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Dwija's hosting a year-end link-up, so I scrolled through the ol' iPhoto events and culled out my winners. Grab a carrot stick and let's go.
1. My little snow babes. Amby now sports the snow suit that little stink-eye Joe's wearing here. I wore a sling wrap for this snow excursion, thinking Amby would be tentative in the white stuff. No. He'll take the highest hill you've got, please. Wheeee!
2. Amby: the original floor-sweeping photobomber.
3. Near the beginning of this year Joe proudly proclaimed GREEN to be his favorite color. And so it came to pass that all things green gradually drifted into his possession. For St. Patrick's Day my Mom sent him some fitting decorations.
4. File this under "stuff my parents have for the kids to ride on at their house, intended or not."
5. Mother's Day. Note our season-appropriate pastels.
6. Even before the green obsession began, Joe loved trains. For his third birthday, my Mom came up and helped throw him a train-themed birthday party. Even though the party got a little rained out and ended up happening in our living room/tiny backyard as opposed to the park, our little engineers still filled their tender cars full of coal and all that. Note Sean's second instance of a yellow shirt.
7. Kids in hats. I cannot get enough.
BONUS. Second instance of "stuff my parents have for the kids to ride on at their house."
8. Weekend lake trip, and Joe's first s'more. I believe he took this bite and said, "But... I'm so sticky."
9. September... highs and lows. Lows: having my gallbladder removed, sending Sean to the Mayo Clinic for 10 days to finally get a diagnosis for his life-long pain. Highs: moving into a new, beautiful home, and a new darling baby nephew for our family. My Mom came up to move us, help us settle in, and take care of all her kids. Like she always does.
10. Being in the new house helped me kickstart this little blog again, hence the homage to my banner photo. A few flowers for my 30th birthday, a sun-filled fall day, an ironed placemat--these are a few of my favorite things.
11. Hosting for Thanksgiving. No turning back from adulthood now.
12. Christmas in California, and the boys with their Poppy. I love this shot because it reminds me of this:
(credit: acartoonchristmas.com)
That's a wrap for us here. You have my prayers and hopes for a blessed 2014. And hey. Go to Mass tomorrow. :)


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This is The Morning Shift, our one-stop daily roundup of all the auto news that's actually important — all in one place at 9:00 AM. Or, you could spend all day waiting for other sites to parse it out to you one story at a time. Isn't your time more important?
1st Gear: Get Those Cars Fixed
After weeks of attempting to find out who knew what when and why the recall didn't happen sooner, the most important part is beginning: The fix.
The repaired ignition switches should start making their way into Cobalts and other recalled vehicles as soon as today. But it isn't an overnight fix for the 2.3 million cars that have been recalled. GM's original timeline had the cars being fixed by October, but that even seems optimistic now. They have asked Delphi to add another shift to make the new parts faster.
So the repairs have begun, and maybe soon we can start to get some answers.
2nd Gear: Record March For Audi
Our favorite car brand from Ingolstadt with four rings on the hood and model lines that start with the letter A or Q (is that enough disclaimers?) had a record number of sales in March.
Audi moved a whopping 170,450 cars in March alone, thanks to demand for the freshly revamped A3 lineup, which sold 28,750 of that total number last month.
That steals some of the thunder from Mercedes, who had earlier bragged about their record month of 158,523 cars sold. So congrats to everyone all around. Swell job folks.
3rd Gear: The 500 Abarth Goes Automatic
We've heard the rumor before, but it seems like it's coming true: The Fiat 500 Abarth, one of the finest and loveliest little cars on the road today, will be adding an automatic transmission to the mix to increase sales.
Booooooo, you say, but it's necessary. The sales of the Abarth are slightly off, and it's because the young people aren't driving cars with a manual transmission. In fact, Fiat thinks the addition of a two pedal setup can help sell 2,000 additional Abarths a year.
No, I'm not a fan of this move either, but more Abarths out there is a good thing. Pus, it isn't replacing the manual, it's just an addition to having the manual out there. So don't shoot the messenger (me, don't shoot me).
4th Gear: How Will GM Compensate Victims?
The GM Recall is a mess for a few reasons, a main one being how to compensate victims and families impacted by deaths caused by the recalled cars.
And it's messy because the current GM is not the same company that existed before the bankruptcy. Technically, they aren't liable for almost anything that occurred pre-bankruptcy, but this is a case where they will almost definitely reach back to compensate those involved with the recalled cars.
This is why they brought in Kenneth Feinberg to help them figure out the best course of action to compensate those involved.
5th Gear: Mercedes Is Dominating F1
Mercedes and their split turbo Silver Arrows are just dominating F1, but that doesn't mean this season isn't exciting.
Quite the opposite.
Yesterday's Bahrain GP had a battle between teammates over the last few laps that could have swung either way, but ended in favor of Lewis Hamilton over Nico Rosberg. There was also a nutso crash from noted crasher Pastor Maldonado, who decided that Esteban Gutierrez seemingly didn't deserve to be on the road anymore.
Still, great race, more like this F1. More like this.
On this day in 1947, Henry Ford, the founder of Ford Motor Company, which developed the first affordable, mass-produced car—the Model T—and also helped pioneer assembly-line manufacturing, dies at his estate in Dearborn, Michigan, at the age of 83.
Instead of going over the GM recall, what do you think of an Abarth with an automatic? Heresy or necessary?


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Intel's Core i7 870 & i5 750, Lynnfield: Harder, Better, Faster Strongerby Anand Lal Shimpi on September 8, 2009 12:00 AM EST
- Posted in
- CPUs
Lynnfield's Turbo Mode: Up to 17% More Performance
Turbo on Bloomfield (the first Core i7) wasn't all that impressive. If you look back at our Core i7 article from last year you'll see that it's responsible for a 2 - 5% increase in performance depending on the application. All Bloomfield desktop CPUs had 130W TDPs, so each individual core had a bit more breathing room for how fast it could run. Lynnfield brings the TDP down around 27%, meaning each core gets less TDP to work with (the lower the TDP, the greater potential there is for turbo). That combined with almost a full year of improving yields on Nehalem means that Intel can be much more aggressive with Turbo on Lynnfield.
|SYSMark 2007: Overall
|Dawn of War II
|Sacred 2
|World of Warcraft
|Intel Core i7 870 Turbo Disabled
|74.3 fps
|84.8 fps
|60.6 fps
|Intel Core i7 870 Turbo Enabled
|81.0 fps
|97.4 fps
|70.7 fps
|% Increase from Turbo
Turbo on Lynnfield can yield up to an extra 17% performance depending on the application. The biggest gains will be when running one or two threads as you can see from the table below:
|Max Speed
|4 Cores Active
|3 Cores Active
|2 Cores Active
|1 Core Active
|Intel Core i7 870
|Intel Core i7 860
|Intel Core i5 750
If Intel had Turbo mode back when dual-cores first started shipping we would've never had the whole single vs. dual core debate. If you're running a single thread, this 774M transistor beast will turn off three of its cores and run its single active core at up to 3.6GHz. That's faster than the fastest Core 2 Duo on the market today.
WoW doesn't stress more than 2 cores, Turbo mode helps ensure the i7 870 is faster than Intel's fastest dual-core CPU
It's more than just individual application performance however, Lynnfield's turbo modes can kick in when just interacting with the OS or an application. Single threads, regardless of nature, can now execute at 3.6GHz instead of 2.93GHz. It's the epitomy of Intel's hurry up and get idle philosophy.
The ultimate goal is to always deliver the best performance regardless of how threaded (or not) the workload is. Buying more cores shouldn't get you lower clock speeds, just more flexibility. The top end Lynnfield is like buying a 3.46GHz dual-core processor that can also run well threaded code at 2.93GHz.
Take this one step further and imagine what happens when you have a CPU/GPU on the same package or better yet, on the same die. Need more GPU power? Underclock the CPU cores, need more CPU power? Turn off half the GPU cores. It's always availble, real-time-configurable processing power. That's the goal and Lynnfield is the first real step in that direction.
Speed Limits: Things That Will Keep Turbo Mode from Working
As awesome as it is, Turbo doesn't work 100% of the time, its usefulness varies on a number of factors including the instruction mix of active threads and processor cooling.
The actual instructions being executed by each core will determine the amount of current drawn and total TDP of the processor. For example, video encoding uses a lot of SSE instructions which in turn keep the SSE units busy on the chip; the front end remains idle and is clock gated, so power is saved there. The resulting power savings are translated into higher clock frequency. Intel tells us that video encoding should see the maximum improvement of two bins with all four cores active.
Floating point code stresses both the front end and back end of the pipe, here we should expect to see only a 133MHz increase from turbo mode if any at all. In short, you can't simply look at whether an app uses one, two or more threads. It's what the app does that matters.
There's also the issue of background threads running in the OS. Although your foreground app may only use a single thread, there are usually dozens (if not hundreds) of active threads on your system at any time. Just a few of those being scheduled on sleeping cores will wake them up and limit your max turbo frequency (Windows 7 is allegedly better at not doing this).
You can't really control the instruction mix of the apps you run or how well they're threaded, but this last point you can control: cooling. The sort-of trump all feature that you have to respect is Intel's thermal throttling. If the CPU ever gets too hot, it will automatically reduce its clock speed in order to avoid damaging the processor; this includes a clock speed increase due to turbo mode.
Lynnfield and its retail cooler
The retail cooler that ships with the Core i7 is tiny and while it's able to remove heat well enough to allow the chip to turbo up, we've seen instances where it doesn't turbo as well due to cooling issues. Just like we recommended in the Bloomfield days, an aftermarket cooler may suit you well.
Lynnfield: Made for Windows 7 (or vice versa)
Core Parking is a feature included in Windows 7 and enabled on any multi-socket machine or any system with Hyper Threading enabled (e.g. Pentium 4, Atom, Core i7). The feature looks at the performance penalty from migrating a thread from one core to another; if the fall looks too dangerous, Windows 7 won't jump - the thread will stay parked on that core.
What this fixes are a number of the situations where enabling Hyper Threading will reduce performance thanks to Windows moving a thread from a physical core to a logical core. This also helps multi-socket systems where moving a thread from one core to the next might mean moving it (and all of its data) from one memory controller to another one on an adjacent socket.
Core Parking can't help an application that manually assigns affinity to a core. We've still seen situations where HT reduces performance under Windows 7 for example with AutoCAD 2010 and World of Warcraft.
With support in the OS however, developers should have no reason to assign affinity in software - the OS is now smart enough to properly handle multi-socket and HT enabled machines.
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nikrusty - Wednesday, November 18, 2009 - linkWith this article Anandtech is Harder, Better, Faster Stronger.
Seriously AWESOME ARTICLE! It cleared many of my doubts FLAT OUT! Now I know i5 is the way to go especially becoz I dont care about overclocking and just want good gaming performance...nothing screamingly extreme. Budget + Performance always keeps you level headed.
shiro - Wednesday, October 21, 2009 - linkwhat is that monster hoop of death heatsink that's on page 3? lol
Eeqmcsq - Saturday, September 19, 2009 - linkI asked a similar question in one of the other articles, so pardon me if this sounds repetitive.
According to the Turbo charts, the slowest Turbo speed is higher than the stock speed. Why is that? For example, why not just make the 750 a stock GHz of 2.8 GHz instead of 2.66GHz?
Eeqmcsq - Saturday, September 19, 2009 - linkArgh, please ignore. Replied using the wrong Firefox tab.
The0ne - Tuesday, September 15, 2009 - linkClear up what you're trying to show on the graphs please. You're getting more FPS at max setting than at min settings? Label the graphs like you did with the others please. With the others I can just look and understand what you're doing. With these, I'm scratching my head.
The0ne - Tuesday, September 15, 2009 - linkAh, turbo mode represented in FPS >.>'
kkara4 - Monday, September 14, 2009 - linkover at bittech.net, they are saying that it is more worth it to go for the i7-920, if we are considering anything above the i5. this is a conflicting story, since anand is recommending the lynnfields. anand or anybody else for that matter could you please see their articles and tell me what they have done wrong? (or perhaps you guys failed to see something). Your article explains things in great technical detail which i can understand since i have studied microprocessors, hence i am more inclined to go for lynnfield. anyway if someone could cross check that would be good
mapesdhs - Tuesday, September 15, 2009 - link
If I've understood Anand's analysis correctly, the conclusion is that,
for application mixes which involve a lot of single and/or dual-threaded
codes, and assuming one is not interested in high-end SLI/CF setups
or hard oc'ing all 4 cores all the time for tasks like video encoding
or animation rendering, the 750/860 are better buys because they
will internally push 1-core and 2-core clocks to a higher rate than
occurs with the 920 via the Turbo function, giving better results
than the 920, and of course the 750/860 are cheaper solutions
(although the 860 price is similar to the 920, the mbd costs less
than an X58, from what people say).
So it depends on what you want to use your system for. No interest
in CF/SLI? Running games that don't hammer 4 cores? An i5 750 or
i7 860 makes more sense. Using apps that don't use more than 2 cores?
Again the 750/860 is more logical, especially from a cost viewpoint.
This ties in with the other advantage of the X58 platform, ie. the
upgrade path to 6-core and 8-core CPUs. If this is something that
holds no value to you, then P55 makes more sense.
As always, it depends on what you want to use the system for. The
attraction of the 860 from a more general point of view is that it
also offers good quad-core performance when one does use all 4 cores
without sacrificing the traditional higher-clocks possible with
single or dual core setups when one is only using 1 or 2 cores. It's
the best of both worlds, at least for out-of-the-box functionality
However, if one does intend to use all 4 cores almost all the time
(I do) with a strong overclock, then the 920 is a better choice
because of the voltage issue and (IMO) the 6/8-core upgrade path.
Likewise, high-end multi-GPU setups work better with X58.
Given that general usage of a PC rarely uses more than 2 cores, this
is why the 750 and 860 are such attractive options.
As for the 870, despite its 1/2-core speed advantages, the price is
too high IMO. For that kind of money, a 920 makes more sense, paired
with better cooling if one has such a spare budget, or buy a better
GPU setup which, for gaming, is where the real bottleneck lies.
Anand, please correct me if I'm wrong with the above.
PS. As always, real-world pricing issues can make a mess of on-paper
technical conclusions. Also, although many games/apps don't exploit
more than 2 cores now, this is likely to change in the near future as
multi-core coding becomes more pervasive in the industry.
mapesdhs - Monday, September 14, 2009 - link
Re your comments about an X58 advantage being the ability to use
later 6 and 8-core CPUs...
I've been planning to build an i7 920 system for video encoding, so
a max oc on all cores is useful to me; from the article I thus infer
the X58 is a better choice.
However, if I did buy such a setup instead of an i5 or i7 860, what
would the cost tradeoff be do you think when the 6-core CPUs arrive
with respect to upgrading? By that I mean, for total processing
throughput, do you reckon a 6-core upgrade would be significantly
cheaper than simply buying a second i7 920 setup? (gfx not an issue)
If not, then the ability to use 6/8-core CPUs later in this context
is somewhat lessened, something that would apply to animation
rendering aswell (ie. extra complete systems perhaps more cost
effective in increased overall throughput compared to upgrading to
more cores). Any ideas? Also, unless the applications used can
exploit more than 4 cores, the later 6-core CPUs won't help. I have
about 1500 hours of material to convert to DivX. Each file is about
40 to 45 minutes (documentary), so converting multiple files on
multiple systems at the same time is very doable.
Given the above, I'm looking forward to more details on how a max
oc'd i860/i870 compares to a max oc'd 920.
At present I'm just using a 6000+ setup to work out the appropriate
format/conversion paths.
PS. May I suggest you don't bother replying to those moaning in such
an obviously ludicrous manner about the Turbo mode being active? I
have the distinct impression their posts are designed purely to
irritate. Please don't encourage them. Anyone with any sense will
read the article and understand the salient points you've highlighted
about Turbo mode being an integral function of the chip.
Milleman - Sunday, September 13, 2009 - linkI would say that i5 750 and Pehnom II X4 965 is fully comparable. AMD just have to adjust the pricetag and the price/performance will be on par. Looking at the Gaming rig performance, both i5 750 and Pehnom II X4 965 are well enough for gaming pleasure. I wouldn't shell out my bucks for the more expensive Intel top models. It's such a waste of money, unless you are working with huge video and image editing processes.


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Senator is the brightest star system in the southern constellation of Toast. It is too far south to be visible in most northern hemispheres.
It is also one of the closest star systems to Earth, at 4.2–4.4 light years. This means if you squint really REALLY hard, like so hard your eye pops out and your Mom comes in and starts screaming and drops your pancakes on the floor and you're really pissed because you wanted those pancakes really bad and you were really hungry because you had been up late last night and hadn't eaten since like 6 o'clock, but there she is screaming her freaking lungs out while your damned pancakes are just sitting there on the floor looking up at you as if to say, "Please, I need to be slathered with butter and drowned in Maple Syrup," you can see it.
System components
Senator is a single star system consisting of the central star, Senate, with 4 planets in orbit around it. These planets were named after the characters on a popular late-1960's TV show, "Banana Splits": Bingo, Fleegle, Drooper and Snorky.
This is a small, rocky planet where there's probably nothing to do. BO-RING
Some people call this planet "Terrance". They're probably too stupid to be able to pronounce a word like "Fleegle", anyway. It's a huge, gas filled planet. (Not unlike Aunt Edna, eh?)
This planet gained a lot of media attention recently, when in the year 2001 a famous pharmaceutical company that were the inventors of Vioxx decided to build a giant billboard on the face of the planet advertising Enzyte, the all natural male enhancement pill. Shortly thereafter, Donald Trump moved to Drooper, and is now applying for it to be renamed Hardandfirm. You can tell what the draw was, selling boner pills to a planet named Drooper. Ha, ha, everyone. Very fucking funny.
Classified. Was the ancient home of a race called the snorks, until some undiscovered disaster involving a bunch of paperclips, some drano, a silver dollar, and some old guy named Andrew Dean Richards.
Star Data
The main star, Senate, is about 5 to 6 billion years old. We think. The Jesus Freaks will tell you otherwise, but we scientists are more than a match for them on the polo field, right chaps?
Seen from Earth, Senator is separated by 2 degrees from Alpha Centauri A and B (about 4 times the angular diameter of the full Moon), and the latter are at an angular distance of up to 40" from each other. One popular observation method involves putting your thumb and forefinger on either side of the distant star, and saying (in a Russian accent), "I krush you, senatorr. KRUSH YOU LIKE A BUG!", while closing your fingers together repeatedly. This method was pioneered by Yakov Smirnoff in his early astronomer days.
- Right ascension (J2000): 14h39m35.9s
- Declination (J2000): -60°50'07"
- Distance from Earth: 4.36 light years
- Parallax: 0.751" ± 0.075"
- Apparent visual magnitude: −0.01
- Absolute visual magnitude: +4.34
- Spectral type: G2V(+K1V)
- Mass: 1.10 (A), 0.92 (B) Solar masses
- Luminosity: 1.57 (A), 0.51 (B) Solar luminosities
- Life Stage: Main Sequence
- Kick-assity: Low, to majorly Geeky
|Featured Article (read another featured article)
|Featured version: 5 April 2005
|This article has been featured on the main page. — You can vote for or nominate your favourite articles at Uncyclopedia:VFH.


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Schedule a one-on-one consultation with Reema to discuss the design and creation of a bespoke jewel.
Reema, Age 4 in India
Shinde Jewels
From The Archive
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Forewing of a blue morpho, rock crystal and sterling silver butterfly wing pendant.
These are handmade for us in Peru, where we obtain the wings from a local butterfly conservancy. Simply, we love butterflies and these are collected at the end of their natural life cycle. Reema was inspired by the Victorians and their use of the natural world in adornment. Special Care Instructions: Please note this pendant should not be submerged in water.
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Rebound redux
By Dan Farber
I've posted previously about the rebound effect. Improving energy efficiency frees up money, which can be used to purchase more of the same product or different products that use energy. This "rebound" cuts away at the energy savings and correspondingly at the carbon reduction achieved through energy efficiency. Everyone seems to agree that the rebound effect is real; the big dispute is over its size and significance. Blake Hudson pointed me toward a new study of the issue on CO2 Scoreboard that concludes that critics of energy efficiency have exaggerated the extent of rebound.
Economists are fond of paradoxical arguments, like the rebound effect or the claim that safer cars cause more deaths. (I'm not making up the auto-safety claim.) Sometimes economists seem to be living n a kind of Bizarro World, where the best way to accomplish any goal is always to do the opposite. Making these claims takes a certain ingenuity, because there's nearly always some feedback effect that tends to push back against the direct effects of a policy. There are also feedback effects that strengthen the impact of a policy, but those are less fun to point out. For instance, energy efficiency makes people better off economically, and the environmental Kuznets Curve holds that more affluence produces greater demand for pollution regulation, which will result in less use of dirty fuels such as coal and thereby cut carbon emissions.
The big issue is the size of the feedback effect, and that's very difficult to establish empirically. The problem is that determining the effect of an event such as a policy or technological change requires holding everything else constant. Since other things rarely are constant, an empirical study has to estimate what would have happened in a world in which everything except the policy change was the same. Not easy to do!
I'd like to suggest the relevance of two economic axioms to this debate. One is familiar: there's no free lunch. Even something as seemingly desirable as improved energy efficiency does not come without some price. The other is less familiar (because I just made it up): you can't lose weight by eating more. Call that the "no miracle diet" rule. This means that the direct effects of an action are rarely completely negated or reversed by feedback effects. Rarely does not mean never, but there's a strong burden of proof on anyone who wants to argue for such exceptionally strong feedback. In the case of energy efficiency, that means that the presumption should be in favor of the common-sense conclusion: greater energy efficiency means less energy use.
Cross-posted from the environmental law and policy blog Legal Planet.


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The 8th International Eugene O'Neill Conference will take place from June 22 through 26, 2011 at New York University, located in the heart of Greenwich Village surrounding Washington Square Park.
Papers and Panel Discussions on the Topic "O'Neill in Bohemia"
The 8th International Eugene O'Neill Conference will take place from June 22 through 26, 2011 at New York University, located in the heart of Greenwich Village surrounding Washington Square Park. It was in this same neighborhood, the center of Bohemian Culture in the early 20th Century, that O'Neill and his colleagues began the Provincetown Playhouse. The conference, with scholars from 13 countries represented, will focus on O'Neill's early career and those of the other Provincetown Playhouse pioneers with papers and panels on topics concerning "O'Neill in Bohemia."
Conference events will be held at numerous locations in Greenwich Village as well as on the NYU campus. Featured events and activities include: a keynote address delivered by playwright Tony Kushner; a presentation on the opera A Blizzard in Marblehead Neck, which is based on an incident in O'Neill's life, by composer Jeanine Tesori with Kushner; a performance by the celebrated actor John Douglas Thompson from O'Neill's The Emperor Jones; the Medallion Award Banquet, this year honoring director Robert Falls, actor Brian Dennehy, and O'Neill Society member Diane Schinnerer; a tour of the newly rebuilt Provincetown Playhouse; and a tour of O'Neill's New York City "haunts" created and written by Arthur and Barbara Gelb and Sheila Garvey.
The conference registration fee is $200 and is open to anyone with an interest in O'Neill and is a current member of the Eugene O'Neill Society. "For more detailed information and a complete schedule of events and activities, visit www.eugeneoneillsociety.org/oneillconference.html.
In conjunction with the conference, an exhibition of drawings by Al Hirschfeld celebrating O'Neill and his canon will go on view in NYU's Kimmel Center Windows Gallery, located at LaGuardia Place and West 3rd Street. Entitled Eugene O'Neill as Seen by Al Hirschfeld, the installation comprises a series of 13 windows each devoted to a single play and its productions over the years. The installation, on view now, will remain through August. For additional information about the exhibition and the Al Hirschfeld Foundation, visit www.alhirschfeldfoundation.org/news/eugene-oneill-seen-al-hirschfeld-free-summer-installation-nyu.


text:
Correction appended at 2:40 p.m.
American travelers began to feel the bite of across-the-board budget cuts known as sequestration this week, as the Federal Aviation Administration furloughed 1,500 air traffic controllers, prompting delays for hundreds of flights. By law, sequestration requires uniform cuts to every "program, project or activity" not explicitly exempted by Congress, including the FAA, and the Republican-led House was explicit about that in its report for fiscal year 2013 appropriations for the agency. President Obama, who opposes the cuts, nevertheless gets to decide some matters of timing, via powers given to the White House Office of Management and Budget under the law — and the furloughing of 10% of the nation's 15,000 air traffic controllers is among the first budget reductions to take effect.
(MORE: Sequestration Begins to Bite)
As the cuts' impact worsens, Sen. Rand Paul (R-Ky.) and White House adviser Valerie Jarrett — both of whom were honored Tuesday night at the TIME 100 gala in New York City — had strikingly different versions of who's to blame.
"I think that it's inexcusable to take important things like travel, air traffic controllers or meat inspectors or something that most of us agree we should have, and play a game with it," Sen. Paul said. "The same day that [President Obama] announces that we have no self-guided tours in the White House, he sends $250 million to Egypt. We've got money. It's a matter of priorities, and a good leader wouldn't cut essential services. So I think it's a bit of a charade and it ought to stop."
Republicans are accusing the White House of playing politics with the budget cuts, arguing that the president is front-loading cuts to vital programs like air traffic control in order to force Congress to lift sequestration altogether. Senate Majority Leader Harry Reid tried and failed on Tuesday to move a bill through the Senate that would have canceled the cuts for the remaining five months of the fiscal year.
(MORE: 'We're Not Bending' to Terrorism: Vice President Biden at Emotional TIME 100 Gala)
But Jarrett, an adviser to the president, says the problem with sequestration isn't about funding priorities. The issue, she says, is the imposition of sequestration itself.
"We don't [have the money]," said Jarrett, in response to Paul's statement. "And that was the whole point of why we wanted to avoid the sequester, because it doesn't provide you with the flexibility that you need. We made it very clear last year what the consequences would be if we didn't take the appropriate action to turn it off. Obviously, this is something we want to avoid if we could."
Correction: A previous version of this article stated that Democrats have accused the White House of playing politics on sequestration. That is inaccurate and the post has been updated.


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Focus on plant foods
It comes down to this: plants have less fat, more fibre, and more cancer-fighting nutrients. These three elements work together to support your immune system and help your body fight off cancer. They also help to support a healthy weight: being obese, along with smoking and being physically inactive, is a risk factor for a number of cancers.
The best diet for preventing or fighting cancer is a predominantly plant-based diet that includes a variety of vegetables, fruits, nuts, grains and beans. The less processed these foods are—the less they've been cooked, peeled, stripped of their nutrients, or otherwise altered from the way they came out of the ground—the better.
There are many ways to add plant-based foods to your diet. A nice visual reminder is to aim for a plate of food that is filled at least two-thirds with whole grains, vegetables, beans, or fruit – three-quarters may be even better. Dairy products, fish, and meat should ideally take up no more than a third of the plate. Keep in mind that you don't need to go completely vegetarian. Instead, focus on adding "whole" foods. Just as important, try to minimize or reduce the amount of processed foods you eat. Eat an apple instead of drinking a glass of apple juice, for example. Or enjoy a small bowl of porridge with raisins instead of a raisin-oat biscuit – more volume to fill you up, too.
Simple tips for getting more plant-based foods in your diet
Breakfast: Add fruit and a few seeds or nuts to your whole grain breakfast cereal (porridge/Weetabix) or yogurt. Spread nut butter, like almond or pumpkin seed, on wholemeal toast and top with sliced bananas, or even berries.
Lunch: Eat a big green salad topped with your favorite beans, seeds and other combination of vegetables. Get in the habit of adding salad vegetables to your rolls, and choose wholegrain bread. Vegetable-based bean soup is a wonderful way to get in a couple servings of vegetables and fibre.
Snacks: Fresh fruit and vegetables. Grab an apple, clementine or banana on your way out the door. Raw vegetables such as carrots, celery, cucumbers, cauliflower, peppers, etc. are great with a low-fat dip such as hummus or raita. Keep a mix of nuts, seeds and a little dried fruit on hand for a quick, no-thought snack. Every now and then add a little dark chocolate to your nibbles stash.
Dinner: Add fresh or frozen vegetables to your favorite pasta sauce or rice dish. Top a baked white or sweet potato with steamed broccoli and yogurt or tahini, sautéed vegetables, or with tomato salsa. Replace creamy pasta sauces, with sautéed vegetables or tomato sauce made with healthy olive oil.
Dessert: Choose fruit instead of a richer dessert. Or nibble on a single square of best quality dark chocolate. The occasional 'blow out' dessert is fine but perfectly ripe fruit is delicious too.
Fill up on fibre
Another benefit of eating plant-based foods is that it will also increase your fibre intake. Fibre, also called roughage or bulk, is the edible part of plants (grains, fruits, and vegetables) that your body can't digest but where many nutrients are found and used by the body. Fibre plays a key role in keeping your digestive system clean and healthy by providing healthy bacteria and promoting regular bowel habits. It helps keep food moving through your digestive tract, and assists in removal of cholesterol and cancer-causing compounds before they can cause harm.
Fibre is found in fruits, vegetables, and whole grains. In general, the more natural and unprocessed the food, the higher it is in fibre. There is no fibre in meat, dairy, sugar, or "white" foods like white bread, white rice, and pastries.
Simple ways to add more fiber to your diet:
Use beans and lentils instead of meat in many dishes such as spaghetti Bolognese, chili, casseroles, stews, tacos, and even burgers (try half bean and half meat too).
Cut down on meat
Research shows that the less meat we eat the less risk from a variety of cancers. So what's the link between meat and cancer risk? First, meat lacks fibre and other nutrients that have been shown to have cancer-protective properties. What it does have in abundance, however, is fat—often high levels of saturated fat. High-fat diets have been linked to higher rates of cancer overall. High levels of heme iron (what makes meat red) has recently been linked to the development of some gut cancers. Finally, depending on how much is eaten and how it is prepared, meat can promote the development of gut-based carcinogenic compounds such as N-nitroso compounds and heterocyclic amines. Even so, moderate amounts are considered by many health experts to be part of a healthy, balanced diet, providing first-class protein, B vitamins and iron.
Making better meat and protein choices
You don't need to cut out meat completely and become a vegetarian. But most people consume far more meat than is healthy. The World Cancer Research Fund advises that we eat no more than 500 grams of cooked red meat (about 700 grams of uncooked) a week. Poultry, fish, seafood, beans, eggs and nuts make a great protein base for most meals. Look out for good quality, leaner cuts when buying red meat.
Eat red meat only occasionally. Red meat is high in saturated fat and has no fibre – eat it sparingly.
Reduce the portion size of meat in each meal. The portion should be able to fit in the palm of your hand, about 100 g.
Add beans and other plant-based protein sources to your meals.
Avoid processed meats such as hotdogs, sausages, bacon, and deli meats such as dried sausages and other salted and cured meats. These meats are generally full of saturated fats and salt, as well as preservatives that are known to be harmful to human health in quantity. See the AICR cancer prevention guidelines for more information.
Choose your fats wisely
A major benefit of cutting down on the amount of meat you eat is that you will automatically cut out a lot of unhealthy fat. Eating a diet high in fat increases your risk for some cancers. But cutting out fat entirely isn't the answer either. In fact, some types of fat not only help us absorb fat-soluble vitamins but may actually protect against cancer. The trick is to choose your fats wisely and eat them in moderation.
Fats that may increase cancer risk – The two most damaging fats are saturated fats and trans fats. Saturated fats are found mainly in animal products such as red meat and whole milk dairy products. Trans fats, also called partially hydrogenated oils, are created by adding hydrogen to liquid vegetable oils to make them more solid and less likely to spoil—which is very good for food manufacturers, but not good for us.
Fats that may decrease cancer risk – The best fats are monounsaturated fats, which come from plant sources and when processed are liquid at room temperature. Primary sources include olives, olive oil, rapeseed oil, nuts/seeds and avocados. Also focus on omega-3 fatty acids, which fight inflammation and support brain and heart health. Good sources include salmon, tuna, trout, mackerel, anchovies, herring and flaxseeds.
Help with choosing the right fats
Watch your consumption of red meat, whole milk and butter as these are the primary source of saturated fats. Eggs have saturated fat too but they are also a source of important nutrients, including the hard-to-get Vitamin D. Butter in modest amounts, although a source of saturates, is more easily handled by the body than most margarines.
Cook with olive oil instead of regular 'no-name'vegetable oil. Rapeseed oil is another good choice, especially for baking. Use other oils for drizzling and flavouring cooked foods (e.g. sesame, argan and walnut oils).
Check the ingredient list on food labels and try and avoid anything with hydrogenated or partially hydrogenated oils, which can be found in margarines, baking fats, salad dressings, and many packaged foods (chilled and ambient). Some supermarkets and major manufacturers have banned these fats, so there is a choice.
Trim the fat off of meat and poultry when you do eat it.
Add nuts and seeds to cereal, salads, soups, or other dishes. Good choices include walnuts, almonds, pumpkin seeds, hazelnuts, pecans, and sesame seeds. Brazils are great too but because of their very high selenium content, we should keep them to no more than 3 a day.
Limit fast food, fried foods, and packaged foods, which can be high in trans fats. This includes foods like crisps, sweet and savoury biscuits and pies, crackers, chips and pastries.
Eat fish once or twice a week. Choose at least one oily fish a week: good choices include wild Alaskan salmon (healthier than Atlantic), sardines, herring, trout and mackerel. Tinned mackerel and red salmon are fantastic store cupboard staples. White fish are low in fat and great for protein and some types have a smidge of Omega 3 fats.
Actively choose cancer-fighting foods
There are many things you can eat to maximise the strength of your immune system, as well as many cancer-fighting foods. But keep in mind that there is no single miracle food or ingredient. Research shows that most of the antioxidants and phytochemicals found in plant foods work best in combination. Eating a colourful and varied plant based diet may optimise dietary protection.
Boost your antioxidants. Antioxidants are powerful vitamins that help protect against cancer and assist the cells to function optimally. Vegetables and fruits are the best sources of antioxidants such as beta-carotene, vitamin C, vitamin E, and selenium. Supplementation has not been shown to be useful and may even be harmful in some instances. Naturally obtained nutrients are better for us, tastier and cheaper, too.
Eat a wide range of brightly coloured fruits and vegetables. Colourful fruits and vegetables are rich in phytochemicals – potent disease–fighting and immune–boosting nutrients. The greater the variety of colours – and tastes – you include, the more you will benefit, since different colours and taste types are rich in different phytochemicals.
Flavour with immune-boosting spices and foods. Garlic, ginger, black pepper and turmeric not only add flavour, but they add a cancer-fighting cache of valuable nutrients. All fresh herbs and dried spices will have phytochemicals. Use them in soups, salads, casseroles, or any other dish, especially in place of salt.
Drink plenty of water. Water is essential to all bodily processes. It stimulates the immune system, removes waste and toxins, and transports nutrients to all of your organs. Have it as green and black teas too. Coffee is fine in moderation and due to its polyphenol content may even be actively helpful.
Aim for two-thirds to three-quarters of the daily diet to be from plant foods. This leaves plenty of room for good quality meat and fish, as well as treats.
Pay attention to food preparation
Choosing healthy food is not the only important factor. It also matters how you prepare and store your food. The way you cook your food can make a difference to the amount of nutrients we absorb and how safe our food is for us.
Preserving the cancer-fighting benefits of vegetables
Try to eat some raw fruits and vegetables. These tend to have the highest amounts of vitamins and minerals, although cooking some vegetables can make the vitamins more available for our body to use. During treatment you may find it easier on your digestion to have your vegetables peeled and cooked, or juiced. See my page on juicing and try my quite fabulous Beetroot Zinger.
When cooking vegetables, steam until just tender using a small amount of water. This preserves more of the vitamins. Overcooking vegetables leaches out the vitamins and minerals. For an extra vitamin boost, use the vegetable cooking water in a soup or another dish.
Wash all fruits and vegetables. Use a vegetable brush for washing. Washing does not eliminate all pesticide and germ residue, but will reduce it.
Cooking and carcinogens
Carcinogens are cancer-causing substances found in our environment but also in food. Carcinogens can form during the cooking or preserving process—mostly in relation to meat—and as foods start to spoil. Examples of foods that have carcinogens are cured, dried, and preserved meats (e.g. bacon, sausage, biltong); burned or charred meats; smoked foods (including smoked salmon); and foods that have become mouldy. Here are some ways reduce your exposure to carcinogens:
Do not cook oils on high heat. Low-heat cooking or baking (less than 200C) prevents oils or fats from becoming carcinogenic. Instead of deep-frying and high heat pan-frying, opt for healthier methods such as baking, boiling or steaming.
A healthier stir-fry. Instead of ultra-high temperature stir frying try adding a small amount of oil to a cold wok, along with an equal amount of water. Gradually heat until starting to sputter. Add in your recipe's ingredients and turn up the heat, stirring quickly to reduce contact with the wok. This method is thought to reduce the molecular changes that can occur in oils at very high temperatures.
Barbeque with caution. Burning or charring meats creates carcinogenic substances. If you do choose to barbeque, don't overcook the meat and be sure to cook at the proper temperature (not too hot!). You may like to start the meat on the grill (to get the marks) and finish cooking it in the oven. They will be juicier that way too.
Store oils in a cool dark place in airtight containers; they quickly go off when exposed to heat, light or air.
Avoid foods that look or smell mouldy, as they likely contain aflatoxin, a strong carcinogen. Aflatoxin is most commonly found on mouldy nuts. Nuts will stay fresh longer if kept in the refrigerator or freezer.
Recommended Reading: American Institute for Cancer Research "CancerResource: Living With Cancer" downloadable handbook – for during treatment and post-treatment guidance


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Baby Bracelet With Enameled Flower Charms In Sterling Silver - 6 Inches
Many in stock
You can count on getting attention with this too-cute-for-words flower bracelet! A charming piece that is crafted with gleaming sterling silver and colorful enameled ladybugs.?ÿThis 6 inches bracelet is rhodium plated for better tarnish resistance, and nickel free to avoid any allergic irritations. Ideal for boys and girls, this bracelet comes in a complimentary gift packaging.
Returns Policy
Jewelry Affairs offers a 30-day return policy on jewelry. If you are not happy with your jewelry purchase within 30 days of receipt, you may return UNUSED merchandise that has not been engraved or customized for a refund, credit or exchange. Jewelry returned must be in original condition and credit is subject to merchandise being reviewed by our Quality Assurance Specialists. Merchandise that is damaged or altered in any way by a jeweler other than Jewelry Affairs cannot be returned. Some estate jewelry and designer jewelry may be fragile and cannot be returned if damaged. A merchandise credit will be issued if merchandise received as a gift is returned by the recipient. Items that have been personalized cannot be returned. Custom made jewelry are not refundable. With the above-mentioned provisions, a refund will be issued as soon as the item is received.


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Film Website
"Let fury have the hour/
Anger can be power/
Do you know that you can use it?"
– "The Clampdown," The Clash
Rough, raw and unapologetically inspirational, LET FURY HAVE THE HOUR is a charged journey into the heart of the creative counter-culture in 2012. In a time of global challenges, big questions and by-the-numbers politics, this upbeat, outspoken film tracks the story of the artists, writers, thinkers and musicians who have gone underground to re-imagine the world – honing in on equality, community and engaged creativity – in exuberantly paradigm-busting ways.
Writer/director Antonino D'Ambrosio unites 50 powerful, of-the-moment voices –from street artist Shepard Fairey to rapper Chuck D to playwright Eve Ensler to musicians Tom Morello and Billy Bragg to novelist Edwidge Danticat to filmmaker John Sayles to comic Lewis Black – who share personal and powerful tales of how they transformed anger and angst into provocative art and ideas. Mix-mastered with historical footage, animation and performances, D'Ambrosio presents a visceral portrait of a generation looking to re-jigger a system that has failed to address the most pressing problems of our times . . . or human potential.
The story begins in the 1980s with the rise of Reagan and Thatcher — and a cultural shift towards fierce individualism and rampant consumerism. Coming of age in a world seemingly gone mad or at least gone shopping, some kids started searching for something more authentic. This was the start of a renegade movement D'Ambrosio calls "creative-response." It was a hybrid, haphazard collective of skateboarders, punk rockers, rappers, street poets, feminists and graffitists whose reaction to this brave new world was not to turn away, but to turn up the volume and have their say.
Now that generation is coming to the fore, sparking a global movement focused not just on pushing the boundaries with guitars, paint, dance, storytelling, graphics and subcultural style – but on coming together around real reasons for hope.
Set to a stirring soundtrack from the film's artists – including Rage Against The Machine, Public Enemy, Billy Bragg, Gogol Bordello, MC5, DJ Spooky and Sean Hayes – LET FURY HAVE THE HOUR is a fast and furious trip into the grass roots of art and activism, 21st Century style. The film is written and directed by author and visual artist Antonino D'Ambrosio in his feature debut. The producers are D'Ambrosio and James L. Reid and the executive producers are Jonathan Gray, Brian Devine, Rob McKay, Mark Urman and Chaz Zelus. The film features original music from composer and MC5 guitarist Wayne Kramer. A CAVU Pictures release.


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OVERVIEW: What every practitioner needs to know
Are you sure your patient has a complement deficiency? What are the typical findings for this disease?
Complement, a part of the innate immune system, is composed of more than 30 plasma- and cell membrane–bound proteins that function cooperatively in antimicrobial and inflammatory reactions. The complement system is composed of three pathways: the classical pathway, the alternative pathway, and the lectin pathway (Figure 1). The classical pathway is typically activated by antibody. The alternative and lectin pathways are evolutionarily older than the classical pathway and do not require antibody for activation.
Most of the genetically determined deficiencies of the complement system are inherited as autosomal recessive traits, with the exception of C1 esterase inhibitor, which is inherited as an autosomal dominant trait, and properdin deficiency, which is inherited as an X-linked recessive trait. A complete deficiency of a complement component is rare, and partial deficiencies are rarely of any clinical significance. Infections are prominent in many complete complement deficiencies, and the kinds of infections are determined by the function of the deficient protein in host defense. Many deficiencies are also associated with rheumatologic disorders for reasons that are not completely clear.
Complement has many functions, including promoting phagocytosis of pathogens by acting as an opsonin, inducing lysis of bacteria or susceptible cells and generatinginflammation by products formed during complement activation. A wide range of diseases are therefore associated with abnormalities or deficiencies in complement and depend on the specific protein that is abnormal.
Continue Reading
The classical complement cascade is composed of 11 proteins and these are, in order, C1q, C1r, C1s, C4, and C2-C9. Activation of the alternative pathway begins with the C3 molecule. C3 is the central protein of all three complement pathways and plays a critical role in the opsonization of pathogens. In addition, all three complement pathways result in the formation of the membrane attack complex, which is vital to bactericidal activity. C5a, a product of C5, also acts as a chemotactic factor and directs migration of phagocytes.
The lectin pathway is initiated by the binding of mannose-binding lectin to certain sugars, which are often present on the cell surfaces of pathogens, and joins the classical pathway at the level of C3. A second set of initiating proteins, the ficolins, interact with acetylated sugars and proceed as in the mannose-binding lectin (MBL) pathway.
In general, C3-deficient individuals therefore have an increased rate of infection involving high-grade pathogens of all types. Individuals with defects in C5-C8 have particular problems with systemic infections involving the genus Neisseria because these pathogens typically require lysis. Abnormalities in the level of MBL are common, and it estimated that one third of the population has levels of MBL below normal. There are reports these patients are subject to an increased incidence of infections with a variety of pathogens.
Complement is often associated with unregulated inflammation, and many mechanisms exist for downregulation of complement activation. This is underscored by a recent report that activation of C5 contributes to tissue damage in pneumococcal meningitis. Although deficiencies in complement components are rare, defects in the proteins that regulate complement are far more common. For example, C1 esterase inhibitor deficiency is the underlying defect in hereditary angioedema, discussed in a separate chapter.
A series of proteins are important in the regulation of C3. Two of these proteins, factors H and I, are circulatory proteins. Defects in factor H have been associated with glomerulonephritis, the presence of macular degeneration in the aged, and atypical hemolytic uremic syndrome. Membrane proteins, CD46 and CD55, also control C3 levels, and defects in CD46 have also been associated with atypical hemolytic uremic syndrome and macular degeneration. Similarly, gain of function mutations in C3 and factor B of the alternative pathway are associated with these diseases.
CD59 on hematologic cells is required to prevent unregulated complement lysis. This protein is bound to cells by a phosphoinositol linkage and this linkage is defective in individuals with paroxysmal nocturnal hemoglobinuria. These patients present with unregulated erythrocyte hemolysis and recently have been treated with a monoclonal antibody to C5.
C1, C2, and C4 deficiencies are associated with pyogenic infections and rheumatologic disorders, particularly systemic lupus erythematosus. C3 deficiency is also associated with pyogenic infections and rheumatologic disorders. Infections are usually caused by encapsulated organisms, including Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis. C5, C6, C7, C8, and C9 deficiencies are associated with increased susceptibility to infection with Neisseria organisms. Properdin deficiency is also associated with increased susceptibility to infection with Neisseria organisms.
MBL deficiency is associated with recurrent infections, including upper respiratory tract infections, abscesses, and sepsis. Low levels may also be associated with more severe lung disease in cystic fibrosis. Heterozygous deficiency of C1 inhibitor is associated with hereditary angioedema. CD46 deficiency is associated with atypical hemolytic uremic syndrome. Factor H deficiency is associated with glomerulonephritis and atypical hemolytic uremic syndrome. A polymorphism of factor H is also associated with age-related macular degeneration. Factor I deficiency is associated with pyogenic infections and atypical hemolytic uremic syndrome. CD59 deficiency leads to paroxysmal nocturnal hemoglobinuria.
What other disease/condition shares some of these symptoms?
Certain conditions can lead to secondary deficiencies in complement proteins. This include systemic lupus erythematosus and related disorders, vasculitis, serum sickness, and sepsis. Any process that results in complement activation or consumption can lead to reduced, but not absent, levels of complement proteins. Certain conditions, for example cirrhosis or malnutrition, may decrease liver synthesis and lead to reduced, but not absent, levels of complement proteins.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Deficiencies of the early components of the classical pathway (C1, C4, and C2), C3, and the terminal components (C5-C9) can be detected with a total serum hemolytic complement (CH50) assay. A deficiency in any one of these proteins leads to a marked reduction or absence of total hemolytic complement activity. The alternative pathway hemolytic assay (AH50) is abnormal with deficiencies of C3, the terminal components (C5-9), and alternative pathway control proteins, including factor D, factor I, and properdin. An enzyme-linked immunoassay is typically used to measure MBL levels. The ability to measure C3 and C4 levels is widely available, and more specialized laboratories can measure the levels of other specific complement proteins.
Would imaging studies be helpful? If so, which ones?
Imaging studies are rarely required for diagnosis but may be useful in the evaluation of associated infectious or rheumatologic complications.
If you are able to confirm that the patient has a complement deficiency, what treatment should be initiated?
Standard therapy includes early detection of infections and aggressive treatment with appropriate antimicrobial therapy. Consultation with an infectious disease subspecialist may be necessary. Overall, the management of inherited complement deficiencies is largely supportive. Patients who have recurrent infections may benefit from antimicrobial prophylaxis. Patients should also receive all routine vaccinations, particularly those against organisms to which they are most susceptible.
Complement proteins have rapid turnover, so replacement of specific complement components is typically not recommended. In addition, a patient may generate an immune response to the infused protein. Autoimmune disorders require management by a subspecialist and careful use of immunosuppressive therapy.
What causes this disease and how frequent is it?
Little is known regarding the incidence and prevalence of complement deficiencies.
How can complement deficiency be prevented?
Families with inherited complement deficiencies should receive genetic counseling.
What is the evidence?
Walport, MJ. "Complement. First of two parts". N Engl J Med. vol. 344. 2001. pp. 1058-66.
Walport, MJ. "Complement. Second of two parts". N Engl J Med. vol. 344. 2001. pp. 1140-4.
Frank, MM, Austen, KF, Frank, MM, Atkinson, JP. "Complement system". 2001.
Botto, M, Kirschfink, M, Macor, P. "Complement in human diseases: lessons from complement deficiencies". Mol Immunol. vol. 46. 2009. pp. 2774-83.
Liszewski, MK, Atkinson, JP, Volanakis, JA, Frank, MM. "Regulatory proteins of complement". 1998. pp. 149-66.
Frank, MM. "Complement disorders and hereditary angioedema". J Allergy Clin Immunol. vol. 125. 1010. pp. S262-71.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has a complement deficiency? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has a complement deficiency, what treatment should be initiated?
- What causes this disease and how frequent is it?
- How can complement deficiency be prevented?
- What is the evidence?


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ASPCA Board of Directors Names Matthew Bershadker President and CEO
NEW YORK--The ASPCA® (The American Society for the Prevention of Cruelty to Animals®) today announced that it has named Matthew E. Bershadker President and CEO. Mr. Bershadker is a 12-year veteran of the ASPCA, serving most recently as Senior Vice President of the Anti-Cruelty Group (ACG). Mr. Bershadker will assume the position June 1, succeeding Edwin Sayres, President and CEO since 2003.
Under Mr. Bershadker's leadership, the ASPCA has risen to new heights in its response to cruelty and natural disasters. The Anti-Cruelty Group evolved from a fledgling team of responders to a robust, national program that confronts animal cruelty and suffering on all levels across the country. Mr. Bershadker helped form the Field Investigations & Response team to provide skilled support to state and federal agencies during large-scale puppy mill busts, dog fighting raids, animal hoarding cases, and other instances of animal cruelty as well as natural disasters such as the Joplin, Mo. tornado and Superstorm Sandy. The team has investigated hundreds of cases around the country. Last year, the ASPCA played a leadership role in the removal of 50 dogs from a Bronx dog fighting ring. Most recently, the ASPCA assisted federal and state authorities in the removal of nearly 100 dogs from a multi-state dog fighting ring.
Prior to leading the Anti-Cruelty Group, Mr. Bershadker served as Vice President of the ASPCA's Development department, where he was responsible for creating fundraising strategy and implementing tactics for major gifts, planned giving, special events, capital campaign, and corporate and foundation grants.
Chair of the Board Tim F. Wray stated: "Matt is far and away the most outstanding choice to be the next leader of the ASPCA. His extensive experience, energy and unwavering commitment to animal welfare, coupled with his strong understanding of business management and the non-profit world, make him the ideal leader for the organization as we pursue our mission. I, along with the rest of the Board, look forward to working with him in his new role. We thank Ed Sayres for all he has contributed to this organization and the welfare of animals. Ed grew the ASPCA by leaps and bounds and changed the fate of countless homeless animals. We wish him the very best."
"I am thrilled to serve the ASPCA, its members and the many communities around the country where we play a vital role," stated Mr. Bershadker. "We have made significant strides on behalf of animals around the country, but there is much more to do. I look forward to working with the executive leadership team and our staff to continue to pursue our mission and develop successful initiatives and programs to take animal welfare to next level."
Mr. Bershadker has been instrumental in the creation of the ASPCA Behavioral Rehabilitation Center at St. Hubert's Animal Welfare Center in Madison, N.J., the first-ever facility dedicated strictly to providing behavioral rehabilitation to canine victims of cruelty, such as those confiscated from puppy mills and hoarding cases.
During Mr. Bershadker's tenure, the ASPCA also launched the Cruelty Intervention Advocacy program, a ground-breaking new initiative to help protect companion animals that are in danger of potential abuse or neglect, helping hundreds of New York City's animals in jeopardy of becoming cruelty victims.
Before joining the ASPCA, Mr. Bershadker worked for ICF Consulting and Share Our Strength (SOS). He received his MBA from Johns Hopkins University Carey Business School and his Bachelor's degree in Communications from Ohio University.
Mr. Bershadker serves on the board of the Gruber Family Foundation and Global Federation of Animal Sanctuaries. He lives in New York City with his wife, Nina, son Elias and their dog, Thelma.


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Isle of Skye: Quiraing – card
Bonnie Scotland
Scotland is widely recognised for its breathtaking beauty. Residents and visitors alike are known to travel the country to see their favourite view and find new ones.
Scenic splendour
There are over seventy views in the Landscapes collection, that will allow you to reminisce from the comfort of your own home, or give the gift to another.
About this location
The Quiraing is a distinctive land formation that comprises part of the Trotternish Ridge in the north of Skye and is the only part of the escarpment that is still moving. The many notable features, including The Needle and The Table, make it a popular location for walkers.
The artwork
The drawing takes inspiration from vintage travel posters, particularly the ones created during the inter-war period. It is offered in a choice of natural colours, or artistic ones that fully explore the creative legacy of those gorgeous old posters.
Product details
- Each card is 5x7 inches (127x178mm).
- Each card is printed on 350gsm silk paper that is Forest Sustainable Certified.
- An envelope is included for every card.
- The inside is blank.


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CJ Eckert Photography
Love and pretty things are all around us. Don't forget to look.
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This consultation closed on 5 June 2018
Consultation period8 May 2018 to 5 June 2018
The APVMA invites comments until 6 pm (Australian Eastern Standard Time), Tuesday 5 June 2018 on the proposal to vary Schedule 20 Maximum Residue Limits of the Australia New Zealand Food Standards Code.
Submissions should be strictly confined to relevant matters that the APVMA must consider (such as public health and safety) which are associated with the occurrence of the proposed residues in foods.
For more information on the proposed amendments and what you need to include when making a submission, see the APVMA Gazette notice (page 18) from 8 May 2018.
Please send your written submission by email, post or fax to:
MRL Contact Officer
Australian Pesticides and Veterinary Medicines Authority
PO Box 6182
Phone: +61 2 6210 4897
Fax: +61 2 6210 4840
Email: firstname.lastname@example.com


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Cancer screening programs: cost and effect questions
In any cancer-screening program it is important to define the population that is to be screened. The population that is defined as having the highest rate of the particular cancer is obviously the most cost effective to scrutinize with the highest number of patients identifies per 1,000 screened. Moreover, the efficiency of the screening will depend on the stringency of the defined risk factors, i.e. the more stringently risk factors are defined; the greater will be the pick-up-rate per 1,000. However, when screening is limited high risk patients, individuals who fall outside these strictly defined risk parameters are not eligible for screening and will therefore be missed.The addition of HPV as a risk factor for oral cancer has made it difficult if not impossible to easily define high risk individuals. OPPORTUNISTIC mass screening is the only viable choice to find oral cancer at precancerous or very early stage high survival stages.
Many professional associations and societies have developed cancer-screening guidelines. Accordingly, in spite of differing views, there has evolved agreements on screening guidelines for colorectal, breast, and cervical cancers (1). However, specific guiding principles have yet to be developed for a number of other cancers, especially for populations that lack any persuasive evidence to indicate that a likelihood of high risk exists. This is particularly true for oral cancers particularly in individuals below the age of 40 who are non-smokers and/or non-consumers of alcohol. In part, this has been caused by the recognition that oral cancer is relatively infrequent accounting for only ~ 3 percent of cancers in men and 2 percent cancers in women in the United States.
Oral cancer screening: defining the problem
Oral cancer is an ideal cancer to identify early by screening. It is frequently preceded by an identifiable pre-malignant lesion and the progression from dysplasia occurs over a period of 2,5-8 years. However, published series (2) show that the majority of oral cancers present at an advanced stage (III and IV), when cure rates abysmal. This may be due to the stereotypical oral cancer patient (an elderly male, who abuses tobacco and alcohol) not presenting to health care professionals. Nonetheless, late diagnosis may be related to the fact that an increasing number of oral cancer patients who do not fall into the "high risk" group are not recognized by health care practitioners as being at risk of developing oral cancer. This concept is exemplified by the rise of the female population that is affected by oral cancer. In the 1930's the male to female ratio for oral cancer was 10:1. With increases in tobacco and alcohol use by women that ratio 2:1 and in our series at the University of Maryland the ratio is 3:2 (unpublished). If screening for oral cancer were restricted to males almost 40% of the cases would be overlooked today, as opposed to only less than 10% of non-diagnosed cases in the 1930'Mw. Interestingly, in this regard there are gender differences between women and men relating to smoking and oral cancer. The relative risk is much higher in women at all levels of smoking (3). Moreover it has also been suggested that women may be more susceptible to cancers that are provoked by alcohol (4).
The two most common approaches of detecting oral cancers are visual inspection and cytology. Neither of these modalities has been shown decrease mortality (5). Consequently, both the United States Preventive Services Task Force (USPSTF) and Canadian Task Force on Preventive Health Care (CTFPHC) have taken a position that although screening can lead to early detection, there is insufficient evidence to recommend for or against routine screening for oral cancer (6, 7). However, both organizations support the principle that educational programs directed toward reducing the use of tobacco and alcohol have merit in sustaining a healthier life. Also the USPSTF recommends a regular dental examination in patients at high risk of oral cancer (7) and the CTFPHC suggests annual examinations by physicians or a dentist to examine for oral cancer in patients older than 60 years with risk factors such as smoking and heavy drinking (6). Based on the fact that the primary risk factors intra-oral (excluding lips) cancer in American men and women is the use of tobacco and alcohol, albeit that infection with HPV-16 and HPV-18 virus has been associated with greater risk of developing squamous cell carcinoma of the oropharynx (8). Despite these recommendations, the National Center for Health Statistics Supplement Survey reported in 1992 that only 14% of the U.S. population has ever had an oral cancer screening (9).
Incidence of oral cancer in young patients: a changing trend
As a result of non collecting population data from screening large populations for oral cancers, little or no attention was initially given to the development of changes in patterns of disease susceptibility. This was especially true for an emergent group of young patients that develop oral cancers, particularly those involving the tongue. Consequently, the increased incidence of tongue cancer was first highlighted by testimonials, letters to the editor, and case reports from Oral Maxillofacial and Head and Neck healthcare professionals. Later, the fact that head and neck cancer, particularly tongue cancer was escalating in young adults in North America, and internationally, began to be recognized from retrospective studies preformed in the late 1980's (10-16) For example, a review of mortality trends in Europe for a 34-year period from 1955 revealed that a number of countries in Central and Eastern Europe had a 2-fold increase in oral cancer. This increase principally involved males that were under 45 years of age. Similar increases were observed in women in a number of countries (14). In the United States, similar studies preformed during a 20 year period began in the 1960's revealed that there was a near four-fold increase of oral cancer in males ages 30-39 in the State of Connecticut (16). Likewise, DePue (13) noted earlier that there was an increase in the mortality rates of adults younger than 30 and indicated that these data suggested that this trend began in the mid 1970's.
Most recently, Schantz and Yu (17) examined the cancer surveillance database from the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) Program. These investigators calculated age-adjusted incidence rates for head and neck cancers using a join point regression model, and described tongue cancer incidence trends and established the statistical significance of temporal changes for this disease. These studies revealed that from 1973 to 1997, there were 63,409 head and neck cancer patients in 9 SEER registries. Among this group of patients, 3339 individuals or 5.2%, were noted to be younger than 40 years of age. While the incidence of head and neck cancer remained stable in patients older than 40 years between 1973-1984 compared to the period 1985-1997, tongue cancers in adults younger than 40 years increased almost 60% during the same intervals of time. Notable, was that the estimated annual percentage change occurred until 1985, after which the incidence rate stopped rising but remained increasingly high. In an attempt to define the change more precisely it was discovered that the change in tongue cancer incidence rates for young adults was associated with birth cohorts between 1938 and 1948 and whites but not blacks. These investigators suggested that these populations might have experienced a changing carcinogenic effect on the tongue, distinct from those contained in tobacco. This conclusion was based on the fact that cigarette smoking has markedly decreased among Americans since the 1960's (18) and among youths in the 1970's and 1980's (19). Moreover, the cancer incidence from other systems as well as the upper aerodigestive tract cancers, except for tongue cancer, had declined (20). It should be noted that these changes were not related to any artifact reports biases, since no changes in tumor coding, improved screening programs or diagnostic methods occurred to distort these results (17, 20).
Comparison of survival between high-risk and non-risk groups: new insights
In assessing survival, the literature is replete with studies of small sample sizes that consider survival independent of anatomic location (21). Several authors have reported that younger patients have diminished survival rate from oral cancer (12, 13, 16, 22). In an extensive review Lewellyn et al. (21) noted that it has been suggested by some (23-26) that patients without typical risk factors for developing cancer of the oral cavity may have a worse prognosis compared with patients with usual risk factors of alcohol and tobacco use. Moreover, Kuriakose et al. (27) have suggested that lesions in young individuals were predominantly invasive as compared to exophytic lesions found in older individuals/ Furthermore, when the periods 1973-1984 and 1985-1997 were compared, the d\stage distribution of tongue cancer did not significantly change and that the local-stage disease was approximately 30% to 40% higher for younger individuals than older patients. These findings, however are disparate from those reported by Sarkaria and Harari (26), which demonstrated that 64% of young patients had Stage I and Stage II disease at presentation. More importantly, Davidson's review (28) of SEER database showed that disease specific morality from tongue cancer increases with age. It may be that this is a reflection of increasing co-morbidities in order patients, which have been shown to adversely affect head and neck squamous cell carcinoma survival (28).
Shantz and Yu (17) found that from 1973 to 1997, 5-year survival rates for tongue cancer increased in all age groups. The absolute increase in survival was greatest in Americans younger than 40 years. Also, survival improvements was more pronounced in young patients that were male, white and at an advanced tumor stage, while survival rates were found to diminish in young non-white patients. There was a greater than 20% survival improvement in young patients with regional or distant stage disease compared to earlier periods. This may be attributed early intervention was selective neck dissections in N0 (non-affected) necks of tongue cancer patients are opposed to the previous "watch and wait" approach. However, the absolute increase in survival was 3% in young patients with localized disease. During these periods there were comparable increases in the survival rates for older individuals when analyzed by sex, race and stages, with the exception of black populations aged 40 to 64, in which a decrease survival rate was observed (17).
Etiologic factors: possible explanations for changing profile in oral cancer.
The temporal and age dependent changes seen with the increase in incidence of oral cancer and specifically tongue cancer have implied the possibility of a changing carcinogen effect on the tongue, particularly distinct from those contained within tobacco (17). A number of etiologies have been proposed as possible explanations for this changing profile of oral cancer.
Although much attention has focused on young patients who are non- smokers (29, 30), non-smokers at all ages can develop oral cancer. Koch et al. (31) found a disproportionate number of females, oral cavity cancers (particularly tongue), and very young and very old patients. In the Maryland experience 99 of the 500 consecutive oral cancers (20%) were found in non-smokers. In this series 60% were females; tongue and gingival accounted for 75% of all sites with only 3% floor mouth cancers. Patients below 40 and above 70 were increased compared to the general group. There was an increase of premalignant lesions particularly white patches in the non-smokers. Interestingly the incidence of second upper aerodigestive tract cancers was the same for non-smokers as smokers (13%). Virtually all-second primaries in non-smokers occurred in the mouth (unpublished data). Koch et al. confirmed a low rate of p53 mutations loss of hetrozygosity, and chromosomal mutations in the non-smokers group. HPV viruses were no different between smokers and non-smokers. He postulated a separate mechanism for carcinogensis in group possibly involving p16. However, no etiology for the development of cancer in this group is known (32).
Alcohol is an independent risk factor for oral cancer (4, 33), and has been cited as the most important risk factor in non-smokers. However, many non-smokers are also non-drinkers, in fact, 50% of our non-smokers never drank and 37% drank less than one alcoholic beverage a day. Although reports have implicated mouthwash use in these patients, a review of seven cases controlled studies on mouthwash and oral cancer failed to show and link (34). Binge drinking of alcohol has become more prevalent with some American youth; however, the duration of exposure appears to fall short of the time required for malignant transformation to occur. Moreover, drinking among Americans in general decreased from the 1930's to the 1990's (17, 35). In comparison with Americans, studies reported from India (36) and more recently from the United Kingdom (UK) indicated that risk factors of tobacco use and alcohol consumption were present in the majority (75%) of patients below the age of 45 years (37). Significant differences in the pattern of alcohol consumption were found in female subjects, who were less likely to consume over the recommended amounts of alcohol compared to the male subjects. Interestingly, daily regular fruit and vegetable consumption during the ten-year period before cancer diagnosis was recorded to be low. However, there was a distinct subgroup of cases, 26%, which had little or no exposure to any major risk factors (37).
Smokeless Tobacco
Among Americans another factor that has been recently advocated as causative for developing cancer has been the use of smokeless tobacco; such agents have been implied in the development of precancerous leukoplakia (16, 38-41). However, in spite of the increased popularity of the use of this form of tobacco, the regional differences in use of these products within the Americas, and Europe, and the fact that American women have shown significant increases in tongue cancer with a low rate of smokeless tobacco use (0.3%) raises doubt as to the significance of these products in accounting for this form of tongue cancer. Intriguingly, West Virginia has highest use of smokeless tobacco and a lower than average rate of oral cancer. Moreover, the incidence of non-tongue oral cancer (cheek and gingival), an area that is used to harbor smokeless tobacco, has remained constant in the United States and the United Kingdom (10, 42).
The reports by Zhang et al. (43) of a dose dependent association between the use of marijuana and head and neck cancer risk, particularly in young patients, has raised the possibility as to the role that such habits may have in causing cancer. It has been estimated that 31% of the population of the United States 12 years and older in 1992 have ever used marijuana. The incidence of marijuana use sharply increased in the United States, in male and female teenagers, and young adults in the 1960's corresponding to the cohort born between 1941 and 1955 (44-46). Such timing would seem to correlate with the increased expression of tongue cancers. Additionally, there exists laboratory and experimental evidence to suggest that there is a carcinogenic effect of marijuana. Correlative human studies verifying this association with oral cancer have yet to be preformed. Moreover, it should be realized that the use of marijuana was not a 20 th century novelty only indigenous to the youth of Central Europe, and the Americas, and the patterns of oral disease in other populations have not mirrored the findings being addressed here. In fact, a comprehensive review of the association of marijuana and squamous cell carcinoma of the head and neck in 2002 concluded that more evidence was necessary to prove marijuana's link to head and neck cancer (47).
Genetic factors
Another consideration that has been raised to account for the increased prevalence of tongue in young individuals has been in the association between various genetic polymorphisms and susceptibility to develop oral squamous carcinoma (30). In fact, a number of studies have established that low does exposure to tobacco increases the risk for the development of oral cancer in individuals with GTS1 and CYP1A1 polymorphisms (48-50). However, the low frequency of such genetic alterations within the population cannot account for the increased rate in tongue cancers. Some have suggested that familial clustering of cancer points to a genetic component in the development of squamous carcinoma at a younger age (21), however; no studies in the offing have provided clear-cut evidence to date to support this view.
The role of viruses in the etiology of oral cancer and particularly the evolving subset of young patients without risk factors that develop tongue cancer has likewise proven to be unconvincing. Although Epstein-Barr virus (EBV) has been implicated in the development of lymphomas, and nasopharyngeal carcinomas, the influence of EBV in emergent oral squamous carcinomas is unresolved. Van Heerden et al. (51) reported that EBV DNA could be identified with near equal frequency in patients harboring SCC that were over the age of 40 years as well as patients less then 40 years of age and control patients with non-neoplastic oral conditions. As such, these investigators were able to conclude that EBV did not distinguish the development of cancer in patients based on age.
The role of human papilloma virus (HPV) in the development of oral cancer is no longer in question. HPV16 is the prime driver of oropharyngeal cancers, and to a much lesser extent oral cancers which are seldom virus related. Oral sex has been identified as the primary mechanism of oral colonization of HPV16. Recent reports (52-54) have shown that a subset of patients that develop oropharyngeal squamous carcinoma have been shown to be less apt to use alcohol and tobacco and rather exhibit a strong correlation with HPV-16. Also, the presence of HPV as the cancer etiology appears to confer a survival advantage among head and neck squamous carcinoma patients, particularly when p53 is wild type (55). However, these patients do not account for increases in incidence in tongue cancers reported over the last decades (56) and the impact of the virus is primarily in the oropharynx.
Future directions: dealing with the problem
The increasing incidence of SCC of the oral cavity particularly tongue cancers, among younger individuals and the evidence that traditional risk factors may not be responsible for this change in disease, raise concern for the need for more definitive and cost effective means to detect SCC in what has been traditionally considered low risk populations.
The development of effective visualizing systems and less invasive cost effective sampling methods should help temper the public health concerns regarding the justification for prudent screening of such populations. At the same time, the assessment to risk needs to be further developed by determining the profiles of molecular alterations seen in young tongue cancer patients. For example, Lingen et al (29) showed that 81% of young patients with tongue cancers over expressed p53 by immunohistochemical analysis. Furthermore, none of these patients demonstrated mutations in exons 5-6, which are known to be "hot-spots" for the gene alterations in conventional oral cancer. Thus, suggesting that young individuals with no risk factors had altered p53 function in oral squamous cell carcinoma that differed from those of more typical population of individuals that develop this malignancy. Unfortunately, this paper and others (57) examined only young patients who were non-smokers/drinkers, confounding the results with 2 variables. It is known that non-smokers have only 14-17% p53 mutations (58) compared to 40-50% in smokers (59). Moreover Atula's study of 34 young patients many of whom were smokers and drinkers found are 51% in advance p53 mutations (60). Similarly, the expression of chromosome g\fragility following the use of marijuana in such populations might prove informative as young adult populations with SCC have shown to express significantly
increased numbers of bleomychin-included chromosome breaks (61).
Recently Mendez et al. (62) using oligonucleotide arrays that contained probes representing approximately 7000 full-length human genes and hierarchical clustering analysis, showed that oral carcinomas are distinguishable from normal oral tissue based on genome-wide transcriptional expression. Recognizing that patients diagnosed with SCC at a young age show evidence of genetic instabilities as well as variant patterns of alteration of the tumor suppressor gene p53, raises expectations that the development of DNA and proteomics chip arrays might well define some of the underlying factors for the development and progression of SCC at a younger age. Such pioneering approaches are likely to have an extraordinary impact on cancer biology, and provide opportunities to unravel the thus far unidentified mechanisms involved in squamous cell carcinogenesis. They are also expected to provide a molecular blueprint for head and neck squamous carcinoma. This will also help to discover appropriate markers for the early recognition of precancerous lesions, and identify novel targets for intervention in this disease.
Salivary Diagnostics
Salivary diagnostics are showing progress as a vehicle for mass screenings of large populations. Samples maybe taken by auxiliary staff, analyzed by computer analysis and results returned in an expedient manner. However currently marketed tests (2017) which have entered the market circumventing FDA approval, are not currently recommended by the Oral Cancer Foundation. The foundation does believe in the core science behind these ideas and hopes that in the future they will prove to be a valuable tool to those who screen for oral cancers. The same holds true for those tests based on molecular markers collected from an oral rinse mechanism.
*** This article has been edited by the Oral Cancer Foundation in 2017 to update the information related to the impact of HPV in oropharyngeal cancers.
Robert A. Ord 1.2, Nikolaos G. Nikitakis 3, and John J. Sauk 2.3
1 Department of Oral and Maxillofacial Surgery
2 Department of Diagnostic Sciences and Pathology
3 Greenebaum Cancer Center
University of Maryland, Baltimore Dental School, Baltimore Maryland


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A group of LibreOffice developers have added experimental collaborative editing capabilities to the open source office suite. The feature allows multiple users to work on the same document simultaneously over the Internet. The collaborative editing functionality was implemented by grafting Telepathy to LibreOffice.
Telepathy is an open source instant messaging framework that supports multiple protocols. One of the key features of Telepathy is that it allows instant messaging protocols to be used as a medium for arbitrary communication between applications, like a form of real-time network IPC. Building LibreOffice's collaborative editing features on top of Telepathy eliminates the need to operate special servers for the purpose.
Four LibreOffice developers recently met for a small hackfest at the Cambridge offices of open source startup Collabora in order to work on the collaborative editing prototype. The hackfest was funded by The Document Foundation, the non-profit organization behind LibreOffice.
The developers published a video that demonstrates the functionality. In the demo, they show two instances of LibreOffice Calc editing the same spreadsheet. When a value was changed in a table on one instance, the change propagated to the other. A formula and chart in the document also updated to reflect the change.
Although much of the underlying code is implemented, there is still a lot of work that needs to be done to advance the feature from the experimental prototype stage to the point where it's ready to be released to regular end users.
The project is included in The Document Foundation's list of ideas for Summer of Code students. Developers who want to contribute to the effort or take a look at the prototype can find the source code in a LibreOffice git branch.


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Scientists all over the world regularly assess the rich body of scientific literature, contributing to an ever-strengthening understanding of how the climate system works, and how it is changing in response to human activity.
The scientific topics assessed by WGI include: greenhouse gases and aerosols in the atmosphere; temperature changes in the air, land and ocean; the hydrological cycle and changing precipitation (rain and snow) patterns; extreme weather; glaciers and ice sheets; oceans and sea level; biogeochemistry and the carbon cycle; and climate sensitivity. The WGI assessment combines observations, palaeoclimate, process studies, theory and modelling into a complete picture of the climate system and how it is changing, including the attribution (or causes) of change.
The WGI assessment provides scientific information relevant for the global community to meet the challenge of climate change. As well as the global scale, WGI looks at variability and changes happening at a regional level, which is closely tied to how impacts and risks to human and natural systems are changing over time. This is, in turn, relates to the assessment of WGII and the need to design effective climate change adaptation policies. Other important policy dimensions of WGI are the assessment of the amount of carbon emissions compatible with climate and energy targets; interactions between land and the climate; and links between climate and air quality. All of these aspects are closely connected with the assessment of WGIII and strategies to mitigate against the impacts of climate change.


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Top length: 65 cm
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100% cotton jersey is slightly stretchy. Lay down a t-shirt or longsleeve on a flat surface. Measure the sleeve length from the tip of the shoulder to the hem of the sleeve. The length and width measurements are taken from the highest and widest points of a flat lying top Slight deviations are rare but possible due to production tolerances.
55 €


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EPA Awards USD 6.5 Million for Ten Restoration Projects (USA)
The U.S. Environmental Protection Agency is awarding $6.5 million in grants to state and local agencies, and non-profit organizations to restore water quality and wetlands throughout the San Francisco Bay watershed. Grants range from $75,000 to $1.5 million and will support ten projects that prevent pollution, restore streams and tidal marshes, and manage floodwaters in an environmentally sound manner.
"This investment by the EPA in important water quality improvement projects will help restore San Francisco Bay, which is so vital to the environment and economy not only of the Bay Area but the entire state of California," said U.S. Senator Dianne Feinstein (D-Calif.). "I applaud the EPA and its local partners for their ongoing commitment to making the Bay clean, healthy, safe and productive for generations to come."
"San Francisco Bay is a magnificent treasure that supports more than 500 species of wildlife, including 128 threatened or endangered species, and the economies of Bay shoreline communities," said Jared Blumenfeld, EPA's Regional Administrator for the Pacific Southwest. "It is critical to safeguard this productive natural resource, and these projects with our state and local partners will make great strides to achieve that goal."
The projects are funded under EPA's San Francisco Bay Water Quality Improvement Fund that has invested over $28 million in 48 projects across the Bay region since 2008. Since the Fund's inception, EPA's investments have been matched with another $100 million from 69 partner agencies and organizations.
The project summaries, partner agencies/organizations, and funding amounts are:
– Restore Wetlands at Creek Mouths ($1.55 million, in partnership with San Francisco Estuary Partnership and the Association of Bay Area Governments): Redesign flood control channels to restore wetland habitat, water quality, and shoreline resilience at three creek mouths: San Francisquito, Lower Novato, and Lower Walnut Creeks. Restore over 100 acres of tidal marsh and re-use 70,000 cubic yards of clean sediment from dredging projects.
– Continue Reducing Sediment Loads into the Napa River ($1.5 million, in partnership with Napa County Flood Control District): Complete instream restoration of the Rutherford Reach and begin restoration of the Oakville Reach to reduce sediment loads into Napa River.
– Restore Quartermaster Reach – Presidio ($1 million, in partnership with Golden Gate National Parks Conservancy): Restore 1,050 feet of creek channel, 3.3 acres of dune-coastal scrub upland, and 4.7 acres of previously buried tidal marsh adjacent to the Crissy Field wetlands.
– Site Preparation of Sears Point Tidal Marsh Restoration ($941,000, in partnership with Sonoma Land Trust): Prepare for restoration of 960 acres of tidal marsh in the San Pablo Bay National Wildlife Refuge through removal of contaminated soil, construction of a 2.5 mile levee to manage floods, and contouring the site to accelerate sediment accumulation.
– South Bay Salt Ponds Mercury Studies ($500,000, in partnership with California State Coastal Conservancy): Conduct methylmercury studies within the 15,000-acre South Bay Salt Pond complex to support tidal wetlands restoration of ponds.
– Reduction in Packaging at Fast Food Establishments ($257,000, in partnership with Clean Water Fund): Develop source reduction programs for takeout food containers, the largest documented contributor of trash in urban waterways that flows into SF Bay, and, with partner cities, conduct outreach at fast food establishments.
– Reduction in Household Use of Toxic Pesticides ($250,000, in partnership with San Francisco Estuary Partnership and the Association of Bay Area Governments): Use social media and direct outreach to consumers and retailers to promote less-toxic pesticides and pesticide free practices. Project aims to reduce Bay Area household use of less-toxic pesticides and pesticide free practices by 5%.
– Improve Water Quality and Wetlands at Sonoma Creek Marsh ($235,000, in partnership with Audubon California): Enhance 300 acres of tidal marsh within Sonoma Creek marsh by excavating a new channel. Dredged channel material will be used to create wildlife habitat and improved tidal exchange will reduce the need for pesticides used to control mosquitoes.
– Restore Alameda Creek ($181,000, in partnership with Alameda County Resource Conservation District): Establish stream buffers, restore stream channels and riparian corridors, improve grazing practices, and upgrade rural roads in three subwatersheds of Alameda Creek.
– Improve Fish Passage on San Francisquito Creek ($75,000, in partnership with San Mateo Resource Conservation District): Remove Bonde Weir and redesign the creek channel to re-open access to 40 miles of upstream spawning habitat for steelhead.
Press Release, October 18, 2012


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|From: Paul Steckler (steck at ccs.neu.edu)
Date: Sat Feb 15 08:00:05 EST 2003
PLT Scheme projects =================== This is a monthly reminder sent to the PLT Scheme mailing list. A list of PLT Scheme Libraries and Extensions is available at http://www.cs.utah.edu/plt/develop/. Please browse this site to find out about software for PLT Scheme, built by PLT and others. If you've built your own software for PLT Scheme, you can add it to this site. Please send email to mflatt at plt-scheme.org for that purpose. If you're looking for a project for yourself or for students, check out the Help Wanted section on the Web page. Each project has a PLT contact person who can provide assistance. If you have a suggestion for a project to be placed on this page, please send email to my address below. -- Paul ------------------------------------------------------------------ | Paul Steckler, Ph.D. | Northeastern University PLT | | steck at plt-scheme.org | DrScheme Project | | Tel: 617/373-4211 | # http://www.ccs.neu.edu/~steck | | FAX: 617/373-5121 | *** Ad astra per hackera *** | ------------------------------------------------------------------
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