Spill some, and you'll probably throw a pinch of it over your shoulder to ward off bad luck. In parts of Africa, 23 Kg (50 pounds) of it is enough to get you a wife. Lack of it lost Napoleon an empire. Escoffier himself couldn't cook without it. A major meat packer uses 31.5 t (35 tons) of it a day. For centuries, it has been one of the most valuable substances known to man. You probably know it as common table salt. But just what is that white stuff in your salt shaker?
Salt is a mineral composed of sodium and chlorine. Neither can exist alone in natural form. Together, they form the stable chemical compound that is sodium chloride, or salt. To geologists, salt is known as halite, from "hals", the Greek word for salt. Halite belongs to the family of minerals which are compounds of the metals with the halogen elements fluorine, chlorine, bromine, and iodine.
Salt is a crystal of the isometric system, which means it is usually cubic and perfectly symmetrical. Pure salt crystals are colourless, although a pile of them will appear white. Impure crystals may be various shades of yellow, red, blue or purple. Salt is one of the earth's most abundant minerals. The world's oceans alone contain an estimated 18,756,000 Km3 (4,500,000 cubic miles) of salt, or enough to cover the entire surface of the globe to a depth of 122 m (400 feet). Millions of tons of salt are extracted each year from the sea and underground deposits.
Salt is such a basic commodity and is used in so many different ways that a chart of salt consumption is almost a barometer of economic conditions. From such charts, economists can trace the rise and fall of national prosperity.
Today, we can find over 14,000 uses for salt in industry, in medicine and in the home. In addition to its direct use in industry, salt plays a vital role as a raw material in the manufacture of other chemicals. Farmers depend on it to keep their stock healthy. Salt adds flavour to almost everything we eat and saves lives in winter by improving the safety of our highways.
Our plentiful supply of salt means that its value must be measured in terms of its versatility. Yet, in times past, salt was so highly prized it was used, like gold, as a medium of exchange. Our early ancestors soon learned that man, like the animals, needed salt in order to live. Ever since, not only our food, but our commerce, our politics, our religion and our superstitions have been flavoured with salt.
Primitive tribes valued salt so highly that coins were made from it. The natives of Africa's Sierra Leone were willing to sell their wives and children for salt. An oppressive salt tax was the final spark that kindled the French Revolution. Many of the world's wars have been fought for strategic salt supplies. During the American Civil War, the men and horses of General Lee's cavalry were decimated by disease because of a salt shortage that affected the future of the entire Confederacy. Salt was the reason for the construction of one of the most famous military roads in history, the Via Salaria, or Salt Road, between the salt works at Ostia and the City of Rome. The Roman legionnaires who guarded this route received a part of their pay in salt. From this ration, the "salarium argentum", derives our modern word "salary". Even today, a good employee is said to be worth his salt".
In many ancient civilizations, salt had great symbolic value. Because of its acknowledged power to purify and preserve, salt spilled on the parchment was a guarantee of good faith in signing a contract or making an agreement. Among the Greeks and the Turks, to eat salt with a stranger was a token of friendship. The Greeks made thank-offerings of salt to the gods they worshipped as givers of life. The ancient Jews offered salt to Jehovah at harvest time. In Jewish tradition today, bread and salt are the first things to be brought into a new house.
In some areas of the far East, people give their children little bags of salt to hang around their necks as protection from the "evil eye". And in parts of Russia no bride and groom would enter a new home without first throwing salt in every corner to protect them from harm and to encourage health and happiness.
Even in modern Christianity, salt has symbolic significance. The Bible contains many separate references to salt. In the ritual of baptism, salt is used as a symbol of protection against evil, representing purity of mind and soul and the power to resist temptation.
According to ancient superstition, when you spill salt, you risk losing the power to triumph over temptation and must banish evil spirits by throwing a pinch of it over your left shoulder.
The association of spilled salt and the appearance of evil is illustrated by the overturned saltcellar of the Last Supper. Judas, who has succumbed to temptation, is identified by Christ through the evil significance of the spilled salt. Which brings us back to the salt on your table. How did it get there? Where does it come from?
The greatest single use for salt is as a feedstock for the production of chemicals. The chlor-alkali industry uses salt, primarily as salt in brine from captive brine wells, to produce chlorine and caustic soda. Demand for salt in to produce chemicals fell from 25 million metric tons in 1974 to a low of 16.7 million metric tons in 1992. However, chemical use rebounded in 1994 to 18.4 million metric tons. Much of the decreased demand for chlorine was attributed to environmental concerns about dioxins. Salt is also used to make sodium chlorate and metallic sodium by electrolysis and, sodium sulfate and hydrochloric acid by reacting with sulfuric acid.
All animals, humans included, require both sodium and chloride for life and health. Since the body cannot manufacture either, they are "essential" nutrients. While developed countries dedicate most of their salt to chemical production, developing countries often use most of their salt for human and animal nutrition.
Livestock, poultry and other animals do not always receive adequate amounts of sodium and chloride from forages and other feeds. They need supplemental salt as part of a nutritionally balanced diet to remain healthy, disease free, and to achieve optimum growth and reproduction rates. Because animals have a natural, definitive appetite for salt - they will eat only a certain amount - it is used to ensure adequate intake of less palatable nutrients and as a means of limiting feed intake. Salt can be mixed with feed or fed free-choice, and is an excellent carrier for trace minerals, It is produced plain or as trace mineralized salt, in 50 lb blocks, smaller spools, and as loose salt, commonly known as mixing salt.
Salt is the most effective, readily available, and economical highway deicer in use today. It assures winter driving safety and continued mobility in snowbelt states, even under the most adverse snow and icing conditions. Rock salt and solar salt are used on U.S. highways. In Europe, because of its availability, evaporated salt is sometimes used. The lowest temperature at which sodium chloride will melt ice (the eutectic point) is -21.12?C (-6.02?F), at a concentration of 23.3% NaCl. Salt works best at temperatures near 0?C (32?F) because melting occurs quickly with a relatively small amount of salt. As the temperature falls, it takes more salt and more time to melt ice because a higher concentration of brine is required. Fortunately, most snowstorms occur when the temperature is near freezing, where salt is very effective. More than 40% of the dry salt produced in the United States is used for highway deicing.
Water is considered hard when it contains calcium and magnesium (hardness ions). Hard water requires more soap and detergent for laundering, cleaning and bathing because suds do not form as well in hard water. The reaction between soap and hard water results in a greasy, curd-like deposit which makes fabrics feel harsh and leaves water spots on dishes and utensils. Mineral scale builds up in hot water appliances and industrial boilers, reducing energy efficiency and shortening appliance and equipment life. Water is conditioned or softened by removing the calcium and magnesium ions from hard water and replacing them with "soft" sodium ions. Water softeners use cation exchange resin to exchange sodium for calcium and magnesium. As supply water flows through the resin bed, the exchange takes place and the water becomes soft. Water softener cation exchange resins are regenerated with a 10% salt brine solution made by dissolving water softener salt.
Pulp & Paper. Salt is used to manufacture chlorine and caustic soda. In paper making, caustic soda is used to process wood fibers and chlorine is used to bleach the pulp. Sodium chlorate, also made from salt, is replacing chlorine as the primary chemical for bleaching pulp.
Other Industries. Salt is used to fix and standardize dye batches in the textile industry; it is used in metal processing and secondary aluminum making, to remove impurities; rubber manufacturers use salt to separate rubber from latex; salt is used as a filler and grinding agent in pigment and dry-detergent processes; ceramics manufacturers use salt for vitrifying the surface of heated clays; soap makers separate soap from water and glycerol with salt; oil and gas drillers use salt in well drilling muds to inhibit fermentation, increase density and to stabilize drilling in rock salt formations; hide processors and leather tanners use salt to cure, preserve and tan hides; and there are more.
Cloud Seeding for Rain. Though perhaps not an "industrial use," salt has been used to "seed" clouds to produce rain in desert areas.


Alabama's bankrupt Jefferson County aims to sell $1.89 billion of municipal debt in late 2013 as part of a bankruptcy-exit plan that will hand historic losses to Wall Street banks and other investors, a lawyer for the county said on Wednesday.
"The buying should start December 2013," Kenneth Klee, a bankruptcy lawyer for the county, told Reuters after a bankruptcy court hearing in Birmingham, Alabama.
"A lot of people out there have money to invest and Jefferson County is going forward with a plan," Klee said of the offerings that were part of a tentative deal reached Tuesday by the county and creditors JPMorgan Chase, hedge funds and bond insurers.
Under the deal, which will be part of a reorganization plan that must be okayed by a federal judge and in a vote by creditors, the county is refinancing the $1.89 billion that will be paid back to creditors in America's largest municipal bankruptcy.
The repayments come after "haircuts", or reductions in claims and bond debts, of a scope unseen in America's municipal bond market since the 1930s. JPMorgan, which struck a $732 million settlement in 2009 related to Jefferson County's debt, on Tuesday agreed to give up about $842 million of the $1.218 billion of Jefferson County sewer debt it owns.
Klee, the county's lead bankruptcy lawyer, told U.S. Bankruptcy Court Judge Thomas Bennett during the hearing that Tuesday's agreements were tentative and relied on the county filing a plan of adjustment by July 1, as well as final approval of the plan by the judge by December 20.
Bennett said he would try to work to that schedule.
With Tuesday's agreements, Alabama's most populous county has negotiated deals in place that cover about 80 percent of the defaulted $3.1 billion of sewer-system debt that was a key driver of it's November 2011 bankruptcy filing.
Klee said the county was still talking with some creditors, including some banks holding about $138 million of warrants. In addition, Klee said, owners of some $534.1 million of debt were so far unknown.
"The parties are committed to going forward in a plan of reorganization," Klee said.


This entry was posted on Sunday, September 9th, 2012 at 4:30 am	and is filed under Accomplished Projects & Activities. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.
blessful are those individuals like you, who has the advocacy to save that poor creatures.that who are victims of cruelty of mankind. hoping that one day, that the world will tip over onto them who does cruelty, and they are the one who will experienced what they did to pitbulls. shame onto them,fame on the advocates.
Our dog just died, i just saw on tv5 about the Pitbull Rehab Project. I want to adopt a pitbull. Problem is, I'm in cebu. And i want to take 1 home in Kidapawan City, Mindanao.
what's up I really like the job you done here.
Please email volunteeratlpb@gmail.com for the requirements and guidelines. Thank you.
Website for the rescued Pit Bulls coming soon!


An ongoing series of illustrations showing my love for period graphics relating to the branding, promotion and advertising for rail transportation. Each label will be designed to reference the style of graphics seen during the 1900′s throughout the world's railways. These are all vector designs, originally created in Adobe Illustrator, then adjusted, realistically aged and weathered in Photoshop.


I am learning that I have to fight for the things I want. I have to fight for the people that I love. I have to fight to hold onto dreams and keep moving forward in life, when all that I really want to do sometimes is sit in a corner, bow my head and say, "Come, Lord Jesus, Come quickly".
So I ask myself tonight, "Do I have a fight left in me?" I've never been one who likes conflict. I'm not one to push the envelope and press in for what I want. I give up too easily. I stop way before the light turns red. I give up long before the breakthrough.
But this year, I want to fight. I want to fight the good fight of faith, to run the race with the joy set before me, which is Christ Jesus. There are so many things I want to accomplish in this life still. So many things I want to do this year, but it will be a fight. I have way too much going on in my life. So I will have to fight to stay focused, to stay balanced and to keep my head above water. Life is a juggling act and I prefer to take the easy way out.
But this year, my eyes are are fixed, my feet are firmly planted, and I will press on with unwavering faith, and find that fight that is within me. I will hold tightly to the promises of God for my life and not let go until I see them fulfilled.
Now it's your turn! What are your thoughts when you think of the word "fight"? I would love for you to share in the comments below.
Thanks so much for stopping by Heather! Have a beautiful week!
Love your post – beautifully written. I wish you luck in fighting this year to live the life you want and not to let it pass you by.
Thanks for stopping by Alecia. Many blessings to you!
Oh yes, I too want to fight the good fight and to finish strong. But I've learned that the way to move forward is by abiding in Him. The Lord is doing a work on my heart within me and that spills over externally. I think that is key to finishing strong and trusting Him.
Your posts always inspire me Barbie…and this one is no exception. I need to fight the good fight and I like what Amy Tilson said about "fighting for" something.
Thanks for your friendship and encouragement Mary! Have a blessed tomorrow.
I'm not a huge fan of conflict either, so combat is not the first thing I think of with fight. I definitely tend to think more in a "fighting for" than with sort of way.
True. I like the thought of fighting for something as well. Have a blessed tomorrow Amy!
This is a wonderful post. I am a mere 35 but finding that the older I get, the harder the fight becomes. Love your thoughts. Thank you for sharing them. They are encouraging.
You're welcome Sarah. I am 47 and yes, I can attest the fight seems harder at times. But God is victorious, AMEN?
Hey! Visiting from FMF! Yes! I too am fighting this year! Fighting to surrender to what God has called me to do and not hide. Love it! Let's fight together!
AMEN Kelly! I'm in your corner!
Yes! Yes! Yes! The good things are always worth fighting for! I love the verse youve applied here!
Fight the good fight of the faith! May we not get sidetracked with fighting fights that will never matter. Things unseen, not temporal things that can be seen. Keep fighting Barbie, but lay down the things that so easily beset us. Remember the victory has been won already and He will make you complete!
Be strong and courageous, my friend.
Oh AMEN Rebekah! Thanks for encouraging my heart!
Loved this post Barbie!! Yes we need to fight the good fight!
Thank you for dropping by Kristin! Blessings!
Love this, Barbie: "But this year, I want to fight. I want to fight the good fight of faith, to run the race with the joy set before me, which is Christ Jesus." Me, too! It is a fight of faith, and there is great joy in the end. The reward of Jesus. As always, thanks for sharing your heart. Beautiful!
Thanks Jaqui! Have a beautiful tomorrow!
Barbie, I love your new look. We have the same taste in blog themes. I love the lovely theme. Reading your words just makes think yes I can do it!
I loved my last design too, but this one will better display my creative side. Yes, we can! Keep up the fight of faith!
I'm not quite sure what I would have written about this word. Maybe about my husband and his willingness to fight for our country. Maybe I would have talked about how grateful I am that He doesn't make this choice without God….that God will be his strength. Now you have me thinking. I'm one that is not quick to step up and fight for my dreams. Has made me a little jealous of my husband. Okay, you really have me in pondering mode.
Oh btw, really LOVE your new look here. So inviting and warm.
Ponder away my friend. Love you!
Your determination to fight forward is so encouraging! Your posts weave beautiful truth together. I enjoy them so much! Have a wonderful weekend, friend!
PS: I love the new look!
Thank you Jennifer! I appreciate you!
Love your new look here, so beautiful, and this? This post was just what I needed.
Love you my friend. Have a beautiful weekend.
Never been much of a fighter here either. I like peace and dislike conflict. Somehow I've ended up smack in the center of something unpleasant (a volunteer position where much was going on behind the scenes, unbeknownst to me) and I am having to navigate some tricky waters. It has required me to stand firm, and speak up for those being treated unfairly. So out of my comfort zone, yet I feel God just nudging me to hang in there, to not be afraid. Honestly I have considered quitting, yesterday in particular, but today fresh eyes, fresh resolve. Thanks for sharing-this was good! Happy New Year!
Thanks for stopping by Joyce. Praying God continues to give you peace and joy as you work through this. Blessings!
I am so used to giving up… I'm used to being a quitter. I have also resolved to fight for things a little harder this year. Thank you so much for sharing this!
Thank you Courtney. Enjoyed your beautiful post today. Blessings!
I love how this word brought out so many different thoughts! Fighting the good fight (not just any old fight) is something I need to remember this year. Rise up to defend the good and not simply my own feeling of being right. Love the verse you chose, too.
Thank you so much for stopping by Kim. Have a blessed weekend!
Oh my friend… I know this fight! This on purpose, working on my follow through Fight! Side by side… we can do this! Here's to going from Victory to Victory in 2014! Love you so!
AMEN! So thankful to have you in my corner! Palms up! Let's go!
Some things are worth fighting for! Welcome back to FMF, my friend! Happy New Year!
Thanks for stopping by Rachael! Blessings!
It is a fight, sometimes, isn't it? I am fighting to lay hold of a deeper dependence on our Good God this year. The verse you've highlighted here, my friend, is a great encouragement to me.
My fight this year is to stay focused on Him. Even being just 3 days in, I've already allowed myself to become distracted and lose sight of my goals. But yes, I will continue to fight. I will be victorious through Him.
May we never let go of the fight to finish well! Great post, Barbie.
Have a beautiful weekend Holly!
Joining you in fighting the good fight this year, lady.
Thank you so much Lori! Thankful to have met you through blogging. Your words always touch my heart and inspire me to be more than I am.
AMEN my friend. So thankful I have you to hold my hand, across the miles, through this journey!
Thanks for the reminder of 1 Timothy 6:12! We do have to fight the good fight of faith and we need to finish the race. I have felt in the most complacent place since October. Since January 1st it has been lifting and I feel more like myself. It was a strange season that I don't care to revisit again.
The Lord is mighty in battle! I know He will fight for you as you lean on Him.
So thankful that season is ending for you. Have a very blessed weekend!
Growing up – I had to fight to be me – or I felt as though I would lose who I was. When I was around 30 I realized I didn't have to fight for me anymore – I'd won that battle – and the last 8 years – I've been fighting for a couple of my boys who took a non-traditional approach to their education – and I had to learn to fight God's way – meaning to give it to Him – but I had to learn what to do in the battle while He fights it. I'm a little worn down – and asking God to fire up the fight in me again – but it's a different kind of fight – it's a jabez kind of thing I'm working out! Wishing you blessing – your 5 minutes spoke to my heart!
Thank you my friend. I understand the education fights. My children have always been in public school as both my husband I work full time. The last two years I attempted to try to homeschool my daughter through 8th grade, while working. It was a totally failure. We are barely schooling now, and we've all decided that public school is where she will go next year. All of my children have excelled there, and love and serve the Lord today. My fight will be to keep her rooted and grounded in His love and Word while being the free spirt that she is. Blessings!
It's amazing how one word could bring out different thoughts from each of us. It's my first Five Minute Friday and I'm being blessed by all the posts. Yours is beautiful like always. Thanks for sharing.
Thanks Jesenia! Your post really spoke to my heart, about the surrendering to gain victory. Have a beautiful weekend!


text:
Police adopt new child safeguarding scheme
Wednesday 10th of January 2018 02:13:26 PM
Tags: emergency services
From Devon & Cornwall Police:
Operation Encompass is helping the force and schools focus on supporting children who are suffering harm in domestic abuse incidents.
Devon and Cornwall Police are working with the Trustees of the Operation Encompass charity and our partners to ensure that schools across Devon and Cornwall are informed promptly of incidents where children have been impacted by domestic abuse.
Operation Encompass is the reporting to schools, before 9am on a school day, when police have attended an incident where a child or young person has been present during or exposed to an environment where there is domestic abuse.
Information is passed by the police to a trained 'Key Adult' within the appropriate school so that silent or overt care can be provided to support the child.
Chief Constable Shaun Sawyer, who also delivered a passionate speech at the Encompass launch event said: "Operation Encompass is an important initiative and directly supports our force mission which is to protect the vulnerable.
"This scheme is now running forcewide meaning that some of the most vulnerable children in society are now receiving the extra help and support from police officers and the school they attend, far earlier than ever before. These are children who may have previously suffered in silence at school after being exposed to domestic abuse in their home.
"Representatives from over 900 schools from across Devon and Cornwall have attended the key adult training, all delivered by David and Elisabeth Carney-Haworth whom I thank personally for their time and commitment in delivering this initiative."
Today (Wednesday 10 January), Devon and Cornwall Police and the charity held a launch event at Pentillie Castle in St Mellion to celebrate the roll-out of Op Encompass across the force.
The event was co-hosted by the Chief Constable, the High Sheriff of Cornwall Sarah Coryton, recently appointed as a Patron of Operation Encompass, and the High Sheriff of Devon Heleen Lindsay-Fynn.
In attendance was Dame Vera Baird a Patron of the Charity and Anneka Rice, an advocate who gave a speech as part of the day. Alison Hernandez, the Police and Crime Commissioner for Devon and Cornwall also attended.
Ms Hernandez, said: "Better connections between the police and the communities they serve is at the heart of my Police and Crime Plan. Operation Encompass allows the police and schools to better connect for the sake of our children. I'm so grateful for the efforts everyone has put in to create a safer environment where children who have suffered trauma will be further supported and helped to cope"
Retired Sergeant David Carney-Haworth, co-creator and founder of Operation Encompass, said: "As the creators of Operation Encompass it is rewarding to see our scheme across the whole of Devon and Cornwall Police Force. Today is a wonderful way to mark and recognise this achievement which has come from a commitment straight from the Chief Constable.
"We can now add Devon and Cornwall to the list of forces supporting Operation Encompass, meaning that parents can rest assured that the child victims of domestic abuse will be recognised and supported in school.
"This scheme is supported by both Her Majesty's Inspectorate of Constabulary and Fire & Rescue Services (HMICFRS) and Ofsted, and we will continue to lobby to ensure that all forces across the country embrace this scheme.
"Our hard work in briefing key adults across Cornwall, Devon, Torbay and Plymouth is a small price to pay to ensure that the children and young people exposed to Domestic Abuse are given the nurture and support that they need, when they need it most: It's every child's right."

redpajama_set_name: RedPajamaCommonCrawl


Team Fortress 2 is the first Source engine game ported to the Linux platform. It is available for free (as in free to play) via the native Steam for Linux client and uses the new SDL 2.
Alternatively you can use driconf to activate S3TC with a graphical user interface.
If you see GL errors in the terminal or video glitches in-game then your video drivers might be outdated. You need Mesa version > 9 and openSUSE 12.2 currently ships 8.0.4 by default. Add this repository and do a vendor change for all packages. You need to switch the repository in YaST software management (or do zypper dup --from "X11:XOrg") to achieve this. Do not commit to the upgrade if it wants to remove either fbdev or vesa drivers. A newport driver is removed with the upgrade, and that is fine.


Our stately medieval hall makes a wonderful setting for your wedding, with its magnificent oak-timbered roof and wide tie beams. The room is framed by heraldic banners and five large candelabras that create a magical and romantic setting for your ceremony. Situated on the ground floor of Tamworth Castle, it is licensed for up to sixty people for a civil marriage or civil partnership. Download the Tamworth Castle wedding pack to find out more.
Weddings take place at: 11.30am, 1.30pm and 3.30pm. Please note the registrar may change these times.
To make a booking or for further details please contact the Wedding Coordinator by telephone, email or in person.
A quick and simple booking form - including a terms and conditions form will be completed and you will be given a copy for your reference.
Wedding bookings, appointments, viewings and enquiries can be taken on a Monday, Tuesday or Friday between 9am and 5pm. And on a Saturday and Sunday between 11.30am and 5.00pm.
Deposit: Please note a £150 non-refundable deposit will be required at the time of the booking.
You will have use of the Great Hall for approximately two hours. This includes half an hour for your guests to be seated, half an hour for the wedding ceremony and an hour to take photographs.
The Great Hall will be set out with 60 chairs for guests, 30 each side of a burgundy aisle carpet consisting of five rows of six chairs. The chairs are attractive dark wooden with burgundy seat cushions. Ribbons and posy like flowers (provided by you) can be tied to the aisle chairs if you wish before the ceremony.
A grand medieval inspired throne chair is provided for the bride and groom.
These can be used to decorate the venue. The wedding coordinator will be able to give you guidance on decorations. any decorations need to be provided and positioned by the bridal party and will need to be removed after the ceremony.
A red Aisle carpet is provided.
To help create a wonderful ambiance on the day, approximately 80 candles will be lit in the Great Hall. These are the only candles which can be used during the ceremony.
The Great Hall has wonderful acoustics for music to accompany your big day. any music needs to be chosen and supplied by the bridal party. However it doesn't have to be a CD or recorded music; it can range from live music such as a harpist, bagpipes, string quartet, singer, piano player to recorded music and the Castle stereo is available for you to use. A member of the bridal party will need to play this music when it is needed.
There are a number of rooms available for you to have your photographs taken. There are two upper rooms - the Victorian Grand With-Drawing room or Tudor Dining Chamber, the Great Hall (generally in bad weather) and the Medieval Courtyard. These beautiful rooms, full of history and splendour, will add something special to your photography.
Photographs can also be taken in our beautiful Castle Grounds, which have spectacular views over the River Tame and beautiful flower beds, packed with colour (season dependent). Please be aware that the grounds are open to the general public through out the year and there may be other wedding parties or event going on.
The floral displays in the grounds around the bandstand give a wonderful backdrop to your photographs, but please bear in mind when they are being replanted from spring bedding to summer, and summer to winter, we unfortunately cannot guarantee that flowers will be there at the time of your wedding. The grounds are also used for other outdoor events which could mean increased members of the public, fuller car parks and additional noise. Please visit the Assembly Rooms website to see when outdoor events are taking place.


text:
Hugh Russell baritone
About Hugh Russell
Canadian baritone Hugh Russell continues to receive high praise for his charisma, dramatic energy and vocal beauty. He is widely acclaimed for his performances in the operas of Mozart and Rossini, and is regularly invited to perform with symphony orchestras throughout North America. At the center of his orchestral repertoire is Orff's popular Carmina Burana, which Mr. Russell has performed with The Philadelphia Orchestra, The Cleveland Orchestra, Los Angeles Philharmonic, San Francisco Symphony, Houston Symphony, Pittsburgh Symphony, Seattle Symphony, Toronto Symphony, and Vancouver Symphony, among others. The New Orleans Times-Picayune said, "Baritone Hugh Russell also grasped the theatrical nature of Orff's work, nearly stealing the show with a voice that ranged from organ-deep rumbles to flute-like falsetto – and an acting style that drew roars of laughter as he captured the bullishness of an intoxicated medieval abbot."
Recent engagements include: Carmina Burana with the Kansas City Symphony and the Milwaukee Symphony Orchestra; Pangloss in Candide in Salt Lake City and Seoul, South Korea, Abimelech in Samson et Dalila with North Carolina Opera, Noah Joad in Grapes of Wrath with Michigan Opera Theater. He also recently sang Carmina Burana with New Mexico Philharmonic and in Mexico City under the baton of Carlos Miguel Prieto, as well as with the Chicago Philharmonic, the Las Vegas Philharmonic, the Louisiana Philharmonic, the Orquesta Nacional de Costa Rica, and the Orquesta Sinfonica del Principado de Asturias in Oviedo, Spain. He also sang Rachmaninoff's The Bells with the Orchestre Metropolitain de Montreal and Yannick Nezet-Seguin, joined Palm Beach Opera in the role of Major General Stanley in Pirates of Penzance, and performed the role of Noah Joad in Grapes of Wrath with Opera Theatre of Saint Louis.
Hugh Russell joined Calgary Opera in 2016 as Papageno in The Magic Flute. He reprised Carmina Burana with the Columbus Symphony Orchestra and the Grand Rapids Symphony, and sang Rachmaninoff's The Bells and with the Cincinnati Symphony. In the 2014-2015 season, Mr. Russell performed the role of Falke in Die Fledermaus with Vancouver Opera. Orchestral engagements included Faure's Requiem with the Dallas Symphony, opera scenes with the Princeton Symphony, and Carmina Burana with the Rhode Island Philharmonic, the West Michigan Symphony, and the Louisville Orchestra.
In 2013-2014, Mr. Russell performed Carmina Burana with the Pittsburgh Symphony, the Israel Philharmonic, and the Detroit Symphony Orchestra. Also that season, he debuted Mendelssohn's Elijah with the Orquesta Sinfonica del Principado de Asturias in Oviedo, Spain. On the operatic stage, he made his company debut with Cincinnati Opera as Father Palmer in Kevin Puts' opera Silent Night, and sang Taddeo in L'italiana in Algeriin his debut with the Calgary Opera.
Selected operatic engagements of recent seasons comprise a return to Opera Theatre of St. Louis as General Stanley in The Pirates of Penzance, Harlequin in Ariadne auf Naxos with Kent Nagano and the Los Angeles Opera, the lead role of the Pilot in Rachel Portman's The Little Prince with Boston Lyric Opera, Taddeo in L'italiana in Algeri with Vancouver Opera, Valentin in Faust with Pittsburgh Opera, Taddeo, Belcore in L'elisir d'amore, and Eisenstein in Die Fledermaus with Arizona Opera, his New York City Opera debut singing the title role in Il barbiere di Siviglia, his UK debut as Virginio in Mercadante's Virginia at the Wexford Festival,and Papageno in Die Zauberflöte and Dandini in La Cenerentola with Atlanta Opera.
Additional notable concert engagements include the Brahms Ein deutsches Requiem and Mahler's Songs of a Wayfarer with the Vancouver Symphony under Music Director Bramwell Tovey, Vaughan Williams's Sea Symphony with Edo de Waart and the Milwaukee Symphony, Fauré's Requiem with Indianapolis Symphony Orchestra and the Orquesta de Sevilla, Rachmaninoff's The Bells with the Madison Symphony Orchestra, Songs of a Wayfarer with the Indianapolis Symphony and the Kitchener-Waterloo Symphony, John Adams's The Wound-Dresser with the Toledo Symphony, and Tobias Picker's Tres sonetos de amor with L'Orchestre Philharmonique de Strasbourg. Mr. Russell has also been a regular performer with the New York Festival of Song and has sung in the Festival's recitals at Merkin Concert Hall, the Kaye Playhouse, and the Kennedy Center in Washington, DC, and was cited by the New York Times for his "lovely sound."
Hugh Russell continued his success as baritone soloist in Carmina Burana with the San Francisco Symphony, the Seattle Symphony, the Detroit Symphony Orchestra under Leonard Slatkin, Vancouver Symphony, Edmonton Symphony, New Mexico Symphony, the National Symphony Orchestra, the Philadelphia Orchestra in Vail, the Kitchener-Waterloo Symphony Orchestra the Sarasota Symphony Orchestra, the Oberlin Conservatory (his alma mater), the Indianapolis Symphony with Music Director Krzysztof Urbanski, the Los Angeles Philharmonic, the Milwaukee Symphony under Andreas Delfs, and the Houston Symphony under Music Director Hans Graf, made debuts with the Danish Radio Symphony under the baton of the late Rafael Frühbeck de Burgos as well as with the Naples Philharmonic.
As a member of the Pittsburgh Opera Center, Mr. Russell sang the roles of Malatesta in Don Pasquale, the title role in Pelléas et Mélisande, and Guglielmo in Così fan tutte, a role he has also performed with Boston Baroque. Reviewing the latter performance, the Pittsburgh Tribune-Review wrote, "Baritone Hugh Russell was magnificent…His was also the most completely acted performance." A further triumph with this company was his performance in Dominick Argento's Postcard from Morocco.
Mr. Russell was both an Adler Fellow and a member of the Merola Opera Program at San Francisco Opera, where he was heard in Ariadne auf Naxos and in Messiaen's St. François d'Assise. The San Francisco Classical Voice proclaimed, "He seems born for the stage. And with a lyrical voice boasting a strong and exciting top end, he is a complete performer."


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As part of The Bridge Teen Center's work study and job readiness training program, specific funding is available to hire a limited number of student workers (ages 16+) at The Bridge Thrift Store. Sales Associate positions involve cashiering, guest relations, stocking and organizing, and sorting/purging donated goods. This is a highly competitive process and only a few positions are available, so student applicants are encouraged to act quickly. Interested parties should download and complete the PDF application found here and email it to jason@thebridgeteencenter.org.
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Amid calls for the team to return on a temporary basis, the NHL is not ruling out the possibility of future New York Islanders games at Nassau Coliseum.
Long term, the Islanders are focusing on Belmont Park, where the team's bid to build a new arena was recently approved. While the Islanders are expected to remain at Brooklyn's Barclays Center through at least the 2018-19 NHL season, they may need a temporary home after that, as the new Belmont Park arena is not expected to open until at least 2020.
Nassau Coliseum reopened with a naming rights deal that makes it known as NYCB Live, home of the Nassau Veterans Memorial Coliseum, and features a reduced seating capacity since the renovation. It has been used for a variety of events, and is currently the home of the Long Island Nets of the NBA Gatorade League.


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Embedded system market size likely to exceed USD 258 billion by 2023
Published Date: March 14, 2016	Authors: Ankita Bhutani, Pallavi Bhardwaj Share
Embedded system market size is likely to be valued USD 258.72 billion by 2023, as per a new research report by Global Market Insights, Inc. Mounting need mainly from application sectors such as healthcare as well as automotive is expected to drive demand. In addition, emergence of IoT is anticipated to fuel industry growth.
Embedded hardware system market size was valued USD 154.82 billion in 2015 and is anticipated to observe significant gains, with USD 240.11 billion at a CAGR of 5.5% from 2016 to 2023. Technological innovation and advancement in emerging nations such as Russia, India, China, Brazil and Taiwan is likely to spur growth. Embedded software was valued at USD 10.46 billion in 2015, and is anticipated to attain USD 18.61 billion by 2023, at an estimated CAGR of over 7.3% over the forecast period.
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Technology innovation in wireless communications, software and digital processing is expected to positively impact embedded system market size. Systems that effectively and efficiently drive the electronic contents within vehicles have also increased significantly in automotive sector. This assists safety systems on the highest priority by monitoring parameters such as tire inflation, antilock braking systems, remote keyless entry, antitheft and airbag systems. However, security risks related to the systems is anticipated to hinder the industry growth.
To access sample pages or view this report in detail along with the table of contents, please click on the link below:
https://www.gminsights.com/industry-analysis/embedded-system-market
Key insights from the report include:
Global embedded system market size was valued USD 165.28 billion in 2015 and is anticipated to attain USD 258.72 billion by 2023 at 5.6% from 2016 to 2023.
Automotive sector valued USD 34.64 billion in 2015 which is likely to attain USD 56.04 billion by 2023, growing at a CAGR of 6% from 2016 to 2023. Increasing acceptance of hybrid as well as electric vehicles in order to control emissions is likely to fuel the industry growth. Healthcare sector is likely to grow at a CAGR of 6.3% over the next few years. Rising need for portable medical devices in this application is predictable to boost the global growth.
U.S. embedded system market share dominated the regional demand, accounting for over 30% of total revenue in 2015. Asia Pacific is anticipated to grow at a CAGR of 6% up to 2023. This can be attributed to the presence of fabrication plants in the region.
Moderately competitive industry consists of top four manufacturers accounting for more than 50% of the embedded system market share. Key manufacturers include Infineon Technologies, Freescale Semiconductor, Atmel Corporation, Renesas Electronics, Samsung, STMicroelectronics, Texas Instruments and Microchip among others.
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Home / Services / Social Mobilization
Social Mobilization
Almost all the community support institutes in Sri Lanka believe that community mobilization is a facilitative instrument that enables positive changes which could help meet the challenges of societies in transition through changed attitudes, values, and behaviors of individuals or groups. Accordingly, individuals or groups are able for better weighing up their needs, to prioritize, to increase potentials of resources and also to produce results. WDF premeditates that the said changes can bring forth required structural changes within communities, with reliable conversion that supports lasting change.
When the self sustenance is concerned many institutions need to struggle in plentiful ways to establish self-driven mechanisms yet, if community mobilization process is not evolved at the inception it would be not possible to change the attitudes of participants in the latter, for a self driven operation.
Mobilization has broader perspectives since different communities prefer different approaches in their mobilization needs. WDF has always made specific effort to diagnose desires of the particular community and the changing leadership pattern is always a challenge Knowing where a community is starting from and progressing toward is helpful for program staff to work appropriately with the community. Also the different layers of mobilization be followed to bring people to the centre. WDF in its long term involvement has assessed the progress of mobilization attended and the quality of results gained that contribute to the overall growth.
Mobilization becomes the most constructive tool in promoting less advantaged segments of respective communities. Basically, to raise awareness on persisting challenges and to prepare the community to go against them becomes the key component to be addressed in the mobilization process. A trained team of Asst. Coordinators have been positioned for this task, at present. Each Asst. Coordinator is paid monthly allowance. WDF has authorized 15% of it's profit to manage these payments.
One of the purposes of mobilizing is to strengthen smooth operation of savings and credit including micro insurance in order to realize economic growth of the poverty stricken women. At present the total membership of WDF has exceeded 70,000 and 1243 member societies are functioning. Members of these societies are used to meet in every two weeks. Also, all the members those who represent 13,500 SHGs (Self Help Group) are extremely important for effective operation of the WDF. These SHGs are practicing weekly meetings and after each meeting they perform, free labour work, savings, sharing goods bought on wholesales prices etc., Progress of each SHG is reviewed at village society meetings which are assembled in every two weeks.
Group guarantee becomes a basic requirement to be qualified for a loan. Administratively, 1,243 trained Assistant Coordinators are employed to facilitate group or society meetings, to resolve inter-personal misunderstandings, while assuring smooth operation of loan activities etc., and in addition there are 36 senior staffs appointed to oversee the accuracy of the said operation. The overall responsibility is being held by a Snr. Manageress assisted by an Asst. Manageress. There are 12 fundamental ethics in use in the process of Mobilization
Living with the respective community
Attitude of learning from the community
Follow collective practices of planning
Work with the community
To start from the level of knowledge of the community members
Also start each activity from what is owned by the community
Learn by doing and through experience
Improving self effort instead of dependency syndrome
Instead of introducing an incident, to introduce method
Rather than working in isolation, to work in collaboration
Instead of static process to enable understanding of change and dynamism
Empowering collective strength.
The Mobilization unit of WDF is responsible for implementation of mobilization along with the above principles. Evidently, the impact of mobilization based action series has contributed in whatever way to minimize poverty from 32.4% in 1990/91 to 6.9 % in 2001. Similarly the life expectancy too, has increased up to 82 years .


Elevated basal, ligand-independent, Wnt signaling in some canine breast cancer cells is not caused by classical mutations in APC, β-Catenin or GSK3β but, at least partially, by enhanced LEF1 expression. We examined the expression and function of EGFR/HER-regulated pathways on the ligand-independent Wnt signaling.
Twelve canine mammary tumor cell lines with previously reported differential basal Wnt activity were used. The expression levels of genes related to EGF-signaling were analyzed by cluster analysis. Cell lines with a combined overexpression of EGF-related genes and enhanced basal Wnt activity were treated with PI3K/mTor or cSRC inhibitors or transfected with a construct expressing wild-type PTEN. Subsequently, effects were measured on Wnt activity, cell proliferation, gene expression and protein level.
High basal Wnt/LEF1 activity was associated with overexpression of HER2/3, ID1, ID2, RAC1 and HSP90 together with low to absent cMET and PTEN mRNA expression, suggesting a connection between Wnt- and HER-signaling pathways. Inhibition of the HER-regulated PI3K/mTor pathway using the dual PI3K/mTor inhibitor BEZ235 or the mTor inhibitor Everolimus® resulted in reduced cell proliferation. In the cell line with high basal Wnt activity, however, an unexpected further increased Wnt activity was found that could be greatly reduced after inhibition of the HER-regulated cSRC activity. Inhibition of the PI3K/mTor pathway was associated with enhanced expression of β-Catenin, Axin2, MUC1, cMET, EGFR and HER2 and a somewhat increased β-Catenin protein content, whereas cSRC inhibition was associated with slightly enhanced HER3 and SLUG mRNA expression. A high protein expression of HER3 was found only in a cell line with high basal Wnt activity.
High basal Wnt activity in some mammary cancer cell lines is associated with overexpression of HER-receptor related genes and HER3 protein, and the absence of PTEN. Inhibition of the PI3K/mTor pathway further stimulated, however, canonical Wnt signaling, whereas the inhibitory effect with the cSRC inhibitor Src-I1 on the Wnt activity further suggested a connection between Wnt and HER2/3-signaling.
Progesterone-induced Wnt signaling plays an important role in the development of the mammary gland during puberty, but may also induce the development of mammary tumors from stem/progenitor cells . There is a high incidence of active Wnt signaling in basal-like breast cancers . Since this activity cannot always be explained by overexpression of Wnt ligand or mutations in players involved in the destruction complex of β- Catenin alone , this high Wnt signaling must have additional causes. One potential candidate, cytoplasmic β-Catenin, functions as a key signaling intermediate in the canonical Wnt/β-Catenin pathway. Wnt proteins, by binding to membrane receptors on the cell membrane, initiate the signal transduction. The total Wnt group consists of multiple genes that are either canonical (Wnt 1, 3A, 8A, 8B) or non-canonical (Wnt 5A, 4, 11). Wnt can also stimulate alternative effectors in the non-canonical pathway that can antagonize the canonical pathway .
Without a Wnt signal, the β-Catenin destruction complex binds and phosphorylates non-cadherin-associated β-Catenin. This targets it for destruction by the proteasome, thereby allowing TCF family of transcriptional factors to bind to transcriptional repressors in the nucleus. The destruction complex is disrupted when active Wnt signaling is stimulated by binding of Wnt proteins to its Frizzled receptor on the cell membrane. As a result β-Catenin accumulates in the cytoplasm, translocates to the nucleus and associates with TCF family of proteins, enhancing transcriptional activation of a program of genes [3–5].
In the non-canonical Wnt pathway, Wnt can act through ROR and RYK tyrosine kinases, which activate Jun N-terminal kinase (JNK). This increases intercellular Ca2+ leading to activation of nuclear factor activated T cells (NFAT) and consequently inhibition of the canonical signaling. The alternative Wnt receptor RYK additionally signals through Dishevelled to cSRC in axon guidance. Traditionally Wnt ligands do not signal through β-Catenin in the non-canonical pathway, but it seems that Wnt 5A had some inhibitory characteristics on the canonical signaling. Likely there is some crosstalk between the canonical and the non-canonical Wnt pathways .
The major drivers of breast cancer risk are 17ß-estradiol (E2) and progesterone (P4). Synthetic progestins are frequently given as oral anticonception or in hormone replacement therapy (HRT) [6, 7]. Apart from stimulating the expression of Wnt4  P4 decreases the presence of the ß-catenin binding adhesion protein E-cadherin, which may result in higher Wnt/β-Catenin signaling . P4 also affects the non-canonical signaling through the transcriptional activity of activator protein 1(AP1) in the signaling cascade of JNK and MAPK . In the dog, P4 also plays an important role in mammary cancer . This makes dogs a useful model, since they share human environmental risk factors and their mammary tumor biology shows a significant overlap with humans: sequencing canine simple mammary carcinomas revealed comparable genomic aberrations to those in human breast cancer. Further, both humans and dogs apparently share pathways that are altered in carcinogenesis, such as cell adhesion, Wnt signaling and PI3K signaling , making them an attractive model for hormone-dependent breast cancer research [5, 12].
Recently we have shown that three canine mammary tumor cell lines with high basal Wnt/β-Catenin activity do not respond to treatment with the Wnt ligand synthesis inhibitor IWP-2 and therefore use a ligand-independent mechanism to activate the pathway. In 4 other cell lines, moderate basal Wnt reporter activity could be inhibited using IWP-2 showing a clear ligand depend Wnt activity, the remaining cell lines had no basal Wnt activity. We furthermore showed that overexpression of LEF1 is one of the contributing factors of the high Wnt/β-Catenin activity in these cells . In this study we demonstrate that these cells also have lost PTEN expression. PTEN is a tumor suppressor gene and a phosphatase that antagonizes the kinase activity of PI3K. PTEN can also target focal adhesion kinase (FAK), the EGF receptor and itself as a binding partner to increase p53 activity . A properly functioning PTEN thus inhibits PI3K/AKT/mTOR and MAPK signaling.
The epidermal growth factor (EGF) is transactivated by the Wnt pathway, which in addition stimulates the ß-catenin/TCF pathway, making Wnt a potent oncogene in the mammary gland . Binding of EGF or related growth factors to the EGF receptors induces homo- and heterodimers leading to phosphorylation on specific tyrosine residues; these residues serve as docking sites for a variety of signaling molecules, leading to activation of intracellular pathways such as the mitogen-activated protein kinase (MAPK), the phosphatidylinositol-3-kinase (PI3K), Stats, RAS and cSRC pathways. Although not binding any ligand, HER2 plays a central role together with the HER3 protein that lacks proper tyrosine kinase activity, with this complex being the strongest activator for downstream signaling pathways [14, 15]. HER3 can also signal ligand independent and its activation is associated with resistance to HER2 targeting tyrosine kinase inhibitors in breast cancer . The HER3 protein, which has no kinase activity, may signal in the nucleus through several C-terminal transactivation domains . Also in the dog, HER2 is overexpressed in some 35 % of malignant mammary tumors whereas HER3 is found in the nucleus of some 42 % of mammary carcinomas .
We therefore investigated in a panel of canine mammary tumor cell lines for a relationship between the canonical Wnt signaling and HER signaling pathways. As shown recently these cell lines varied in basal Wnt/ß-Catenin signaling from high ligand-independent to moderate ligand-dependent or absent basal .
Canine mammary tumor cell lines used in this study were CMT1, CMT-U229, CMT-U335, CMT-U27, CMT9, P114, CHMp, CHMm, CNMp, CNMm, CIPp and CIPm [19–21]. The cell lines were generous gifts of the Prof Dr Hellmen (SLU, Uppsala, Sweden), Prof Dr Sasaki (Laboratory of Veterinary Surgery, University of Tokyo, Japan), and Dr Rutteman (Utrecht University, The Netherlands). All cell lines were cultured in DMEM/F12 (Invitrogen, Bleiswijk, The Netherlands) supplemented with 10 % fetal bovine serum (FBS) (FBS Gold, PAA, Cӧlbe, Germany). Cells were tested to be free from mycoplasma with a Mycosensor QPCR assay according to manufacturer's protocol (Agilent technologies, Middelburg, The Netherlands).
Cells were seeded in a 24 well plate (Primaria, BD Biosciences, Breda, The Netherlands) at a density of 100,000 CMT1, CMT-U27 and CMT9 cells and 80,000 CIPm cells, to reach an 80 % density 24 h before transfection. Transfection was performed in FBS-free medium using 3 μl Lipofectamine 2000 (Invitrogen), 800 ng pTOPFLASH (TOP) or pFOPFLASH (FOP) (gift from Prof Dr Hans Clevers, Hubrecht Institute, The Netherlands) and 0.5 ng human ß-actin-promoter renilla construct  as an internal control. Transfection was stopped after 5 h by adding the same volume DMEM/F12 supplemented with 20 % FBS. Cells were treated with 100 nM Everolimus (Selleckchem, Munich, Germany), 50 nM BEZ235, (Selleckchem), 20 μM Src-I1 (Enzo, Lausen, Zwitserland), or 1 μM FAK Inhibitor 14, (Santa Cruz, Heidelberg, Germany) for 40 h. All the compounds were dissolved in DMSO and diluted in medium to a final concentration of 0.2 % DMSO. The firefly and renilla luciferase activities were measured using a Dual-Luciferase Assay System (Promega, Leiden, The Netherlands) in a Centro LB 960 luminometer (Berthold Technologies, Vilvoorde, Belgium).
From each cell line, total RNA was isolated and treated with DNase using RNeasy mini kit (Qiagen, Venlo, The Netherlands) according to manufacturer's protocol. Using iScript kit (BioRad, Veenendaal, The Netherlands), cDNA synthesis was performed. Specific primer sets were used to amplify gene products in a qPCR reaction (Table 1). The reactions were performed and measured using a BioRad MyIQ detection system (BioRad) with SYBR green fluorophore. Relative target gene expression was normalized to a set of eight reference genes (tested in Genorm with a pairwise variation (PV) of 0.07) for the transfection experiments. For the cluster analysis, 6 reference genes were used with a PV 0.07 (HNRPH, TBP, SRPR, HMBS, RPS5 and RPS19). A relative induction of gene expression was statistically assessed using paired, 2-tailed student's T-test. Relative expression was calculated by the delta-delta Ct (ΔΔCt) method .
Cell viability was determined by means of the colorimetric 3-[4,5-dimethylthiazol-2-yl] 2,5-diphenyltetrazolium bromide assay (MTT) (Sigma Aldrich, Zwijndrecht, The Netherlands). Briefly, cells were seeded in 96 wells plates (Primaria, BD Biosciences, Breda, The Netherlands) and after 24 h incubation to attach and stretch, treated with the different compounds for 40 h. Cell viability was determined by incubating 20 μl 5 mg/ml MTT in 100 μl medium in each well. After a 2 h incubation, the media was removed by decanting and 100 μl DMSO was added to each well, incubated for 30 min and the absorbance was measured at 595 nm in a spectrophotometer Anthos Multimode Detector (Anthos Mikrosystem GmbH, Krefeld, Germany). IC50 curves were plotted with Sigma-plot version 12.5.
Cells were seeded in 75 cm2 bottles and after 24 h incubation to attach and stretch, treated with the different compounds. After 40 h cells were washed with cold HANK's balanced salt solution and lysed and scraped with RIPA buffer . After 20 min incubation on ice, samples were centrifuged for 15 min at 16,000 g and 4 °C. Protein concentration was determined using Bio-Rad Dc Protein Assay (Bio-Rad Laboratories). Twenty micrograms of protein from total cell lysates was subjected to SDS-PAGE and analyzed by Western blot. Primary antibodies used in this study were directed against β-Catenin (Ab6302 1:4000) (Abcam, Cambridge, UK), HER2 (PA5-14635 1:500) (Pierce-Thermo Scientific), HER3 (PA1-86644 1:2500 (Thermo Scientific), with β-Actin pan Ab-5 (MS-1295-P1 1:2000) (Thermo Scientific) as a reference protein. And as secondary antibody, goat anti-mouse HRP-conjugated (HAF007), goat anti-rabbit HRP conjugated (HAF008) and donkey anti-goat HRP conjugated (HAF109) (R&D Systems, Abingdon, UK) was used in a 1:20.000 dilution. HRP was visualized using Advance TM_Enhanced chemiluminescence (ECL, Amersham, GE Healthcare, Eindhoven, The Netherlands) and analyzed using GelDoc 2000 (Bio Rad). With the Quantity One software, version 4.6.9 (BioRad), densities were measured, corrected for the background and related to β-Actin expression as loading control.
Cluster analysis with qPCR results from all the cell lines was done in RStudio (version 3 software (R Core Team (2013) R: A language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria; http://www.r-project.org)) with a Pearson:Spearman test (genes: Pearson; samples: Spearman average) to find a correlation between the TOP/FOP ratio, related target genes and the cell lines.
Transfection and incubation studies, and also the MTT assays, were done in three independent experiments (n = 8 for MTT and n = 4 for each transfected/incubation compound). After background subtraction, the cell viability, the Wnt-signaling and the protein levels were calculated as a percentage of the non-treated cells. IC50 curves were done in a single experiment with n = 8 and the HER3 Western blots were done in triplicate. Differences in TOP/FOP activities, RNA, cell viability and protein expression levels were statistically assessed using unpaired, two tailed Student's t test, a P value less than 0.01 was considered significant.
In a continuation of our previous findings of a variation in basal Wnt/β-Catenin activity in canine mammary tumor cell lines  we searched for the mRNA expression of members of the EGF receptor family of proteins and the associated signal-transduction pathways. In the present paper, the three cell lines with high ligand-independent basal Wnt activity (CMT1, CMT-U27 and CMT9) were, through cluster analysis of the gene expression data, shown as a clear grouping, but no clear association for absent or low Wnt-ligand induced basal Wnt/β-Catenin activity in the other cell lines (Fig. 1). High basal Wnt activity is clearly grouped together with an up-regulated expression of LEF1, ID1, ID2, EGFR (only in CMT1), HER2/3, HSP90 and RAC1 mRNA and a down regulation of SLUG, NCOA3, MUC1, CYCLIN D1, BCL2, cMET and PTEN mRNA. In these highly activated Wnt cell lines, PTEN expression is completely lost. PTEN deficiency occurs in 5 to 14 % of primary human breast cancers and PTEN is also lost in human T47D and MCF7 cell lines . The cluster analysis confirmed our previous finding that in the cell lines with active Wnt signaling, LEF1 is overexpressed and acts as a contributing factor of the high canonical Wnt pathway . New is our finding of a strong association of the expression of the EGF pathway both at the receptor level (HER expression) as in the silencing of PTEN with high ligand independent Wnt signaling. Previously, it has been shown that binding of Wnt proteins to the Frizzled receptor may activate the EGFR. EGFR can be further activated by homo or hetero-dimerization with HER2, HSP90 as its chaperone, or HER3. These activated complexes functions as an oncogenic unit to drive the proliferation of breast cancer cells [14, 24]. In human and mouse mammary glands, the activated Wnt/β-Catenin is related to enhanced HER2 expression , something also found in 30 % of canine malignant mammary tumors . Combining the up regulation of both HER2 and HER3 in our canine mammary cell lines and the fact that the HER2/HER3 complex is the strongest activator for downstream signaling pathways makes this an interesting area for further research [15, 27, 28].
We concluded that the association between high Wnt signaling (high TOP/FOP ratios), high LEF1 levels, loss of PTEN and high HER2/3 mRNA levels all point to the activation of the PI3K/AKT/mTor pathway [29–32]. We therefore investigated the effects of PI3K/mTor inhibitors on cell viability, Wnt signaling, expression levels of the differently expressed genes from the clustering analysis and the cellular content of β-Catenin, and HER2/3 protein as an experimental model for HER2+/PTEN- breast cancer.
Cell lines with high Wnt activity and a cell line lacking basal Wnt activity (CIPm) were incubated with Everolimus as a specific mTor inhibitor and BEZ235 as a dual inhibitor of PI3K and mTOR. Both BEZ235 and Everolimus equally inhibited the viability of the highly activated Wnt cell lines and have only a slightly inhibitory effect on the CIPm cells (Fig. 2).
This inhibitory effect on viability was clearly dose-dependent and present in both the high basal Wnt cell line CMT-U27 and the CIPm cell line (Fig. 3 and Table 2). Comparable concentrations of BEZ235 were also used in human studies with different cell lines [33, 34]. In human MCF7 cells, Everolimus (Rad001) was tested in a range from 0-1000 nM and only the 1000 nM concentration showed a 50 % reduction in cell number . Incubation of these cells with BEZ235 and Everolimus resulted in unexpected further significant enhancement of Wnt activity of CMT1, CMT-U27 and CMT9, with a more than 2-fold increase in the TOP/FOP ratios (Fig. 4).
BEZ235-induced inhibitions of cell proliferation have been reported previously in MCF-7/shPTEN cells and in 21 other tested human cancer cell lines . The only difference is that in these cell lines, BEZ235 had a stronger effect than Everolimus on cell proliferation . In human breast cancer, loss of PTEN is associated with activation of the PI3K/AKT Pathway , which may result in increased nuclear stabilization of β-Catenin in mammary stem cells using human breast tissue xenografts . This is in contrast to the absence of any inhibitory effect in the TOPFlash reporter assays of several breast and prostate cancer cell lines treated with another inhibitor of the PI3K pathway (Wortmannin) and suggests that the PI3K pathway has no relation with Wnt-mediated transcriptional activity . In our cell lines as well, neither Wortmannin nor the introduction of a PTEN-expressing plasmid inhibited Wnt signaling, indicating that PI3K inhibition alone does not influence the active Wnt signaling and that mTor inhibition is needed (data not shown). CIPm, which lacks basal Wnt activity, did not respond to both inhibitors with increased reporter activity.
We conclude that inhibition of PI3K and/or mTor in the highly activated Wnt cell lines inhibits cell viability, but further stimulates Wnt activity. Because the mechanism behind this remained unclear, we tested the effect of these inhibitors on the expression of genes from the cluster analysis.
Inhibition of the PI3K/mTor pathway with BEZ235 (a dual PI3K mTor inhibitor) or with Everolimus (a single mTor inhibitor) in cell lines with high ligand-independent canonical Wnt activity resulted in comparable upregulation of a number of candidate genes (Fig. 5). A moderate twofold increase was detected in the expression of β-Catenin, Axin2, HER2 and cMet mRNA. Only the expression of EGFR and MUC1 mRNA was higher, especially in the CMT-U27 and CMT9 cell lines. β-Catenin and Axin2 are markers for an activated Wnt/β-Catenin signaling in mammary tissues . Protein levels of β-Catenin were not significantly different after treatment with both inhibitors (Fig. 6). The stable total protein expression of β-Catenin may reflect predominantly binding to E-cadherin, which is comparable high in both cell lines [5, 7] and may not be related to the cytoplasmic or nuclear ß-Catenin content. No significant effect of both inhibitors was seen on HER2/3 protein content although HER3 expression was only found in the cell line with high basal Wnt activity (Fig. 6). Apart from the expression of HER2 at the cell surface it can also form a complex with AP-1/Stat3/PR in the nucleus. This nuclear HER2 can act as a transcription factor and modulate genes involved in breast cancer proliferation . In contrast with the absence of HER3 in the CIPm cell line, the CMT-U27 cells have a HER3 band visible at 180kD, which correspond to a glycosylated form. This glycosylated HER3 protein is also found in human MDA-MB-445 and MDA-MB-453 cells . In MDA-MB-453 and other mammary tumor cell lines, there is strong evidence for the role of HER3 in cancer. HER3 plays a role in EMT and activated HER3 can also increase the expression of the cMET proto-oncogene independently from EGFR and HER2 , which may be in line with the 2-3 fold increased expression shown in Fig. 5. EGFR and HER2 expressions are upregulated after treatment with BEZ235 in a human breast cancer cell line with a lack of PTEN (MDA-MB-468). In contrast with this BCL2 is not upregulated in all tested canine cell lines and HER3 is only, although significantly, 1.5 times upregulated in some cases . The most prominent change was the 7-fold increase in MUC1 expression. At the same time, in all tested cell lines, basal MUC1 protein concentrations showed no difference, even in the presence of considerable amounts of the cytoplasmic domain MUC1-CD (data not shown). Still, overexpression of MUC1 plays a role in tumor formation and progression in > 90 % of the breast cancers . It has been reported that the Wnt activity is directly affected through the binding of the Wnt effector β-Catenin on MUC1-CD  through binding of several proteins, including cMET, cSRC and EGFR/HER. Consistent with this is the enhanced EGFR and oncoprotein MUC1 mRNA concentrations in our experiment together with the upregulation of cMET. Enhanced cMET expression has been linked to poor prognosis in human breast cancer, since it influences extravasation/angiogenesis, enhances resistance to endocrine therapy and trastuzumab treatment and may influence the regulation of β-Catenin/TCF transcription [29, 43]. The basal expression of cMET in the cell lines with elevated Wnt activity is low, but stimulated when the PI3K/mTOR pathway is blocked; blocking this pathway also affects the EGFR and HER2 expression. Overexpression of MUC1 is associated with the induction of anchorage-independent growth and tumorigenicity in human carcinomas. MUC1 overexpression is also directly associated with stabilization of β-Catenin either via MUC1 binding to E-Cadherin, or by inhibition of the adenomatous polyposis coli (APC)/GSK3β/ MUC1-CD complex, whereas phosphorylation of MUC1-CD by EGFR and cSRC increases β-Catenin [42, 44–46].
Leaving aside the question of how EGFR/HER2/HER3 signaling is involved in high basal Wnt activity, it is clear that the upregulation of the MUC1 and EGFR/HER2 expression have a relationship with the increased Wnt activity that occurs after inhibition of the PI3K/mTor pathway. The presence of glycosylated HER3 protein in the highly activated Wnt cell line is new, and because our results suggest that activation of cSRC could play a role [15, 46], we next studied the influence of cSRC inhibitors on the Wnt activity and HER3 levels.
Activation of EGFR initiates the activation of PI3K/AKT/mTor and MAPK as well as various other signaling pathways, including the PLC-Υ1, JAK/STAT, and cSRC pathway [15, 47]. Because the EGFR can form a complex with cSRC, FAK (focal adhesion kinase), integrins and β-Catenin resulting in growth, viability, survival and migration , we tested the effect of the cSRC inhibitor 1 (Src-I1) and a FAK inhibitor [48, 49]. Treatment with the FAK inhibitor resulted in a small non-significant decreases in the TOP/FOP ratio with no effect on cell proliferation (data not shown), however Src-I1 had a clear effect on cell viability and was found to be an inhibitor of the Wnt activity via inhibition of cSRC signaling [50, 51]. The same inhibition on the Wnt pathway was found in the human cell lines NIH 3 T3 with the cSRC inhibitor PP1 . The used concentration of Src-I1 reduced cell proliferation for some 20 % and acted as a weaker inhibitor in comparison with BEZ235 and Everolimus (Fig. 2). Unlike BEZ235 and Everolimus, the cSRC inhibitor Src-I1 reduced the Wnt/β-Catenin signaling by almost half in canine mammary tumor cell lines with high canonical Wnt activity, but not in the CIPm cells that lack basal Wnt activity (Fig. 4). Inhibiting mouse cells with cSRC inhibitors PP2 and Genistein gave comparable results on LEF/TCF sensitive transcription and on the level of activated phosphorylated cSRC. This indicates that cSRC is a positive regulator of the Wnt/β-Catenin signaling . To investigate the Wnt-regulation by both the PI3K pathway and the cSRC pathway, we tested the same target genes used in the clustering analyses (Fig. 1).
The cSRC inhibitor Src-l1 decreased the cell viability (Fig. 2), decreased Wnt signaling (Fig. 4) without affecting MUC1, EGFR and HER2/HER2 expression levels (Figs. 5 and 6). The inhibition of Wnt activity as measured by a decrease in TOP/FOP ratios was also clearly dose-dependent (data not shown) in the activated Wnt cells. Marginal increases were found in SLUG and HER3 mRNA concentrations (Fig. 5c) after cSRC inhibition. Remarkably inhibition with Src-I1 showed a significant decrease in HER3 protein concentrations whereas the HER3 mRNA expression was slightly elevated indicating that cSRC inhibition is associated with a higher turnover or a decreased glycosylation of HER3 at the protein level. At the moment information on the regulation of HER3 expression is scarce. Several microRNAs regulate the expression levels and also epigenetic effects have been shown to influence HER3 expression in breast cancer cells .
We see an association between the Wnt pathway and the EGFR/HER2/HER3 stimulated cSRC (motility) route. The role of MUC1 is less clear and needs further research. In mice, however, data are available showing that MUC1 activates cSRC signaling by influencing the association of PI3K and β-Catenin leading to a delay in mammary tumor progression . Prior research indicates that activation of the PI3K/mTor pathway may be related to resistance to hormonal therapies. Administration of the mTor inhibitor Everolimus has therefore been studied extensively in women with HR+, HER2+ or TNBC breast cancer. Reports on various studies, i.e. BOLERO (Breast Cancer Trials of Oral Everolimus), TAMRAD and EFECT, have shown an increased progression free survival (PFS) when Everolimus was combined with aromatase inhibitors . If the effects shown in this paper on the in vitro inhibition of cell viability but increased Wnt signaling are also present in a subset of breast cancer patients then treatment with Everolimus could have an adverse effect on Wnt regulated aspects such as stemness and metastasis.
cSRC may play a crucial role in tumor growth and metastasis. Metastasis involves loss of cellular adhesion, increased motility, intravasation, invasion, extravasation, resistance to anoikis, and colonization at distant sites. High cSRC expression is found in various breast cancers in association with reduced survival. Recently the cSRC inhibitors Dasatinib and Bosutinib were studied as a monotherapy in humans, but showed no clear reduction of antitumor activity, indicating that before further studies are done, clear biomarkers should be found for proper patient selection . The search for these biomarkers is being aided by research on dogs with spontaneous mammary carcinomas. For example, the successful treatment with Dasatinib of a dog with osteosarcoma, reported in a recent case study, shows that the dog is an interesting animal for further clinical studies using cSRC inhibitors in HER2+/PTEN- tumors [26, 55, 56]. Binding of cSRC to HER2 is crucial for the formation of HER2:HER3 heterodimers. Both phosphorylated and total levels of cSRC are upregulated in anti-estrogen resistant T47D cell lines that show growth reduction by cSRC inhibitors. EGFR homodimers also play an important role in growth. The individual contributions of EGFR, HER2 and HER3 in Wnt pathway activation require further study. Our results on highly activated Wnt signaling cells require further research into the role of HER3, cSRC, and Wnt on tumor growth and metastasis .
In summary, inhibition of the PI3K/mTor pathway in tumor cell lines with ligand-independent Wnt activity further increases canonical Wnt signaling. As we have shown, this Wnt activity can be effectively inhibited by a cSRC inhibitor. While very recently, loss of PTEN has been associated with worse outcomes in HER2 positive breast cancer patients, no data are available on their Wnt activity . Although a number of human breast cancer cell lines have active ß-catenin signaling (summarized in ), this relation between HER2/3 expression and PTEN loss appears not to have been previously documented.
Further studies will need to identify optimal biomarkers for selecting breast cancer patients most likely to benefit from concerted treatment with combination therapies of mTor and cSRC inhibitors. Such research is very likely to include studies in dogs with spontaneous mammary carcinomas.
We greatly acknowledge Hans Clevers, Hubrecht Laboratory, Utrecht The Netherlands for the supply with TOP- and FOP-Flash reporter constructs. Andrew Aplin, Thomas Jefferson University, Philadelphia USA for the gift of the PTEN expression plasmid. Frank Riemers for the clustering analysis, Monique van Wolferen for several qPCR data and Ms Linda McPhee (write-research.com) for language advice. This work was supported by the Mozaiek Grant 017.004.081 (to A.G.) from the Dutch Society for Scientific Research (NWO).
EPMTS, AG and JAM conceived and designed the experiments. EPMTS and AG performed the experiments and analyzed the data. EPMTS and JAM wrote the paper. All authors read and approved the final manuscript.


text:
Film Junk Podcast Episode #703: Hellboy
Posted by Sean on April 16th, 2019 Filed under: Featured, Film Junk Podcast
0:00 – Intro: The Deaner
16:30 – Review: Hellboy
39:30 – Headlines: Star Wars: The Rise of Skywalker Trailer
51:25 – Other Stuff We Watched: The Kid Who Would Be King, The Lineup, Nightfall, The Burglar, Experiment in Terror, Guava Island, Game of Thrones
1:23:30 – This Week on DVD and Blu-ray
1:23:55 – Outro
» Download the MP3 (44 MB)
» View the show notes
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Sean. I bet you heard the Fantomas cover of Experiment In Terror.
https://www.youtube.com/watch?v=e74k2Gi2-Fg
Todd S. Gallows
You beat me to it.
yonato
Agree with you 100% on Game of Thrones Frank.
It's possible although I don't think I ever owned this album.
I did find an old Henry Mancini tribute album called Shots in the Dark that *may* have been where I heard it originally.
IMO the sound quality is noticably better now! Keep up the good work guys!!
devolutionary
The Rosemary's Baby track is my favourite. I would recommend you also check out Petra Haden's (ex-Decemberists) album "Petra Goes to the Movies". Classic vocal-pop tributes to film scores.
https://youtu.be/FIl7CkgYYMM
I really need to rewatch Nightfall. I love Jacques Tourneur and noir but that was one I watched maybe 2 years ago and did not like it. Quality wasnt great so maybe a Criterion channel revisit is in order.
I did enjoy The Burglar and The Lineup watching those around the same time too though.
Moratorium on Frank whining about ADR in movies or being a killjoy on anything that's super-popular like Game of Thrones.
tyler mikol
I loved hearing about The Criterion Channel viewings Jay and Sean has this week. I watched a few Noirs this week also. THE BIG HEAT which is a masterpiece and probably in my top 3 Noirs of all time. Then I watched PUSHOVER with Fred MacMurray and a 20 year old Kim Novak. It's great as well. I'll be checkin out the ones our boys talked about, and Frankie, stay away from TCC. It ain't for ya bud.
I'm happy I'm not as smart as Frankie. It would suck to be able to predict every piece of dialogue and to figure out how every film
Is going to end before watching it.
I kinda given up on Frank actually watching some interesting stuff. I love Frank but it seems like 90% of what he watches outside of something within the current year is a rewatch.
For someone who dislikes a lot of whats popular and says he likes hidden gems, he really doesn't do much digging for those gems. Instead, he tries to polish rocks in plain sight into gems with force feeds.
Love ya though Frank! Just some times wish I coule hear some of those irrational thoughts applied to a wider range of movies.
Haven't seen it in ages either. I recall mixed feelings over the change in tone and characters throughout. Remember loving the setup so it definitely deserves a rewatch.
Beat_C
perfect sound quality ???????? thanks for another great show.
You are spot on. I also love our dear Frank but he should try to dig some more. Instead of watching Major League for the 300th time he could go check out some True under seen gems. Let's bring back Prescribing Frank!
The Big Heat is one of my favourites out of the ones I've seen as well. It occurs to me that when Reed was asking for recommendations a month or two ago I mentioned White Heat when I really meant The Big Heat.
Andrew James
Not bullshit Frank. I absolutely remember the reel change pop in Return of the Jedi during the Jabba's Palace scene. I saw that film 4 or 5 times at the same theater. This particular pop was slightly more noticeable than others, so for years I always expected it to be there even on VHS.
sansho1
We had the album of the Mancini score when I was a kid, and a friend and I used to terrorize my younger sister by playing it and telling scary stories of murder and abduction by monsters. It really is quite creepy and holds up great.
People should watch this while they wait for next week's episode:
https://www.youtube.com/watch?v=zckMQrryJX0
That Death Proof into is amazing. I can't believe it's been almost 12 years.
OsoDuck
I'm pretty sure Llorona would be pronounced Yo ro na. Off the top of my head, I think It's a traditional mexican tale about a ghoul woman who murders children, and apparently the traditional song associated with it was incorporated into Pixar's Coco, from what I've just gleaned from a quick youtube search.
https://www.youtube.com/watch?v=Ukp_EFEDOl4
White Heat is great too! But yeah, The Big Heat is also a favorite of mine.
I first watched probably like 10 years ago and I think I had it rated at 4/5, but after rewatching recently, it's a 5-banger easy and a Top 10 noir for me.
filmstache
The Fantomas cover is really great!
Yeah, La Llorona is kind of an equivalent to something like Bloody Mary in terms of folklore.
Your pronunciation is basically right. It's more of a soft/short R, so it's kind of like Yor-o na. Almost like saying "Euro" but with a "yo" instead of "you" sound
colin the dude
This reminds me. Been meaning to ask, how come Roman never comes on the show?
These are big facts.
But it's also the reason the Jay/Frank push and pull is such gold.
This listener is really enjoying the new Criterion Channel too; especially the Columbia Noir series that Jay and Sean mentioned in this week's podcast. Also rewatched Blood Simple for the 1st time in 10 years including the many related accompanying Criterion features. Hoping future podcasts continue to mention offering on this channel. Fingers crossed that this great service can sustain and succeed for many years.
I have bad news, folks.
IMDB has finally hit rock bottom:
https://uploads.disquscdn.com/images/0829da8f1fae7059a9b7b67951c8e5dce09357efbf09265ab8975725b20e3e63.jpg
He's got 3 kids and travels a lot for work so he's got a lot going on. He does still make it out to the drive-in from time to time though. It would be great to get him back on at some point!
This video is like a lost treasure. I have never seen it. The video podcast thing must make a comeback!
This video is like a lost treasure. I have never seen it. The video podcast thing must make a comeback!!
I just blind-bought this from Indicator even though I knew it's gonna be on the Criterion Channel… have yet to watch.
Sean, George RR Martin has stopped writing scripts for the TV show after season 4 so that he can concentrate on his novels.
As we can all see, that has not achieved the desired result since book 6 is not out yet, and from season 7 onward the scripts are based on Martin's general outlines but obviously not any completed works. We can debate whether that compromised the quality of the show, but people love what they are seeing. The show has never been bigger. Of course we all have preferred that the novels stay ahead of the show but that was not to be.
Yeah I just meant that they are still working from his basic plan, it's not like they cut him off and took it in some completely unauthorized different direction. But I don't doubt that the show would have benefited from having him more directly involved throughout.
TimC
Frank's analysis of Game of Thrones' most recent seasons is spot-on.
It was a little frustrating to hear Jay accuse him of just being anti-COPO, as I think Jay would probably actually agree if he was caught-up.
Hopefully the guys can reprise this discussion once everyone finishes watching the complete series.
I also agree with Frank about Game of Thrones. I feel there's been a steady decline in quality even as its popularity has skyrocketed, with overly contrived or convenient plotting/character behavior becoming common features of the show.


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