(Taken from a transcript of Nicola?s weekly private client Business &?Internet Marketing Mentoring?Call)
I just want to make sure that you?re all aware of two events coming up ? one is the event Neil Asher and myself are hosting in London on the 20th October, which is all about how to build a real business selling real ? physical ? products to real people. ?Online. ?Things that actually have to get posted to folks!? Not that you?d be posting them, mind!
Neil has made a massive success of that in several businesses so far and you can find out more about that here >>> and read more about that further on in this post.
I?d also like to recommend Martin Avis? forthcoming workshop, the Kiss Workshop in London, 13th and 14th of October.? It?s going to be absolutely brilliant, I know Nick?s already booked.? I?m going to be there as well for the whole two days, I?m staying overnight.? Nick and I are going out for dinner, if anyone of you would like to come and join us you would be most welcome.? Really it?s a collection of under the radar internet marketers who are seriously making money online but who don?t necessarily shout about it, teach about it, mentor about it or whatever.? I know several of them personally and I know they?re really serious people who are earning significant sums every month.
I know it?s still a dream of many of you to create a second income online and while I?ve made a lot of money online it?s always been through coaching and mentoring, and occasionally selling the odd product and occasionally recommending someone else?s product.? But like many of you I?d really, really like to have something rolling in the background that brings in significant sums every month ? on an automated basis.?
It?s interesting because a lot of the people that will be there are actually making money from affiliate marketing ? just from recommending other people?s stuff.? Old school and bloomin? hard work nowadays but still apparently do-able. ?Martin only recently branched out into having his own membership site and creating his own product which is a private label company that he and his wife Delia were running together.? He?s built a six-figure income literally with just a text on e-zine that he sends every week recommending other people?s stuff, all the stuff that he?s used himself, all the stuff that he?s recommending personally.? But it can be done.
Martin was one of our chosen speakers for the really useful internet day with Brett McFall and he was the obvious person to ask.? Also there that day was Sarah Starr who used to own ? well, she still does actually ? a video production company.? She was videoing it for us.? Sarah is dyslexic, which is why she uses video a lot, and she is another person who?s going to be speaking in this Kiss Workshop event in London.? I think it?s ?147 for the two days.? It?s going to be absolutely dynamite content from people who are not trying to sell you big ticket items or big ticket coaching, and it?s going to be great fun.? I wouldn?t miss it for the world.
Selling Physical Items Online
On the topic of building a business, one of my colleagues in one of the other businesses I?m involved in ?. Neil?s actually created a couple of business selling physical products rather than digital or ?info products.? Two or three that I know about.? One?s called Kidz 5 A Day, which is where he figured that he wanted his daughter Isabella to be eating more vegetables but she only liked tomatoes! ?Well do you know the SuperGreens stuff that you can buy ? good for adults but good luck getting kids to drink it! ?
I didn?t realise this, I thought Neil just licensed his products from overseas.? But it turns out he actually got what?s called a private label manufacturing company to make it for him.? It?s really delicious, I actually got it in my fridge.? His daughter loves it, it?s like chocolate milkshake.? It?s like Ovaltine mixed with chocolate milkshake.? He sells this stuff all around the world from a website.?
He?s also got a company called Advanced Child Academy, and we?ve got a lot of ACA boxes in our cupboard.? When he goes away, my daughter Phoebe takes over the packing and dispatch of the said items to the people who are buying these physical products online.? Again, they?re all over the country, they?re all over Europe.? So I know that he can do what he says he does.?
We had an interesting conversation about it the other day and he said, ?Look, why are you going to this Martin Avis thing in London??? I said because I really want to learn how to create a passive income online rather than having to coach and mentor for it all the time, although I do love doing that as well obviously.
He said it?s easy.?
I said, ?It might be easy for you Neil but it?s not easy for your average person.?? He said, ?Okay.? That sounds like a challenge to me, why don?t I teach you how to do it then we can perhaps turn it into a product or something if you want to or we might be able to turn it into a seminar in Brighton.? But the main thing is I want to prove to you that it?s a lot easier than you think it is.??
I said, ?Okay.? So then how would you do it??? He said, ?Well, I?d outsource it.? I know what to do and I?d outsource it.??
I said to him ?The problem with lots of people is that they might be able to afford to come to a seminar or come to a webinar or whatever, or even buy a tuition product, but they probably wouldn?t have the resources to then outsource it all like you would. ?You?ve got to teach them how to do it on a limited budget, otherwise you?re not moving them from knowing it?s possible for you to knowing it?s possible for them, to thinking it?s probable.? That?s what you have to do with marketing, move people from possible for them to probable for them, otherwise you won?t make any sales.??
So that?s something I wanted to share with you.? We?re doing two webinars next week.? I don?t know how he managed to talk me to doing that actually.? He?s very persuasive and very enthusiastic.? It?s difficult to say no.?
So, next week we?re doing two webinars that you really ought to come along to one or other of them.?
The other thing you want to think about is if you?re trying to sell something online, whether it?s a product or a service ? I haven?t mastered this completely yet ? you need to think about moving people from thinking that the outcome is possible for other people to moving them to think it?s possible for them, to moving them to think that it?s probable for them if they buy your product or service or invest in your product and service.
That?s why it?s easier to sell to business people really because they think in terms of investment rather than spending / buying ? although Neil is selling both Kidz 5 A Day and Advanced Child Academy to people who have jobs, have kids and who are buying stuff, they?re not investing in anything.?
So again, he?s out to blast my limiting beliefs out of the waters as he put it.? So, if you want to watch that happening that will be quite interesting.
?
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Supporters cheer as U.S. President Barack Obama arrives to speak at a campaign event at Desert Pines High School??Looking to his first face-to-face clash with Mitt Romney, President Barack Obama told a cheering crowd of supporters in Las Vegas on Sunday that his Republican foe was "a good debater" while he himself was "just ok."
The Democrat, addressing a crowd of 11,200 packed onto the soccer field of Desert Pines High School, said Wednesday's debate ought to be "a serious discussion" about boosting economic growth and helping the middle class.
The media is focused on "who's going to have the best zingers" and "who's going to put the most points on the board," he said, looking to manage expectations for what could be a punchy back-and-forth. "Governor Romney, he's a good debater. I'm just ok."
"But what I'm most concerned about is having a serious discussion about what we?need to do to keep the country growing and restore security for hard-working Americans," Obama said. "That's what people are going to be listening for. That's the debate that you deserve."
Both camps have been trying to shape the expectations for Wednesday's debate -- the first of three pitting the presidential candidates against each other.
Blocking key protein could halt age-related decline in immune system, Stanford study finds Public release date: 30-Sep-2012 [ | E-mail | Share ]
Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center
STANFORD, Calif. The older we get, the weaker our immune systems tend to become, leaving us vulnerable to infectious diseases and cancer and eroding our ability to benefit from vaccination. Now Stanford University School of Medicine scientists have found that blocking the action of a single protein whose levels in our immune cells creep steadily upward with age can restore those cells' response to a vaccine.
This discovery holds important long-term therapeutic ramifications, said Jorg Goronzy, MD, PhD, professor of rheumatology and immunology and the senior author of a study to be published online Sept. 30 in Nature Medicine. It might someday be possible, he said, to pharmacologically counter aging's effects on our immune systems.
In the study, the Stanford team fingered a protein called DUSP6 that interferes with the capacity of an important class of immune cells to respond to the presence of a foreign substance, such as those appearing on the surface of an invading pathogen or in a vaccine designed to stifle that invasion.
The researchers also identified a potential lead compound that, by inhibiting DUSP6's action, restores those cells' responsiveness to a more youthful state.
A person's immune response declines slowly but surely starting at around age 40, said Goronzy. "While 90 percent of young adults respond to most vaccines, after age 60 that response rate is down to around 40-45 percent. With some vaccines, it's as low as 20 percent." Vaccine failure among seniors poses a serious health problem: Some 90 percent of influenza deaths are among people over age 65.
A vaccine is, in essence, a "mug shot" of one or more of a pathogen's most prominent features, akin to a photo of a giant wart on a suspect's nose. This chemical snapshot or antigen, in scientific parlance is nailed into customized "frames" and displayed on the surface of "desk cop" cells specializing in signaling T cells, the "beat cops" of the immune system.
One important type of beat cop, the so-called T-helper cell, stimulates other immune cells called B cells that play a key role in our response to infection-preventing vaccines. On exposure to an antigen from a vaccine or the pathogen itself, along with appropriate interactions with T-helper cells, B cells proliferate, mature and get down to brass tacks: producing and secreting antibodies. These molecules are designed to snare and immobilize the pathogen, flagging it for incarceration and, quite likely, a death sentence meted out by still other very tough immune cells.
For poor responders, there are a few ways of increasing a vaccine's potency. One is to simply boost the dose. A second is the use of adjuvants: chemicals, or combinations of them that, like a cup of strong coffee, wake up the desk cops whose job is to display the description of the pathogen's distinguishing feature (the antigen) to the beat cops. A recently published large, multicenter study, one of whose co-authors was Cornelia Dekker, MD, professor of pediatrics (infectious disease) at Stanford, showed that adding an experimental adjuvant to the standard seasonal flu vaccine substantially improved seniors' response to the vaccine.
But just waking up the desk cops won't cut it if the beat cops are too sluggish. Older people's T-helper cells suffer from a diminished capacity to activate, proliferate and secrete crucial signaling chemicals in response to infections or vaccines. This limits even an adjuvant-containing vaccine's ability to get the job done.
"Some age-associated defect or defects raise the threshold of responsiveness to the presented antigen, so a vaccine dose that triggers T-cell activation in a younger person doesn't in an older person. Adjuvants can't compensate for these defects," Goronzy said.
So he and his team sought to identify the defects that cause this age-related sluggishness in T-helper cells, and to see how to counter them.
Circulating T-helper cells fall into two broad categories. "Nave" T-helper cells have never encountered an antigen before (as in the case of, say, a rare or emerging pathogen or a new vaccine), but are capable of wheeling into action once they do. It takes a week or two to reach full tilt.
"Memory" T-helper cells have previously been exposed to an antigen. These cells are long-lived and narrowly fixed on that particular antigen. They can rapidly transition to an activated state should the same antigen ever cross their path again. That's why prior exposure through infection or a vaccine renders us more resistant.
In a Proceedings of the National Academy of Sciences study published earlier this year, Goronzy's team showed that faulty regulation in memory T-helper cells, due to aging-related increased levels of a protein called DUSP4, inhibits the activation of those cells, with their consequent failure to ignite a good B-cell (antibody-producing) response.
This time around, the investigators uncovered a similar effect with a related protein, DUSP6, on nave T-helper cells. In test tubes, they compared blood cells drawn from people ages 20-35 versus 70-85 in response to stimulation. In nave T-helper cells (but not in memory cells), there were age-associated differences in a specific chain of biochemical events involved in the cells' activation, proliferation and differentiation. Laboratory tests showed that the culprit behind the cells' fecklessness in older people was DUSP6, an enzyme that works by hacking phosphate groups off of other enzymes, thus dialing down their activity. Those "downstream" enzymes are crucial to nave T-helper cell activation. DUSP6 levels were much higher in older people's nave T-helper cells.
Further experimentation revealed that DUSP6's increase in aging nave T-helper cells was caused by an age-associated easing up on a brake pedal called miR-181a, one among hundreds of small molecules made of RNA (called microRNA) that regulate proteins' production. All microRNA molecules work by affixing themselves to larger protein-template RNA molecules, also made of RNA, gumming things up and stalling the procedure. Each distinct variant of microRNA molecule can bind to several different varieties of protein-prescribing RNA molecule, thereby swiftly redirecting a cell's overall behavior.
Goronzy and his colleagues saw that miR-181a directly interferes with the production of DUSP6 and noted that the amount of miRNA-181 present in nave T-cells declines steadily, bottoming out around age 65-70, causing levels of DUSP6 in these cells to increase with age. Artificially boosting miRNA-181a levels in nave human T cells caused DUSP6 levels to plummet, commensurately increasing those cells' readiness to activate on exposure to a given dose of influenza vaccine. In contrast, artificially increasing the levels of DUSP6 blocked the beneficial effects of heightened miR-181a levels.
A study conducted by University of Pittsburgh researchers and published in Nature Chemical Biology in 2009 had shown in zebrafish that a particular compound with an extremely long chemical name (abbreviated in Goronzy's study as "BCI") appeared to block DUSP6's action in certain heart cells, leading to cardiac hypertrophy. (In this case, DUSP6's proliferation-preventing function was beneficial.)
So Goronzy and his colleagues incubated blood cells from 10 60- to 85-year-old individuals with activation-stimulating molecules in the presence of increasing concentrations of BCI. The greater the BCI dose, the more evidence of nave T-helper cell activation they saw.
"We are still far from application in the clinic," cautioned Goronzy. "We need to keep tweaking the compound and testing it in mice to make absolutely sure it's safe enough to try in humans. But improving vaccine responses to overcome age-related immune defects represents a unique opportunity to attain healthy aging."
###
First authorship of the study, funded by the National Institutes of Health, was shared by Guangjin Li, PhD, Mingcan Yu, PhD, and Won-Won Lee, PhD, all postdoctoral scholars in Goronzy's lab. Other Stanford co-authors were Eswar Krishnan, MD, assistant professor of medicine; and Cornelia Weyand, MD, PhD, professor of medicine.
Information about the medical school's Department of Medicine and its Institute for Immunity, Transplantation and Infection, which also supported the work, is available at http://medicine.stanford.edu and http://iti.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACTS:
Margarita Gallardo at (650) 723-7897 (mjgallardo@stanford.edu)
Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT:
M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Blocking key protein could halt age-related decline in immune system, Stanford study finds Public release date: 30-Sep-2012 [ | E-mail | Share ]
Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center
STANFORD, Calif. The older we get, the weaker our immune systems tend to become, leaving us vulnerable to infectious diseases and cancer and eroding our ability to benefit from vaccination. Now Stanford University School of Medicine scientists have found that blocking the action of a single protein whose levels in our immune cells creep steadily upward with age can restore those cells' response to a vaccine.
This discovery holds important long-term therapeutic ramifications, said Jorg Goronzy, MD, PhD, professor of rheumatology and immunology and the senior author of a study to be published online Sept. 30 in Nature Medicine. It might someday be possible, he said, to pharmacologically counter aging's effects on our immune systems.
In the study, the Stanford team fingered a protein called DUSP6 that interferes with the capacity of an important class of immune cells to respond to the presence of a foreign substance, such as those appearing on the surface of an invading pathogen or in a vaccine designed to stifle that invasion.
The researchers also identified a potential lead compound that, by inhibiting DUSP6's action, restores those cells' responsiveness to a more youthful state.
A person's immune response declines slowly but surely starting at around age 40, said Goronzy. "While 90 percent of young adults respond to most vaccines, after age 60 that response rate is down to around 40-45 percent. With some vaccines, it's as low as 20 percent." Vaccine failure among seniors poses a serious health problem: Some 90 percent of influenza deaths are among people over age 65.
A vaccine is, in essence, a "mug shot" of one or more of a pathogen's most prominent features, akin to a photo of a giant wart on a suspect's nose. This chemical snapshot or antigen, in scientific parlance is nailed into customized "frames" and displayed on the surface of "desk cop" cells specializing in signaling T cells, the "beat cops" of the immune system.
One important type of beat cop, the so-called T-helper cell, stimulates other immune cells called B cells that play a key role in our response to infection-preventing vaccines. On exposure to an antigen from a vaccine or the pathogen itself, along with appropriate interactions with T-helper cells, B cells proliferate, mature and get down to brass tacks: producing and secreting antibodies. These molecules are designed to snare and immobilize the pathogen, flagging it for incarceration and, quite likely, a death sentence meted out by still other very tough immune cells.
For poor responders, there are a few ways of increasing a vaccine's potency. One is to simply boost the dose. A second is the use of adjuvants: chemicals, or combinations of them that, like a cup of strong coffee, wake up the desk cops whose job is to display the description of the pathogen's distinguishing feature (the antigen) to the beat cops. A recently published large, multicenter study, one of whose co-authors was Cornelia Dekker, MD, professor of pediatrics (infectious disease) at Stanford, showed that adding an experimental adjuvant to the standard seasonal flu vaccine substantially improved seniors' response to the vaccine.
But just waking up the desk cops won't cut it if the beat cops are too sluggish. Older people's T-helper cells suffer from a diminished capacity to activate, proliferate and secrete crucial signaling chemicals in response to infections or vaccines. This limits even an adjuvant-containing vaccine's ability to get the job done.
"Some age-associated defect or defects raise the threshold of responsiveness to the presented antigen, so a vaccine dose that triggers T-cell activation in a younger person doesn't in an older person. Adjuvants can't compensate for these defects," Goronzy said.
So he and his team sought to identify the defects that cause this age-related sluggishness in T-helper cells, and to see how to counter them.
Circulating T-helper cells fall into two broad categories. "Nave" T-helper cells have never encountered an antigen before (as in the case of, say, a rare or emerging pathogen or a new vaccine), but are capable of wheeling into action once they do. It takes a week or two to reach full tilt.
"Memory" T-helper cells have previously been exposed to an antigen. These cells are long-lived and narrowly fixed on that particular antigen. They can rapidly transition to an activated state should the same antigen ever cross their path again. That's why prior exposure through infection or a vaccine renders us more resistant.
In a Proceedings of the National Academy of Sciences study published earlier this year, Goronzy's team showed that faulty regulation in memory T-helper cells, due to aging-related increased levels of a protein called DUSP4, inhibits the activation of those cells, with their consequent failure to ignite a good B-cell (antibody-producing) response.
This time around, the investigators uncovered a similar effect with a related protein, DUSP6, on nave T-helper cells. In test tubes, they compared blood cells drawn from people ages 20-35 versus 70-85 in response to stimulation. In nave T-helper cells (but not in memory cells), there were age-associated differences in a specific chain of biochemical events involved in the cells' activation, proliferation and differentiation. Laboratory tests showed that the culprit behind the cells' fecklessness in older people was DUSP6, an enzyme that works by hacking phosphate groups off of other enzymes, thus dialing down their activity. Those "downstream" enzymes are crucial to nave T-helper cell activation. DUSP6 levels were much higher in older people's nave T-helper cells.
Further experimentation revealed that DUSP6's increase in aging nave T-helper cells was caused by an age-associated easing up on a brake pedal called miR-181a, one among hundreds of small molecules made of RNA (called microRNA) that regulate proteins' production. All microRNA molecules work by affixing themselves to larger protein-template RNA molecules, also made of RNA, gumming things up and stalling the procedure. Each distinct variant of microRNA molecule can bind to several different varieties of protein-prescribing RNA molecule, thereby swiftly redirecting a cell's overall behavior.
Goronzy and his colleagues saw that miR-181a directly interferes with the production of DUSP6 and noted that the amount of miRNA-181 present in nave T-cells declines steadily, bottoming out around age 65-70, causing levels of DUSP6 in these cells to increase with age. Artificially boosting miRNA-181a levels in nave human T cells caused DUSP6 levels to plummet, commensurately increasing those cells' readiness to activate on exposure to a given dose of influenza vaccine. In contrast, artificially increasing the levels of DUSP6 blocked the beneficial effects of heightened miR-181a levels.
A study conducted by University of Pittsburgh researchers and published in Nature Chemical Biology in 2009 had shown in zebrafish that a particular compound with an extremely long chemical name (abbreviated in Goronzy's study as "BCI") appeared to block DUSP6's action in certain heart cells, leading to cardiac hypertrophy. (In this case, DUSP6's proliferation-preventing function was beneficial.)
So Goronzy and his colleagues incubated blood cells from 10 60- to 85-year-old individuals with activation-stimulating molecules in the presence of increasing concentrations of BCI. The greater the BCI dose, the more evidence of nave T-helper cell activation they saw.
"We are still far from application in the clinic," cautioned Goronzy. "We need to keep tweaking the compound and testing it in mice to make absolutely sure it's safe enough to try in humans. But improving vaccine responses to overcome age-related immune defects represents a unique opportunity to attain healthy aging."
###
First authorship of the study, funded by the National Institutes of Health, was shared by Guangjin Li, PhD, Mingcan Yu, PhD, and Won-Won Lee, PhD, all postdoctoral scholars in Goronzy's lab. Other Stanford co-authors were Eswar Krishnan, MD, assistant professor of medicine; and Cornelia Weyand, MD, PhD, professor of medicine.
Information about the medical school's Department of Medicine and its Institute for Immunity, Transplantation and Infection, which also supported the work, is available at http://medicine.stanford.edu and http://iti.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACTS:
Margarita Gallardo at (650) 723-7897 (mjgallardo@stanford.edu)
Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT:
M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Well, it looks like Sony's in-house software developers have decided this isthe perfect week to deliver delicious treats to a large portion of the company's mobile lineup. Not long after outing updates for the Tablet S and Xperia Ion (in the US), the electronics giant is now bringing Ice Cream Sandwich to handsets such as the Xperia go, Xperia U and Xperia sola. The refresh itself brings a slew of novel traits to the trio of Xperia slabs, including a "new way to experience" music, photos and video, improvements to the lockscreen, the ability to resize widgets and the addition of a "multitasking" button. While the standout features remain the same across the board, the Xperia sola does get an added bonus in the form of a so-called, self-explanatory glove mode -- which is made possible by the device's "floating touch" technology. Sony does note that availability of the 4.0 upgrade will vary by market and, not surprisingly, carrier requirements. Let's just hope you get to enjoy the changes soon.
Although transaction remained sluggish given cautious sentiment, the local market extended gains to the second straight session on Wednesday thanks to support of a number of large-caps, with the VN-Index advancing 3.35 points, or 0.86%, from the day earlier to close at 395.12.
The market opened sharply higher but dropped back into the red and bottomed at 392.56 points before trading in a narrow range around Tuesday?s close until the end of the morning session. In the afternoon, stocks rallied again and pushed the index to the highs where it closed.
Liquidity on the southern exchange stayed weak with 23.8 million shares worth VND390.5 billion traded, both dropping by over 10% against the previous session. The put-through market was quiet with only a handful of small transactions.
Gainers outnumbered losers by 142 to 76 while 92 stocks closed at the reference prices. BVH, VIC and VNM were the largest contributors to the VN-Index.
Viet Capital Securities Co. (VCSC) noted that BVH reversed strongly after plunging to the floor prices for two days in a row, although this time the support no longer came from foreigners as it was last week. VIC, on the other hand, has been enjoying steady performance since September 14, gaining 13% over the period.
Tan Tao Investment Industry Corporation (ITA) again took the lead for liquidity, going up to the ceiling price of VND4,600 per share with nearly 1.8 million shares changing hands. Eximbank (EIB) was the second most actively traded stock but it fell 1.3% to VND14,600 on a volume of 1.1 million shares.
The Hanoi market managed a modest gain as PVX hit the ceiling price with nearly four million shares traded. With 135 rising stocks versus 54 falling tickers, the HNX-Index inched up 0.07 point, or 0.12%, from the previous day to close at 56.29.
Ending the day, there were 21.4 million shares worth VND149 billion traded on the bourse. Value increased by 8.8% from the session earlier but mostly thanks to penny stocks, evidenced by a remarkable volume increase of 26.6%.
VCSC said that while the VN-Index is approaching closer to 400 points, the HNX-Index is still struggling far below the 60-point thresholds. It believes the levels are important to observe.
?The key point is that except for some isolated sessions, liquidity remains low. That we believe exactly reflects investors? uneasiness to make a decision at the moment. Markets are moving in an attractive valuation region but mixed macroeconomic indicators and enterprise results means it is hard for investors to identify turnaround point,? it said.
Cut your time bartering and still get the wheels you want with online research and even peer-to-peer lending.
In a recent survey, more than half of respondents said they would rather go to the dentist than negotiate a car purchase. I don?t know of anyone who enjoys the process, except for the father of a friend of mine. He simply goes into the dealership already knowing what is on the lot and which vehicle he wants. He brings with him a briefcase full of cash in the amount of a few thousand less than the MSRP. He simply offers them the briefcase in return for the vehicle.
He hasn?t been turned down yet. He?s in and out ? with his new car or truck ? in 15 minutes.
Unfortunately, most of us do not have backyards with strategically placed coffee cans full of cash. This weekend it was time for my wife and I to face the crucible, as her lease is about to run out and she?s interested in a bigger SUV.
During the four or five trips our salesperson made between us and her manager to see if we could strike a deal (we couldn?t), I had plenty of time to ruminate on how technology can help this process and what solutions are already out there. As it turns out, the Web already offers quite a few resources that can help save time and make the process of buying a new car less of a headache.
The most important piece of information you can have before stepping into the fire is what the dealer paid for the car, or the factory invoice number. One of the most popular sites to find that number is TrueCar, which also shows you a graph of what other buyers have been paying for the car at the dealerships around your area. If one dealership seems a little more flexible than another, it will show up there. TrueCar also has a network of dealers it has already negotiated pricing with, so you can go in knowing exactly what you will pay. The site did come under fire recently for some aspects of their relationships with dealers, forcing changes in their business model. It seems to make the site more transparent for all involved.
One of the tried-and-true sites of car buying, the Kelley Blue Book site, recently underwent a renovation to make it more TrueCar-like. It also shows the keys numbers involved with a car purchase, but also provides an estimated five-year cost of ownership figure based on things like insurance and gas mileage. If you?re not sold on a particular model yet and want to compare multiple vehicles, KBB makes an informative first stop.
These solutions are definitely a step in the right direction towards shifting the balance of power in the auto sales industry, but I don?t think they truly eliminate the aspects of the car purchase experience that people abhor. The dealership will still try to play numbers games using their ?hypothetical? forms and their four corners sales sheets. Even with TrueCar?s pricing deals, I?m sure you will still have to sit through multiple rounds of ?I don?t know if this is going to work. Let me talk to my manager?? They will still try to sell you add-ons and upgrades you don?t need.
What we really need is a way for more people to experience the kind of power my friend?s father experiences when he goes car shopping: bypassing the ambiguity of financing.
Perhaps that solution already exists.
Thanks to TrueCar and KBB.com, you can know the terms and amounts you need ahead of time. Then, through sites like LendingClub and Prosper, you can negotiate your own financing at terms that are comfortable for you ? funded by private financiers. You have none of the hoops to jump through when financing through a regular bank or credit union. You then get a check for the amount you need (I guess you can cash the check and put it in a briefcase, if you really want to experience my example at the next level) and take it to the dealership. One ultimatum later, you?re driving away in your new sled, or whip, or whatever the kids are calling it these days.
Through this plan, everyone wins? except the car dealerships, that is. But I doubt anyone will shed a tear for them.
As the impact investing industry marks five years since the term ?impact investing? was coined, Omidyar Network has developed a series of six articles that highlight key issues and opportunities for the industry. Presented in partnership with Stanford Social Innovation Review, the online series, ?Priming the Pump for Impact Investing?, begins today and extends through October 2.
Omidyar Network makes the case for a fundamental shift from a firm-based to a sector-based approach to impact investing. By re-directing investments, re-evaluating the role of subsidies and policies, and re-examining returns across the investment continuum, we believe that impact investors can accelerate greater social and financial returns impacting millions of people worldwide.
Join Omidyar Network and the SOCAP?12 community in this dialogue about the approaches and ideas that can help prime the pump to spark, nurture and scale new sectors.
The first article in the series, ?Sectors, Not Just Firms,? can be read on the Stanford Social Innovation Review website.?
Join the conversation on Twitter by following #primingthepump.?
Did you honestly think Eric Schmidt went all the way to Seoul just to launch the Nexus 7 for South Korea, hang out with Samsung's JK Shin and moan about the patent war with Apple? Of course not. The Google chairman also found some time to learn the legendary "invisible horse" dance with PSY, the charismatic oppa in the Korean chart-topper Gangnam Style. While Google Korea was happy to supply a few photos, the only video we could dig up was a surprisingly short one hosted by Daum -- it's embedded right after the break.
Brian: "Man, not being the CEO of a multinational corporation sure is hard work."
Terrence: "I see you are a fellow disciple of the Carlton Banks school of dance."
Don: "Gangnam Style, 2012-2012."
Billy: "This song is really about the time I set my socks on fire. I see you still have yours. One moment."
Edgar: "Hm... I think we forgot the horse."
Richard Lai: "OK Eric, now let's do the elevator scene."
Dan: "Doenjang Girls, would you like to buy a Nexus 7? It's wayyy more expensive than a latté."
Darren: "Soooo glad this guy put this video on YouTube and not Vimeo. $$$$$$$$"
Jon Fingas: "Oppan Google sty-- no, even I can't go that far."
BEIRUT (AP) ? Syrian rebels struck deep in the fortress-like inner sanctum of President Bashar Assad's rule Wednesday in Damascus, detonating two car bombs that engulfed the army headquarters in flames.
The suicide bombings and subsequent gun battles in the Syrian capital killed at least five people, including a reporter for Iranian TV. The carefully orchestrated attacks highlighted the regime's growing vulnerability, even as the 18-month battle to bring down Assad is locked in a stalemate.
International diplomacy has failed to stop the bloodshed.
Making his debut on the global stage at the United Nations, Egypt's new President Mohammed Morsi said he will not rest until Syria's civil war is brought to an end. He called it the "tragedy of the age" and one that "we all must end."
Morsi has launched an "Islamic Quartet" of regional powers to seek an end to the violence, but he has not offered a specific plan of action.
The explosions targeting the Syrian military compound went off about 10 minutes apart, around 7 a.m., with the first blast possibly meant to create a diversion to enable the second attacker to get into the compound.
Security camera footage aired by Syrian state TV showed a white van driving on a busy thoroughfare outside the military compound, then veering to the right and exploding. The footage showed a second blast going off inside the complex, with flames rising up behind trees.
After the second explosion, rebel fighters and regime forces exchanged fire for more than three hours, including inside the military compound, said Rami Abdul-Rahman of the Britain-based Syrian Observatory for Human Rights, an activist group. The fighting spilled over into nearby Omayyad Square, with regime troops ? some wildly firing in the air ? chasing after rebel gunmen, witnesses said.
Syrian state TV reported that four army guards were killed and 14 people were wounded, including civilians and military personnel.
The Iranian English language Press TV said one of its Syrian correspondents, 33-year-old Maya Nasser, was killed by a rebel sniper following the blast. The station replayed Nasser's last report, in which he was on the phone from Damascus during a live broadcast, when the line suddenly went silent. The Damascus bureau chief for Press TV, Hosein Mortada, was wounded in the clashes.
Abdul-Rahman said the regime was underreporting casualties in an attempt to play down the severity of the attacks.
Fear spread among residents of the nearby Malki area, an upscale district that has largely been sheltered from the battles that usually rage in the city's impoverished belt of suburbs.
"It is obvious that there are no more safe areas in Syria," said Hala, a 28-year-old resident who only gave her first name for fear of repercussions. "We are all under fire."
Rebels have targeted the center of Damascus with bomb attacks in the past, most dramatically in July when they detonated explosives inside a high-level crisis meeting in Damascus that killed four top regime officials, including Assad's brother-in-law and the defense minister.
However, predictions that such attacks could accelerate the regime's demise have proven premature, and both sides have dug in, each unable to deliver a knockout blow.
The two sides are deadlocked in the northern battle for Aleppo, Syria's largest city. In the western slice of Syria that is most heavily populated, rebels control large swaths of the countryside, while the regime is clinging to urban centers.
Fighting has accelerated over the summer, and the Observatory said the death toll has broken the 30,000 mark, with nearly two-thirds of the casualties reported in the past six months.
The number of people killed rose from about 11,000 by mid-April to 30,109 people as of Wednesday, said the Observatory. Of those, more than two-thirds ? or 21,594 ? were either civilians who did not take part in the fighting or took up arms to topple the regime. In addition, 7,345 regime soldiers were killed, along with 1,170 army defectors fighting on the side of rebels, he said.
The Observatory, which compiles information from a network of activists in Syria, says it only includes named victims in its count or those whose death was verified by other means, such as amateur video.
Wednesday's blasts, while potentially demoralizing for the regime, won't likely shift the momentum in the rebels' favor, analysts said.
"The rebels are able to penetrate here and there and catch the regime off guard," said Paul Salem of the Carnegie Middle East Center, a Beirut-based think tank. "It's an important event, but does not change ... the balance of power, which is right now in a deadly stalemate."
In Damascus, Syrian Information Minister Omran Zoubi played down the significance of the attacks. "Everything is normal," he told Syrian state TV. "There was a terrorist act, perhaps near a significant location, yes, this is true, but they failed as usual to achieve their goals."
Yet for several hours Wednesday, rebels were able to create fear and confusion in the heart of the capital. The explosions set off a huge blaze that engulfed the military complex in flames and sent columns of thick black smoke over Damascus for several hours.
The blasts shattered windows of the Dama Rose hotel and other nearby buildings, as well as windshields of parked cars. Footage by another state-run TV channel, Ikhbariya, showed heavy damage inside the compound, with glass shards scattered across the floor and broken ceiling tiles.
Witnesses reported heavy gunfire for hours near Omayyad Square and the military compound. One witness reported seeing panicked soldiers shooting in the air randomly as they ran. A group of army soldiers standing outside the buildings shouted pro Assad slogans, including: "Shabiha, forever, for your eyes, Oh Assad!" in reference to pro-regime militiamen.
The Syrian army said "terrorists" ? a term the regime routinely uses for the rebels ? in the area opened random fire at the same time as the bombings to scare people. The army said authorities were pursuing the gunmen.
The rebels' Free Syrian Army claimed responsibility for the attacks, which came just a day after a Damascus school used by regime forces, according to activists, was bombed Tuesday, wounding several people.
Damascus has been targeted repeatedly by the rebels. Previous bombings raised concerns that the al-Qaida terror network is becoming increasingly active in Syria. Jebhat al-Nusra, an extremist Syrian group, claimed responsibility for many of them.
Also Wednesday, the Observatory and another activist group, the Local Coordination Committees, said dozens of bodies were found in the southern Damascus suburb of Thiyabiyeh. The reports could not be independently confirmed because of strict restrictions on foreign media.
The Observatory said 40 bodies, including some of women and children, were discovered, but it was not clear under which circumstances the victims were killed.
Another group of activists, the Local Coordination Committees, said 107 bodies were found, including women and children killed execution-style. It said the dead included nine members of the Al-Rifaie family whose throats were slit.
An amateur video, which could not be verified, showed the bodies of 18 men lined up on the floor of a room, some of them with marks of deep wounds.
___
Associated Press writer Bassem Mroue in Beirut and Albert Aji in Damascus contributed reporting.
Nokia's Lumia 920 packs the industry's best image stabilization -- there's no questioning that -- thanks to a camera module that pairs both sensor and lens-based optical IS. The iPhone 5 also offers a notable improvement over its Apple-made predecessor on the video front, but considering that its stabilization is of the digital variety, we wouldn't expect it to top Nokia's new flagship. We had an opportunity to test both smartphones in a head-to-head demo at Nokia's research and development facility in Tampere, Finland, about two hours north of the company's Espoo headquarters. In fact, we're told that this is the very first such comparison shoot in the world, considering that the iPhone made it to market just last week and the only opportunity to shoot with a Lumia 920 is currently in the European country where the device was born.
As expected, the Nokia phone was able to capture far smoother video than what we snapped with the iPhone, with both devices secured side-by-side in a homemade foam holster. Unlike our handheld interview shoot earlier today, we pushed the limits a bit further this time, running through Nokia's parking lot and turning every which way as well. It's important to note that the Lumia 920 we used was a prototype, but its performance was still quite solid. You'll find the side-by-side video just past the break -- the Lumia 920 is on the left, with the iPhone clip on the right.
Buy a copy of guitar-teaching game Rocksmith at HMV and ?5 will be donated to the Teenage Cancer Trust.
Publisher Ubisoft and HMV will each stump up ?2.50 for every game sold.
Rocksmith, which allows you to plug a real guitar into your console and turn into Carlos Santana, launches in the UK on Friday after numerous delays.
"We are exceedingly excited to be launching Rocksmith in the UK this week," Ubisoft UK boss Rob Cooper said. "The game literally provides real-life benefits by teaching people how to play an actual guitar, and we hope to inspire the next generation of rock stars in the UK and beyond.
"Moreover, I couldn't be more pleased to be partnering with HMV to raise much-needed funds for Teenage Cancer Trust."
The charity helps improve the quality of life and chances of survival for those with cancer aged between 13 and 24, and has so far set up nearly two dozen specialist units within UK NHS hospitals. So if you're thinking of buying Rocksmith, HMV isn't a bad place to do so.
Lil Wayne launched a lawsuit against Quincy Jones III over the alleged unauthorized use of the rapper’s music including hits like “Lollipop” and “A Milli” [...]
The Hope College football team could not muster an upset on Saturday at home, losing to 15th-ranked Illinois Wesleyan 23-13.
Illinois Wesleyan improved to 3-0 on the season in front of a Holland Municipal Stadium crowd of 1,810, while the Flying Dutchmen fell to 1-3 with their third consecutive loss.
Read more The Sentinel's analysis of the game in Sunday's newspaper and e-edition.
Illinois Wesleyan built a 23-0 lead before Hope scored on Vincent Boddy?s 5-yard touchdown catch from Michael Atwell with 3 minutes, 51 seconds remaining in the third quarter.
Hope added another score with 5:07 remaining the game when Christian Subdon recovered the fumble of teammate Brian Lynn in the end zone for a touchdown.
?The thing that hurt us in the first half was that it was one guy here and there,? Hope coach Dean Kreps said. ?It wasn?t like it was a play that wasn?t working or they were dominating, but we?d have a breakdown over here or on the other side. You can?t do that.?
The Flying Dutchmen limited Illinois Wesleyan to 33 yards rushing and the fewest amount of points to an opponent this season. Hope yielded 112 points in the previous two games combined.
?We made some personnel changes,? Kreps said. ??We moved (Mark) Karam back to nickel back and we moved Santino (DeCesare) to free safety and I think that helped us. They were in on a lot of plays.?
Hope scored a season-low 13 points and was outgained in yards 336-119, including 60 yards rushing.
First quarter IWU-Dan O?Neill 46 pass from Mike Heaton (Michael Kelley kick), 3:58 IWU-Parker Carroll 33 pass from Rob Gallick (Kelley kick), 1:44 Second quarter IWU-Cameron Blossom 6 run (run failed), 13:23 Third quarter IWU-Michael Kelley 39 field goal, 9:23 Hope-Vincent Boddy 5 pass from Michael Atwell (Evan Finch kick), 3:51 Fourth quarter Hope-Christian Subdon 1 run with recovered fumble (run failed), 5:07
Naked mole-rats may hold clues to pain reliefPublic release date: 21-Sep-2012 [ | E-mail | Share ]
Contact: Jeanne Galatzer-Levy jgala@uic.edu 312-996-1583 University of Illinois at Chicago
Naked mole-rats evolved to thrive in an acidic environment that other mammals, including humans, would find intolerable. Researchers at the University of Illinois at Chicago report new findings as to how these rodents have adapted to this environment.
The study was published online this week on PLOS ONE.
In the tightly crowded burrows of the African naked mole-rats' world, carbon dioxide builds up to levels that would be toxic for other mammals, and the air becomes highly acidic. These animals freely tolerate these unpleasant conditions, says Thomas Park, professor of biological sciences at UIC and principal investigator of the study -- which may offer clues to relieving pain in other animals and humans.
Much of the lingering pain of an injury, for example, is caused by acidification of the injured tissue, Park said.
"Acidification is an unavoidable side-effect of injury," he said. "Studying an animal that feels no pain from an acidified environment should lead to new ways of alleviating pain in humans."
In the nose of a mammal, specialized nerve fibers are activated by acidic fumes, stimulating the trigeminal nucleus, a collection of nerves in the brainstem, which in turn elicits physiological and behavioral responses that protect the animal -- it will secrete mucus and rub its nose, for example, and withdraw or avoid the acidic fumes.
The researchers placed naked mole-rats in a system of cages in which some areas contained air with acidic fumes. The animals were allowed to roam freely, and the time they spent in each area was tracked. Their behavior was compared to laboratory rats, mice, and a closely related mole-rat species that likes to live in comfy conditions, as experimental controls.
The naked mole-rats spent as much time exposing themselves to acidic fumes as they spent in fume-free areas, Park said. Each control species avoided the fumes.
The researchers were able to quantify the physiologic response to exposure to acidic fumes by measuring a protein, c-Fos, an indirect marker of nerve activity that is often expressed when nerve cells fire. In naked mole-rats, no such activity was found in the trigeminal nucleus when stimulated. In rats and mice, however, the trigeminal nucleus was highly activated.
The naked mole-rats' tolerance of acidic fumes is consistent with their adaptation to living underground in chronically acidic conditions, Park said.
###
The study was supported by a grant from the National Science Foundation. Pamela LaVinka, graduate student in biological sciences at UIC, was first author on the study.
[Video link: http://youtu.be/jHm0jmg-sbc]
[Photos for download: http://newsphoto.lib.uic.edu/v/naked+mole-rats/]
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Naked mole-rats may hold clues to pain reliefPublic release date: 21-Sep-2012 [ | E-mail | Share ]
Contact: Jeanne Galatzer-Levy jgala@uic.edu 312-996-1583 University of Illinois at Chicago
Naked mole-rats evolved to thrive in an acidic environment that other mammals, including humans, would find intolerable. Researchers at the University of Illinois at Chicago report new findings as to how these rodents have adapted to this environment.
The study was published online this week on PLOS ONE.
In the tightly crowded burrows of the African naked mole-rats' world, carbon dioxide builds up to levels that would be toxic for other mammals, and the air becomes highly acidic. These animals freely tolerate these unpleasant conditions, says Thomas Park, professor of biological sciences at UIC and principal investigator of the study -- which may offer clues to relieving pain in other animals and humans.
Much of the lingering pain of an injury, for example, is caused by acidification of the injured tissue, Park said.
"Acidification is an unavoidable side-effect of injury," he said. "Studying an animal that feels no pain from an acidified environment should lead to new ways of alleviating pain in humans."
In the nose of a mammal, specialized nerve fibers are activated by acidic fumes, stimulating the trigeminal nucleus, a collection of nerves in the brainstem, which in turn elicits physiological and behavioral responses that protect the animal -- it will secrete mucus and rub its nose, for example, and withdraw or avoid the acidic fumes.
The researchers placed naked mole-rats in a system of cages in which some areas contained air with acidic fumes. The animals were allowed to roam freely, and the time they spent in each area was tracked. Their behavior was compared to laboratory rats, mice, and a closely related mole-rat species that likes to live in comfy conditions, as experimental controls.
The naked mole-rats spent as much time exposing themselves to acidic fumes as they spent in fume-free areas, Park said. Each control species avoided the fumes.
The researchers were able to quantify the physiologic response to exposure to acidic fumes by measuring a protein, c-Fos, an indirect marker of nerve activity that is often expressed when nerve cells fire. In naked mole-rats, no such activity was found in the trigeminal nucleus when stimulated. In rats and mice, however, the trigeminal nucleus was highly activated.
The naked mole-rats' tolerance of acidic fumes is consistent with their adaptation to living underground in chronically acidic conditions, Park said.
###
The study was supported by a grant from the National Science Foundation. Pamela LaVinka, graduate student in biological sciences at UIC, was first author on the study.
[Video link: http://youtu.be/jHm0jmg-sbc]
[Photos for download: http://newsphoto.lib.uic.edu/v/naked+mole-rats/]
[ | E-mail | Share ]
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Public release date: 30-Sep-2012
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One of the tried-and-true sites of car buying, the Kelley Blue Book site, recently underwent a renovation to make it more TrueCar-like. It also shows the keys numbers involved with a car purchase, but also provides an estimated five-year cost of ownership figure based on things like insurance and gas mileage. If you?re not sold on a particular model yet and want to compare multiple vehicles, KBB makes an informative first stop.
As the impact investing industry marks five years since the term ?impact investing? was coined, Omidyar Network has developed a series of six articles that highlight key issues and opportunities for the industry. Presented in partnership with Stanford Social Innovation Review, the online series, ?Priming the Pump for Impact Investing?, begins today and extends through October 2.
