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Coolnicknameguy: flat grind isn't as good as saber at splitting.. it tends to get stuck, the condor only split better cause its so much thicker then the bk. Had the condor ben 3/16ths and not 1/4 you woulda had trouble and you ould have clearly seen the bk was better.. I have an sp46 that always gets stuck and my buddy has a sp47 that splits wood like a champ.
Wendy Price: RBC Life Sciences is a notorious American MLM company. There is almost no one is interested in the United States, in American local no market. In recent years, the vast majority of sales come from the mainland China and Taiwan MLM pyramids. The company background of RBC Life Sciences is suspected fraud. The founder posing as "physician", "Father of Aloe" bewitched MLM gangs! Mr.Clinton Howard, RBC Life Sciences MLM company founder, He only got a master's degree from Southwestern Medical School. in the United States, anybody to presided over the medical research projects or to become a licensed physicians, should normally obtain a doctorate (Ph.D.).The results of numerous studies aloe, but in addition to RBC MLM pyramid schemes, no one had heard Clinton Howard. Free radicals: What doesn't kill you may make you live longer Date:May 8, 2014 Source:McGill University Summary: What is the secret to aging more slowly and living longer? Not antioxidants, apparently. Many people believe that free radicals, the sometimes-toxic molecules produced by our bodies as we process oxygen, are the culprit behind aging. Yet a number of studies in recent years have produced evidence that the opposite may be true. A team of researchers discovered that free radicals -- also known as oxidants -- act on a molecular mechanism that, in other circumstances, tells a cell to kill itself. What is the secret to aging more slowly and living longer? Not antioxidants, apparently. Many people believe that free radicals, the sometimes-toxic molecules produced by our bodies as we process oxygen, are the culprit behind aging. Yet a number of studies in recent years have produced evidence that the opposite may be true. Now, researchers at McGill University have taken this finding a step further by showing how free radicals promote longevity in an experimental model organism, the roundworm C. elegans. Surprisingly, the team discovered that free radicals -- also known as oxidants -- act on a molecular mechanism that, in other circumstances, tells a cell to kill itself. Programmed cell death, or apoptosis, is a process by which damaged cells commit suicide in a variety of situations: to avoid becoming cancerous, to avoid inducing auto-immune disease, or to kill off viruses that have invaded the cell. The main molecular mechanism by which this happens is well conserved in all animals, but was first discovered in C. elegans -- a discovery that resulted in a Nobel Prize. The McGill researchers found that this same mechanism, when stimulated in the right way by free radicals, actually reinforces the cell's defenses and increases its lifespan. Their findings are reported in a study published online May 8 in the journal Cell. "People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect," says Siegfried Hekimi, a professor in McGill's Department of Biology and senior author of the study. "We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat -- not cause -- aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life." The findings have important implications. "Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules," Hekimi says. "It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging." "Since the mechanism of apoptosis has been extensively studied in people, because of its medical importance in immunity and in cancer, a lot of pharmacological tools already exist to manipulate apoptotic signaling. But that doesn't mean it will be easy." Stimulating pro-longevity apoptotic signaling could be particularly important in neurodegenerative diseases, says Hekimi. In the brain the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them, explains Hekimi. That's because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neurons. Story Source: The above story is based on materials provided by McGill University. Note: Materials may be edited for content and length. Journal Reference: Callista Yee, Wen Yang, Siegfried Hekimi. The Intrinsic Apoptosis Pathway Mediates the Pro-Longevity Response to Mitochondrial ROS in C. elegans. Cell, 2014; 157 (4): 897 DOI: 10.1016/j.cell.2014.02.055 'Free Radical Theory Of Aging Incorrect': Scientists Say There Is A Link Between Cell Suicide And Longevity By Sabrina Bachai May 8, 2014 What is the secret to anti-aging? It’s a question that people all over the world for thousands of years have been trying to figure out. To some, the culprit is free radicals, which are sometimes toxic molecules that our bodies produce. Not only can they incite aging, but they can also lead to heart attacks, stroke, and cancers — or so it was previously believed. Now further information and a number of studies have substantial evidence opposing these theories. In a study published in Cell, researchers at McGill University in Canada have discovered that free radicals — by way of the mechanical makeup — tell cells when it’s time to kill themselves. They used an experimental model organism, a roundworm, to show how free radicals will promote longevity. "People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect," says Siegfried Hekimi, a professor in McGill's Department of Biology and senior author of the study, in a press release. "We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat – not cause – aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life." In 2010, the same researchers published a study regarding this exact theory. They also found that roundworms with genetic mutations that slowed their metabolism lived longer than regular roundworms — even though the mutated worms showed no evidence of increased protection from free radicals, Live Science reported. This new research is important because it is "showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules," Hekimi said. "It also means that apoptosis signaling [physiological process for killing cells] can be used to stimulate mechanisms that slow down aging." Hekimi also says that since apoptosis signaling has already been studied in great depth on people because of its links to cancer and immunity, there are also a number of pharmacological tools that scientists can use to manipulate apoptosis. He also says that Pro-longevity apoptotic signaling could open doors for more research on neurodegenerative diseases. In the brain, the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them, he continued to explain. That's because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neuron signaling. But that doesn't mean it will be easy. Source: Yee C, Yang W, Hekimi S. The Intrinsic Apoptosis Pathway Mediates the Pro-Longevity Response to Mitochondrial ROS in C. elegans. Cell. 2014.
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