text:
Home Health & Fitness 15minutes4me: A personalized app for eliminating stress, anxiety, and depression
15minutes4me: A personalized app for eliminating stress, anxiety, and depression
by Businesszag April 28, 2022
written by Businesszag April 28, 2022
Getting stressed has become a common thing nowadays. Every second person is going through depression. If you are one of them and want a good doctor then you should know about 15minutes4me. At this place, you can resolve your stress and anxiety.
In this article, you will get the complete guide. We will explore what is 15minutes4me and how you can get in touch with doctors in 15minutes4me.
Definitely, all of us want to remain mentally and physically fit in our ups and downs. But how it can be? How can we remain consistent during our hard times?
Let us explore 15minutes4me.
What is "15minutes4me"?
15minutes4me is providing a free self-help program to resolve stress, anxiety, and depression through an online program. This online website is especially for those people who get more stressed and depressed.
Doctors and experts are available 24 hours and also they are available on weekends. The interesting fact is, you don't need to be waiting for an appointment and no wait for calls. It's upon you when you are free to get a complete service. Services are available at your home, offices, and anywhere.
This is a personalized app designed to give guidance for just 15 minutes per day for a month. You can proceed with this service for the long term if you want. They will provide you with some questions which help you to come out from stress and move on. These questions will help you to find out the way to problem solve and gives you confidence.
What kinds of offers does 15minutes4me provide?
The most important part of moving forward is "Confidence". You should have enough confidence to solve the problems by yourself and get rid of anxiety.
They will help you in avoiding negative thoughts and taking your life positively. They will provide you with different videos, charts, and theoretical insights which will be very helpful for moving on in life.
How can I log in to the self-help program?
The login process is as easy as 123. Just create an account and get into login access. Make Sure that you followed all the instructions and rules for login into the 15minutes4me anxiety test free.
Firstly, visit the official link "https://app.15minutes4me.com/login".
Click on the "subscribe now" button mentioned on the right side.
There mentioned that provide self-help courses just for $77 for 15 minutes per day for 30 days.
You can avail of this offer for just $77.
You have to enter the "First Name", "Last Name", "Email address", and as well as choose the "Language" in which language you want to take the course.
Then select the "Payment Method", there will be four options Visa, American Express, Mastercard, and PayPal. You can choose the appropriate option.
Then accept the GDPR privacy policy and terms of use and click on "Confirm your order".
Now you have done it and your order will be confirmed and you will be promoted for the next sessions.
How to start a free 15minutes4me test?
If you want to start a free 15minutes4me test, then follow the steps mentioned below:
Open an official website "https://www.15minutes4me.com/"
Click on "Start your self-test now"
Same here, click on "Start your self-test now".
After this, your 15minutes4me test will start and they will ask you different questions like your past, health condition, etc. give them the right answers about your life. When you complete the MCQs question and answer session, some more questions will appear having dropdown options.
The next step is to choose the problem to solve according to your choices like stress, depression, anxiety, etc
It is reported that a large number of mental health patients have been reported. 15minutes4me is the best place where you can get relief from stress, mental sickness, and depression. Undoubtedly, we can say that the 15minutes4me computerized program is the best ever self-help program in the world. You must try it in your busy life.
15minutes4mehow can i login to 15minutes4mewhat is 15minutes4me
Businesszag
Businesszag is an online webpage that provides business news, tech, telecom, digital marketing, auto news, website reviews in World.
Kedplasma rewards: how to log in and registration process latest 2022
Why and which technology is used to design custom Muffin boxes
Where to Buy Soma Online Overnight By Credit...
What are the Reporting Options for Eligible Clinicians...
How Vitamin D3 K2 Drops Can Help You
What Are the Long-Term Side Effects of Vitamin...
Anger Management- Beneficial or not?
Have You Had the Best Homemade Fig Newtons...
Periodontitis Treatment In Houston: What Works Best?
Treatment for Allergic Rhinitis using Ayurveda
5 Reasons You Need a Smartwatch in 2023
Find Out 7 Best Restaurants For Grilled Fish in Lahore
IS SHOPIFY PERFECT CHOICE FOR ONLINE STORE in 2023
by Uneeb Khan January 3, 2023
What City In Florida Has The Best Healthcare?


text:
'Ngog's future never in doubt - says Roy
Andy Hampson
July 30 2010 10:08 AM
Roy Hodgson hailed the performance of David Ngog after the Frenchman's double got the new Liverpool manager's reign off to a winning start last night.
Ngog, playing alone up front, struck in each half as an under-strength Liverpool emerged from a potentially tricky Europa League test against FK Rabotnicki in Macedonia with a 2-0 win.
Ngog's future has been uncertain since Hodgson took charge a month ago with reports linking the 21-year-old with a move to West Brom.
The player, however, has expressed a desire to remain at Anfield and Hodgson said: "I can't stop players being linked with other clubs.
"I certainly have never discussed him leaving.
"I think Ngog has done well in the pre-season matches so far and he has worked very hard in the training sessions.
"I was pleased that he crowned his performance with two goals.
"I thought his target play, his general movement and his ability to keep the ball for us was also very good.
"But front players need goals and that will be a very big weight off his mind.
"It will mean he doesn't have to worry too much about the coming matches."
With their Premier League opener still 17 days away, Liverpool were without 10 of their World Cup players for the third qualifying round first leg.
The likes of Steven Gerrard, Joe Cole, Jamie Carragher and Glen Johnson were left to train on Merseyside while Fernando Torres, Jose Reina and Dirk Kuyt are still on holiday.
Vindicated
Ngog was one of only a handful of recognised senior players on duty along with Lucas, Sotirios Kyrgiakos, Martin Skrtel, Daniel Agger and Alberto Aquilani.
Youngsters David Amoo, Jay Spearing and Martin Kelly all took the chance to impress against a limited Rabotnicki side and Hodgson's selection was fully vindicated.
"I am very satisfied," Hodgson said. "It was a game that could have been very difficult for us.
"It was a big crowd and some of our players that played are not used to big crowds.
"I was really pleased with the way everyone went about their business and we can go back to Anfield with a margin of victory which will enable us to feel a little more comfortable."
However, Rabotnicki could face action if UEFA authorities are alerted to an incident of racist crowd behaviour.
Pictures have emerged from Skopje of supporters directing monkey taunts towards the English side's players.
Liverpool started the third qualifying round tie at the Philip II Stadium with two black players in their side in double goalscorer Ngog and 19-year-old winger Amoo.
Macedonian football has had a problem with racist behaviour in the past.
In September 2003, England players Emile Heskey, Sol Campbell and Ashley Cole were all the subject of abuse in an international against Macedonia at the same stadium.
An English flag was also burned and European governing body UEFA later fined the Football Federation of Macedonia £10,730.

redpajama_set_name: RedPajamaCommonCrawl


RIKEN's K computer belongs to the highest caliber of supercomputers on this planet. Hi Alex, thanks for stopping by and commenting. Am glad you preferred this text. I am so excited concerning the future, particularly by way of the technologies we may develop. It is wonderful to think about how the world regarded like one hundred years earlier than and the way it looks like now. There isn't any motive to consider we may not have some very fantastic technologies 100 years hence.
A subtype of notebooks, called subnotebook , has a lot of the options of an ordinary laptop computer computer, however with smaller bodily dimensions. Subnotebooks are larger than hand-held computers , and often run full versions of desktop or laptop computer working systems. Extremely-Cell PCs (UMPC) are often thought-about subnotebooks, or extra specifically, subnotebook pill PCs , which are described below. Netbooks are typically considered to belong to this class, although they're typically separated into a class of their own (see beneath).
CSE 557: Computer Graphics Introduction to image synthesis and computer modeling, emphasizing the underlying concept required for endeavor computer graphics research. Subjects embody colour theory, picture processing, affine and projective geometry, hidden-surface willpower, photorealistic picture synthesis, advanced curve and floor design, dynamics, life like character animation. Prerequisite: CSE main, stable information of linear algebra.
Others argued that cheaply printed books and broadsheets would undermine spiritual authority, demean the work of students and scribes, and spread sedition and debauchery. As New York University professor Clay Shirky notes, Many of the arguments made in opposition to the printing press had been appropriate, even prescient." But, once more, the doomsayers had been unable to imagine the myriad blessings that the printed word would deliver.
On the 2006 World Financial Forum in Davos, Switzerland, the United Nations Growth Program (UNDP) announces it'll create a program to ship technology and assets to focused colleges in the least developed countries. The undertaking became the One Laptop per Child Consortium (OLPC) founded by Nicholas Negroponte, the founder of MIT's Media Lab. The first providing to the public required the buyer to purchase one to be given to a child in the growing world as a situation of buying a machine for themselves. By 2011, over 2.4 million laptops had been shipped.


The Air Quality Advisory Board advises the Division on day-to-day operations, and recommends control programs, regulations, and standards. The Air Quality Advisory Board consists of five (5) members appointed by the Governor.
Each board shall have one (1) member who represents industry, one (1) member who represents agriculture, one (1) member who represents political subdivisions and two (2) members who represent the public interest. Each board shall hold at least four (4) regularly scheduled meetings each year, and special meetings may be called by the chairman at any time. To determine if the Air Quality Advisory Board has a scheduled meeting, click here.


As I pointed out in a previous series of articles on PJ Media, it is customary in Orthodox synagogues to read a portion of the Five Books of Moshe from a traditionally hand-written scroll. These readings are identified as the sidra (Aramaic for "order") or parasha (Hebrew for "division"). These readings, which take place every sabbath and Jewish holiday, are followed by a reading from Nach, as the rest of the Hebrew Bible is called, which is in some way linked to the general subject of the weekly parasha. This series is intended to explore these supplemental readings, which are termed Haftara, or "taking leave" of the Torah reading.
This week's parasha begins the story of Yosef, whose story will occupy the rest of the Book of Genesis. In it, we learn of the conflict that arose between Yosef and his brothers, a conflict which led to his being sold by them into slavery in Egypt. The haftara to this parasha is Amos II, 6 - III, 8).
Amos was an older contemporary of the prophets Hoshea and Yisha'yahu ("Isaiah"), living and teaching during the reign of Yerov'am ("Jeroboam") II, King of the northern kingdom of Israel. Early in his career, Yerov'am II succeeded in subduing Israel's enemies in Syria, Mo'av, and Ammon. He brought those pagan nations under tribute to Israel and initiated a lengthy period of peace and prosperity in the northern kingdom. However, it was also a time of increasing influence of the more numerous subject nations upon Israel, a time in which the standards of Torah observance were greatly debased and the ethics of the surrounding world accepted in their place.
This is why Amos, though his origin lay in the southern kingdom of Yehuda, saw his calling in Yerov'am's realm. Amos took his cue from the Torah's juxtaposition of qedusha ("holiness") and tzedeq ("justice"). Qedoshim tihyu, the Torah enjoins us, ki qadosh Ani Ha-Shem Elo-heichem ("You shall be holy, for I, Ha-Shem your G-d, am holy," Leviticus XIX, 2) and then relates all of the principles of justice and morality to that commandment.
The connection of our haftara to our parasha is found at the beginning, when Amos chastises Israel 'al michram bakesef tzaddiq ("for their sale for silver of a tzaddiq;" II, 6). The Rabbis see this as an oblique reference to the sale of Yosef, known throughout Jewish literature as Yosef haTzaddiq ("Yosef the Just/Righteous").
He lays out a thorough indictment of the moral failings in the northern kingdom of his day: greedy selfishness; sexual looseness; engaging in the foul, idolatrous rites which characterized the Canaanites in their day, as well as their contemporary neighbors, corrupting even those who sought sanctity. They were vederch 'anavim yattu ... lema'an challel eth shem qodshi ("turning away the path of the humble" -- humility being a foundational necessity of the Torah way of life -- "in order to profane My holy name," ibid., 7). All of these practices are enjoined, as I have already noted, in parshath Qedoshim, which begins with the quotation from Leviticus above.
The prophet then offers the most damning possible indictment of this behavior, which would lead inevitably to Israel's downfall: Raq ethchem yada'ti mikol mishpechoth ha'adama; 'al ken efqod 'aleichem eth kol 'avonotheichem ("Only you have I known of all the families of the Earth; therefore I shall impose upon you all your sins," VII, 2). All of Israel, both the northern and the southern kingdom, were elected by G-d to be the bearers of Torah and the principles of Torah. This is the only purpose of Israel's existence, to be the 'am haTorah, the world's mamlecheth kohanim vegoy qadosh ("kingdom of priests and holy nation," Exodus XIX, 6). As the Torah makes clear, to be a goy qadosh Israel must also be a goy tzaddiq.
The haftara concludes with the reminder that Israel's fate is in Israel's hands: Ki lo ya'ase Ad-nai HaShem davar, ki im gala sodo el 'avadav hanevi'im. Arye sha'ag mi lo yara? Ad-nai HaShem dibber, mi lo yinnava? ("For my L-rd, Ha-Shem, will not do a thing, save reveal His secret to His servants the prophets. A lion roars: Who is not afraid? My L-rd Ha-Shem has spoken: who will not prophecy?" III, 7-8).
In our day, the voice of G-d speaks to us from the Torah, the Prophets, and the writings of Tanach as viewed through the rabbinical lens. As the Radaq points out, just as one trembles at the sound of the lion's roar, so too should one tremble at the words of the prophets.
This is why the common term for the most scrupulously observant segment of the Jewish nation is chareidim; they tremble (chared) at the word of Ha-Shem.


text:
Shuswap Lake (udtales /ˈʃuːʃwɑːp/) er en sø beliggende i det sydlige indre af British Columbia, Canada, der dræner via Little Shuswap River ud i Little Shuswap Lake. Little Shuswap Lake er kilden til South Thompson River, en gren af Thompson River, en biflod til Fraser River. Søen befinder sig i hjertet af en region kendt som Columbia Shuswap eller "the Shuswap", der kendt for sine rekreative søsamfund, herunder byen Salmon Arm. Navnet "Shuswap", som er afledt af Shuswap eller Secwepemc, betegner en stamme af et oprindeligt canadisk folk, det nordligste af Salishfolkene, hvis territorium omfatter Shuswap. Shuswap kalder sig selv /ʃǝxwépmǝx/ på deres eget sprog, som kaldes /ʃǝxwepmǝxtʃín/.

Geografi
Det centrale indre plateau i British Columbia er drænet af Fraser- og Okanagan-floderne og er en del af Shuswap jordskorpen i British Columbia og den nordlige del af Washington stat. Den gennemskæres af adskillige aflange søbassiner, som er dannet gennem gletsjeres overuddybning på samme måde som kystnære fjorde er opstået.

Shuswap Lake består af fire flodarme, der danner en form, der minder om bogstavet H. De fire arme hedder Salmon Arm (sydvest), Shuswap Arm (vest), Anstey Arm (nordøst) og Seymour Arm (nord). Shuswap Lake forbinder sig med Little Shuswap Lake via Little River, som løber fra enden af Shuswap Lake.

Mod nordvest fødes Shuswap Lake af Adams River, som dræner Adams Lake. Laksearmen fra Shuswap-søen forbinder til Mara-søen ved Sicamous-kanalen. Shuswap River forbinder via Mara Lake. I sydvest løber Salmon River ud i søen ved Salmon Arm. Eagle River løber ned fra Eagle Pass i Monashees for at komme ind i søen ved Sicamous, i øst. Seymour River munder ud i den nordlige ende af Seymour Arm. Ud over disse floder leder adskillige åer vand ud i søen, inklusive Scotch Creek, som løber sydpå til den nordlige bred af hovedarmen, nær samfundet af samme navn.

Referencer

Britisk Columbia
Søer i Canada

redpajama_set_name: RedPajamaWikipedia


text:
Q: getProductUrl() taking url without giving any url in magento 1.9 I have a custom product page and have a button too on that page below the product. I added a link on the product and the link is
<a href="<?php echo $_product->getProductUrl() ?>">

so When I'm clicking on this link the page is redirecting to "product_name.html" . So my question is, where would i find this "product_name.html" or is there any way that I could add a custom page on that link and edit that page according my need?

A: You can use url rewrites:
Go to Catalog>URL Rewrite Managment and add a URL Rewrite for product. It will walk you though and then in the last step you need to modify the Request Path (this will be your custom prodcut_name.html), click save and you have your custom url added to your product.

A: You can use $product->getUrlPath() instead of $product->getProductUrl().

redpajama_set_name: RedPajamaStackExchange


text:
Home/EU statement in response to the Address by the GUAM Secretary General
EU statement in response to the Address by the GUAM Secretary General
The European Union warmly welcomes the Secretary General of the Organisation for Democracy and Economic Development – GUAM, Mr. Altai Efendiev, to the Permanent Council and thanks him for his presentation.
We are supportive of non-exclusive regional cooperation initiatives that can contribute to improving stability and security at the regional level. The EU's framework for cooperation with the GUAM countries is the Eastern Partnership, is based on a shared commitment to the principles of international law and to fundamental values, including democracy, the rule of law and the respect for human rights and fundamental freedoms, as well as to market economy, sustainable development and good governance. Our cooperation aims at stabilisation and strengthening the state and societal resilience in the region.
At the same time, we continue to witness grave violations of Ukraine's sovereignty and territorial integrity. Russia's violation of international law, its illegal annexation of Crimea and Sevastopol, and its destabilising actions in eastern Ukraine, on top of protracted conflicts in the wider Black Sea region, challenge the European security order at its core. The EU remains firm in its support to the sovereignty, territorial integrity, unity and independence of Ukraine within its internationally recognised borders.
Also the resolution of the protracted conflicts – in the Republic of Moldova, Georgia and of the Nagorno Karabakh conflict – is a top priority for the European Union and enhanced efforts should be made at all levels to stir political will in order to make tangible progress for conflict resolution based on the principles and norms of the OSCE and of international law. We furthermore encourage progress towards the resolution of the conflicts within the existing agreed formats, namely the 5+2 Process, the Geneva International Discussions and the OSCE Minsk Group. The status quo is highly detrimental to the security of the whole OSCE area.
As stated in the EU's Global Strategy for the Union's Foreign and Security Policy which was adopted last year, it is in the interest of our citizens to invest in the resilience of states and societies in our neighbourhood. We are committed to driving forward the Eastern Partnership agenda and, where appropriate, to cooperate with regional organisations.
The Candidate Countries the FORMER YUGOSLAV REPUBLIC OF MACEDONIA*, MONTENEGRO* and ALBANIA*, the Country of the Stabilisation and Association Process and Potential Candidate BOSNIA and HERZEGOVINA as well as UKRAINE, the REPUBLIC OF MOLDOVA and GEORGIA align themselves with this statement.
* The Former Yugoslav Republic of Macedonia, Montenegro and Albania continue to be part of the Stabilisation and Association Process.
Vienna, June 8, 2017
GUAM2017-06-19T15:34:32+03:0008.06.2017|Documents, GUAM and OSCE, International Cooperation, Joint Declarations, Statements, Communiques, Statements and documents of partners and GUAM Member States|
Statement of the Delegations of GUAM member states on the Secretary General's 19th consolidated report on the Conflict in Georgia
Statement of the Group of GUAM Observers in connection with the second round of the election of the President of Ukraine 2019
Meeting of Ambassadors of Visegrad Group and GUAM Member States
Statement of the Group of Observers of the Organization for Democracy and Economic Development – GUAM on the election of the President of Ukraine 2019
GUAM-Japan Workshop on Investment Promotion


text:
Archaeology Tour Of Croatia: See It Through Ancient Ruins
by Yanna N. 1 Comment
The lovely Croatia has more than just Game Of Thrones tours and beach resorts on the Adriatic coastline. It's a country with rich and varied history, colorful culture and plenty of sites to explore. If you're a history buff or just a fan of ancient archaeology findings and remnants of the old days, you should definitely include these places on your bucket list.
Pula Arena
Often regarded as the Croatian Colosseum, the amphitheater in Pula is a better destination than the one in Rome for two main reasons. The first one is that Pula Arena is the one and only ancient amphitheater, which still has all of its original architectural orders and four side towers. The second reason is that you'd be able to actually see the arena, unlike the one in Rome, which is so overcrowded that you wouldn't be able to see anything but the sky above your head. Equipped with an underground arena, a 29.4 meter high enclosure and lots of well-preserved décor, Pula Arena is splendid any time of year.
Diocletian's Palace
Contrary to its name, the palace is actually a full-blown complex, which takes up most of Split's Old Town. Remains from the original structures are scattered all over the town with the most famous being the courtyard's peristyle, the Temple of Jupiter and the Golden Gate. Adorned with mystical sphynxes, marble quarries, granite columns and exquisite stonework, the complex used to house more than 9,000 people on its grounds.
Walls of Ston
As far as historical findings go, the Walls of Ston are still holding the spot for the second-longest fortification system on Earth after the Great Wall of China, hence their nickname "the European Wall of China". Dating back to the 14th century the limestone walls once spanned over 7 kilometers in length. Due to being demolished and damaged during wars and invasions on numerous occasions throughout the years, their total length has been shortened to nearly 5.5 kilometers. The walls used to be additionally fortified with 40 towers, half of which are preserved today, several fortresses and guarded by thousands of Dalmatian soldiers.
Stećak tombstones
A stećak is a type of monumental inscribed tombstone from medieval times. These tomstones are scattered on numerous sites in Croatia. They were enlisted as official World Heritage Sites by UNESCO in 2016. Cista Velika and Dubravka are the two main necropolis sites with stećak tombstone concentration. The stećak movement kicked off at some point during the 12th century and reached its peak around the 15th, being denounced shortly afterwards during Ottoman rule.
Fortress of Klis
Initially built by Illyrians and later developed into a fortress with royal residential quarters, the Fortress of Klis has served quite a few kings throughout the history of Croatia while guarding crucial routes of economic and military importance. Albeit mostly ruined, what's left of the once glorious royal castle and the fortification system is still open to the public. Battle reenactments are organized from time to time and if you happen to miss them, you can still see authentic armory and medieval uniforms on display at the fortress' museum.
City ruins of Salona
Ancient Salona, now known as Solin, was one of the capitals of Dalmatia. After being occupied by Croats it became a vital political center in the medieval Kingdom of Croatia. Nowadays Solin is just a tiny fraction of land and a rather scarce outskirt of the larger Split conurbation. The ruins of the city of Salona are still standing and fortunately, they don't get overcrowded with curious tourists. A pagan necropolis, amphitheater, chapel, fortified walls, public baths and remains of other constructions can be seen across the archaeological park.
Our site 1
Leslie Kell says:
Your way of telling all in this piece of writing is truly pleasant, all be able to simply be aware of it, Thanks a lot.
archaeologycroatiaruins
Romanian Artist Turns Tree Stumps Into Beautiful Carved Artworks
When Babushka Loves you: Slav school breakfast


text:
WND's Kupelian Does Not Like Cities, City Folk
You know you're in for a doozy of a piece when David Kupelian begins his Aug. 16 WorldNetDaily column by likening all big cities to Babel:
There is something a little strange about big cities.
The enigmatic biblical story of the tower of Babel revolves around this strange something that occurs when large numbers of people come together in one place and form a great hive.
It's not that something bad has to happen – it doesn't, especially if the people governing that city are highly principled and grounded in reality. But how often does that happen?
Kupelian ghoes on to cite "the abandonment of traditional Judeo-Christian values that has led to today's devastating social, moral and financial corruption," which mostly happens in big cities.
This leads, inevitably to invoking the urban liberal/rural conservative divide with a map of presidential voting by county -- utterly irrelevant since people, not counties, vote for president -- and then perhaps not so inevitably to bashing transgenders:
My childhood home was just outside of D.C., in Montgomery County, Md., one of the most affluent and – especially today – ideologically progressive counties in the nation. To illustrate, Montgomery County has been in the news for passing county ordinances permitting men to frequent women's restrooms if they "feel" that they are really women – you know, "inside." Behaviors and "orientations" that a generation ago would have been regarded as both pathological and possibly criminal are today enshrined in law and culture alike. And such upper middle-class suburban communities that serve as enclaves for the federal government's hundreds of thousands of well-paid employees – most of them liberal – serve as natural proving grounds for such wildly progressive policies.
Then, back to the utterly inevitable side, Kupelian blames the ills of big cities on liberals in general and Obama in particular:
The real reason America's big cities are dragging the rest of the nation kicking and screaming into socialism is that, for decades, those cities have been run by arrogant, power-mad, progressive leftists. Want to know why Detroit looks like a war zone bombed by an enemy power? It's because it has been run for so long by leaders like former Mayor Coleman Young, who reigned over Detroit for almost two decades. Young was secretly a member of the Communist Party USA – an organization loyal to an enemy power!
What on earth do we expect to happen when, instead of elevating worthy statesmen as leaders, we instead turn our cities over to parasitic unions and plundering politicians dedicated to tearing down everything America has traditionally stood for, everything that has made this nation – including her shining cities – the envy of the world?
What could be worse than turning our thriving metropolises, the engines of civilization and progress, over to corrupt leftist "progressives" – a euphemism for neo-Marxists – with no clue how to run a candy store, let alone a great city? The only thing worse would be to make the same mistake with the entire country – which of course is exactly what we have done in elevating a corrupt Chicago politician and leftist revolutionary to the presidency of the United States of America.
Of course it Obama's fault. Why wouldn't it be?
Posted by Terry K. at 8:49 PM EDT


text:
Icon Fetch
About Icon Fetch
About Tony Peters
Bob Seger – 4/5/11 – (Concert review)
April 6, 2011 Tony Peters
Bob Seger – US Bank Arena – Cincinnati – April 5, 2011 (Concert Review) There was no smoke, no video screens, and no synthesizers; just a no-frills rock n' roll show from Bob Seger. The singer, who will turn 66 in May, put together a 2 ½ hour show with a bulletproof setlist of hits and rockin' albums cuts, mostly focusing on his four biggest albums: Live Bullet, Night Moves, Stranger in Town and Against the Wind. Augmenting Seger was the ever-present horn section, led by longtime bandmate Alto Reed as well as three female backup singers.
His core band featured longtime members Chris Campbell on bass and Craig Frost on keyboards, as well as Don Brewer of Grand Funk (another Michigan native) on drums. Because of his age and recent health issues, you might have expected a mellow show—absolutely not. Seger dug back for high-octane LP tracks like "Betty Lou's Getting Out Tonight," and "Horizontal Bop," as well as a fun take on Chuck Berry's "You Never Can Tell." The only "new" songs he touched on were the early Seger chestnut "Gets Ya Pumpin'" (recently issued on Early Seger volume one), and his cover of Tom Waits' "Downtown Train," which is the first single off an album expected out later in the fall. "Turn the Page" was a breathtaking highlight, featuring Reed's signature sax, while "We've Got Tonight" had a gentle, aching quality not found on the record. He mentioned during the show that he was battling a sore throat and did sound a little more raspy than usual, but the crowd didn't seem to mind. Seger ended the regular set with the spirited "Katmandu," before launching into two encores, ending with the telling "Rock n' Roll Never Forgets." Judging by the deafening howl of the audience (I've NEVER heard a louder crowd), they haven't forgotten either.
A new country duo, Steel Magnolia, opened the show. Giving further proof that the line between country and rock is almost non-existent, they opened with the Stevie Nicks/Tom Petty classic "Stop Draggin' My Heart Around," segued later into Rod Stewart & the Faces' "Stay With Me," and ended off with Johnny & June Carter Cash's "Jackson."
Previous Post#81 – Joe Robinson – Let Me Introduce YouNext PostSmithereens – 2011 (album review)
349 – Myles Goodwyn – April Wine and Friends of the Blues
Rush – Clockwork Angels Tour (vinyl edition)
Creedence Clearwater Revival – Willy and the Poor Boys (vinyl edition)
348 – Franke Previte – The Knockouts Complete & Dirty Dancing
347 – Kim Simmonds of Savoy Brown – City Night
Great music interviews, reviews and more!
Random Shows
#84 – Todd Park Mohr – 100 Years of Robert Johnson
#187 – Greg Lake – Songs of a Lifetime
Various Artists – Lipstick, Powder & Paint (review)
Ben Wilkins – sef titled (review)
Another Free MP3 from Icon Fetch
He Almost Drowned


Don't let downtown road construction stop you; the Friends of Morrisson-Reeves Library are having their annual fall book sale this weekend.
RICHMOND, Ind. — The Friends of Morrisson-Reeves Library's annual fall book sale will be Thursday-Saturday, Nov. 2-4, despite road construction making it more difficult to get to the library.
On the plus side, more parking will be available for the sale than to last year, now that work on Elstro Plaza across from the library is complete.
The Books, Movies, Music and More Sale will be open 3-7 p.m. Thursday, 12:30-4:30 p.m. Friday and 10 a.m.-2 p.m. Saturday at 80 N. Sixth St.
More than 8,000 donated DVDs, CDs, videos, books on CD/cassette, games, puzzles and magazines as well as fiction and non-fiction books for all ages will be replenished throughout the weekend.
Paperback books are 50 cents, and hardbacks are $1, with other items ranging from 10 cents to $2. Children and teens can receive a free book by showing their library card or a flyer distributed at local schools.
Money raised at the Friends' three annual book sales helps pay for library programs, such as free summer reading events, storytimes, children's events, concerts, book discussions and movies, according to a release.
Shoppers with large orders or those who aren't able to carry their purchases to their vehicles can request help as available. Volunteers will assist with curbside pickup for customers.


Black or White: What Difference Does it Make?
I recently completed a book called 'Why are all the Black Kids Sitting Together in the Cafeteria?' written by Dr. Beverly Tatum, an expert on race relations in the classroom and the development of racial identity. Dr. Tatum introduces a concept called 'smog-breathing,' where individuals who are consistently exposed to stereotypical images, messages, or behaviors in their environment consequently associate these stereotypes with certain racial or ethnic backgrounds. She likens these stereotypes to 'smog' and oftentimes, given that the 'smog' can be so thick (through media exposure, comments made by others around us, etc.), we cannot help but only breathe it in.
No one likes to be considered racist or prejudiced. As Americans, we embrace 'unity in diversity' and flaunt this to the rest of the world.
However, if I sit down and examine my own stereotypes in my workplace, I am astonished at how many I can come up with. I work predominantly in a county hospital serving largely our poor and underserved population in Atlanta, Georgia; therefore, it probably isn't surprising that different stereotypes and prejudices abound, whether intentionally or unintentionally. As examples, if I see a patient presenting with cocaine-induced congestive heart failure exacerbation, or learn that another patient has a history of non-adherence to medications, or discover that a patient is unable to read his prescription bottles and therefore has not been appropriately taking his medications, I am not surprised when I find out that these patients are African-American. In reality, most of my patients' behaviors are a ramification of their socio-economic environments rather than their racial/ethnic background. However, over time, after continuously witnessing certain behaviors with a particular race, I inadvertently fall into the trap of associating the behaviors to the racial background. Then, I am stereotyping.
Well, one may ask, are these really stereotypes or prejudices? Sometimes these behavioral associations appear to reflect reality. Maybe sometimes, they are. Health disparities research has shown that there are differences in overall rate of disease burden and opportunities to achieve optimal health among different populations, including different racial and ethnic populations. However, they need to remain as simply observations to not be considered 'stereotypes' and 'prejudices.' If, however, our 'simple observations' affect how we provide care among different racial/ethnic groups in that one racial group may benefit over another, then perhaps we are actually stereotyping. Dr. Tatum defines racism as a system of advantage based on race. Our stereotypes may in fact be perpetuating, even if without malicious intent, racism.
For example, would we educate our illiterate, African-American man with chronic obstructive pulmonary disease who continues to smoke 1 pack per day on the harms of smoking with as much tenacity as we would our educated, Caucasian male? Would we provide the same aggressive and invasive treatment options to a poor African-American man as we would to the wealthy Caucasian man? Sure, socio-economic factors have a tremendous role in our management, but perhaps we may need to examine our racial stereotypes a little more closely as they may also be influencing our decisions.
'Is that all we can do?' I wonder.
Perhaps, we are folding much earlier than we should.
Once we all as physicians, individually and collectively, bring our stereotypes to our conscious awareness, realize how our stereotypes affect our care of individuals and different groups of people in society, and strongly affirm that all our patients must be equally treated but within reason given socio-economical constraints, then we can be motivated to action. Let us take those extra few minutes at each patient visit to counsel on tobacco cessation and appropriate dietary practices for all of our patients, despite the seeming absence of motivation in some of our patients. Let us take that cultural competency training class offered to health care professionals at our institution to better educate us on how to close the disparities gap in health care. Let us not let a racial remark by a colleague go unhindered. Let us actively speak out against racial stereotyping and profiling in our workplace.
Let us not become smog-breathers, and let us achieve the 'unity in diversity' that America so cherishes.


text:
Socio-Economics
Anti-discrimination law took hold during an era in which "good jobs" involved "narrow portals of entry" into secure career ladders. The predominant economic theory of discrimination at the time suggested that different treatment involved employment and consumer "tastes" or dislike of other groups. Today's economy has dismantled the secure employment and predictable career ladders of mid-century America. In the process, inequality has grown, and the dominance of white (and in some cases Asian) men has increased in the upper reaches of the economy. Indeed, while the gendered wage gap has narrowed overall, the gap has increased for college graduates since the early nineties. This panel will consider how to understand the redefinition of "good jobs" in a networked economy, the new remade terms of competition among employees, and the implications for gender and racial diversity.
Business meeting at program conclusion.
Naomi R. Cahn, The George Washington University Law School
June Rose Carbone, University of Minnesota Law School
Jessica Clarke, Vanderbilt University Law School
Lisa M. Fairfax, The George Washington University Law School
Josephine Sandler Nelson, Villanova University Charles Widger School of Law
Frank A. Pasquale, University of Maryland Francis King Carey School of Law
Steven A. Ramirez, Loyola University Chicago School of Law
Michael L. Selmi, The George Washington University Law School
[4200] Socio-Economics - Gender, Race and Competition in the New Economy: $0.00


This Service is operated by Lawdeck Limited "Homeshift", which is a company registered in England and Wales with company number 08442448. Its registered office is at 86-90 Paul Street, London, EC2A 4NE.
Our website collects personal information about you when you use a link or a contact form to send us an email or when you sign up for an online account. If, in that email or any attachment to the email, you voluntarily provide us with personally identifiable information about yourself, such as your name, email, address or telephone number, we will collect and store that personal information. By using that link or contact form you or by signing up to an account you consent to us doing so.
Contact Data includes your email address, telephone number and postal address.
Profile Data includes your username and password, preferences, feedback and survey responses as well as information about the service providers you use and that you set up via our Service.
If you do not wish to provide this information to us you should not use the Service. If you have already begun using the Service, you should stop using it immediately.
Technical Data from analytics providers such as Google Analytics [INSERT OTHERS] based outside the EU.
We process personal data on behalf of our customers, who use our Service to gather information about an application made to them. However, when we Homeshift, do this we do so as a Data Processor under UK and EU data protection law. This means we do not make independent decisions about how personal information is processed in order to provide the Services to our users and customers. For example, we may store your personal information in our user database, and on our servers, accounting, credit card processing and customer relationship management software in order to record and process your personal data so as to be able to provide you with the Service that you have signed up to, but in providing the Service to you we do not perform any processing activities without your consent or at your request.
anyone who may purchase any or all of our assets, including your personal information (we will contact you using the details you provide if there is any change in the person controlling your information).
We are mindful of the importance of upholding the security of information under our control. All data collected through our website that is stored electronically, is stored on secure servers, and we have stringent security and confidentiality procedures covering the storage and disclosure of such information, in accordance with UK and EU data protection law.
Other companies in the FF Frisbee Group and who are based [SPECIFIC COUNTRIES] and provide [IT and system administration services and undertake leadership reporting].
Sometimes we might need to use your personal data to provide you with information, services and facilities that you have asked for. For example, if you ask us for a brochure for one of our products, more information about one of our websites or apps.
We may use information such as how different people navigate around our websites, how long they spend on particular pages, whether they download any of our content (including product brochures, white papers and so on that we publish from time to time) or watch videos in order to help improve the user experience of our websites and your experience of them.
Generally speaking, we rely on your consent to make contact with you by email for marketing purposes. You can withdraw that consent and ask us to delete your information at any time by contacting us directly via hello@homeshift.com – please see section 6 below.
Necessary for performance of a contract with the relevant individual, or to take steps for entering into a contract. For example, if you sign up to one of our products or services online or download our app, it will often be necessary for us to use your details in order to provide that product or service and you must consent to our use of your details to the extent required to provide that product or service in order to use that product or service.
Necessary in order to comply with a legal obligation. For example, some regulators, government bodies and courts have powers to order us to provide personal information and, like any other organisation, we sometimes have to comply with their requests and we whilst we may make commercially reasonable efforts to defend personal information from unjustified regulatory or governmental access, we cannot make any guarantee about the extent to which we are able to do so.
Your personal data may be shared between the employees and agents of Homeshift and any of its group companies to allow them to perform their job functions and current or future members of Homeshift's group companies and their employees and agents.
We use Amazon Web Services to host our servers.
We also use the credit card payment processing services provided by [INSERT] for taking subscription and other payments.
We may use printing companies to produce and send personalised direct mail.
Our database of personal data may be hosted by, but not accessible to, third parties on our behalf.
We are based in the United Kingdom, and will normally access and use your information from here. However, we also have operations in the Philippines and personal data may be accessed from there too. In both cases, the use of the information in those locations is protected by European data protection standards.
We will normally keep your personal data while you have an ongoing relationship with us or if you have demonstrated an interest in our products and services within the past two years. You can request us to delete it earlier as explained in section 6.
6. WHAT RIGHTS DO YOU HAVE IN RESPECT OF THE INFORMATION THAT WE HOLD ABOUT YOU?
You have several different rights in relation to the personal data that we hold about you. These are briefly described below.
Withdrawal of consent / objection: Where we rely on your consent to use your personal data, you are free to withdraw that consent at any time. In any other cases, you can let us know that you object to us using your personal data (for example, if you do not want to receive marketing calls from us any more).
Restriction: You can ask us to restrict our use of your personal data in some circumstances, such as while we are verifying whether the information is accurate. While the information is restricted, it can only be used for certain limited purposes such as bringing or defending legal claims, or protecting another person. It cannot be used or shared for ordinary purposes.
We use Amazon Web Services (AWS) to provider our servers. AWS maintain their servers in a highly secure server environment with 24 X 7 monitoring, surveillance and support to prevent unauthorized access and data security. Advanced security measures including firewalls, security guards and surveillance are taken to ensure the continued service and protection of our services from natural disaster, intruders and disruptive events. Your data is encrypted both when in transit and at rest.
Your passwords and other login credentials may pass through Homeshift servers or those of its service provider partners, in particular our server provider which is Amazon Web Services. When you enter this confidential information, it goes straight to the secure website.
Neither Homeshift's employees nor any of its contractors or service provider partners can obtain or access your passwords or other login credentials entered by you. We will also never ask you for your passwords or other login credentials via mail, email or telephone or in any other unsolicited manner and you should not give them out to someone claiming to be from Homeshift who is asking for them.
Our Service collects, encrypts and securely transfers confidential, personal information. By accessing the Service and entering information required from time to time to complete a form on our website or in our Service customers consent to Homeshift providing this information to service provider partners, such as Amazon Web Services or our analytics or payment processing partners. We may store this confidential information, for so long as you are actively involved with Homeshift and then for a period of 2 years after you have ceased to use our Services.
If you have any further questions about our Privacy Policies, email us at hello@homeshift.com.


text:
Q: Setup automated build\deployments to my Azure VM using VSTS? I have my source control in Visual Studio Team Services and push my code via web deploy to my Azure VMs. Just going thru several Azure related articles, it's hard to figure the easiest way to setup continuous delivery where the latest code is pushed to VMs per developer check-ins?

A: Have you tried some of the deployment articles in VSTS? You can setup continuous deployment in a more flexible way (to VMs for instance) using Build and RM in VSTS.
https://www.visualstudio.com/en-us/docs/release/examples/examples-index


Finding a reliable VPN provider in these technological times can be a daunting prospect. For a novice just getting into using VPNs, it can be hard to know what factors are important and which are less so. So long as you bear in mind a few determining factors your decision might be simpler than you expect.
A VPN is a Virtual Private Network that tunnels your internet connection through a server located somewhere else. As it does this, it will assign you a new IP address based on where that server is located (In this case somewhere in Europe) and will also encrypt the data stream keeping your data safe. You may want a VPN for a couple of reasons. You may want or need to keep your internet viewing and usage away from prying eyes or you just want to have access to a secure and stable connection to the web and in some cases maybe both reasons apply.
How Many VPN Servers Should I Look For?
One of the easiest factors to get an idea how a VPN will perform for you is to look at how many servers the provider has available for your use. The number of servers available is important as a provider with only a handful of servers may suffer severe quality degradation if many users are all trying to use that handful of servers at the same time. This can lead to input lag, packet loss, and more. The more servers the provider has available means a better potential connection for you. You should also consider where the servers are located in relation to you. If you want to watch a locally streamed football match in France while you're in Germany you will want to aim for the closest French server in relation to you. If you're aiming only for a secure and steady connection you will want to find a server that is located as close to you as possible.
Downtime often represents the average time servers may be unavailable for your use. This is due largely in part to servers requiring maintenance to ensure they continue running at optimal conditions and it helps to avoid the second cause of downtime, malfunction. This service relies upon machines and machines sometimes break, most providers have backups ready to go in the case of this happening but their downtime estimates should be considered when deciding whether or not to use them.
At the base level of VPN encryption your data is sufficiently safe, the way your VPN functions guarantees a level of protection already. If security is a big issue to you either by preference or necessity most providers offer alternative plans that offer a higher level of encryption for your VPN though this always comes with greater cost.
If idea of trying to figure out the best VPN provider has you stumped, we can help! Our team of experts have created an easy to read table highlighting the best VPN providers as well as their pros and cons. This can make the process a lot simpler whether you're a newcomer to VPN or seasoned consumer.


It started on January 11th, 2014/2015 Men's Milan Fashion Week, international festival of ready-to-wear men's fashion house presented by the most important Italian fashion. Forty fashion show, more than a dozens of presentations, outside fashion catwalks. Milan Design Agenda, got between others thousands journalists and thousand buyers not to mention bloggers, that came from all places….Besides Milan.
The trends follow in the wake of those proposed 85th edition of Pitti Immagine Uomo. Camouflage printing details, search on tailoring coats, double-breasted from the coat, unexpected mix of fabrics, hints rock, new metropolitan gentleman. Even between a thousand attendees, Milan Design Agenda notice that 4 in 7 women, were drawn these clothes to fit on woman.
Minimal hand for fall/winter 2014, Sergio Corneliani honed in on the suit, perfecting and expanding upon the ultimate wardrobe staple.
Showing his second collection for Ermenegildo Zegna, Stefano Pilati sent his men down the catwalk against a backdrop of the universe.
Keeping fall/winter 2014 young and fresh, MSGM creative director Massimo Giorgetti weaved the label's signature prints into a cohesive lineup for the urban jungle.
Exuding a fearless confidence, Donatella Versace merged theItalian fashion house's trademark flamboyance with the romantic idea of the cowboy for fall/winter 2014.
Tomas Maier celebrated a younger Bottega Veneta man for today's show. A breath of fresh air, Maier embraced a certain casualness, presenting relaxed luxury for fall/winter 2014.
Salvatore Ferragamo creative directorMassimiliano Giornetti put the spotlight on inspired by Aztec blankets, with contrasting stripes at the hem and cuffs, faded blots of color woven onto the back, or thick bands of alternating color, such as sage and camel.
Taking in the surfer as this season's muse, Angela Missoni dressed long slouchy separates in the fashion house's signature prints.
Trust Miuccia Prada to deliver food for thought alongside a healthy serving of fashion. Her Milan men's show delivered plenty of both, referencing European culture from the Weimar period up through the early Eighties.


text:
AGTR1 overexpression defines a subset of breast cancer and confers sensitivity to losartan, an AGTR1 antagonist
Daniel R. Rhodes, Bushra Ateeq, Qi Cao, Scott A. Tomlins, Rohit Mehra, Bharathi Laxman, Shanker Kalyana-Sundaram, Robert J. Lonigro, Beth E. Helgeson, Mahaveer S. Bhojani, Alnawaz Rehemtulla, Celina G. Kleer, Daniel F. Hayes, Peter C. Lucas, Sooryanarayana Varambally, and Arul M. Chinnaiyan
PNAS June 23, 2009 106 (25) 10284-10289; https://doi.org/10.1073/pnas.0900351106
Daniel R. Rhodes
Bushra Ateeq
Qi Cao
Scott A. Tomlins
Rohit Mehra
Bharathi Laxman
Shanker Kalyana-Sundaram
Robert J. Lonigro
Beth E. Helgeson
Mahaveer S. Bhojani
Alnawaz Rehemtulla
Celina G. Kleer
Daniel F. Hayes
Peter C. Lucas
Sooryanarayana Varambally
Arul M. Chinnaiyan
For correspondence: arul@umich.edu
Edited by Owen N. Witte, David Geffen School of Medicine at the University of California, Los Angeles, CA, and approved April 10, 2009
↵1D.R.R., B.A., Q.C., and S.A.T. contributed equally to this work. (received for review January 12, 2009)
Breast cancer patients have benefited from the use of targeted therapies directed at specific molecular alterations. To identify additional opportunities for targeted therapy, we searched for genes with marked overexpression in subsets of tumors across a panel of breast cancer profiling studies comprising 3,200 microarray experiments. In addition to prioritizing ERBB2, we found AGTR1, the angiotensin II receptor type I, to be markedly overexpressed in 10–20% of breast cancer cases across multiple independent patient cohorts. Validation experiments confirmed that AGTR1 is highly overexpressed, in several cases more than 100-fold. AGTR1 overexpression was restricted to estrogen receptor-positive tumors and was mutually exclusive with ERBB2 overexpression across all samples. Ectopic overexpression of AGTR1 in primary mammary epithelial cells, combined with angiotensin II stimulation, led to a highly invasive phenotype that was attenuated by the AGTR1 antagonist losartan. Similarly, losartan reduced tumor growth by 30% in AGTR1-positive breast cancer xenografts. Taken together, these observations indicate that marked AGTR1 overexpression defines a subpopulation of ER-positive, ERBB2-negative breast cancer that may benefit from targeted therapy with AGTR1 antagonists, such as losartan.
A central aim in cancer research is to identify genetic alterations involved in the pathogenesis of cancer, thereby providing an opportunity to develop therapies that directly target the alterations. In breast cancer research, this strategy has been realized with the study of ERBB2, which is amplified and overexpressed in 25–30% of breast tumors (1, 2), directly contributing to tumorigenesis (3, 4). Targeting this genetic lesion with trastuzumab, a humanized monoclonal antibody directed against ERBB2, has significant clinical benefit in breast cancer management (5–7). Cancer genes are activated or inactivated by a variety of mechanisms, including those that alter the activity of proteins (e.g., activating Ras mutation, BCR-ABL fusion protein) and those that change expression levels of proteins (e.g., ERBB2 gene amplification, Ig-Myc DNA translocation, or p53 homozygous deletion). It is likely that only a fraction of such "driver" alterations have been identified to date, and furthermore, many of the identified alterations are not thought to be "druggable" by conventional means.
DNA microarrays have been widely applied to the study of gene expression in cancer. Although microarrays are not capable of directly detecting alterations affecting the activity of proteins, they are theoretically well suited to detect alterations that change the expression of genes and proteins, although it can be difficult to identify driver alterations directly related to tumorigenesis among hundreds or thousands of differentially expressed genes. As a strategy for using microarray data to identify genes directly related to cancer pathogenesis that may thus serve as therapeutic targets, we hypothesized that genes that show the most profound changes in gene expression (10-fold to more than 100-fold increase relative to baseline), termed "pathogenic overexpression," even if in only a small subset of cases, may play a direct role in cancer progression and may serve as optimal therapeutic targets for the subpopulations with overexpression. Because cancer is heterogeneous, distribution statistics that compare average expression values between classes of samples (e.g., cancer vs. normal) will often fail to identify these profound changes in expression, especially if the alterations occur in subsets of cases (e.g., Her2/neu amplification and overexpression in 25% of breast cancer). We previously developed a simple analytical method, termed "Cancer Outlier Profile Analysis" (COPA), to identify such gene expression profiles, nominating ERG and ETV1 as novel cancer genes in prostate cancer, which were shown to be activated by gene fusions with the androgen-regulated gene TMPRSS2 (8). Here, we extend the COPA approach to include a meta-analysis strategy, combining the search for profound changes in expression with multistudy validation. We focus our analysis on breast cancer because this disease has been most extensively analyzed by gene expression profiling. Interestingly, the majority of such analyses have focused on disease classification and prediction of patient outcome, rather than target discovery. We present a large-scale analysis spanning 31 gene expression profiling studies comprising nearly 3,200 microarray experiments. In addition to objectively identifying the prototypical breast cancer target, ERBB2, our analysis also nominates a number of previously unidentified genes which, based on their profound overexpression in subsets of tumors across independent cohorts, may play a role in tumorigenesis and may serve as therapeutic targets in their respective subpopulations.
We hypothesized that genes directly involved in breast tumorigenesis may be activated via pathological overexpression in specific subsets of tumors. Thus, we developed a methodology to identify genes that display substantial changes in expression in subpopulations of tumors across independent cancer microarray datasets. The methodology, MetaCOPA, combines MetaAnalysis and COPA, 2 approaches that we have applied previously but separately to identify cancer genes (8, 9) (Fig. S1). We analyzed 31 breast cancer profiling datasets, comprising 3,157 microarrays (Table S1). We defined per dataset "outliers" as genes with the most dramatic overexpression in a subset of tumors, and"meta-outliers" as genes that were identified in a statistically significant fraction of datasets. We identified 159 significant meta-outliers (P < 1E-5) (Fig. 1A and Table S2), of which ≈20 genes were identified as outliers in the majority of datasets examined (Fig. 1B and Table S3).
MetaCOPA analysis of breast cancer gene expression data. (A) MetaCOPA map. Each column in the map represents a breast cancer gene expression dataset. The numbers at the base of the map correspond to dataset details (Table S1). Each row indicates a gene. A red cell indicates that the gene was deemed to have an outlier expression profile in the respective dataset because it scored in the top 1% of COPA values at 1 of 3 percentile cutoffs. The line graph along the y axis indicates the P value for a gene based on the number of datasets in which the gene was deemed an outlier. A total of 158 genes were called outliers in a significant fraction of datasets (P < 1E-5). The bar graph indicates the number of samples in the respective datasets and the contribution of the dataset to the meta-analysis. The black bar on the left of the map indicates the top 25 meta-outliers, which are detailed in B for 3 datasets marked with an asterisk. (B) Heatmaps of COPA-normalized values for top-scoring meta-outliers across 3 highly contributory datasets: Miller et al. (26), Hess et al. (27), and Wang et al. (28). Genes are ranked by their MetaCOPA P values. For each gene, samples are ordered from left to right by their COPA-normalized expression values. Highest intensity of red indicates a COPA-normalized value of 6 or greater. White indicates a value of zero or less.
Notably, considering all human genes represented in the analysis, ERBB2 was the most significant meta-outlier, identified in 21 of 29 independent datasets (72%; P = 3.6E-26), indicating that this established therapeutic target shows the most substantial and consistent overexpression in a fraction of breast tumors (Fig. S2A). Although ERBB2 did not have a no.1 ranked outlier expression profile in any individual dataset, it did score highest in the meta-analysis. Several other top-scoring meta-outliers localize within 1 Mb of ERBB2 on chromosome 17q. As expected from the past observation that ERBB2 and genomic neighbors are coamplified and coexpressed in breast cancer (10, 11), we observed a clear coexpression pattern of the 17q meta-outliers (Fig. S2B).
The next most consistently scoring outlier, excluding ERBB2 and genomic neighbors, was AGTR1, the gene encoding angiotensin II receptor type I, which is the target of the antihypertensive drug losartan (12) and has previously been linked to cancer (12–17) and cancer-related signaling pathways (18, 19). AGTR1 was called an outlier in 15 of 22 datasets (68%; P = 2.0E-18). The microarray data clearly indicated that AGTR1 is highly overexpressed in a subset of tumors relative to normal tissue (Fig. 2A) and that high overexpression occurs exclusively in a subset of estrogen receptor-positive (ER+) tumors (Fig. 2C). Furthermore, a coexpression analysis of AGTR1 and ERBB2 revealed a mutually exclusive relationship, with breast tumors overexpressing ERBB2 or AGTR1, but never both (Fig. 2 B and D). Additional evidence for the marked overexpression of AGTR1 in 10–20% of breast tumors, specifically ER+, ERBB2− breast tumors, is presented in SI Materials and Methods (Figs. S3 and S4). AGTR1 overexpression was not significantly associated with 5-year recurrence-free survival in ER+, ERBB2− breast cancer across 2 independent datasets (Fig. S5). We validated and quantified AGTR1 overexpression by quantitative RT-PCR in formalin-fixed, paraffin-embedded tissue from normal breast, primary breast cancer, and metastatic breast cancer. Consistent with the microarray data, we found AGTR1 to be more than 20-fold overexpressed in 7 of 45 tumors (15.5%) and more than 100-fold overexpressed in 2 primary tumors and 1 metastatic tumor (Fig. 2E).
AGTR1 outlier expression in breast cancer. (A) AGTR1 expression profile in the Perou et al. (29) cDNA microarray dataset (n = 55). (B) In the same dataset, AGTR1 expression vs. ERBB2 expression. (C) AGTR1 expression profile in the van de Vijver et al. (30) oligonucleotide dataset, segregated by ER status (n = 295). (D) AGTR1 expression vs. ERBB2 expression in the same dataset. (E) AGTR1 expression by quantitative RT-PCR in formalin-fixed, paraffin-embedded tissue. Expression of AGTR1 was assessed in 3 normal breast tissue specimens, 36 primary breast tumor specimens, and 9 metastatic breast cancer specimens. Expression levels were normalized to GAPDH expression and then scaled by the median AGTR/GADPH ratio.
Given the remarkable overexpression of AGTR1 in tumor subsets, we investigated potential mechanisms by which AGTR1 becomes overexpressed. First, using Oncomine, we examined AGTR1 coexpression data from 5 independent datasets, and in each case we found no more than one additional gene correlated with AGTR1 (R > 0.5), providing preliminary evidence that AGTR1 is not regulated as part of a larger transcriptional program. Second, we examined AGTR1 overexpression in the context of genes that neighbor AGTR1 on chromosome 3q. Unlike ERBB2, AGTR1 did not display any correlated expression with genomic neighbors (Fig. S6).
Next, we performed FISH on tissue microarrays to test the AGTR1 locus for gene rearrangement or DNA copy number aberration. Using a split probe strategy (8), we found that 5′ and 3′ AGTR1 probes never demonstrated consistent split signals, and thus concluded that rearrangement of the AGTR1 locus is not involved in AGTR1 overexpression. AGTR1 copy number was also evaluated in 112 breast carcinoma cases. Definitive copy number gain [locus/control (L/C) > 1.5] was observed in 7 of 112 cases (6.25%), of which 6 were invasive ductal carcinoma and 1 was ductal carcinoma in situ (Fig. 3 A and B). To study the association between DNA copy number and overexpression, we identified available cases for qRT-PCR analysis, including 14 cases with no gain (L/C < 1.2), 3 cases with questionable gain (1.2 < L/C < 1.5), and 4 cases with definitive DNA copy number gain (L/C > 1.5). We observed a significant concordance between high AGTR1 expression and definitive copy number gain (P = 0.006; Fig. 3C). All 4 cases tested with definitive copy number gain also had high AGTR1 expression; however, high expression was also observed in 3 of 17 cases without definitive copy number gain. Thus, in this small sample set, copy number gain was always associated with overexpression, but overexpression also occurred without copy number gain.
Copy number analysis of the AGTR1 locus. (A) A schematic of probes used for FISH analysis. (B) Representative image from FISH analysis. Left is taken from a representative negative case. Middle and Right are images from a representative case with definitive copy number gain of AGTR1. Red signal is the AGTR1 locus probe, and green signal is the probe near the chromosome 3 centromere. (C) Association of AGTR1 overexpression with copy number gain. Three expression bins were defined based on AGTR1/GAPDH ratios: low (<1.0), moderate (1.0–2.0), and high (>2.0).
To study the function of AGTR1 overexpression in breast epithelial cells, we generated an adenovirus construct expressing AGTR1. Human mammary epithelial cells (H16N2 and HME) were infected with AGTR1-expressing virus or control LacZ-expressing virus and cultured in serum-free media (Fig. S7). We assayed AGTR1-overexpressing cells and control cells for cell proliferation and invasion both in serum-free media and upon stimulation with angiotensin II (AT), the ligand of AGTR1. Overexpression of AGTR1 alone or in combination with AT did not affect cell proliferation. However, in both cell lines, we did observe that overexpression of AGTR1 with AT stimulation did significantly promote cell invasion in a reconstituted basement membrane invasion chamber assay (Fig. 4 A and B). The control experiment, in which the LacZ gene was transfected, did not exhibit increased invasion with AT stimulation. Importantly, AGTR1 and AT-mediated invasion was attenuated in a dose-dependent manner with inclusion of the AGTR1 blocker, losartan. Losartan had no effect on the LacZ-transfected cells or the AGTR1-transfected cells not stimulated with AT (Fig. 4B). To confirm that losartan inhibition of invasion is specific to AGTR1 transfection, we also infected H16N2 and HME cells with EZH2-expressing adenovirus, a gene known to induce invasion and, as expected, found that EZH2-mediated invasion was not attenuated by losartan treatment (Fig. S8). Thus, in 2 benign breast epithelial cell lines, AGTR1 overexpression in the presence of AT led to a markedly invasive tumorigenic phenotype, which is specifically reversed by treatment with losartan. We also tested the AGTR1-overexpressing mammary epithelial cells for activation of the MAPK and PI3K pathways, as measured by ERK phosphorylation and AKT phosphorylation, respectively. We found that AGTR1 overexpression combined with AT stimulation did increase ERK phosphorylation but not AKT phosphorylation. Losartan treatment (10 μM) inhibited the AT-stimulated increase in ERK phosphorylation (Fig. S9).
AGTR1 overexpression and analysis of angiotensin II (AT) and losartan effects on cell invasion. (A) Matrigel invasion assays of H16N2 cells infected with adenovirus expressing AGTR1 or LacZ. Cells were cultured in serum-free media and were pretreated with and without AT and losartan. Similar results were observed for HME cells. (B) Colorimetry readout of invasion assays from transfection experiments. LacZ- or AGTR1-expressing adenovirus was infected into H16N2 and HME immortalized mammary epithelial cells, and cells were treated with or without 1 μM AT and losartan. Because of absent baseline invasion, the optical density (OD) measurements were background subtracted, and values below 0.01 were set to 0.01. (C) Colorimetry readout of invasion assays from a panel of cancer cell lines. Seven breast cancer cell lines and a prostate cancer cell line, DU145, were examined for invasion after treatment with or without 1 μM AT and losartan. AGTR1 expression levels are indicated and were obtained from published microarray data and qRT-PCR analysis (Fig. S7). The quantification of invasion was done as described in B.
Next, we identified and tested a panel of breast cancer cell lines with endogenous AGTR1 overexpression. By using Oncomine (20), we identified 4 breast cancer cell lines with validated AGTR1 overexpression and 3 breast cancer cell lines with little or no expression of AGTR1 (Fig. S10). As an additional negative control, we also included the highly invasive prostate cancer cell line DU145, which has low expression of AGTR1. By using the reconstituted basement membrane invasion chamber assay, we tested the cell line panel with and without 1 μM AT and losartan. In each of the 4 AGTR1-overexpressing cell lines, we observed an increase in invasion upon stimulation with 1 μM AT, which was reversible by addition of losartan, whereas none of the 3 breast cancer cell lines with low AGTR1 expression, nor DU145, showed an increase in invasion upon 1 μM AT stimulation (Fig. 4C). Thus, we confirmed that our ectopic AGTR1 overexpression results can be generalized to breast cancer cells with endogenous overexpression but not those with low expression, and that losartan-mediated decrease in invasion is specific to invasion related to AT stimulation and AGTR1 overexpression.
Next, we stably transfected AGTR1 into MCF7 human breast cancer cells and performed mouse xenograft studies. We implanted MCF7-AGTR1 cells or MCF7-GUS control cells into the mammary fat pad of nude mice and treated animals with 90 mg/kg losartan per day or vehicle control. We studied the impact of losartan on tumor growth at 2 weeks and 8 weeks. Ten mice were studied in each group: MCF7-AGTR1 plus saline, MCF7-AGTR1 plus losartan, MCF7-GUS plus saline, and MCF7-GUS plus losartan. MCF7-AGTR1 tumors did not display increased growth at 2 weeks or 8 weeks relative to MCF7-GUS control tumors. Losartan treatment did, however, significantly reduce early and late tumor growth in MCF7-AGTR1-implanted mice but had no effect on tumor growth in MCF7-GUS control-implanted mice. At 2 weeks after implantation, the median tumor size of MCF7-AGTR1 tumors treated with losartan was 20% smaller than MCF7-AGTR1 tumors treated with vehicle control (P = 1.4E-4; Fig. 5A). On the contrary, there was no significant change in tumor size at 2 weeks in MCF7-GUS tumors treated with losartan relative to vehicle control (P = 0.67). Similarly, at 8 weeks, median tumor size of MCF7-AGTR1 tumors treated with losartan was 31% smaller than those treated with control (P = 0.016; Fig. 5B). Again, no significant change in median tumor size of MCF7-GUS tumors was observed upon losartan treatment (P = 0.24). In summary, although AGTR1 transfection into MCF7 breast cancer cells did not increase tumor size, it did significantly sensitize tumors to growth inhibition with losartan treatment.
Effect of losartan treatment on AGTR1- or GUS-overexpressing MCF7 cell xenografts. Female BALB/C nu/nu mice were implanted with 2.5 × 106 stable MCF7 cells overexpressing AGTR1 or GUS resuspended in 100 μL of saline with 20% Matrigel into the mammary fat pad of anesthetized mice. Mice from both groups: MCF7-AGTR1 or MCF7-GUS (n = 10 for each group) were treated every day with losartan (90 mg/kg body weight) or vehicle control. All animals were monitored at weekly intervals for tumor growth, and tumor sizes were recorded using the formula (π/6) (L × W2), where L = length of tumor and W = width. Box plots of log2 tumor volumes are shown. P values from 2-sided Student's t tests indicate statistical significance. (A) Xenograft tumor size at 2 weeks. (B) Xenograft tumor size at 8 weeks.
In summary, we performed a large-scale meta-analysis of outlier expression profiles across several large cohorts of breast tumors. Our analysis prioritized genes with marked overexpression in subsets of tumors. This approach correctly prioritized the prototypical breast cancer oncogene and drug target ERBB2. In addition, several new genes were identified, demonstrating consistent and dramatic overexpression in tumor subsets. We suspect that our analysis has uncovered a new crop of potentially important breast cancer genes.
AGTR1, the angiotensin II receptor, was found to be one of the most highly overexpressed genes in 10–20% of breast cancers across independent breast cancer microarray studies. This has potential clinical importance because AGTR1 is antagonized by commonly prescribed antihypertensive agents (12), such as losartan, which have been shown to have antitumorigenic effects in model systems (12–17). Interestingly, AGTR1 always displayed high overexpression in ER-positive, ERBB2-negative tumors, potentially providing insights into the selective pressures governing AGTR1 activation in breast cancer. Contrary to expectation, ER in fact down-regulates the AGTR1 transcript via cytosolic mRNA-binding proteins (21). Thus, we hypothesize that the paradoxical marked overexpression of AGTR1 in a subset of ER+ breast tumors may be the result of a genetic aberration that put the AGTR1 transcript under the positive control of the ER. Based on the mutually exclusive expression pattern with ERBB2 and the reported overlapping downstream pathways affected by AGTR1 and ERBB2, we suspect that AGTR1 activation and ERBB2 activation may represent alternative but functionally related events in tumorigenesis. Our AGTR1 transfection experiments in HME cells confirmed that ERK phosphorylation, a MAPK pathway readout, increases upon angiotensin stimulation.
We applied computational and experimental strategies to uncover mechanisms for AGTR1 overexpression. Coexpression analysis revealed that AGTR1 is not likely to be part of a larger transcriptional program, because other genes were not found to be highly coexpressed with AGTR1. FISH analysis demonstrated that chromosomal rearrangements do not occur at the AGTR1 locus, making gene fusions an unlikely cause of overexpression. DNA copy number analysis did identify a small fraction (6.5%) of breast tumors with increased copy number at the AGTR1 locus, and copy number gain occurred only in cases with overexpression. However, some overexpressing cases did not have copy number gain, and the level of copy number gain observed in positive cases was not proportional to the degree of overexpression observed. Thus, we suspect that copy number gain contributes to overexpression in some cases but is not likely to be the predominant mechanism. Future studies to investigate the mechanism of AGTR1 overexpression should include high-resolution array comparative genomic hybridization and sequencing of the AGTR1 locus.
Regardless of the mechanism, AGTR1 undergoes profound deregulation in a subset of breast cancers, and our in vitro and in vivo studies demonstrate a functional role for AGTR1 overexpression in breast cancer and, more importantly, the potential for targeting AGTR1+ breast tumors with an available therapy. Past work has shown that in breast cancer cell lines, angiotensin II stimulation evokes an invasive phenotype, which is inhibited by losartan treatment (22). Furthermore, it was demonstrated that the increase in invasion is coincident with decreased expression of integrins, possibly via protein kinase C signaling. Although these observations were made in transformed breast cancer cells naturally expressing AGTR1, our work shows that activated AGTR1 pathway, by way of artificial AGTR1 overexpression, in normal breast epithelial cells is sufficient to activate an invasive phenotype, suggesting that this pathway may be especially important in breast tumors with high overexpression. Furthermore, we studied a panel of cell lines with either high or low levels of AGTR1 and showed a clear correlation between AT-mediated invasion and level of AGTR1 expression.
Our in vivo data provide further evidence that losartan may be a viable therapy for women with AGTR1-overexpressing breast tumors. Breast cancer xenografts overexpressing AGTR1 were differentially sensitive to losartan treatment, demonstrating a 30% reduction in growth at 8 weeks, whereas control xenografts had no reductin in tumor size. It is interesting that MCF7-AGTR1 xenografts did not display increased growth relative to MCF7 control xenografts, but they did display a significantly increased losartan effect. This suggests that AGTR1 does not provide an additive growth signal to MCF7 cells, which do harbor an activating PI3K mutation. We suspect that the stable transfection of AGTR1 reprogrammed MCF7 cells to be at least partially dependent on AGTR1 as a growth or survival signal; hence, the differential response to losartan. We anticipate that de novo AGTR1-positive primary tumors may be even more dependent on the AGTR1 signal, and thus more sensitive to inhibition.
Interestingly, past studies have linked polymorphisms in the angiotensin pathway with breast cancer incidence (23, 24), documenting a significant increase in breast cancer incidence in women with the D/D angiotensin-converting enzyme (ACE) allele, which is associated with increased circulating ACE levels, and thus increased levels of angiotensin II, the ligand for AGTR1. Other studies have examined the relationship between antihypertensive therapy (AHT), which often involves modulation of the angiotensin axis, and breast cancer incidence. The largest of such studies did not observe a significant relationship (25); however, the study examined a variety of AHT modalities and was likely not powered to detect a small change incidence that might be expected from a response only in the AGTR1+ subpopulation.
In summary, this study provides a rationale for a clinical trial that includes losartan in the treatment of breast cancer patients with tumors positive for AGTR1. We demonstrated that AGTR1 transcript levels and DNA copy number can be effectively measured from formalin-fixed, paraffin-embedded tissue specimens, thus enabling the identification of the appropriate patient population.
MetaCOPA Analysis.
COPA analysis was performed on 31 breast cancer gene expression datasets in Oncomine (www.oncomine.org) as described previously (8). Genes scoring in the top 1% of COPA scores at any of the 3 percentile cutoffs (75th, 90th, and 95th) were deemed outliers in their respective datasets. Meta-outliers were defined as genes deemed outliers in a significant fraction (P < 1E-5) of datasets as assessed by the binomial distribution. Analysis details are provided in SI Materials and Methods.
Quantitative PCR (QPCR).
QPCR was performed by using SYBR Green dye on an Applied Biosystems 7300 Real Time PCR system (Applied Biosystems) essentially as described previously (8). Details and primer sequences are available in SI Materials and Methods.
AGTR1 Transfection.
The benign human mammary epithelial cells HME and H16N2 were transfected with AGTR1-expressing adenovirus and assayed for cell invasion with or without losartan and angiotensin II treatment. Details are available in SI Materials and Methods.
Cell Invasion Assay.
Breast cell lines BT-549, Hs578T, HME, H16N2, HCC1528, HCC1500 and prostate carcinoma line DU145 were assayed for cell invasion with or without losartan and angiotensin II treatment using Matrigel invasion chambers. Details are available in SI Materials and Methods.
AGTR1 Amplification Assessment.
A breast cancer tissue microarray containing 311 cases of invasive breast cancer was tested for AGTR1 locus amplification by flourscence in situ hybridization. Details are available in SI Materials and Methods.
Mammary Fat Pad Xenograft Model.
Balb/C nu/nu mice were implanted with MCF7 cells stably overexpressing AGTR1 or Gus and then treated daily with losartan vehicle control. Details are available in SI Materials and Methods.
We thank V. Mahavisno, R. Varambally, T. Barrette, and D. Gibbs for Oncomine support, and Diane Roulston and Lisa Smith for assistance with FISH. We thank Merck USA for providing losartan. This work is supported by the Department of Defense Era of Hope Scholar Award (to A.M.C., C.G.K, and D.F.H.), the Early Detection Research Network Biomarker Developmental Lab Grant UO1 CA111275-01 (to A.M.C.), Department of Defense Grants PC040517 (to R.M.) and PC020322 (to A.M.C.), and the Cancer Center Bioinformatics Core Support Grant 5P30 CA46592. S.A.T. is supported by a Rackham Predoctoral Fellowship. A.M.C. is supported by a Clinical Translational Research Award from the Burroughs Welcome Foundation and a Doris Duke Charitable Foundation Distinguished Clinical Scientist Award.
2To whom correspondence should be addressed. E-mail: arul{at}umich.edu
Author contributions: D.R.R., B.A., S.A.T., S.V., and A.M.C. designed research; D.R.R., B.A., Q.C., S.A.T., R.M., B.L., B.E.H., and S.V. performed research; M.S.B., A.R., C.G.K., and S.V. contributed new reagents/analytic tools; D.R.R., B.A., S.A.T., R.M., S.K.-S., R.J.L., D.F.H., P.C.L., S.V., and A.M.C. analyzed data; and D.R.R., S.A.T., and A.M.C. wrote the paper.
This article contains supporting information online at www.pnas.org/cgi/content/full/0900351106/DCSupplemental.
King CR,
Kraus MH,
Aaronson SA
(1985) Amplification of a novel v-erbB-related gene in a human mammary carcinoma. Science 229:974–976.
Slamon DJ,
(1987) Human breast cancer: Correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science 235:177–182.
Di Fiore PP,
(1987) erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science 237:178–182.
Hudziak RM,
(1989) p185HER2 monoclonal antibody has antiproliferative effects in vitro and sensitizes human breast tumor cells to tumor necrosis factor. Mol Cell Biol 9:1165–1172.
Piccart-Gebhart MJ,
(2005) Trastuzumab after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J Med 353:1659–1672.
Romond EH,
(2005) Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med 353:1673–1684.
(2001) Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med 344:783–792.
(2005) Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science 310:644–648.
(2004) Large-scale meta-analysis of cancer microarray data identifies common transcriptional profiles of neoplastic transformation and progression. Proc Natl Acad Sci USA 101:9309–9314.
Bertucci F,
(2004) Identification and validation of an ERBB2 gene expression signature in breast cancers. Oncogene 23:2564–2575.
Kauraniemi P,
Barlund M,
Monni O,
Kallioniemi A
(2001) New amplified and highly expressed genes discovered in the ERBB2 amplicon in breast cancer by cDNA microarrays. Cancer Res 61:8235–8240.
Timmermans PB
(1999) Angiotensin II receptor antagonists: An emerging new class of cardiovascular therapeutics. Hypertens Res 22:147–153.
Miyajima A,
(2002) Angiotensin II type I antagonist prevents pulmonary metastasis of murine renal cancer by inhibiting tumor angiogenesis. Cancer Res 62:4176–4179.
Fujimoto Y,
Sasaki T,
Tsuchida A,
Chayama K
(2001) Angiotensin II type 1 receptor expression in human pancreatic cancer and growth inhibition by angiotensin II type 1 receptor antagonist. FEBS Lett 495:197–200.
Rivera E,
Arrieta O,
Guevara P,
Duarte-Rojo A,
Sotelo J
(2001) AT1 receptor is present in glioma cells; its blockage reduces the growth of rat glioma. Br J Cancer 85:1396–1399.
Uemura H,
(2003) Angiotensin II receptor blocker shows antiproliferative activity in prostate cancer cells: A possibility of tyrosine kinase inhibitor of growth factor. Mol Cancer Ther 2:1139–1147.
Suganuma T,
(2005) Functional expression of the angiotensin II type 1 receptor in human ovarian carcinoma cells and its blockade therapy resulting in suppression of tumor invasion, angiogenesis, and peritoneal dissemination. Clin Cancer Res 11:2686–2694.
Muscella A,
Greco S,
Elia MG,
Storelli C,
Marsigliante S
(2003) PKC-zeta is required for angiotensin II-induced activation of ERK and synthesis of C-FOS in MCF-7 cells. J Cell Physiol 197:61–68.
Amaya K,
(2004) Angiotensin II activates MAP kinase and NF-kappaB through angiotensin II type I receptor in human pancreatic cancer cells. Int J Oncol 25:849–856.
(2004) ONCOMINE: A cancer microarray database and integrated data-mining platform. Neoplasia 6:1–6.
Krishnamurthi K,
(1999) Estrogen regulates angiotensin AT1 receptor expression via cytosolic proteins that bind to the 5′ leader sequence of the receptor mRNA. Endocrinology 140:5435–5438.
Puddefoot JR,
Udeozo UK,
Barker S,
Vinson GP
(2006) The role of angiotensin II in the regulation of breast cancer cell adhesion and invasion. Endocr Relat Cancer 13:895–903.
Gonzalez-Zuloeta Ladd AM,
(2005) Angiotensin-converting enzyme gene insertion/deletion polymorphism and breast cancer risk. Cancer Epidemiol Biomarkers Prev 14:2143–2146.
(2007) Differential roles of Angiotensinogen and Angiotensin Receptor type 1 polymorphisms in breast cancer risk. Breast Cancer Res Treat 101:299–304.
Fryzek JP,
(2006) A cohort study of antihypertensive medication use and breast cancer among Danish women. Breast Cancer Res Treat 3:3.
Miller LD,
(2005) An expression signature for p53 status in human breast cancer predicts mutation status, transcriptional effects, and patient survival. Proc Natl Acad Sci USA 102:13550–13555.
Hess KR,
(2006) Pharmacogenomic predictor of sensitivity to preoperative chemotherapy with paclitaxel and fluorouracil, doxorubicin, and cyclophosphamide in breast cancer. J Clin Oncol 24:4236–4244.
Wang Y,
(2005) Gene-expression profiles to predict distant metastasis of lymph-node-negative primary breast cancer. Lancet 365:671–679.
Perou CM,
(2000) Molecular portraits of human breast tumours. Nature 406:747–752.
van de Vijver MJ,
(2002) A gene-expression signature as a predictor of survival in breast cancer. N Engl J Med 347:1999–2009.
You are going to email the following AGTR1 overexpression defines a subset of breast cancer and confers sensitivity to losartan, an AGTR1 antagonist
Daniel R. Rhodes, Bushra Ateeq, Qi Cao, Scott A. Tomlins, Rohit Mehra, Bharathi Laxman, Shanker Kalyana-Sundaram, Robert J. Lonigro, Beth E. Helgeson, Mahaveer S. Bhojani, Alnawaz Rehemtulla, Celina G. Kleer, Daniel F. Hayes, Peter C. Lucas, Sooryanarayana Varambally, Arul M. Chinnaiyan
Proceedings of the National Academy of Sciences Jun 2009, 106 (25) 10284-10289; DOI: 10.1073/pnas.0900351106


text:
The 2014–15 Ethiopian Premier League is the 69th season of top-tier football in Ethiopia. The season began play on 25 October 2014. Saint George SC are the defending champions, having won their 23rd championship.

The league comprises 14 teams, the bottom two of which will be relegated to the National League for 2015–16.

Teams
A total of 14 teams will contest the league, including 12 sides from the 2013–14 season and two promoted from the National League. The two newcomers are Welayta Dicha and Dashen Beer FC.

Weha Serawoch and Adama City F.C. were the last two teams of the 2013–14 season and play in the National League for the 2014–15 season. Saint George SC are the defending champions from the 2013–14 season.

League table

References

Premier League
Premier League
Ethiopian Premier League
Ethiopian Premier League


Each minute God has His hand and eye on all of it.
This entry was posted in art, Life, Poetry, Uncategorized and tagged Art, encouragement, God, Inspiration, life, motivation, Poetry, protection from danger, Religion. Bookmark the permalink.
Thank you! Paul's art really is responsible for inspiring the words.