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August 12, 1985- Japan Airlines flight 123 left Tokyo, Japan at around 6:10 in the evening, fourteen minutes later at an altitude of twenty four thousand feet, and three hundred knots, an explosion, oscillations, and cabin decompressions was heard and captured on the plane's on board recorder. The captain on duty was seated at the right side of the plane and his co-pilot, who was at that time training for promotion to be a captain, was sitting on the left seat.
A few moments later, the captain signals an SOS on the transponder and suggests that the flight return to Tokyo.
The airplane went down to twenty two thousand feet and went on doing violent movements; the plane, for about two minutes was doing a Phugoid, or longitudinal motion and rolls. The captain and his co-pilot were helpless and had no means in controlling the airplane's heading through the usual flight control inputs. Their only way of limited control is done through thrust differentials.
The plane was able to maintain an altitude of twenty two thousand feet and two hundred and fifty knots for an approximate duration of twenty minutes.
At around 6:39 in the evening, the main landing gear was deployed which caused the erratic movements of the plane to intensify. The plane then did a controlled turn to the left while descending to eight thousand feet. Erratic movement of the plane meanwhile, continue. At 6:47 PM, the plane was in a mountainous area, the plane increased power, and they were at five thousand and three hundred feet. The flaps of the plane were extended at 6:51 PM that caused the roll angle of the plane to be sixty degrees, the crew starts to move the flaps and increase thrust.
The plane was at ten thousand feet when it began a nose dive at a very fast eighteen thousand feet per minute. The crew countered this by lifting the nose. 6:56 PM – the airplane crashed at the mountains on an altitude of five thousand feet and three hundred and forty knots. Roughly forty six minutes since take-off and thirty two minutes since the decompression. Boeing, as owners of the plane, are somehow responsible for the crash but definitely they are not the only ones to blame and do not deserve to be blamed in entirety.
Part of the responsibility lies with Japan Airlines who maintains the plane. In fairness to Boeing, they have provided specific repair instructions to the plane that was not followed by those who were responsible for the repairs. The plane had previously suffered damage to the bulkhead in 1978 but was not repaired properly. As stated in the report, "The initiation and propagation of the fatigue cracks are attributed to the improper repairs of the bulkhead, conducted in 1978, and since the fatigue cracks were not found in the later maintenance inspection, this contributed to the accident.
" (Aviation Safety Network, 2008). Boeing did its part by providing proper instructions but their failure to see to it that they were carried out properly contributed to the crash which makes them partly guilty of neglect. There was confusion on the rescue operation, A US owned helicopter was the first at the scene, about twenty minutes after impact. The US chopper in turn, informed Yokota Air Base and offered backup. But the US helicopter was ordered to return to base because Japanese forces were to handle the mission.
Poor visibility at the crash site prompted the Japanese team to report that there were no survivors and made it impossible to land. Thinking that there were no survivors the rest of the rescue team waited till the next morning to check out the site. But there were survivors, reports show that injuries on the bodies found imply that they survived the crash but were not given immediate medical attention which caused their deaths.
If the helicopter pilot hadn't reported abruptly that there were no survivors, there could have been.
Aviation Safety Network. (2007).
Applying Lessons learned from Accidents. from: http://aviation-safety. net/database/record. php? id=19850812-1 Air Disaster. com (n. d).
Special Report: Japan Airlines 123. from: http://www. airdisaster. com/special/special-jal123. shtml Jackson, H. (1985). 524
Killed in worst single air disaster. from: http://www. guardian. co. uk/fromthearchive/story/0,,1017027,00. html
Cite this essay
Japan Airlines Flight 123. (2016, Aug 28). Retrieved from https://studymoose.com/japan-airlines-flight-123-essay


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Albert Hammond Jr has said The Strokes will release a new album before they tour again.
The guitarist previously stated that the band, who are onfirmed to make their live return at the Governors Ball Music Festival in New York on June 7, will hopefully record a new album next year (2015).
Speaking to Gigwise about the band's live dates and hopes for new material, the guitarist revealed that he expects there will be a new album before the band embark on a full tour again.
"I know that when The Strokes tour again, it will be because we put something out – even though we didn't tour the last one," he says. "Doing a few festivals before you put something out is kind of gearing up the big machine, it just kind of helps everyone get ready, mentally, financially and it brings you back to your audience. You can see the audience's reaction to your music and you just 'feel' again."
Speaking about the Governors Ball show, Hammond continues: "I think it was just that Julian was trying to figure out his solo thing and I don't know when he's doing it, but we got this offer and we all agreed on it – but more importantly he agreed on it. He's the leader of the band, and we usually say yes to playing shows. I imagine that'll start something, it always does but it's just too soon. He's swamped with his solo stuff and I can't even begin to stress him out with, like, 'What are doing?' I know he's singing a song that we recorded and he's in the studio trying to do something, so we'll see."
Albert Hammond Jr is currently on tour in UK and he has been playing material from The Strokes' 2013 album 'Comedown Machine' in his set. Fan footage of him playing 'One Way Trigger' at Newcastle's O2 Academy 2 on May 6 can be seen here.
Albert Hammond Jr's UK tour continues throughout May. He will play:
Oxford O2 Academy 2 (May 9)
Birmingham Glee Club (11)
Nottingham The Bodega (12)
Bristol Fleece (13)
London Village Underground (15)

subset: commoncrawl


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Additionally, refinances for FHA and VA loans jumped by 11 percent. The average contract interest rate for 30-year fixed-rate mortgages with jumbo loan balances (greater than $484,350) decreased to.
Today's Mortgage Rates and Refinance rates. 15-year fixed-rate jumbo 4.375% 4.391% 7/1 ARM Jumbo 4.125% 4.649% Rates, terms, and fees as of 8/24/2018 10:15 AM Eastern Daylight Time and subject to change without notice. Select a product to view important disclosures, payments, assumptions, and APR information. Please note we offer additional home loan options not displayed here.
Offers custom fixed-rate loan terms that are between eight and. and adjustable home loans and mortgage refinancing, as well as jumbo loans and home equity financing. Pros Embraces FHA-backed home.
Where you're planning to buy your home can play a role in what kind of loan is best for you. FHA and conventional loan guidelines allow wide latitude for borrowers in expensive areas, but in some.
"Because mortgage rates have recently fallen and home price growth. The Jumbo and Conforming MCAIs are a subset of the.
Data suggests differences in jumbo loan rates are about twice as high each day as they are for conforming loans, so check lender rates carefully. Keep in mind too that sometimes – as has been the general case for the past five years – interest rates for jumbo loans are actually slightly lower than for conforming loans.
This allows our clients to avoid the tighter loan guidelines and higher rates and costs generally associated with Jumbo loans including options with less than 20% down. At a glance: The current single-family conforming loan limit for most counties in Washington State is $484,350 (an increase over the 2018 cap of $453,100).
Putting 20 Down On A House fha vs conventional loan conventional fha Q: I have good credit of about 730. I meet the requirements for both FHA and Conventional 97.I plan to live in the home for 6+ years. Which has lower payments and what is the difference between the FHA loan and conventional loan?*In February 2019, according to Ellie Mae. Which loan is right for me? Choosing between an FHA or conventional mortgage remains a personal decision. luckily, you can make it easier to decide by taking a long look at your income, financial assets, immediate spending needs and the type of home you'd like or are willing to consider.The scheme involved a lady convincing her 20 boyfriends to buy her 20 new iPhone 7s, which she then sold for enough money to put a down payment on a house. Using the pseudonym Proud Qiaoba, a blogger.
FHA and conventional loan guidelines allow wide latitude for borrowers in expensive areas, but in some cases you may end up needing a jumbo loan, which is bigger. on the insurer the lender uses..
Fha Arm Loan 2019 FHA HOME LOAN GUIDELINES AND REQUIREMENTS – FHA.co – fha adjustable rate mortgage. adjustable rate mortgage, on the other hand, is an option where the interest rate is not fixed beforehand. An introductory period is determined, such as 3 or 5 or 7 years for which the interest rate remains the same.
MBA: Mortgage applications decline as economic uncertainty grows – "Government refinances provided a bright spark, picking up over 10%, as both FHA and VA refinancing activity. The average contract interest rate for 30-year fixed-rate mortgages with jumbo loan.
This lender offers conventional, FHA, VA and jumbo loans along with fixed or adjustable rates. 580 minimum credit score required for FHA; 620 for VA and conventional. Fast, online application.


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Schools of the Future
Save the date for the SOTF annual conference on October 3-4, 2019 at the Hawai'i Convention Center. Join teachers and administrators from Hawai'i's public, private, charter and parochial schools as they focus on how to best transform our existing schools and create new learning environments for the 21st Century.
This collaborative event is presented by the Hawai'i Association of Independent Schools, the Hawai'i Department of Education and the Hawai'i Community Foundation in partnership with the Pillars of Peace Fund of the Hawai'i Community Foundation and the Hawai'i Society for Technology in Education to highlight the best practices that are taking place in our learning environments today and being planned for those of tomorrow.
For more information: SOTF 2019 Conference
Three lucky teachers won the Digital Media Kits that HENC awarded in the Digital Media Playground at the SOTF Conference on Nov. 4, 2015:
Teacher: Deb Anderson
Teacher: Kapiʻolani Nee
Teacher: Elena Chan
Each kit had a value of just under $1,000 and is being treated as one of the Hawaiʻi Schools Digital Media (HSDM) grants for the 2015/16 school year.
According to the organizers of the Digital Media Playground, more than 150 teachers visited the playground on Nov. 4 and participated in all four of the digital media "stations" (Olelo, PBS, Kamehameha Schools, and Hiki No) to learn about the various aspects of digital video production and the HSDM grant program.


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Softball Pitching Tool Pennsylvania
Compete at a Higher Level
Big league players and coaches attest to the effectiveness of Armtrak as a Softball Pitching Tool for Pennsylvania athletes. Armtrak allows players to perfect the proper throwing motion to gain command of the ball, balance, and achieve top velocity. Most importantly, Armtrak will assist your arm to remain healthier for a longer period of time.
How it Works
Simply set up Armtrak to practice to keep your arm's throwing motion within the natural arm track lanes. Armtrak will prevent or break bad throwing habits. Best of all, Armtrak may extend a player's career by preventing unnecessary stress to a player's joints.
Whether it's practice or in games, young players often do not use proper throwing techniques. This is a big concern with young kids in Pennsylvania . Armtrak can safeguard athletes from harming themselves from improper throwing techniques and protect both their bodies and careers. This device is specially designed to develop a fluent movement when throwing which will reduce stress and prevent injury.
Take Control of the Field
Armtrak is the first portable and patented Softball Pitching Tool invented to teach athletes of all ages a proper and repeatable throwing motion. Invented by former Major League pitcher and professional pitching instructor Fernando Arroyo, Armtrak helps develop muscle memory to increase speed and accuracy when throwing.
Armtrak is the world's only sturdy Softball Pitching Tool of its kind and provides a visual aid for athletes to use while perfecting their throw. By giving Pennsylvania athletes a visual indicator of where they should be throwing, Armtrak allows training to be more engaging and results more noticeable.
Armtrak is a simple to set up, easy to use Softball Pitching Tool that provides striking results. This device teaches career saving techniques while increasing performance. If you would like more information on how Armtrak can change your game, please contact us today!
In your area:
- Softball Pitching Tool Wisconsin
- Softball Pitching Tool Colorado
- Baseball Pitching Tool North Carolina
- Baseball Pitching Trainer North Carolina
- Softball Pitching Aid North Carolina
- Softball Pitching Tool North Carolina
- Softball Pitching Trainer North Carolina
- Baseball Pitching Aid Arizona
- Baseball Pitching Tool Arizona
- Baseball Pitching Trainer Arizona
Perfect Your Throw
Sports legends achieved their stardom through mastering the basics and applying them in game situations. Armtrak teaches the fundamentals of throwing regardless of your individual role on the field. This device will ingrain the user with the basics of a fluent and effective throw so they can compete at a higher level on the field. Of course, results will vary with level of dedication.
Armtrak provides athletes of all ages the opportunity to obtain game changing results through career saving techniques. The device allows the user to perfect their follow through and delivery with reduced stress on the arm. Armtrak is simple to set up, fun to use with outstanding results.


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Form 990 – Not Just a Tax Return
Blog by Dan Billingsley, Vice President of External Affairs
Your 990 is not just a tax return, it is an important tool to tell a story about your nonprofit. And while it presents important financial information, it's a way for the public to engage with your organization.
Financial Tool
The 990 is a financial overview of your organization's fiscal stability. Over time (say three to five years), it can give the public a picture of your growth, changes in funding and increases in your programmatic cash outlay. This gives donors a perspective of your organization that helps to paint a picture beyond just your program descriptions and outcomes.
Transparency Tool
Most importantly, the 990 is your organization's tool for transparency. It lets the public know about your governance, your fiduciary position, and so much more. Your board list is public, your highest salaries are listed, expenditures on your programs are outlined, and if you lobby, that information is available to the public. Schedules within the 990 also let the public know if you have related staff and board members, those salaries, whether or not you compensate board members, etc. We recommend that you post at least three years of your 990s on your website even though these documents are also regularly available through Guidestar.
Marketing Tool
Many of us don't realize that the 990 is actually a good marketing tool for organizations. We can use it to not only describe our programs, but link those outcomes to the financials within those 990s. In addition to our annual reports, websites and other materials, the 990 can give even greater perspective of program effectiveness and efficiencies with the information contained within its dense pages.
One Caveat
A 990 is not exactly "easy to read" which is why nonprofits should be educating their staff and board about what is within their pages. However, the general public doesn't normally understand how to read a 990 which is why you should also pull out pertinent information from the document and put it into something easy to understand for the general public (such as percentages of administrative, fundraising and program expenses along with explanations).
We encourage you to come to our 990 trainings so that YOU can learn more about this most important financial tool!


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Music City USA (U S A, 80 min)
Directed by: Chris McDaniel
Written by: Chris McDaniel
Chris McDaniel
Nashville, currently based on music, wasn't always Music City. Find out how this printing and Insurance mecca became the music capital of the world, and see how the devastating flood of 2010 tried to get them down, but thanks to this thriving music community, a city was reborn. Resilience in the form of the artists, entertainers and musicians that put the MUSIC in MUSIC CITY. This documentary begins by showing you what Nashville used to be. Why Nashville was settled and how she grew into such a rich cultural town. From the Opry to the current superstars of ALL kinds of music, Nashville boasts the greatest musicians and recording studios on earth. Country superstars call Nashville home, but non country musicians have been recording there for years; Lionel Richie, Air Supply, Tesla, The Wailers, Brett Michaels, Queen of Rock a billy Wanda Jackson and more, none of which have country roots, but all make a point to call Nashville their recording homes. From Gospel to Bluegrass and Rockabilly to Country, heartland's music has been generated here, but the days of country being the only influence are long gone. Rock superstars like The Black Keys, The Kings of Leon, and Jack White of the White Stripes all call Nashville home. These musicians helped a city pull together after the flood of 2010 and I feel that this story is not only important and educational, but a must see for anyone that believes in the empowering qualities of art, music and creativity.


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Boyce, Ralph Edward, Jr.
Birth: Tuesday, August 28, 1951 in Washington, D.C.
Residence: Waldorf, Maryland
Death: Wednesday, September 07, 2016 at the age of 65
Condolences: Click to View or Post
Ralph Edward "Ed" Boyce Jr., of Waldorf, Maryland died on Wednesday, September 7, 2016 at his home. He was 65 years old. In addition to his father, Mr. Boyce was preceded in death by his wife of 42 years, Mary Ruth Boyce.
Born on August 28, 1951 in Washington, DC, he was the son of Mary Kathryn "Kitty" Boyce and the late Ralph Edward Boyce Sr. Mr. Boyce was an automotive painter and worked with several car dealerships until his retirement. He enjoyed hunting, crabbing, and being around his family and friends. He was a devoted father and grandfather.
And in addition to his mother, he is survived by his daughters Christina Washington, Brenda (Keith) Curtis; sons Wayne (Michelle) Boyce and Eddie Boyce; siblings Kathy Campbell and Russ (George Smith) Boyce; grandchildren Frank, Jewel, Gabby, Ciera, Morgan, Lil Wayne, Bella, Jasmine, Victoria and Marcus; great grandchildren Frank Jr., Adrian, Damien and Stiles; his loving companion Peggy Cannon; lifelong friend/brother Billy (Tammy) Arnold.
A visitation will be held on Saturday, September 10, 2016 from 2:00 PM until 4:00 PM with Services to begin at 4:00 PM at the Raymond Funeral Service, P.A. 5635 Washington Avenue La Plata, MD 20646. Interment will be private. In lieu of flowers, memorial contributions may be made to the Go Fund Me Account set for Mr. Boyce at https://www.gofundme.com/2gph3ec?pc=em_co_dashboard_a or to Hospice of Charles County 2595 Davis Road Waldorf, MD 20603. Arrangements by Raymond Funeral Service.


text: Hey all....Welcome to the NEW Savage Soldiers Open Recruiting Thread SAVAGE SOLDIERS 2.0... UPGRADED AND READY TO KICK A%# About us: We are a close bunch of friends that like to play games and have fun. We maintain a clan of both Wii players and PS3 players. We DO NOT welcome drama here. If you like to cause problems, this is not the place for you. We have open recruiting with only a few minor requirements that must be met. There are no tryouts or applications, we ask that you register on our site ( http://WWW.SAVAGESOLDIERS.NET ), read the rules outlined there and post up an intro. Come and play a few games with us and you're in. We are a self financed clan (paid for by the owners) who own and maintain our own internet forum site. We laugh and play and joke around and do not care if you are 15th prestige or 1st...We do not care if you have a 2.9 kdr or a 0.25 kdr. If you are looking to get serious and mad at the game then look elsewhere...here at dollar dollar you will find all sorts of different people with all sorts of different idea on what fun...we welcome them all (as long as you stay withing the rules of fair play as explained below) YOU MUST BE AT LEAST 17 YEARS OLD TO JOIN..... Our most important rule is the one that we insist be met is to always under all circumstances, enjoy the game. We are a fun and happy clan who enjoys the relaxation and stress relief that these games bring us....if you're not enjoying it...stop playing it! Please post up here and then come see us on our site http://WWW.SAVAGESOLDIERS.NET


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What Is A Partial Knee Replacement
If it's not broke, don't fix it. That could be a mantra for younger people with knee arthritis who are reluctant to undergo major joint replacement surgery. "A lot of people are resistant to doing a knee replacement. They want an alternate that will relieve their pain and keep them more functional," says Dr. John Kagan, orthopedic surgeon on Lee Memorial Health System's medical staff. The solution they seek may be a less traumatic procedure. An alternative option, a partial knee replacement restores only the side of the knee damaged by arthritis. "The knee joint is comprised of three compartments. When you do a total knee replacement you replace all three compartments. When you do a partial knee replacement you replace one compartment, usually the inside compartment. Basically what you're doing is going to the involved area, removing a small amount of bone and resurfacing it with metal and plastic. Rather than cutting both sides of the joint, removing the ligament or possibly two ligaments," says Dr. Kagan. With a third of the impact, it restores the knee to full function. The partial or unicompartmental replacement is performed surgically through a small opening. The downsized option also shrinks recovery time. "Whereas a regular knee replacement might take 4-6 weeks, the partial knee replacement takes 2-4 weeks," says Dr. Kagan. For people who have normal knee function and arthritis in only one compartment, a partial knee replacement may be a step in the right direction. View More Health Matters video segments at leememorial.org/healthmatters/ Lee Memorial Health System in Fort Myers, FL is the largest network of medical care facilities in Southwest Florida and is highly respected for its expertise, innovation and quality of care. For nearly a century, we've been providing our community with everything from primary care treatment to highly specialized care services and robotic assisted surgeries.


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GP Bikes beta18c available!
Started by janaucarre, October 04, 2017, 12:19:52 PM
Quote from: Verdi on February 10, 2018, 05:23:58 PMI have the same problem. Bought the sim today, so still figuring everything out; mod bikes are also invisible to me and almost any mod I download makes my game crash.I will figure things out at some point tho Sorry if I posted this on the wrong thread btw. Just glad I'm not alone with my troubles.[edit] I have figured out how it works! I was not downloading the tyres! (should I delete this post?)


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Join us for our Community Hub every Tuesday in the Radley Room from 11.30am to 3pm.
The Community Hub was born out of the regular lunches that we served at St George's during the months after the floods of December 2015 for those who had had to leave their homes or were affected in any way by the trauma of that time. We were so inspired by the new friendships that were made with our neighbours then that we decided to continue holding community lunches and drop-ins regularly at the heart of our local community.
Everyone is welcome with lots of games and other activities on offer or just the opportunity for a good chat with friends.
Lunch is served between 11.30am and 1.30pm.


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Located in an established and well maintained middle to upper class neighborhood, this residence is a rancher home, wi...View Property
Close to Shopping & Dining
This charming residence is a modern home with pale pink coral siding in a quiet, established middle to upper middle cl...View Property
This home is in a well-established neighborhood with mature landscaping. The homeowner is from the southwest and the h...View Property
Not all available homes and rooms are shown here. Call or complete a reservation request and let us find the perfect room for YOU! Furnishings and décor may have changed since pictures were posted.


text: B2B Telemarketing – 6 Top Tips for success!B2B Telemarketing – 6 Top Tips for success!Despite the notion that Telemarketing is a dinosaur that it is being replaced by email and social media, we find that many businesses (including our own) still rely on the telephone for lead generation purposes.B2B Telemarketing and lead generating after all, has a very different dynamic than that of B2C. However, it is still difficult to get right. Getting it right has a lot to do with the decision-maker.Doesn't it drive you crazy when… There isn't a business owner out there that doesn't give a cold call short shrift – who's got the time? And doesn't it always get your back up when –Someone you've never heard of says 'Hi, how are you doing today?' Seriously??They speak too quickly, rattling off a tonne of information leaving you feeling like you don't know who they are, what they do or why they rang you.They assume you're dying to spend money with them.They assume you're a complete idiot and they're here to save the day.They get a bit shirty when you close the call insisting you are not interested.We've all been there, and sometimes we are still there. However, there is a better way, one that can help to make lead generation more successful.6 Top Tips for Effective Telemarketing CallsSo here it is, sound, tried and tested advice in no particular order –Know who you are talking toIt's overlooked, but the more you know about the person you are talking to the better. What are their problems, obstacles and requirements? How does what you are offering help them? But how to go about finding out? –Targeted DataBy far the most effective use of your Telemarketing time is having good quality data. Data you can rely on to be clean and up-to-date. Data that you can closely target your audience with. This means that you know that you are going to be talking to the right person in the right industry about what you do.'Manners maketh man'Be courteous. Not curt, nor with saccharine platitudes. Just good old-fashioned manners. It will get you a lot further'What's it all about Alfie?'Don't witter. What you are doing is passing on information that might be of benefit to the person you are talking to. So be informative but succinct. Believe in what you are talking about, know it inside out and how it advantages the person you are talking to.ChillOur dogs chillingThe last thing you want to do is take up any more of their valuable time than is necessary, but speak slowly and clearly – it will take up less time in the long run, cause less irritation and might get you further.'It's good to talk'Lead generation is about starting a conversation, the first steps in any relationship. Always remember who you are talking to. What is there industry? What are their challenges? It also helps to be clear about what you wish to achieve from this conversation – their agreement for you to send further information or to set up a meeting.The Bigger PictureHaving a lead nurturing strategy in place is key. When someone says 'no' it may not be definitive. Perhaps they might not need your product or service just at that moment, but that doesn't mean they never will. If you have targeted data that puts you in contact with people who will at some point need you, it's good to have a strategy in place that allows you to follow up with them without being a nuisance. Other Blogs that might Interest You (Click to Read)Do You Fear Talking to Prospects?Top 5 Telemarketing Tips to Ease the FearIn the Mix – Telemarketing's New Groove


text: Editing Jason Genao 0 You do not have permission to edit this page, for the following reasons: The action you have requested is limited to users in one of the groups: Users, FANDOM Staff, FANDOM Helpers, Wiki Managers, Content Team Members. Please log in to edit this wiki.Joining X-Men Movies Wiki is free, and it only takes a minute.We hope that you sign in, and become a member of the community!Click here to log in or create an account more + You can view and copy the source of this page: {{Actor |image = Jason_Genao_(Logan).png |movie =''[[Logan (film)|Logan]]'' |character = [[X-23]] }} '''Jason Genao''' is Dominican-American actor who portrayed [[Rictor]] in ''[[Logan (film)|Logan]]''. He currently plays Ruby Martinez on the Netflix original series ''On My Block''. ==External links== *{{WP}} *{{IMDb|# = 7535414}} Templates used on the current version of this page: Template:Actor (view source) Template:IMDb (view source) Template:WP (view source) Return to Jason Genao. Retrieved from "https://xmenmovies.fandom.com/wiki/Jason_Genao" Edit summary Preview Mobile Desktop Show changes


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The Shadow at the Edge of the World was the second story of the audio anthology, Charlotte Pollard: Series One. It was written by Jonathan Barnes and featured India Fisher as Charlotte Pollard and Michael Maloney as the Viyrans.
Publisher's summary Edit
The Ever-and-Ever-Prolixity has granted Charlotte Pollard her dearest wish and set her loose once more in time and space. But where has it brought her? Waking amid the minatory darkness of a forest floor, she has no notion of where she is, or when.
Welcomed at gunpoint and beset by danger, Charley finds herself immediately embroiled in a frantic struggle for survival. For there are perilous shadows in this night-time forest. There are hungry, watchful eyes. And there is something ancient also, something tracking her, something implacable and ruthless which knows Miss Pollard of old...
Plot Edit
to be added
Cast Edit
- Charley Pollard - India Fisher
- Viyran - Michael Maloney
- The Slaverings - Nicholas Briggs
- Susan Broadstairs - Abigail McKern
- Charity Savage - Nicola Weeks
- Emmeline Leigh/Viyran - Lucy May Barker
- Mrs Turnerman - Jacqueline King
References Edit
- Charley described the Slaverings as a "cross between a silver-backed gorilla and Mr. Hyde."
- Charley tells Charity that she learned never to give up from a "a man [she] knew a very long time ago."
Notes Edit
- This story was recorded on 11, 18, 19 and 20 November 2013.
Continuity Edit
- Charley refers to the British airship R101. (AUDIO: Storm Warning)
- Charley mentions that she has previously encountered people with psychic abilities. (AUDIO: Scaredy Cat, Something Inside, Memory Lane, Patient Zero)
- Charley tells the Viyran that she has already made the choice between death and spending the rest of her life as their prisoner. (AUDIO: The Lamentation Cipher)
- The message from the future Viyrans refers to the fact that Charley possesses the Lamentation Cipher. (AUDIO: The Lamentation Cipher)
External links Edit
- Official The Shadow at the Edge of the World page at bigfinish.com


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The World Super Bikes kicked off their season right here at Phillip Island over the weekend of Feb 22- 24 2019. With new colour schemes and rider combos as well to show to the world. Everyone was keen to see the new liveries and riders in action. With the action actually kicking off the Monday before the event, teams were already in Australia testing man and new machine at the Island getting dialed in for the action that lay ahead.
So when the actual event started on the Friday, everyone was ready and riders already dialled in for the track. It was going to be a cracker of a weekend ahead. Weatherwise it was a great low 20c day with cloud cover on the friday for FP1. It looks like things kicked off from last year, with Jonathan Rea leading FP1 in his Kawasaki Racing Team WorldSBK – Kawasaki ZX -10RR with a 1'30.341. 2nd was new comer to WSBK Alvaro Bautista, on the ARUBA.IT Racing – Ducati Panigale V4 R with a 1'30.362. Third was another Kwaka of Leon Haslam also on a Kawasaki Racing Team WorldSBK – Kawasaki ZX -10RR with a time of 1'30.499. Not much at all seperating the top 3!
Fp2 saw the same 3 but this time a different order. This time it was the Ducati of Alvaro Bautista in 1st, followed by the 2 Kawasakis of Rea and Haslam for the day! It certainly shaped up a great battle for the Superpole on Saturday!
Saturday and everyone was greeted by beautiful sunny weather and a nice breeze. Not that the riders will get to enjoy it as the battle for Superpole had to be decided. So with the riders setting off it was on for everyone! but only 1 can be at the top of the pile. So with Superpole continuing on from FP1 and 2 the same trio had locked out the top 3. With Alvara Buatista taking his first ever Pole in WSBK !! Rea and Haslam on their Kawasakis respectively in 2nd and 3rd.
It was Bautista on his Red rocket that blasted off into the distance leaving everyone in his wake. Winning the race by almost 15 seconds over Jonathan Rea's Kawasaki and Marco Melandri in 3rd on his Yamaha.
The Island had put on its best weather for the Sunday having already seen action packed racing, could it get any better? It seems Alvaros Ducati was on fire and no one could catch him, again winning the 10 lap Supersprint ahead of the Kawasakis of Rea and Haslam. With only 1 race left for the weekend, could Alvaro and Ducati make it a clean sweep?
Debutante Alvaro Bautista not only smashed everyone, he left em for dead and left everyone stunned for someone on his first appearance. The Ducati Panigale V4 R and Bautista made the perfect combo at Phillip island!! Again team mates Rea and Haslam left fighting for the scraps, but hauling valuable points.
"Thanks to Ducati and the whole team, because they have all worked so hard."
Round 2 sees the 2019 MOTUL FIM Superbike World Championship of to Thailand.
Enjoy the pics below.


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Erol CERASI,MD, PhD, DHC
Endocrine Services Department of Medicine
Hebrew University Hadassah Medical Centre
Jerusalem, ISRAEL
by E. Cerasi, Israel
The idea that type 2 diabetes (T2DM) is mainly due to insulin resistance stems from the 1930s, but became dominating from the 1980s. However, evidence since the 1960s indicates that insulin response to glucose is markedly diminished from the earliest signs of glucose intolerance. Insulin pump treatment induces near-normoglycemia in T2DM with doses similar to type 1 diabetes, indicating that hyperglycemia is caused by lack of insulin, insulin resistance acting as an amplifier. Insulin secretion is genetically controlled. T2DM risk gene polymorphisms hint toward mechanisms of reduced insulin secretion in diabetes-prone subjects, in whominsulin response decreases as the number of diabetic alleles increases. I hypothesize that the genetic background of the β cell determines its adaptation capacity to increased insulin demand imposed by augmented caloric intake and insulin resistance; failure to adapt eventually leads to T2DM. Therefore, I regard the "prediabetic" β cell as a normal cell with limited adaptability, diabetes risk being entirely context-dependent (nutritional load and insulin sensitivity). Once hyperglycemia is established, β cells are exposed to continuous nutrient stimulation, with consequent oxidative and endoplasmic reticulum (ER) stresses. The result is increasing functional deficiencies and β-cell apoptosis, hence reduced β-cellmass. Some of itsmechanisms are discussed. An intriguing as yet unanswered question is whether the mechanisms of β-cell deficit in the diabetic environment operate before hyperglycemia in overfed, insulin-resistant subjects. Therapeutic agents preventing β-cell oxidative and ER stress could stop the progression and perhaps initiation of T2DM.
The formal separation of type 1 diabetes as an autoimmune entity is of relatively recent date1; nevertheless, the heterogeneity of diabetes, as well as the fact that for some patients insulin treatment is a lifesaving procedure while others may more or less control their metabolic state with dietary or pharmacological means, has been known to clinicians and clinical investigators since long ago. As insulin became more widely used it also appeared that in many patients whom today we identify as typical type 2 diabetics, achieving metabolic control with insulin treatment was difficult, sometimes impossible. Thus, several decades before the insulin receptor and its signaling pathways were identified, an astute clinician such as H. P. Himsworth could write "…I would suggest the possibility of the existence of a type of diabetes due not to diminished secretion of insulin by the pancreas, but to a greater or less impairment of the organism's susceptibility to insulin."2,3 In short, the idea that diabetes may be the result of insulin resistance is not new. Indeed, the presence of obesity in the vast majority of patients with type 2 diabetes (T2DM) makes it a reasonable assumption that some degree of insulin resistance must exist in this disorder.
The striking advancements over the past three decades in the field of insulin action, including the detailed understanding of the molecular biology of the insulin receptor and its signaling pathways as well as of the regulation of glucose transporters, have naturally further attracted the attention of investigators to insulin resistance as a main pathophysiological factor in type 2 diabetes, sometimes presented as the sole factor. Thus, as recently as 2000, the Journal of Clinical Investigation stressed this by publishing a "Perspective" series entitled On diabetes: insulin resistance.4 Yet, many investigators demonstrated as soon as insulin immunoassays became available in the early 1960s that the insulin response to a glucose challenge is markedly reduced in type 2 diabetics, including in normoglycemic subjects with glucose intolerance (IGT) only.5-9 The adoption of dogmatic, monolithic views by many investigators of both "camps" did not facilitate the development of open-minded approaches to analyze the etiopathology of diabetes in its full physiological context, notwithstanding some balanced views10-12 pointing to the fact that the biology of type 2 diabetes is not simple, and that pure β-cell deficit or exclusive insulin resistance are rare events since in fact these two factors are interlinked, as would be expected from any closed-loop feedback regulatory system.
Insulin resistance, plasma insulin levels, and β-cell function
The variability of the insulin response to glucose as well as that of the sensitivity to insulin is remarkably large in the normal population.13-15 he obese, while insulin sensitivity is reduced and insulin response is augmented, variation is as wide, with considerable overlap with the levels of lean subjects. Thus, there exist substantial numbers of subjects with either a markedly low insulin response or a low sensitivity to insulin who nevertheless retain normal glucose tolerance. Indeed, at least 2/3 of obese subjects never develop IGT or type 2 diabetes; yet they are insulin resistant and hyperinsulinemic. In type 2 diabetic patients, except in its very severe forms, both fasting and postprandial plasma insulin levels are normal or higher than normal. This observation provides the rationale for insulin resistance in diabetes: if blood glucose remains high despite substantial levels of insulin, hormone action must be defective. This is a static view of a highly dynamic regulatory system, confusing cause and effect: what are "substantial" levels of insulin, ie, what degree of hyperinsulinemia is adequate for a given degree of hyperglycemia? Glucose vs insulin dose-response curves have been constructed from acute experiments (eg, see reference 16); however, lacking data on long-term experimentally induced hyperglycemia in normal subjects, how can we determine whether a given plasma insulin value in a chronically hyperglycemic diabetic is higher or lower than normally expected?
Figure 1. Fasting plasma insulin levels in 15 type 2 diabetic patients
prior to and following 6-month treatment with the sulfonylurea
gliclazide. Data calculated from reference 17.
Two examples strikingly demonstrate how lack of consideration for physiological regulation leads to erroneous conclusion. The first relates to fasting insulin concentration. Many investigators, including our group, find that the fasting plasma insulin level in type 2 diabetic patients is higher than normal; however, fasting glucose also is higher: does it contribute to the fasting hyperinsulinemia of the patient? In 15 mildly obese type 2 diabetics treated with the sulfonylurea gliclazide for 6 months we found that, in parallel with the normalization of blood glucose, the initially high fasting plasma insulin levels fell to the range found in weight-matched normoglycemic controls despite the use of the β-cell stimulator gliclazide17; this is illustrated in Figure 1. Thus, fasting insulin is also under the control of ambient blood glucose concentration. The second example relates to the bell-shaped insulin curve often used to describe changes in β-cell function during the fall of glucose tolerance from normal to IGT and T2DM. This is an artefact due to the use of 120-minute plasma insulin values in the oral glucose tolerance test (OGTT): patients with IGT having higher glucose levels throughout the test generate a strong signal for amplifying the secretion of insulin at a time when blood glucose is still high enough to stimulate the β-cell, resulting in a typical late insulin peak. In fact, if earlier (eg, 30 min) time points are chosen, the insulin response to OGTT shows a linear fall from normal via IGT to T2DM.18-20 In short, provided the plasma insulin data are interpreted with full reference to the physiology of regulated insulin secretion, it becomes clear that β-cell responsiveness to glucose is lower than normal in IGT, and even less so in T2DM.
Table I. Effect of continuous subcutaneous insulin infusion (CSII) treatment on fasting and postprandial blood glucose control in moderately obese type 2 diabetic patients (calculated from references 17, 21, and 22; Mean ±SEM).
Figure 2. Schematic illustration of the plasma insulin response to a hyperglycemic clamp, showing the gradual decrease in firstphase as well as second-phase insulin secretion as glucose tolerance deteriorates from normal to IGT and further to mild and advanced diabetes.
The above discussion does not mean that I negate the existence of insulin resistance in type 2 diabetic patients; the scientific literature is replete with data convincingly showing that insulin resistance is part of the pathogenesis of T2DM. Nevertheless, I remain convinced that T2DM is a disorder of insulin deficit, the input of insulin resistance to its pathogenesis increasing with the severity of obesity. To my mind, the best demonstration of the above was achieved in mildly obese type 2 diabetic patients treated with continuous subcutaneous insulin infusion (CSII). In pilot studies in 23 white patients, we could achieve fasting and postprandial normoglycemia with a mean daily insulin dose around 0.6 units per kg body weight.17,21 Similar results were obtained in a larger group of Chinese patients.22 The amounts of insulin administered through CSII in these studies were not strikingly higher than the doses routinely used in insulin pump–treated type 1 diabetic patients (Table I). Thus, a similar degree of insulin deficit seems to exist in both types of diabetes, which leads me to conclude that insulin resistance in T2DM is not the main factor inducing hyperglycemia.
β-Cell function during the development of type 2 diabetes
The earliest modifications of the insulin response to glucose that can be detected as glucose tolerance starts deviating from normal are the early or first-phase insulin response, and the physiological oscillations of secretion.5,6,8,23,24 The latter requires numerous blood samplings, and therefore has not gained popularity among clinicians and investigators. In contrast, early insulin response to glucose can be measured during oral or IV glucose tolerance tests; however, glucose clamps allow the most detailed definition of the kinetics of the plasma insulin response to glucose. The first-phase response is markedly reduced in subjects with IGT, and further diminishes as fasting hyperglycemia appears. At these stages of the disease, the later or second-phase insulin response to glucose is normal, but with the progression of the severity of diabetes also this phase collapses. These changes are schematically illustrated in Figure 2.
Low first-phase insulin response is found also in some subjects with normal glucose tolerance.5,6 Several studies over the past few years have demonstrated that a low insulin response is a predictor of future glucose intolerance and T2DM, both in lean and obese subjects belonging to various ethnic groups.25-27 In our study, lean and physically active Swedish subjects with normal glucose tolerance were followed for a mean period of 25 years; the only initial parameter that was significantly correlated to later glucose intolerance was first-phase insulin response corrected for insulin sensitivity (disposition index).25 These results are summarized in Table II (page 38).
What is the genetic/molecular basis of the low insulin response in nondiabetic subjects? Extensive studies over 4 decades in family members related or unrelated to diabetic patients, in-cluding in monozygotic twin pairs, have shown that several aspects of the insulin response to glucose in man are under strong genetic control.28-31 However, it is only now that we are gaining some insight into the possible cellular mechanisms that may be responsible for the decrease of β-cell function in subjects at risk of developing diabetes. Indeed, the numerous whole genome association studies that have been performed over the past decade have identified allelic variants of several genes, mostly involved in β-cell development, function and survival, that collectively participate in the risk of diabetes development. As the number of risk alleles that a subject carries increases, several aspects of β-cell function deteriorate; most pertinently, the insulin response to oral or IV glucose decreases in proportion to the number of risk alleles.32,33
Table II. Prediction of the 2-hour blood glucose concentration
during OGTT in 269 healthy lean subjects after a mean of 25 years.
performed 25 years later.
Abbreviations: (ΔI5/ΔG5)/HOMA-IR: glucose-induced insulin response measured at 5 minutes of a glucose clamp, corrected for HOMA-IR; HOMA-IR, homeostasis model assessment of insulin resistance; NS, nonsignificant; OGTT, oral glucose tolerance test.
Modified from reference 25: Alvarsson et al. Diabetologia. 2005;48:2262-2268. © 2005, Springer-Verlag.
By which cellular mechanisms these risk alleles impair insulin secretion is not known. However, recent findings from Gloyn et al suggest that, at least regarding the highest-risk gene, transcription factor 7–like 2 (TCF7L2), the association of insulin granules with the voltage-gated calcium channels in the β may be disturbed, thus reducing the efficiency of the insulin exocytotic machinery.34 stands to reason that within a short space of time, the mechanisms of low insulin response to glucose, which is a strong risk factor for T2DM, will be fully clarified at the molecular level.
Progression of diabetes and deterioration of β-cell function: decrease in cell function or cell mass?
It has been the experience of most clinicians that as the duration of diabetes increases so does the severity of the disease. This old observation has received its scientific approval through the United Kingdom Prospective Diabetes Study (UKPDS): whatever the treatment modality chosen, the level of HbA1c increases with time (for a review, see reference 35). However, it is also the experience of most clinicians that, whatever the treatment modality chosen, induction of strict normoglycemia throughout the day over a period of years in type 2 diabetics is nearly impossible; therefore, it is not clear whether T2DM is an inherently progressive disorder due to the nature of its pathogenesis, or whether progression is secondary to the unregulated metabolic state which reflects our inability to provide adequate treatment (the latter is my belief, entirely unproven). Whether primary or secondary, the progression of diabetes is paralleled by the progressive decline of β-cell function, as measured by the plasma insulin response to glucose35 (see Figure 2 also). Plasma insulin may decrease either because β-cell function, ie, the function of individual β cells, is reduced, or because the number of β cells declines, ie, β-cell mass is reduced.
_ Is β-cell mass reduced in type 2 diabetes?
There is consensus that some degree of β-cell mass reduction does occur at some stage in T2DM,36-38 but there is also considerable disagreement as to the extent of the reduction and its significance for diabetes development. Presently the dominating view, most strongly advocated by the Butler group in Los Angeles,37 is that β-cell mass is markedly reduced already at the stage of IGT, a further deficit being apparent in overt diabetes even if treated only by diet. By contrast, studies in Europe36,38 find considerably less reduction in β-cell mass. It has to be stressed that real β-cell mass was calculated only by Rahier et al,38 while Butler et al37 measured β-cell area, which reflects β-cell mass less adequately. Perhaps more importantly, the Rahier laboratory in Brussels points to the extraordinarily wide range of β-cell masses
both in the diabetic and nondiabetic groups, with the existence of major overlap between the hyperglycemic and normoglycemic subjects. These observations make it difficult to ascribe a definitive role to reduced β-cell mass in the genesis of hyperglycemia. Obviously, it may be argued that the hyperglycemia of the patient should have driven β-cell mass to increase substantially as a compensatory mechanism, which is not observed.
To gain some insight into the dynamics of β-cell mass changes during the development of diabetes, we utilized an animal model of nutrition-dependent type 2 diabetes, the gerbil Psammomys obesus. These animals have an inborn insulin resistance, but retain normal glucose tolerance under caloric restriction; when given a diet with circa 40% higher calories and low fiber content, they rapidly become hyperglycemic.39 Figure 3 shows that as the animals develop hyperglycemia, they rapidly lose pancreatic insulin stores, since the cells are forced to secrete all their insulin granules in the face of the unrelenting hyperglycemic stimulation. Nevertheless, β-cell mass remains normal for a considerable period; it even increases slightly due to increased β-cell proliferation induced by the high glucose levels.39 β-Cell mass collapses only after prolonged diabetes, with severe worsening of the hyperglycemia (so-called end-stage diabetes). Thus in this model, possibly in analogy with European type 2 diabetic patients, from a pathophysiological viewpoint significant β-cell mass reduction occurs only in long-standing and advanced T2DM. In earlier stages, the β-cell deficiency seems to be more of a functional nature. I therefore prefer to use the term "function- al β-cell mass" to denote a globally insufficient insulin delivery situation, until we gain access to in vivo imaging techniques to allow in situ β-cell mass determination in our patients.
Figure 3. The evolution of nutritional diabetes in Psammomys obesus.
mass also collapses.
Abbreviations: FFA, free fatty acid; HE, high energy.
Modified from reference 39: Kaiser et al. Diabetes. 2005;54:138-145. © 2005,
American Diabetes Association.
Why do β cells die in a diabetic environment?
Extensive work over the past decade has shown that mimicking the diabetic environment in vitro, ie, exposure to high concentrations of glucose and fatty acids over extended periods, causes death of β cells by apoptosis (for a review, see reference 40). Both oxidative stress and endoplasmic reticulum (ER) stress in the β cell, induced by the high nutrient exposure, contribute to initiating programmed cell death. Our laboratory has been interested in &beat;-cell ER stress over the past few years. In β-cells exposed continuously, ie, in a noncyclic manner, to high glucose levels proinsulin biosynthesis is under continuous stimulation; this puts the ER system under high pressure, since proinsulin has to be correctly folded and exported to the Golgi apparatus for processing and further maturation in insulin granules. The ER responds to the increase in proinsulin mRNA translation and chaperone-guided proinsulin folding by what is named the unfolded protein response (UPR), which is an adaptive feedback response aimed at reducing the workload by partially blocking the translation of mRNAs and degrading them, and augmenting chaperones to prevent misfolding of newly formed proteins as well as removing misfolded proteins from the ER. If the load on the ER persists despite these measures, then the UPR activates several mechanisms that end in apoptosis, leading to the removal of the deficient cell (for a short-but-comprehensive overview, see reference 41). We have shown that exposure to chronic high glucose levels activates the inositol-requiring enzyme 1 (IRE-1 ) arm of the UPR both in β-cell lines and in Psammomys obesus islets.42 Furthermore, fatty acids (palmitate) and glucose exhibited a high degree of synergism in activating IRE-1 . This eventually leads to activation of c-jun N-terminal kinase (JNK) and increase in -cell apoptosis; by using specific JNK inhibitors we could demonstrate that JNK is indeed responsible for initiating the caspase cascade and β-cell death.42 Importantly, the effect of glucose on the IRE-1 cascade is mammalian target of rapamycin (mTOR)-dependent, since it could be inhibited by reducing the activity of mTOR complex 1 (mTORC-1) with rapamycin, thus rescuing cells from glucolipotoxicity-induced death.42 This unfortunately does not mean that rapamycin can be used as a therapeutic agent against type 2 diabetes. To our dismay, when we administered rapamycin to diabetic Psammomys obesus, the animals developed even higher hyperglycemia together with extreme lipemia and massive β-cell apoptosis.43 Thus, the in vivo situation is more complex than that observed under well-controlled in vitro experiments. Intensive efforts are ongoing in numerous laboratories to design means for counteracting ER stress (as well as oxidative stress) in cells; these may eventually lead to the generation of new classes of antidiabetic drugs aimed at prolonging the life of the cell, thus preventing the seemingly ineluctable progression of type 2 diabetes.
Is T2DM a disease of insulin deficiency or insulin resistance? Obviously both. Nevertheless, I am comforted in my nearly 50-year-old belief in the primacy of insulin deficiency for the pathogenesis of T2DM by the consensus that has emerged in the last decade over the fact that hyperglycemia is not possible in the absence of β-cell deficiency. Compared to the near-total lack of insulin of the type 1 diabetic, the β-cell deficiency of the type 2 diabetic patient is modest, and therefore would not be sufficient to lead to the full diabetic state in such a high proportion of subjects without additional environmental factors. This is a classic gene-environment interaction. It is a fascinating idea that, had the whole genome association studies been performed immediately after World War II in the undernourished populations of Europe and Asia, none of the polymorphic genes being hotly investigated today would have been found to be associated with type 2 diabetes. Indeed, these polymorphic alleles seem to render the cell somewhat less efficient, ie, place it at the lower end of normal variation in terms of its functional adaptability and resistance to stress; nevertheless, these cells are normal until faced with unreasonable demands. I think too much emphasis is put on insulin resistance; I believe that the greatly augmented caloric intake, ie, the greatly increased nutrient flux in the cell, is the real problem, insulin resistance acting as a potent amplifier. The consequence of this thought is that the risk for an individual to develop T2DM would be inversely correlated with the magnitude of adaptability of his cells and directly correlated with the degree of caloric intake/ insulin resistance to which he would be exposed. Thus, the "stronger" the cell, the greater the degree of obesity that can be tolerated while maintaining normal glucose tolerance. There are cases of lean, insulin-sensitive T2DM, as there are cases of diabetes with severe insulin resistance and extreme hyperinsulinemia. However, these are rare. For the majority of type 2 diabetics, to prevent hyperglycemia and its consequences either food intake has to be reduced drastically, or the cell enforced to cope with the increased workload. Neither seems easy. Almost all research today on the cell in connection with T2DM deals with the cells' reaction to various stresses, ie, the glucolipotoxicity situation. That this is most relevant to the fate of the cell in the diabetic environment, and therefore to diabetes progression, is clear. A legitimate question does arise, however: Are the various mechanisms of -cell stress discussed above (and in the literature) responsible also for the initiation of hyperglycemia? In other words, is -cell stress a secondary reaction to diabetes (glucolipotoxicity), almost a complication of the disease, or is it the etiopathogenic event that leads to the gradual impairment of glucose homeostasis until glucose intolerance and diabetes appear? This is an important question that awaits its solution through future research. _
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Keywords: insulin secretion; first-phase response; low insulin response; insulin resistance; IGT; type 2 diabetes; &bata-cell function; β-cell mass; ER stress


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I was telling my therapist how I never feel that I'm good enough as a writer and he suggested that I might be suffering from "the imposter syndrome." No matter what accolades come my way, or how hard I worked to earn them, I always feel like they were given to me by mistake. The first time I was paid for something I wrote was in 1994. The publication was Ladies' Home Journal and I was paid $700. I was floored. But instead of thinking that my writing was good enough, I felt that they accepted what I wrote only because the topic was timely. I imagined the editors shaking their heads and saying, "Well, it's all we have to work with." The worst part was that I didn't even get a by-line; the column for which my piece was accepted was written anonymously because it was about things that women keep secret. (I won't divulge here what my secret was.)
My next sale I was a little more proud about even though I didn't get paid nearly as much. But it was an essay that I dashed off late one night in a fit of inspiration and so I figured that was just a fluke. It's when things don't come so easily that I get caught up in the imposter syndrome. Who am I to call myself a writer? I haven't published anything in years. Yes, I write everyday, but I never finish anything so I'm not a writer. What I really mean is that I'm not a famous writer, but how many writers are? And what do I mean by fame? How famous do I have to be before I'll stop feeling like I'm pulling something over on my readers?
The main reason I rarely write in this blog is because I feel presumptuous writing about the writing life as if I was really a writer. As if I had a thing to say that would be helpful or interesting to (other) writers. And the fact that no one except for my husband has visited this blog proves to me that I don't. It's easy for me to come to this conclusion because that's how I view everything I do: as uninteresting, unhelpful, unimportant. As my therapist says, "You never cut yourself a break, do you?" No, I don't. And I don't think I deserve to.
The other day it dawned on me that maybe I've been trying to write in the wrong voice. After all, I'm a gloomy and pessimistic person and I've been trying to write like Ms. Well-Adjusted. No wonder what I write comes out sounding false. It might not always be pleasant reading, but if I want to write "true," I have to let the real me come out. That's the only way I can stop feeling like an imposter. Or at least not as much of one.
If I do have anything to say to other writers it's that I know what it's like to doubt yourself. I wallow in doubt everyday. Some days the only reason I think I'm a writer is because I can't stop writing. I've tried to give it up and I can't. But most days that's not enough to make me feel like a "real" writer. Dr. S (the aforementioned therapist) says that I need to be realistic about what I'm shooting for. It's all right to shoot for the stars as long as you know what is likely to happen–or not happen. He told me that his father made him apply to Harvard and Yale when it came time for him to apply to medical school, even though he didn't have a chance in hell of getting in. Being rejected probably hurt even though he knew he wouldn't be accepted. But he also applied to other schools and was accepted into one of them and became a very good psychiatrist with a thriving practice. Is he a failure because he didn't go to an Ivy League school? If that's all you care about, yes. But if you look at things realistically, it's obvious that he has made it.
I don't submit to or query the top magazines for the same reason that I wouldn't have applied to Harvard or Yale: I don't want to be rejected. And I'm sure I would be. Dr.S's father reasoned that sometimes "ordinary" people get into Ivy League schools, but not if they don't try. I just don't have the guts to put that to the test with the big publications. If I did get something accepted, I would feel like they made a mistake, but that my piece might slip through if no one takes a really good look at it.
Years ago, I got up the nerve to say that I was a writer. I needed to be able to do that. Now I'm going through the same crisis of confidence. I'm older, I haven't published for a while, I'm harder on myself than I was then. I'm afraid that when I say I'm a writer, others are thinking, "Right." But they would probably think that unless I became the next Anne Tyler or Elizabeth Berg. And even then they might not be impressed. Why do I worry about the impression I make on people? The only one who can really say whether I'm a writer or not is myself. So I'm going to try to stop feeling like an imposter and say it proudly: "I am an authentic writer." And then get about the business of writing authentically.


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Hold onto those fleeing users
It's not a secret that 23% of users abandon an app after only one use. Is your app in danger?
As the importance of mobile technology grows in our daily lives, so does user expectations of it.
People will mercilessly leave an app that fails to fully engage them. The question is, can you afford to lose users?
No, so how to keep them?
You have to think of your users as individuals – using your app should connect to their personal interests and desires. You have to make sure you provide them with the types of experiences relevant to them. Don't overload your user with information they don't need and aren't interested in. Just like yourself, they all just want to get on with their lives.
What if you could present your new users with some fresh, relevant content already on the sign in screen? Something new, but related to their personal interests. Now you've caught their attention. Localize and time it. Know where your users are and what content is relevant to them at that specific place, at that specific time. Use our powerful technologies to deliver an experience that's relevant and personally interesting to your individual end user.
Calldorado lets developers add Caller ID functionality as an app extension. With the Calldorado SDK the screen at the end of a call includes a re-engagement field, drawing the user back to the core app, and a targeted ad alongside the Caller ID info.
Sign up for our SDK today to boost your app revenue while keeping your app users engaged.


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TIMESGRESIK, MALANG – https://timesindonesia.co.id/read/news/249701/mengenal-sosok-bejo-pembuat-karinding-yang-hampir-punah
Karinding is a folks music instrument of Malang. This music instrument could be categorized as a rare or could be said almost extinct one since there are no much people left to be able to play it.
Nowadays, people are tend to choose to play the modern instruments rather than the traditional one. But a guy named is trying to bring back the old music instrument to live.
Bejo who lives in Sukun Malang stated his concern towards the Karinding for no one has ever been played the instrument for a long time.
Karinding is also well known as jaw harp. You need to put it on your mouth and with a little help of your finger to use it. This instrument usually made of bamboo or metal.
Bejo works from his workshop to make this instrument. His concern was started when he saw a video about a music museum in Holland that kept almost all Indonesian folks instrument.
"I started making Karinding once I saw the video, if Holland could have done it, why wouldn't we as Indonesian?," he stated his concern.
Bejo made all the Karinding from Bamboo. Bamboo is chosen for it's easier to find and more eco friendly. He hope that someone or may be the government will stand and help him to preserve this music instrument. (*)
Baca Berita Peristiwa dan Politik terbaru di Indonesia dan luar negeri lainnya hanya di TIMES Indonesia.


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The District 13 rebels are at it again! Yep, getting their rebellious, little mole hands on TheCapitol.PN once again, and getting the fandom all apoplectic…again. Perhaps "apoplectic" is the wrong word? Maybe concerned, or attentive, maybe excited could work in a pinch? Whatever word works best for you individually, hold fast to it and run!
This is not a new phenomena though, i.e, we're no strangers to the fictional D13ers and co. (co being Beetee), tapping away at their advanced computer arrays, and throwing cogs into The Capitol's watch-works. What, was it less than three weeks ago that this message went up on the site for all to see?
I think the collective reaction to that particular hack was, um… well, "yay"? What is it about the D13 rebels that gets us happy? Is it the simple, and inevitable glimpse of a propo featuring Katniss in all her Mockingjay glory? And yes, since we finally got the first official teaser trailer, we do have viewable footage of her in her Cinna designed Mockingjay uniform, but it's kind of not the same as seeing her, say… delivering her impassioned rooftop speech directed at President Snow.
The rebels are at it again though! Making us double click, and get messages like this.
So, what's going to be different this time guys? We're waiting!
Them There Eyes


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Website https://ccseit2020.org/sigml/index.html | Edit Freely
Category signal processing;Digital and Signal Processing;Machine Learning;Deep Learning;Electronic and Electrical Communications;Mechanical engineering
Deadline: March 07, 2020 | Date: March 28, 2020-March 29, 2020
Venue/Country: Sydney, Australia, Australia
Updated: 2020-03-03 21:48:17 (GMT+9)
Keywords: Accepted papers list. Acceptance Rate. EI Compendex. Engineering Index. ISTP index. ISI index. Impact Factor.
Disclaimer: ourGlocal is an open academical resource system, which anyone can edit or update. Usually, journal information updated by us, journal managers or others. So the information is old or wrong now. Specially, impact factor is changing every year. Even it was correct when updated, it may have been changed now. So please go to Thomson Reuters to confirm latest value about Journal impact factor.


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As usual we are closing for the week commencing August 24th. We will be re-opening for all CD & DVD duplication on Tuesday 1st September 2009. Any urgent correspondence should be emailed to:- email@example.com
We will despatching CD and DVD duplication orders from Tuesday 1st September 2009 and will be dealing with any jobs that are sent in during the week. Any pending free of charge and obligation approvals will be despatched on this day too.
We thank you for your continued support. We have lots of exciting enhancements coming to the site and our CD and DVD printing processes which will be rolled out during the next few weeks-just in time for the seasonal rush.
Tags: Office Closed


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It's the most magical time of the year. And although most people don't realize it, the tradition of telling stories during the Yule season goes back hundreds of years. And who better to tell you a story than the big man himself, Santa Claus!
If you are a Santa that does special events, home visits, corporate events, or any place where Santa is expected to entertain for any length of time, being a good storyteller is a very useful skill to have indeed.
Christmas Performer Workshops
What are the Christmas Performer Workshops?
The concept of Christmas Performer Workshops is that it's not a school, per se. These are ongoing resources, and I and others will help guide and develop programs for the Santa Community. If you have performing or folklore related questions, please don't hesitate to ask.
If you are looking for the Discover Branson 2016 handouts from Santa True, please head over to the Christmas Performer Workshops Branson resources.
Reasons to Build Storytelling Skills
Here are three very good reasons to add storytelling to your skill set.
- You are already half way there. You have created a character and brought it to life! Every time you answer a question about the life of Santa, Reindeer, and anything about life on the North Pole, you are touching on storytelling.
- Learning to be a good storyteller takes work. But after you have some good stories, you will be able to offer storytelling to your clients. When someone insists they want an hour and everything else is done, YOU can gather people around to share in stories that will enthrall young and old alike. And that will make the time fly. You can pull special things about that event into your stories to give them a unique story that they will remember for years.
- The various tools used by a storyteller are also used in almost every aspect of performance. They overlap and re-enforce each other. As a storyteller, your techniques for voice, pacing, characterization, and physicality are also used as a performing Santa. So many of the skills you use as a storyteller can help with doing magic, emceeing, and narrating (The Night Before Christmas, among others).
In short, training as a Storyteller will help you be a better Santa or Mrs. Claus and will give you new ways to entertain clients for longer periods of time. It can also help you have more fun and land better paying gigs.
Topics in the Workshops
Here are some of the topics that can be covered (depending on the length of the workshop).
- What IS Storytelling?
- How is the human brain hard-wired for Stories?
- The History of Storytelling and its role in society
- How was storytelling used and how will it be used today and in the future?
- Where do stories come from?
- The different types of stories: Myth, Legend, Folktale, and modern Personal Stories, Shared stories
- Storytelling Styles and Techniques (Rhyming, Call and response, Improv)
- Finding the Right Story
- Polish and Practice: the Art of the perfect story
- Speaking to truth and relevance: Connecting with your audience
- Coaching and getting the feedback YOU need
- Performance (an entire workshop in itself: Voice, Physicality, Working your Environment)
- Characterization and transitions (first person, third person, narrative)
- Improvisation
- Beginnings and Endings
- Storytelling Resources
Specific Services
These are some services I offer.
- Free advice for my Brothers and Sisters in Red
- One-on-One Instruction Coaching
- Storytelling workshops for one or more people via Skype
- Performance video evaluations
- Workshops at your site: by the Hour, Day, Weekend or longer. Specific workshops include:
- Storytelling
- Performance
- Coaching
- The History and Folklore of Santa and the Yule season
Additional Info
I am a professional, traditional storyteller. My specialty is bringing stories to life with fun, energy, and passion. One of the ways I do that is by delivering my stories in character. My personas come from a wide variety of cultures including Celtic, Norse, Western, and more. And one of my most requested characters is Santa True: the storytelling, singing, FUN Santa.
Teaching at the Nationwide Santa's Convention in Las Vegas, 2015 (photo courtesy of Santa Gordon Bailey)


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84 Green St
Huntington, NY 11743
Dr. Salvatore Tangredi is a popular Huntington area children's dentist known for his easy going and friendly approach. Our caring team is dedicated to your child's dental health.
We're happy to answer all of your questions. We want you and your children to feel comfortable, whether we're treating your toddler's baby teeth or your teenager's permanent teeth.
Salvatore Tangredi, D.D.S. is pleased to provide laser teeth whitening in the Huntington area. You'll enjoy how gentle the treatment is, as well as having teeth that are immediately several shades lighter.
Our patients tell us how comfortable they feel, and how much they appreciate their whiter teeth. We'll make sure you're happy with your healthy new smile, too!
Salvatore J. Tangredi, D.D.S is fully accessible to disabled patients. With designated handicapped parking spaces, a wide entrance that can accommodate a wheelchair, and fully accessible facilities throughout, patients in wheelchairs will be very welcome to their next appointment with Huntington area dentist Dr. Salvatore Tangredi.
Distinguished Huntington area mini dental implants dentist Salvatore Tangredi, D.D.S. can provide you with the highest quality results. At Salvatore J. Tangredi, D.D.S, we use state-of-the-art materials and techniques that make them less invasive and more affordable.
You deserve the best treatment available to replace missing teeth. Whether you're missing a single tooth or experiencing pain from slipping dentures, mini dental implants can be a faster way to regain your beautiful smile.
For comfortable dental hygiene treatment in the Huntington, New York area, Dr. Salvatore Tangredi is known for having a gentle touch. The friendly team at Salvatore J. Tangredi, D.D.S provides teeth cleaning for a whiter smile.
Maintaining good dental hygiene is the foundation for healthy teeth and gums. We're committed to helping you have a lifetime of oral health.
245 Bay Shore Rd
Bay Shore, NY 11706
A negative self image can be detrimental to many facets of your life. Bay Shore area dentist Dr. John McLoughlin understands the positive life-changing power that a healthy and beautiful smile can bring to you. Here at John T. McLoughlin, D.D.S, we don't want you to be embarrassed any longer. Why not take your smile - and even your life - to a new level of self-confidence and beauty?
Don't let untreated dental problems get you down. Rebuild your confidence with a beautiful new smile. From simple treatments that make a big difference, to more extensive work, unveiling the smile you were meant to have can have profound life-changing effects. Serving the Bay Shore, NY area and offering sleep apnea, Dr. McLoughlin can help you develop an affordable treatment plan you'll feel good about.
At John T. McLoughlin, D.D.S, we offer quality, personalized care. Serving the Bay Shore, NY area, we're happy to discuss the variety of treatment options available to you. If you're interested in sedation or sleep dentistry options, please schedule an appointment with John McLoughlin, D.D.S., and we can provide you with all the information you need.
If you're looking for dentures that look great and last, look no further than John T. McLoughlin, D.D.S located in the Bay Shore, NY area. John McLoughlin, D.D.S. will assess your needs and fit you with durable, comfortable, natural-looking dentures - at a price you can afford.
Here at John T. McLoughlin, D.D.S, your comfort is our number one priority. We will do our utmost to put you at ease and keep you feeling relaxed and secure. Under the experienced leadership of Dr. John McLoughlin, our dedicated team of professionals is at your service to explain your treatment thoroughly and answer any questions you may have.
61-34 188th Street, Suite 201
Fresh Meadows, NY 11365
Fresh Meadows area restorative dentistry at Alan L. Rosenberg, D.D.S can produce natural-looking results. If you have a damaged or missing tooth, we can help.
Our highly skilled team will assess your need for a crown, bridge, implant or other procedure to restore or improve your smile. Our goal is to provide quality dental care for your life-long oral health.
Dr. Alan Rosenberg at his Fresh Meadows area dental implants practice offers extensive experience restoring your dental implant crown.
Our dedicated team uses state-of-the-art materials and techniques for stability and longevity. You'll enjoy the comfort and confidence of natural-looking teeth.
If you're looking for denture repair in the Fresh Meadows area, our team at Alan L. Rosenberg, D.D.S offers friendly service. Dr. Rosenberg understands the importance of reliable dentures that fit properly.
We'll get your repairs done professionally and quickly. You'll be able to eat and smile again with confidence as soon as possible.
Dr. Alan Rosenberg is a trusted Fresh Meadows area veneers dentist. Our professional team is dedicated to providing you with quality results in a comfortable and pleasant atmosphere.
You won't have to feel embarrassed any longer by crooked, chipped or discolored teeth. With your new dental veneers, you'll be thrilled to show off your healthy teeth and beautiful smile.
Dr. Rosenberg provides secure implant dentures in the Fresh Meadows area. Implant retained dentures won't slip, and are a long-lasting solution to missing teeth.
You'll talk, eat and smile with more confidence. Your self esteem will return with your new natural-looking teeth.
Dr. Amy L. LudwigD.D.S.,PC
630 5th Avenue,Suite 1810
New York, NY, 10111
Smile Solutions
16 Old Riverhead Road
Westhampton Bay, NY, 11978
(631) 288-9000
Marinbach, Mark-CDT
221 Hempstead Turnpike
West Hempstead, NY, 11552
(516) 489-5200
School of Dental Medicine
SUNY at Buffalo
Buffalo, NY, 14214
(716) 348-1880
Sleep apnea appliances are another way your sleep apnea dentist can help you sleep soundly. Worn while you sleep, oral appliances like CPAP masks can hold your mouth and jaw in such a way that makes breathing easier and will stop snoring. A sleep apnea oral appliance fits into your mouth like a mouth guard, night guard or orthodontic retainer.
Oral appliance therapy is a popular alternative to CPAP treatment. There are many options, and your dentist can help you choose which sleep apnea appliance will be best for your obstructive sleep apnea (OSA).
One sleep apnea remedy is the mandibular advancement system (MAS), also known as a mandibular advancement device (MAD). This oral splint is a dental appliance that moves the lower jaw slightly forward, which can effectively treat sleep apnea and also provide snoring prevention.
There are many other types of sleep apnea equipment. Generally, oral appliances for snoring and sleep apnea are made of soft plastic or hard acrylic. Some incorporate wires or rubber bands to provide the right sort of pressure. Almost all of them require a prescription and a professional fitting by your dental sleep medicine dentist or sleep apnea physician. If a dental appliance doesn't fit properly, it can lead to orthodontic problems and trouble breathing.
Snoring is one of those problems that often bothers other people more than the person who does it. Many people who snore don't even know it. However, it can drive others crazy: spouses, roommates, neighbors, even dogs.
The noise of snoring happens when a person's airways are partially obstructed during sleep. When the airways are totally blocked, an apnea happens: that's when a person stops breathing briefly during sleep. So it's hardly a surprise to learn that people with obstructive sleep apnea also snore.
Snoring can be loud and disturb others, but snoring in and of itself isn't bad for your health. However, missing breaths during sleep is indeed a health problem. Snoring can be a symptom of a more serious sleep disorder, like sleep apnea. If your snoring is a symptom of sleep apnea, then you should discuss it with your doctor or dentist. Sleep apnea treatment can stop snoring and make your sleep more restful.


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#01 Sun Moon Lake
One of the island's most relaxing retreats, with nature walks, cool breezes, calming views and a shoreline brimming with cultural interest.
Sun Moon Lake, Taiwan © CHEN HSI FU/Shutterstock
#02 Kinmen
This island is the frontline between Taiwan and China – the latter is literally a stone's throw away – and now an absorbing blend of former battlefields and well-preserved imperial Chinese monuments.
© Philos Chen/Shutterstock
#03 Hot springs
Taiwan has over 150 hot springs, most set among mountainous landscapes and piped into hotel resorts, ranging from the ultra-hip to the cheap and cheerful.
© totogo1015/Shutterstock
#04 Kenting National Park
Studded with fine-sand beaches and rolling surf, this resort-fringed national park covers Taiwan's southern tip and is a haven of snorkelling and diving.
© StephanScherhag/Shutterstock
#05 Taroko National Park
Taiwan's most visited national park is sliced in half by narrow, deep-cut Taroko Gorge, one of Asia's top natural wonders and an absolute must-see.
© Watchara Tawongsa/Shutterstock
#06 Lugang
Taiwan's most attractive old town, with traditional architecture, beautiful temples, tasty snack food and shops stocked with the work of the island's most accomplished craftsmen.
© chungphoto/Shutterstock
#07 Lanyu (Orchid Island)
Inhabited almost solely by the seafaring Tao tribe, whose traditional ways of life give this lush Pacific island an almost Polynesian flavour.
© weniliou/Shutterstock
#08 Aboriginal culture
Taiwan's indigenous peoples, divided into fourteen officially recognized tribes and several other distinct groups, have their own vibrant cultures quite separate from the Chinese majority.
© topimages/Shutterstock
#09 Tainan
The old capital of Taiwan remains an important stronghold of Taiwanese culture, its myriad temples the perfect places to absorb its complex religious traditions.
© The HippoZoom/Shutterstock
#10 Surfing
The island's lengthy stretch of Pacific coastline has vastly underrated surfing, with countless breaks – and plenty of typhoon swell – to challenge both beginners and serious shredders.
© Wayne0216/Shutterstock
#11 Chung Tai Chan Monastery
Nothing else quite looks like this enormous Buddhist monastery, packed with artistic gems, elegant shrines and innovative architecture.
© Suchart Boonyavech/Shutterstock
#12 Alishan National Scenic Area
Gorgeous, rugged valleys, high mountain tea plantations and Tsou villages culminating in the misty forests of Alishan itself, home of the spectacular "sea of clouds".
© NH/Shutterstock
#13 National Palace Museum
View the former contents of Beijing's Forbidden City in this world-famous museum, an extraordinary collection of Chinese art and historical artefacts.
Gugong National Palace Museum, Taiwan © Avigator Fortuner/Shutterstock
#14 Dajia Mazu Pilgrimage
One of the world's biggest festivals involves thousands of pilgrims on an animated seven-day parade circuit between the revered Mazu temples in Dajia and Xingang.
© Lewis Tse Pui Lung/Shutterstock
#15 Climbing Yushan
At 3952m, Yushan (Jade Mountain) is far and away northeast Asia's highest peak, but a spectacular and well-trodden trail to the summit makes it surprisingly accessible.
© Kriangkrai Thitimakorn/Shutterstock
#16 East Coast National Scenic Area
From the north's towering cliffs to the south's expansive beaches, the east coast is a feast for the eyes and is a hotbed of aboriginal cultures.
© Chen Liang-Dao/Shutterstock
#17 Night markets
Taiwan's night markets are the best and cheapest places to try a selection of the island's famous "little eats".
© Baiterek Media/Shutterstock
#18 Taipei 101
At 509m, East Asia's tallest building dominates central Taipei, providing mind-blowing views of the surrounding area.
© Sean Hsu/Shutterstock