Jump to content

cso1

Member
  • Posts

    492
  • Joined

  • Last visited

cso1's Achievements

Newbie

Newbie (1/14)

0

Reputation

  1. A New Shot at Life Friday, November 4, 2011 Video and transcript here http://sixtyminutes.ninemsn.com.au/stories...ew-shot-at-life "The doctors there believe Alzheimer's disease can be reversed and they have the results to prove it." "It clearly has a marvelous, immediate and prolonged effect" "It’s called perispinal etanercept, an anti-inflammatory drug that was designed to treat rheumatoid arthritis. Now, it targets a protein called TNF – we all have it – but it’s 25 times higher in patients with Alzheimer’s. Dr Tobinick discovered that this, just a few ‘mls’ of it, can shrink excessive levels of that protein in the brain. And his patients say it’s like a fog clearing from their mind." "Researchers at Queensland’s Griffith University hope to begin the first Australian trials on perispinal etanercept early next year."
  2. "The findings could offer a relatively simple approach for Alzheimer’s prevention and treatment." "The mice were injected with Gleevec twice a day for seven days; then plasma and brain tissue were collected, and the amount of beta amyloid in the blood and brain was measured. The findings: the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate" www.kurzweilai.net/scripps-research-study-points-to-liver-not-brain-as-origin-of-alzheimers-plaques Scripps Research study points to liver, not brain, as origin of Alzheimer’s plaques March 4, 2011 by Editor Unexpected results from a Scripps Research Institute and ModGene, LLC study could completely alter scientists’ ideas about Alzheimer’s diseaseâ€â€ÂÂÂÂpointing to the liver instead of the brain as the source of the “amyloid†that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer’s prevention and treatment. The study was published online today in The Journal of Neuroscience Research. In the study, the scientists used a mouse model for Alzheimer’s disease to identify genes that influence the amount of amyloid that accumulates in the brain. They found three genes that protected mice from brain amyloid accumulation and deposition. For each gene, lower expression in the liver protected the mouse brain. One of the genes encodes presenilinâ€â€ÂÂÂÂa cell membrane protein believed to contribute to the development of human Alzheimer’s. “This unexpected finding holds promise for the development of new therapies to fight Alzheimer’s,†said Scripps Research Professor Greg Sutcliffe, who led the study. “This could greatly simplify the challenge of developing therapies and prevention.†An estimated 5.1 million Americans have Alzheimer’s disease, including nearly half of people age 85 and older. By 2050, the number of people age 65 and over with this disease will range from 11 million to 16 million unless science finds a way to prevent or effectively treat it. In addition to the human misery caused by the disease, there is the unfathomable cost. A new report from the Alzheimer’s Association shows that in the absence of disease-modifying treatments, the cumulative costs of care for people with Alzheimer’s from 2010 to 2050 will exceed $20 trillion. A Genetic Search-and-Find Mission In trying to help solve the Alzheimer’s puzzle, in the past few years Sutcliffe and his collaborators have focused their research on naturally occurring, inherited differences in neurological disease susceptibility among different mouse strains, creating extensive databases cataloging gene activity in different tissues, as measured by mRNA accumulation. These data offer up maps of trait expression that can be superimposed on maps of disease modifier genes. As is the case with nearly all scientific discovery, Sutcliffe’s research builds on previous findings. Several years ago, researchers at Case Western Reserve mapped three genes that modify the accumulation of pathological beta amyloid in the brains of a transgenic mouse model of Alzheimer’s disease to large chromosomal regions, each containing hundreds of genes. The Case Western scientists used crosses between the B6 and D2 strains of mice, studying more than 500 progeny. Using the results from this study, Sutcliffe turned his databases of gene expression to the mouse model of Alzheimer’s, looking for differences in gene expression that correlated with differences in disease susceptibility between the B6 and D2 strains. This intensive work involved writing computer programs that identified each genetic difference that distinguished the B6 and D2 genomes, then running mathematical correlation analysis (known as regression analysis) of each difference. Correlations were made between the genotype differences (B6 or D2) and the amount of mRNA product made from each of the more than 25,000 genes in a particular tissue in the 40 recombinant inbred mouse strains. These correlations were repeated 10 times to cover 10 tissues, the liver being one of them. “A key aspect of this work was learning how to ask questions of massive data sets to glean information about the identities of heritable modifier genes,†Sutcliffe said. “This was novel and, in a sense, groundbreaking work: we were inventing a new way to identify modifier genes, putting all of these steps together and automating the process. We realized we could learn about how a transgene’s pathogenic effect was being modified without studying the transgenic mice ourselves.†Looking for a Few Good Candidates Sutcliffe’s gene hunt offered up good matches, candidates, for each of the three disease modifier genes discovered by the Case Western scientists, and one of these candidatesâ€â€ÂÂÂÂthe mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer’s diseaseâ€â€ÂÂÂÂwas of special interest to his team. “The product of that gene, called Presenilin2, is part of an enzyme complex involved in the generation of pathogenic beta amyloid,†Sutcliffe explained. “Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer’s-like pathology.†This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain. To test this hypothesis, Sutcliffe’s team set up an in vivo experiment using wild-type mice since they would most closely replicate the natural beta amyloid-producing environment. “We reasoned that if brain amyloid was being born in the liver and transported to the brain by the blood, then that should be the case in all mice,†Sutcliffe said, “and one would predict in humans, too.†The mice were administered imatinib (trade name Gleevec, an FDA-approved cancer drug), a relatively new drug currently approved for treatment of chronic myelogenous leukemia and gastrointestinal tumors. The drug potently reduces the production of beta amyloid in neuroblastoma cells transfected by amyloid precursor protein (APP) and also in cell-free extracts prepared from the transfected cells. Importantly, Gleevec has poor penetration of the blood-brain barrier in both mice and humans. “This characteristic of the drug is precisely why we chose to use it,†Sutcliffe explained. “Because it doesn’t penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease.†The mice were injected with Gleevec twice a day for seven days; then plasma and brain tissue were collected, and the amount of beta amyloid in the blood and brain was measured. The findings: the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer’s. As for the future of this research, Sutcliffe says he hopes to find a partner and investors to move the work into clinical trials and new drug development. Ref.: “Peripheral reduction of β-amyloid is sufficient to reduce brain Aβ: implications for Alzheimer’s disease†http://onlinelibrary.wiley.com/doi/10.1002....22603/abstract
  3. cso1

    GIP

    "(just in case investors/potential off-takers don't understand JORC............LOl LOL LOL!!!!!!)" ... the Canadian listing requirements are significantly different to the U.K., Germany and Australia for a company like GIP. GIP is sort of sending a warning shot across the bows of the weakened and formerly boastful Commerce in Canada and might be preparing to reveal information (BFS pricing etc), it would not before for commercial reasons, which stopped it from listing in Canada. Another set of problems preventing listing has included fees, GFC and the crowded space over there, where companies which made a point of NOT having uranium "contamination" were previously most unwelcome. Anyway, a spin off at an opportune time to help raise funds for the main game would be welcome (at least versus another fund raising effort at $0.01, while giving so much of the company away). Eritrean and Arab gold as well as Tassy tin have long been on the cards for a possible spin off (there was one failed attempt relating to the AIM listing), while the tin, tantalum and feldspar in Egypt awaits a funding sign off, which if achieved, would set Noventa back somewhat.
  4. cso1

    GIP

    You've improved since your days of 100's of just one-liner put downs in a row.
  5. "918-megaherz of frequency twice a day for an hour each time over nine months" "exposure to the electromagnetic fields caused the erasure of deposits of beta-amyloid - a protein fragment that accumulates in the brain of Alzheimer's sufferers to form the disease's signature plaques. Memory impairment in the older mice disappeared, too ... young adult mice with no apparent signs of memory impairment were protected against Alzheimer's disease after several months of exposure to the mobile phone waves." "The memory levels of normal mice with no genetic predisposition for Alzheimer's disease were also boosted after exposure to the electromagnetic waves." www.abc.net.au/news/stories/2010/01/07/2787526.htm Mobile phone use may reverse Alzheimer's 07/01/2009 The electromagnetic waves emitted by mobile phones could protect against and even reverse Alzheimer's disease, according to a US study. Researchers at the University of South Florida exposed 96 mice, most of whom had been genetically altered to develop the Alzheimer's disease as they aged, to electromagnetic waves generated by mobile phones. The mice were zapped with 918-megaherz of frequency twice a day for an hour each time over nine months - the equivalent of several decades in humans. In older mice with Alzheimer's, long-term exposure to the electromagnetic fields caused the erasure of deposits of beta-amyloid - a protein fragment that accumulates in the brain of Alzheimer's sufferers to form the disease's signature plaques. Memory impairment in the older mice disappeared, too, the study showed. It also found that young adult mice with no apparent signs of memory impairment were protected against Alzheimer's disease after several months of exposure to the mobile phone waves. The memory levels of normal mice with no genetic predisposition for Alzheimer's disease were also boosted after exposure to the electromagnetic waves. The study was the first to look at the long-term effects of mobile phone exposure in mice or humans, and its findings took the researchers by surprise. "I started this work with a hypothesis that the electromagnetic fields would be deleterious to Alzheimer's mice," lead author Professor Gary Arendash said. "When we got our initial results showing a beneficial effect, I thought, 'give it a few more months and it will get bad for them'. "It never got bad. We just kept getting these beneficial effects in both the Alzheimer's and normal mice." Based on the findings, the researchers are hopeful electromagnetic field exposure could be an effective, non-invasive and drug-free way to prevent and treat Alzheimer's in humans.
  6. cso1

    GIP

    All time record volume http://bit.ly/26C6yC and a breakout looming suggest GIP is at a most interesting juncture. At the least, the gold, feldspar, tin and world class tantalum deposits are all in play thanks to recent funding moves and potential, untainted tantalum shortages.
  7. "According to a study by the Massachusetts Institute of Technology, if we tapped 40 percent of the geothermal heat under the United States, it would meet demand 56,000 times over. MIT said an investment of $800 million to $1 billion could produce more than 100 gigawatts of electricity by 2050, equaling the combined output of all 104 nuclear power plants in the U.S." http://www.energy-daily.com/reports/Electr...ricity_999.html ElectraTherm Green Machine Turns Geothermal Heat Into Electricity by Staff Writers Carson City NV (SPX) Jun 19, 2009 ElectraTherm has announced use of the ElectraTherm Green Machine in a significant geothermal application. ElectraTherm's Texas partner, Gulf Coast Green Energy, will employ Green Machines to make clean electricity at two projects funded by the Research Partnership to Secure Energy for America. The first of those projects will make power from heat captured in geothermal brine, a common byproduct of drilling for oil. ElectraTherm Green Machines can convert low temperature (200 degree F) geothermal heat into electricity for onsite consumption, or to sell power to the grid. ElectraTherm launched the 50 kW ElectraTherm with an installation at Southern Methodist University's Geothermal Laboratory in June 2008. Since then, ElectraTherm has fielded interest from all over the world in the company's fuel-free, emissions-free systems. The ElectraTherm Green Machine can produce power from a wide array of heat sources including industrial waste heat, stationary engines, biomass, and solar thermal installations. Recently interest in geothermal applications has taken center stage. "Generating electricity from geothermal sources is ideal because it harnesses local energy sources and provides a secure domestic energy supply with stable output," said Bill Olson, ElectraTherm Sr. VP of Business Development. "Given the modularity and scalability of ElectraTherm's technology, the company plans to introduce geothermal systems from the current 50 kW size up to 500 kW. ElectraTherm's smaller units can economically address smaller geothermal resources - including the tens of thousands of oil and gas wells in the U.S. and Canada alone. ElectraTherm's larger units can be installed in parallel to rapidly construct multi-megawatt plants for larger geothermal resources." According to a study by the Massachusetts Institute of Technology, if we tapped 40 percent of the geothermal heat under the United States, it would meet demand 56,000 times over. MIT said an investment of $800 million to $1 billion could produce more than 100 gigawatts of electricity by 2050, equaling the combined output of all 104 nuclear power plants in the U.S. The Geothermal Energy Association and the Geothermal Resource Council have recognized ElectraTherm's renewable energy systems with their top awards as an innovative, low-cost solution for geothermal applications. By invitation of the Canadian Geothermal Energy Association, Olson recently presented a session titled, "The Green Machine: Innovative Power Technology" at the CanGEA annual conference in Vancouver, BC.
  8. "as expected, the rats that had gone for the six-hour swim showedpreliminary molecular changes that would increase endurance. But the second rodent group, which exercised for less than five minutes also showed the same molecular changes." "six minutes or so a week of hard exercise (plus the time spent warming up, cooling down, and resting between the bouts of intense work) had proven to be as good as multiple hours of working out for achieving fitness. The short, intense workouts aided in weight loss, too" "similar, intense, brief sessions of exercise improve cardiac health, even among people with heart disease" "There's a catch, though. Those six minutes, if they're to be effective, must hurt. "We describe it as an 'all-out' effort," Gibala says. You'll be straying "well out of your comfort zone." That level of discomfort makes some activities better-suited to intense training than others." http://well.blogs.nytimes.com/2009/06/24/c...-minutes-a-week June 24, 2009, 12:26 pm Can You Get Fit in Six Minutes a Week? By Gretchen Reynolds A few years ago, researchers at the National Institute of Health and Nutrition in Japan put rats through a series of swim tests with surprising results. They had one group of rodents paddle in a small pool for six hours, this long workout broken into two sessions of three hours each. A second group of rats were made to stroke furiously through short, intense bouts of swimming, while carrying ballast to increase their workload. After 20 seconds, the weighted rats were scooped out of the water and allowed to rest for 10 seconds, before being placed back in the pool for another 20 seconds of exertion. The scientists had the rats repeat these brief, strenuous swims 14 times, for a total of about four-and-a-half minutes of swimming. Afterward, the researchers tested each rat's muscle fibers and found that, as expected, the rats that had gone for the six-hour swim showed preliminary molecular changes that would increase endurance. But the second rodent group, which exercised for less than five minutes also showed the same molecular changes. The potency of interval training is nothing new. Many athletes have been straining through interval sessions once or twice a week along with their regular workout for years. But what researchers have been looking at recently is whether humans, like that second group of rats, can increase endurance with only a few minutes of strenuous exercise, instead of hours? Could it be that most of us are spending more time than we need to trying to get fit? The answer, a growing number of these sports scientists believe, may be yes. "There was a time when the scientific literature suggested that the only way to achieve endurance was through endurance-type activities," such as long runs or bike rides or, perhaps, six-hour swims, says Martin Gibala, PhD, chairman of the Department of Kinesiology at McMaster University in Ontario, Canada. But ongoing research from Gibala's lab is turning that idea on its head. In one of the group's recent studies, Gibala and his colleagues had a group of college students, who were healthy but not athletes, ride a stationary bike at a sustainable pace for between 90 and 120 minutes. Another set of students grunted through a series of short, strenuous intervals: 20 to 30 seconds of cycling at the highest intensity the riders could stand. After resting for four minutes, the students pedaled hard again for another 20 to 30 seconds, repeating the cycle four to six times (depending on how much each person could stand), "for a total of two to three minutes of very intense exercise per training session," Gibala says. Each of the two groups exercised three times a week. After two weeks, both groups showed almost identical increases in their endurance (as measured in a stationary bicycle time trial), even though the one group had exercised for six to nine minutes per week, and the other about five hours. Additionally, molecular changes that signal increased fitness were evident equally in both groups. "The number and size of the mitochondria within the muscles" of the students had increased significantly, Gibala says, a change that, before this work, had been associated almost exclusively with prolonged endurance training. Since mitochondria enable muscle cells to use oxygen to create energy, "changes in the volume of the mitochondria can have a big impact on endurance performance." In other words, six minutes or so a week of hard exercise (plus the time spent warming up, cooling down, and resting between the bouts of intense work) had proven to be as good as multiple hours of working out for achieving fitness. The short, intense workouts aided in weight loss, too, although Gibala hadn't been studying that effect. "The rate of energy expenditure remains higher longer into recovery" after brief, high-intensity exercise than after longer, easier workouts, Gibala says. Other researchers have found that similar, intense, brief sessions of exercise improve cardiac health, even among people with heart disease. There's a catch, though. Those six minutes, if they're to be effective, must hurt. "We describe it as an 'all-out' effort," Gibala says. You'll be straying "well out of your comfort zone." That level of discomfort makes some activities better-suited to intense training than others. "We haven't studied runners," Gibala says. The pounding involved in repeated sprinting could lead to injuries, depending on a runner's experience and stride mechanics. But cycling and swimming work well. "I'm a terrible swimmer," Gibala says, "so every session for me is intense, just because my technique is so awful." Meanwhile, his lab is studying whether people could telescope their workouts into even less time. Could a single, two- to three-minute bout of intense exercise confer the same endurance and health benefits as those six minutes of multiple intervals? Gibala is hopeful. "I'm 41, with two young children," he says. "I don't have time to go out and exercise for hours." The results should be available this fall. The Phys Ed column will appear here in Well every Wednesday and also in print once a month, in the Sunday magazine. In it, Gretchen Reynolds, who is working on a book about the frontiers of fitness, will write about what the latest science can tell us about how to make ourselves stronger, more flexible, less prone to pain and generally fitter and healthier. We want to hear what you think, so stay tuned and offer your comments and questions.
  9. "the technique improves patients' vision within weeks" "We've gone from patients that are legally blind ... to being able to read letters on a standard visual chart." http://www.abc.net.au/news/stories/2009/05/28/2582954.htm Stem cell lenses give sight to sore eyes 28/5/09 Australian scientists have found they can restore the sight of people with one damaged eye using contact lenses coated with stem cells from their healthy eye. Researchers at the University of New South Wales say the technique improves patients' vision within weeks. Dr Nick Di Girolamo says they cultured stem cells from the patients' eyes inside contact lenses, then placed them onto their damaged corneas for 10 days. "We're quietly excited about the technique because we don't know how long the ocular surface is going to remain healthy," he said. "At the moment, we're out to 18 months. We've gone from patients that are legally blind, meaning that they probably can only count their own fingers at a certain distance in front of their eyes. "Going from that to being able to read letters on a standard visual chart."
  10. cso1

    CRICKET

    The rot has set in. The selectors deserve to go the way of Breaker Morant. First they send the mighty magnificent Magoffin to South Africa http://content.cricinfo.com/rsavaus2009/co...ory/393329.html and we see South Africa humbled to the surprise of most "experts" http://www.news.com.au/dailytelegraph/stor...5017479,00.html Then we see the marvellous Magoffin sent home and what do we note happens straight away? http://content.cricinfo.com/wwc2009/conten...ory/395146.html . The Gods are not pleased! ;-)
  11. http://news.bbc.co.uk/2/hi/health/7813072.stm Page last updated at 00:01 GMT, Sunday, 8 March 2009 Enzyme behind cancer spread found Scientists say they have discovered a way to stop cancer spreading to other parts of the body. Cancer metastasis, where the cancer spreads from its original location, is known to be responsible for 90% of cancer-related deaths. Institute of Cancer Research scientists have found that an enzyme called LOX is crucial in promoting metastasis, Cancer Cell journal reports. Drugs to block this enzyme's action could keep cancer at bay, they hope. The researchers studied breast cancer in mice, but are confident that their findings will apply to humans with other cancer types too. Lead researcher Dr Janine Erler LOX (lysyl oxidase) works by sending out signals to prepare a new area of the body for the cancer to set up a camp. Without this preparation process the new environment would be too hostile for the cancer to grow. Lead researcher Dr Janine Erler described the discovery as "the crucial missing piece in the jigsaw that scientists have been searching for." She said it was the first time one key enzyme has been identified as responsible for effectively allowing the cancer to spread. "If we can interrupt the body's ability to prepare new locations for the cancer to spread to, we can effectively prevent cancer metastasis. "Cancer metastasis is very difficult to treat and this new discovery provides real hope that we can develop a drug which will fight the spreading of cancer," she said. Dr Julie Sharp, Cancer Research UK's science information manager, said: "A better understanding of how cancer spreads is crucial to improving the treatment of the disease. This research takes scientists a step closer to understanding this major problem - the next stage will be to find out if the LOX protein can be switched off to stop cancer spreading."
  12. http://style.ekoliving.com/archive/38-Envi...al%20News/83-80 80% Efficient Solar Panel?! Works at Night?! Written by Matt Thursday, 31 January 2008 The most expensive, carefully designed, and complicated solar panels in the world operate at about 40% efficiency. That means that, for every bit of sunlight that hits the panel, only 40% of it is turned into electricity. Scientists think that this is just about as good as silicon panels can do and are now looking at ways to make it cheaper, instead of making them more efficient. But suddenly, from nowhere, comes Steven Novack of the Idaho National Laboratories with an inexpensive, foldable solar panel that may turn out to be up to 80% efficient. The trick is nanotechnology. The surface of the material is printed with miniscule nano-antennae that capture infra-red radiation, the kind that the sun puts out in abundance, and is even available at night. Television antennas absorbe large wavelength energy, so in order to absorb ultra-small wavelength energy (photons) they had to create ultra-small antennas. The material is fairly simple to create, and scientists are confidient that it would scale easily out of the laboratory. But there is a bit of a hitch: There's currently no way to capture the energy being created. So while there are electrons pouring out of the nano-antennas when exposed to the sun, there is no way to capture those electrons. But don't worry, those geniuses in Idaho are working on that already. By putting a tiny capacitor, or AC/DC converter in the center of every tiny tiny antenna, they think they could make this new kind of solar panel export all that energy it's created without raising the price, or lowering the efficiency too much.
  13. cso1

    CRICKET

    Hair implants? ;-)
  14. cso1

    CRICKET

    At long last, what I have been posting about on this forum and suggesting the selectors do for years has finally been noted. This is surely the beginning of a new era - a renaissance - in Australian cricket! I trust a week long holiday will be declared in honour of this devastating speed demon's promotion. ;-) http://content-www.cricinfo.com/rsavaus200...ory/393329.html "he has been a consistent cricketer in the Australian interstate competition for a long time now." Magoffin, a tall bowler capable of gaining uncomfortable bounce, currently sits second on the wicket list for the Sheffield Shield with 38 and has 191 first-class victims" Magoffin joins injury-hit Australia Cricinfo staff March 4, 2009 Steve Magoffin, the Western Australia fast bowler, will fly to South Africa as cover for Australia's struggling attack following niggling injuries to Ben Hilfenhaus and Peter Siddle. The squad has already been expanded by Brett Geeves, who is there in case Doug Bollinger fails to recover from a stomach problem in time to be considered for Friday's second Test in Durban. Siddle and Hilfenhaus played key roles in Australia's opening victory in Johannesburg as the inexperienced line-up out-gunned the home team. However, Siddle's left foot is aching following the game - he spent most of January out with a similar injury - and Hilfenhaus, who made his debut, has lower-back soreness. "With such a short turnaround between the first and second Test, the panel has taken the precaution of adding another bowler to the squad," the chairman of selectors Andrew Hilditch said. "Steve Magoffin has been added as a stand-by player, but that being said he has been a consistent cricketer in the Australian interstate competition for a long time now." Magoffin, a tall bowler capable of gaining uncomfortable bounce, currently sits second on the wicket list for the Sheffield Shield with 38 and has 191 first-class victims at 27.90. "We are sure he will step up should the opportunity present itself in South Africa," Hilditch said. Siddle and Hilfenhaus will continue to receive treatment in the lead-up to the second game. The young attack was chosen for the tour due to long-term injuries to the regulars Brett Lee and Stuart Clark.
  15. cso1

    CRICKET

    After a Test match like we've just seen, following on from an exceptional finish last year (same time and place), once again with not many spectators, it makes sense that the whole concept should now be dumped in favour of Double wicket and French cricket competitions. ;-)
×
×
  • Create New...