10 Universities to Form Semester Online Consortium

Starting next fall, 10 prominent universities, including Duke, the University of North Carolina at Chapel Hill and Northwestern, will form a consortium called Semester Online, offering about 30 online courses to both their students — for whom the classes will be covered by their regular tuition — and to students elsewhere who would have to apply and be accepted and pay tuition of more than $4,000 a course.

Semester Online will be operated through the educational platform 2U, formerly known as 2tor, and will simulate many aspects of a classroom: Students will be able to raise their hands virtually, break into smaller discussion groups and arrange and hold online study sessions.

The virtual classroom is a cross between a Google+ hangout and the opening sequence of “The Brady Bunch,” where each student has his or her own square, the equivalent of a classroom chair. However, with Semester Online courses, there is no sneaking in late and unnoticed, and there is no back row.

Unlike the increasingly popular massive open online courses, or MOOCs, free classes offered by universities like Harvard, M.I.T. and Stanford, Semester Online classes will be small — and will offer credit.

“Now we can provide students with a course that mirrors our classroom experience,” says Edward S. Macias, provost and executive vice chancellor for academic affairs at Washington University in St. Louis, one of the participants.

“It’s going to be the most rigorous, live, for-credit online experience ever,” said Chip Paucek, a founder of 2U.

For many of the participating schools, which include Brandeis, Emory, Notre Dame, the University of Rochester, Vanderbilt and Wake Forest, Semester Online offerings will be their first undergraduate for-credit online courses, and the first to offer credit to students from outside the universities.

One draw for the colleges is the expansion in their course catalogs.

“No university can deliver the full range of courses that both might be interesting and useful and enlightening to our students,” said Peter Lange, the provost of Duke. “Imagine if you don’t have a person who works on the Sahel region in Africa, but another school does.”

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Jerusalem Targeted by Rockets for First Time in Gaza Conflict

JERUSALEM — Palestinian militants fired rockets for the first time at Jerusalem on Friday in a daring new escalation of hostilities with Israel on the third day of their latest lethal conflict over Gaza, triggering air raid sirens and panicking residents who had thought themselves secure from such attacks because of the holy city’s multireligious heritage and large Palestinian population.

The Israeli authorities did not immediately confirm the origin of the rocket fire but responsibility was claimed by the Palestinian militant group Hamas in Gaza, which has amassed arsenals of smuggled rockets with increased ranges and more accurate trajectories in recent years. On Thursday, Hamas rocket squads launched at least two at Tel Aviv, Israel’s biggest city, for the first time, and on Friday launched more as part of a response to a large-scale aerial assault by the Israelis on targets in Gaza and indications that Israel was close to launching its first ground invasion there in four years.

“We are sending a short and simple message: There is no security for any Zionist or any single inch of Palestine and we plan more surprises,” said Abu Obeida, a spokesman for the military of wing of Hamas, in a message quoted by The Associated Press.

Jerusalem, a city holy to Jews, Muslims and Christians, had been previously thought off-limits to rocket attacks by militant Palestinians and others who reject Israel’s claim to the city as its capital. Even Saddam Hussein, the Iraqi leader, had avoided targeting the city when he aimed Scud missiles at Israel during the first Persian Gulf War in 1991. The city is about 48 miles from the Gaza border.

The police in Jerusalem said no rockets fell within city limits, but one crashed harmlessly near a Jewish West Bank settlement just south of Jerusalem. A police spokesman, Micky Rosenfeld, said other explosions were heard in the same area but security forces had not located the landing sites.

The Jerusalem rocket attack came hours after scores of rockets were fired from Gaza into Israel, striking major cities of the south, causing widespread panic and damage and shattering plans for a temporary cease-fire during a remarkable visit to Gaza by the Egyptian prime minister that showed the shifting dynamics of Middle East politics since the turmoil of the Arab Spring uprisings.

The rocket fired at Tel Aviv on Friday probably landed in the sea, Mr. Rosenfeld said. Israeli officials say the only rockets in Gaza with a range that can reach Tel Aviv are the Iranian-made Fajr-5 projectiles that Israel has been targeting in its hundreds of airstrikes over the last few days.

That these rockets were still being fired seemed to weigh heavily in Israeli military calculations about a ground invasion. After a meeting with President Shimon Peres, Prime Minister Benjamin Netanyahu said the Israeli Army was “continuing to hit Hamas hard and is ready to expand the operation into Gaza,” according to a statement from his office.

Mr. Netanyahu said the aim was “to take out the terrorist infrastructure in Gaza while doing everything possible not to harm civilians.”

The rapidly escalating confrontation between Hamas and Israel followed an Israeli airstrike on Wednesday that killed the top commander of Hamas, and the tit-for-tat violence is widely seen as a potential catalyst for broader hostilities at a time of spreading turmoil in Syria and elsewhere in the region.

The Israeli military said Col. Amir Baram, commander of the Israel Defense Forces’ paratroopers brigade, had addressed his forces during a preparatory briefing in the field, saying: “We are already 48 hours into an operation that we knew would have to happen. We have spoken about it during training, exercises and conferences. There is no doubt that we have to operate. This is why we enlisted, and why we have trained.”

Witnesses on the Gaza-Israel border said Israeli tanks had massed in several places.

Early on Friday, the Israeli military said it had called up 16,000 army reservists to move against what Israel considers an unacceptable security threat from smuggled rockets amassed by Hamas, which does not recognize Israel’s right to exist.

It was not initially clear whether the show of Israeli force on the ground was meant as more of an intimidation tactic to further pressure Hamas leaders, who had all been forced into hiding on Wednesday after the group’s military chief, Ahmed al-Jabari, was killed in a pinpoint aerial bombing. But Israel’s preparations seemed to pick up on Friday after the attempts to land rockets in Tel Aviv, while Hamas itself seemed emboldened by Egypt’s support.

“The time in which the Israeli occupation does whatever it wants in Gaza is gone,” said Ismail Haniya, the Hamas prime minister.

Isabel Kershner reported from Jerusalem, Jodi Rudoren from Gaza City and Alan Cowell from Paris. Reporting was contributed by Fares Akram from Gaza, Rick Gladstone from New York, Rina Castelnuovo from the Gaza-Israel border, Mayy El Sheikh and David D. Kirkpatrick from Cairo, and Gabby Sobelman from Jerusalem.

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Ikea Admits Use of Forced Labor in the 1980s

BERLIN — Ikea has long been famous for its inexpensive, some-assembly-required furniture. On Friday the company admitted that political prisoners in the former East Germany provided some of the labor that helped it keep its prices so low.

A report by auditors at Ernst & Young concluded that Ikea, a Swedish company, knowingly benefited from forced labor in the former East Germany to manufacture some of its products in the 1980s. Ikea had commissioned the report in May as a result of accusations that both political and criminal prisoners were involved in making components of Ikea furniture and that some Ikea employees knew about it.

“Even though Ikea Group took steps to secure that prisoners were not used in production, it is now clear that these measures were not effective enough,” the company said in a statement on Friday.

The use of political prisoners as forced labor, even decades ago, is a publicity disaster for a company that with its familiar blue and yellow logo seems at times like a cultural ambassador for Sweden. Inexpensive Ikea furnishings have filled countless student apartments and the homes of millions of young families around the world.

Accusations against Ikea started to appear about a year ago in news media reports in Germany and Sweden. Ikea’s admission has given new impetus to efforts by victims’ groups to receive compensation for work they were forced to perform under the Communist government in East Germany, an issue that has long been overshadowed here by the large and deadly slave-labor program under the Nazis.

“There’s little recognition,” said Hugo Diederich, the chairman of the Association of Victims of Stalinism, himself a former forced laborer, after a news conference here a short walk from the former Checkpoint Charlie border crossing, in a building that stands along the path of the Berlin Wall.

Ikea is not the only company that has been linked to forced labor in the former East Germany by purchasing goods from suppliers there, though the actual number may never be known.

Mr. Diederich said that after an attempt to escape from East Germany, he was forced to make steel pipes for the firms Klöckner & Company and Mannesmann.

At least two well-known mail-order companies in the former West Germany, Neckermann and Quelle, which have since run into financial trouble, have also been accused of using forced labor.

Christian Sachse, a Berlin historian, said forced labor permeated institutions across East Germany, and that it would take “years of research to properly understand the field.”

Mr. Diederich said that more needs to be done for the victims, many of whom today live under worse circumstances than their former tormentors. “This will raise the pressure enormously on politicians to act,” he added.

Ikea’s announcement received a mixed response. There was praise that the company had made an effort to uncover unpleasant facts about its past, but also criticism that it had not been transparent enough with the results. Rather than releasing the entire report, the company made only a four-page summary available, citing privacy concerns.

But Steffen Alisch, a researcher on prisons in the former East Germany at the Free University in Berlin, said, “They have to make the entire report available and they have to do it quickly.”

The fact that Ikea retained Ernst & Young for the inquiry instead of using independent academic experts also raised questions. “Ernst & Young has no experience with research into dictatorships and is clearly not objective,” said Ronald Lässig, chairman of the East German victims’ group DDR-Opfer-Hilfe. “What Ikea did today was little more than an event for show.”

Investigators examined 20,000 pages of internal Ikea records, as well as 80,000 pages of documents from federal and state archives. They interviewed about 90 people, including current and former Ikea workers and witnesses from East Germany.

A political prisoner in Naumburg, about an hour’s drive from Leipzig, told investigators that he was sent to VEB Metallwaren Naumburg, one of East Germany’s state-owned enterprises. He was put to work placing metal pegs in chair legs and furniture rollers, and remembered seeing boxes with the Ikea logo.

A purchaser for the company said that “the use of prison labor was not an official Ikea strategy, but that there was an awareness within the company about the issue.”

“The G.D.R. did not differentiate between political and criminal prisoners,” Ernst & Young wrote, referring to East Germany, adding that “during this time period, many innocent individuals were sent to prison.” Ikea repeatedly raised concerns about the possible use of forced labor at the time but no action was taken, the report said.

Jochen Staadt, a professor at the Free University of Berlin, said it was well known at the time that East Germany was using prisoners to work in factories but West Germany encouraged the production of goods in the East because it allowed the East to reduce its debt. At the same time, companies liked to move production to East Germany because costs were lower.

Professor Staadt said companies like Ikea would still have paid for the work in East Germany but that the pay never reached the workers. “It was pocketed by the G.D.R.,” he said.

Employees of Ikea did visit the production sites in East Germany but rules governing such visits were strict, that way reducing the effectiveness of site inspections. Any visit had to be registered and approved in advance, could take place only in selected parts of the plants and a representative of the East German government had to be there.

Ikea said Friday it was sorry about the episodes and pledged to donate money to research on forced labor in the former East Germany.

“We deeply regret that this could happen,” Jeanette Skjelmose, sustainability manager at Ikea, said in a statement.

Rainer Wagner, chairman of the victims’ group UOKG, said at the news conference here that “a broad public clarification” was necessary, not just from Ikea but “all the firms” that used forced labor. But Mr. Wagner also thanked Ikea for its “pioneering role” in helping to bring greater public attention the subject.

Nicholas Kulish reported from Berlin, and Julia Werdigier from London. Chris Cottrell contributed reporting from Berlin.

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I Was Misinformed: The Time She Tried Viagra

I have noticed, in the bragging-rights department, that “he doesn’t need Viagra” has become the female equivalent of the male “and, I swear, she’s a real blonde.” Personally, I do not care a bit. To me, anything that keeps you happy and in the game is a good thing.

But then, I am proud to say, I was among the early, and from what I gather, rare female users.

It happened when the drug was introduced around 1998. I was 50, but after chemotherapy for breast cancer — and later, advanced ovarian cancer — I was, hormonally speaking, pretty much running on fumes. Whether this had diminished my sex drive I did not yet know. One may have Zorba-esque impulses when a cancer diagnosis first comes in; but a treatment that leaves you bald, moon-faced and exhausted knocks that out of your system pretty fast.

But by 1998, the cancer was gone, my hair was back and I was ready to get back in the game. I was talking to an endocrinologist when I brought up Viagra. This was not to deal with the age-related physical changes I knew it would not address, it was more along the feminist lines of equal pay for equal work: if men have this new sex drug, I want this new sex drug.

“I know it’s supposed to work by increasing blood flow,” I told the doctor, “But if that’s true for men, shouldn’t it be true for women, too?”

“You’re the third woman who asked me that this week,” he said.

He wrote me a prescription. I was not seeing anyone, so I understood that I would have to do both parts myself, but that was fine. I have a low drug threshold and figured it might be best the first time to fly solo. My memory of the directions are hazy: I think there was a warning that one might have a facial flush or headaches or drop dead of a heart attack; that you were to take a pill at least an hour before you planned to get lucky, and, as zero hour approached, you were supposed to help things along by thinking beautiful thoughts, kind of like Peter Pan teaching Wendy and the boys how to fly.

But you know how it is: It’s hard to think beautiful thoughts when you’re wondering, “Is it happening? Do I feel anything? Woof, woof? Hello, sailor? Naaah.”

After about an hour, however, I was aware of a dramatic change. I had developed a red flush on my face; I was a hot tomato, though not the kind I had planned. I had also developed a horrible headache. The sex pill had turned into a bad joke: Not now, honey, I have a headache.

I put a cold cloth on my head and went to sleep. But here’s where it got good: When I slept, I dreamed; one of those extraordinary, sensual, swimming in silk sort of things. I woke up dazed and glowing with just one thought: I gotta get this baby out on the highway and see what it can do.

A few months later I am fixed up with a guy, and after a time he is, under the Seinfeldian definition of human relations (Saturday night date assumed) my official boyfriend. He is middle aged, in good health. How to describe our romantic life with the delicacy a family publication requires? Perhaps a line from “Veronika, der Lenz ist da” (“Veronica, Spring Is Here”), a song popularized by the German group the Comedian Harmonists: “Veronika, der Spargel Wächst” (“Veronica, the asparagus are blooming”). On the other hand, sometimes not. And so, one day, I put it out there in the manner of sport:

“Want to drop some Viagra?” I say.

Here we go again, falling into what I am beginning to think is an inevitable pattern: lying there like a lox, or two loxes, waiting for the train to pull into the station. (Yes, I know it’s a mixed metaphor, but at least I didn’t bring in the asparagus.) So there we are, waiting. And then, suddenly, spring comes to Suffolk County. It’s such a presence. I’m wondering if I should ask it if it hit traffic on the L.I.E. We sit there staring.

My reaction is less impressive. I don’t get a headache this time. And romantically, things are more so, but not so much that I feel compelled to try the little blue pills again.

Onward roll the years. I have a new man in my life, who is 63. He does have health problems, for which his doctor prescribes an E.D. drug. I no longer have any interest in them. My curiosity has been satisfied. Plus I am deeply in love, an aphrodisiac yet to be encapsulated in pharmaceuticals.

We take a vacation in mountain Mexico. We pop into a drugstore to pick up sunscreen and spot the whole gang, Cialis, Viagra, Levitra, on a shelf at the checkout counter. No prescription needed in Mexico, the clerk says. We buy all three drugs and return to the hotel. I try some, he tries some. In retrospect, given the altitude and his health, we are lucky we did not kill him. I came across an old photo the other day. He is on the bed, the drugs in their boxes lined up a in a semi-circle around him. He looks a bit dazed and his nose is red.

Looking at the picture, I wonder if he had a cold.

Then I remember: the flush, the damn flush. If I had kids, I suppose I would have to lie about it.

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I Was Misinformed: The Time She Tried Viagra

I have noticed, in the bragging-rights department, that “he doesn’t need Viagra” has become the female equivalent of the male “and, I swear, she’s a real blonde.” Personally, I do not care a bit. To me, anything that keeps you happy and in the game is a good thing.

But then, I am proud to say, I was among the early, and from what I gather, rare female users.

It happened when the drug was introduced around 1998. I was 50, but after chemotherapy for breast cancer — and later, advanced ovarian cancer — I was, hormonally speaking, pretty much running on fumes. Whether this had diminished my sex drive I did not yet know. One may have Zorba-esque impulses when a cancer diagnosis first comes in; but a treatment that leaves you bald, moon-faced and exhausted knocks that out of your system pretty fast.

But by 1998, the cancer was gone, my hair was back and I was ready to get back in the game. I was talking to an endocrinologist when I brought up Viagra. This was not to deal with the age-related physical changes I knew it would not address, it was more along the feminist lines of equal pay for equal work: if men have this new sex drug, I want this new sex drug.

“I know it’s supposed to work by increasing blood flow,” I told the doctor, “But if that’s true for men, shouldn’t it be true for women, too?”

“You’re the third woman who asked me that this week,” he said.

He wrote me a prescription. I was not seeing anyone, so I understood that I would have to do both parts myself, but that was fine. I have a low drug threshold and figured it might be best the first time to fly solo. My memory of the directions are hazy: I think there was a warning that one might have a facial flush or headaches or drop dead of a heart attack; that you were to take a pill at least an hour before you planned to get lucky, and, as zero hour approached, you were supposed to help things along by thinking beautiful thoughts, kind of like Peter Pan teaching Wendy and the boys how to fly.

But you know how it is: It’s hard to think beautiful thoughts when you’re wondering, “Is it happening? Do I feel anything? Woof, woof? Hello, sailor? Naaah.”

After about an hour, however, I was aware of a dramatic change. I had developed a red flush on my face; I was a hot tomato, though not the kind I had planned. I had also developed a horrible headache. The sex pill had turned into a bad joke: Not now, honey, I have a headache.

I put a cold cloth on my head and went to sleep. But here’s where it got good: When I slept, I dreamed; one of those extraordinary, sensual, swimming in silk sort of things. I woke up dazed and glowing with just one thought: I gotta get this baby out on the highway and see what it can do.

A few months later I am fixed up with a guy, and after a time he is, under the Seinfeldian definition of human relations (Saturday night date assumed) my official boyfriend. He is middle aged, in good health. How to describe our romantic life with the delicacy a family publication requires? Perhaps a line from “Veronika, der Lenz ist da” (“Veronica, Spring Is Here”), a song popularized by the German group the Comedian Harmonists: “Veronika, der Spargel Wächst” (“Veronica, the asparagus are blooming”). On the other hand, sometimes not. And so, one day, I put it out there in the manner of sport:

“Want to drop some Viagra?” I say.

Here we go again, falling into what I am beginning to think is an inevitable pattern: lying there like a lox, or two loxes, waiting for the train to pull into the station. (Yes, I know it’s a mixed metaphor, but at least I didn’t bring in the asparagus.) So there we are, waiting. And then, suddenly, spring comes to Suffolk County. It’s such a presence. I’m wondering if I should ask it if it hit traffic on the L.I.E. We sit there staring.

My reaction is less impressive. I don’t get a headache this time. And romantically, things are more so, but not so much that I feel compelled to try the little blue pills again.

Onward roll the years. I have a new man in my life, who is 63. He does have health problems, for which his doctor prescribes an E.D. drug. I no longer have any interest in them. My curiosity has been satisfied. Plus I am deeply in love, an aphrodisiac yet to be encapsulated in pharmaceuticals.

We take a vacation in mountain Mexico. We pop into a drugstore to pick up sunscreen and spot the whole gang, Cialis, Viagra, Levitra, on a shelf at the checkout counter. No prescription needed in Mexico, the clerk says. We buy all three drugs and return to the hotel. I try some, he tries some. In retrospect, given the altitude and his health, we are lucky we did not kill him. I came across an old photo the other day. He is on the bed, the drugs in their boxes lined up a in a semi-circle around him. He looks a bit dazed and his nose is red.

Looking at the picture, I wonder if he had a cold.

Then I remember: the flush, the damn flush. If I had kids, I suppose I would have to lie about it.

Read More..

Hurt by Rivals From Asia, Dell Profit Falls 47%

SAN FRANCISCO (Reuters) — Dell’s third-quarter profit fell 47 percent, the company said on Thursday, hurt by lower PC sales and weaker demand from large corporations. But Dell said it expected revenue to grow as much as 5 percent in the current quarter compared with sales in the previous one.

The company, once the world’s top PC maker and a pioneer in computer supply chain management, is struggling to defend its market share against Asian rivals like Lenovo. It is trying to bolster growth by focusing on products and services to corporations.

The company, founded by its chief executive, Michael Dell, said that it saw “the challenging global macroeconomic environment continuing in the fourth quarter.”

Net income was $475 million, or 27 cents a share, compared with $893 million, or 49 cents a share, in the period a year earlier. Excluding certain items, it earned 39 cents a share, compared with an average forecast of 40 cents.

Revenue fell 11 percent, to $13.7 billion, slightly less than the average analyst estimate of $13.89 billion, according to Thomson Reuters.

Dell’s chief financial officer, Brian T. Gladden, said in an interview that corporate customers continued to postpone technology spending.

“It’s not clear what’s going to cause them to increase their spending in the short term, given the uncertainty in the economy,” he said.

Dell’s enterprise solutions revenue rose 3 percent to $4.8 billion, while server and networking revenue climbed 11 percent. In contrast, consumer revenue plummeted 23 percent to $2.5 billion, underscoring the plight of the broader PC market. And sales to large corporations declined 8 percent to $4.2 billion.

The consumer market is improving with the introduction of the Windows 8 operating system from Microsoft, which has been designed with touch-screen devices and Internet-based computing in mind, Mr. Gladden said.

Part of the spending weakness among corporate customers comes from worry over early next year, when trillions of dollars in tax increases and automatic spending cuts will begin to go into force unless lawmakers agree on legislation to reduce the budget deficit, Mr. Gladden said.

The cuts could take a toll on consumer and government spending and cause the economy to stall.

“I would tell you that the behavior we are seeing from our customers today is actually driven by that uncertainty,” Mr. Gladden said. “It’s not like it’s all going to happen overnight. It’s affecting our business today.”

Dell is ensuring that it has access to cash in case there is no Congressional action.

“I would say there are several things we are doing from a planning standpoint,” Mr. Gladden said, “to ensure that we are in a position to have appropriate access to liquidity.” He said Dell was making sure it would have access to lines of credit and commercial paper.

Dell shares fell around 2 percent in late trading from their close of $9.56. The shares initially rose after the release of the results.

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Palestinian Rockets Kill Three Israelis and Trigger Air Sirens in Tel Aviv

KIRYAT MALACHI, Israel — Israel and Hamas widened their deadly conflict over Gaza on Thursday, as militants fired dozens of rockets — including one that killed three civilians in an apartment block in this small southern Israeli town — and two longer-range rockets aimed at Tel Aviv, causing no harm but triggering the first air raid warning there set off by incoming fire from Gaza. The death toll in Gaza from Israeli airstrikes rose to at least 19, including five children and a pregnant teenager.

There was no sign that either side was prepared to dial back the confrontation that has threatened a new war in the Middle East, despite entreaties for restraint by world leaders including President Obama and Ban Ki-moon, the United Nations secretary general, who planned a visit there in coming days. If anything, the Israelis intensified their attacks on Gaza after the Tel Aviv scare and made new moves toward a possible ground invasion.

The Israeli deaths were the first since Israel’s military launched ferocious aerial assaults on Wednesday to stop the chronic rocket fire from Gaza, the Palestinian coastal enclave controlled by Hamas, the militant Palestinian group.

The Israel Defense Forces said in a cryptic statement that one of the two longer-range rockets aimed at Tel Aviv landed but did not hit the ground — meaning that it likely crashed into the Mediterranean Sea — and that the other appeared to have landed far outside the city. Exact locations were not specified.

But the Tel Aviv air raid warnings — which residents of Israel’s largest metropolis had not heard except for drills or malfunctions since Saddam Hussein’s Scuds threatened them in the first Persian Gulf War, more than two decades ago — were a reminder of their vulnerability to an attack from Gaza, less than 40 miles away. They also underscored Israel’s stated reason for seeking to destroy the missile-launching sites in Gaza.

Ehud Barak, the minister of defense, said the targeting of Tel Aviv and the scope of the Palestinian rocket fire “represents an escalation, and there will be a price for that escalation that the other side will have to pay.”

Mr. Barak also dropped a further hint that planning for a ground invasion of Gaza had begun, saying he had instructed the army to broaden its draft of reservists to “be prepared for any kind of development if and when it will be required.” Israeli officials said 30,000 reservists could be called, and heavy machinery and tanks rumbled south along Israeli roads leading to Gaza on Thursday in preparation for a possible invasion.

The Israel Defense Forces said that within hours of the Tel Aviv air raid warning, they had attacked 70 underground rocket-launching sites in Gaza, and “direct hits were confirmed.” There were also unconfirmed reports that Israeli rockets had struck near Gaza’s Rafah crossing into Egypt, forcing the Egyptians to close it.

.

Brig. Gen. Yoav Mordechai, a spokesman for the Israel Defense Forces, said its aerial assaults had hit more than 200 sites in Gaza by late Thursday, and “we’ll continue tonight and tomorrow.” He also said militants in Gaza had fired about 300 rockets into southern Israel and at least 100 more had been intercepted by Israel’s Iron Dome antimissile defense system.

The Israeli aerial assault on Gaza that began on Wednesday was the most intense military operation by Israel in Gaza since an invasion four years ago.

The regional perils of the situation sharpened as President Mohamed Morsi of Egypt warned that his country stood by the Palestinians against what he termed Israeli aggression, echoing similar condemnation on Wednesday.

“The Egyptian people, the Egyptian leadership, the Egyptian government and all of Egypt is standing with all its resources to stop this assault, to prevent the killing and the bloodshed of Palestinians,” Mr. Morsi said in nationally televised remarks before a crisis meeting of senior ministers. He also instructed his prime minister to lead a delegation to Gaza on Friday and said he had contacted President Obama to discuss strategies to “stop these acts and doings and the bloodshed and aggression.”

Isabel Kershner reported from Kiryat Malachi, Israel, and Rick Gladstone from New York. Reporting was contributed by Fares Akram from Gaza, Rina Castelnuovo from Kiryat Malachi, Mayy El Sheikh and David D. Kirkpatrick from Cairo, Gabby Sobelman from Jerusalem and Alan Cowell from Paris.

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DealBook: In a Switch, Investors Are Buying European Bank Bonds

LONDON — European bank debt, once an investment pariah, is suddenly popular.

In recent weeks, money managers have been readily buying the new bonds of the region’s financial institutions, deals that just months ago would have seemed unpalatable. Bank of Ireland, which received a bailout in 2010, sold $1.3 billion of bonds on Tuesday and found strong demand. It was the largest offering by an Irish bank without a government guarantee in almost three years.

The gradual thawing of the capital markets is a good sign for the region’s banks. In the midst of the crisis, institutions, especially in troubled economies like Ireland and Portugal, have been struggling to raise money from private investors. The latest deals will help bolster banks’ capital levels and strengthen their balance sheets.

But the bonds could leave investors exposed, especially given the precarious situation in Europe. The sovereign debt crisis continues to weigh on the economy. The financial markets remain volatile. And profit at the region’s banks is flagging.

“It’s a great time to be issuing high-yield debt but not to be investing in it,” said Robin Doumar, managing partner at the private equity firm Park Square Capital.

For now, bondholders are taking comfort in the policy makers’ response to the sovereign debt crisis.

In late August, the European Central Bank began an unlimited bond-buying program aimed at lowering countries’ borrowing costs and breathing life into local economies. By essentially offering a blank check to help Europe’s troubled governments, policy makers calmed short-term fears that some of the region’s banks might need to be bailed out, reviving interest in the companies’ bonds.

“The biggest driver of demand has been the policy responses from the European Central Bank,” said Melissa Smith, head of European high-grade debt capital markets at JPMorgan Chase in London. “It’s provided stability as policy makers have stated their commitment to preserving the euro zone.”

With interest rates at record lows, European bank debt looks especially appealing to investors.

On Thursday, the British bank Barclays sold $3 billion of 10-year bonds at 7.6 percent. The Portuguese lender Banco Espírito Santo recently issued $958 million worth of debt at 5.9 percent.

By comparison, a 10-year Treasury is paying 1.8 percent. Germany has offered a negative yield on some of its sovereign debt maturities this year.

Even the yields on junk bonds, the risky corporate debt that pays high interest rates, are coming down as investors pile into such securities. The average yield is now just 5.8 percent, according to a Bank of America Merrill Lynch index. Historically, they have paid 10 percent or even more.

“There’s been a huge contraction,” said Robert Ellison, head of European debt capital markets for financial institutions at UBS in London.

The industry has been quick to capitalize on investors’ desperate hunt for returns. Banks in Europe have issued a combined $318 billion of unsecured debt so far this year, almost triple the amount raised by their American counterparts, according to the data provider Dealogic.

The capital markets are being discerning. This year, well-financed companies in Northern Europe, like Nordea Bank of Sweden, have been able to sell the largest lots of bonds at relatively reasonable rates. Smaller banks, particularly in Southern Europe, have had to offer investors better rates to win support for their bond deals.

Even so, it is a stark contrast from almost a year ago. With the capital markets paralyzed, the European Central Bank then had to step in to stabilize the banks, offering $1.3 trillion in short-term, low-cost loans to financial companies.

As they find renewed interest from private investors, European banks can more easily raise money, fortifying their balance sheets in case of unexpected losses. At regulators’ behest, financial institutions in the region have been increasing their capital levels.

But bond investors, in their thirst for yield, may be overlooking signs of potential trouble.

Barclays, for instance, sold a controversial type of debt, known as contingent convertible bonds. With these so-called CoCo bonds, investors can be wiped out if the bank’s capital falls below a certain threshold. While Barclays’ balance sheet is in good shape, bondholders’ willingness to accept such conditions highlights the risks in the market. Traditional bondholders can usually recoup at least some of their principal even if a company goes bankrupt.

At the same time, many European financial institutions are still in fragile shape. The Bank of Ireland, in which the Irish government still has a small stake, is struggling to divest itself of many risky loans that it made before the financial crisis. Portugal’s economy is also expected to contract 3 percent this year, which will probably depress the earnings of Banco Espírito Santo.

The question for investors is whether the reward is worth the risk.

Read More..

Alzheimer’s Tied to Mutation Harming Immune Response

Alzheimer’s researchers and drug companies have for years concentrated on one hallmark of Alzheimer’s disease: the production of toxic shards of a protein that accumulate in plaques on the brain.

But now, in a surprising coincidence, two groups of researchers working from entirely different starting points have converged on a mutated gene involved in another aspect of Alzheimer’s disease: the immune system’s role in protecting against the disease. The mutation is suspected of interfering with the brain’s ability to prevent the buildup of plaque.

The discovery, researchers say, provides clues to how and why the disease progresses. The gene, known as TREM2, is only the second found to increase Alzheimer’s risk substantially in older people.

“It points very specifically to a potential metabolic pathway that you could intervene in to change the course of Alzheimer’s disease,” said William Thies, chief medical and scientific officer of the Alzheimer’s Association.

Much work remains to be done before scientists understand precisely how the newly discovered gene mutation leads to Alzheimer’s, but already there are some indications from studies in mice. When the gene is not mutated, white blood cells in the brain spring into action, gobbling up and eliminating the plaque-forming toxic protein, beta amyloid. As a result, Alzheimer’s can be staved off or averted.

But when the gene is mutated, the brain’s white blood cells are hobbled, making them less effective in their attack on beta amyloid.

People with the mutated gene have a threefold to fivefold increase in the likelihood of developing Alzheimer’s disease in old age.

The intact gene, says John Hardy of University College London, “is a safety net.” And those with the mutation, he adds, “are living life without a safety net.” Dr. Hardy is lead author of one of the papers.

The discovery also suggests that a new type of drug could be developed to enhance the gene’s activity, perhaps allowing the brain’s white blood cells to do their work.

“The field is in desperate need of new therapeutic agents,” said Alison Goate, an Alzheimer’s researcher at Washington University in St. Louis who contributed data to Dr. Hardy’s study. “This will give us an alternative approach.”

The fact that two research groups converged on the same gene gives experts confidence in the findings. Both studies were published online Wednesday in The New England Journal of Medicine. “Together they make a good case that this really is an Alzheimer’s gene,” said Gerard Schellenberg, an Alzheimer’s researcher at the University of Pennsylvania who was not involved with the work.

The other gene found to raise the odds that a person will get Alzheimer’s, ApoE4, is much more common and confers about the same risk as the mutated version of TREM2. But it is still not clear why ApoE4, discovered in 1993, makes Alzheimer’s more likely.

Because the mutations in the newly discovered gene are rare, occurring in no more than 2 percent of Alzheimer’s patients, it makes no sense to start screening people for them, Dr. Thies said. Instead, the discovery provides new clues to the workings of Alzheimer’s disease.

To find the gene, a research group led by Dr. Kari Stefansson of deCODE Genetics of Iceland started with a simple question.

“We asked, ‘Can we find anything in the genome that separates those who are admitted to nursing homes before the age of 75 and those who are still living at home at 85?’ ” he said.

Scientists searched the genomes of 2,261 Icelanders and zeroed in on TREM2. Mutations in that gene were more common among people with Alzheimer’s, as well as those who did not have an Alzheimer’s diagnosis but who had memory problems and might be on their way to developing Alzheimer’s.

The researchers confirmed their results by looking for the gene in people with and without Alzheimer’s in populations studied at Emory University, as well as in Norway, the Netherlands and Germany.

The TREM2 connection surprised Dr. Stefansson. Although researchers have long noticed that the brain is inflamed in Alzheimer’s patients, he had dismissed inflammation as a major factor in the disease.

“I was of the opinion that the immune system would play a fairly small role, if any, in Alzheimer’s disease,” Dr. Stefansson said. “This discovery cured me of that bias.”

Meanwhile, Dr. Hardy and Rita Guerreiro at University College London, along with Andrew Singleton at the National Institute on Aging, were intrigued by a strange, rare disease. Only a few patients had been identified, but their symptoms were striking. They had crumbling bones and an unusual dementia, sclerosing leukoencephalopathy.

“It’s a weird disease,” Dr. Hardy said.

He saw one patient in her 30s whose brain disease manifested in sexually inappropriate behavior. Also, her bones kept breaking. The disease was caused by mutations that disabled both the copy of TREM2 that she had inherited from her mother and the one from her father.

Eventually the researchers searched for people who had a mutation in just one copy of TREM2. To their surprise, it turned out that these people were likely to have Alzheimer’s disease.

They then asked researchers around the world who had genetic data from people with and without Alzheimer’s to look for TREM2 mutations.

“Sure enough, they had good evidence,” Dr. Hardy said. The mutations occurred in one-half of 1 percent of the general population but in 1 to 2 percent of patients with Alzheimer’s disease.

“That is a big effect,” Dr. Hardy said.

Read More..

Alzheimer’s Tied to Mutation Harming Immune Response

Alzheimer’s researchers and drug companies have for years concentrated on one hallmark of Alzheimer’s disease: the production of toxic shards of a protein that accumulate in plaques on the brain.

But now, in a surprising coincidence, two groups of researchers working from entirely different starting points have converged on a mutated gene involved in another aspect of Alzheimer’s disease: the immune system’s role in protecting against the disease. The mutation is suspected of interfering with the brain’s ability to prevent the buildup of plaque.

The discovery, researchers say, provides clues to how and why the disease progresses. The gene, known as TREM2, is only the second found to increase Alzheimer’s risk substantially in older people.

“It points very specifically to a potential metabolic pathway that you could intervene in to change the course of Alzheimer’s disease,” said William Thies, chief medical and scientific officer of the Alzheimer’s Association.

Much work remains to be done before scientists understand precisely how the newly discovered gene mutation leads to Alzheimer’s, but already there are some indications from studies in mice. When the gene is not mutated, white blood cells in the brain spring into action, gobbling up and eliminating the plaque-forming toxic protein, beta amyloid. As a result, Alzheimer’s can be staved off or averted.

But when the gene is mutated, the brain’s white blood cells are hobbled, making them less effective in their attack on beta amyloid.

People with the mutated gene have a threefold to fivefold increase in the likelihood of developing Alzheimer’s disease in old age.

The intact gene, says John Hardy of University College London, “is a safety net.” And those with the mutation, he adds, “are living life without a safety net.” Dr. Hardy is lead author of one of the papers.

The discovery also suggests that a new type of drug could be developed to enhance the gene’s activity, perhaps allowing the brain’s white blood cells to do their work.

“The field is in desperate need of new therapeutic agents,” said Alison Goate, an Alzheimer’s researcher at Washington University in St. Louis who contributed data to Dr. Hardy’s study. “This will give us an alternative approach.”

The fact that two research groups converged on the same gene gives experts confidence in the findings. Both studies were published online Wednesday in The New England Journal of Medicine. “Together they make a good case that this really is an Alzheimer’s gene,” said Gerard Schellenberg, an Alzheimer’s researcher at the University of Pennsylvania who was not involved with the work.

The other gene found to raise the odds that a person will get Alzheimer’s, ApoE4, is much more common and confers about the same risk as the mutated version of TREM2. But it is still not clear why ApoE4, discovered in 1993, makes Alzheimer’s more likely.

Because the mutations in the newly discovered gene are rare, occurring in no more than 2 percent of Alzheimer’s patients, it makes no sense to start screening people for them, Dr. Thies said. Instead, the discovery provides new clues to the workings of Alzheimer’s disease.

To find the gene, a research group led by Dr. Kari Stefansson of deCODE Genetics of Iceland started with a simple question.

“We asked, ‘Can we find anything in the genome that separates those who are admitted to nursing homes before the age of 75 and those who are still living at home at 85?’ ” he said.

Scientists searched the genomes of 2,261 Icelanders and zeroed in on TREM2. Mutations in that gene were more common among people with Alzheimer’s, as well as those who did not have an Alzheimer’s diagnosis but who had memory problems and might be on their way to developing Alzheimer’s.

The researchers confirmed their results by looking for the gene in people with and without Alzheimer’s in populations studied at Emory University, as well as in Norway, the Netherlands and Germany.

The TREM2 connection surprised Dr. Stefansson. Although researchers have long noticed that the brain is inflamed in Alzheimer’s patients, he had dismissed inflammation as a major factor in the disease.

“I was of the opinion that the immune system would play a fairly small role, if any, in Alzheimer’s disease,” Dr. Stefansson said. “This discovery cured me of that bias.”

Meanwhile, Dr. Hardy and Rita Guerreiro at University College London, along with Andrew Singleton at the National Institute on Aging, were intrigued by a strange, rare disease. Only a few patients had been identified, but their symptoms were striking. They had crumbling bones and an unusual dementia, sclerosing leukoencephalopathy.

“It’s a weird disease,” Dr. Hardy said.

He saw one patient in her 30s whose brain disease manifested in sexually inappropriate behavior. Also, her bones kept breaking. The disease was caused by mutations that disabled both the copy of TREM2 that she had inherited from her mother and the one from her father.

Eventually the researchers searched for people who had a mutation in just one copy of TREM2. To their surprise, it turned out that these people were likely to have Alzheimer’s disease.

They then asked researchers around the world who had genetic data from people with and without Alzheimer’s to look for TREM2 mutations.

“Sure enough, they had good evidence,” Dr. Hardy said. The mutations occurred in one-half of 1 percent of the general population but in 1 to 2 percent of patients with Alzheimer’s disease.

“That is a big effect,” Dr. Hardy said.

Read More..