerene nanoparticle suspensions using the alkaline single-cell gel electrophoresis assay (Comet assay) to quantify breaks in single and double stranded DNA. The team chose these particular nanoparticle types because they are commonly used commercially – in electronics, textiles and sporting goods – and easy to work with in the laboratory setting.– “We observed both dose-dependent and time-dependent increases in DNA damage in breast cancer cells exposed to either aqueous colloidal silica or C60 fullerenes,” Pacheco said. “The DNA damage could potentially lead to mutations and ultimately increase the risk of cancer- One problem is that, while it’s clear that some nanoparticles can be more toxic than others, there’s not enough data as yet to determine the most dangerous types “A lot is unknown about nanoparticle function, but clearly both size and composition are important,” Pacheco said. “Several studies have shown that smaller particles are more likely to enter cells and cause more toxicity-According to Pacheco, what makes matters worse is the fact that so far, aside from preventing their release, there are no known ways to prevent the harmful effects of environmental nanoparticles[F7].-“It is important to know whether the nanoparticles are entering the cell and causing DNA damage directly or if they are acting on the membrane and inducing a cascade of events resulting in DNA damage,” Pacheco said. “Once we understand the mechanisms by which nanoparticles induce their toxicity, we will be better able to prevent or mitigate their harmful effects.”–In the meantime, the experimental team suggests that great caution should be taken in handling such nanoparticle suspensions and that any uncontrolled release should be avoided-Until we understand which types of nanoparticles are harmless and which have the potential to be harmful, I think it is prudent to limit their introduction into the environment,” recommended Pacheco.–Source: American Association for Cancer Research
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Explosion rocks nuclear power plant in New York
An explosion has rocked a nuclear facility in the US state of New York, triggering fears across the country, reports say.
The explosion happened on Saturday at the Indian Point nuclear plant in the upstate part of New York.–According to the company running the plant, Entergy Corporation, the affected parts of the facility were “safely shut down” and in “safe and stable condition.”–There was no damage to the reactor[F8], the most important part of a nuclear facility, according to US media reports. Authorities at the scene reported no human casualties either[F9]. –“The plant’s unit 3 reactor was closed after the explosion but the other one, Unit 2 is still operating,” Entergy Corporation spokesman Jerry Nappi told reporters.–“No threat to public safety at any time,” said the company, attempting to comfort the public as many expressed fears across the state.–People who were nearby the nuclear plant and witnessed the explosion said that there was a large blast followed by fire and then smoke.–The same nuclear plant was just brought back online on Friday after it was shut down for technical repairs[F10].–The plant was built in 1962, but the current reactors operating went online in the late 70s.–The Indian Point nuclear center produces 25 percent of New York City’s and many suburbs across the state.–Over 1,600 employees work there and it produces over 2,000 megawatts of energy annually
TOP B
 
[F1]Don’t you love the sales pitch here –incredible —actually putting spyware in a human —and utilizing this as a
health aide to sell this concept—when anyone who is anyone knows that nano does not opeate the way normal cells do and with the inclusion of nano in the body would overwrite the genetic codes—it would insert it’s artificial intelligence into a person and take over
[F2]Am I hearing
bioweapon
[F3]This is all meaningless—you add a nano program into the person and what it is going to show is the rate of exposure and rate of decay –if there is not the equipment to repair then what would be the point
[F4]The laboratory would be the general public—morgellons is a form of nano poisoning—they have released this to see how the bugs can e taken out
Before they perfect this for military use
[F5]This is how the nano particles work on us as well
[F6]This sounds good in theory But the reality is —not accurate—and what happens once they are in those organs or tissue?? And hw does one extract them out?
[F7]Some have seen these dyes on the skin they glow
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TOP C
 
 
Show of the Month May 23 2015
 
Pooled analysis confirms vitamin E as a treatment for non-alcoholic steatohepatitis
How vitamin E keeps muscles healthy
 
Obesegons
 
Contaminants that cause Obesegons
 
Atrazine –Endocrine Damaging –and Disorienteering Sexual Development
 
 
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Pooled analysis confirms vitamin E as a treatment for non-alcoholic steatohepatitis
Date:April 23, 2015
Source:European Association for the Study of the Liver
Summary:
Vitamin E (d-alpha-tocopherol) is an effective treatment for non-alcoholic steatohepatitis[F1] (NASH), according to new research. NASH occurs when the liver becomes inflamed due to the accumulation of fat. Over time, persistent inflammation can lead to the formation of fibrous scar tissue in the liver and around its blood vessels, which can eventually cause cirrhosis.
 
CITE Page
European Association for the Study of the Liver. “Pooled analysis confirms vitamin E as a treatment for non-alcoholic steatohepatitis.” ScienceDaily. ScienceDaily, 23 April 2015. <www.sciencedaily.com/releases/2015/04/150423085348.htm>
Results revealed at The International Liver Congress™ 2015 show that vitamin E (d-alpha-tocopherol) is an effective treatment for non-alcoholic steatohepatitis (NASH). NASH occurs when the liver becomes inflamed due to the accumulation of fat. Over time, persistent inflammation can lead to the formation of fibrous scar tissue in the liver and around its blood vessels, which can eventually cause cirrhosis.— A pooled analysis of data from two randomised trials comparing vitamin E versus placebo, and the placebo group from another trial comparing vitamin E use versus non-use, demonstrates that the efficacy of vitamin E is comparable to other treatments for NASH, including pioglitazone, metformin and obeticholic acid. In addition, treatment with vitamin E is associated with significant improvements in both NASH histology (45% vs 22% in those not treated with vitamin E) and resolution of disease (38% vs 20% in those not treated with vitamin E). There was no increase in cardiovascular events and no adverse lipid profiles were observed with vitamin E treatment– A total of 347 patients (155 treated with vitamin E, 192 not treated with vitamin E) were included in the analysis which compared data from three clinical trials that investigated the efficacy and safety of vitamin E as a treatment for NASH: the PIVENS, TONIC and FLINT trials. Histologic improvement was defined as ? 2 point improvement in NAS with no worsening of fibrosis, and NASH resolution measured effectiveness.– The study supports the use of vitamin E as a treatment for NASH-Story Source–The above story is based on materials provided by European Association for the Study of the Liver. Note: Materials may be edited for content and length
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How vitamin E keeps muscles healthy
Date:
May 19, 2015
Source:
Medical College of Georgia at Georgia Regents University
Summary:
Body builders have it right: Vitamin E does help build strong muscles, and scientists appear to have figured out one important way it does it. Vitamin E has long known as a powerful antioxidant, and now scientists have shown that without it, the plasma membrane, which essentially keeps a cell from spilling its contents and controls what moves in and out, cannot properly heal.
 
 
Body builders have it right: vitamin E does help build strong muscles, and scientists appear to have figured out one important way it does it.
Vitamin E has long known as a powerful antioxidant, and now scientists have shown that without it, the plasma membrane, which essentially keeps a cell from spilling its contents and controls what moves in and out, cannot properly heal.
That’s a big problem for many cells, such as muscle cells, which get membrane tears just from being used.-“Every cell in your body has a plasma membrane, and every membrane can be torn,” said Dr. Paul L. McNeil, cell biologist at the Medical College of Georgia at Georgia Regents University and corresponding author of the study in the journal Free Radical Biology and Medicine.-The scientist suspects knowing the cell membrane repair action of vitamin E has implications for muscular dystrophy, and common diabetes-related muscle weakness, as well as traumatic brain injury, resulting from collisions on a football field, battlefield, or roadway. With a traumatic brain injury, for example, one of the first events that happens is that the plasma membrane of the neurons, key cells in the central nervous system, tear. “Part of how we build muscle is a more natural tearing and repair process — that is the no pain, no gain portion — but if that repair doesn’t occur, what you get is muscle cell death. If that occurs over a long period of time, what you get is muscle-wasting disease,” said McNeil. The association between vitamin E and healthy muscles is well-established; for example, mammals and birds deprived of the vitamin experience muscle-wasting disease, in some cases lethal disease. A poor diet resulting in low vitamin E levels in the elderly contributes to frailty syndrome, a condition where muscles are weak and people are unsteady on their feet. The ubiquitous vitamin’s well-established role as a powerful antioxidant has led to its use in antiaging products and in helping delay the onset of Alzheimer’s by protecting neurons from free radicals. Exactly how vitamin E protects muscle, as well as other cell types, has been unknown. “This means, for the first time, 83 years after its initial discovery, we know what the cellular function of vitamin E is, and knowing that cellular function, we can now ask whether we can apply that knowledge to medically relevant areas,” McNeil said.For the new study, rats were fed either normal rodent chow, chow where vitamin E had been removed, or vitamin E-deficient chow where the vitamin was supplemented. First, there was a period of training to ascertain the rats’ innate ability to run downhill on a treadmill — a challenging move for muscles, called an eccentric contraction. The exercise helps lengthen muscles and can produce the most soreness in athletes because of the high mechanical stress as the muscle contracts and lengthens simultaneously. Gravity is an additional force. They found vitamin E-deficient rats were generally deficient in their running ability compared with controls and made significantly more visits to a grid, despite the fact that they received a mild electric shock when they stood there. The scientists also administered a dye that could not permeate an intact plasma membrane and found it easily penetrated the muscle cells of vitamin E-deficient rats. McNeil notes that a healthy cell makes a patch within a minute and has completely restored the cell membrane within a few minutes. Later examination of the quadriceps muscle fibers under a microscope showed rats fed normal chow or chow where vitamin E had been restored were essentially the same. The large thigh muscle fibers in rats fed vitamin E-deficient chow were smaller and inflamed. While exactly how free radicals, or reactive oxygen species, interfere with important cell membrane repair remains a mostly unanswered question, McNeil suspects they basically get in the way. Free radicals are essentially waste products produced by normal body functions, such as using oxygen, as well as exposures to cigarette smoke and other air pollutants and chemicals. Because it’s lipid-soluble, vitamin E can actually insert itself into the membrane to prevent free radicals from attacking. It also can help keep phospholipids, a major membrane component, compliant so they can better repair after a tear. For example, exercise causes the muscle cell powerhouse, the mitochondria, to burn a lot more oxygen than normal and so produce more free radicals while the physical force tears the membrane. Vitamin E enables adequate plasma membrane repair despite the oxidant challenge, helping keep the situation in check. McNeil’s finding that vitamin E is essential to rapid cell membrane repair, and ultimately cell survival, likely holds up across different cell types because, in culture at least, when the scientists have treated a number of different cells types with vitamin E, they documented similar enhanced cell membrane repair. “The major medical significance here is yet to be uncovered,” McNeil said, but could one day mean not just supplements to aid sluggish membrane repair in diseases such as muscular dystrophy, but preventive therapy for high-risk individuals such as astronauts or soldiers. McNeil’s 2011 study in Nature Communications indicated that, at least in cell culture, one way vitamin E keeps muscles healthy is by enabling cell membrane repair. Those studies linked the antioxidant and membrane repair benefits of vitamin E. Muscle cells in culture repaired better when vitamin E was added; when cells were exposed to free radicals, repair failed. Those findings led McNeil to see if the findings held up in research rats. Still earlier work showed that muscle cells were more fragile and membrane tears more common in muscular dystrophy. Good sources of vitamin E include vegetable oils; nuts; seeds such as sunflower seeds; green leafy vegetables; Wheat Germ Oil 200
Per 3 oz( 100mls), Sunflower (28%), Grapeseed (19%)-  Nuts (such as almonds, peanuts, and hazelnuts/filberts)  Seeds (such as sunflower seeds)
Reduced Risk of Heart Disease – Vitamin E is thought to help prevent heart disease by inhibiting oxidation of low-density lipoprotein (LDL) cholesterol, and helping to prevent blood clots which could lead to a heart attack.3,4 Studies report mixed results as to the effectiveness of supplements.5,6
Reduced Cancer Risk (*Controversial) – Vitamin E may help reduce cancer risk by acting as an antioxidant and by preventing formation of carcinogenic nitrosamines formed in the stomach from nitrites in foods.7,8
Promoted Eye Health (Prevention from Macular Degeneration) (*Controversial) – At least one study has shown intake of the DV for vitamin E reduces risk of age related eye damage (macular degeneration) by 20%.9,10 Other studies, however, fail to find any association.11,12
Alleviation of Chronic Inflammation – Preliminary studies show that vitamin E can help mediate the inflammatory response, and may help those with type II diabetes, or chronic heart failure, who suffer from chronic inflammation.13-15
Reduced Risk of Dementia (Cognitive Decline) (*Controversial) – Preliminary findings have shown increased levels of vitamin E to have a protective effect on mental functioning as people age. Further studies need to be conducted to confirm this finding.16
Reduced Risk of ALS (Amyotrophic Lateral Sclerosis, Lou Gehrig’s Disease) (*Controversial) – A long range study found that increased intake of Vitamin E over 5 years could reduce risk of ALS. Further studies are needed as the sample size was small.17
 
Story Source-The above story is based on materials provided by Medical College of Georgia at Georgia Regents University. Note: Materials may be edited for content and length.-Journal Reference-Mohamed Labazi, Anna K. McNeil, Timothy Kurtz, Taylor C. Lee, Ronald B. Pegg, José Pedro Friedmann Angeli, Marcus Conrad, Paul L. McNeil. The antioxidant requirement for plasma membrane repair in skeletal muscle. Free Radical Biology and Medicine, 2015; 84: 246 DOI: 10.1016/j.freeradbiomed.2015.03.016
 
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Obesogen
Obesogens are foreign chemical compounds that disrupt normal development and balance of lipid metabolism, which in some cases, can lead to obesity.[2][3][4] Obesogens may be functionally defined as chemicals that inappropriately alter lipid homeostasis and fat storage, change metabolic setpoints, disrupt energy balance or modify the regulation of appetite and satiety to promote fat accumulation and obesity.[5]
There are many different proposed mechanisms through which obesogens can interfere with the body’s adipose tissue biology. These mechanisms include alterations in the action of metabolic sensors; dysregulation of sex steroid synthesis, action or breakdown; changes in the central integration of energy balance including the regulation of appetite and satiety; and reprogramming of metabolic setpoints.[6][7] Some of these proposed pathways include inappropriate modulation of nuclear receptor function which therefore allows the compounds to be classified as endocrine disrupting chemicals that act to mimic hormones in the body, altering the normal homeostasis maintained by the endocrine system.[8]
Obesogens have been detected in the body both as a result of intentional administration of obesogenic chemicals in the form of pharmaceutical drugs such as diethylstilbestrol, selective serotonin reuptake inhibitor, and thiazolidinedione and as a result of unintentional exposure to environmental obesogens such as tributyltin, bisphenol A, diethylhexylphthalate, and perfluorooctanoate.[6][7] Emerging evidence from laboratories around the world suggests that other chemicals will be confirmed as falling under this proposed classification in the near future, and that there may be some serious biological effects due to exposure to these chemicals that still remain undiscovered.[6][7] Until now, 20 chemicals have been found responsible for making one fat.
The term obesogen was coined by Felix Grün and Bruce Blumberg of the University of California, Irvine.[3] The topic of this proposed class of chemical compounds and how to counteract their effects is explored at length in the book The New American Diet. Paula Baillie-Hamilton,[9] a doctor in the UK, was the first one to have identified how obesogens make it difficult to lose weight. She published her results in the Journal of Alternative and Complementary Medicine in 2002
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Metabolic sensors–Both obesogenic drugs and chemicals have been shown to target transcription regulators found in gene networks that function to control intracellular lipid homeostasis and proliferation and differentiation on adipocytes. The major group of regulators that is targeted is a group of nuclear hormone receptors known as peroxisome proliferator activated receptors (PPARα, δ, and γ). These hormone receptors sense a variety of metabolic ligands including lipophilic hormones, dietary fatty acids, and their metabolites, and, depending on the varying levels of these ligands, control transcription of genes involved in balancing the changes in lipid balance in the body.[6][7] In order to become active and properly function as both metabolic sensors and transcription regulators, the PPAR receptors must heterodimerize with another receptor known as the 9-cis retinoic acid receptor (RXR). The RXR receptor, itself, is the second major target of obesogens next to the PPAR receptors.[6][7]
The PPARα receptor, when complexed with RXR and activated by the binding of a lipid, promotes peroxisome proliferation leading to increased fatty acid β-oxidation[F2].[10] Substances, such a xenobiotics that target and act as agonists of PPARα typically act to reduce overall serum concentrations of lipids. In contrast, the PPARγ receptor, when complexed with RXR and activated by the binding of fatty acids or their derivatives promotes lipid biosynthesis and storage of lipids is favored over fatty acid oxidation. In addition, activation promotes differentiation of preadipocytes and the conversion of mesenchymal progenitor cells to preadipocytes in adipose tissues. Substances that target and act as agonists of PPARγ/RXR complex typically act to increase overall serum concentrations of lipids.[11]
Obesogens that target the PPARγ/RXR complex mimic the metabolic ligands and activate the receptor leading to upregulation of lipid accumulation which explains their obesogenic effects[F3]. However, in the case of obesogens that target the PPARα/RXR complex, which when stimulated reduces adipose mass and body weight, there are a few different explanations as to how they promote obesity.[6][7]
The ligand binding pockets of PPARs are very large and unspecified, allowing for different isoforms of the receptor(PPARα, δ, and γ)to be activated by the same agonist ligands or their metabolites. In addition, fatty acid oxidation stimulated by PPARα requires continuous stimulation while only a single activation event of PPARγ is required to permanently increase adipocyte differentiation and number.[6][7] Therefore it may be the case that metabolites of PPARα targeting obesogens are also activating PPARγ, providing the single activation event needed to potentially lead to a pro-adipogenic response.[12][13]
A second explanation points to specific PPARα targeters that have been shown to additionally cause abnormal transcriptional regulation of testicular steroidogenesis when introduced during fetal development. This abnormal regulation leads to a decreased level of androgen in the body which, itself is obesogenic.[14][15][16]
Finally, if PPARα activation occurs during critical periods of development, the resulting decrease in lipid concentration in the developing fetus is recognized by the fetal brain as undernourishment. In this case, the developing brain makes what will become permanent changes to the body’s metabolic control, leading to long term upregulation of lipid storage and maintenance.
 
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Sex steroid dysregulation
Sex steroids normally play a significant role in lipid balance in the body. Aided by other peptide hormones such as growth hormone, they act against the lipid accumulation mediated by insulin and cortisol by mobilizing lipid stores that are already present. Exposure to obesogens often leads to a deficiency or change in the ratio between androgen and estrogen sex steroid levels, which modifies this method of lipid balance resulting in lowered growth hormone secretion, hypocortisolemia (low levels of circulating cortisol), and increased resistance to insulin effects.[18]
This alteration in sex steroid levels due to obesogens can vary enormously according to both the sex of the exposed individual as well as the timing of the exposure.[6][7] If the chemicals are introduced at critical windows of development, the vulnerability of an individual to their effects is much higher than if exposure occurs later in adulthood. It has been shown that obesogenic effects are apparent in female mice exposed to both phytoestrogens and DES during their neonatal periods of development, as they, though born with a lower birth weight, almost always developed obesity, high leptin levels, and altered glucose response pathways.[19][20][21] Both phytoestrogen and DES exposed male mice did not develop obesity and rather, showed decreased body weights with increased exposure confirming the role of gender differences in exposure response.[20][21][22] Further studies have shown positive correlations for serum BPA levels with obese females in the human population, along with other xenoestrogen compounds suggesting the parallel roles that these effects may be having on humans.[23]
 
Potential chemical obesogens