[ [ [['A picture is worth a thousand words', 5]], ‘http://news.yahoo.com/why-facebook-bought-instagram-4-theories-160400376.html’, ‘[Related: Why Facebook bought Instagram: 4 theories]‘, ‘ ‘, ’630′, ‘ ‘, ‘ ‘, ], [ [['He was in shock and still strapped to his seat', 9]], ‘http://contributor.yahoo.com/join/yahoonews_virginiabeach’, ‘[Did you witness the jet crash? Share your story with Yahoo! News]‘, ‘ ‘, ’630′, ‘ ‘, ‘ ‘, ], [ [['A JetBlue flight from New York to Las Vegas', 3]], ‘http://yhoo.it/GV9zpj’, ‘[Related: View photos of the JetBlue plane in Amarillo]‘, ‘ ‘, ’630′, ‘ ‘, ‘ ‘, ], [ [['Dick Clark', 11]], ‘http://news.yahoo.com/photos/dick-clark-dies-at-82-slideshow/’, ‘Click image to see more photos’, ‘http://l.yimg.com/a/p/us/news/editorial/c/21/c217c61aa2d5872244c08caa13c16ec5.jpeg’, ’500′, ‘ ‘, ‘Reuters’, ], [ [['the 28-year-old neighborhood watchman who shot and killed', 15]], ‘http://news.yahoo.com/photos/white-house-stays-out-of-teen-s-killing-slideshow/’, ‘Click image to see more photos’, ‘http://l.yimg.com/cv/ip/ap/default/120411/martinzimmermen.jpg’, ’630′, ‘ ‘, ‘AP’, ], [ [['Titanic', 7]], ‘http://news.yahoo.com/titanic-anniversary/’, ‘ ‘, ‘http://l.yimg.com/a/p/us/news/editorial/b/4e/b4e5ad9f00b5dfeeec2226d53e173569.jpeg’, ’550′, ‘ ‘, ‘ ‘, ], [ [['He was in shock and still strapped to his seat', 6]], ‘http://news.yahoo.com/photos/navy-jet-crashes-in-virginia-slideshow/’, ‘Click image to see more photos’, ‘http://l.yimg.com/cv/ip/ap/default/120406/jet_ap.jpg’, ’630′, ‘ ‘, ‘AP’, ], [ [['xxxxxxxxxxxx', 11]], ‘http://news.yahoo.com/photos/russian-grannies-win-bid-to-sing-at-eurovision-1331223625-slideshow/’, ‘Click image to see more photos’, ‘http://l.yimg.com/a/p/us/news/editorial/1/56/156d92f2760dcd3e75bcd649a8b85fcf.jpeg’, ’500′, ‘ ‘, ‘AP’, ] ]
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Homer was a shy guy, but he let me throw him a cativersary party anyway.
I always feel like a sappy jerk when I tell the story of how I adopted my cat Homer. It was six or seven years ago. I was fresh off a devastating break-up. I was living a thousand miles from anyone I knew, in a graduate program I realized might be ill-suited for me. I was crying in public a lot. It was, as they say, the worst of times.
As an adult, I?d never had a pet of my own, though I?d swooned over rescue cats in college and dreamed of having my own menagerie of furry friends. So when I happened upon the offer to adopt 13-year-old Homer, I figured our love was fated.
Anyone who has ever used Craigslist knows that there?s a free section. Despite all of the things I?ve gotten from the site — roommates, furniture, two cars, several jobs — I had no idea people were just giving stuff away. One particularly sad night, I was cruising around the site and saw the section listing. Free?! I thought.
Even more shocking, three listings down, a family was trying to offload a recently deceased parent?s cat. They lived in some far-flung suburb, and I was convinced I?d have to act fast or miss out on the opportunity of a lifetime. (I later realized, to my horror, that dozens of animals are listed for free on a daily basis. Duh, Brittany.)
I ran in to ask my roommates. Did they care if I got a cat? Probably not used to seeing me excited about anything, they shrugged and told me to go for it.
The next morning, I called to ask where we could arrange a mutually convenient pick-up. The woman on the phone sounded startled that anyone was inquiring. Still, she humored me.
Three days later, I nervously arrived to pick up Homer in a dingy Sears Auto Center waiting room. Still knowing nothing about what I was getting into, the carrier I?d brought was a bit too small for my medium-sized homeboy. Homer gamely climbed in anyway, apparently knowing we were meant to be.
Homer had two teeth and matted hair on his back when he came into my life. From what I could tell, he?d been confined to a bathroom, where he wouldn?t be a nuisance to his temporary family?s other animals. He had a pitiful mew and a gentle demeanor, which made it hard to determine if he?d been outright abused (nevermind the obvious neglect).
The first low-cost community vet we visited gave him some eardrops and suggested a more thorough exam elsewhere. The bills for various screenings and pills quickly piled up.
But I wasn?t worried about the money, even though I had none. My new buddy slept curled around my head at night. He gave me a reason to get up every morning, and a reason to come home at night. When you?re depressed and feeling especially self-destructive, sometimes the best thing you can do for yourself is foster some accountability — in my case, with a living, breathing friend who needed me as much as I needed him.?
The perks of king-sized pillows: big enough for two!
It?s a clich?, but clich?s exist for a reason. Homer taught me things about myself that, at that depressive juncture in my life, no one else could have helped me understand. I did things I didn?t know I was capable of, like giving him subcutaneous fluids through an IV ion the kitchen table with no one there to spot me.
When he was diagnosed with cancer, I lived with the daily knowledge of his inevitable fate, and I prioritized relationships and life choices accordingly. My academic and professional life suffered, but I felt like my life finally made sense.
When Homer died in my arms in the veterinary emergency room a year after I brought him home, I thought I might drop dead, too. Consumed by grief, I skipped more classes and hid from the friends I?d managed to make. When searching for a new roommate after one?s lease ended, I chose the girl who cried when I told her my cat had just died.
And then, one afternoon, I did the thing that I swore I wouldn?t do. I went to the shelter — the SPCA attached to the animal ER, no less. I was just there to feel less lonely, I told myself. I assured everyone I was cool. I wouldn?t get there and have a meltdown.
Instead, I walked into the cat adoption center and met Cloe.
Who wouldn’t love such a big, serious lioness face?
Cloe was sitting in a basket, her toddler-sized bigness spread out to the edges, screaming at a ferocious volume at anyone who walked in the room. At first, the noise startled me so badly that I almost turned around and walked back out. (I would not have been the first.)
Instead, I sat down with the 23-pound giant. After studying her yowling for a couple of minutes, I figured it must just be her way of communicating. After figuring out how to lift her with both hands onto my lap, she stopped yelling.
Her nametag indicated that she was 10, and that both her cat brother and human mama had recently passed away. Turned out she and I were both grieving — her more loudly than me — and that day, we decided to help each other through it.
Needless to say, we became inseparable. I bought her a dog bed and some low-cal food, and she charmed everyone who entered my life. Like Homer, she became the reason some friends came over.
Her good-natured disposition meant she followed me everywhere and purred when I brushed her belly or hauled her off the bathtub floor when I wanted to shower. My now-husband Andreas moved in, and we became a fiercely loving family of three.
Cloe abruptly stopped eating a year later, which, for such an enormous cat, proved to be fatal within a very short period of time. The vet didn?t seem to realize the severity of the situation, and by the time we once again ended up in the ER, there wasn?t much they could do for her.
I wish I did not know that they make animal-sized oxygen masks. I wish I did not forever have to live with the memory of how one looked strapped on my best pal?s nose as she struggled to breathe through it. I wish I didn?t know what it?s like to tell one love of your life that the other one is about to die. I wish I didn?t remember how his face looked when the meaning of my words sunk in.
Maybe because I was sharing the pain with someone else, Cloe?s death somehow felt acute in a way that Homer?s passing had not. That isn?t to say that both losses were not equally tragic. But for months after Cloe died, Andreas and I both slept badly. We?d wake up crying, Cloe?s physical mass missing from our small bed.
Along with seven other grieving animal parents, we even ended up in a pet loss grief support group, which is a story for another time.
I realize none of this sounds like a sales pitch for senior pet adoption. I?m very far into this personal account of pet loss without telling you why it matters that both of my cats were in the double digits when I adopted them. And in a way, that?s sort of my point. It didn?t and doesn?t matter (except, perhaps, to the fine money-lending folks at American Express). An open love letter to the animals who have lived with me is about celebrating their awesomeness, not pointing out their age. As much as any younger or healthier kitten, my cats deserved a loving home, and for one year each, respectively, we lived full, joyous lives together.
Which is why, about eight months later, I felt reasonably prepared for what I might encounter when I walked into a cat shelter in Copenhagen, where Andreas and I were living at the time.
?I?ve done it all,? I said when the shelter caretaker asked if I was looking for any particular type of cat. ?I?ll take whoever needs me the most.?
Malcolm apparently swatted away a number of prospective humans in the weeks before we arrived. When I walked in to meet the chunky, 10-year-old tuxedo cat with an X-shaped scar on his neck, he immediately began purring and bonked his blocky head against my leg. We signed the paperwork and began building our family once again.
If he’s really a senior cat, he sure doesn’t act like it.
This story has a happy ending. For the last three years, aside from my occasional (and thankfully unwarranted) anxiety about his health, Malcolm has lived the good life without incident. We all have, because we have each other.
(We?re also quite unconvinced that he?s as old as they said he is. Aside from some minor issues with his teeth, he?s in perfect health. I have a hard time believing the maniac furball I live with is pushing 14.)
Even though we travel a lot, sometimes we talk about adopting a dog. Malcolm is a bossy terror when he wants to be, but we like to think he might get along with another older animal pal. If and when the time comes, we?ll probably call the good people at Muttville, a local non-profit rescue group that specializes in finding good homes for senior dogs.
If it isn?t obvious, I feel lucky to have shared my life with so many amazingly sweet animals. I grew up with pets, but it wasn?t until I had my own that I felt like I understood the depth of their patience and forgiveness with people who, generally speaking, do a pretty terrific job of letting them down.
Maybe the lesson isn?t that I adopt senior pets, but that I?m open to animal friends who need a little extra help and might otherwise be deemed undesirable and subsequently overlooked.?
Time and again, my pets have proven that age is often just a number. When it?s been emotionally or financially taxing, I?ve still felt nothing but extraordinarily fortunate to share my home with such wonderful friends. Even if my foray into senior pet adoption was a Craigslist fluke, I can?t think of another spontaneous, uninformed choice I?d go back and so willingly make again.
Finance, in the sense in which it will be used in this article, means the machinery of money dealing. That is, the machinery by which money which you and I save is put together and lent out to people who want to borrow it.
Finance becomes international when our money is lent to borrowers in other countries, or when people in England, who want to start an enterprise, get some or all of the money that they need, in order to do so, from lenders oversea.
The biggest borrowers of money, in most countries, are the Governments, and so international finance is largely concerned with lending by the citizens of one country to the Governments of others, for the purpose of developing their wealth, building railways and harbours or otherwise increasing their power to produce.
Money thus saved and lent is capital. So finance is the machinery that handles capital, collects it from those who save it and lends it to those who want to use it and will pay a price for the loan of it. This price is called the rate of interest, or profit. The borrower offers this price because he hopes to be able, after paying it, to benefit himself out of what he is going to make or grow or get with its help, or if it is a Government because it hopes to improve the country?s wealth by its use. Sometimes borrowers want money because they have been spending more than they have been getting, and try to tide over a difficulty by paying one set of creditors with the help of another, instead of cutting down their spending. This path, if followed far enough, leads to bankruptcy for the borrower and loss to the lender.
If no price were offered for capital, we should none of us save, or if we saved we should not risk our money by lending it, but hide it in a hole, or lock it up in a strong room, and so there could be no new industry.
Since capital thus seems to be the subject-matter of finance and it is the object of this book to make plain what finance does, and how, it will be better to begin with clear understanding of the function of capital. All the more because capital is nowadays the object of a good deal of abuse, which it only deserves when it is misused. When it is misused, let us abuse it as heartily as we like, and take any possible measures to punish it. But let us recognize that capital, when well and fairly used, is far from being a sinister and suspicious weapon in the hands of those who have somehow managed to seize it; but is in fact so necessary to all kinds of industry, that those who have amassed it, and placed it at the disposal of industry render a service to society without which society could not be kept alive.
O ye unfaithful, believe. For those of you who saw Rimac‘s preview of its Concept_One electric supercar and were skeptical of that claimed 2.8-second 0-62MPH time given all the leisurely putting around, the Croatian automaker has followed up with a video proving that this isn’t your daddy’s EV. It turns out that the 1,088HP-equivalent motor is quick enough to leave a lot of rubber on the tarmac, thank you — both from a very enthusiastic start and from a healthy amount of drifting. This won’t change the need to both drop $980,000 and get in quick on that 88-unit production run, but if you were worried that there wouldn’t be a torch-bearer for high-speed EVs during the Tesla Roadster’s hiatus, Rimac just put that anxiety to bed.
An unusual brightness, documented by NASA’s Chandra telescope appears to be coming from a black hole.
A NASA space telescope has detected an incredible energy burst from a distant black hole, an explosion so intense that it boosted the black hole’s X-ray brightness by at least 3,000 times, scientists say.
Skip to next paragraph A NASA-hosted news conference in Washington highlights imagery and data captured by the Chandra X-Ray Observatory about the early universe’s growth of supermassive black holes in galaxies.
The outburst came from a black hole in the spiral galaxy M83, about 15 million light-years away from Earth. Using NASA’s Chandra X-ray Observatory, astronomers found a new object, called an ultraluminous X-ray source (ULX), ?that emits more X-rays than most “normal” systems in which a companion star orbits around a black hole or neutron star, the researchers said.
The observations from Chandra spanned several years, and scientists noticed that the ULX in M83 increased its X-ray brightness by at least 3,000 times.
This surprisingly sudden brightening is one of the largest changes in X-rays ever seen for this type of object, according to the researchers. In fact, ultraluminous X-ray sources do not typically have periods of dormancy. [Photos: Black Holes of the Universe]
In the accompanying image, the left is an optical view of M83. On the right is a composite image showing X-ray data from Chandra in pink and optical data from the Hubble Space Telescope in blue and yellow. The ULX is located near the bottom of the composite image.?
Optical images of the black hole in M83 were taken by the European Southern Observatory’s Very Large Telescope in Chile. These images revealed a bright blue source where the ULX is located during the X-ray outburst. Yet, before the outburst, this blue source cannot be seen, the scientists said.
The discrepancy suggests that the companion to the black hole in M83 is a red giant star that is more than 50 million years old. The mass of this object is less than four times the mass of the sun, and according to theoretical models that predict the evolution of stars, the black hole in M83 should be almost as old as this companion red giant star.
The bright blue emission that could be seen during the X-ray outburst could be the black hole’s disk brightening significantly as it acquires more material from its companion star, the astronomers said.
Another strangely behaved ULX from a black hole with an old, companion red giant star was found recently in the galaxy M31. These new discoveries in M83 and M31 show that there could be a population of similar black holes that are older and more volatile, the researchers said.
The mass of the ULX in M83 is estimated to be between 40 to 100 times the mass of the sun.
The astronomers also found that the black hole in this system may have formed from a star surprisingly rich in “metals,” or elements that are heavier than helium. Based on previous observations, the ULX is located in a metal-rich region.
Large concentrations of metals increase the rate of mass lost from massive stars, siphoning mass before they collapse. This also decreases the mass of the resulting black hole.
Current theoretical models suggest that in regions highly rich in metals, only black holes with masses less than about 15 times that of the sun should form. As a result, the findings based on the ULX in M83 could dispute these models, the researchers said.
Another plausible explanation is that the black hole is so old that it formed at a time when heavy elements were much less abundant in M83, before metals were sprinkled throughout by later generations of supernovas. Astronomers are also investigating the possibility that the mass of the black hole in M83 is only about 15 times that of the sun.
Follow SPACE.com for the latest in space science and exploration news on Twitter @Spacedotcom and on Facebook.
Public release date: 7-May-2012 [ | E-mail | Share ]
Contact: Mika Ono mikaono@scripps.edu 858-784-2052 Scripps Research Institute
LA JOLLA, CA May 7, 2012 Scientists at The Scripps Research Institute have made an important discovery about the internal programming of B cells, the immune cells that make antibodies against infections. The finding opens the way for the development of vaccines that can work more efficiently and hints at therapies for conditions in which B cells cause harmsuch as the autoimmune disease lupus erythymatosus, severe allergies, and B-cell lymphomas.
The discovery reveals that B cells produce special proteins to maintain themselves in a particular functional “class,” even as they lie dormant in the memory-cell state, awaiting a new infection. The class of a B cell determines how its antibodies marshal other components of immunity, and thus how well they can remove a certain type of threat, say bacteria on the skin versus intestinal parasites.
“This is a real breakthrough, in the sense that we now have a much better understanding of how B cell class is regulated, and how we might target that regulatory process in vaccine and drug design,” said Michael McHeyzer-Williams, a Scripps Research professor who was the principal investigator for the study, published in Nature Immunology‘s advance online edition on May 6, 2012.
Specialized Infection Fighters
Young, “nave” B cells begin their careers as infection fighters when they are exposed, in the right way, to pieces of an invading microbe that happen to match their main receptor (the B cell receptor, or BCR). Some then become plasma B cells, and slowly ramp up the active production of antibodies. Others instead become memory B cells, which can lie in wait for years, primed to respond very rapidly and nip in the bud any reinfection.
Either way, as B cells move out of the nave state, helper T cells secrete chemical signals that typically force the B cells into particular classes. IgG-class B cells are the most common in humans, and are broadly effective against viruses and bacteria. IgA-class B cells are predominantly found on mucosal surfaces such as in the throat and intestines. IgE-class cells and their antibodies protect against intestinal worms and other parasites. Some B cells stay in the default IgM class. The class of a B cell is marked by the type of “stem” it has on its Y-shaped antibodies; this stem, or effector, can mobilize other elements of the immune system, such as inflammatory chemicals, when the antibody binds to an invader.
It had been long assumed that the switching of a B cell to a particular class is the result of a one-time signaling event. “The idea was that the signals that produce this switch don’t persist in B memory cells, for example,” said Nathaniel Wang, a graduate student in the Scripps Research Kellogg School of Science and Technology working in the McHeyzer-Williams laboratory who was first author of the new study.
Testing Assumptions
In the study, Wang, McHeyzer-Williams, and their colleagues tried to determine whether that assumption is true. They knew, for example, that when T cells cause nave B cells to switch to the IgG2a class, a potent antiviral class, they do so by inducing the production in B cells of a particular protein called T-bet. To clarify T-bet’s role, the researchers engineered transgenic mice whose B cells lack the protein.
Without T-bet, they found, the mouse B cells could not be switched to the IgG2a class, even when presented with all the normal stimuli, and even though other IgG classes could be produced normallyor even in higher amounts. Even more surprisingly, in existing IgG2a memory B cells, the abrupt knockdown of T-bet levels caused the cells to lose their ability to respond to a new infection. In fact, most of the T-bet-deprived memory B cells became undetectable within a few days.
“T-bet turns out to be the central molecule that enforces the IgG2a class in B cells, and if its production stops in IgG2a memory cells, they become dysfunctional and die,” Wang said.
The finding that T-bet has this all-important, ongoing function in IgG2a memory cells suggested that other proteins play analogous roles in other classes of memory B cell. Wang therefore turned to memory B cells of the IgA class, and, with a similar set of experiments, showed that these memory B cells depend on the transcription factor ROR?. “It essentially does for IgA memory cells what T-bet does for IgG2a memory cells,” said Wang.
Implications for Science and Medicine
Wang and McHeyzer-Williams and their colleagues are now searching for the proteins that keep other memory B cells healthy and in their classes. But already the work has clarified how memory B cells work. “Until now we haven’t really had a good conceptual framework for the development and maintenance of these cells,” McHeyzer-Williams said.
The findings clearly also have implications for medicine. By supplying a particular class-enforcement protein at the same time that it exposes B cells to microbial proteins, a vaccine could induce a long-term immunity that is heavily weighted towards a desired antibody class. “If you’re designing a vaccine for certain types of virus, for example, you would like to have lots of IgG2a and IgA memory cells,” said McHeyzer-Williams. “So the goal would be to design a chemical adjuvant for the vaccine that drives B cells into those classes.”
Similarly, therapies that knock down class-enforcement signals such as T-bet could usefully reduce or eliminate memory B cells in certain classes. “Some autoimmune, allergic and lymphoma conditions are driven by B cells of a particular class, for example IgE cells in allergies,” said McHeyzer-Williams. “Being able to target just that class of B cell would be an obvious advantage over existing therapies, such as steroids, that knock down large parts of the immune system.”
###
Other contributors to the paper, “Divergent Transcriptional Programming of Class-Specific B Cell Memory by T-bet and ROR?,” were Louise J. McHeyzer-Williams and Shinji L. Okitsu of the McHeyzer-Williams lab; Thomas P. Burris of the Jupiter, Florida campus of Scripps Research, who provided crucial reagents for manipulating ROR? levels; and Steven L. Reiner of Columbia University’s College of
Physicians and Surgeons, who supplied transgenic mice.
Nathaniel Wang is a CTSA TL-1 scholar in association with the Scripps Translational Science Institute (STSI).
Professor McHeyzer-Williams’s research is funded in part by the National Institutes of Health.
[ | E-mail | Share ]
?
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Public release date: 7-May-2012 [ | E-mail | Share ]
Contact: Mika Ono mikaono@scripps.edu 858-784-2052 Scripps Research Institute
LA JOLLA, CA May 7, 2012 Scientists at The Scripps Research Institute have made an important discovery about the internal programming of B cells, the immune cells that make antibodies against infections. The finding opens the way for the development of vaccines that can work more efficiently and hints at therapies for conditions in which B cells cause harmsuch as the autoimmune disease lupus erythymatosus, severe allergies, and B-cell lymphomas.
The discovery reveals that B cells produce special proteins to maintain themselves in a particular functional “class,” even as they lie dormant in the memory-cell state, awaiting a new infection. The class of a B cell determines how its antibodies marshal other components of immunity, and thus how well they can remove a certain type of threat, say bacteria on the skin versus intestinal parasites.
“This is a real breakthrough, in the sense that we now have a much better understanding of how B cell class is regulated, and how we might target that regulatory process in vaccine and drug design,” said Michael McHeyzer-Williams, a Scripps Research professor who was the principal investigator for the study, published in Nature Immunology‘s advance online edition on May 6, 2012.
Specialized Infection Fighters
Young, “nave” B cells begin their careers as infection fighters when they are exposed, in the right way, to pieces of an invading microbe that happen to match their main receptor (the B cell receptor, or BCR). Some then become plasma B cells, and slowly ramp up the active production of antibodies. Others instead become memory B cells, which can lie in wait for years, primed to respond very rapidly and nip in the bud any reinfection.
Either way, as B cells move out of the nave state, helper T cells secrete chemical signals that typically force the B cells into particular classes. IgG-class B cells are the most common in humans, and are broadly effective against viruses and bacteria. IgA-class B cells are predominantly found on mucosal surfaces such as in the throat and intestines. IgE-class cells and their antibodies protect against intestinal worms and other parasites. Some B cells stay in the default IgM class. The class of a B cell is marked by the type of “stem” it has on its Y-shaped antibodies; this stem, or effector, can mobilize other elements of the immune system, such as inflammatory chemicals, when the antibody binds to an invader.
It had been long assumed that the switching of a B cell to a particular class is the result of a one-time signaling event. “The idea was that the signals that produce this switch don’t persist in B memory cells, for example,” said Nathaniel Wang, a graduate student in the Scripps Research Kellogg School of Science and Technology working in the McHeyzer-Williams laboratory who was first author of the new study.
Testing Assumptions
In the study, Wang, McHeyzer-Williams, and their colleagues tried to determine whether that assumption is true. They knew, for example, that when T cells cause nave B cells to switch to the IgG2a class, a potent antiviral class, they do so by inducing the production in B cells of a particular protein called T-bet. To clarify T-bet’s role, the researchers engineered transgenic mice whose B cells lack the protein.
Without T-bet, they found, the mouse B cells could not be switched to the IgG2a class, even when presented with all the normal stimuli, and even though other IgG classes could be produced normallyor even in higher amounts. Even more surprisingly, in existing IgG2a memory B cells, the abrupt knockdown of T-bet levels caused the cells to lose their ability to respond to a new infection. In fact, most of the T-bet-deprived memory B cells became undetectable within a few days.
“T-bet turns out to be the central molecule that enforces the IgG2a class in B cells, and if its production stops in IgG2a memory cells, they become dysfunctional and die,” Wang said.
The finding that T-bet has this all-important, ongoing function in IgG2a memory cells suggested that other proteins play analogous roles in other classes of memory B cell. Wang therefore turned to memory B cells of the IgA class, and, with a similar set of experiments, showed that these memory B cells depend on the transcription factor ROR?. “It essentially does for IgA memory cells what T-bet does for IgG2a memory cells,” said Wang.
Implications for Science and Medicine
Wang and McHeyzer-Williams and their colleagues are now searching for the proteins that keep other memory B cells healthy and in their classes. But already the work has clarified how memory B cells work. “Until now we haven’t really had a good conceptual framework for the development and maintenance of these cells,” McHeyzer-Williams said.
The findings clearly also have implications for medicine. By supplying a particular class-enforcement protein at the same time that it exposes B cells to microbial proteins, a vaccine could induce a long-term immunity that is heavily weighted towards a desired antibody class. “If you’re designing a vaccine for certain types of virus, for example, you would like to have lots of IgG2a and IgA memory cells,” said McHeyzer-Williams. “So the goal would be to design a chemical adjuvant for the vaccine that drives B cells into those classes.”
Similarly, therapies that knock down class-enforcement signals such as T-bet could usefully reduce or eliminate memory B cells in certain classes. “Some autoimmune, allergic and lymphoma conditions are driven by B cells of a particular class, for example IgE cells in allergies,” said McHeyzer-Williams. “Being able to target just that class of B cell would be an obvious advantage over existing therapies, such as steroids, that knock down large parts of the immune system.”
###
Other contributors to the paper, “Divergent Transcriptional Programming of Class-Specific B Cell Memory by T-bet and ROR?,” were Louise J. McHeyzer-Williams and Shinji L. Okitsu of the McHeyzer-Williams lab; Thomas P. Burris of the Jupiter, Florida campus of Scripps Research, who provided crucial reagents for manipulating ROR? levels; and Steven L. Reiner of Columbia University’s College of
Physicians and Surgeons, who supplied transgenic mice.
Nathaniel Wang is a CTSA TL-1 scholar in association with the Scripps Translational Science Institute (STSI).
Professor McHeyzer-Williams’s research is funded in part by the National Institutes of Health.
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The Veterans Affairs (VA) Maryland Health Care System will observe National Nurses Week (May 6-12) with an awards ceremony on May 7, at 3 p.m. in the auditorium at the Baltimore VA Medical Center. Janet D. Allan, PhD, RN, FAAN, dean of the University of Maryland School of Nursing, will deliver the keynote address on the future of nursing. During the ceremony, nurses will be honored with the VA Secretary?s Award for Excellence in Nursing and the 2012 DAISY Award.
Baltimore, MD (PRWEB) May 06, 2012
The Veterans Affairs (VA) Maryland Health Care System will observe National Nurses Week (May 6-12) with an awards ceremony on May 7, at 3 p.m. in the auditorium at the Baltimore VA Medical Center. Janet D. Allan, PhD, RN, FAAN, dean of the University of Maryland School of Nursing, will deliver the keynote address on the future of nursing. During the ceremony, nurses will be honored with the VA Secretary?s Award for Excellence in Nursing and the 2012 DAISY Award.
?We consider our nurses?the largest of our workforce at more than 900 strong, of which 700 are RN?s and Nurse Practitioners?to be the compassionate backbone of our health care system,? said Dennis H. Smith, director of the VA Maryland Health Care System. ?We are thrilled to honor the dedicated men and women who have mastered the art and science of caring for our nation?s heroes with compassion. No other health care professional is closer to the Veterans we serve than VA nurses. Our patients rely on them for their compassion, and the VA relies on them for setting the highest clinical care standards.?
The VA Maryland Health Care System?s nursing staff includes licensed practical nurses, registered nurses, nurse practitioners, health technicians and nursing assistants who serve Veterans at three inpatient facilities and six community based outpatient clinics throughout the state. During the ceremony, four nurses will be recognized as the VA Maryland Health Care System?s winners of the Secretary?s Award for Excellence in Nursing. Of the four winners, two will be recognized as the awardees for the VA Capitol Health Care Network, with the nurse that is named as the national VA Secretary Award recipient selected from the pool of Network winners.
The VA Secretary?s Award for Excellence in Nursing consists of three major categories: Excellence in Nursing, Advancement of Nursing Programs by a Medical Center or Health Care System Director, and Advancement of Nursing Programs by a Medical Center or Health Care System Nurse Executive.
During the ceremony, one VA nurse will also be recognized as the DAISY Award recipient. Established by the DAISY Foundation, a non-profit organization designed to eliminate diseases attacking the immune system ? in memory of J. Patrick Barnes ? the DAISY Award for Extraordinary Nurses recognizes the very special work nurses do every day.
The ceremony?s keynote speaker, Janet Allan, who has served as dean of the University of Maryland School of Nursing since June 2002, has emerged as a leader in nursing education. She has collaborated with nurse educators and health care providers to develop the Nurse Support Program II, a 10-year grant program providing $10 annually to fund educational initiatives aimed at alleviating the state?s shortage of faculty and bedside nurses. Dean Allan is one of nine nurses in the nation honored by the U.S. Assistant Secretary of Health for contributions to the care of people with AIDS and HIV infection. Allan created a hospice for HIV/AIDS patients that serves as a national model. Many students from the University of Maryland School of Nursing rotate through the VA Maryland Health Care System as part of the VA?s commitment to the training of tomorrow?s clinicians.
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The VA Maryland Health Care System (VAMHCS) provides a broad spectrum of medical, surgical, rehabilitative, mental health and outpatient care to veterans at two medical centers, one community living rehabilitation center and five outpatient clinics located throughout the state. More than 52,000 veterans from various generations receive care from the VAMHCS annually. Nationally recognized for its state-of-the-art technology and quality patient care, the VAMHCS is proud of its reputation as a leader in veterans? health care, research and education. It costs nothing for Veterans to enroll for health care with the VA Maryland Health Care System and it could be one of the more important things a Veteran can do. For information about VA health care eligibility and enrollment or how to apply for a VA medical care hardship to avoid future copayments for VA health care, interested Veterans are urged to call the Enrollment Center for the VA Maryland Health Care System, Monday through Friday, from 8 a.m. to 4:30 p.m. at 1-800-463-6295, ext. 7324 or visit http://www.maryland.va.gov.
For the original version on PRWeb visit: http://www.prweb.com/releases/prweb2012/5/prweb9476107.htm
Many individuals need to make their life a lot more green, but do not know steps to start. There are lots of environmentally friendly power systems open to support help save vitality and funds. This content listed below covers some great ways to go green.
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1 clever method to save money and be natural is to help keep your hot water heater temperatures at 120 degrees maximum. Achieving this is able to reduce your electric bill by around 10 percent and keep temperatures at a harmless level.
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After looking at the content, you ought to have a greater understanding of eco-friendly power. Are you prepared to present environmentally friendly energy a shot? Use the tips in this article and you could produce a better life for yourself. .Use the tips to see ways to be eco-friendly.
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Viatical Settlement Benefits Immediate cash inorder to ease financial burdens Additional cash to compensate for loss of income relief from Premium paid funds to seek treatment not covered by health insurance
Viatical settlement definition A viatical settlement is selling a life insurance policy issued on the life of a person, who has a terrible illness or condition that is expected to result in death within 84 months, for an amount that is less than policy?s face value. The person with the life-threatening illness who is insured under the policy is called a viator. He may or may not be the owner of the policy. But only the holder of the policy has the right to sell it. If you do not own the policy, owner cannot sell it without your consent. The unit that buys the policy is called a viatical settlement provider, also, there are persons called brokers, who help with the sale of the policy. This settlement offers you the chance to receive a portion of your policy?s death benefit as you are still alive, giving you an option to ease the financial stress that goes with an illness or condition.
How Viatical settlement works Most of the providers or brokers will ask you to fill an application and medical release forms so that they could collect information from your insurance company and your doctors. All that gathered is to be kept confidential and cannot be given to someone without your written approval. If you meet the criteria, the provider will make an offer for your policy. The amount offered for your insurance policy will be purely based on the facts such as how long you are likely to live, the sum you pay for premiums, the rating of your life insurance company, and your policy?s other provisions. If you accept the offer, you would be asked to sign a viatical settlement contract.
investing in viatical settlement contract Viatical Settlement Contracts are nowadays being sold as securities, and even though there is nothing inherently wrong with investing in viatical settlements, the potential investors need to be alert of a few basic facts and the difference between viatical settlements and other kinds of securities. The first thing to keep in mind is that most often the investor in a contract is reliant upon the viatical settlement provider, or other party selected by the viatical settlement provider, see to it that the viatical settlement contract and the fundamental life insurance policy is maintained. This can involve everything from determining the life expectancy of the viator to safeguarding of the life insurance policy.
Most states consider a viatical settlement contract that is sold as an investment, as a security and regulate these investments as such. As always, anybody considering investing money in any security should carefully research the product, the individual, and the company that is offering the security.
Tags: Bonded Life Settlement, Life insurance settlements, life settlement policies
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Finance, in the sense in which it will be used in this article, means the machinery of money dealing. That is, the machinery by which money which you and I save is put together and lent out to people who want to borrow it.
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Public release date: 7-May-2012
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