Thursday, 10 December 2015

What Is Antimatter? Why It Does Matter?!

What Is Antimatter? Why It Does Matter?
| On 09, Dec 2015Increase Text Size Decrease Text Size

If it matters… it’s matter, but if you’re antimatter I guess you just don’t care about anything anymore. Matter is everything around us. It’s you, me, the tree, the rock, everywhere! Even the land, and the ship! Matter is considered every physical substance in the universe; if it has mass, it’s matter. But then… there’s this other thing called antimatter.
During the Big Bang, the universe should have created half-and-half: 1 atom of matter, 1 of anti-matter. But look around you, matter is everywhere. Where’d all the anti-matter go?! It’s one of the great mysteries of physics…
Anti-matter is the same as matter, but opposite. Scientists have been looking for antimatter since it was theorized in the 1920s. Physicist Paul Dirac was trying to reconcile two new chapters in physics… Einstein’s theory of relativity, and quantum mechanics. Think of it this way, when solving for X-squared equals four, X can be either 2 or negative 2. Up to this point, physicists had spent most of their energy — physics joke — on the positive solution — not the negative one. But since both give you the same result, antimatter must exist!
Obviously that’s very simplified, but that’s the idea. So, if you picture hydrogen, one positively charged proton, one negatively charged electron: that is matter. Balanced. Simple. ANTIhydrogen: is made of a negatively charged antiproton, and positively charged positron! This evil antimatter twin version has the same mass, by the way.
Experiments with antimatter in the journal Nature from November 2015 found antimatter behaves exactly like matter, which is actually confusing, shouldn’t the opposite particle behave… oppositely? More research is needed.
The base rule of old physics, is matter cannot be created or destroyed, but, that’s not strictly speaking true. In fact, when an electron hits a positron they annihilate one another, turning into energy in the form of gamma rays — specifically gamma rays at 511 kiloelectron volts! To scale that up, if 1 kilo of antimatter hit a kilo of matter — based on E=mc squared — the resulting explosion would be 3,000 times the Hiroshima bomb.
So, new physics, energy cannot be created or destroyed; because matter and energy are the same. But this annihilation is a big clue as to where antimatter went. We know this annihilation happens because of particle accelerators. When high energy particles are smashed together, or go through beta decay naturally, tiny bits of antimatter are created. They clearly want to study this, but they need to hold onto it, and therein lies the rub.
LHC Smash: antimatter
LHC Smash! – Starts With A Bang. ©Wikipedia/Lucas Taylor

Our universe is full of matter. Whenever scientists create a particle of antimatter, it hits the mattery walls of the container and instantly annihilates itself! How frustrating would that be? There was literally no way to hold antimatter in place and get a look at it — until now.
In 2002, the ALPHA collaboration team at CERN announced they’d trapped 38 antihydrogen atoms for 172 milliseconds each. A breakthrough at the time, but not a lot of stuff, or a long time. Then in 2010, scientists trapped hundreds of antimatter atoms for more than 15 minutes! Giving them time to explore how these mysterious things work! With this study, published in Nature Physics, as a base, cosmologists believe the Big Bang somehow created more matter than antimatter. Not much more… mind you, but more.
A piece in The Guardian describes it as an “infinitesimally small excess.” Then, in the seconds after the Big Bang — all the antimatter and matter annihilated each other leaving just matter, and creating HUGE amounts of energy! Of course, that’s just a hypothesis. So far, the lack of asymmetry — or the fact that matter and antimatter seem to behave exactly the same — is super confusing for scientists… IF there was asymmetry, then they could predict why the matter survived this great annihilation, but so far… they don’t know.
One study is currently using supercomputers to try and find any tiny difference between the two. We’ll see. Otherwise, antimatter is dead useful, Star Trek famously uses it to power spacecraft, which makes sense and might actually work out of fiction, but closer to home, antimatter could be combined with traditional nuclear technologies to kick off fusion reactors.
Positron Emission Tomography involves putting these antimatter positrons into the human body, knowing they’ll annihilate and emit the predictable 511 keV gamma rays, revealing tumors and mapping the patient. 1.1 million of these PET scans were performed in 2005 alone. And, with a little more energy in the right place, those antimatter-matter annihilations could even be used to hyperlocally treat cancer without harming surrounding tissues!
Matter matters! But it’s not just about matter vs antimatter. There are also states… Solid, liquid, gas, plasma… And maybe a new one too! After all this research, I am so PRO antimatter! But what do you think? Does it even matter?

Wednesday, 2 December 2015

Kepler’s second law of planetary motion


“A line joining a planet and the Sun sweeps out equal areas during equal intervals of time” (Meaning that each triangle seen there has equal area.)

The black dot represents a planet, the point where the black lines intersect represent the sun.
The green arrow represents the planet’s velocity,
The purple arrows represents the force on the planet.
Know more:
http://www.physicsclassroom.com/mmedia/circmot/ksl.cfm
http://www-spof.gsfc.nasa.gov/stargaze/Skepl2nd.htm

Animation credit: Antonio González Fernández/ University of Seville (Spain)

Tuesday, 13 October 2015

Mapping the Genes that Increased Lifespan

Mapping the Genes that Increase Lifespan

   Comprehensive study finds 238 genes that affect aging in yeast cells.
October 5, 2015/Novato, California Following an exhaustive, ten-year effort, scientists at the Buck Institute for Research on Aging and the University of Washington have identified 238 genes that, when removed, increase the replicative lifespan of S. cerevisiae yeast cells. This is the first time 189 of these genes have been linked to aging. These results provide new genomic targets that could eventually be used to improve human health. The research was published online on October 8th  in the journal Cell Metabolism.
“This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is,” said Brian Kennedy, PhD, lead author and the Buck Institute’s president and CEO. “It also sets up a framework to define the entire network that influences aging in this organism.”
The Kennedy lab collaborated closely with Matt Kaeberlein, PhD, a professor in the Department of Pathology at the University of Washington, and his team. The two groups began the painstaking process of examining 4,698 yeast strains, each with a single gene deletion. To determine which strains yielded increased lifespan, the researchers counted yeast cells, logging how many daughter cells a mother produced before it stopped dividing.
“We had a small needle attached to a microscope, and we used that needle to tease out the daughter cells away from the mother every time it divided and then count how many times the mother cells divides,” said Dr. Kennedy. “We had several microscopes running all the time.”
These efforts produced a wealth of information about how different genes, and their associated pathways, modulate aging in yeast. Deleting a gene called LOS1 produced particularly stunning results. LOS1 helps relocate transfer RNA (tRNA), which bring amino acids to ribosomes to build proteins. LOS1 is influenced by mTOR, a genetic master switch long associated with caloric restriction and increased lifespan. In turn, LOS1 influences Gcn4, a gene that helps govern DNA damage control.
“Calorie restriction has been known to extend lifespan for a long time.” said Dr. Kennedy. “The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes.”
 A number of the age-extending genes the team identified are also found in C. elegans roundworms, indicating these mechanisms are conserved in higher organisms. In fact, many of the anti-aging pathways associated with yeast genes are maintained all the way to humans.
The research produced another positive result: exposing emerging scientists to advanced lab techniques, many for the first time.
“This project has been a great way to get new researchers into the field,” said Dr. Kennedy. “We did a lot of the work by recruiting undergraduates, teaching them how to do experiments and how dedicated you have to be to get results. After a year of dissecting yeast cells, we move them into other projects.”
Though quite extensive, this research is only part of a larger process to map the relationships between all the gene pathways that govern aging, illuminating this critical process in yeast, worms and mammals. The researchers hope that, ultimately, these efforts will produce new therapies.
“Almost half of the genes we found that affect aging are conserved in mammals,” said Dr. Kennedy. “In theory, any of these factors could be therapeutic targets to extend healthspan. What we have to do now is figure out which ones are amenable to targeting.”
Other Buck Institute researchers involved in the study include: Mark A. McCormick (first co-author), Mitsuhiro Tsuchiya, Scott Tsuchiyama, Arianna Anies, Juniper K. Pennypacker, Shiena Enerio, Dan Lockshon, Brett Robinson, Ariana A. Rodriguez, Marc K. Ting, and Rachel B. Brem.  A full list of authors is included in the paper.
This research was supported by NIH grants R01AG043080, R01AG025549, R01AG039390 and P30AG013280, as well as NIH training grants T32AG000266, T32AG000057 and T32ES007032 and the Ellison Medical Foundation.
 Citation: A comprehensive analysis of replicative lifespan in 4,698 single-gene deletion strains uncovers novel mechanisms of aging
About the Buck Institute for Research on Aging
The Buck Institute is the U.S.’s first independent research organization devoted to Geroscience – focused on the connection between normal aging and chronic disease. Based in Novato, CA, The Buck is dedicated to extending “Healthspan”, the healthy years of human life and does so utilizing a unique interdisciplinary approach involving laboratories studying the mechanisms of aging and those focused on specific diseases. Buck scientists strive to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer’s and Parkinson’s, cancer, cardiovascular disease, macular degeneration, osteoporosis, diabetes and stroke.  In their collaborative research, they are supported by the most recent developments in genomics, proteomics, bioinformatics and stem cell technologies.
Related Posts Plugin for WordPress, Blogger...