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For the longest time, the press and the Republicans have whined that in the current government shutdown and impending default threats, President Obama has failed to lead. You cannot turn on any 24-hour cable news channel without hearing some pundit whining about the lack of presidential leadership. Even those who correctly place the blame on the Republicans for the suicide-bombing caucus inflicted wound on America don't miss a chance to brandish their pundit credentials by charging President Obama as MIA in a leadership role.
They base this accusation on the fact that the president has refused to negotiate with a gun to America's head and to pay ransom to the Tea Party. What these pundits miss is that that refusal is the leadership the president needed to provide at this critical juncture in history, and he has passed that test with flying colors.
Think about this with a long term view. Seeing the presidency slip from them, the far Right radical Republicans are attempting to write a dangerous new norm into American policymaking: government by extortion. They are trying to normalize the behavior of a fringe to demand ransom for the simple fact that Congress would do its job. The idea is to get with extortion what they could not - and likely have decided no longer can - win at the ballot box, or they break the government and wreck the world economy. They are trying to turn democracy on its head.
This cannot be allowed to happen. America cannot indefinitely continue to govern by manufactured crises, or give into extortion to end one such crisis only until another is manufactured. We especially cannot accept that a small fringe can manipulate the political process to effectively end a law that they cannot outright repeal.
And so, the president's job, as not simply the head of government but the leader of our republic, is not to attempt to Congress' job for them. The president's job is to ensure that the American form of government - a representative democracy - is protected not just for his presidency but for future presidents and future Congresses. What the president needed to do as a leader is to crush the forces of government-by-extortion and make them understand, once and for all, America does not negotiate with economic terrorists.
I should note here that this dynamic is fundamentally different from what happened in 2011. Too many on the Left and the Right confuse the 2011 debt ceiling crisis with this one - and sometimes misguidedly believe that the only reason the president is standing firm now is because he does not want a repeat of 2011. That is in part true, however, in 2011, the president was dealing with a new Congress that - for better or for worse (and generally, for the worse) - was the result of a legitimate, and severe, electoral loss for Democrats. At that time, despite the pattern of behavior being similar, the Republicans were not trying to achieve through extortion what they could not achieve through the ballot box. They won a big victory. They may have legitimately believed that they won a mandate to use any means necessary to cut the budget.
Which brings us to the second, and perhaps the more key, difference - the 2011 turmoil, terrifying as it was, still was entirely about the budget, and the Republicans, politically in a much stronger position than now, did not attempt to repeal or delay the Affordable Care Act through the budget process. They did not try to extort the president and the Democratic Senate into repealing a law they could not repeal through regular order. This time is different. This time, Republicans planned this crisis to reverse a law they could not reverse by winning elections, or challenging it in the courts.
What the Tea Party controlled GOP launched with this crisis is a war on the American form of government. In war, a president leads as the Commander in Chief, and leadership is about finding a strategy to crush the enemy - America's domestic enemy, the Tea Party. To say that the president has been successful in his is an understatement. He has, from the beginning, laid out a clear principle: Congress does not get to collect ransom in exchange for doing its basic duty, and Congress does not get to drag laws they cannot otherwise repeal into budget fights. The president has been strong, decisive, and effective in making the GOP face the consequences of its own actions. That the Senate Republican leader today is left negotiating the terms of his party's surrender is in good part a result of the president's resolve.
The president has brought the Republican establishment and the Republican party's backers face-to-face with their own Frankenstein, and forced them to take on the Tea Party. The president has exposed the radical Republican agenda and made Republicans on the Hill face down their Tea Party colleagues, and left them scurrying to put this politically disastrous episode behind them.
That is leadership. That is exactly the leadership a president at this moment needed to provide. That is precisely the leadership this president has provided. Chew on that for a minute, pundits.
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Life is about Experiencing, Learning and Moving On To Next
The JOY of it all Tears are filling my eyes.
I can feel the room full of people getting ready to move on. It is a big room, actually a hockey rink most of the time, a hockey rink where in an earlier time I watched Kamen play on community and school teams from age 6 to 17. And it is where I have watched Rensselaer play for the last dozen years. But today it is so different - no ups and downs, no mistakes, no cheering when RPI scores and being disappointed when the other school accomplishes the exact same feat. No wondering about the outcome. No winning and losing.
Everybody is a winner today. There are only ups, and that is why the tears are flowing down my face.
There are not many occasions where the joy is so pure. Even weddings have that sense of the loss of what was. And even on this day of so much joy there is probably some sorrow...the passing of an era in a family, in a person's life...but the sorrow is hard to find, hard to feel, hard to hear because the JOY is so loud.
There are 758 people waiting to walk across the stage to receive their college degrees. Many times that number are sitting in the stands with smiles on their faces and pride in their hearts and hopes about the future in their thoughts. As one of the trustees of the Sage Colleges, I march down the aisle and take a seat on the stage. This is my fifth year of this graduation ceremony, this community joy. It brings tears every year, starting with seeing the grads line up outside, then walk in with such pure joy - a joy I have experienced nowhere else.
I have had the privilege of witnessing the birth of a child, and nothing is so precious and filled with such awe. But a birth is a private, intimate revelation, rarely shared with more than a few. It is not, at least in our culture, a public event.
This is a different experience. The sheer volume. The number of people who are experiencing joy all at the same time. Everyone in the Fieldhouse is happy. Thousands of happy people in one place, being joyous about life and about the achievements of people.
The cheers are fun to hear. As people walk across the stage, family members or friends in the audience call out their names. There is yelling and applause - just for them. How many times in life do people walk across a public stage and have other applaud them? For most, not too many times. For some, it is the first and possibly the only time it will happen.
And the grads ...they can't stop smiling. Some have writing on their caps. Others are wearing very special outfits, dressed up for their big day...maybe the biggest day of accomplishment in their lives so far. And for some of the families, they are seeing the first person in the family history achieve a college degree, or a masters or a doctorate.
The air is alive with joy. I feel the joy in all of my being and I am overwhelmed with a feeling of life in one of its finer moments. Seven hundred and fifty eight new graduates celebrating themselves, with their loved ones there as witnesses to the moment.
In this sacred space, all I can do is let the tears flow and know how blessed I am to experience such a moment and to share it with thousands of people in Rensselaer Polytechnic Institute's Hockey Fieldhouse in Troy, New York. And in that moment, I realize we are not alone in our joy. Graduations like this are happening all over the country and the world. It is one of the gifts we give ourselves as human beings.

subset: commoncrawl


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Landscape Rock
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text:
On this week's "Name Check," Grammy Award-winning singer and Brooklynite Melanie Fiona stops by The Post to chat with Michael Riedel about her evolution as a singer, working with Jay-Z and Kanye West, and her Canadian-Caribbean roots. The songstress is scheduled to perform tracks from her new album, "The MF Life," while touring with Mary J. Blige and D'Angelo.
Page Six's Ian Mohr also stops by to dish on how Rihanna and Chris Brown can't stay away from each other and Kristen Stewart's cheating scandal.


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March 9 2012
Well I guess you have guessed that I have not been keeping up with this 365 project...
I thought I would be able for another year in pics but I think to be honest 2011 was enough. i really enjoyed my 365 and I am so very glad I did it and finished (2011 anyway!) but I fear if I go on I will suffer from permanent irreversible burnout! I don't want to risk that as I love photography too much!
So for now anyway this is all I have for 2012!
Funny thing is I probably haven't missed many days taking a pic!
Please come back to my site as I am trying to add new things. And I'm sure I will start a new blog soon.
Thanks to everyone that has followed my journey!
Leave a Reply.
Take 2-012
I decided to go for another year in photos! i didn't think at the start of 2011 I would ever be doing this again but well hey it had to be the way!
I have an Etsy shop now! Check it out here!!!!
Visit me on Flickr!


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Help us raise £2 million for a twin operating theatre suite
The ARCHIE Foundation is the official charity of Tayside Children's Hospital at Ninewells
We're the official charity of Tayside Children's Hospital at Ninewells, Dundee. We're currently raising £2 million for a new twin operating theatre suite which will transform the experience of having an operation for thousands of local children.
Help make the experience of having an operation as good as it can be for children in Tayside
The ARCHIE Foundation is the official charity of Tayside Children's Hospital at Ninewells
ARCHIE Tayside is part of a family of funds. Read about how we began, and how we've grown.
We provide specialist equipment, support families, create amazing hospital environments, enhance staff training, buy toys, fund research and provide specialist staff. Supporters just like you make all of this possible.
We need your help – can you fundraise, volunteer, support our events or donate? There are lots of ways you can support us. Find out more about what we do and how we help make the difference to local sick children.
All the staff at Ninewells Hospital have been brilliant looking after Amber - they are caring, dedicated and supportive. We have been in pretty much all the different children's areas - ICU, HDU, outpatients, inpatients, and theatre. They are all on different floors and areas. It would be lovely if they could be closer together.
Carole, Amber's Mum, Dundee


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The Ghost Ones was the name given to the mysterious and nomadic clan of Senali that lived without family ties. Considered troublemakers by the other Senali, they were known for creating rivalries between other clans over trivial matters. The Ghost Ones spoke out against the custom of Rutan and Senali royalty exchange children.
It was later discovered, after the Mission to Rutan, that the Ghost Ones were a work of fiction, created by Prince Taroon in order to discredit his brother, Prince Leed, so that Taroon himself would gain the throne of Rutan.
Community content is available under CC-BY-SA unless otherwise noted.


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Code for blog?
Answered Public 2 comments
The Feisty Ginger 12/17/2015 10:43
Is there some sort of code I have to put into the header or footer of my blog in order for my review to verify? It's saying I need to put in some sort of ID, but it's not my ID or the product ID.
Paul Blum 12/18/2015 02:00
Dear Feisty Ginger, Yes there is a code that you have to put in the content of your review. We use that code to verify and validate your post. The code is unique for every promotion you participate in. When you click on the "Manage tasks" button for the promotion you want to review under task 1.Publish Blog Post you will find the code. Best Regards, Paul
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my name is Michael Schuster and I'm a German guy who is fascinated by the art of photography.
Ever since I was a young teenager I couldn't resist to capture beautiful scenes and places on camera.
Over the years the "hobby" became a real passion of mine and it made me see the world around me with different eyes.
Walking through the streets and thinking of what the buildings and sceneries would look like in unusual angles or in black and white are pretty common thoughts already.
I'm hunting for my biggest dream - becoming a professional photographer. Let your project or vision be part of that hunt and let's get things started together...


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MV compact switchboard (Ring Main Unit) up to 36kV for wind farms
Ring main units
DVCAS switchgears functional groups have been designed as compact units, and built as the union of modular switchgears.
Each of the modular functions is composed of:
- Metal base frame
- Operating mechanism and relay compartment
- MV cable compartment
- Stainless steel, gas-tight cubicle which uses SF6 gas as insulating medium and houses the busbar system and the breaking devices.
General electrical/Constructive data:
- Frequency Hz 50
- Rated voltage kV 36
- Insulation level
> Power frequency withstand voltage kV 70
> Lightning impulse withstand voltage kV peak 170
- Rated current of the main busbar A 630
- Short time withstand current kA/s 20/3
- Short circuit breaking current capacity kA 20
- Short circuit making capacity kA peak 50
- Internal arc withstand IAC AFL kA/1s 20
- Degree of protection
> HV compartment IP 67
> LV and operating mechanism compartment IP 3X
- SF6 gas pressure at 20ºC bar 0.3
For other values, please consult Schneider Electric.
The Wind Main Unit
Choosing DVCAS switchgears ensures installations safety through the experience of a world leader in the field of wind power.
Experience in wind farms
- More than 8200 transformer substations
- More than 450 collecting substations
- More than 10500 MW.
Advantages of the DVCAS range
- Maximum availability: service continuity
- Minimum width: < 600 mm
- Maximum safety conditions for staff personnel
- Environment insensitivity: SF6 insulation
- Certificates: IEC
- Approved quality: ISO 9001:2000
- Environmentally friendly: ISO 14001:2004
- Simple installation
- Economical.
- DVCAS switchgears have been specifically designed to meet all the needs of networks up to 36 kV, inside wind farms.
- These DVCAS switchgears can be installed in wind farms up to 2000 m over the sea level.
Have a question?Search our library of technical questions, videos, guides, and answers created by our support team. Find an answer
Looking for a distributor?A simple tool to locate easily your nearest Schneider Electric distributor Find your local distributor
Ready to order?Save time by starting your sales enquiry online and an expert will connect with you! Please follow the link below, and supply your details. Contact sales


text: This is the neighborhood where Jamie Lee Curtis had that tragic evening of babysitting in the 1978 John Carpenter movie, Halloween. The houses are located in the heart of Hollywood, right off Sunset Blvd. Unlike many of the neighborhoods in Hollywood, this one looks like middle America. The Myers house is not here. That is located in Pasadena, California.


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I am exhausted. Like...wowza...tired. I spent the week in Chicago hanging with my little brothers and dad while my mom visited my sister overseas. And let me tell you--I am NOT a mother, I do not have my own children but man, I LOVE my little brothers. They are 10 and so funny but man...they are sometimes a handful...and I am exhausted! I played pseudo mom--I made lunches, did carpool, was "cool big sister" at times and grouchy "evil big sister" at others...and bottom line is I am WIPED OUT. So this is my official ROUND OF APPLAUSE to any and every mother, father, aunt, uncle, friend, sibling, grandparent or godparent that has ever raised a child or children.
Sit down and have a glass of wine on me.
I'm applauding you from my couch.
Below is a picture of me and my two brothers after they WON their football game!!! Woooohoo!!!! Yes, I made a homemade "TEAM RAPIER" shirt for my dad and me...how freakin' handsome are my brothers? Sheesh. I love them....a lot.
Hugs & a wee bit of exhaustion :)


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Eddie came to work Monday and his co-workers asked him how his weekend was. He said he played a little golf. So his co-worker asked him how well he did.
"I hit two of my best balls," he said.
"Tell me about it," said his co-worker.
"I stepped on a rake."


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As a follow up to yesterday's post about GOING VIRAL having its Boston premiere at the Boston Theater Marathon, I just learned that REGULARLY SCHEDULED—a one-minute play I wrote as part of last year's 31 Plays in 31 Days challenge—will have its world premiere during the BTM's Warm-Up Laps on May 10th.
Suffice it to say that I will definitely be doing this year's 31 Plays in 31 Days. I wrote them because they made me laugh—I never imagined that so many would get staged (or published)!


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California's Highway 1 reveals adorable otters, friendly towns, and fabulous local flavors.
Photo creditPhoto: David H. Collier
Photo creditPhoto: David H. Collier
Photo creditPhoto: Christopher Chan/Monterey Bay Aquarium
Photo creditPhoto: David H. Collier
Photo creditPhoto: David H. Collier
Photo creditPhoto: David H. Collier
Photo creditPhoto: Philip Bird/Alamy
Late one day, as a sunset painted the ocean pink, I paused along a footpath in Point Lobos State Natural Reserve, south of Monterey, Calif. Standing on a bluff, I watched a sea lion loll in the shallows as a pair of otters backstroked through an eddy, clacking shellfish like castanets. They already knew what I'd been learning: This swath of the California coast isn't just a smorgasbord of beautiful sights and unexpected diversions. It's also a darned good place to eat.
I was at the tail end of a three-day road trip along Highway 1 from Moss Landing to Big Sur. The route is roughly 60 miles and can be driven in less than two hours, but I had set aside a long weekend to digest it all.
The bayside village of Moss Landing seemed a fitting place to start. Its tiny downtown is a draw for antique seekers, while its inland edges attract hikers and kayakers to Elkhorn Slough, an estuary, marine research center, and ecological reserve. I joined a long lunch line at Phil's Fish Market & Eatery, an iconic seafood joint with a patio that overlooks the beach and a menu of freshly caught items broiled, boiled, and battered. One table over, a family of four launched a group assault on a large bowl of cioppino. I slurped from a cup of red chowder, its peppery broth brimming with potatoes and clams.
A few minutes' drive away, a menu in the window of Moss Landing Café announced its status as the home of "world famous" deep-fried artichokes. Certainly, they were hearts with soul: earthy, bite-size, and coated in crispy, herb-flecked batter.
"Tarragon?" I asked Mark Couts, who has owned the café for 30 years, but he wasn't nibbling. "If I told you every little secret," he said, "it wouldn't be a secret anymore."
No mystery surrounds the main ingredient, which grows abundantly in nearby Castroville, a quiet farm town. As I pulled back onto the highway, the spiky plant spread out in neat green grids in the fields on either side. The day wasn't yet beachworthy, but the sky was clear and the morning's marine layer had begun to lift. Along the coast summer often feels only a breath away, even in winter.
Lunch hour had given way to happy hour by the time I pulled into Monterey, where a maritime past meets a mercantile present. At the waterfront, a crowd gathered around the bar for the specials at Sandbar & Grill, a locals' hangout in the literal sense: The building hangs off the side of Municipal Wharf No. 2. One taste of the sand dabs, panfried and splashed with lemon, and I understood why the place was packed.
"They get 'em right here in the bay," the barman, John Chezem, said of the fish, even if their price—just $6.95 for a happy-hour appetizer serving—suggested that they'd come from another place and time.
The next morning, I rose with the sun and found that Cannery Row had gotten up before me, a historic set piece stirring with the promise of saltwater taffy and souvenirs. Skirting the bustle, I walked along the Monterey Bay Coastal Recreation Trail. The paved pedestrian and bicycle path curves northwest along the water for about a mile to the next city. Pacific Grove may be overshadowed in fame by Monterey, but it remains unsurpassed in its sweet appeal, a salt-sprayed city of grand Victorian houses and a refuge for wintering monarch butterflies. At Holly's Lighthouse Café, a homey downtown haunt, a breakfast of blackberry pancakes was all the fuel I needed for the hike back to Monterey.
At the Monterey Bay Aquarium, a nonprofit showcase of nearly 200 marine exhibits, a regularly scheduled event was getting under way. Listed on the program as the Open Sea Feeding, it was more like a frenzy, a flashing spectacle of bluefin tuna, sharks, sardines, and other marine life in a ravenous display that called to mind an underwater fireworks show.
Those bluefin eat a lot of squid. And we humans eat a lot of bluefin—enough, anyway, to make the fish a no-no on the aquarium's Seafood Watch list, a program to raise awareness about sustainable fishing and farming. Albacore, an eco-conscious alternative, was offered instead at Cindy's Waterfront, the site's new restaurant, helmed by accomplished Napa Valley chef Cindy Pawlcyn. The grilled fish, the centerpiece of a tostada, was perched on a crispy tortilla with black beans, given a headdress of cabbage slaw, and spiked with chile heat.
Just southwest of Monterey and Pacific Grove lies an oasis of midcentury manses and Spanish-style villas: Pebble Beach, with its famous 17-Mile Drive, the name both factual and insufficient. On this serpentine private road, nearly every turnoff deserves a postcard. Yet nothing tops its panoramic view at Cypress Point Lookout or the pristine vistas from the beach opposite Bird Rock. There, a 1.5-mile dirt path led me along the sand and tide pools to Point Joe, which doomed early mariners who mistook its craggy elbows for the entrance to Monterey Bay.
Exiting 17-Mile Drive through the Carmel gate, I eased into Carmel-by-the-Sea, where shaded streets abundant in art galleries, day spas, and chic boutiques slope toward a white-sand beach. Carmel strives to keep the spirit of the village it once was: no streetlights, no addresses, no chain restaurants. There's even a law requiring a permit to eat ice cream on the street.
As its centennial approaches in 2016, the city has caught up with the culinary times. That's apparent at Carmel Bakery, which not only scoops ice cream but also turns out treats such as éclairs, shortbread, and sweet pretzels—flaky figure eights of pastry dusted with cinnamon and sugar. A vibrant restaurant scene stars newcomers like La Balena, where a rustic Italian menu includes wild mushroom risotto and ricotta gnocchi in hearty Bolognese sauce.
Carmel hosts the four-day GourmetFest, February 25 to 28 this year, to highlight the region's food and wine. Many of those local vintages pour year-round at more than a dozen tasting rooms clustered around downtown, in what amounts to a walkable urban wine trail. The oldest belongs to Jack Galante of Galante Vineyards, whose great-grandfather, J.F. Devendorf, was a founder of Carmel.
Galante grows his grapes in Carmel Valley, Carmel's sunnier, sleepier inland neighbor. Carmel Valley is also where chef Cal Stamenov gets much of the produce for Bernardus Lodge & Spa. As part of the luxe property's recent renovation, its formal restaurant, Marinus, morphed into Lucia, a more laid-back venue stripped of white tablecloths, with a terrace and a retractable roof. Stamenov puts his relaxed but sophisticated spin on contemporary dishes such as scallops Wellington with black truffle emulsion and chicken-fried quail with saffron-horseradish crème fraîche.
At Lucia, the menu also included abalone, a scrumptious mollusk that once thrived in local waters. A reminder of its place in California history came on the last day of my trip, during a hike around Point Lobos, the oldest marine reserve in the United States. Though one-third of the park lies beneath the Pacific, its headlands are laced with walking trails. I followed one to Whalers Cabin, now a museum. Its walls are lined with fishing and whaling implements as well as photos from the late 1800s, when the waters teemed with abalone.
The ribbon of Highway 1 that spools south from Point Lobos toward Big Sur is not a route to rush. Safety commands a leisurely pace, and so does the coastline, a necklace of coves and cliffs ornamented by such jewels as Julia Pfeiffer Burns State Park, where I pulled off for one last scenic stop.
Enough daylight remained to illuminate my short walk down Waterfall Overlook Trail, which faces McWay Falls, an 80-foot cascade spilling to a small beach. A squadron of pelicans winged by. Breaking formation, one of the birds dive-bombed for dinner. My belly rumbled. It was almost time to eat again.
This article was first published in Winter 2016. Some facts my have aged gracelessly. Please call ahead to verify information.


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As a social innovation specialist you would think that becoming an RSA fellow was right up my street. I mean on paper (well, screen) its a perfect fit. A group of people far more intelligent than I will ever be coming together to create solutions for the world. I would have the chance to learn, to grow, to connect and to create with others who could really do something to tackle the problems I love to solve. You know the ones. The really niggly ones that just get more complex the more you niggle them.
But something about an old institution left me flat, even to the point that I guiltily didn't chase up my offer of nomination. But after tonight I will chase it down. Hard.
I was invited to a "reboot" night, an informal night of mini talks introducing projects and speed networking that left the room buzzing. Not just nice and friendly buzzing. I mean the walls were literally reverberating long after the bells rang to call the session to a temporary halt while we heard from the next group of speakers.
The fellows are an extraordinary bunch. I didnt have a single conversation that left me thinking "how do I get out of this one". In fact, even with those with no obvious connection to explore I found myself determined to learn more about these fascinating individuals. Well travelled, well read, informed by the old, excited by the new. I left feeling that this was in no uncertain terms down to the organisers, most notably Roxanne Persaud, whose enthusiasm for those present to mingle and discover just how damn fine each other were, was infectious and welcome.
Which leaves me to wonder just how under the radar this event was. It seems that those present were not so much part of the hierarchy of RSA, but rather willing fellows who care enough to take a risk and do rather than stay safe and discuss. In short, my kind of people.
If this is the future of RSA, I commend you heartily. As a representative of a new generation of self organising, self motivated social innovators I feel duty bound to tell you that this is what we need.
If this is not the future of RSA, please let me know where I sign, so I can come on in and explain to you why all you very smart people are wrong.


text: Motorola recently announced the release of the TEAM Enterprise Wireless badge, a miniature push-to-talk (PTT) over WLAN voice communicator. This compact and lightweight device improves the productivity and efficiency of workers within your four walls. It is ideal for a wide range of employees, including retail, warehouse, maintenance staff and hospital workers. This video from Motorola gives an overview of the features and benefits offered by the new TEAM Badge.


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With Valentine's Day approaching, we thought it's about time we share our tips for places where you should go if you want to impress someone special. The chosen places offer a romantic atmosphere, nice food and friendly service - a combination that will surely do the trick -- whether it's Valentine's Day, an anniversary or another special occasion.
La Degustation If you want to get dressed up and indulge in some truly out-of-this-world cuisine, reserve a table at possibly the best dining place in Prague. The ambience is intimate, modern and elegant, featuring very soft lightning with a dark wooden decor, yet still keeps a sense of cheekiness and fun. The food is delicious, exciting, innovative and artistic. It's pricey but we think it's really worth a visit. Even if only for a lunch when the prices are significantly lower...
V Zatisi Here you will find a pleasant atmosphere with flying candles and great service; the menu is evenly as striking. We recommend the wonderful Bohemian degustation menu paired with great local wines. The restaurant has also prepared a special Valentine's menu. The charming houses and cobblestone streets around the restaurant invite you to wander aimlessly through the streets.
Divinis Wine BarWalk thorough the Old Town Square on a frosty evening and enjoy the night view of the Tyn Church, then walk into this wonderful place with eclectic, yet warm and inviting interior and taste excellent Northern Italian cuisine and top-notch wines. The kitchen is open until midnight, so if you wanna go to the opera first, this might be for you.
Aromi"Simplicity, tradition, passion" is the motto of this pleasant Italian restaurant. The interior has a warm, rustic feeling with dark wood floors and brickwork accents. The food is simple, yet delicious and the stuff very attentive and helpful.
SaSaZuWell, the atmosphere of this place is clubby and might not be exactly welcoming, but it's very stylish and we simply love this place's kitchen. The food with the authentic and exotic flavours of Vietnam, Cambodia, Indonesia is served in small portions in the middle of the table. Can it get more romantic than serving each other colorful dishes that will definitely bring a smile to your faces?
We also have some tips for those on a budget:
Al CafeteroThis small, non-smoking, family run café with a wonderful atmosphere is truly a "coffee-lover's" paradise. Reserve a place on the couch, try unique coffee-making procedures such as the vacuum pot and savor home-made cakes. We promise, your Valentine will love it.
Vinograf This wine bar and cellar that focuses on Czech/Moravian wines has a comfortable, cosy, intimate atmosphere. The food selection is short but the wine range fully makes up for it. Sip on wine and share a plate of local cheeses while enjoying the company of your significant other.
Of course, this list is not exhaustive. However, when it comes to a special occasion, not just any place will do. Therefore, we've chosen the ones we like. They all have an excellent food or drink menu in addition to a special romantic ambiance. Don't forget to make reservations asap if you're planning a Valentine's Day dinner!


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Brennan Center President Michael Waldman issued a statement decrying Pres. Trump's approval of the release of a House Republican memo on the FBI investigation into his campaign.
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Redemption or Renaissance?
Guest: Cole Campbell, Dean of the Donald W. Reynolds School of Journalism, University of Nevada - Reno In between the second and third presidential debates, there was a flurry of blogosphere-driven chatter about a suspicious bulge in President Bush's suit coat during the second debate. A photo showing telltale shadows on the president's back was blown up, analyzed, explained away by the White House tailor, speculated about by everyone else drawn to the idea of conspiracy. Was this some device by which the president's handlers -- presumably people smarter than him, or at least with better syntax -- could coach the president to a more palatable performance in the debate? Was this whole contretemps a clever ruse by White House insiders to divert public discussion from substantive matters of war, jobs, the environment and schooling? What gives speculation over a shadow on a jacket such resonance -- besides our national appetite for conspiracy theories -- is that it fits with what we know about the deterioration of public discourse. Candidates are not free to speak their minds, bare their souls or open their hearts. They are assigned -- by handlers, pollsters, pundits, press commentators and others -- two specific roles: Consolidate and mobilize their base of supporters, and persuade as many undecided voters to align with them. Vision is reduced to a memorable metaphor -- President Reagan's "morning in America," President Clinton's "bridge to the future." So however disappointing it may be that the final presidential debate was reduced to redundant mantras and rhetorical semaphore signals, it's not surprising. It's the embodiment of a cynical kind of pragmatism. This is what the political elite knows from experience moves poll numbers and shifts momentum in the days leading up to balloting. What we need is a return to the older, nobler pragmatism -- the kind Rich encounters on Wisconsin public radio, in conversations with community leaders, in reflecting on community desires in a place like Las Vegas. This pragmatism is a search for solutions to real public problems, not a search for competitive advantage in an electoral contest. We can blame the candidates, and hope they can redeem themselves, or we can accept responsibility to use our own work, our own professions, our own institutions to reclaim public discourse. That's what Rich is doing through the work of the Harwood Institute -- and even through this blog. Are the rest of us doing the same? It's not two politicians who need redemption, but a system of political conversation and decision-making that needs to be reborn. The shadow we need to worry about is not on candidates' clothing but on our own political culture.


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ANZAC Kokoda Track - Doc's Wrap
- Published in AdventureFit Blog
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So, here we were. Landed in the (not so) far away land of Papua New Guinea, in the infamous city of Port Moresby, we nervously pack our gear with our new best friends and lifelines in our Papua New Guinean boys. The banter level is relatively low. New scenery, new people, a few familiar faces but the realisation of what we were about to take part in was looming large over everyones psyche. No matter what we did we couldn't escape the fact we were about to chalenge ourselves in a way not many people have done before. Fortunately for us we were able to take part in this challenge of our own accord, rather than some of the unfortunate men that went before us.
For those who aren't aware, the Kokoda Track is a 96km strecth of land that runs across Papua New Guinea's Owen Stanley Range all the way from the capital of Port Moresby to the small village of Kokoda. The signifigance of such a track is that there was a very important WW2 battle waged through this steep, muddy, wet thouroughfare between Allied, primarily Australian and Japanese military troops in 1942. The Japanese who had invaded, very successfully for the most part, many other destinations in the Pacific, had planned to take Port Moresby to provide them with what would be a perfect springboard for a base to launch a military invasion of mainland Austraia. Many lives were lost in this epic battle between the two forces as I will discuss in some more detail later in this blog. Now, the Kokoda Track itself serves as right of passage for Australian's, New Zealander's and others to pay homage to what our troops went through in order to keep Australia and our population safe.
And we were just such a group ready to take it on. Doc, Roysy, Coro, Rakey, Em, Mac & Perri. We made a good team. Add to the fold our amazing local team, headed by Clement (Clemmo) and my porter Ivan we were in good hands. Ivan himself had crossed the track "70 or something times mate", "yes mate, 70 plus" but Clemmo had him well covered crossing the track on triple digit occasions. Add to that, the personal porters the rest of the guys had and our food porters and chefs and we had a 19 person strong squad.
So after packing our bags, getting ourself briefed and getting in what was looked at as the final supper down at the amazing Port Moresby Yacht Club we were awoken much too early for all of our likings to jump in the bus and head down to Owen's Corner to begin our trek. There are two different ways you can attack the Kokoda Track. One is to start from Owen's Corner and head towards Kokoda and the other is to start at Kokoda and head back. We were startinfg from Owen's Corner.
So here we were at Owen's Corner, overlooking the amazingly lush, forests of the area and taking some last minute photographs and we were away. "How many hours today Clemmo" somebody asked as we set off......"Today is a nice one mate, an easy one, yes mate, today is 5 hours"......An easy one you say Clemmo? 5hrs is an easy one.
As we took off and began to walk we were fashioned walking sticks by the boys, straight from the jungle to assist in the walking as it's an absolute nightmare walking the muddy hills of the area without assissatance. So now the game was on. Who would be first? We were all placing bets on who would be the first to go and sure enough, it took no more than 5 mintes and the first of us, Emily was down. "White hawk down, white hawk down" yelled Gary, Corey's porter. And then another went down. "White hawk down, white hawk down". And then another. It felt as if no one could string more than three or four steps together without down and then, THUD. Another. But this time it was not 'white hawk down', it was Gary, Corey's legendary porter who had taken a spill. Everyone was in shock. Everyone was thinking 'well if these guys have walked this thing hundreds of times and they can't even hold their feet then what hope are we'.
And then someone said it. "BLACK HAWK DOWN, BLACK HAWK DOWN"! The crowds burst into raucious fit of laughter. And we were mates. It was the perfect ice breaker.
So after a long slog up and down some serious inclines we got to camp at Ua'Ule Creek. Muddy, sweaty, tired and hungry we arrived at camp. As the gang helped show us around we were lead down to the local watering hole where we could wash our clothes and ourselves in some of the most refreshing water known to man. One of the highlights of the whole trip was the fact that we got to finish every single day with a swim in a local river like this. It was one of lifes simple pleasures. It makes you realise that nature is perfect in every way and the bullshit we have built around it is sometimes quite sad to think of what we are losing. Anyhow, an amazing first day of hiking was in the books.
Day two started off slow....I guess we weren't really used to pushing our bodies to the extreme like we did on day one so getting out of our nice warm sleeping bags was always going to a little bit of a struggle. A quick brush of the teeth, some porridge mixed with cereal from our ration packs and we were off on the road again. Another short day today to really give us a false sense of what we were in for got us in by a decent hour and to Ofi Creek for the night. Ofi Creek was a beautiful little village along the track where the children played and the adult came to sell their local foods and drinks to weary travellers. Ofi Creek was another highlight for it was the first night we began to get into our campfire stories with Clemmo. A historian of the track Clemmo was able to regale us in the stories of the heroes and brave soldiers that fought in what a lot of war historians call the 'worst conditions man has faced in the field of battle'. This became a regular staple of our nights from this day forward.
And the trek went on. We pushed through our first big day on day threee with aplomb. Things even seemed to be going pretty smoothly, that was unil we reached 'the wall'......
Aptly named, the wall was a long strecth of near straight up hill climbing for hours on end. It was one of those times where you thought you eyes were failing you. At so many point throughout this day it was almost like you could see the top only to reach what you thought was the top to look up and see a brand new wall staring you right in the face. But step after step we climbed. And we climbed some more. It's times like these where we gain another instinct. A feeling without speaking kind of skill where you are talking to your mates, spurring them on, getting them through it as they are to you. But all without words. There is an energy in the air that is palpable. An energy that cannot be summed up succinctly without someone being there with you. Working hard and battling through things together is known to bring us closer. And that's what today was for us. We were under no illusions that we were doing this in a much easier and nicer fashion than the military troops that did it before us. So we knew it they could do it carrying their own bags, malnurished, exhausted and under attack then we could do it too. And just like those who went before us we were going to do it as a team.
This is the kinda stuff you dream of.
Once the wall was past us we were able to rest and enjoy each others company once more knowing that we had just worked through one of the most gruelling days on the track. And whatever came up against over the coming days we were going to be ready for it.
And then the rains came. We'd been getting wet for a good period each day so far but it started to become blatently obvious that we were in it up to our necks on this partilcuar day, but the best thing about it was. Nobody cared. There was not a poncho or a jacket in sight. Here we were, a team of mates, working hard together, sweating it out through the mud, with rain pelting down on us and we couldn't be happier. The levels of banter were probably reaching an all time high in fact. The level of adventure had been raised and so had the spirits. And so we reached Brigade Hill and kicked on to our home for the night.
The next day was filled with another new adventure entirely. Mud. Just when you thought you'd seen it all we are blessed with a strecth of the track that seemed never ending whilke trudging through the shin deep mud. But again. It was an epic adventure. Add to that the waist high water we battled in the river crossings this day and we were really starting to get through the track.
A few more days passed by on the track and although they were amazing they were also semi-uneventful. It was just consistent beautry of nature and great chats with great friends day after day. The biggest highlights you might say may have been the micro-marketplace that had been established each night when we would sit and swap out way through our ration packs. Emily would die for a LeSnak while I would give my left leg for a jelly cup. Mac seems to love to hoard the chicken in a can and everyone had their own little favourites. It was more like a game of Monoploy that a simple barter session with all involved trying to be Scrooge McDuck and find themselves owner of a monopology on Mayfair and Park Lane. Or in this case the tuna with biscuits and barbeque chips (or crisps if that's what you know them as).
As the days passed it was amazing what we learnt from Clemmo and the gang about the history of the battles that were fought along the track. They were the grandest type of horror for both parties to endure and no battle was more famous than the Battle Of Isurava. Many Australian's and Japanese troups were killed during this 5 day battle and once we reached Isurava we could tell we swere standing on a place of much signifigance. To hear the stories day after day after day of what went on during this battle really affects you. You begin to understand how lucky you are.
But we were beginning to realise we were coming to the end of our trip and although we were beat up mentally and physically we weren't wanting the trip to end. Loved ones aside who really wants to go back to Facebook, Instagram, billboard, phonecalls, emails and all the other bullshit that we fill our lives with. The simple life is truly where it is at. Good challenges, good conversation and good people is all we had and all you need.
The last evening was something special. Unfortunately for the rest of the group the incident that is for sure one of the highlights of my life was only shared by myself and Matt. But I will share it anwyay.
So as we came to camp on the last night of the trek we arrived in the dark. In fact we had to switch out headlamps on as we were walking in the dark for much of the last part of the day. As we arrived, headlamps on, absolutely exhausted to our final nights resting place we could hear something? It sounds very angelic but also very far away. As we walked through the dark camp we realised we were listening to a choir. The church choir was singing in candlelight in the middle of the village. We stood in amazement while we listened to the local children sing their songs under the starlit night. When they finished we all started cheering and they all started giggling. But it didn't ene there. Once the singing was over the rest of the crew walked off our huts while Matt and I stood around chatting and taking pictures. A few minutes later we turned around and we saw a sea of 100 or so children walking towards us. The village pastor then approached Matt & I and asked if the kids could come down after dinner and sing to us, to which we both accepted of course. But what happened next was the killer. As we were about to leave Matt & I put our hands in the air for a HI-5 from a few of the kids and then what happened was insane. The kids all starting giggling and stirring and pushing through each other to get to our hands to HI-5 us. The energy was insane. Everyone started laughing, then everyone started screaming and then I started dancing, so everyone started dancing! It was one of those 'had to be there moments' but a moment Matt & that we will never ever forget.
So then it was our final day. A few hours left of chats, a swim in one final stream, a couple of hours of pretty flat, pretty stright walking and we were done. We'd reached Kokoda. We congratulated ourselves, thanked the amazing boys who we couldn't have done it without and then we headed to Clemmo's mums place to enjoy a few well earned beers. What an adventure.
The next days were filled with much relaxing and capped off by a trip to the Bomana War Cememtary for the dawn service on ANZAC day. An amazing way to cap the trip and another highlight we will never forget.
So this is my wrap. Thanks if you made it all the way through and hopefully you reading this has the chance to share in this epic adventure at some point of your life too.
Cheers, Doc.
We have another Kokdoa adventure coming up in 2018. If you want informnation please fill in the box below.


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Turn Stress & Stuggle Into Joy, Vitality & Money - Tip 1
YES! Good for you that you've made the decision to take charge of STRESS and transform it into more joy, energy and FREEDOM!
I'm so happy you'll be joining me in this enlightening, inspiring and motivating audio course "7 ½ Tips to Turn Stress into JOY."
Each session is short (about 5 minutes) and has an action step that reinforces what you're learning AND supports you to do something new – which is how we transform STRESS into JOY.
Are you ready to get started?
Here is Tip 1
P.S. I recommend doing the action step right after you listen to each session. That way, by the end of the course, you'll have all the steps in place and FEELING energized and in charge!
P.P.S. Here's what's coming next
Tip 2 – The Two Minute Miracle
Tip 3 – Yes, Stress Can Make You Fat
If you'd like to listen to the tips again here's a link that has all of them listed.
I would love to hear how these tips touched you so please feel free to email me at firstname.lastname@example.com
Lots of JOY & Blessings,
The Health, Wealth & Happiness Coach for Women in Business


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Accumulating evidence indicates that platelets play a critical role in the pathogenesis of experimental severe malaria (ESM) elicited by infection with Plasmodium berghei. Mice injected on day 1 of P berghei infection (early) with either anti-CD41 or anti-CD61 monoclonal antibodies (mAbs) exhibited significantly (P < .001) increased survival from ESM compared with infection controls, indicating that platelets function early in the disease. In contrast, groups of mice treated on days 4, 5, and 6 (late) with anti-CD41 mAb exhibited similar mortality as controls. Because platelet depletion by anti-CD41 mAb on day 4 of infection did not protect mice, and platelet adherence occurs on day 6, platelet adherence to endothelium is not required to mediate malarial pathogenesis. Few platelet microparticles were detected in the blood during the course of malaria, but large numbers of erythrocyte vesicles, microparticles, and debris were detected. The protective effect of early anti-CD41 mAb treatment was independent of the number of platelets, platelet microparticles, erythrocyte-platelet conjugates, and erythrocyte vesicles. Mice treated early with anti-CD41 mAb exhibited markedly altered cytokine production on day 4 of P berghei infection (increased interleukin 10 [IL-10], IL-1α, IL-6, interferon-γ [IFN-γ], and tumor necrosis factor α [TNF-α]; decreased IL-2) but no decline in coagulation factors compared with rat immunoglobulin G (IgG)–treated controls, indicating that platelets regulate the levels of pathogenic cytokines.
One of the hallmarks of cerebral malaria, which is caused by infection with Plasmodium falciparum, is petechial hemorrhaging into the brain, indicating that platelets may play a crucial role in malarial pathogenesis.1 Clinical studies of patients with P falciparum indicate a marked procoagulant state with consumption of clotting factors, the presence of fibrin dimers, and decreased levels of the anticoagulants protein C and S2-4; the procoagulant state correlates with the development of severe malaria. Grau and colleagues5 have proposed that platelet activation and adherence contributes to the development of severe malaria. Patients with severe falciparum malaria exhibit profound thrombocytopenia, and platelet accumulation in the brains of children who have succumbed to severe falciparum malaria is significantly higher than platelet accumulation in the brains of patients who died from other coma complications.6-9
These clinical results in humans with malaria provide the impetus for parallel mechanistic studies in animal models. Extrapolation of results from mouse models of severe malaria must be cautious because the P falciparum species of the malarial parasite cannot be used in rodent models of severe malaria because they do not replicate in mouse erythrocytes, and there are also differences between rodents and humans. Nevertheless, direct evidence for the importance of platelets in malarial pathogenesis has come from the P berghei model of severe malaria.10,11
CD41/CD61 (αIIb/β3 integrin heterodimer, also known as gpIIb/IIIa) is an important molecule in platelet biology and its major function is contributing to expansion of clot formation and platelet adhesion to the microvasculature.12-14 Our previous studies indicate that platelet adhesion during experimental severe malaria (ESM) occurs primarily in venules within the pial microvasculature and that CD41 plays an important role in this platelet adhesion.15 We therefore determined whether treatment with anti-CD41 or anti-CD61 monoclonal antibody (mAb) functions early or late in mediating protection against ESM, and what effect anti-CD41 mAb has on (1) platelet numbers, (2) platelet microparticle and erythrocyte vesicle formation, (3) the developing immune response, and (4) malarial coagulopathy. Early treatment with the mAb occurs just after infection, whereas late treatment corresponds to parasitemia being readily detectable (0.5%-5%) in blood. The early treatment corresponds to prophylaxis and the late time points corresponds to when a patient infected with P falciparum might present at the clinic, up to the development of severe complications. We elected to perform our studies in the P berghei model of ESM rather than the P yoelii model because P berghei–infected mice exhibit (1) a marked systemic inflammatory response, (2) profound thrombocytopenia, and (3) obtundation.16,17
Materials and methods
Infection and treatment of mice
Plasmodium berghei ANKA was stored as a frozen stabilate and this stabilate was injected into source mice to generate an inoculum for the experiments. The experimental C57BL/6 female mice were obtained at 4 to 5 weeks of age from Harlan (Indiapolis, IN) or Jackson Laboratories (Bar Harbor, ME) and injected with 1 × 106 P berghei parasitized erythrocytes when they were between 6 and 10 weeks of age. The animals were housed in microisolator cages and provided food and water ad libitum. Parasitemia was assessed by counting the number of infected erythrocytes among 200 and 1000 erythrocytes in Giemsa-stained thin blood films. The institutional animal use committees of Louisiana State University Health Sciences Center, Targeted Molecules Corporation, and La Jolla Bioengineering Institute approved all procedures. Anti-CD41 mAb (clone MwReg30), anti-CD61 (clone 2C9.G2), and anti-Ter119 (Ly-76; clone Ter119) were purchased from Becton Dickinson (San Diego, CA).
Flow cytometry
Flow cytometry and determination of cell number was performed essentially as described previously.18,19 Briefly, the tail was pricked with a lancet and 2 μL blood was immediately transferred to 40 μL of citrate solution (Sigma, St Louis, MO) to prevent coagulation. All incubations were performed at room temperature. Anti-CD41 mAb conjugated with fluorescein isothiocyanate (FITC) and anti-CD61 conjugated with phycoerythrin (PE) were added to the blood and incubated together for 15 minutes. In selected experiments, anti-Ter119 mAb conjugated with PE-cyanin5 (PE-Cy5) was added to label erythrocytes. Cells were resuspended in 1 mL phosphate-buffered saline (PBS), and then the cells were analyzed on a FACSCalibur (Becton Dickinson, San Diego, CA). Data acquisition was performed using the CellQuest program (Becton Dickinson) on at least 5000 cells with size (forward scatter) and granularity (side scatter) of platelets. The data were analyzed using the Attractors program (Becton Dickinson). Propidium iodide (5 μg/mL) was added to selected samples to exclude permeable cell debris. For the first 3 experiments, Tru-count beads and tubes were used from Becton Dickinson for cell counting.18 In other experiments, Spherotech beads (Libertyville, IL) were used. The beads are easily distinguished from cells based on their unique forward- and side-scatter and fluorescence in all 3 channels. They are indicated in the flow cytometry figures. The number of cells was calculated using the following formula: No. of cells/μL = No. of positive events × bead count/test no. of beads collected sample volume (μL).
Cytokine protein and coagulation factor analysis
Blood (400 μL) was obtained from the retro-orbital plexus from anesthetized mice via heparinized capillary tubes and bled into collection tubes containing EDTA (ethylenediaminetetraacetic acid; Becton Dickinson). The blood samples were centrifuged at 500g to obtain plasma, which was frozen and stored at –80°C. Plasma (25 μL; 3 replicates) was analyzed in a modified enzyme-linked immunosorbent assay (ELISA) using Luminex beads (Luminex, Austin, TX) for levels of selected cytokine and coagulation factor protein. The cytokines analyzed in this multiplex assay were: IFN-γ, TNF-α, IL-1α, -1β, -2, -4, -5, -6, -7, -10, -12p70, -17, and -18. The coagulation factors analyzed were: fibrinogen, factor VII (fVII), tissue factor, and von Willebrand factor (VWF).
Statistical analysis
Analysis of variance (ANOVA) with the Statview program (SAS Institute, Cary, NC) with Fisher post-hoc test was performed to statistically compare all measurements with a P value cut-off of .05. The mean and standard deviation of the results are reported in the text and figures. The survival times are compared with nonparametric log rank test with a P value cut-off of .05.
P berghei infection of mice is a very reproducible model of cerebral malaria with C57BL/6 infected mice usually succumbing between day 6 and day 8 of infection. Moribund mice exhibit obtundation, marked weight loss, rapid breathing, and minimal responses to neurologic tests (such as righting and gripping responses). Mice exhibiting these clinical signs die hours later. Mice surviving beyond day 12 of P berghei infection develop hyperparasitemia and die after day 20 of infection from anemia, and they do not exhibit impaired neurologic tests. Thus, day 12 of infection is considered by most investigators to be the last time point when the mice will develop cerebral malaria and is the rationale for terminating our experiments assessing the pathogenic mechanisms of cerebral malaria at this time point.20
Either anti-CD41 or anti-CD61 mAb injected on day 1 of P berghei infection protects against the development of ESM
To determine whether either anti-CD41 mAb or anti-CD61 mAb treatment protects against the development of severe experimental malaria, we injected groups of 8 to 10 mice intraperitoneally with 106 parasitized erythrocytes and then injected 0.1 mg antibody intraperitoneally on day 1 of infection when parasites were not detectable in the Giemsa-stained thin blood films. Only 1 of 8 mice treated with anti-CD41 mAb on day 1 of infection succumbed between day 6 and day 12 of infection, whereas all control mice injected with PBS died by day 8 of infection (Figure 1A). The difference in survival between anti-CD41 mAb–treated mice and controls was significant (P = .0002).
Mice treated with anti-CD61 mAb on day 1 of P berghei infection exhibited a significantly (P = .0007) increased survival compared with rat IgG–injected controls (Figure 1C). In fact, 5 of 10 mice survived beyond day 12 of infection (Figure 1C). We have previously reported that there is no difference in parasitemia or survival between PBS-injected mice and rat IgG–injected mice, so both groups of mice are appropriate infection controls.21,22 The similar parasitemia in anti-CD41 mAb–injected mice and PBS-injected controls (Figure 1B) as well as in the anti-CD61 mAb–injected mice and rat IgG–injected controls indicates that protection against the development of severe experimental malaria by these mAbs cannot be attributed to altered replication of the parasite or inadequate infection (Figure 1B,D). Rather, the effects of the host response to the parasite determine whether the animal develops severe malaria.
To determine the effects of anti-CD41 mAb and anti-CD61 mAb on platelet number, we assessed the number of platelets during the course of P berghei malaria in all mice by flow cytometry using only 2 μL blood from the tail vein. This low volume of blood meant that our assay method had a minimal effect on the course of the disease (stress or anemia). Platelets have a distinct forward scatter (measure of size) and side scatter (measure of granularity) being smaller and less granular than erythrocytes and leukocytes. However, some cell debris may also fall within this platelet region, which was excluded by propidium iodide (PI) labeling. The flow cytometric analysis encompassed only cells within the platelet region defined by forward and side scatter. The flow cytometric analysis of all groups of mice indicated there were few, if any, platelets that were single positive for CD41 or CD61 only (< 0.1%). In uninfected controls, the majority of cells within the platelet region were CD41+CD61+ (95% ± 1%) with few CD41–CD61– cells (5% ± 1%). Treatment with either anti-CD41 mAb or anti-CD61 mAb resulted in a marked decrease in the number of circulating CD41+CD61+ platelets on day 4 of P berghei infection compared with infection controls (Figure 2). In the platelet region, CD41–CD61– cells were detected in all groups of P berghei–infected mice (Figure 2), and the number of CD41–CD61– cells increased modestly with infection. On day 4 of P berghei infection, there were few if any detectable CD61+CD41– or CD41+CD61– cells (< 0.1%) in anti-CD41 mAb–, or anti-CD61 mAb–treated mice and infection control mice. Thus, antibody masking of its epitope cannot explain the lower platelet detection after treatment with either anti-CD41 or anti-CD61 mAb because the anti-CD41 and anti-CD61 mAbs recognize distinct epitopes and we detected few CD61+CD41– cells in the anti-CD41 mAb–treated mice and few CD41+CD61– cells in the anti-CD61 mAb–treated mice.
Late (therapeutic) treatment with anti-CD41 does not protect against the development of severe experimental malaria
Because early (prophylactic) treatment with anti-CD41 mAb protected mice against the severe malarial pathogenesis, we next determined whether late (therapeutic) anti-CD41 mAb treatment had a similar capacity to protect against malarial pathogenesis. Similar to the above results of the early treatment with anti-CD41 mAb (Figure 1), mice (n = 10) injected with anti-CD41 mAb on day 1 were protected (Figure 3A). In contrast, mice (n = 10) injected intraperitoneally with 0.1 mg anti-CD41 mAb on day 4, 5, or 6 of infection did not exhibit significant protection from severe malarial pathogenesis compared with infected controls. The late treatment (day 4 only) versus early treatment (day 1) with anti-CD41 mAb was repeated twice with similar results. We did not test late depletion with anti-CD61 mAb because both antibodies depleted platelets to a similar extent (Figure 2); thus, testing late administration of anti-CD61 was unlikely to provide additional information. Mice treated early or late with anti-CD41 mAb and control mice injected with rat IgG all exhibited similar levels of parasitemia (Figure 3B), indicating that differences in parasite replication or infection of mice were not causing the marked differences in survival.
To verify that the intraperitoneal injections of anti-CD41 mAb on day 4, 5, and 6 of P berghei infection had similar effects on the circulating platelet count as injection on day 1, 2 μL blood was obtained from the tail vein of each of the mice in the groups of mice on day 6 of P berghei infection and then analyzed by flow cytometry. P berghei–infected control mice exhibited a profound thrombocytopenia on day 6 of infection compared with uninfected controls (Figure 4). The number of CD41–CD61– cells in the platelet region remained relatively the same across the different treatment groups and increased modestly during the course of P berghei infection. Mice injected with anti-CD41 mAb on day 1, 4, 5, or 6 of P berghei infection had few CD41+CD61+ platelets detectable by flow cytometry. A comparison of the numbers of cells in (1) protected mice treated with anti-CD41 mAb on day 1 of infection, (2) susceptible mice treated with anti-CD41 mAb on day 4, 5, or 6 of P berghei infection, and (3) susceptible controls showed similar numbers of CD41–CD61–; CD41+CD61–; or CD41–CD61+ cells in all groups of mice on day 6 of P berghei infection (Figure 4). The numbers of CD41+CD61+ platelets were slightly higher in protected mice treated with anti-CD41 mAb (39 734 ± 33 317) on day 1 of P berghei infection compared with susceptible mice treated with anti-CD41 mAb on day 4, 5, or 6 (day 4: 2042 ± 1580; day 5: 2391 ± 1836; day 6: 3803 ± 2976) but lower than the susceptible infection controls (127 274 ± 139 274).
Flow cytometric analysis of platelets during P berghei malaria
Because we had detected by flow cytometric analysis of blood from mice on day 6 of P berghei infection large numbers of CD41–CD61– PI– cells in the platelet region, we next determined whether these CD41–CD61– cells represented platelets, erythrocyte vesicles, or cell debris. To determine whether CD41–CD61– cells were viable cells, we labeled blood cells in a group of 10 mice on day 6 of P berghei infection with a vital dye fluorescein diacetate. The CD41–CD61– cells all labeled positively with fluorescein after 10 minutes of incubation (Figure 5A-B) but they did not label with propidium iodide. These data indicate CD41–CD61– cells contained active esterases in their cytosol to render the fluorescein diacetate fluorescent, but exhibited intact membranes to prevent propidium iodide from entering.
To determine whether CD41–CD61– cells represented erythrocyte ghosts that have formed vesicles, we analyzed the blood of mice by flow cytometry during the course of P berghei malaria in 5 infected mice and 5 uninfected controls by using anti-CD41 (platelets) and anti-Ter119 (erythrocyte) mAbs. The parasitemia on day 4 was 2.6% ± 0.9% and on day 6 was 8.8% ± 2.9%, and all 5 infected mice became moribund on day 7 of P berghei infection. The Attractor program was used to perform subset analysis. Cells with the distinct forward scatter and side scatter of platelets were within the orange platelet region (Figure 6A,C). The level of surface CD41 and Ter119 labeling on cells was used to define subsets within the platelet set (Figure 6B,D) and each subset was color coded so the forward and side scatter of these cell populations was apparent. Virtually all the CD41– cells in both the infected and uninfected mice labeled with anti-Ter119 mAb, indicating these cells within the platelet region were of erythrocyte origin (Figure 6A-B). Anti-CD41 mAb–treated mice infected with P berghei exhibited only the CD41–Ter119+ cell population (not shown). Pattanapanyasat et al23 have termed these Ter119+ events in the platelet region as erythrocyte vesicles, and these vesicles are larger and exhibit greater granularity than microparticles.
Platelet microparticles have been reported by Piguet et al24 to be present in high numbers in the platelet-rich plasma of mice infected with P berghei. In our analysis of whole blood from animals infected with P berghei, most (89% ± 2%) of the microparticles exhibited surface Ter119 protein whereas few (0.4% ± 0.2%) exhibited surface CD41 protein (Table 1). The ratio of CD41+ platelets to CD41+ microparticles when the animals were moribund from P berghei malaria was about 20:1 in our analysis compared with about 1:4 in Piguet's analysis, indicating a greater creation of platelet microparticles in platelet-rich plasma of infected mice than in whole blood.
The platelet microparticles exhibited similar forward scatter during the course of P berghei malaria (uninfected: 2.9 ± 0.1; day 4: 3.0 ± 0.1; day 6: 2.8 ± 0.1) but levels of surface CD41 on the microparticles declined about 25% from 80 ± 6 mean fluorescence intensity (MFI) in uninfected mice to 60 ± 2 on day 6 of P berghei infection. In uninfected control animals, platelet microparticles exhibited significantly (P < .0001) less surface CD41 than intact platelets (0.5-fold: microparticles: 80 ± 2; platelets: 175 ± 21). The intact platelets increased significantly in forward scatter (size) during the course of P berghei malaria (uninfected: 16.2 ± 1.9; day 4: 19.2 ± 2.1; day 6: 40.6 ± 3.4; P = .04 for comparison of day 4 with uninfected and P < .0001 for comparison of day 6 with uninfected) but their levels of surface CD41 were constant.
To assess platelet erythrocyte conjugate formation during the course of P berghei infection, we assessed the number of CD41+ (platelet) and Ter119+ (erythrocyte) events by flow cytometry analysis on data obtained from the infected mice and uninfected controls described above (Figure 6). The percentage of platelets forming platelet and erythrocyte conjugates (CD41+Ter119+ cells) was similar in uninfected controls at each of the time points and to day 0 controls just prior to infection, indicating there was no significant day-to-day variability in the assay. However, the percentage of CD41+ cells forming erythrocyte-platelet conjugates increased significantly (P < .0001) from 8.6% ± 2.5% in uninfected controls (day 0) to 36% ± 5% in infected mice on day 6 of P berghei malaria (Table 1). In contrast to the increase in percentage of platelets forming conjugates with intact erythrocytes, the actual number of platelet-erythrocyte conjugates decreased significantly (P = .04) in infected mice on day 6 of P berghei malaria compared with uninfected controls (Table 1), and this decline in the number of conjugates reflects the profound decrease in the number of circulating platelets on day 6 of P berghei malaria.
Levels of blood cytokines but not coagulation factors are altered after anti-CD41 mAb treatment on day 1 of P berghei infection
Because the anti-CD41 mAb treatment was functioning early in P berghei infection to protect mice, we determined whether the presence or absence of platelets altered the inflammatory response or coagulopathy by assessing the levels of selected cytokines and coagulation factors in the blood of mice on day 4 of infection. The mice treated with anti-CD41 mAb on day 1 of P berghei infection exhibited similar parasitemia on day 4 of infection as the rat IgG–injected control mice (2.0% ± 0.4% and 1.3% ± 0.9%, respectively), indicating both groups of mice were appropriately infected. The number of CD41+ platelets was 10 074 ± 1949 per μL blood for anti-CD41 mAb–treated mice, 591 129 ± 376 921 for rat IgG–treated controls, and 731 254 ± 328 765 for uninfected mice, indicating that anti-CD41 mAb on day 1 had depleted platelets. The anti-inflammatory, protective cytokine IL-10 increased (2-fold) and the inflammatory, pathogenic cytokine IL-2 decreased (about 5-fold) in anti-CD41 mAb–treated mice compared with rat IgG–injected controls (Table 2). The inflammatory cytokines IFN-γ, IL-1α, TNF-α, and IL-6 were all increased in anti-CD41 mAb–treated mice compared with rat IgG–treated controls (Table 2). The cytokines IL-1β, -5, -7, -12p70, -17, and -18 were similar on day 4 of P berghei infection in rat IgG–injected mice, uninfected controls, and anti-CD41 mAb–treated mice. The coagulation factors fVII, tissue factor, and VWF were similar in all 3 groups of mice. The fibrinogen levels were significantly increased in the anti-CD41 mAb–treated mice compared with rat IgG–injected controls (Table 2).
The platelet adhesion hypothesis proposes that platelets function late in the disease by adhering to activated endothelial cells in the brain and lung, which then signal the endothelial cells to loosen their intracellular junctions or become more sensitive to apoptosis signaling by TNF; this process leads to increased vascular leak and then hemorrhage.11 Radiolabeled platelet studies, immunohistochemical analysis with anti-CD41, and intravital microscopic analysis of fluorescence labeled platelets all indicate that platelets accumulate in the brain late in the disease when the animals become moribund.5,15 In contrast to stroke and atherosclerosis, platelets roll and adhere primarily late in the P berghei infection to pial venules but not to the arterioles. ICAM-1, P-selectin (both platelet and endothelial), and anti-CD41 are required for platelet adhesion to pial microvasculature during experimental malaria, and mice lacking ICAM-1 or P-selectin are significantly protected from malarial pathogenesis.15,25,26 Massberg et al27 and Frenette et al28 report that P-selectin is critical for platelet adhesion during ischemia/reperfusion injury, a condition that also causes inflammation and platelet adherence in venules; this observation suggests that platelet adhesion via P-selectin is a conserved and important platelet adhesion molecule during diseases that elicit an inflammatory response.
A prediction of the platelet adhesion hypothesis is that removal of the platelets (either early or late) should protect mice from severe P berghei malaria. Mice treated early in the infection with antiplatelet serum or with anti-CD41 and anti-CD61 mAbs are protected from developing severe experimental malaria.5,29 Both the anti-CD41 mAb and the anti-CD61 mAb rapidly depleted platelets from the circulation so that few circulating platelets are detected 30 minutes after injection of the antibodies. The level of protection conferred by anti-CD41 mAb appeared to be greater than that of the anti-CD61 mAb (Figure 1). One possible explanation is interexperimental variation caused by using different parasite inocula or mice. However, we had included a group of 5 anti-CD41 mAb–treated mice in this anti-CD61 mAb experiment and only 1 of 5 mice injected with anti-CD41 mAb became moribund. A more likely explanation is that the level of platelet depletion on day 4 of P berghei infection is lower in the anti-CD61 mAb–injected mice compared with anti-CD41 mAb mice, suggesting that maintaining low levels of platelets early in the infection is critical for protection to occur. It is also possible that the effect of anti-CD61 mAb on endothelial β3 integrin is detrimental and reverses some of the protective effects of the platelet depletion by this mAb.
Although early treatment with anti-CD41 mAb is protective, which supports the platelet adhesion hypothesis, our data also show that mice treated late (day 4, 5, or 6 of P berghei infection) with anti-CD41 mAb are not protected from severe malaria, which contrasts with this hypothesis. It is unlikely that mice treated late with anti-CD41 mAb exhibit platelet adhesion to the brain microvasculature for the following reasons. Platelet adhesion during experimental malaria only occurs on day 6 of infection, just before the animals become moribund.15 Anti-CD41 mAb injection on day 4 or day 5 of infection when mice exhibit no overt clinical symptoms removes virtually all circulating platelets within 30 minutes. Thus, it is unlikely that any circulating platelets remain in the blood to adhere days later to the inflamed brain microvasculature when these unprotected animals start developing the disease. Further, our intravital microscopic analysis indicates that anti-CD41 mAb inhibits platelet adhesion to the inflamed pial endothelium on day 6 of P berghei infection.15 Finally, there is no apparent relation between the low numbers of circulating platelets and malaria morbidity (Figures 3 and 4) as is predicted by the platelet adhesion hypothesis. Mice protected from malarial pathogenesis by anti-CD41 mAb on day 1 of P berghei infection had fewer platelets than PBS-injected controls but more platelets than mice treated with anti-CD41 mAb on day 4, 5, or 6 of infection; both the PBS controls and mice treated late with anti-CD41 mAb all succumbed to severe experimental malaria.
Our finding that early but not late anti-CD41 mAb treatment protects against development of ESM suggests that platelets function as initiators of a pathogenic response rather than as effectors. Indeed, the removal of platelets by anti-CD41 mAb has a marked effect on the immune response elicited by infection, indicating that the coagulation system can control the immune system. It is well established that anti-inflammatory cytokines (IL-4 and IL-10) are not required for the development of ESM, whereas inflammatory cytokines (IL-1, IL-2, IFN-γ, and TNF-α) are all required.22,30,31 Differences in resistance and susceptibility to ESM in different strains of mice correlate with the development of inflammatory versus anti-inflammatory cytokines.20,32 Because administration of IL-10 actually protects against the development of ESM,33 we propose that the increased levels of anti-inflammatory IL-10 and lower levels of IL-2 in the protected anti-CD41 mAb–treated mice may account for the increased survival by counteracting the detrimental effect of increased proinflammatory cytokines.
Because coagulation factors are consumed during malaria and platelets assemble coagulation protease complexes,2-4,34 it is possible that depletion of platelets may ameliorate consumption of coagulation factors during malaria that in turn reduces hemorrhage and vascular leak. Senaldi et al observed no significant depletion of fibrinogen during P berghei malaria whereas injection of either TNF or lipopolysaccharide (LPS; which elicits another TNF-mediated systemic inflammatory response) depletes fibrinogen.35 Fibrinogen depletion by ancrod has no effect on P berghei–, TNF-, or LPS-induced mortality.35 Indeed, we also observe no fibrinogen depletion on day 4 of P berghei infection, but anti-CD41 mAb treatment leads to increased levels of fibrinogen. The similar levels of tissue factor, VWF, and fVII on day 4 of P berghei infection after treatment with anti-CD41 mAb and in rat IgG–injected controls indicates that the protective effect is not likely due to early changes in coagulation factor levels.
In inflammatory diseases such as atherosclerosis and stroke, there is adhesion of leukocytes via platelet P-selectin, followed by apoptosis of the platelets and formation of pro-coagulant microparticles; these events are critical for pathogenesis.36-38 In contrast, platelet-leukocyte conjugates are not detected by flow cytometry during experimental malaria, and leukocyte adhesion to brain microvasculature is not affected by the absence of P-selectin, indicating that P-selectin (platelet or endothelium) is not required for leukocyte adhesion to the activated endothelium during malaria.26,39 Our flow cytometric analysis of blood CD41+ cells obtained directly from the venous circulation indicate there are only about 600 detectable platelet microparticles/μL blood when the animals are moribund from P berghei malaria compared with 60 000 in blood of uninfected controls, indicating it is unlikely that platelet microparticles are being generated during experimental malaria. Indeed, mice with experimental malaria exhibit lower blood pressure and shear stress and increased shear stress is required to generate platelet microparticles, which makes it unlikely that platelet microparticles are formed during ESM.12,21,40 Platelet microparticles are therefore unlikely to contribute to the pro-coagulant state observed during malaria and removal of platelet microparticles by early anti-CD41 mAb treatment does not explain the protective effect of this treatment.
Platelet-erythrocyte conjugates or mini-thrombi are postulated to play an important role in the pathogenesis of septic shock, and clinical isolates of P falciparum often form in vitro conjugates with platelets, which is associated with the development of severe malaria.41 Our flow cytometric analysis of platelet-erythrocyte conjugates reveal that a greater percentage of platelets are coupled with erythrocytes. The actual number of these conjugates is low because of the profound thrombocytopenia observed during P berghei malaria. This low number may be due to adhesion of the platelet-erythrocytes conjugates to inflamed microvasculature during malaria or the rapid clearance of these conjugates by the spleen. Alternatively, few conjugates are formed during experimental malaria because platelets are removed from the circulation. Thus, prevention of mini-thrombi formation does not explain the protective effect of early anti-CD41 mAb treatment. Because the number of erythrocyte vesicles (CD41–CD61– cells in Figure 4) is similar in protected mice treated early with anti-CD41 mAb and in unprotected mice treated late with anti-CD41 mAb, prevention of erythrocyte vesicle formation cannot explain the protective effect of early treatment with anti-CD41 mAb.
Collectively, our data indicate that the role of platelets in malarial pathogenesis is very complex and they challenge our current understanding of the role of platelets in the development of severe malaria. These results indicate that malarial pathogenesis cannot be described by a domino effect in which removal of a domino prevents the cascade from reaching its conclusion. Rather, several parallel and interacting processes may best describe malarial pathogenesis with platelet activation representing one important process. These results also indicate that the major role of platelets in malarial pathogenesis is early in the infection. Platelet adhesion, which occurs just prior to death, is not required for the development of disease. In addition, there is no detectable development during experimental malaria of pro-coagulant microparticles, leukocyte-platelet or erythrocyte-platelet conjugates, all of which have been implicated in the pathogenesis of other inflammatory diseases. Our results indicate an unrecognized regulation of the immune response during malaria by platelets and this regulation is critical for the development of the pathogenic immune response leading to the development of ESM.
We thank Clara Polizzi, Zaid Yusufi, John Nipkur, and Dennis Young for their technical assistance and Drs Elias Lazarides, John Frangos, and Barry Coller for their helpful discussions of the data. Dr Herman Sahlin and Mr Peter Sobolewski kindly reviewed the manuscript.
- Reprints:
Henri C. van der Heyde, La Jolla Bioengineering Institute, 505 Coast Blvd, Suite 405, San Diego, CA 92037; e-mail: hvande{at}ljbi.org.
Prepublished online as Blood First Edition Paper, October 19, 2004; DOI 10.1182/blood-2004-06-2206.
Supported by National Institutes of Health grant AI40667 (H.C.v.d.H.).
The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
- Submitted June 10, 2004.
- Accepted September 8, 2004.
- Copyright © 2005 by The American Society of Hematology


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Splatterhouse Xbox 360 Cheats
- Game: Splatterhouse
- Publisher: Namco Bandai
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- Genre: Action Adventure
- Game Description: Welcome to Splatterhouse, where you'll use your bare hands as well as weapons, and the energy of your dead enemies to splatter and maim your way back to Jennifer, your lost girlfriend. She has been kidnapped by the diabolical Dr. West. You are Rick, left for dead in a world of darkness, where creatures straight out of nightmares are waiting. In West Mansion, Rick makes a pact with a Terror Mask, saving his life in return for blood. Rick transforms into a ruthless killer, pursuing the evil Dr. West through time, fighting against the undead and risking his very soul to save Jennifer.
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text: Mishelle has been a pleasure to have in Rough-Fit, is always positive, and works hard to achieve her goals. She has had great success not only with becoming physically fit, but with making healthy eating choices and pursuing an overall healthy life. She has found support in the Rough-Fit community and continues to support others in the same way. Congratulations Mishelle on your health and success!


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Howarth Windows and Doors has given a family from Stourbridge a whole new point of view after volunteering to provide new windows as part of a competition run by the Wood Window Alliance.
The Wood Window Alliance recently ran the competition to find the three houses in the UK that would benefit most from having their windows replaced with real wood windows. The prize was a £5,000 contribution each towards the new windows, with over 4,000 people entering.
Howarth Windows and Doors came forward and volunteered to supply and install new windows throughout one of the winning houses, which included double-glazed traditional vertical sliding sashes for the front façade of the property.
The home, a much older building that had been refaced in the 19th century, was bought as a wreck at auction. To lessen the strain on budget the homeowners decided not to replace the PVC-U units but as the house is in a conservation area in a small village this decision left the property as a sore thumb in a community of listed buildings.
The homeowners entered the competition to try and remedy this and have their home better match the classic look of their neighbour's homes.
Helen Reeves, the winning homeowner, said: "I thought sliding sashes would be draughty but I'm thrilled, the new windows are just as warm as the old windows and we have not had to sacrifice comfort for style; in my eyes the house is now perfect, and with no compromise. For me, value isn't just about money; good windows change the way you live in a property, it's great to go in any room and love the windows – I'm so glad we've done it."
Naomi Cleaver, the competition judge, said: "The difference in quality, function and feel is immeasurable. Performance is faultless, with the satisfying solidity of these new fittings matching up to the traditional visual appeal."
Local estate agent Allan Morris & Peace has since confirmed that an extra £20,000 has been added to the sale price of the property as a result of the new windows and doors being installed.


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We haven't really mentioned The Chew lately -- mainly because the daytime talker for foodies hasn't mentioned Miami lately.
Call it childish, but why should we give a shout out to a show that shows no love for the 305 ... until now.
Apparently The Chew crew's ears were burning because today's show features a segment filmed on location in Little Havana.
Chew correspondent Evette Rios will report from Calle Ocho, visiting some iconic spots along the way including Versailles,
El Palacio de los Jugos, and Azucar.
Coincidentally, that's two times this week that El Palacio de los Jugos will be featured on national television (Andrew Zimmern and
Michelle Bernstein sipped fresh coconut water at the juice palace on
Monday's Bizarre Foods America).
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Tune in to ABC today at 1
p.m. to watch. We're excited that Calle Ocho is featured on national
television, but next time you come to Miami Chew -- bring Michael Symon and Carla Hall, will ya?
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Global climate science sometimes comes head to head with policymakers and corporations in ways that make us feel like there is no way that we, as sustainability professionals, can really 'save the world.'
It can be difficult to keep things in perspective. But we must.
If you quit, then you really have no hope of effecting change. And you're still here, still on this planet, and you likely still need a job. So, find some internal motivation and keep going.
Here is our take on the Six Ways for Staying Motivated When You Really Want to Quit:
1. Practice looking at Things From the Other Side
If you think it's futile to 'keep fighting' when change is so incremental and what is at risk in our world seems so great, look at it from a different perspective. Don't be afraid to spend a few minutes looking back in time and celebrating some of the that have been accomplished in our world, or in your own career, to feel reenergized.
2. Identify your Intention
Are you going head-to-head with the CEO because you want to win, or because you truly believe what you're doing will help the company achieve its goals? Look at what you hope to achieve as a sustainability professional, assess whether it lines up with what you're actually doing, and then realign your action steps so you're doing what you intend to do. If you have a clear intention, you're more likely to feel motivated because you'll feel like you're getting somewhere.
3. Find a Different Way to do Things
If you come up against a hurdle, use some creative genius to work around it. Or just evaluate whether to reprioritize this activity. It may not be the right time to implement a certain policy in your industry, but there may be other areas you can focus on and have equal impact.
4. Lose Your Ego (and your High Horse)
Ego can get in the way of a lot of good ideas. In sustainability, a combination of ego and that sustainability, because of its focus on the lofty 'world saving' type goals, can immediately be off-putting.
You are likely a good person and working in sustainability is likely going to make the world a better place, overall, but focusing on that can be so self-centric that you'll lose your motivation. Instead, go back to the first item on our list, and challenge yourself to get projects going by putting others first.
5. Beware of your Habits
Don't get trapped by the status quo. Sustainability best practices are always rapidly changing, so get motivated by learning something new on the cutting edge of the field. Enroll in a class or learn to use a new assessment tool. You'll likely want to run out and start working on applying the new knowledge.
6. Realize that Nothing is Perfect
Whether it's a big project or a small one, everything we do as sustainability professionals is about incremental change that helps add up to big impact. Nothing will ever be perfect, but don't let that hold you back. Just get up, get a project started, and then celebrate what you did accomplish.
Staring for too long at the big picture may be counterproductive in any field, but especially in sustainability. Instead, find internal motivation and understand that there are thousands of us, like-minded professionals in all sectors, who are working alongside you.
Together we will create change.
How do you stay motivated? Let us know in the comments.


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6 weekly drawing classes with professional artist and teacher Kerry Wilson start TUESDAY 26TH JULY 2016.
Each week different subjects, materials and techniques will take you through the elements of drawing. Explore a variety of media such as graphite, charcoal, ink, pastels, collage and mixed media.
Still life, landscape, portrait, natural history and abstraction are all addressed in stimulating and informative classes.
Discover ways of seeing, creating form, depiction, expression and just how liberating drawing can be.
If you have always wanted to draw you will see how easy it is to start. Experienced artists will find these classes provide fresh approaches and expand their practice.
Venue: Butter Factory Arts Centre, 10 Maple St, Cooroy
Dates: Tuesdays 26 July, 2, 9, 16, 23, 30 August.
Time: 9.30am – 12.30pm
Cost: $270 (sample materials are supplied; students encouraged to bring own materials, list provided when booking)
Tea and coffee provided
Enquiries, Bookings and Payment directly to Kerry
Contact Kerry: 0428 502 251
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Tuesday Drawing Classes at the Butter Factory
9:30am - 12:30pm
Every Tuesday from 26 July - 30 August
Butter Factory Arts Centre
Butter Factory Arts Centre, Cooroy
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Pinnacle Shows offers a number of co-promotional materials to help you boost your numbers at our shows. Click here to download the full 2019 Panama City Beach Gift Show Exhibitor Marketing Kit. Below you'll find a description of these tools and links to the forms included in the exhibitor marketing kit. You will need to use Adobe Acrobat to open these pdf files. If you do not have Adobe Acrobat, you can download it for free by visiting www.adobe.com.
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