Networked Politics ? Blog Archive ? Naples Web Design Companies ...

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This entry was posted on Thursday, February 2nd, 2012 at 9:20 pm and is filed under News. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed.

Source: http://www.networked-politics.info/?p=50523

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Sony's Q3 earnings are in: wider than expected full year loss, lowered sales projections

Sony already revealed Kazuo Hirai will take over for Howard Stringer as CEO and President April 1st last night, and with the big shocker out of the way it's time for the fiscal Q3 reports. After posting a net loss of $346 million last quarter, Sony is now expecting a bigger loss for 2011 than it had previously estimated, as well as lower sales. It's currently showing a net loss for the quarter of 159 billion yen ($2~ billion), or a $1.2 billion operating loss. Blame is put on a larger than expected effect from the flooding in Thailand, strong yen and weakness in cellphones. Sales for the quarter were about $23 billion, down 17.4 percent from the same quarter last year. The consumer products and services division (HDTVs, PS3s, etc.) in particular caught a brick, with an operating loss of over a billion dollars on sales that dropped 24 percent from last year. It recorded a loss on its sale of shares in the S-LCD venture with Samsung, LCD TVs sold for prices lower than its cost reductions, and the PlayStation 3 had the killer combo of higher marketing costs and lower unit sales. Check the PDF and slides linked below for more bad news. We'll let you know what we hear on the earnings call in a few, but until then, Kaz, may we suggest bringing in Jimmy Rollins for tips on breaking out of a slump?

Continue reading Sony's Q3 earnings are in: wider than expected full year loss, lowered sales projections

Sony's Q3 earnings are in: wider than expected full year loss, lowered sales projections originally appeared on Engadget on Thu, 02 Feb 2012 01:04:00 EDT. Please see our terms for use of feeds.

Permalink   |  Sony Q3 2011 earnings (PDF), Slides  | Email this | Comments

Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/jPdLAaGOJDI/

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The State of the American Small Business | RedState

The State of the American Small Business

Posted by Caleb Howe (Diary)

Wednesday, February 1st at 6:00PM EST

6 Comments

Today, the House Small Business Committee held a hearing ?to examine obstacles to small business job creation and economic growth in America.? The below video highlights some excerpts from that meeting.

?I?ve never been more concerned with our prospects as a company than I am right now.? Last October, Gallup released a poll regarding the most significant challenges facing small businesses in America today. It is from that poll that the statistics in the opening of the video were taken. Listening to the video excerpts above, nothing has changed since October.

Best takeaway quote? ?I can tell you exactly how many jobs were created on net by the stimulus, it was zero point zero zero zero. Because if you take a trillion dollars out of the economy, and spend a trillion dollars back into the economy, you haven?t done anything for the economy on net. It?s old-fashioned, out-dated, Keynesian economics, which is a proven failure.?

Consider this an Open Thread.

Source: http://www.redstate.com/absentee/2012/02/01/the-state-of-the-american-small-business/

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Bold Ford Plan To Slash Waste | Car Reviews,finance,lease ...

The five door VW up!

Volkswagen have just increased the appeal of their award-winning Up! model, with the launch of a five-door version.

The five-door model of the VW up! adds an extra touch of practicality to the versatile and remarkably good value city car range.

Passengers in the five-door VW will enjoy exactly the same amount of room as in the three-door, with an impressive 947mm of headroom and 789 mm of legroom, with a slightly raised seat base compared to the front, allowing for a clearer view through the windscreen.

However, they will benefit from easier accessibility, which may give the five door Volkswagen Up! an advantage with young families in particular.

Still the same award-winning car

Despite the first deliveries of cars not being expected to be made to owners until the second half of this year, the VW up! has already won a slew of prestigious automotive awards, including WhatCar? Car of the Year 2012 and taking the TopGear Small Car of the Year.

It?s built on the same 2.42m wheelbase, and so has the same interior spaciousness and impressive boot capacity as the three-door model.

And this is on top of the kind of safety and infotainment features that in some cases are unique to this class of car, with Volkswagen setting a new benchmark for what can be expected in an economic city car.

Five star safety

VW is justly proud of the Up!s five star rating from NCAP, becoming the first car in its class to score so highly and achieve an Advanced Award for affordable safety technology.

As standard each VW Up! comes with ABS with hydraulic brake assist, Isofix child seat fittings and front and side airbags. On every model except the entry level Take Up!, the VW Up! has an Electronic Stabilisation Programme.

And for an extra ?225, you can enjoy the security of the Volkswagen City Emergency Braking system, the kind of cutting-edge safety technology more commonly found on luxury cars.

The system uses sensors to scan the road in front of the VW Up!, and will brake automatically if it notices an object within a certain distance to the car.

Maps and more

VW have created their own infotainment system, to streamline your access to audio, navigation and telephone systems.

A touchscreen device with voice-activated control, it also connects with the car?s integral systems to allow you to check information like parking sensor readings. For your security, the system is also easily removable.

Again, this high-end system is included in the price of the top of the range Volkswagen High Up!. It might surprise you that a new car with such advanced technologies is available to purchase, finance or lease from just ?10,390 on the road.

The entry level VW Take Up!, meanwhile, starts from an incredibly reasonable ?7,995. Even then, you can add the Maps & More system for ?275.

All VW Up! models are available to order now.

Keep yourself updated with the latest motoring news by liking us on facebook, following us on twitter or connecting with us on LinkedIn.

If you?re looking to purchase or lease a new VW contact our sales team. Alternatively, visit our website where you will find new and used VW?s available for sale or on finance.

Thanks for visiting us today.

Source: http://www.osv.ltd.uk/latestnews/main-osv-news/vw-up-new-model-uk/

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Why the brain is more reluctant to function as we age

Public release date: 1-Feb-2012
[ | E-mail | Share ]

Contact: Caroline Clancy
caroline.clancy@bristol.ac.uk
44-011-792-88086
University of Bristol

Researchers reveal a novel mechanism through which the brain may become more reluctant to function as we grow older

New findings, led by neuroscientists at the University of Bristol and published this week in the journal Neurobiology of Aging, reveal a novel mechanism through which the brain may become more reluctant to function as we grow older.

It is not fully understood why the brain's cognitive functions such as memory and speech decline as we age. Although work published this year suggests cognitive decline can be detectable before 50 years of age. The research, led by Professor Andy Randall and Dr Jon Brown from the University's School of Physiology and Pharmacology, identified a novel cellular mechanism underpinning changes to the activity of neurones which may underlie cognitive decline during normal healthy aging.

The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to underpin age-dependent changes to cognitive abilities.

The researchers examined the brain's electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. In this way they characterised what is known as "neuronal excitability" this is a descriptor of how easy it is to produce brief, but very large, electrical signals called action potentials; these occur in practically all nerve cells and are absolutely essential for communication within all the circuits of the nervous system.

Action potentials are triggered near the neurone's cell body and once produced travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.

The Bristol group identified that in the aged brain it is more difficult to make hippocampal neurones generate action potentials. Furthermore they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurones.

Professor Randall, Professor in Applied Neurophysiology said: "Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer's disease. We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.

"Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability."

###

The research, entitled 'Age-related changes to Na+ channel gating contribute to modified intrinsic neuronal excitability' by Andrew D Randall, Clair Booth and Jon T Brown, is published in the journal Neurobiology of Aging and funded by Pfizer who are long-standing collaborators with Randall and Brown. The paper is available to download from the following website: http://www.sciencedirect.com/science/article/pii/S0197458011005756

---

[ | 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.

Public release date: 1-Feb-2012
[ | E-mail | Share ]

Contact: Caroline Clancy
caroline.clancy@bristol.ac.uk
44-011-792-88086
University of Bristol

Researchers reveal a novel mechanism through which the brain may become more reluctant to function as we grow older

New findings, led by neuroscientists at the University of Bristol and published this week in the journal Neurobiology of Aging, reveal a novel mechanism through which the brain may become more reluctant to function as we grow older.

It is not fully understood why the brain's cognitive functions such as memory and speech decline as we age. Although work published this year suggests cognitive decline can be detectable before 50 years of age. The research, led by Professor Andy Randall and Dr Jon Brown from the University's School of Physiology and Pharmacology, identified a novel cellular mechanism underpinning changes to the activity of neurones which may underlie cognitive decline during normal healthy aging.

The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to underpin age-dependent changes to cognitive abilities.

The researchers examined the brain's electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. In this way they characterised what is known as "neuronal excitability" this is a descriptor of how easy it is to produce brief, but very large, electrical signals called action potentials; these occur in practically all nerve cells and are absolutely essential for communication within all the circuits of the nervous system.

Action potentials are triggered near the neurone's cell body and once produced travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.

The Bristol group identified that in the aged brain it is more difficult to make hippocampal neurones generate action potentials. Furthermore they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurones.

Professor Randall, Professor in Applied Neurophysiology said: "Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer's disease. We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.

"Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability."

###

The research, entitled 'Age-related changes to Na+ channel gating contribute to modified intrinsic neuronal excitability' by Andrew D Randall, Clair Booth and Jon T Brown, is published in the journal Neurobiology of Aging and funded by Pfizer who are long-standing collaborators with Randall and Brown. The paper is available to download from the following website: http://www.sciencedirect.com/science/article/pii/S0197458011005756

---

[ | 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.

Source: http://www.eurekalert.org/pub_releases/2012-02/uob-wtb020112.php

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David Guetta Brings Nicki Minaj to Life in Video for "Turn Me On"

David Guetta has unveiled his official music video for the track "Turn Me On," and it's pretty awesome.

Featuring Nicki Minaj, the spot stars Guetta as a mad scientist who brings his 29-year old rapping counterpart to life. It's really like a mini movie, as you can see here:

David Guetta (ft. Nicki Minaj) - Turn Me On (Official Video)

The collaboration itself currently resides at number four on the Billboard Hot 100 and is off Guetta’s latest album, "Nothing But the Beat." Hit up iTunes of a music store nearby today to pick up a copy.

Source: http://www.thehollywoodgossip.com/2012/01/david-guetta-brings-nicki-minaj-to-life-in-video-for-turn-me-on/

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In lab, Pannexin1 restores tight binding of cells that is lost in cancer

Monday, January 30, 2012

First there is the tumor and then there's the horrible question of whether the cancerous cells will spread. Scientists increasingly believe that the structural properties of the tumor itself, such as how tightly the tumor cells are packed together, play a decisive role in the progression of the disease. In a new study, researchers show that the protein Pannexin1, known to have tumor-suppressive properties, plays an important role in keeping the cells within a tissue closely packed together, an effect that may be lost with cancer.

"In healthy tissues, the recently discovered protein Pannexin1 may be playing an important role in upholding the mechanical integrity of the tissue," said first author and Brown University M.D./Ph.D. student Brian Bao. "When we develop cancer, we lose Pannexin1 and we lose this integrity."

The results appeared in advance online in the Journal of Biological Chemistry on Jan. 20.

To conduct their research, the group at Brown University and the University of British Columbia employed a "3-D Petri dish" technology that allows investigators to watch closely how cells interact with each other, without scientists having to worry about additional interactions with surrounding scaffolding or the culture plate itself. How readily the cells form large multicellular structures therefore reflects their interactions with each other, not their in vitro surroundings.

Bao's advisor, Jeffrey Morgan, associate professor of medical science, developed the 3-D Petri dish technology. Morgan is the paper's senior author.

Cancer cells converge

Starting with rat "C6" glioma (brain tumor) cells that do not express Pannexin1, the researchers left some unaltered and engineered others to express Pannexin1. After putting the different cells into the 3-D Petri dishes and watching them interact for 24 hours, they saw that the Pannexin1 cells were able to form large multicellular tissues much faster and more tightly than the unaltered cancer cells.

To confirm that Pannexin1 was indeed causing these changes, Bao and his colleagues treated their samples with the drugs Probenecid and Carbenoxolone, which are well known inhibitors of Pannexin1. They saw that sure enough, the drugs negated Pannexin1's accelerating effect.

Then the team was ready to achieve the the study's main aim, Bao said, namely to determine how Pannexin1 was able to drive these cells to clump together faster and tighter. They found that Pannexin1 sets off a chain reaction involving the energy-carrying molecule ATP and specific receptors for it.

When all experiments were done, Bao, Morgan, and their collaborators had found that as soon as the cells touched each other, Pannexin1 channels were stimulated to open and release ATP. The ATP then bound to cell surface receptors, kicking off intracellular calcium waves that ultimately remodeled the network of a structural protein called actin. This remodeling increases the forces between the cells, driving them to bind together more tightly.

Figuring out that sequence, and Pannexin1's role in it, is perhaps the study's biggest contribution to cancer research, Bao said.

"Using their single-cell systems, others have been able to carefully study individual pieces of this cascade," he said. "We came from a different perspective. Because the strength of our assay is that we can look at gross multicellular behavior in 3-D, we could ask, 'Does this actually manifest into something tangible on the multicellular level?'"

Having gained this understanding of Pannexin1's role in the mechanics of tumors, Bao is now engaged in research to answer the obvious next questions: Does Pannexin1 affect the tumor's ability to spread and invade? When cancerous cells regain Pannexin1 expression, are they less likely to spread and leave the tumor?

###

Brown University: http://www.brown.edu/Administration/News_Bureau

Thanks to Brown University for this article.

This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.

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Source: http://www.labspaces.net/117181/In_lab__Pannexin__restores_tight_binding_of_cells_that_is_lost_in_cancer

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