These new 91探花online courses, under the name UWashingtonX, will be free and open to the public. The courses will be in addition to the such courses already available on , where the 91探花was an early innovator with both free and for-credit classes, announced in July 2012.

The 91探花plans to start with four new courses for edX, ready in January 2014. Courses under consideration will build on the university鈥檚 online teaching expertise since the 1990s that includes: more than a dozen Massive Open Online Courses launched in 2012-13, plus 15 , , 40 , 58 online undergraduate courses, and 14 other made available during the last decade.

In addition to Harvard and MIT, edX elite partners also include such universities as California, Berkeley; Georgetown; Toronto; Cornell; Boston and Texas, plus leading institutions in Asia, Europe and Australia. Each partner shares a commitment to transforming educational quality, efficiency and scale through technology and research for the benefit of campus-based students and the worldwide community of online and blended learners.

鈥淭he 91探花 remains committed to learning more about the impacts, reach, challenges and benefits of MOOCs,鈥� said 91探花President Michael K. Young. 鈥淎s a large, public research institution with a mission to increase access to education, we鈥檒l continue to explore the forefront of educational delivery, evaluate teaching and learning effectiveness, consider trends, and drive research to improve higher education. MOOCs are part of this, and joining with edX adds to our portfolio of high-quality, free offerings for the public.鈥�

Among institutions offering new Massive Open Online Courses the last year, the 91探花was the first university to provide a way for those online students to obtain credit. Many 91探花Coursera students are provided an option to convert from the free online courses to an enhanced, small cohort, instructor-led, 91探花online for-credit class that requires additional homework, assignments, evaluations, and a fee.

鈥淭he research focus and Harvard/MIT roots of edX will allow us to further our knowledge of MOOCs and their efficacy,鈥� said David P. Szatmary, vice provost of 91探花Educational Outreach. 鈥淎s a leader in online education, we want to help shape this important innovation and define what鈥檚 possible.鈥�

Currently, the 91探花offers 14 Massive Open Online Courses on Coursera. Some are new courses, launching soon. Enrollments for representative 91探花courses on Coursera are listed below. Numbers reflect the top instance for each individual course to date, since some courses are repeated multiple times throughout the year:

• Introduction to Computational Finance and Financial Econometrics: 30,578
• Information and Risk Management: 25,077
• *Introduction to Public Speaking: 15,929 (*growing daily; course starts June 24, 2013)
• Computational Methods for Data Analysis: 15,179
• High Performing Scientific Computing: 14,977
• Scientific Computing: 13,374
• Building an Information Risk Management Toolkit: 10,533
• Designing and Executing Information Security Strategies: 9,206

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91探花is planning courses that will be made available in multiple ways, tailoring innovative options to match consumer needs. Free, non-credit versions will use the Coursera platform, providing access to high-quality education for anyone.聽 In addition, enhanced, instructor-led versions will result in 91探花credit and/or certificate credentials when successfully completed.

“Increasing access to meet a variety of educational needs is vital to building an informed community and has been a key part of the 91探花鈥檚 mission for 150 years,” said Provost Ana Mari Cauce. “We鈥檙e pleased to align with Coursera’s online learning platform and join other institutions in using technology to reach a variety of learners in innovative ways.”

Initial 91探花offerings on Coursera are currently under development for the 聽2012-13 academic year. They will include several free classes with an option for enhanced, instructor-led versions for a fee that lead to 91探花credit and/or a certificate. Pricing for the credit offerings is under review and will be comparable to current 91探花credit courses and certificate programs.

Offerings ready for launch this year include:

• An applied mathematics program in scientific computing.
• Computer science courses, including several in programming.
• A linked sequence in computational finance.
• A three-course certificate in information security and risk management.

Each of these online programs focuses on student and employer demand using transferable resources, including video that 91探花has available and can be developed for use on Coursera鈥檚 platform. More courses are expected to launch once initial offerings have been developed. In each case, the course will increase access to world-class 91探花educational resources for a large population of online learners around the globe. Expanding access to the expertise of the university has been the mission of 91探花Educational Outreach since 1912.

“Going forward, we anticipate using Coursera’s platform as a gateway to offer more 91探花 courses that are free to the general public, with enhanced versions of our Coursera classes that will be overseen by an instructor and allow students to earn a 91探花credential with additional work,” said David Szatmary, vice provost of 91探花Educational Outreach. “All 91探花classes on Coursera and the 91探花credentialed options will be approved and taught by world-class departments at the 91探花. We are very pleased to be part of this new movement that provides ever greater access to the best classes in the world.”

A recent study in mice shows the ability of the fetal heart to grow healthy cells to compensate for cardiac tissue lost to disease. The mice are normal at birth and their hearts function well during their youth. However, these gains can be short-lived. About 40 percent had signs of heart disease in early adulthood, and 10 percent died of heart failure.

Results published in the Oct. 14 edition of Development Cell describe the capacity of a mouse heart to repair extensive damage while in the womb, even after all the heart’s major cell types and structures have developed. The finding that so many of these mice grew up to have heart disease suggests that some human heart diseases in adults may have originated from damage in the womb. An international group of scientists from Australia, Germany, and the United States conducted the study.

Most organs in developing embryos and fetuses have moderate leeway in changing their growth in response to external and internal influences. However, except for the liver, extensive regeneration of diseased or damaged tissue has not been observed before in mammals. This phenomenon was previously thought to occur only in fish and in amphibians, like frogs and newts.

Timothy Cox, 91探花  research associate professor in pediatrics and the study’s senior author, said, “What’s noteworthy about this study is that it suggests that a diseased or damaged heart in a developing embryo can largely repair itself. The mice were born with normal cardiac function that persisted, according to our monitoring, during the first months of life.”

Nevertheless, he added, despite the fetal heart self-repairing and the newborn mice appearing healthy, their hearts started to give out as they entered adulthood.

In addition to his work on congenital disorders at the UW, Cox is a member of the Center for Tissue & Cell Sciences at Seattle Children’s Research Institute and a researcher at the 91探花Center for Human Development & Disability. He moved to Seattle recently from Australia, where he was a researcher in anatomy and developmental biology at Monash University and in biomedical and molecular science at the University of Adelaide.

In their study, the researchers bred mice that had a sex-linked genetic defect that caused a disorder in the mitochondria, or tiny powerhouses, inside their heart cells. Mitochondrial disorders are one of the leading causes of fatal heart disease early in life, and they may possibly contribute to failure of aging hearts as well. The researchers found that most of the male mice with this genetic defect on their single X chromosome, and the female mice with the defect on both their X chromosomes, died midway through gestation.

The researchers assumed that the female mice with the defect on only one X chromosome would have the genetic deficiency in about 50 percent of their heart cells. Females generally have only one of their two X chromosomes activated in each cell. The de-activation of one or the other X chromosome is random. To the researchers’ surprise, none of the females carrying both the normal and the defective X chromosome died before birth. Analysis of cardiac tissue from newborn and two-month old female mice showed few cellular changes and no major pathology. Measurements of specific protein marker and of cellular respiration were normal.

At about the middle of gestation, female embryos with one defective X chromosome had an abundance of heart cells with enlarged and disorganized mitochondria, but also many cells containing normal mitochondria. By the time females of this genetic type were born, their hearts appeared to be remarkably normal.

Additional analysis suggested that this normalcy was likely due to such a proliferation of healthy cells that the proportion of defective cells became smaller and smaller, yet remained resident amongst the predominantly healthy cells. The proportion and the location of these residual defective cells, the authors surmised, might have contributed to heart problems later in life. The heart’s conduction system, which helps control the heartbeat, might have become more severely affected than it appeared at birth.

Future research in the area of fetal heart self-repair, Cox said, will probably be geared toward identifying the signals that turn on the regenerative response in healthy heart cells. If these signals could be identified, Cox said, switching them on again might help repair adult heart tissue. Scientists are also interested in when or if the heart loses the capacity to repair itself, and what governs the timing and the mechanisms of this loss.

Researchers also are hoping, he added, to understand why some of the apparently healthy baby mice in this study ended up showing signs of heart disease in young adulthood or dying early from heart failure. This information might someday help pinpoint which children are at risk for heart disease as the enter adulthood.

In addition to Cox, other researchers on the fetal mouse heart regeneration study were Jorg-Deltef Drenckhahn, Max-Delbruck Center for Molecular Medicine in Berlin, Germany; Quenten P. Schwarz, Department of Molecular Biosciences at University of Adelaide, Australia; Stephen Gray, Monash University, Clayton, Australia; Adrienne Laskowski and David R. Thorburn, both of the Murdoch Children’s Research Institute, Melbourne, Australia; Helen Kiriazis, Ziqiu Ming, and Xiao-Jun Du, all of the Baker Heart Research Institute in Melbourne; and Richard Harvey, Victor Chang Cardiac Research Institute, Sydney, Australia.

Research funding was from the Australian National Health and Medical Research Council, German Research Council, and Muscular Dystrophy Association.

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