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Cognitive neuroscientists are the Cassandras of education.
Recall that in Greek mythology, Cassandra was blessed with the gift of prophecy by the god Apollo. But when she refused to sleep with him, Apollo didn't rescind the gift, he added a curse: poor Cassandra could still see the future, but she was doomed never to be believed. Mark Seidenberg probably envies Cassandra. He writes like someone who wonders exactly whom he has to sleep with to get people to pay attention to him.
Seidenberg is a University of Wisconsin cognitive neuroscientist who has been studying reading "since the disco era." His indispensable new book, Language at the Speed of Sight, lays out in clear, readable English much of what we have learned over the past several decades about reading; he labors to "cheerfully destroy a few myths" about how we process and make sense of the printed word, but Seidenberg is no happy warrior. He wants his readers to share his fury at the "profound disconnection between the science of reading and educational practice" that he deftly unpacks.
The first two-thirds of the book covers the current state of reading science, starting with a brief history of human language development and...
Every day I learn about another charter school that has found a way to help low-income, often minority, students graduate from high school and get accepted into college at an unbelievably high rate.
For the community that I work with, Latinos, this is fantastic news. Statistics from the Pew Research Center show that the high school dropout rate for Latinos is higher than all other groups: 12 percent. Additionally, 66 percent of Latino high school graduates polled told the National Journal that they intended to enter the workforce or join the military directly after high school.
Sure, not every kid has to go to college, but the benefits of a college degree are well known, so I wholeheartedly cheer on the work of these charters. The reality is that the kids in the neighborhoods these schools serve haven't been avoiding college to follow some other fruitful path—they're falling into a seemingly inescapable cycle of poverty. When charter schools break that cycle, they change the trajectory of entire families.
But, in a dubious new trend, critics of charters—and even some supporters—are focusing on their graduates' college drop out rate. Not long ago, an article in USA Today...
There's a lot that's appealing about personalized learning, properly construed. Rather than march a classroom of students through academic material at the exact same pace, regardless of their discordant levels of readiness or their varying degrees of background knowledge, personalized settings allow schools to target instruction to the exact needs of individual children. It's not meant to be a euphemism for "computer-based instruction," but a version of differentiation that uses a variety of approaches, from tutoring to peer discussions to teacher-led lessons and, yes, some digital resources. Done right, it doesn't give up on academic standards, either. Instruction may be personalized but all students are still expected to master all the knowledge and skills that will prepare them for the next step in their learning and for eventual success beyond school.
Hooray for all that. But after seeing a version of personalized learning in action recently, I'm worried that it may be reinforcing some of the worst aspects of standards-based, data-driven instruction. Namely: It might be encouraging a reductionist type of education that breaks learning into little bits and scraps and bytes of disparate skills, disconnected from an inspiring, coherent whole.
Personalized learning enthusiasts might look to the food industry...
The release of this latest report from Bellwether Education Partners is fortuitously timed as school districts large and small reach the end of another school year beset by transportation problems. Authors Phillip Burgoyne-Allen and Jennifer O'Neal Schiess dissect those challenges and argue convincingly that the difficulties in providing effective and efficient service are the result of archaic structures, bureaucratic inertia, and siloed responsibilities. It is less a question of money, as some would argue, than a lack of wherewithal to change how that money is spent.
The authors begin by describing the main models of student transportation: district-operated, contractor-operated, public transit, and various combinations of the three. While all of these models are decades old, the district-centered model still predominates: school systems own and operate two-thirds of all school buses on the road today. Various state funding models are also described. Some are aimed at maintaining the district-operated status quo, others are more student and family-centric and agnostic on form, and still others incentivize contracting out transportation or seeking economies of scale with parallel public transit systems.
Rural and suburban districts face challenges of distance and inefficient routes. Urban districts face myriad challenges posed by...
The Fordham Institute recently released Three Signs that a Proposed Charter School is at Risk of Failing, a study of over six hundred charter applications that aims to identify risk factors that make a potential charter school more likely to perform poorly during its early years. As the leader of Fordham's authorizing team in Ohio, I was eager to read the report to see whether it aligns with what we see when reviewing applications and, subsequently, authorizing brand new schools.
Indeed, one or more of the report's top three identified "flags"—in our experience—are usually present in weak charter applications:
These "flags" make sense. Self-managed schools—those not supported by a larger network—typically lack access to deep and consistent talent pipelines, and often have a harder time finding and retaining high quality school leaders. Misalignment of programming is another problem. If an application proposes to serve...
It's time for charter school advocates who've doubled down against private school choice to "see the light." We need to put aside old grudges and commit ourselves to cooperation.
As a new administration works to make education savings accounts and vouchers palatable to Washington, reform advocates should remember that when any type of educational option is strengthened, all options benefit. Families benefit. After all, freedom isn't easily taken away once people experience it. So let's open the floodgates and not argue about whether charters are better than private schools.
The charter/private school divide isn't new. I remember my first tour of a charter school as the executive director of an organization with "school choice" in its name. The principal greeted me warmly, but was quick to point out, "We're a public charter school. School choice isn't our thing." She would be the first of many to highlight this seemingly metaphysical difference.
What many in the charter camp wish to assert is that there are "good" choices and "bad" choices. And this isn't a statement about school quality. It's a position that private school choice in the form of vouchers and other funding mechanisms should not exist. It's something like a...
Far too few students have access to the kind of high-quality, career-focused high school education that'll put them on a path to postsecondary credentials connected to high-demand, high-wage jobs. Charter schools, however, may hold the most promise for quickly scaling up these models.
While well intentioned, pushing all students toward four-year college immediately after high school may do more harm than good. Despite rising enrollment rates over the past three decades, less than 40 percent of students who enroll in a four-year college graduate after four years. Graduation rates for minority students are shockingly low: 21 percent for black students and 30 percent for Hispanic students. Those students who do graduate typically enter the workforce carrying significant debt: among the class of 2015, more than two-thirds had student loan debt, and this debt averaged around $30,000.
These statistics underscore the need for robust career preparation and work-based learning in high school that puts students on a path to success in adulthood. The evidence suggests that high-quality, career-focused education in high school can boost graduation rates, increase future employment and earnings, and lead to higher enrollment in postsecondary education and training. Career pathway approaches hold promise for sustaining...
Students of history know that governments rarely give up power without a fight. To paraphrase Edmund Burke, those who have been intoxicated with power never willingly abandon it. Yet, last year, the federal government passed a new education law which returns a significant amount of power and decision-making authority to states, districts, and schools.
The bi-partisan passage of the Every Student Succeeds Act creates a unique and exciting opportunity for improving American education. The law explicitly bars the Department of Education from dictating or influencing standards or curricula at the federal level, and states and districts have a wide range of new liberties when it comes to developing accountability systems, testing, and content.
But with this newfound freedom from Washington comes a newfound responsibility for excellence at the state and district level. We cannot confuse local control with laissez faire. State and local leaders must embrace this opportunity and lift expectations, not relax them.
This is a large task and will require some heavy lifting, though. For years, states have been in compliance mode—overly focused on meeting detailed federal criteria—and that mindset has lulled some states into complacency. But that is the case no longer. Authority over American education has...
When I moved from California to Texas at age four, I was reading full books and writing at a first-grade level. After being iced out of one upscale community that wasn't keen on having a single black mother as a neighbor, my mom moved us into a different district, specifically for its public schools. But when she went to enroll me in kindergarten, she was told that under no circumstances would I be allowed to enter kindergarten as a four-year-old, no matter what grade level I tested into.
School staff recommended I attend preschool for a year to wait it out. My mom did not accept that recommendation. Instead, she sent me to a nearby private school where I was welcomed into kindergarten with open arms. I excelled, and instead of falling behind a year, I stayed in private school through fourth grade. Then I transferred to public school, where I took part in programs for gifted students. When I graduated from high school at seventeen and went on to the Ivy League, it looked like the public education system had served me well, but the real reason I made it was the commitment of my mother.
Earlier this year,...
A new report examines whether the effect of a teacher's value added persists over one to two years and across subject areas. In particular, it asks if the impact of an English language arts teacher has any bearing on a student's math achievement. Prior research has provided some evidence that ELA instructional effects may be generalizable across subjects, given the applicability and transferability of reading and language skills.
Using data from the New York City and Miami-Dade school districts, Benjamin Master and colleagues use student records in grades four through eight, where current and prior year achievement data are available for students. They investigate the persistence of teachers' value added effects on student achievement in the first and second year after they teach a student, distinguishing between short-term, test-specific knowledge and longer-term, generic knowledge that accumulates. The methods are complex: They attempt to isolate teacher-specific value added that persists both in the same subject and into another subject (either ELA or math), and to isolate this from teacher spillover effects that stem from same-year instructional collaboration with peers—while also estimating how much typical "decay" one might expect of student's prior long-term knowledge—and also controlling for various student, school, and classroom...


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MSPPM Alumna Named One of New Jersey's Top 50 Real Estate Professionals
Jan 10, 2013
The third annual list of New Jersey's top 50 most powerful and influential leaders in the real estate industry has been released, and Carnegie Mellon University's H. John Heinz III College was represented by 2001 Master of Science in Public Policy Management alumna Monique King-Viehland.
The NJBIZ 50 list not only represents the big deals that transpired in New Jersey real estate; it also notes the leaders who are pushing development policy behind the scenes. King-Viehland is currently the president of Campus Gateway Development Inc., a New Jersey Institute of Technology (NJIT) subsidiary that's working to redevelop the area around the campus and transform it into a community populated by housing and retail projects.
"Truthfully, I was stunned when I saw my name," said King-Viehland. "I have been reviewing the list since they started it three years ago, and I never thought I would see my name on it."
"And to be one of four women and the only African American," she said. "I was honored."
King-Viehland said she leveraged her Heinz College education to immediately begin adding value to her organization.
"I could absorb information quickly, which allowed me to hit the ground running, and I had a battery of tools -- both quantitative and qualitative -- at my disposal to attack problems," said King-Viehland. "Heinz gave me a strong foundation on which I have built my career."
"I have been doing this type of work for more than a decade, not for the glory, but to make a real difference in people's lives."
Interested in supporting Heinz College students and initiatives like those featured in this story? Click here for more information.

subset: commoncrawl


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A couple of former prime ministers have had bold declarations come back to haunt them. Bob Hawke's line about no child living in poverty and Julia Gillard's insistence about no carbon tax will continue to haunt them.
And right now a feted football coach probably knows how they feel. The following is what Mick Malthouse told Carlton supporters less than 14 months ago in a program for the Blues' second intra-club practice match under his command:
"'I want a healthy side, a good game plan and an attitude of 'we are hungry enough'. Take those ingredients, along with the stars and planets aligning, and we may very well have the makings of a premiership side."
Yep, that's the Blues he's talking about. The same side which now sits 15th 0-3 and on Sunday night at the MCG was humiliated to the tune of 81 points against a bitter rival, looking barely competitive from the first moments.
To put it in context, that's Carlton's worst losing margin for nearly seven years. It's been 142 games since the Blues were beaten by more – round 21 2007 against North Melbourne – to be precise, just weeks after they'd dispensed with their last so-called coaching saviour Denis Pagan.
This latest search for a coaching messiah hasn't yet reached the depths the Blues did in the early to mid-2000s, but it sure isn't going to plan. So much so that even a coach as confident in his methods as Malthouse continues to be taken aback by how things are working out.
Certainly, the extent to which he has changed his tune since those comments about potential flags has been remarkable.
Malthouse recently met the Carlton board and reportedly told them the list wasn't nearly good enough, that a top-four team needed eight A-grade players, but the Blues had five (not including Chris Judd, who he felt was too near the end to factor into a discussion about the longer-term future) and few B-graders capable of making the jump to the next bracket.
To be brutally frank, can Carlton even claim to have five A-graders right now? Skipper Marc Murphy at his best, sure; but then who? Even Lachie Henderson, as valuable as he's been at either end of the ground, hasn't yet earned an All-Australian nomination.
The gameplan is a big issue. It's stodgy, the Blues having seemingly forsaken much of their flair for what was supposed to be more dependability. Change it? Well, Malthouse says he already has. Midway through last season, in fact.
After another big win in round 10 of 2013 against GWS, Carlton's sixth from seven games, Malthouse said: "We've started to cut off bits and pieces that I had, and cut off bits and pieces that I perhaps didn't like ... and what's happened is that we've got a game structure that [now] meets the criteria. And as long as we don't stray from it now we can be a good football side."
It goes without saying if the Blues have strayed from it, the message isn't getting through.
But if they haven't? Well, since that moment, Carlton has won just six of 17 games, a strike rate of 35 per cent.
We continue to ask: has Carlton improved under Malthouse? And few now could realistically argue that the answer is yes. Certainly not in the most tangible ways.
Under Brett Ratten in 2012, Carlton scored an average 94.5 points a game. Under Malthouse last year, that went up by just two points, and after three games this season the average is 76.6. But was defence supposed to be the biggest improvement? The figures there are even starker.
In 2012 under Ratten, the Blues conceded 87.5 points a game. Last year, that crept up to 90.5 a game. And right now, after Sunday night's belting, they're conceding 118.7, the second-worst defensive record in the competition.
Carlton's free kick into last year's finals then its stunning elimination final win over Richmond has proved a potentially damaging mirage. This list patently isn't good enough.
But if Malthouse is now committed to rebuilding, why haven't the younger players on the list been played more?
Dylan Buckley, Troy Menzel, Nick Graham have all shown plenty of ability. Buckley is now in his third season with the Blues, and the other two their second. But all up the trio has played just 15 games.
You can't continue to talk about talent coming through without being prepared to actually have it out on the park and see what difference it makes. Carlton has been doing that for some time now, even before Malthouse's arrival. And that's another area in which little seems to have changed since.
Mixed messages have been the recurring theme over the past 18 months: in recruiting, at selection, and in the brand of football the Blues have been playing. Does Carlton itself even know just where it is at?
Sunday night's belting may have helped provide an answer. But it leads to an even more problematic question. Is the coach Carlton picked to take it the next step up the ladder still the same man it wants to oversee another climb from closer to the bottom? Because that, clearly, isn't the job Malthouse was hired to do.


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$4000 3-D Money Shoot at Limerick Bowmen.
Limerick Bowmen: Third Annual 2-Person 3-D Team Money Shoot.
It's that time again! Mark you calendars and get registered. We will be holding this years Money Shoot on Saturday, April 16th rain or shine. We will again host two classes: Hunter and Unlimited. Each classification will be shooting at 20 separate targets on two separate courses. With a full complement of teams, the payout this year will be $4,000. Early registration is required. First come first serve! A registration form with further detailed information will shortly be available for download at our website on limerickbowmen.com. Keep in mind that space in this shoot is limited to 40 teams per classification so get your registration in A.S.A.P. If you need more personalized information contact me by e-mail at firstname.lastname@example.com or Gary Gerhart at 610-636-0095. Hope to see you there!
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I'm 26 and have RA, how do i explain to my BF family i cant do things without being told i'm lazy
This question has not been answered by one of our experts yet.
Hi Jessica,
I am 49 and have had RA for 20 years. I had to give up work 12 months ago I am due for knee and wrist surgery in the next few months. If you don't feel able to do something don't, everyone has different experiences with RA - Your BF should tell his family and if anyone accused me of being lazy - God help them. If your BF does not understand the pain you can be in, then bring him with you for your next checkup. Every single person I know with RA has had different experiences with medication, doctors etc., so no two people's disease progresses at the same rate. So at 26 it can be as advanced as someone elses at 66 so listen to your body and if you don't want to do something don't
I wish you the very best of luck in managing your disease.
MaryREAD MORE
Tell your family that you have a chronic autoimmune disease that leads to significant discomfort and disability. Although rheumatoid arthritis most often affects the joints, it is a disease of the entire body. It can affect many organs and body systems besides the joints. This is what is meant by systematic disease. Let them know that:
* Many people with rheumatoid arthritis have difficulty carrying out normal activities of daily living, such as standing, walking, dressing, washing, using the toilet, preparing food, and carrying out household chores.
* The symptoms of rheumatoid arthritis interfere with work for many people. As many as half of those with rheumatoid arthritis are no longer able to work 10-20 years after their condition is diagnosed.
* On average, life expectancy is somewhat shorter for people with rheumatoid arthritis than for the general population. This does not mean that everyone with rheumatoid arthritis has a shortened life span. Rheumatoid arthritis itself is not a fatal disease. However, it can be associated with many complications and treatment-related side effects that can contribute to premature death.
Let them know that symptoms of RA, like fatigue, pain, limited mobility can manifest for several years before the disease is diagnosed. If they still think that you are lazy, instead of ill, find a competent psychologist to see to find ways to deal with the lack of support from your family.
Good luck,
Hi Jessica,
I was diagnosed with RA when I was 33 years old an am now 46. You can do everything everyone else done as long as you don't have a flare or have been told not to by a doctor.
There were many many times when I had to use stairs on my behind and had casts on my wrists to contend with but the problem among many with people with Ra is that you appears normal on the outside so what I did was to gather pamplets about the condition and let everyone read them as people know very little about the disease.
Good luck.READ MORE
Jessica, your friends will never understand unless they go through it. I was 26 when I found out I had RA and I am 57 now and I am still working. Before I married my husband he never understood what I was going through until he started having medical problems. When I met him 13 years ago there was times when he thought I was just lazy when I didn't do certain things. He use to say things like,"if you get up and move around you will feel better." He didn't realize there were times when I couldn't get out of the bed. In the last 5 years he has had 2 hip replacements, lung surgery and his ankle was broken in 3 places. Now that he knows what pain is, he has apologized to me about the way he thought. Now both of us has our bad days and all we can do is look at each other and laugh. We love each other so much, that's only 1 of many things that we share together. Be strong and remember you are not alone there are a lot of us out there. One thing that keeps me going is I always tell myself there are many others out there who are worst off than me. Good luck to you and keep the faith.READ MORE
I am 30 and I have been diagonosed with RA since I was around 2 yrs old and have had 3 surgeries on one knee alone. For those of whom stated below you can't be that progressed at 26, please bite your tongue. They didn't officially know that it was RA with me, I was a guinea pig for years and still to this day are they testing me for lupus and more things as well. I have had surgeries, I have a sway in my hands, I limp, and can barely fasten my bra at times! Regardless of your pain, remember bodies in motion, stay in motion. YOU ARE NOT LAZY! but be honest with everyone. If you are having a flare up, let them know that unfortunately you can't but that you would love to when you are feeling better. Remember although it's a disease, you are alive! Live your life! I have accomplished plenty of activities throughout my life, but don't let it consume you. Gather up information about RA, ask your doctor questions, bring your boyfriend to your appointments, but don't fall into being "lazy" because you just don't feel great that day. Sometimes getting up and going for a walk will make you feel a lot better than curling up on the couch! And remember, having RA you need to excercise to help your body! Good luck!READ MORE
Your arthritis cannot be that much progressed at 26 - I've had it since I was 28 and I'm 69 in 3 weeks and still working part-time (typing all my life). I've had surgery on both hands for Carpal tunnel syndrome, and Osteoarthritis in my hands as well as RA all throughout my other joints! One HAS to keep moving and do what they can - I live alone and am the mother of 4 adult children and 1 grandchild. I know what you get as I've gotten "By now, everyone on the planet must know," but they still don't understand until probably I am long gone and they now have RA/OA themselves. That's when I too realized what my parents went through and without much treatment except for an odd aspirin or topical cream rub like Ben Gay or Icy Hot, which I would send from America!! However, before I go I have to be honest and tell you that finally, I gave my notice for end of year as I don't want to be a burden rather than a help, and whilst I always worked hard and fast some here admit that I "gave them everything, including my hands, eyes and heart." So keep going as long as you can, maybe there'll be a breakthrough for you still - you're young and there's always hope!
Rita Hynes at MGH or email@example.com MORE
Thank you for your comment. I'm 58 and trying my best to work. This morning it was all I could do to get out of bed and walk even to the bathroom, kitchen etc. Then to have to climb stairs at work is even more painful. My husband says, "Go on in to work
and try to get in to see the doctor. I know he doesn't understand how much pain I'm in most of the time. I know I have to keep going or I will really get stoved up. I work,
am active in my chruch and sing in a Sweet Adelines Chorus. The one thing that helps
is that I have a wonderful support group through my church and the many prayer
warriors I have praying for me helps so much.
Phyllis MREAD MORE
I was diagnosed at 23 years old with RA. I don't know what medications you have tried, but my doctor put me on Humira and methotrexate. I would also take celebrex for pain as needed, along with folic acid and vitamin D. After two years I felt completely cured so I stopped taking my medicine. Now, at 26, my symptoms have returned but are even worse now. So, if I were you I would definetly explore medications, they are life savers, but stay on them because when you get off the symptoms do return and you can cause more damage. And like the others have said, when you feel tired, rest. You know your body and your limitations. But stay as active as you can because keeping your joints active and building muscle can help you live a healthy life much longer. Good luck!READ MORE
Do not pay any attention to anyone that says your arthritis cannot be that progressed at 26, that is by far one of the stupidest statements that I have ever heard or read. Rheumatoid Arthritis does not decide what age you are as to how bad it will affect you. Tell your boyfriend's family that you have RA and that you do not have it under control yet. Print out information on RA so they will understand it and if they do not understand or try to understand what you are going through then just stay away from them so they do not bring you down. You feel bad enough when you are in pain and suffering from the fatigue that RA causes to let anyone make you feel worse.
Too many people watch the commercials for RA medication on TV and believe that all you have to do is take whatever is being advertised and you are 100% recovered. You do not respond to medication as fast as the commercials imply and not everyone can take the medications that are advertised on TV or want to them because of the side effects. Good luck with getting your RA under control and do not let any make you feel quilty or embarrassed about your condition.READ MORE
Hi Jessica: First, I want to say in response to Margaret's comment about 'you cannot be that progressed at 26' - please ignore that. I am 38 years old and have been fighting this disease for years in which time I have had weeks to which I cannot walk, open jars, brush my teeth, walk stairs, go to work, cook or even open my jaw wide enough to eat. Everyone's experience is different and you can absolutely be very progressed in this disease at any age. Secondly, I too have had experience with comments of being lazy. I hold a full time job and many nights when I come home I simply need to rest my body when I should probably be doing housework or making dinner. However, I don't feel guilty on those evenings and I certainly won't put up with anyone insinuating that I'm lazy. Take it one day at a time and listen to your body. It's hard to make people who don't experience this pain understand what it feels like, so sometimes you just have to stop trying and just worry about yourself and not so much of what others are thinking.READ MORE
Hi jessica!
I was diagnosed with severe RA in january of 08, I am 31. I was told that if I did not do anything about it...to help myself. Then I would be crippled by the end of the year. My body feels like I've been in a 'flare" since I was diagnosed. After 6mo. I finally found a combination that takes the edge off. Yet I still cant do MANY things I could before. My family is very understanding...I'm lucky for that. But I too get funny looks and dumb comments about not looking like i'm "sick." I am a bit of a smart alec..I reply with some quick replies (but not mean) just to make them realize that, their comments are not needed. ((My huny and I were getting out of the car one day (I have a handicap sticker, for the bad days) A woman that is aquianted with my huny made the comment.."You dont look handicaped!"..So I smiled at her and said.."I wish i wasn't!" and walked on by. She stood quietly and her husband told her to "behave".)) In the simplicity of it all, I dint explain anything to her but I made her realize that she should think before she makes rude comments.
but as for family members i usually try to give them examples of how i feel that may relate to something they've done. Such as I told my cousin..."you know when you work out really really hard and every muscle is completely sore the next couple days....thats how i usually feel everyday." It helps to find something they can relate to. i did try handing out information but they never read it...lol. But one thing my family did was a lot of research on my situation...we have a lot of health professionals in our family so their a lil more understanding of my situation. I hope I helped you in some way.READ MORE
Hi Jessica
I've read all these posts and agree with most. So saying that, there is only one person you need on your side and that is your boy friend. He will be the one to see
you at your worst and at your best.
I know this because it was my mother who could'nt or would'nt understand. Her ansewer was you have irish blood in your veins. so buck-up and ignor your pain. So I stoped
taking my meds.for a few years.But as eveyone knows bad idea. Finely I had gone to my family doctor I couldn't take it any more. I wanted to put a gun to my head, so he put me pain meds sent me to a speicalist. That was 5yrs ago. Mother still didn't know until a few days before my fathers death.I had to fly to fla. And when I tried to get out of the taxi and I needed help. She finely started to ask questions about RA. this was sept 2008. oct 2008 I had knee surgery and the damage is from the RA. So tell them what you have and if they don't care. Tell them to piss off and live your lives.Because you only have one life live. and no regrets.
Hi Jessica! I know exactly what you're going thru. I'm 21 and I have severe rheumatoid arthritis. My hands are severely deformed-Fact is, RA progresses differently for everyone. I was a guinea pig for years for my doctors. I've had RA since I was 16 and my doctor kept telling me to take ibuprofen, meanwhile my hand pain got worse and my hair kept falling out. I'm afraid of dating because I don't know how to explain to a man what RA is. :-P Dating is already stressful enough, try having deformed hands that you can't hide...It's best to be honest and upfront with people about having RA. Let them know your limitations and leave it at that. I know what its like to be told your lazy though. Try being 16 years old in excruciating pain and everyone around you telling you you're faking it and just don't want to work or go to high school. It's hard. You'll become much more confident in who you are in time because of RA though. :-) I haveREAD MORE
I would just tell them what you have, and if they don't know about RA explain to them the best you can. Just let them know about your pains etc... Do not be hidding it.I have RA for 7 years now ,sometimes it is hard and not easy to talk about it. But it is important for your moral.READ MOREI would just tell them what you have, and if they don't know about RA explain to them the best you can. Just let them know about your pains etc... Do not be hidding it.I have RA for 7 years now ,sometimes it is hard and not easy to talk about it. But it is important for your moral. READ MORE
Hi there:
Just tell them what you have and that it may limit some things you are unable to do. I just went through the same thing in May with my boyfriend (I am 28 and have had RA for six years), he moved down to the city I'm in to be with me and we had to move what he didn't bring here to his parents house. They understood and didn't mind at all, I felt bad for not being able to help, but in the end, you have to do what is best for you, you have to protect your joints and body.
If you have a job, do the same thing there, as well. I've learned that people are more understanding that I thought they were and it's really helped me when there are things I just can't do. For example, my supersvisor wanted me to help her move some very heavy file cabinets this morning, she knew I couldn't do this, so I stood off to the side while another coworker who was able to move the files did so. I would also say take a stance if someone is pushing you to do something that you know you physically are not able to do, sometimes you have to be assertive.
If you educate people on RA and what it does to the body, they really get a picture of what it is you deal with on a daily basis. I've found with me, I put more pressure on myself thinking that I can do the same things I did prior to becoming "sick"...I've slowly (and still am) realizing that although I am limited in what I can do, there's nothing stopping me from accomplishing the goals that I want in life. RA also makes you creative! In order to better function, you learn to use your resources to open, move, etc. things that you can no longer do as well as you use to. You also get to research all kinds of RA friendly gadgets! There are some neat items out there!READ MOREYou should know Answers to your question are meant to provide general health information but should not replace medical advice you receive from a doctor. No answers should be viewed as a diagnosis or recommended treatment for a condition. Content posted by community members does not necessarily reflect the views of Remedy Health Media, which also reserves the right to remove material deemed inappropriate.DISPLAY TEXTLINK URL
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Above video is set to start at 9 min 46 sec.
Megyn Kelly: Do you think that President Obama is dangerous?
Liz Cheney: Yes … I think there's no question. I think he is unique in terms of a president who is sitting in the Oval Office who has made very clear that his desire is to weaken the nation.
And whether you say it's his intent, whether it's naivety, you can now look at the result of the policy of the past six years.
… There's no question that he's a dangerous president, and that we've got to fight back and we've got to ensure that people understand the importance of American power in securing our freedom and security.
Dick Cheney and his daughter, Liz Cheney, have started a new organisation, Alliance for a Strong America
Report This Post]]>
… of the Institute of Public Affairs refers to "Brat's attack on immigration" and writes:
… what could be more respectful of the tenets of individual liberty than allowing individuals and families to travel across national borders to make a better life for themselves?
I haven't seen anything from David Brat that opposes this.
What David Brat states on his campaign website is:
When addressing the issue of immigration, we must start by securing our border. An open border is both a national security threat and an economic threat that our country cannot ignore. I reject any proposal that grants amnesty and undermines the fundamental rule of law.
… I support proposals that will secure our border, enforce our current laws, and restore an orderly and fair process to allow law abiding individuals to work towards becoming citizens of this great nation.
Repeat: "… to allow law abiding individuals to work towards becoming citizens …"
… in his article on David Brat's defeat of Eric Cantor explains the importance of "law abiding":
A key issue in this campaign was amnesty for illegal immigrants.
… Immigration laws are the only laws that are discussed almost entirely in terms of what can be done to help those who have broken the law. Some want to help a little and some want to help a lot. But amnesty lite is still amnesty.
… Amnesty is not some esoteric concept. It means that you are not going to be punished for breaking the law — and that simply brings laws into contempt. Denying citizenship is not a punishment because crossing the border illegally does not entitle you to citizenship. Providing a legal status short of citizenship is not punishment either.
… If you are serious about controlling the borders, then you pass laws to control the borders first.
Some years later, after you can see whether the border has been controlled or not — you can start discussing what our national immigration laws should be.
Chris Berg says it's time for …
… politicians who proclaim the virtues of liberty to discover its connection with the free movement of people
I support the "free movement of people" and the "virtues of liberty".
That's why I think it's great that:
Over a million people a year are granted permanent residence (green card) status in the USA (link to PDF)
Between 600,000 and 750,000 people are granted citizenship each year in the USA (link to PDF)
Between 5,000,000 and 9,000,000 non-immigrant visas are granted each year in the USA (link to PDF)
That's a lot of people following the law, isn't it?
That's a lot of people who have made the effort, paid the fees, passed the tests — in order to be in the USA.
The USA has a lot of legal immigrants and visitors. To me, this represents a lot of "free movement of people".
And demonstrates that America is quite "respectful of the tenets of individual liberty … allowing individuals and families to travel across national borders to make a better life for themselves".
And it's nice to meet people who get visas or green cards or citizenship by means of respecting the laws of a country which is so much in favour of the "free movement of people".
I haven't heard David Brat complain about any of the above, wonderful people. Have you?
If he was "anti-immigration" you'd think he'd be quite annoyed about all or most or some of those millions of people, wouldn't you?
But he doesn't seem to be bothered.
I have been unable to confirm Chris Berg's claim about David Brat "attacking" immigration.
Get acquainted with David Brat ….
Mark Levin talks about Brat, Conservative principles, and unleashing the American economy …
Report This Post]]>
David Woods ponders the inexplicable:
How do so many Muslims keep misunderstanding Islam and concluding that it commands them to "fight those who do not believe in Allah" (Qur'an 9:29)?
Why do so many Muslims think that they are supposed to "strive hard against the unbelievers and the hypocrites and be unyielding to them" (Qur'an 9:73)?
Why do so many converts to Islam decide that they must be "severe against disbelievers, and merciful among themselves" (Qur'an 48:29)?
Where are they getting this stuff from?
Haven't Muslim groups like CAIR and ISNA explained to them that Allah always means the opposite of what he says?
PS: Above video of David Woods in drag is from his presentation, "Muhammad, Cross-Dressing, and the London Muslim Patrol".
Report This Post]]>
Theodore Dalrymple writes:
Jihad is a concept perfectly suited to giving psychopaths the idea that their viciousness serves an ideal other than their own gratification.
That doesn't mean all Jihadists are psychopaths, but the Jihad aspect of Islam — and that's no small part of Islam — does provide opportunities for individuals without conscience or moral qualms.
Report This Post]]>
UK writer and activist, Brendan O'Neil, editor of Spiked Online, in The Australian:
IMAGINE if there were a women's rights organisation that said women should stay in the kitchen and leave the world of work to men.
Or a gay rights group that argued homosexuality was sinful. We would think that was weird, right?
Well, it is no more weird than having a human rights commission that has devoted itself not to the expansion of freedom but to the strangling of it, to the straitjacketing of liberty in the name of protecting people from offence and defending public morals.
Australia's Human Rights Commission must be one of the worst cases of Orwellian doublespeak in the modern world.
… this vast bureaucratic outfit that is funded by government to the tune of $25 million a year does far more to thwart freedom than it does to promote it.
… Without the freedom to speak our minds, publish our ideas and hawk our ideologies, everything from the right to vote to artistic rights becomes meaningless, impossible even.
… in the debate about section 18C, in this key ideological clash over whether the state should have the authority to tell individuals what they can think and say, most of the HRC has come down on the side of the state control rather than the individual liberty.
via Abolish the Human Rights Commission, and return us to the Enlightenment's positive values | The Australian.
Report This Post]]>
David French @ NationalReview.com
A successful rescue typically results in the death or capture of enemy soldiers, costs the enemy its valued asset — in this case an American prisoner — and discourages hostage-taking by raising the price for no return.
A ransom, on the other hand, gives the enemy an additional asset (in this case, five valued commanders), leaves his capturing forces intact, and encourages future hostage-taking.
The defeat of ransom is compounded when we give far more than we receive: giving away the Taliban "dream team" for a sergeant who apparently deserted his post.
Good points.
But as for whether or not Bergdahl deserted his post, that needs to be established by an appropriate court. We need to get both sides of the argument. We need to hear Bergdahl's side.
The media statements of his fellow soldiers may be compelling, but it's still not proper proof.
And of course even an alleged deserter deserves to be rescued.
The other thing I'd like to know is: Why did the United States government exchange FIVE hardcore Jihadists for this soldier? Why not fewer?
Doesn't that reduce its future negotiating ability? If it had only traded ONE Jihadist, it would then have four more Jihadists than it does now for use in any future trade — should the need and opportunity arise.
Furthermore, the USA government must now keep tabs on all these Jihadists.
Robert Tracinski @ The Federalist describes the Taliban Dream Team who were swapped for Bergdahl:
These were top officials in the Taliban regime:
a provincial governor,
a deputy defense minister,
a deputy intelligence minister,
a top arms smuggler,
and a top Taliban military commander.
Two of them are wanted by the United Nations for war crimes committed against Afghanistan's Shiites.
Report This Post]]>
Greg Sheridan on the election of Narendra Modi:
Here is a big tip.
Modi will get Indian economic growth back to 8 per cent a year well within his first term.
This will change everything.
… He is a supply-side economic reformer.
He wants to free up the constraints on the supply side of the economy.
As much as Tony Abbott in this country (Australia), Modi wants to be known as the infrastructure prime minister.
via Plug into the Modi moment | The Australian.
Report This Post]]>
Report This Post]]>
Report This Post]]>
Robert Tracinski's friend and colleague, Jack Wakeland says:
Obamacare can't be fixed because it was designed to break.
Obamacare was designed to fail; to fail slowly and incrementally; to fail in a way that would convince people that private, for-profit health insurance companies are the reason why America's catastrophically overpriced and malfunctioning health care system hasn't worked, doesn't work, and will never work.
The architects of the Affordable Care Act wanted to 'prove' that third-party private insurance should be scrapped entirely and replaced with a single-payer system: straight socialism.
The ACA was supposed to fail slowly and painfully over the course of two or three or four presidential election cycles (which is why Obamacare's namesake, Barack Obama, saw to it that it wouldn't be implemented until the second half of his second term).
When the backlash came, it was supposed to come on some other president's—preferably a Republican president's—watch.
But instead of failing on schedule, four or eight or twelve years from now—it has failed instantly, upon contact with reality
…. Obama, Reid, and all of the other architects of the Affordable Care Act have created a problem for themselves that was designed to be insoluble.
In early 2012, Dr Jill Vecchio explained Obamacare, step-by-step, in a series of clear, well-presented, non-partisan video presentations.
Here is the first of her video series:
(Thanks to Barboo for drawing my attention to these.)
Report This Post]]>


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|Message view
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|« Date » · « Thread »
|"Rahul Jain (Created) (JIRA)" <j...@apache.org>
|[jira] [Created] (HADOOP-7822) Hadoop startup script has a race condition : this causes failures in datanodes status and stop commands
|Tue, 15 Nov 2011 00:04:51 GMT
Hadoop startup script has a race condition : this causes failures in datanodes status and stop commands ------------------------------------------------------------------------------------------------------- Key: HADOOP-7822 URL: https://issues.apache.org/jira/browse/HADOOP-7822 Project: Hadoop Common Issue Type: Bug Reporter: Rahul Jain The symptoms are the following: a) start-all.sh is able to start both hadoop dfs and map-reduce processes, assuming same grid nodes are used for dfs and map-reduce b) stop-all.sh stops map-reduce but fails to stop dfs processes (datanode tasks on grid nodes) Instead, the warning message 'no datanode to stop' is seen for all data nodes. c) The 'pid' files for datanode processes do not exist therefore the only way to stop datanode processes is to manually execute kill commands. The root cause of the issue appears to be in hadoop startup scripts. start-all.sh is really two parts: 1. start-dfs.sh : Start namenode and datanodes 2. start-mapred.sh: Jobtracker and task trackers. In this case, running start-dfs.sh did as expected and created the pid files for different datanodes. However, start-mapred.sh script did end up forcing another rsync from master to slaves, effectively wiping out the pid files stored under "pid" directory. -- This message is automatically generated by JIRA. If you think it was sent incorrectly, please contact your JIRA administrators: https://issues.apache.org/jira/secure/ContactAdministrators!default.jspa For more information on JIRA, see: http://www.atlassian.com/software/jira
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text:
DNA-R1B1C7-L ArchivesArchiver > DNA-R1B1C7 > 2008-12 > 1230441841
From: "David Wilson" <>
Subject: Re: [R-M222] DYS385a,b
Date: Sat, 27 Dec 2008 21:24:01 -0800
References: <email@example.com><B5AF1C5DDA504CFB819953BDD9BC404D@Mercedes>
In-Reply-To: <B5AF1C5DDA504CFB819953BDD9BC404D@Mercedes>
I have wondered this myself. One would like to be able to assert that a
single individual with 11-12 at 385 was the ancestor of all individuals who
have those results today, but we need to be cautious. If you can find a
cluster of distinguishing markers (the more the better) that include
385b=12 and define a subcluster within the overall M222 group, then you
would have something to work with. But I have not yet seen such a cluster
myself. Also, remember that mutations go both directions. It is possible
that some 11-13 individuals today descend from an 11-12 individual who lived
two, four or eight centuries ago, and in one of whose descendants the modal
value re-established itself and prospered in succeeding generations.
I'm not trying to rain on your parade, but I have seen too many of my own
notions and enthusiasms fail to play out as I expected. I'm just really
cautious these days.
David Wilson
-----Original Message-----
[mailto:] On Behalf Of Richard B. Hare
Sent: Saturday, December 27, 2008 8:54 AM
Subject: Re: [R-M222] DYS385a,b
I'd love to hear anything anyone knows about DYS 385 b as a 12. Is it a
mutation of DYS 385b to 12 from it's modality of 13? Is there any
significance to it? There are a measurable number of us so it may be more
than a random event.
Dick Hare
-----Original Message-----
[mailto:] On Behalf Of Colin Ferguson
Sent: Friday, December 12, 2008 10:57 AM
To: DNA-R1b1c7
Subject: [R-M222] DYS385a,b
In the Fergus(s)on DNA Project we have a cluster of 6 people of no
konwn genealogical relation wherein DYS385a,b=12,12; see
A searched YSearch, SMGF and the R-M222 Haplogroup project revealed
few instances DYS385a,b=12,12. This got me to wondering just how far
removed 12,12 is from the modal 11,13. On the face of it I would say a
genetic distance of 2 but being a palindromic marker I know that it
can be more complicated than that. How many ways can 11,13 mutate to
Related question: what is the modal Kittler test for R-M222?
Colin Ferguson
R1b1c7 Research and Links:
This thread:
|Re: [R-M222] DYS385a,b by "David Wilson" <>


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News Corporation has sold its 44 per cent stake in New Zealand television provider Sky Network Television for $NZ815 million ($658 million).
Investment banks Deutsche Bank and Craigs Investment Partners placed shares with institutional investors across the weekend.
It's understood the shares were sold for $NZ4.80 each, which represented a 7.2 per cent discount to Friday's $NZ5.17 closing price.
News Corporation, through local arm News Ltd, owned 169.9 million SkyTV shares as at August 13, according to SkyTV's most recent annual report.
SkyTV is listed on the New Zealand and Australian exchanges and has a $1.6 billion market capitalisation. The company provides pay and free-to-air television in New Zealand.
Sunday's sale was the biggest ever New Zealand block trade and comes only months after the Todd family's Todd Communications Ltd sold its 11.11 per cent SkyTV stake in a separate deal.
SkyTV reported a strong first-half result last month, with net profit after tax up 8 per cent to $NZ67.2 million and ahead of consensus estimates ($NZ60 million).
The company also lifted its full-year profit guidance expectation to between $NZ125 million and $NZ130 million.
News' sale comes as it trims its portfolio ahead of the media conglomerate's demerger, scheduled for later this year.
The Australian Financial Review


text:
Paul Ollila Named to Michigan Tech Board of Trustees
Last Modified 2:57 PM on Mon Jun 15, 2015
February 25, 2009—
Paul Ollila, the former superintendent of the Copper Country Intermediate School District, has been appointed to an eight-year term on the Board of Trustees of Michigan Technological University, Governor Jennifer Granholm has announced.
Ollila fills the seat vacated by outgoing Board Member Rodger Kershner, whose term expired Dec. 31.
"I'm very pleased and proud to be asked to serve," said Ollila, a 40-year resident of Painesdale. "I've always been very interested in Tech, so I view this as both an honor and an opportunity."
In 1964, Ollila started the first special education senior high school program in the Copper Country, located at Jeffers High School in Painesdale. He accepted a position as a consultant with the Copper Country ISD in 1969, placing handicapped students in jobs throughout the area.
In 1975, he was appointed CCISD's director of special education, with responsibility for personnel, collective bargaining, federal projects, curriculum development and compliance. He was named assistant superintendent in 1979 and in 1993 became superintendent of the CCISD, retiring in 2004.
Since then he has served briefly as the elementary principal for the Ontonagon Area School District, following the previous principal's death, and as acting superintendent of the Adams Township School District, following the retirement of the superintendent.
Ollila is a member of the Portage Health Foundation Board, the Keweenaw Community Foundation Board, the Finlandia Community Advisory Committee, the Range Lions Club and the Keweenaw Economic Development Alliance. In addition, he serves on the board of the Michigan Tech Employees Federal Credit Union as secretary/treasurer.
Ollila has earned a bachelor's degree in social work/sociology and economics and psychology, a master's in special education/educational administration, and an EdS in educational administration, all from Northern Michigan University.
The Board of Trustees is responsible for the general supervision of the institution and the control and direction of its funds. It also determines compensation for services and property, confers degrees, fixes tuition and other fees and charges and promotes the purposes of the institution.
Michigan Technological University (www.mtu.edu) is a leading public research university developing new technologies and preparing students to create the future for a prosperous and sustainable world. Michigan Tech offers more than 120 undergraduate and graduate degree programs in engineering; forest resources; computing; technology; business; economics; natural, physical and environmental sciences; arts; humanities; and social sciences.


text:
serifed is a valid word in this word list. For a definition, see the external dictionary links below.
The word "serifed" uses 7 letters: D E E F I R S.
Direct anagrams of serifed:
Words formed by adding one letter before or after serifed (in bold), or to deefirs in any order:
b - debriefs e - redefies f - seriffed i - deifiers edifiers fireside l - defilers fielders n - definers o - foreside t - resifted
Shorter words found within serifed:
de dee deer deers dees defer defers defi defier defies defis dere desire die dies dire dis dree drees dries ed eds ef efs eide eider eiders er ere ers es fed feds fee feed feeds fees fer fere feres fid fids fie fir fire fired fires firs free freed frees fried fries frise frisee id ides ids if ifs ire ired ires is re red rede redes reds ree reed reeds reef reefs rees ref refed refs rei reif reifs reis res resid reside rid ride rides rids rif rife rifs rise seder see seed seer sei seif ser sere sered serf serif si side sir sire sired siree sri
List shorter words within serifed, sorted by length
Words formed from any letters in serifed, plus an optional blank or existing letter
Try a search for serifed in these online resources (some words may not be found):
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Each search will normally open in a new window.
List all words starting with serifed, words containing serifed or words ending with serifed
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Other words with the same letter pairs: se er ri if fe ed
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text:
I have linked my live account to my Windows Mail but now my live inbox is
empty. How can I bring back all those important messages to my live-hotmail
inbox? This means I can not check my hotmail-live inbox any more from a
different computer than mine? What if I'm traveling around the world without
my laptop?
HELP Please !!! I need to reverse this


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Corby 'terrified' ahead of verdict
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Accused drug smuggler Schapelle Corby is terrified ahead of today's verdict, her Australian lawyer said today.
The 27-year-old Gold Coast woman, accused of smuggling 4.1kg of marijuana into Bali last October, faces Denpasar District Court today to hear the verdict in her trial.
"She's probably the worst I've ever seen her," lawyer Robin Tampoe told the Nine Network.
"She tries to put on a brave face but there was a lot of crying, she's pretty well terrified about the worst case scenario, what might happen today, so it's very hard to console her in that sort of situation.
"We're trying not to dwell on anything negative, we're trying to keep very upbeat and positive with her, as is her family.
"She knows the possible scenarios today and that's what we don't talk about, we're just dwelling on the positive."
Still hope
The Indonesian prosecutor said yesterday that he hoped Australians would accept the judges' decision, but Mr Tampoe said he was still hoping for a positive result.
"I think a lot of people are preparing for a bad decision," he said.
"We're all still pretty optimistic about a good result today. I mean, a good result as far as we're concerned is obviously an acquittal, that's what we're asking for.
"But even a sentence that would allow her to go home very quickly or immediately would be a great result. Fingers crossed we'll achieve that."
Appeals could hold the case up for some time, Mr Tampoe said, and that would put further strain on his client.
"She's very fragile at the moment and the thought of spending more time I think is not a good thing.
"But I know she's trying very very hard for all of us just to maintain herself, maintain her composure and she's very very hopeful that today will be positive."
Nervous wait
Schapelle Corby's financial backer also says she is not faring well.
"She's in pretty bad shape," Gold Coast businessman Ron Bakir told the Nine network today.
"She believes in her heart they can't keep here there. She keeps saying 'they can't keep me here, I've done nothing, I've got to go home, This is so wrong'.
"I can only hope that she can get through today. It is the most important day of her life and everybody's pretty uptight and nervous about today."
A three-judge panel will hand down its decision sometime after 9am (1100 AEST) in Denpasar District Court.
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This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
Cancer stem cells or tumor-initiating cells (CSC/TICs), which can undergo self-renewal and differentiation, are thought to play critical roles in tumorigenesis, therapy resistance, tumor recurrence and metastasis. Tumor recurrence and chemoresistance are major causes of poor survival rates of ovarian cancer patients, which may be due in part to the existence of CSC/TICs. Therefore, elucidating the molecular mechanisms responsible for the ovarian CSC/TICs is required to develop a cure for this malignancy. Recent studies have indicated that the properties of CSC/TICs can be regulated by microRNAs, genes and signaling pathways which also function in normal stem cells. Moreover, emerging evidence suggests that the tumor microenvironments surrounding CSC/TICs are crucial for the maintenance of these cells. Similarly, efforts are now being made to unravel the mechanism involved in the regulation of ovarian CSC/TICs, although much work is still needed. This review considers recent advances in identifying the genes and pathways involved in the regulation of ovarian CSC/TICs. Furthermore, current approaches targeting ovarian CSC/TICs are described. Targeting both CSC/TICs and bulk tumor cells is suggested as a more effective approach to eliminating ovarian tumors. Better understanding of the regulation of ovarian CSC/TICs might facilitate the development of improved therapeutic strategies for recurrent ovarian cancer.
Although high response rates to initial treatments, including surgical debulking and chemotherapy, have been achieved in patients with ovarian cancer, this disease remains the most lethal gynecological malignancy [
One of the current emerging concepts concerning tumorigenesis is that tumors are composed of heterogeneous populations of cells with different biological properties and tumorigenic potentials. The cancer stem cell or tumor-initiating cell (CSC/TIC) subpopulation, which has a high tumorigenic potential, is thought to play a crucial role in tumor development, chemoresistance and relapse after initial treatment [
In this review, we briefly summarize the recent findings regarding genes and signaling pathways that regulate ovarian CSC/TICs, which have helped improve understanding of the mechanisms that contribute to ovarian pathophysiology, including the high level of recurrence and chemoresistance associated with this malignancy. Important microRNAs (miRNAs) and tumor microenvironment features that are responsible for the maintenance and function of ovarian CSC/TICs are also described. Furthermore, current and potential approaches targeting ovarian CSC/TICs will be illustrated to provide insight into future treatment strategies for recurrent ovarian cancer.
The concept of CSC/TICs has emerged based on the identification and characterization of a subpopulation of stem-like cells in several distinct malignancies; however, there remain several controversies concerning CSC/TICs. More recently, this concept has evolved into a more comprehensive model that better explains the complex processes involved in tumorigenesis [
In terms of the origin of CSC/TICs, it is currently thought that CSC/TICs are derived from stem cells or from more differentiated cells that acquire CSC/TIC features through the accumulation of genetic and epigenetic alterations. Intriguingly, recent works have demonstrated that CSC/TIC phenotypes, such as self-renewal and pluripotency, can be acquired by the activation of oncogenic genes or the inactivation of tumor suppressor genes [
Recent discoveries have helped develop an updated model of CSC/TICs in cancer. This model suggests that CSC/TICs are more dynamic than previously thought, that a tumor can contain multiple genetically diverse CSC/TIC clones, and that the frequency and phenotype of CSC/TICs can vary during tumor progression [
Since Bapat
The hyaluronic acid receptor CD44 and the stem cell factor receptor CD117 (c-kit) are cell surface markers of ovarian CSC/TICs. CD44+CD117+ cells isolated from human ovarian adenocarcinomas are a subpopulation with an ovarian tumor-initiating capacity, which can recapitulate original tumors from which they are derived when injected into mice [
Several developmental pathways, including Notch, Wnt, Hedgehog, and transforming growth factor-β (TGF-β), are crucial for the regulation of the self-renewal and maintenance of CSC/TICs [
First, the Notch pathway plays a role in the regulation of ovarian CSC/TICs. Amplification and overexpression of the Notch 3 gene are frequently found in ovarian cancer tissues [
Second, the Hedgehog signaling pathway, which is another well-known pathway involved in embryonic development, is implicated in several cancers, including ovarian cancer [
Third, EMT is a cellular reorganization process that is essential for embryonic development and also occurs during tumorigenesis, allowing some cancer cells to become more migratory and invasive [
Lastly, although genetic mutations in the Wnt pathway are rare in epithelial ovarian cancer, recent studies showed that activation of Wnt signaling mediated by the unique ovarian tumor microenvironment may play a role in ovarian tumorigenesis [
In addition to the aforementioned stem cell pathways, the NF-κB signaling pathway, which is commonly activated by inflammatory cytokines, affects the survival of ovarian CSC/TICs. NF-κB is constitutively active in ovarian CD44+ CSC/TICs, and inhibition of constitutive and TNF-α-induced NF-κB activity results in apoptotic cell death [
Growing evidence suggests that cancer-associated genes play functional roles in the development and maintenance of CSC/TICs, in addition to their roles in ovarian cancer cells. These genes include well-known tumor suppressor genes, CSC/TIC marker genes and EMT-related genes.
First, loss of p53 function, a tumor suppressor protein, is related to the pathogenesis of high-grade serous adenocarcinoma of the ovary [
Twist is a transcription factor implicated in several processes in human malignancies, including EMT, invasion, survival and drug resistance [
The clinical relevance of stem cell-associated genes in ovarian cancer has been uncovered. For instance, Lin-28 is a reprogramming factor that can convert somatic differentiated cells into induced pluripotent stem cells [
Given that these stem cell-associated genes are involved in the regulation of CSC/TICs in several tumors, it is likely that
Silencing of developmental genes in embryonic stem cells and pluripotent embryonic carcinoma cells by bivalent histone modifications containing active H3K4me3 and repressive H3K27me3 [
MiRNAs have recently emerged as an important regulator of CSC/TICs. In addition to their role in the functions of normal stem cells, including self-renewal and differentiation, miRNAs are involved in tumorigenesis [
In most studied breast CSC/TICs, miRNAs such as let-7, miR-30 and miR-200 regulate critical properties of CSC/TICs by targeting their respective downstream genes; for example, let-7 targets
An association between miR-214 and ovarian CSC/TIC properties was demonstrated by a recent study, which found that miR-214 regulates ovarian CSC/TICs in association with p53/NANOG [
MiR-200a is also involved in the regulation of ovarian CSC/TICs. In ovarian cancer cell lines, miR-200a is downregulated in CD133+ cells in comparison to its level in CD133− cells. Overexpression of miR-200a reduces the migration and invasion of CD133+ ovarian CSC/TICs, suggesting that miR-200a functionally inhibits ovarian CSC/TICs [
Additionally, profiling of dysregulated miRNA expression in the CD133+ subpopulation of ovarian cancer cell line indicated that several miRNAs are upregulated, including miR-205, miR-146a, miR-200a and miR-200b, whereas miR-1202 and miR-1181 are downregulated, which indicates that miRNAs can modulate the properties of ovarian CSC/TICs [
Consistent with the effect of let-7 on tumorigenesis in other tumor types, the let-7 pathway is deregulated in a specific molecular subtype of high-grade serous ovarian cancer tissues [
It is noteworthy that the aforementioned miRNAs, including miR-214, miR-200 and let-7, also play important roles in ovarian cancer cells [
As discussed above, a variety of genes, pathways, and miRNAs are implicated in the regulation of ovarian CSC/TICs. In addition, CSC/TIC traits, for example being undifferentiated and the capacity for self-renewal, might be maintained by their surrounding environment, termed the "CSC/TIC niche" [
Several recent studies have reported that hypoxia is one of the key attributes of the tumor microenvironment that regulates the properties of ovarian CSC/TICs. For instance, hypoxia increases the survival and chemoresistance of ovarian CSC/TICs isolated from ovarian cancer cell lines through the induction of c-kit expression mediated by HIF-1α [
TGF-β that is secreted into the ovarian tumor microenvironment also affects the growth of ovarian CSC/TICs [
Importantly, McLean
Cancer-associated fibroblasts (CAFs) are a type of stromal cells that constitute the tumor microenvironment and promote tumorigenesis by enhancing cell proliferation, angiogenesis, invasion and metastasis [
The main focus of ovarian cancer therapy is to overcome chemoresistance and recurrence after initial therapy since these are the major causes of mortality in ovarian cancer patients. Chemoresistance can be classified into two major forms: "de novo or inherent" and "acquired," both of which are ultimately linked to disease recurrence [
Several studies have explored the mechanisms underlying chemoresistance in ovarian cancer. Steg
Similarly, it was recently reported that endoglin, a member of TGF-β pathway, is involved in ovarian chemoresistance [
On the basis of the involvement of Notch signaling in the chemoresistance of ovarian cancer, a recent study [
In addition, the ovarian CSC/TIC marker c-kit is involved in chemoresistance in ovarian cancer cells by regulating ABCG2 through β-catenin [
The current approach of anti-cancer drug discovery has shifted from conventional cytotoxic drugs to molecular targeted therapy. High-throughput approaches have identified numerous potential therapeutic targets specific to cancer cells. However, this approach has focused on the killing of bulk tumor cells rather than targeting CSC/TICs.
The current failures in cancer therapy are mostly due to tumor recurrence after therapy and not to a defective response to initial therapy. A major challenge now is to discover agents and strategies that eliminate the sources of tumor recurrence and chemoresistance along with bulk cancer cells. As discussed above, CSC/TICs have crucial roles in tumor recurrence after therapy; therefore, targeting CSC/TICs has been suggested as a promising way to achieve a long-term cure for cancer without further recurrence.
Progression has been made in developing strategies that target CSC/TICs. Recent searches for therapeutic agents and drugs that efficiently eradicate CSC/TICs can be classified into two main approaches: (1) the identification of agents that inhibit CSC/TIC markers or CSC/TIC-specific pathways believed to be critical for the regulation of CSC/TIC properties [
Similar approaches have been used to identify therapeutic agents against ovarian CSC/TICs; such agents deplete the CSC/TIC population, inhibit CSC/TIC growth, or induce CSC/TIC death, and thereby have anti-tumor activity. These agents may be useful in the treatment of patients with recurrent ovarian cancer; however, these studies are at an early experimental stage and further validation is required (
The targeting of CSC/TIC markers, such as CD44, CD123, EpCAM, and ATP-binding cassette transporters have been explored as a means of eliminating CSC/TICs [
With regards to targeting pathways relating to CSC/TICs, treatment with γ-secretase inhibitors, which target the Notch pathway [
Based on previous successful identification of CSC/TIC-specific inhibitors in breast cancer [
More recently, novel attempts targeting the unique properties of CSC/TICs that are distinct from those of non-CSC/TICs was also used to identify ovarian CSC/TIC-specific inhibitors. Alvero
As mentioned above, targeting of CSC/TICs has been reported to successfully suppress tumor progression, which supports the belief that CSC/TIC-targeting therapies are promising anti-cancer strategies. However, CSC/TICs may be generated from non-CSC/TICs. This means that CSC/TIC-targeting therapies may eliminate CSC/TICs, but further CSC/TICs may be generated from non-CSC/TICs, leading to incomplete regression of tumors [
Metformin, which is clinically used as an anti-diabetic drug, selectively targets CSC/TICs [
It has been suggested that combination treatment of retinoids with platinum therapy is likely to affect both ovarian cancer cells and ovarian CSC/TICs, whereas carboplatin treatment alone does not [
Since accumulating evidence suggests that the tumor microenvironment plays crucial roles in the regulation of CSC/TICs, targeting of the CSC/TIC niche should be considered in the development of anti-cancer therapies in ovarian cancer.
Taken together, ovarian tumors are composed of heterogeneous populations, including CSC/TICs, cancer cells and various cells in the tumor microenvironment, including stromal cells. Although CSC/TICs are currently thought to be the main cause of tumor recurrence and chemoresistance, targeting of CSC/TICs alone might not provide the ultimate cure for ovarian cancer since CSC/TICs appear to be induced or emerge from differentiated non-CSC/TICs in response to signals from the tumor microenvironment. Accordingly, targeting both the bulk tumor, including the tumor microenvironment, and CSC/TICs may provide a more effective means of overcoming tumor recurrence and thereby provide a cure for ovarian cancer (
Growing evidence supporting the existence of ovarian CSC/TICs and their crucial roles in the recurrence and chemoresistance of ovarian cancer has helped identify more effective therapeutic strategies for treating recurrent ovarian cancer. Recent studies have begun to report the genes, pathways, and miRNAs that regulate ovarian CSC/TICs. However, further studies are required to fully understand how the properties of ovarian CSC/TICs are regulated in order to assist the development of therapeutic strategies that target ovarian CSC/TICs. Notably, current evidence suggests that the microenvironment in which CSC/TIC reside, the so-called "CSC/TIC niche," is pivotal to the maintenance of CSC/TICs; therefore, how the tumor microenvironment regulates CSC/TICs should be considered. A comprehensive understanding of how ovarian CSC/TICs are regulated will allow novel anti-cancer drugs targeting CSC/TICs to be identified. Ultimately, this will facilitate the development of better treatments for recurrent ovarian cancer using combinations of drugs that target both CSC/TICs and non-CSC/TICs in tumors and the tumor microenvironment.
This work was supported by Basic Science Research Program grant (No. 355-2011-1-E00124) and by the Global Core Research Center (GCRC) grant (No. 2012-0001194) from the National Research Foundation (NRF), funded by the Ministry of Education, Science and Technology, Republic of Korea.
The authors declare no conflict of interest.
The tumor microenvironment involved in the maintenance and regulation of ovarian CSC/TICs. The maintenance and properties of the ovarian CSC/TIC population are influenced by the surrounding microenvironment, termed the "CSC/TIC niche." Growth factors, such as bone morphogenetic protein (BMP) and transforming growth factor-β (TGF-β) released from ovarian cancer cells, increase the self-renewal and proliferation of CSC/TICs. Ovarian carcinoma associated-mesenchymal stem cells (CA-MSCs) are also reported to regulate ovarian CSC/TICs through BMP signaling. Moreover, hypoxia, which is a common feature of the ovarian cancer microenvironment, enhances the survival and chemoresistance of ovarian CSC/TICs through the upregulation of c-kit mediated by HIF-1α. Conversely, hypoxic induction of HIF-1 expression can promote the differentiation of ovarian CSC/TICs by inducing TWIST1 expression. A high level of NF-κB activity in ovarian CSC/TICs may be induced by cytokines, such as TNF-α, that are generated as a result of inflammation in the ovarian tumor microenvironment.
Strategies for the effective treatment of recurrent ovarian cancer. (
Genes, pathways, and miRNAs involved in the regulation of ovarian cancer stem cells or tumor-initiating cells (CSC/TICs).
|Gene symbol
|Gene name or target gene name
|Types of ovarian CSC/TICs
|Notch signaling (
|Notch 3
|Side population
|Expansion of ovarian CSC/TIC population Resistance to platinum
|Hedgehog signaling
|Growth of ovarian cancer spheroid-forming cells
|TGF-β signaling (
|Transglutaminase 2 (C polypeptide, protein-glutamine-gamma-glut amyltransferase)
|CD44+CD117+ cells
|Self-renewal and expansion of ovarian CSC/TIC population
|NF-κB signaling
|CD44+ cells
|Survival (apoptosis)
|TLR2-MyD88-NF-κB signaling
|CD44+MyD88+ cells
|v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog
|Self-renewal and expansion of ovarian CSC/TICs Resistance to chemotherapy
|EpCAM+ cells
|Expansion of ovarian CSC/TIC population
|Lin-28 homolog (
|ALDH+ cells
|Expansion of ovarian CSC/TIC population
|Twist basic helix-loop-helix transcription factor 1
|CD44+MyD88+ cells
|miR-214 (
|Tumor protein p53
|ALDH1+ cells
|Self-renewal and expansion of ovarian CSC/TIC population
|miR-199a (
|CD44 molecule
|CD44+CD117+ cells
|Proliferation and invasion Resistance to chemotherapy
|miR-200a (
|Zinc finger E-box binding homeobox 2
|CD133+ cells
|Migration and invasion
Agents and drugs targeting ovarian CSC/TICs.
|Agent or drug
|Ovarian CSC/TICs targeted
|Mechanism of action
|Small hyaluronan oligosaccharides
|Cells highly expressing CD133
|Hyaluronan-CD44 interaction
|Inhibition of growth of ovarian carcinomas with high levels of CD133
|Inhibition (dissociation) of the hyaluronan-CD44 interaction
|Clostridium perfringens enterotoxin (CPE)
|CD44+ cells
|Claudin-4 in CD44+ ovarian CSC/TICs
|Inhibition of tumor progression of mice harboring xenografts of chemotherapy-resistant CD44+ ovarian CSC/TCS
|CPE-induced cytotoxicity
|γ-secretase inhibitors
|Side population
|Notch pathway
|Increased sensitivity to cisplatin
|Depletion of CSC/TICs
|Side population
|Metabolic pathways
|Inhibition of ovarian CSC/TIC growth
|Disruption of multiple metabolic pathways
|Isoflavane derivate, NV-128
|CD44+MyD88+ cells
|Mitochondria (Mitochondrial bioenergetics)
|Induction of apoptosis in ovarian CSC/TICs
|Inhibition of mitochondrial function
|Eriocalyxin B
|CD44+ cells
|NF-κB pathway
|Induction of apoptosis in ovarian CSC/TICs
|Inhibition of the NF-κB pathway
|ALDH+ cells
|Inhibition of ovarian CSC/TIC growth
|Depletion of CSC/TICs, and inhibition of the formation of CSC/TIC spheres


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Yo, Adiran. I started saying Yo at inappropriate times because of this film.
Eh this movie is SO nerve racking. Samuel L. Jackson is TERRIFYING.Tags: dvd, movies, film, drama, entertainment, Philadelphia, cinema, action, fantasyAdded 8 Years Ago from Amazon.com
This movie horrified me. It was so good and it annoyed me when people used to tell me it wasn't scary, because they are obviously lying. Also Mischa Barton has a great performance in this movie.Added 9 Years Ago from Amazon.com


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Right to walk away???
I've been looking for a M3 for a while and today I went to check out a Carbon Black vert at the local BMW dealership. The car had a little over 67,000 miles and the test drive was great. I asked for any service history that they could find but the salesperson was only able to get info up to around 39,000 miles. I asked if they could find out if Stage II inspection was done in which they told me no. The manager said they would do the inspection and take care of any problems if I would buy the car, I told him to call me after the inspection was done then we can talk. The manager then stated, "That's the best solution he could offer." I walked out. Was I right?
In my opinion...YES
Funny thing about cars...."There's another one just down the street".
Keep looking, you'll find your baby
No as in they didn't know if it was done. The manager claimed the car was checked out by his service dept but could not say it has been done. Shouldn't that be tracked with the VIN once its done by a BMW dealer?
First rule of buying a car: don't get attached to the car! Oh and BTW, never EVER trust someone when they tell you not to worry and that everything would be fixed when you come back or if you buy the car on the spot. Guess what? They ain't fixing shjt.
Sent from my G6
Yes you did the right thing. I wouldn't of done anything different.
I wouldn't be scared off right away. If it's a nice, clean car, maybe the PO had an indy do all the work when the warranty ran up? If it's at a BMW dealership and they're selling it and not sending it to auction, chances are it's a decent car.
Plus they said they'd do inspection 2 for you, that's a big chunk of change there.
I'm missing specifically why you walked away from the car. No-one is going to do a major Inspection on a car when you are making zero commitment to it. They said they would do the Inspection if you bought it. Thats reasonable. Just get an independent PPI, then agree to buy contingent upon the Inspection being done before delivery.
Re: no records after 39K miles - that means it was done at indy shops - which is probably true of >95% of cars that old. Short of finding a single owner car (probably about 1% of M3s out there now) - I'm not sure how you plan to improve upon that.
The car in question:http://www.bmwofmobile.com/used/BMW/...af731a82c2.htm
inspection II being done by the dealer, thats a HUGE amount of cash being saved, i did mine at an indy shop for 1300ish. i dont see why you walked away, get a PPI done if it checks out ok, and has SOME service records, why not buy?
Your first instinct is usually right.. Keep looking if felt uncomfortable..
They're not going to do Inspection II "on spec." Most buyers won't insist, and if they end up sending it off to auction, they won't get that investment back.
I'd have a PPI done, and then buy it contingent on Inspection II being done.
Sounds like the sales guy is a jerk, but you're not marrying him. Guy who sold me my car was a jerk too but the car was perfect.
I'd think a cold and snowy January is a good time to buy a convertible M3.
They don't even know how to do math. Stay away.
The ad states "at $1050 below Kelly Blue Book..." They list the car at 23,990 and KBB price is 24,600 (again, these numbers are in THEIR ad)
To me, that is only $610 under KBB.
When sellers are this stupid, I tend to stay away. But that's just me.
IDK maybe u do math differently...
Just list the items on a make-ready. That way they know you're definitely buying, and the dealer MUST take care of everything on the list, as it's an integral part of the contract.
this is it right? http://www.cars.com/go/search/detail...nal&listType=1
This car has an accident, minor or major doesn't really matter, it drops the price because it had bodywork.
also the previous guy bought it on 06/25/2012! Why did he sell it?
I wouldn't buy this car. I consider you lucky for walking away!
Vert... yup walk away... But in all srs if they are willing to stand behind the car and do inspection two I would consider it. Inspection 2 is pricey.
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Atletico Madrid president Enrique Cerezo is confident of keeping hold of striker Diego Forlan. The Uruguay international is threatening to clinch the Spanish Golden Boot ahead of Barcelona star Samuel Eto'o and is under consideration at the Nou Camp as a replacement for the contract rebel. Tottenham and Sunderland are also keen to bring the former Manchester United forward to England.
However, Cerezo says of Forlan: "I believe his buyout clause of £32 million is enough and he will not leave."
"Here I am happy with my life," chimed in Forlan at a media conference yesterday.