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This would be the page for creating our final presentation script. On this page, basically write what you're planning to present in the final presentation. So what you're going to write here would be something that would convey your points to the listners.
It doesn't have to be a perfect script at start, but we can gradually make it into a complete presentation script.
In General
Write up the presentation by 1/7 night. Meanwhile, you can use the main page to develop the flow and the outline of the script on this page.
As of 1/7 23:00, this presentation script took more than twelve minutes when I read it out loud. (And that was at a fairly fast speed.) Maybe we can cut some contents? --Asahiko
The following is the script for the presentation.
U-learning, or ubiquitous learning has the following characteristics.
Anytime, Anywhere, Any media
Context aware
Provide the most efficient learning environment by detecting the user's position, learning situation, information, and requirements.
E-learning --> M-learning --> U-learning
The availability of handheld, networked devices, such as Pocket PCs, enables their use both in the development of mobile learning environments (m-learning) and in the ntegration m-learning into e-learning environments to form ubiquitous learning environments (u-learning).
Problems and limitations
1.How do students access a flexible learning environment when the methods of access are restricted to a desktop computer? A:more portable devices, such as personal digital assistants (PDAs)
2.Not all features of a desktop web site can be replicated for mobile web browsers.
Adaptive learning with ULE
Adaptive learning
Adaptive learning is based on the idea of adapting learning methodologies to students' learning styles.
The concept is that an individualised method of teaching will help students learn at a faster pace, more effectively, and with greater understanding.
Some elements of adaptive learning may include:
- 1. monitoring student activity
- 2. interpreting the result
- 3. understanding student's requirements and preferences
- 4. using the newly gained information to facilitate the learning process =>able to provide *specific* and *personalized* knowledge when required.
Ubiquitous learning environment (ULE)
- 1. Students can become totally immersed in the learning process. They may not even be conscious of the learning process. Source data is present in the embedded objects. Students don't have to DO anything to learn. They just have to BE there in ULE.
- 2. It provides props and stimuli needed to easily encourage student involvement but without needing the active attention of the student.
- 3. U-learning's many-to-one relationship allows an ULE to service an unlimited number of individuals at once.
- 4. It allows students to intuitively interpret their surroundings and construct their own knowledge ==> Students can retain the information within their own knowledge base. Ex. Instead of being told that "a seed will sprout in soil and not in rocks" is true, students can understand *why* and *how* it happens.
The development of a ubiquitous learning environment (ULE) combines the advantages of an adaptive learning environment with the benefits of ubiquitous computing and the flexibility of mobile devices. Students have the freedom to learn within a learning environment which offers adaptability to their individual needs.
In order to practice the ubiquitous spirit not only in learning but in developing economics and social welfare, Japan, Korea and Taiwan government all issue their u-policies roughly since 2004. They mainly focus on the enhanced wireless sensor network, ICT and ICT development, RFID (Radio Frequency ID), and upgraded enabling environment. Creating U-school, U-home, and U-city are some ideal stages in these policies.
U-Japan since2004
- Goal:100% population have access to wireless network with 80% comfortablely using ICT technology by 2010.
U-Korea since2005
- Goal: establish U-city with advanced IT and U-home with home-banking e-passport, and home-shopping.
U-Taiwan since2005
- Goal: create an ubiquitous environment with IT technology applied in life.
Subgroup 2: Dream Device
In order to describe how people will learn in the u-society, we imagined up our dream device for use in u-learning. A website can help us understand more what the functions of dream devices are. Examples of ICT Usage in u-Japan Society: http://www.soumu.go.jp/menu_02/ict/u-japan_en/j_r-menu_u.html
The device will help us learn various things, including language, culture, cooking, etc. It can also have other functions like alarm clock, watch, GPS and so on.
- One type is like the watch, it is already put to practical use. It is very light, so you can put it on in the body and progress, it is enough to recording voice, taking picture, and check your schedule. But, because of its size, it is difficult to equip with large screen, so it is not suitable for learning and complicated work. In some Cinemas, it appears floating display; it is difficult to come true.
- The other type is like a note pad, it is also already realized, and it called PDA. You can pen input, pen input is very useful for character learning, in particular, Chinese character learning, teacher can check student's order to write, not only figure, it is superior to notebook, in Japan, some elementary school uses UMPC(Ultra-Mobile PC) for learning Chinese character.
- And.... another type is an ultimate form, wearable computer. It has Head Mounted Display (HMD), and you have large amount of information, it is under development now.
Language learning
1.Choose language: The device has many kinds of languages, and it can also connect to the country where you want to learn its local language, so you can learn many languages through the device.
2.Choose teacher: You can choose which teacher you like. For example, if you would like to learning Japanese, you can choose "Kuraki Mai" (a woman star) to be your teacher. If you want to learn English, then you can choose "Bush." You can also choose cartoon character like Conan or Doraemon. The teacher's face will appear on the screen. The functions can make you learn pleasantly.
3.Choose course: There are many articles and courses, and you can use the functions of listening, speaking, reading, writing, grammar, spelling, and vocabulary to improve your language ability. The design of the course is similar to TOEFL learning software. Beside, if you require real person to explain for you, you can connect to the Internet and there are many teachers who can help you. http://www.bbc.co.uk/skillswise/words/grammar/[1]
4.Translate: When people speak a language which you don't understand, you can open the function and it will translate soon for you. The language you listen will be your first language. You can also change the language which you understand into the language you want to practice. By the way, you can learn form conversation.
5.Record: The device can record what you learn today. It is convenient for your review. For example, it can record what language you learn, how effects you gain and the dialogic contents. In particular, using those records, you can review what you learn during sleeping.
- Culture learning: Because the device can connect to other countries and real persons, it can also provide their culture information. You can truly feel that you are in other country, interacting with local residents and learning their culture.
- Cooking learning(adaptive learning): If you want to cook delicious dishes, but you don't know how to do, the device will teach you! When you are in the kitchen, it will tell you the steps. It can identify whether your steps are right or not, and make corrections and suggestions. So, follow the instructions that the device gives, and you can simply finish a delectable dish.
- Learning in a sleep(learning anytime): The functions are so magical! Before you go to bed, you can open the device. When you feel asleep, the device will release a frequency which is as the same as your brain wave, so it's safe and doesn't influence your sleep quality. Then the device will help you review what you learn today by extracting the record. By the way, your memory can maintain in a good condition, and can continuously learn when you sleep.
Social Effects Evaluation
Finally keeping our dream device in mind, we evaluated the effects u-learning will have on the society.
A change in the roles of schools
U-learning technologies, by definition, releases learning from schools. The role of the school would be greatly affected. A ubiquitous device, like the watch-shaped one we showed you earlier, can be used anywhere, anytime. Which means, learning does not have to take place in schools anymore.
However, schools have been a place for children's interaction and communication with each other. U-learning might weaken this, and problems might arise. On the other hand, a network-capable u-learning device would allow communication around the world, some of which we are already experiencing.
Life-long learning
In relation to the school-free nature of u-learning technologies, u-learning opens up education to areas outside traditional education. For example, they can be used to learn cooking, along with many other cultural education. Since the device can be used anytime anywhere, the user does not have to be a student. Therefore, it would help greatly to adults in "life-long learning".
Remove regional barriers
U-learning devices must be small, and must be able to carry anywhere. This characteristic allows the device to be used in a remote environment, for example, areas sparcely populated. It will reduce discrepancies in educational levels between urban and rural areas.
Motivate users to learn
U-learning devices can adapt itself to each learner's preferences. One example of this can be seen in the device we showed earlier: choosing a teacher you like. Functions like this would make learning a fun experience and would motivate users to learn more.
Individualized learning
A u-learning device could record the learner's progress and achievements, and based on that record, it can adapt its content to suit the learner. The context awareness of u-learning devices would allow each learners to study at their own pace. This might solve the problems in traditional teaching methods that arise from differences in each learner's achievements.
Ubiquitous technologies provide us a whole new approach to learning. U-learning is not without problems, but it will open up new possibilities. For a better environment in the future, what we could do is get to know u-learning better. We think we understood the general idea of u-learning through this project, and we hope you did too.


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Descended from a long line of powerful New York business tycoons, Anderson Cooper's maternal Vanderbilt line is no stranger to the public eye. In Episode 3: Our American Storytellers, the Finding Your Roots team focused on Anderson's lesser known heritage — that of his father, Wyatt Emory Cooper, who passed away when Anderson was just a child.
Roll over each branch of Anderson Cooper's interactive family tree to view images from the series and learn more about the award-winning journalist's fascinating genealogical journey.
Note: the family tree is best viewed on a computer.
- June 3, 1967
- Wyatt Emory 'Buddy' CooperFatherWyatt Emory 'Buddy' Cooperb. 1927 (Pleaseant Grove, Mississippi)Anderson's father, who passed away from a heart attack when Anderson was just 10 years old, was a charismatic man with deep Southern roots. 'My Dad loved Mississippi,' remembered Anderson. 'He loved being from Mississippi and he loved the stories that he grew up with and all the people he grew up with.'
- GrandfatherEmmett Debro Cooperb. 1888 (Quitman, Mississippi)Anderson's paternal line can be traced through back several generations of Mississippi and Alabama cotton farmers. Unlike his famous maternal lineage, Anderson's father's family, including his grandfather Emmett Cooper, were modest, small farmers who owned very little land.
- Great-GrandfatherWilliam Preston Cooperb. 1864 (Hinton, Alabama)Anderson's Great-Grandfather, William Preston Cooper, moved his family from Alabama to Mississippi before his son, Anderson's grandfather was born. The Coopers were part of a wave of settlers seeking their fortunes cultivating cotton.
- Great-Great-GrandfatherBurwell Cooperb. 1836 (Alabama)Anderson's Great-Grandfather Robert Campbell was just one of several of Anderson's Southern relatives who fought for the Confederacy, despite the fact that none of them owned slaves. His Great-Great-Grandfather, Burwell Cooper, also volunteered, as evidenced in this enlistment document.
- Great-Great-Great-GrandfatherWilliam Harrison Cooperb. 1803 (Alabama)
- Great-Great-Great-GrandmotherAnnie Margaret Boykinb. 1816 (Mississippi or Georgia)Annie Margaret's father, Anderson's 4th Great-Grandfather Burwell Boykin, was a bit more well-to-do than the Cooper line, and the family owned several slaves according to this register. However, in 1860, Burwell was killed by a rebellious slave.
- Great-Great-GrandmotherLaura Safronia Bullb. 1846 (Alabama)Many of Anderson's southern ancestors volunteered to fight for the Confederate army, even though most of them, including his Great-Great-Grandmother Laura Bull, never owned slaves.
- Great-GrandmotherRoxieann Safronia Flowersb. 1865 (Choctaw County, Alabama)The invention of the cotton gin in the early 1800's created the biggest economic boom in American history, and by the early 1800's, planters like Anderson's paternal relatives wanted in on the action.
- GrandmotherRixie Annie-Jane Andersonb. 1896 (Clarke County, Mississippi)
- Great-GrandfatherWilliam Michael Andersonb. Unknown (Alabama)The 'Finding Your Roots' research team uncovered this census record from the cotton fields of Mississippi, listing Anderson's Great-Grandfather, William Anderson, as 'William Anderson, farmer, owning a hundred dollars worth of land.'
- Great-GrandmotherSarah Ann Elizabeth Campbellb. 1876 (Clarke County, Mississippi)
- Great-Great-GrandmotherRixie Ann Jane Leeb. 1848 (Unknown)
- Great-Great-GrandfatherRobert Fletcher Campbellb. 1822 (Alabama or Mississippi)Robert Fletcher Campbell, Anderson's Great-Great-Grandfather, was born in 1822. This enlistment document shows that he volunteered to fight for the Confederacy in the Civil War.
- Gloria Laura Madeleine Sophie VanderbiltMotherGloria Laura Madeleine Sophie Vanderbiltb. 1924 (New York City, New York)As a young girl, Anderson's mother found herself at the center of a heated and public custody battle between her mother, Gloria Laura Morgan and her father, Reginal Claypoole Vanderbilt. It tore the family apart, and estranged Anderson's immediate family from the rest of the Vanderbilt clan.
- GrandfatherReginald Claypoole Vanderbiltb. 1880 (Staten Island, New York)
- Great-GrandfatherCornelius Vanderbilt, IIb. 1843 (Brooklyn, New York)
- Great-Great-GrandfatherWilliam Henry 'Billy' Vanderbiltb. 1821 (New Brunswick, New Jersey)
- Great-Great-Great-GrandfatherCornelius Vanderbiltb. 1794 (Staten Island, New York)Anderson's Great-Great-Great-Grandfather, Cornelius Vanderbilt, transformed his small ferry boat operation into one of the largest shipping and railroad companies in the world. When he died in 1877, the Commodore was worth more than 100 billion dollars in today's currency, making him one of the wealthiest men in the history of the United States.
- Great-Great-Great-GrandmotherSophia Johnsonb. 1795 (Staten Island, New York)The Vanderbilt family made their fortune by investing railroads and shipping throughout the 1800's.
- Great-Great-GrandmotherMaria Louise Kissamb. 1821 (Coeymans, New York)
- Great-GrandmotherAlice Claypoole Gwynneb. 1845 (Cincinnati, Ohio)
- GrandmotherGloria Laura Mercedes Morganb. 1904 (Lucerne, Switzerland)
- Great-GrandfatherHarry Hays Morgan, Sr.b. 1859
- Great-GrandmotherLaura Delphine Kilpatrickb. 1869 (Santiago, Chile)

subset: commoncrawl


text:
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You know those songs we loved too much but wondered why they never had music videos to rape our minds with the genius concepts we had already thought of every time we heard them? This post has taken account of 10 (and maybe, one more) such songs that really deserved but never got the music video treatment.
Have a good time reading and digesting our list picks, and feel free to even add yours.
M.I Abaga – "Millionaira Champagne" ft. DJ Lambo, Ice Prince & Sarkodie
This song is arguably the hottest hip-hop offering from Jude Abaga's The Chairman album. There was chatter that he was going to shoot a music video for this song but I'm guessing that was just cheap talk. It would have been good to see Ice Prince at his best (he gave a most epoch delivery on this song) alongside Sarkodie voicing out those intriguing lines. Moreso, the club banger came with very twerk-worthy instrumentals for some epic booty shaking and waist grinding action.
Tiwa Savage – "Ileke"
Tiwa led the women empowerment movement in the Nigerian music industry with how she stormed the arena with everything loud, uber sexy and proud. Plus she was unapologetic to no one for it. Ileke is one of those songs that talks about a woman's natural gifting – only this time it was a woman singing about it. Tiwa would have worked seriously in the video (I mean, we all know how much she loves to dance)
Modenine – "Some More" ft. Don Jazzy
Modenine's Some More with Don Jazzy is one of my favourite materials from the rap rabbi. The two bosses brought some unusual heat on this track. Yes, Modenine was damn too compliant with his lines, and on form just like always but the enigmatic addition of Don Dorobucci's vocals especially on the hook (he even had a verse too) was lit af! Who says 2 captains can't steer one ship? Mode9 and Jazzy already pulled that shxt off… just not in pictures 🙁
Runtown – "Ghetto University"
Ghetto University reminds you a lot about the legendary afrobeats king, Fela. Runtown's tribute track sampled elements of the revered genre but with stylized lyrics to fit his own musical context. All the same, Runtown should have topped off this release with a modern adaptation of a Fela-inspired picture. Hopefully, he's got plans for that 'cos it would totally rock!
Olamide – "Oga Nla" ft. Pasuma & Lil Kesh
Oga Nla. This was the perfect starter for Olamide's fourth studio LP, Street OT. The song served musical prowess that was a crossbreed of the industry high flyers – from veteran to staunch alumnus and then badass sophomore. The chante-esque record sampled a dictatorship vocal cut at the beginning which would have been a good prelude for a military-styled music video, one that reclaims all their boss status and in their different hierarchies.
Wizkid – "For Me" ft. Wande Coal
Best buds, Wizkid and WC have always enjoyed some sort of music chemistry, either in showing vocal prowess or WC lending his acuity in the lyrical writing artistry. At the time of Wizkid's prime when he enjoyed massive support from fans and lovers nationwide, he joined forces with Wande Coal on For Me off his debut album, Superstar. We enjoyed a variety of videos off that album but certainly not the one where two of music's finest breds had to sing about what they loved the most – GIRLS! Oh wait, I think it's the booty.
D'Prince – "Amarachi"
When it comes to D'Prince and musical choices, I'm kind if neither here nor there about it. But if there's anything guy knows how to do best with his records, it is to get you up on your feet and working it hard on the dance floor. Amarachi of course wasn't any different. Off the new Mavins (first order) label compilation, Solar Plexus, the groovy tune came backed with the vocal undercoat of production maestro, Don Jazzy who also produced the track. Sola and I would have given top bucks to see (or even star) in this video but then we're reminded again that the Mavins (even from the time of Mo'hits) have always hit a brick wall with their music videos.
P-Square – "Do As I Do" ft. Tiwa Savage & May D
P-Square's collaboration with Mr May D and Tiwa Savage fits appropriately into just one descript – music & dance! Obviously, the Okoye brothers made for the vocal spice by having Mrs Billz on this song while May D was simply for the hype (he was really buzzing as at that time). However, all parties would have totally slayed a choreographed routine, Nigerian afropop video style, and of course directed by brother Jude 'Engees' Okoye.
M.I Abaga – "One Naira" ft. Waje
MI and Waje's powerful rap ballad, One Naira has remained a love classic since it's inception. It would have been another one of the many epoch sights where Waje unleashes her vocals of a lifetime on us, with Mr Incredible serving that signature short black boy swag that has specially endeared him to our hearts for a long long time now, in a carefully plotted music video. And then again, you remember that these two have got chemistry… they've got it!
Iyanya – "Story Story" ft. Oritsefemi
The musical genius brought by both artistes on Story Story was the kind that was perhaps never imagined or even believable if someone dared to think of it. The bad part about this utterly creative music piece was that it suffered lack of proper hype for it to gain the deserving commercial reception. If I belonged to Iyanya's camp, I'd have advised him to unleash a panache visual on us. That would have catapulted the song's impression on the general public.
Skales – "OMG" ft. Victoria Kimani
I wont lie, even I didn't see this one coming. Victoria Kimani and Skales served some sexually tensioning heat on this track. OMG is one of those underrated tracks off Skales' long-awaited debut LP, Man of the Year. And it was smooth and so stylishly slide, you can literally picture Ms Kimani bathing her seductive nature all over Skales' suaveness when you're jamming the song. And that's exactly what we'd love to see in this video. Nothing too serious, and plainly the usual guy meets girl concept. Skales, bruh, you still gat time to make this happen!
ALSO READ: Top 7 Nigerian Artistes Who Are Kings Of Vulgar And Profane Lyrics
We obviously couldn't have put all the great songs without music videos on this list. So if you by chance happen to think of/remember any others, please do well to share them with us!
Also Download
Chopstix Ft. El Phizzy & Stormexy – High
Olu maintain Nawti remix.
Chairman 2 by MI featuring Oritsefemi and Frank Edwards
u guys forgot to mention I love my baby by wizkid
For the first am so in love with this list…MI Abaga take over the list that is my happiness. MI Abaga ft Olamide Middle it also deserve a video.
aboki remix by ice prince ft wizkid, sarkodie,
mercy johnson
Yung6ix-SAY YES (to the altar)
Air brush – Seyi Shay
MI's all over this list.. let's forget about #MI2.. But we must talk about the Chairman Album cos it's not too late to see the videos.. at least.. Shekpe, Millionaira Champagne should have had videos.. Even #ThirdMainlandBridge from TICBN.. we the fans need to These Videos to brag to our friends about how legit MI is.. #TeamMI
very cool nd 9ice
Burnaboy smoke some weed also need a video tho


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Doctor insights on:
Treatments For Melanosis
Is there any homeopathic treatment for neurocutaneous melanosis?
Homeopathy: Homeopathy is an older treatment method, where small amounts of a substance that produce a symptom, are used to treat the symptom in microscopic amounts. Homeopathy is very popular in europe and is still in use all over the world. Homeopathy is symptom based and they do not "treat" named diseases. ...Read moreSee 1 more doctor answer
It seems I have Penile lentiginosis. I don't think it is Penile melanosis cause of my age,18, and no sexual activity. Is there any treatment possible?
See a dermatologist.: A dermatologist can diagnose and treat your condition. If you are correct, and these spots are benign lentigos, topical treatments include hydroquinone, azelaic acid, corticosteroids, and tretinoin. Laser surgery can provide definitive treatment. The dermatologist can provide accurate diagnosis and definitive treatment. Take care. ...Read more
Dear docs! What is melanosis on the white sclera of the eyes and is there a treatment.My son 4 year old has been diagnozed,he has black spotson sclera?
Nevi: It is a nevus in the sclera of the eyes. Most likely it is benign. It is common in Asian population ...Read more
I have gastropathy secondary to bile fluid & mild melanosis coli with looping of sigmoid colon. My value bumps bile into stomach not bowel. treatment?
Dumping: You would be best to find a surgeon or gastroenterologist who could help you with your problem. ...Read more
Is melanosis a type of cancer?
Melanosis Coli: I think you are referring to melanosis coli. This is a discoloration of the inner lining of the colon, which is not cancerous, but can make it difficult to notice irregularities. ...Read moreSee 1 more doctor answer
Can taking rifampicin cause melanosis coli?
Med side effect: Doubtful. Melanosis coli is very common and can occur more frequently in females, those who use laxatives or who have inflammatory bowel disease. In general it can just happen so no need to try and see if a medication caused it. Speak to your md for more details if you are concerned but you may just "have it for no reason". ...Read moreSee 1 more doctor answer
What exactly is melanosis cutaneous fibromatosis?
Disease: Depends where the lesion is. Likely it is a benign tumor (fibroma) that has skin color changes (melanosis) that need to be followed and biopsied on a regular basis. Autoimmune disease might also be a contributing factor. Ur dermatologist could best answer this. ...Read moreSee 1 more doctor answer
What is pustular melanosis in infants and how is it treated?
Transient change: This is a transient skin condition of unknown origin.It presents in a fraction of infants with tiny blisters, pustules or open blisters with a scaley margin. The blisters or pustules are usually gone by 5 days but the pigmentary change may last for weeks to a few months. They resolve without treatment so no treatment is recommended. Exclusion of other conditions is part of the evaluation. ...Read more
What are the tests for transient neonatal pustular melanosis?
Visual Diagnosis: This benign skin condition seldom warrants any tests. A scraping of the pustules reveals white cells & eosinophils without germs.The eruption pattern & lack of inflammation separate it from other entities. ...Read more
What is a melanosis coli?
Coloration of colon: The inside lining of the colon can become darkened oftentimes from laxative use but it is a benign finding seen on colonoscopy. ...Read moreSee 1 more doctor answer


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Separate names with a comma.
Discussion in 'Landscape Architecture and Design' started by Landrus2, Oct 3, 2010.
are they worth the money. around here they go for $3100
I got mine for $2,799
I've used a walk behind blower a couple of times and it just didn't seem to work for what I do.
If the piles get too big with a blower, then I just use a tarp. Or, I'll take my little simplicity mower with the bagger blade and push them around that way.
Regardless with the process, I always bag the yard when I'm done just to clean it up completely, so having a few leaves left behind isn't a big deal.


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Product Description: This cute small bag can be taken over as a sling bag and even can be hold in a hand to show-off. The color of this bag is very eye catchy and it is the best accessory a girl can carry.
Product Detail: Material: PU
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Width: 10.2(inch)
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Color: Navy Blue
Bag Size: Small
Width (cm): 26.5
Height (cm): 20
Depth (cm): 11.5
Strap Length (cm): 131
Handle Drop (cm): 8.5
Weight (Kg): 134.50000000
Outside zip pocket(s): One
Inside zip pocket(s): Two
Inside open pocket(s): Two
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Achillion Pharmaceuticals, Inc. (NASDAQ:ACHN)
Barclays Global Healthcare Conference
March 13, 2013 8:00 am ET
Milind S. Deshpande - Chief Scientific Officer and President of Research & Development
Unknown Analyst
Good morning. My name is [indiscernible], I'm the U.S. biotech analyst here at Barclay's. So I welcome everyone to the first session of the second day of our conference. I'm very pleased to announce that our next presenting company is Achillion Pharmaceuticals. And then presenting for the company is the Dr. Deshpande, Chief Scientific Officer of the company. Milind?
Milind S. Deshpande
Thank you, and good morning. My name is Milind Deshpande, and I'm the President of R&D and Chief Scientific Officer at Achillion Pharmaceuticals. It is my pleasure to present to you, to give you an overview of our HCV pipeline and strategy.
During my presentation, I will be making some forward-looking statements. There are some risks and uncertainties associated with these statements, and these are fully disclosed in our SEC filings.
The current treatment for hepatitis C is interferon-based, and there are -- aside from the suboptimal activities that is seen with this interferon-based treatments, there are severe side effects that are associated with these treatments such as, severe rash as well as anemia. Our goal in developing our portfolio for treatment of hepatitis C is to deliver an all-oral interferon-free regimen. And we have 2 combination regimens, which are in Phase II clinical trials, that we are currently evaluating for treatment of hepatitis C. The first combination is of sovaprevir, which is an NS3 protease inhibitor and ACH-3102, which is an NS5A inhibitor. We envision that this combination will be used for -- broadly used for treatment of genotype 1, as well as other genotypes. Because of the high barrier to resistance that is provided by ACH-3102, we are also evaluating a very simple combination of ACH-3102 plus ribavirin for treatment of genotype 1b. This combination also currently is in Phase II clinical trials. Aside from these 2 combinations that we are developing for our treatment of HCV, we also have a next-generation protease inhibitor, which is, ACH-2684, which has completed Phase I clinical trials.
HCV is a global disease that affects about 170 million people. There are 6 different genotypes or subtypes of hepatitis C virus, and the distribution of these different subtypes is shown on this particular slide. Genotype 1a is the predominant subtype or genotype of HCV that is found in the United States, where about 60% of the patient population is infected with genotype 1a.
Genotype 1b is the predominant subtype, and is found in Japan as well as certain parts of Europe. Genotype 3 is found predominantly in Russia and some other parts of Eastern Asia, and genotype 4 is predominantly found in Egypt.
Aside from the diversity that is seen in the HCV virus itself, there is a significant diversity in patients also. There are multiple factors that are seen in patients that affect the treatment outcomes. Stage of the liver disease are -- if some patients have advanced liver disease or cirrhosis, that tends to affect the outcome of the treatment. About 10% of the patient population is also co-infected with HIV. And for HIV/HCV co-infected patients, there are multiple drugs, or these patients are on multiple concomitant medications, elevating the importance of drug-drug interactions. And this is one important aspect that I'll touch upon as we look at our portfolio of HCV compounds.
So aside from the diversity in the virus itself, there are numerous factors in patients that affect their treatment response. And as I'll discuss in the next few slides, our portfolio is well-suited to address the diversity in the virus, as well as the complexity in patients that is observed in this particular disease.
Because of the multiplicity of the viral subtypes, as well as the varied responses that are seen in patients, we believe that the HCV market is ideally suited for segmentation. Subsets of patients can be treated with different regimens. For example, genotype 1b is an easier to treat patient population and can be addressed with a very simple treatment regimen. Genotype 1a and patients with advanced liver disease are difficult to treat, as well as patients who have had prior experience with interferon are also difficult to treat. Comorbidities, as well as co-infection with HIV, as well as the stage of the liver disease, also play an important role in treatment outcomes. So we believe that ability to launch regimens that are tailored to specific geographic needs, different HCV subtypes, as well as different patient populations is going to be important as different treatment regimens are brought to the market to treat hepatitis C.
So if you look at our development strategy, our base case scenario is that a combination of NS5A inhibitor, such as ACH-3102, plus protease inhibitor, which is sovaprevir, with pegylated [ph] ribavirin, will be able to treat genotype 1 as well as, other genotypes. This is the base case scenario for our value proposition.
Aside from treating different genotypes, because of the high barrier that is provided by both 3102, as well as sovaprevir, we believe that this combination is also ideally suited to address different types of patient factors that we discussed earlier, such as patients with cirrhosis, as well as patients that are co-infected with HIV.
I briefly mentioned that ACH-3102 provides a high barrier to emergence of resistance. We were not able to generate resistance with ACH-3102 in genotype 1b. And based on that finding, we believe that a combination of ACH-3102 and ribavirin will be able to deliver sustained viral response in genotype 1b. We see this as an upside scenario for our base case value proposition, where we are developing a combination of NS5A and a protease inhibitor.
We are also actively engaged in developing these 2 compounds in combination with other direct-acting antiviral agents, and we believe that these collaborations, represent a value-added scenario to our portfolio.
In today's presentation, I'll go through our strategy for the base case, as well as the upside in our portfolio, which is talk about the development of sovaprevir in combination with 3102, as well as 3102 by itself for treatment of genotype 1b.
Since the presentation of the first clinical data for NS5A inhibitors, going back in 2008, there has been very active interest in pursuing NS5A inhibitors as a component of the backbone of the combination treatment. NS5A inhibitors display pico-molar activity against HCV. Another attractive feature of NS5A inhibitors is that these compounds intervene at multiple stages in viral life cycle. They block viral secretion, they block HCV RNA synthesis and they also reduce the stability of HCV RNA. Because these compounds intervene at multiple stages in HCV life cycle, one of the hallmarks of NS5A inhibitors is that you see a very rapid decrease in HCV RNA. Our "The Phase I Decline" which is seen in the first 24 to 48 hours is very profound, and if not for any other reason, just for this reason, I think NS5A inhibitors will continue to play a very important role in treatment of HCV. However, the main challenge for NS5A inhibitors has been a low genetic barrier to resistance. The baseline amino acid variants in NS5A protein confer resistance to inhibitors, and as a consequence of that, on-treatment rapid emergence of resistant variants are seen when patients are exposed to NS5A inhibitors.
So our goal in designing the second-generation NS5A inhibitors was really to identify a compound that provided a high barrier to resistance, while maintaining the pico-molar activity that is seen with NS5A inhibitors. And that was accomplished by making 2 key changes to the structure of first-generation inhibitors. The first change was in the core structure or in the central part of the NS5A inhibitors, where we modified that core structure, and to go along with that, we also modified the "end pieces" to NS5A inhibitors. ACH-3102 was optimized to retain activity against these resistant variants. And the activity was optimized due to the 2 key changes that I just highlighted. The first change was in the core structure of the molecule and the second change was to the end pieces or the end groups of first-generation NS5A inhibitors.
ACH-3102, in it's Phase I clinical trials was dosed up to 14 days in healthy volunteers. The compound was safe and well-tolerated up to 1,000 milligrams. And as you'll see in subsequent slides, the therapeutic dose of ACH-3102 is either 50 milligrams or 75 milligrams. So we have established a significant safety margin from the Phase I studies that were done with ACH-3102, where we dosed it up to 1,000 milligrams.
ACH-3102 clearly demonstrates a biphasic elimination. The first phase of elimination is about 25 to 30 hours, and the terminal elimination phase is about 250 hours. About 90% of the drug is eliminated from the body within the first 24 to 48 hours, and about 10% of the drug is eliminated at a much lower rate, resulting in a long terminal half-life.
In HCV-infected patients we treated, we used doses of 50, 150 and 300 milligrams. So a single dose of ACH-3102 was administered to genotype 1a treatment-naive patients. And with all these doses, we achieved an average of 3.74 log reduction in HCV RNA, and this is clearly profound. So a single dose of 3102 gave us very robust reductions in HCV RNA.
Not shown on this slide is the genotypic analysis that we completed with some of the -- with all -- actually, all of the patients that were treated with ACH-3102, and it was very gratifying to see that ACH-3102 did retain activity against some of the key resistant mutations that confer resistance to other NS5A inhibitors, for example, the L31M mutation. In all the Phase I studies, including the proof-of-concept study, ACH-3102 was safe and well-tolerated.
Because of the unique virology of ACH-3102, i.e. the high barrier to resistance that ACH-3102 provides, which is actually not seen in any of the other NS5A inhibitors, we decided to undertake a study where we are now testing ACH-3102 in combination with ribavirin for 12 weeks in genotype 1b patients.
There are 3 groups in this ongoing study. In the first group, we are treating ACH-3102 with a loading dose of 225 milligrams and 75 milligrams for the rest of the treatment duration, plus wave-based ribavirin for 12 weeks. This cohort is completed and I'll show you the results from this particular cohort. There are 2 additional cohorts that we will undertake after a full analysis of this first cohort. The key objectives of this study were to establish 12 weeks of safety and tolerability. Since this is the first 12-week treatment that we are evaluating with ACH-3102, it was important for us to see the safety and tolerability of this drug. We also wanted to see if the high barrier to resistance that we saw in all our preclinical studies would translate into a clinical study. And finally, we also wanted to evaluate the ability to achieve SVR4 and SVR12 with a single DAA NS5A inhibitor in combination with ribavirin.
The patient demographics from this trial are fairly straightforward. Majority of the patients were male, majority of them were caucasian, majority of them were slightly on the heavier side and the HCV RNA median was 6.43 logs at baseline.
The next slide shows the study status as of last month. There are 3 subjects who completed our 12-weeks of dosing and we have SVR4 data for these subjects, and the other subjects are in different stages of their treatment regimen. And in the next few slides, I will summarize the data for all these patients in terms of their antiviral response.
Overall, if you look at the efficacy of ACH-3102 plus ribavirin, 8 patients completed our 4-weeks of dosing, so we are looking at RVR, and 6 out of 8 patients achieved RVR, that is HCV RNA levels were less than 25 international units per mil, that is 75%. So 75% of the patients achieved RVR. 3 patients have not completed end-of-treatment, and all 3 subjects had undetectable HCV RNA after 12-weeks of dosing. So at this time, the end-of-treatment response is 100%, and these 3 same -- and same 3 subjects have SVR4 data and these 3 subjects also are undetectable 4 weeks after completing the treatment regimen. So SVR4 is also 100%.
What was really instructive for us to see in this particular trial? Well, there were 2 things. One is the response on a weekly basis in these patients. That is, we monitor the reduction in HCV RNA on a weekly basis, and it was good to see the rapid reduction in HCV RNA in the subjects that were enrolled in this trial. And the second important aspect was the clinical virology that came out from this trial. We were very much interested in looking at whether 3102 provides a high barrier to emergence of resistance. So not seeing viral breakthrough while on treatment was an important aspect of this study.
So in the next 4 slides, I'll walk you through the individual patient data that we have in terms of reductions in HCV RNA. This slide shows the reductions in HCV RNA for the first 3 subjects who completed 12-weeks of dosing and achieved sustained viral response. What we see in these subjects is a very rapid reduction in HCV RNA. By week 3, these subjects are undetectable. They don't have HCV RNA that can be detected by the current sensitivities of the assay, and the viral suppression is maintained throughout treatment duration. So again, we did not see viral breakthrough with these patients and we see sustained viral response up to 4 weeks after completion of dosing.
The next 3 patients, again, we see very rapid reduction in HCV RNA in these patients. By week 4, all 3 patients achieved undetectable HCV RNA, again indicating the potency of ACH-3102. In these patients, again, we did not see any viral breakthrough while on treatment, which highlights that 3102 does provide a high barrier to emergence of resistance and we are eagerly awaiting response from these patients as they continue treatment with ACH-3102.
It's important to note that one of the subjects here, which is shown in blue, this subject had the highest baseline viral load. So this subject came in, had about 12 million copies of HCV RNA at baseline. And as we know, one of the factors that affects treatment outcomes in HCV-infected patients is the amount of viral load. So it was, again, very gratifying to see that a patient with a very high viral load at baseline achieves undetectable HCV RNA by week 4.
The last 2 patients that I'll discuss are very interesting. These 2 patients did not achieve undetectable HCV RNA, as I showed for the previous 6 patients, but nonetheless, both these patients are responding to treatment. We have not seen viral breakthrough, and so the question was why is it that these patients have a slow response as compared to the other 6 patients that I showed you early on? And the answer to that is in the clinical virology that we are completing for these patients. So this patient, which we refer to as patient E, has demonstrated clear [ph] log reduction from baseline to week 1, but after that, the sloping HCV RNA reduction is tapered.
Baseline sequencing for this particular subject demonstrates that this subject has at least 3 simultaneous substitutions at baseline. We are now completing the phenotypic analysis for this particular subject. But what we are seeing is that, again, this patient has at least 4 mutations at baseline, which is a fairly unusual situation. And the probability of a subject having 4 mutations, linked mutations, at baseline to an NS5A inhibitor prior to exposure is highly unlikely.
The same point can be illustrated with the next subject that I'm going to discuss, which is patient F. This patient had a slow response to ACH-3102. And again, we have not seen any viral breakthrough with this particular subject. What was really interesting with this subject is that, when we completed the baseline sequencing or completed the clinical virology at base line, this patient had 6 mutations that confer resistance to NS5A inhibitors. More importantly, the mutations at L31M and the Y93H mutations were present 100% at baseline. So this patient did not have any wild-type virus coming into this clinical trial, which is a very, very unlikely situation. And at this time, we cannot rule out the possibility that this patient may have had prior exposure to another NS5A inhibitor before enrolling in this trial. But the good news is that, even with these 6 mutations that confer high level of resistance to other NS5A inhibitors, we are seeing a continued decrease in HCV RNA with ACH-3102. We have not seen viral breakthrough in any of the patients that have been treated with ACH-3102, which again supports our thesis that ACH-3102 does provide a very high barrier to emergence of resistance.
So if you take a broader view in terms of what we are learning from this trial, as I mentioned earlier, this is the first trial that we are doing where we are exposing 3102 for 12 weeks, and so far, ACH-3102 appears to be safe and well-tolerated. The second important question for us was does ACH-3102 provide on-treatment, continued viral suppression and does it provide a high barrier to resistance? And based on the individual viral kinetics that I showed you early on, we do see very rapid viral suppression, indicating that ACH-3102 is indeed a very potent direct-acting antiviral agent. We have not seen any viral breakthrough or relapse to date, again, indicating that 3102 provides a high barrier to resistance. And we are seeing continued viral progression [ph] in presence of multiple NS5A resistant mutants, again, supporting our thesis that ACH-3102 is unique as compared to the other NS5A inhibitors that are currently in development. And the final question is can ACH-3102 plus ribavirin, in a 12-week treatment regimen, provide a high barrier to resistance? And the answer to that is yes, so far.
So moving on to outside [ph] scenario, where we are evaluating a combination of protease inhibitor and ACH-3102 for treatment of genotype 1 broadly. Before I go there, I would just like to briefly capture some of the key characteristics of ACH-1625. As I mentioned, this is a protease inhibitor that provides, again, a high barrier to resistance. This is a once daily drug that does not require boosting and has minimal potential for drug-drug interactions. We did a 12-week trial with sovaprevir in combination with peg/riba and the results from these trials indicate that 1625, in combination with peg/riba, provides SVR12 at 80% -- 80% to 85%, depending on the dose that is used.
So we have 2 compounds in our portfolio now, which are 1625, a protease inhibitor, and 3102, which is an NS5A inhibitor. And the base case in our value proposition is that development of 3102 and sovaprevir, in combination with ribavirin or without ribavirin, for treatment of genotype 1 patients. The Phase II trials with this combination will begin second quarter of this year, and there are multiple Phase II trials that we are undertaking from now and about 15 months. And these trials, in these trials, we will be exposing about 500 patients by third quarter of 2014, and the first results are expected in summer of 2013 from this particular combination.
In terms of capitalization, we are very well-funded. We have about $220 million in cash. And our top 5 shareholders are listed on this slide. We have a number of milestones that are coming up in 2013, which include data from 3102 and ribavirin, as well as data from sovaprevir and NS5A combination.
So to summarize, based on the compounds that we have in our portfolio, as well as the strategy that we have put in place, we believe that we are well-positioned to provide therapies for different HCV patient populations, as well as different HCV genotypes. We will be reporting clinical trial results throughout 2013, and our goal is to rapidly advance optimal treatment regimens and to compete globally in this very important HCV market. Thank you.
Unknown Analyst
Thank you very much, Milind. The breakout session will be held at the New York [indiscernible] room, which is across from your hallway.
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Obit - Willie "Bill" Popp
Expand Messages
- Victoria Advocate, 1 Jul 2008
LOUISE - Willie Edward "Bill" Popp, 92, passed away on June 30, 2008. He was born on June 20,1916, in Hillje to the late Edward and Pauline Kainer Popp. He was an honorary member of the Louise Volunteer Fire Department.
He is survived by his wife of 69 years, Ruby Kainer Popp of Louise; daughter-in-law, Shirley Popp of Louise; three grandchildren, Robin Sless of Louise, Michelle "Peanut" Nunnelly and husband Gary of Sheridan, and Kendra Charbula and husband Scott of Louise; six great-grandchildren, Dustin Sless and wife Catherine of El Campo, Destiny Sless of Beeville, Justin Lipinski of El Campo, Jessica Lipinski of Sheridan, and Colby and Clayton Nunnelly of Sheridan; and one great-great-grandson, Daylan Wayne Sless of El Campo; and a sister, Rosalie Popp Hlavaty of Hillje.
He was preceded in death by his parents; sons, Warren Popp in 1972 and Wayne E. Popp in 2006; sisters, Mary Kovar and Annie Popp; and brother, Frank Popp.
Visitation will begin on Tuesday from 2-5 p.m. at Triska Funeral Home. A rosary will be held on Tuesday at 7 p.m. at St. Andrew's Catholic Church in Hillje. Funeral services will be on Wednesday at 2 p.m. at St. Andrew's Catholic Church with the Rev. Clement Quainoo. Burial will follow at St. Andrew's Cemetery.
Pallbearers will be Philip Huvar, Paul Feagin, Clarence Kovar, Norbert Popp, Larry Hlavaty, Dwayne Courville, Raymond Poncik, and James Heard.
Honorary pallbearers Joe Henderson, Jay Heard, Jimmy Trojcak, Cecil Sanchez, R.J. Strnadel, Jr., Steve Henderson, Mike Prasek Sr., Larry Knebel, and Donald Huvar.
Memorial donations may be made to St. Procopius Church or Louise Volunteer Fire Dept.
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News, Interviews, Live Streams, Upcoming Events, Tweets..
Tuesday, October 25, 2016
Donald Trump Rally in Tallahassee, FL - Oct 25, 2016
8 comments:
- AnonymousOctober 25, 2016 at 10:13 PM
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My friend Mr.Donald J.Trump for presidentReplyDelete
tu sera le président des états unis d'amerique avec succès mon ami Donald J.TrumpReplyDelete
- AnonymousOctober 26, 2016 at 7:41 AM
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- AnonymousOctober 26, 2016 at 7:45 AM
TRUMP USED ALL CAPITAL LETTERS IN HIS TWEET-NAUGHTY-NAUGHTY-VOTE FOR TRUMP!ReplyDeleteReplies
- AnonymousOctober 26, 2016 at 2:22 PM
MSM: It has been proven by the Wikileaks emails and the videos that Hillary lies, cheats and steals and much more, but we have breaking news that Donald Trump used all capital letters in his tweet and we must bring in our panel to discuss this for an entire week because writing in all caps is not presidential. This post was all in fun, but not too far from what the MSM is doing. VOTE TRUMP AND BRING SOME SANITY BACK TO AMERICA.Delete
The Trump Tsunami is on the way!ReplyDelete
- AnonymousOctober 26, 2016 at 6:19 PM
In Germany today was reported that children ages around 5 yrs. old were taught to memorize ALLAH AKBAR and recite a Muslim prayer today. Also in England a Muslim immigrant with 6 wives and 23 children will receive over 300,000 a year in govt. benefits for his family...NO WONDER England HAD BREXIT...we must too. VOTE THE ELITES OUT TODAY .this kind of giveaway is probably why our National debt is so high...and not just because of refugees or big Muslim families but also because of all illegal immigrants that must be taken care of by the govt. of the USA ... the sheer volume of dependents , non-citizens, must be staggering...and we don't know what the current amount is....this increasing cost to our already huge welfare and entitlement programs must be why we are failing.today they reported that England's people are more concerned about increasing immigration than they are of the E.U. WE MUST BE CONCERNED TOO ABOUT HILLARY'S PLEDGED 550 % increase in Syrian refugees if she wins..get out there if you can and work for Trump...go Trump.ReplyDelete


text:
Nuclear factor I-A represses expression of the cell adhesion molecule L1
The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression.
We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse
Our findings suggest that NFI-A, in particular its brain-specific isoform, represses
Neural adhesion molecules of the immunoglobulin superfamily mediate cell-cell recognition by homo- or heterophilic Ca2+-independent cell surface interactions
In the control region of the mouse
Plasmid constructs
The L1 reporter plasmid L1-11
The CMX expression plasmid coding for β-galactosidase
Cell culture
Mouse neuroblastoma cells (N2A) were maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum, 1 mM sodium pyruvate, 2 mM L-glutamine, and antibiotics (100 units/ml penicillin and 100 μg/ml streptomycin). For reporter gene assays, N2A cells were grown in Opti-MEM without phenol red (Invitrogen, Karlsruhe. Germany) supplemented with 5% fetal calf serum, 200 units/ml of penicillin G, and 200 μg/ml streptomycin. Chinese hamster ovary cells (CHO) were grown in Glasgow minimum essential medium (GMEM), which contained 10% fetal calf serum, 4 mM L-glutamine, and antibiotics (100 units/ml penicillin and 100 μg/ml streptomycin). All cell types were grown at 37°C under a 5% CO2 atmosphere.
Electrophoretic mobility shift assays (EMSAs)
For EMSAs, HA-NFI-A constructs were expressed in CHO cells. Cells were plated onto 90-mm dishes in CHO culture medium. After reaching confluence, cells were washed once with CHO culture medium without serum and antibiotics. Transfections were performed with Lipofectamine (Invitrogen) according to the manufacturer's instructions. Per dish, 13 μg of the respective plasmid were transfected with 26 μl Lipofectamine and 39 μl Plus Reagent (Invitrogen). Three h later, the transfection reaction was stopped by addition of 6.5 ml CHO culture medium. 24 h after transfection, cell monolayers were washed once with PBS and harvested by scraping into PBS supplemented with Complete protease inhibitor (Roche). Cells were pelleted by spinning for 10 min at 4°C (300 × g), the supernatant was removed and the pellet resuspended in low salt lysis buffer (20 mM HEPES pH 7.8, 100 mM NaCl, 5 mM DTT, 1 × Complete protease inhibitor (Roche)). The cell suspension underwent three freeze-thaw cycles in dry ice/ethanol. Cell debris were removed by centrifugation (15 min, 4°C, 15000 × g), and the supernatant was used for DNA binding analysis. The electrophoretic mobility shift experiments were essentially performed as described
Oligonucleotides used were as follows: L, 5'-gctatTTGGCTTGGTGCCAAgcatc-3'; Lc, 5'-gctatTTCGCTTGGTGCCAAgcatc-3'; N, 5'-aggtCTGGCTTTGGGCCAAgagccgc-3'; Nc, aggtCTCGCTTTGGGCCAAgagccgc-3'; SIS, 5'-agcttaccagaaggtcaaggtcaaatgaagctagct-3' Sequences corresponding to the NFI binding site are capitalized; mutations in the negative control oligonucleotides are shown in boldface. The sequence of one strand is shown after the fill-in reaction.
Western Blot
In order to check HA-NFI-A expression by Western Blot, transfection of CHO cells was performed as described for EMSAs. However, 6-well plates were used, with DNA amounts and volumes of media and reagents adjusted accordingly. 24 h after transfection, cells were lysed by incubating in Ripa buffer (50 mM Tris pH 7.4, 150 mM NaCl, 1 mM EDTA, 0.5% (w/v) NP-40, 1 × Complete protease inhibitor (Roche)) for 1 h at 4°C. Cell debris were removed by centrifugation (15000 × g, 4°C, 10 min). The supernatant was mixed with sample buffer and boiled for 5 min. Proteins were separated by SDS-PAGE, transferred to a nitrocellulose membrane, and immunologically detected as described (Kalus
Chromatin immunoprecipitation assay (ChIP)
Myc-tagged NFI-A expression for ChIPs was carried out in N2A cells, cultivated on 90-mm dishes until confluency. 13 μg of the respective plasmid were transfected with 26 μl Lipofectamine and 39 μl Plus Reagent (Invitrogen) per dish according to the manufacturer's instructions. 48 h later, ChIP analysis was essentially performed as described
Luciferase-based reporter gene assays
For transient transfections, 1 × 104 mouse neuroblastoma (N2A) cells were seeded in 96-well tissue culture plates (Greiner, Frickenhausen, Germany) and transfected the next day with 2.5 μl Lipofectamine 2000 (Invitrogen) per microgram of DNA. 80 ng reporter plasmid (L1-11), 60 ng of the effector plasmids (pCHBNFI-A or pCHBNFI-Am) or control CMX plasmid coding for β-galactosidase were applied per well. EGFP fluorescence generated by cotransfection of 60 ng pEGFP-C3 (Clontech, Heidelberg, Germany) was determined after 48 hours with a Wallac 1420 Multilabel Counter (PerkinElmer, Wiesbaden, Germany). Luciferase activity was measured with the Bright-Glo Luciferase Assay System according to the manufacturer's instructions (Promega, Mannheim, Germany). Light emission was normalized to the level of EGFP fluorescence activity from the EGFP control plasmid. Transfections were generally performed in septuplicate. Average relative luciferase light units and standard deviations were calculated using the Prism-4 program (GraphPad Software, La Jolla, CA, USA).
Identification of a full NFI binding site in the first intron of the mouse
To ask whether NFI-A binds to the murine
Figure 1
The regulatory region of the mouse
The regulatory region of the mouse
NFI-A binds to the regulatory region of the mouse
To assess binding of NFI-A to the full NFI recognition motif in the
Figure 2
Expression of HA-tagged NFI-A isoforms in CHO cells
Expression of HA-tagged NFI-A isoforms in CHO cells. A, Schematic drawing of the brain-specific isoform ("NFI-A bs") and the ubiquitous "standard" isoform ("NFI-A st") of mouse NFI-A. The isoform-specific N-termini (
Figure 3
NFI-A binds to its full binding site in the mouse
NFI-A binds to its full binding site in the mouse
Figure 4
In competition experiments, the L oligonucleotide was more effective than the N oligonucleotide (Fig.
The brain-specific isoform of NFI-A binds to the regulatory region of the mouse
To ask whether the interaction between NFI-A and its binding motif in the mouse
Figure 5
NFI-A binds to the
NFI-A binds to the
NFI-A represses activity of the
For a functional analysis, the effect of forced NFI-A bs expression on the activity of a previously described L1-luciferase reporter construct, L1-11
Figure 6
NFI-A represses mouse
NFI-A represses mouse
The cell adhesion molecule L1 plays a crucial role in mammalian nervous system development, but regulation of its expression at the transcriptional level is only partly understood. Here, using EMSA and antibody supershift experiments, we showed that the site-specific transcription factor NFI-A specifically interacts with a full NFI recognition site in the first intron of the murine
ChIP analysis confirmed that the brain-specific isoform of NFI-A (NFI-A bs) binds to the regulatory region of the mouse
In order to understand how binding of NFI-A to the
How could NFI-A activity at the
Interactions with other site-specific transcription factors might also regulate transactivation/transrepression by NFI-A. NFI proteins physically interact with TTF-1
In summary, our data suggest that NFI-A is a repressor of mouse
Authors' contributions
TS designed and performed experiments shown in Fig.
We thank Ute Süsens and Peggy Putthoff for expert technical assistance. Pekka Kallunki (H. Lundbeck A/S, Valby, Denmark) generously provided us with L1-luciferase reporter constructs. The galactosidase plasmid was a gift of Ronald M. Evans (Salk Institute, La Jolla, CA, USA). This work was supported by the European Union program "Role of CAMs in ageing", QLK6-CT-1999-02187 (to M.S.), and the German Federal Ministry of Education and Research, project no. 0311762/8 (to M.S.).
Neural cell recognition molecule L1: relating biological complexity to human disease mutations
The role of L1 in axon pathfinding and fasciculation
Tissue-specific expression of the L1 cell adhesion molecule is modulated by the neural restrictive silencer element
The neural restrictive silencer element can act as both a repressor and enhancer of L1 cell adhesion molecule gene expression during postnatal development
Characterization of Pax-6 and Hoxa-1 binding to the promoter region of the neural cell adhesion molecule L1
A binding site for homeodomain and Pax proteins is necessary for L1 cell adhesion molecule gene expression by Pax-6 and bone morphogenetic proteins
L1, a novel target of beta-catenin signaling, transforms cells and is expressed at the invasive front of colon cancers
Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons
Roles of the NFI/CTF gene family in transcription and development
Nuclear factor one transcription factors in CNS development
Expression patterns of the four nuclear factor I genes during mouse embryogenesis indicate a potential role in development
Purification of a RAS-responsive adenylyl cyclase complex from Saccharomyces cerevisiae by use of an epitope addition method
The genes for transcription factor nuclear factor I give rise to corresponding splice variants between vertebrate species
Disruption of the murine nuclear factor I-A gene (Nfia) results in perinatal lethality, hydrocephalus, and agenesis of the corpus callosum
Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors
Domains of ERRgamma that mediate homodimerization and interaction with factors stimulating DNA binding
Cofactor dynamics and sufficiency in estrogen receptor-regulated transcription
Analysis of multiple forms of nuclear factor I in human and murine cell lines
The proprotein convertase PC5A and a metalloprotease are involved in the proteolytic processing of the neural adhesion molecule L1
Identification of DNA binding-site preferences for nuclear factor I-A
The transcription factor nuclear factor I mediates repression of the GLUT4 promoter by insulin
Regulation of brain fatty acid-binding protein expression by differential phosphorylation of nuclear factor I in malignant glioma cell lines
Nuclear Jak2 and transcription factor NF1-C2: a novel mechanism of prolactin signaling in mammary epithelial cells
Nuclear factor I/thyroid transcription factor 1 interactions modulate surfactant protein C transcription
The Oct-1 POU homeodomain stabilizes the adenovirus preinitiation complex via a direct interaction with the priming protein and is displaced when the replication fork passes
DNA binding and transcriptional activation by the Ski oncoprotein mediated by interaction with NFI
CREB binding protein coordinates the function of multiple transcription factors including nuclear factor I to regulate phosphoenolpyruvate carboxykinase (GTP) gene transcription
The Transcription Factor NFIA Controls the Onset of Gliogenesis in the Developing Spinal Cord
Specific glial populations regulate hippocampal morphogenesis
Committed neuronal precursors confer astrocytic potential on residual neural precursor cells
Nuclear factor I isoforms regulate gene expression during the differentiation of human neural progenitors to astrocytes
NFIA haploinsufficiency is associated with a CNS malformation syndrome and urinary tract defects


text: Blastertal was a company that engineered a war so they could make a profit selling the viewing rights. When Bernice Summerfield learned of this, through the illegal acquisition of records at the Braxiatel Collection, she became a contestant on Blastertal's game show Eat the Poor, sabotaged their equipment, and sent out a transmission of the records. The populace of Collasac rose up against Blastertal. (PROSE: Something Broken)


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(952) 545-3953
Rental History Reports
23 years in business701 5th St S
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BBB File Opened: 05/20/2003
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Home > Product Categories > Pro-Audio > Microphones > Condenser Microphones > 2200A II C
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The sE2200a II C (Cardioid) replaces the best-selling and multi-award winnning sE2200a large diaphragm condenser mic from sE Electronics.
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China pledges more reform on tourism development
- Posted by Newsdesk
- On 30th July 2015
- arlt, china, reform, tourism
China will carry out more reforms to boost investment and consumption in tourism industry, the State Council, or China's cabinet, decided on July 29, 2015 according to a statement released after an executive meeting of the State Council presided over by Chinese Premier Li Keqiang.
In the statement it is confirmed that "Tourism development is significant in fostering the country's modern service sector. ... Better and colorful tourism activities will enrich people's life, and also boost economic development."
The meeting urged improving tourism consumption including the construction of regional airports especially in less-developed central and western China.
Public-private-partnerships (PPP) in developing tourism projects will be promoted with more government investment and individual capital participation.
Prof. Dr. Arlt, Director COTRI: "The statement is another example of the increased level of attention the current Chinese government is paying to tourism, including domestic, inbound and outbound as a way to boost consumer spending."


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text: Harry Lawrence General information Occupation(s) Actor Matrix role Old Man Other works Flirting Outback [Source]Harry Lawrence is an Australian actor who portrayed the Old Man in The Matrix. Contents[show] FilmographyEdit The Matrix 1999 Flirting 1992 Outback 1971 Adam's Woman 1970 Retrieved from "http://matrix.wikia.com/wiki/Harry_Lawrence?oldid=29758" Ad blocker interference detected! Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers Wikia is not accessible if you've made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected. Categories: Actors Add category Cancel Save


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Read our pocket guide to Verbier
Verbier: A pocket guide
One of the most popular ski resorts in Europe, Verbier is one that has kept its charm and traditional style village despite its ever growing popularity and indulgent luxury chalets.
Gorgeous Chalets & Fabulous Skiing
Verbier offers a wide choice of exclusive catered chalets and luxury ski hotels. Verbier is home to some of the best off-piste skiing in the world and is primarily focused on intermediate and advanced grade skiers. The resort lies in a sunny, south-facing valley with stunning panoramas of the surrounding summits. It is also the largest and most popular resort of the 4 Vallées ski region, linking with other resorts including Nendaz, Veysonnaz, Thyon and La Tzoumaz.
Great Events & Excellent Shopping
Aside from skiing, Verbier hosts many annual events. Not to be missed is the Freeride World Tour, Xtreme Verbier, at the end of March. If you buy one thing on your visit to Verbier, make sure to visit Surefoot. The boutique, in Verbier town centre, is a custom-made ski boot designer. Offering a snug and perfect fit for your feet, Surefoot ensures that you ski to the best of your ability.
For food, there are a couple of stellar restaurants to choose from.Restaurant Fer à Cheval is always full with locals, seasonaires and holidaymakers. It has a cosy and lively bar and bistro upstairs and quieter seating downstairs. Chalet d'Adrien has the only Michelin Star in the centre of Verbier, and offers a beautiful variety of locally inspired fine dining and stunning views. Book in advance.


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Personal Property only being conveyed. Convenience of in-town living, close to shopping and medical facilities. This year round mobil home is in a desirable area just off Hwy 47 in Arbor vitae in Hiawatha Mobile Home Estates a 55 and over park. The home is in an estate and the sellers are saying that the home can be sold, "as-is" with all items currently on the property at the time of the offer including furnishing and tools, etc. The property is being sold with two garages one adjoining and one across the street.The montly dues are $300 which include plowing, garbage removal road maintenance, sewer, water. Just minutes from town conveniences, bike trails, etc. Affordable living can be yours.
Features Residential
|Style: Other
|Lake Chain:
|Garage: 2 Car, Detached, Multiple Garages
|Lake Name:
|Year Built: 1979
|River Name:
|Basement Type: None
|Water Frontage (feet): 0
|Fin SqFt Total: 980
|Lake Size-Acres: 0
|Lot Size: 0
|High School: ON Lakeland Union
|Site Influence: 55+ Community, Easy Access, Recreation Nearby, Senior Oriented, Shopping Nearby
|School District: Lakeland UHS
|Construction: Manufactured/Mobile


text:
Nice photos of your upper teeth!
The upper teeth should be able to be straightened using Invisalign or braces.There is quite a bit of teeth overlap, and, consequently, a fair amount of movement has to occur. That means a longer amount of time! That said, we can't see your lower teeth in the photos. So, we are giving you a partial answer based on the available information.


text:
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Questions 31-40
In the context of global oil prices, "Brent crude oil" is frequently referred to in the news. What does this term imply?
1. It is a major classification of crude oil.
2. It is sourced from North Sea.
3. It does not contain sulphur.
Which of the statements given above is/are correct?


text:
Aqua Mundo at Les Bois-Francs
Whatever your age, you'll be sure to have fun in total safety. Enjoy being splashed in the Water Tree, watch out for the current and the bends in the Wild Water Slide and the other slides. Everything is there to ensure that you have a really great time.


text:
1997 was a memorable year in many ways. The National Championship and Charles Woodson's Hesiman campaign highlight the year. One moment in particular that year was against Michigan State, and Woodson made a statement.
Michigan held a 13-7 lead against Michigan State late in the third quarter. The Spartans quarterback, Todd Schultz was facing pressure during a routine throw-away pass. Little did Schultz know that Woodson was lurking in the area. Woodson soared to make an unbelievable one-handed interception. A play that certainly helped Woodson's Heisman hopes.


text:
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Description: From one of America's iconic writers, a stunning book of electric honesty and passion. Joan Didion explores an intensely personal yet universal experience: a portrait of a marriage- and a life, in good times and bad- that will speak to anyone who has ever loved a husband or wife or child. Several days before Christmas 2003, John Gregory Dunne and Joan Didion saw their only daughter, Quintana, fall ill with what seemed at first flu, then pneumonia, then complete septic shock. She was put into an induced coma and placed on life support. Days later- the night before New Year's Eve- the Dunnes were just sitting down to dinner after visiting the hospital when John Gregory Dunne suffered a massive and fatal coronary. In a second, this close, symbiotic partnership of forty years was over. Four weeks later, their daughter pulled through. Two months after that, arriving at LAX, she collapsed and underwent six hours of brain surgery at UCLA Medical Center to relieve a massive hematoma. This powerful book is Didion's attempt to make sense of the " weeks and then months that cut loose any fixed idea I ever had about death, about illness . . . about marriage and children and memory . . . about the shallowness of sanity, about life itself,"""
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List price: $26.95Copyright year: 2005Publisher: Knopf Doubleday Publishing GroupPublication date: 10/4/2005Binding: HardcoverPages: 240Size: 5.50" wide x 8.00" long x 1.00" tall Weight: 1.034Language: English
Born in Sacramento, California, on December 5, 1934, Joan Didion received a B.A. from the University of California, Berkeley in 1956. She wrote for Vogue from 1956 to 1963, and was visiting regent's lecturer in English at the University of California, Berkeley in 1976. Didion also published novels, short stories, social commentary, and essays. Her work often comments on social disorder. Didion wrote for years on her native California; from there her perspective broadened and turned to the countries of Central America and Southeast Asia. Her novels include Democracy (1984) and The Last Thing He Wanted (1996). Well known nonfiction titles include Slouching Towards Bethlehem (1968), The White Album (1979), The Year of Magical Thinking (2005) and Blue Nights (2011). In 1971 Joan Didion was nominated for the National Book Award in fiction for Play It As It Lays. In 1981 she received the American Book Award in nonfiction, and was nominated for a National Book Critics Circle Prize in nonfiction for The White Album. Didion has received a great deal of recognition for The Year of Magical Thinking, which was awarded the National Book Award for Nonfiction in 2005. In 2007, Didion received the National Book Foundation's annual Medal for Distinguished Contribution to American Letters. In 2009, Didion was awarded an honorary Doctor of Letters degree by Harvard University. On July 3, 2013 the White House announced Didion was one of the recipients of the National Medals of Arts and Humanities presented by President Barack Obama.
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Give Now
Charles Dickens' Mystery of Edwin Drood sings and dances
...a mostly light hearted atmosphere with occasional serious moments and even a bit of irony...
With name recognition of the show and the rising reputation of IU's musical theatre program, Chicago was sold out two weeks before opening night.
There was always something to look at while you listened.
Characters rendered with all those little dots, literally step out onto the stage in sharp detail.
Playing "Sunday in the Park with George" is no picnic!
The fine acting, very good singing and spirited dancing are a testament to the growth of IU's BFA Musical Theatre program.
"What I'm after in our summer offerings is to really making a festival." Artistic Director Jonathan Michaelsen
"We wanted to bring a 'here and now' approach...".Contemporary Dance Director Elizabeth Shea
The IU Theatre opens their season with the American tribal love-rock musical 'Hair,' in a production directed by Patti Wilcox.


text:
Fort Siloso
Website: www.sentosa.com.sg
Address: 33 Allanbrooke Road, Sentosa Singapore 099981
Getting there:
Take the MRT to HarbourFront MRT Station (NE1/CC29).
Take Sentosa Express monorail in Vivo City (Level 3) or Sentosa Bus at Harbourfront Interchange to get to Sentosa. On Sentosa, take either the Blue or Red Line buses, or the Siloso Beach Tram.
Contact: (+65) 6736 8672
Operating Hours:
Daily from 10am - 6pm (Last entry 5.30pm).
Get a real taste of World War Two at Fort Siloso, the only preserved coastal fortress filled with both indoor and outdoor exhibitions, and catch a glimpse of Singapore's colonial past as soldier at the site sought to protect Singapore's precious harbour. Enjoy free guided tours and tram rides and explore old tunnels, discover original guns, cannons, film clips and old photographs in-depth, and catch a glimpse of the life led by the soldiers of yesteryear. Serious history buff and war enthusiast can also get their hands on pieces of 1940s military collectibles and souvenirs at the QuarterMaster Store. View Fullscreen Map
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Email us at email@example.com
PolyTable SUPER12
Hi my name is George Merrill I have designed and produced turntables since 1979. I enjoy seeing the smiles on peoples face when they are swept away in a musical presentation. The concerns and feedback from many would be audiophiles is the cost of excellent equipment. My goal has always been to provide the best possible performance at a price that is affordable. Over the years my Energy Management designs have been the cutting edge. Some of the innovations include: Fluid Damped Motor, Oilwell bearing, Constant Resonant Tuning System, Periphery clamping ring and Spectrum analyst resonant tuning. If you are looking for a music reproduction system that will send the goose bump factor through the roof, you must start with the heart of the system, the turntable.
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text:
Available ebook formats: epub mobi pdf rtf lrf pdb txt html
Mitchell Willie's love of the written word was born the day he saw his first book. Since then, his love of good stories and the art of storytelling has never waned. A member of the National Forensic League, Willie is a student of acting, music, literature, and language. He enjoys cooking, classic science fiction, a good cup of tea, and speaking out in favor of the power of imagination and literacy. From reading with his grandmother as a child, to penning fiction in his Kentucky home, Willie continues to, in his words, "bleed ink."


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Discussion in '1969-1972 K5 Blazer | Truck | Suburban' started by chevyin, Jan 9, 2007.
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