text:
SiriusXM to Launch Holiday Music Channels
15 commercial-free channels featuring a wide collection of holiday music from classic to country to acoustic and beyond
Mannheim Steamroller to launch exclusive new channel to celebrate the holiday season
Sirius XM Holdings Inc.
Oct 22, 2018, 10:00 ET
NEW YORK, Oct. 22, 2018 /PRNewswire/ -- SiriusXM today announced its extensive holiday music lineup featuring 15 commercial free channels, including 5 available exclusively on SiriusXM's streaming platforms. To kick off the festive season, 7 of the music channels start broadcasting Thursday, November 1.
SiriusXM's holiday music channels will offer listeners a variety of traditional holiday songs, classic Christmas carols, country Christmas classics, contemporary holiday tunes, soul music, Hanukkah music and Latin seasonal music.
New to the holiday music channel lineup this year includes an exclusive Mannheim Steamroller channel, featuring music by Manheim Steamroller which is known for their blend of symphonic music with elements of new age and rock and modern recordings of Christmas music.
In addition, SiriusXM will also launch four new holiday music online channels including 70s/80s Christmas, Rockin' Xmas, Holiday Chill-Out and Jazz Holidays which subscribers are able to listen to online, on-the-go with the SiriusXM mobile app and at home on a wide variety of connected devices including smart TVs, Amazon Alexa devices, Apple TV, PlayStation, Roku, Sonos speakers and more. Go to www.SiriusXM.com/streaming to learn more.
SiriusXM's holiday channel lineup features:
Holly (via satellite on channel 4)
Will feature contemporary holiday hits including songs by Michael Bublé, Ariana Grande, Josh Groban, Pentatonix and Mariah Carey.
Thursday, November 1 – Friday, December 28 at 3:00 am ET
Holiday Traditions (via satellite on channel 3)
Will feature traditional holiday music from the '40s through the '60s and beyond by artists such as Bing Crosby, Dean Martin, Burl Ives, Carpenters, Glenn Miller, Nat King Cole, Andy Williams, Ella Fitzgerald, Mel Tormé and Elvis Presley.
Thursday, November 1 – Wednesday, December 26 at 3:00 am ET
Radio Hanukkah (via satellite on channel 77)
Will feature an extensive collection of Hanukkah-themed music, including contemporary, traditional and children's selections as well as daily reflections and prayers related to the holiday.
Saturday, December 1 – Tuesday, December 11 at 3:00 am ET
Country Christmas (via satellite on channel 58)
Will feature traditional holiday favorites and original sounds of the season from classic country artists like Willie Nelson and Merle Haggard to contemporary country stars like Blake Shelton and Carrie Underwood. You'll also hear artists such as Garth Brooks, Alan Jackson, LeAnn Rimes, Brett Eldredge, Lady Antebellum and Reba McEntire.
Monday, December 3 – Wednesday, December 26 at 3:00 am ET
Holiday Soul (via satellite on channel 49)
Will feature R&B Christmas classics from The Temptations, Charles Brown, The Jackson 5, New Edition, Whitney Houston, The O'Jays, Aretha Franklin, TLC, Kool & The Gang, as well as newer tracks by Fantasia, Babyface, and Toni Braxton.
Acoustic Christmas (via satellite on channel 14)
Will feature acoustic holiday classics from well-known singers and songwriters such as Jack Johnson, George Ezra, Norah Jones, Maroon 5, The Lumineers, Jewel and Jason Mraz.
Friday, December 14 – Wednesday December 26 at 3:00 am ET
Christmas Spirit (via satellite on channel 63)
Will feature Christmas music and holiday favorites from contemporary Christian artists including Michael W. Smith, Amy Grant, MercyMe, for KING & COUNTRY, Matthew West, Chris Tomlin, Francesca Battistelli, and Lauren Daigle.
Friday, December 21 – Wednesday, December 26 at 3:00 am ET
Mannheim Steamroller Channel (via satellite on channel 30)
Will feature Mannheim Steamroller which is known for their blend of symphonic music with elements of new age and rock and modern recordings of Christmas music.
Monday, December 17 – Tuesday, December 25 3:00 am ET
Holiday Pops (via satellite on channel 76)
Will feature classical Christmas carols and other holiday favorites performed by the world's most popular classical performers including the Choir of King's College, Cambridge, New York Philharmonic, Boston Pops Orchestra, Luciano Pavarotti, The King's Singers, Chanticleer, Mormon Tabernacle Choir and James Galway.
Monday, December 24 – Wednesday, December 26 at 3:00 am ET
New Year's Nation (via satellite on channel 4)
The ultimate soundtrack to New Year's Eve parties around the country and will feature the biggest, upbeat party hits from genres across SiriusXM's music platform. Artists include Lady Gaga, Bruno Mars, The Chainsmokers, Pitbull, Drake, Britney Spears, Maroon 5, Cardi B, Imagine Dragons and Justin Bieber.
Friday, December 28 – Wednesday, January 2 at 3:00 am ET.
70s/80s Christmas (via streaming on channel 780)
Will feature the biggest and most familiar Christmas and holiday hits from the 70s and 80s featuring artists such as Elton John, Carpenters, Paul McCartney, The Jackson 5, Bruce Springsteen, Wham!, Madonna and Hall & Oates.
Rockin' Xmas (via streaming on channel 781)
Will feature classic Christmas songs that rock including hits, rarities and live tracks from artists including AC/DC, Bon Jovi, U2, Twisted Sister, REO Speedwagon, Bruce Springsteen, The Pretenders, Tom Petty & The Heartbreakers.
Holiday Chill-Out (via streaming on channel 783)
Will feature downtempo electronic holiday music from artists like Kaskade, Lost Frequencies, DJ Style and more.
Jazz Holidays (via streaming on channel 784)
Will feature Christmas favorites from classic legends and contemporary jazz stars including Ella Fitzgerald, Vince Guaraldi, Diana Krall, Joey DeFrancesco, David Benoit, Wynton Marsalis, Dianne Reeves and Dave Koz.
Navidad (via streaming on channel 786)
Will feature a festive blend of contemporary and traditional classic favorites, including El Gran Combo, Héctor Lavoe, Laura Pausini, Ricky Martin, Tito El Bambino, Gloria Estefan, José Feliciano, Marco Antonio Solís, Celia Cruz and Juanes.
Thursday, November 1 – Monday, January 7 at 3:00 am ET
SiriusXM offers people without a subscription the chance to sample SiriusXM's content on the SiriusXM app and the streaming web player at SiriusXM.com, seamlessly and without any registration requirements. Go to https://siriusxm.us/2AVma2a to tune in.
About SiriusXM
Sirius XM Holdings Inc. (NASDAQ: SIRI) is the world's largest radio company measured by revenue and has approximately 33.5 million subscribers. SiriusXM creates and offers commercial-free music; premier sports talk and live events; comedy; news; exclusive talk and entertainment, and a wide-range of Latin music, sports and talk programming. SiriusXM is available in vehicles from every major car company and on smartphones and other connected devices as well as online at siriusxm.com. SiriusXM radios and accessories are available from retailers nationwide and online at SiriusXM. SiriusXM also provides premium traffic, weather, data and information services for subscribers through SiriusXM Traffic™, SiriusXM Travel Link, NavTraffic®, NavWeather™. SiriusXM delivers weather, data and information services to aircraft and boats through SiriusXM Aviation™ and SiriusXM Marine™. In addition, SiriusXM Music for Business provides commercial-free music to a variety of businesses. SiriusXM holds a minority interest in SiriusXM Canada which has approximately 2.6 million subscribers. SiriusXM is also a leading provider of connected vehicles services, giving customers access to a suite of safety, security, and convenience services including automatic crash notification, stolen vehicle recovery assistance, enhanced roadside assistance and turn-by-turn navigation.
To download SiriusXM logos and artwork, visit http://www.siriusxm.com/LogosAndPhotos.
This communication contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements include, but are not limited to, statements about future financial and operating results, our plans, objectives, expectations and intentions with respect to future operations, products and services; and other statements identified by words such as "will likely result," "are expected to," "will continue," "is anticipated," "estimated," "believe," "intend," "plan," "projection," "outlook" or words of similar meaning. Such forward-looking statements are based upon the current beliefs and expectations of our management and are inherently subject to significant business, economic and competitive uncertainties and contingencies, many of which are difficult to predict and generally beyond our control. Actual results and the timing of events may differ materially from the results anticipated in these forward-looking statements.
The following factors, among others, could cause actual results and the timing of events to differ materially from the anticipated results or other expectations expressed in the forward-looking statements: our substantial competition, which is likely to increase over time; our ability to attract and retain subscribers, which is uncertain; interference to our service from wireless operations; consumer protection laws and their enforcement; unfavorable outcomes of pending or future litigation; the market for music rights, which is changing and subject to uncertainties; our dependence upon the auto industry; general economic conditions; the security of the personal information about our customers; existing or future government laws and regulations could harm our business; failure of our satellites would significantly damage our business; the interruption or failure of our information technology and communications systems; our failure to realize benefits of acquisitions or other strategic initiatives; rapid technological and industry changes; failure of third parties to perform; our failure to comply with FCC requirements; modifications to our business plan; our indebtedness; our principal stockholder has significant influence over our affairs and over actions requiring stockholder approval and its interests may differ from interests of other holders of our common stock; impairment of our business by third-party intellectual property rights; and changes to our dividend policies which could occur at any time. Additional factors that could cause our results to differ materially from those described in the forward-looking statements can be found in our Annual Report on Form 10-K for the year ended December 31, 2017, which is filed with the Securities and Exchange Commission (the "SEC") and available at the SEC's Internet site (http://www.sec.gov). The information set forth herein speaks only as of the date hereof, and we disclaim any intention or obligation to update any forward looking statements as a result of developments occurring after the date of this communication.
Source: SiriusXM
Media contact for SiriusXM:
Carolina Dubon
Carolina.dubon@siriusxm.com
SOURCE Sirius XM Holdings Inc.
http://www.siriusxm.com
SiriusXM Announces Extensive Broadcast Lineup for 2020 PGA...
SiriusXM and Pandora Present The Chainsmokers & Lizzo Live...


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Married Biography / Biography / Toni Braxton
Toni Braxton Bio
(Singer)
Last Modified April 12, 2019
Facts of Toni Braxton
Horoscope:
Severn, Maryland, U.S.
Height / How tall :
5 feet 2 inches (1.57m)
Father's Name:
Michael Conrad Braxton
Mother's Name:
Evelyn Braxton
Bowie State University
Waist Size:
Bra Size:
34B inch
Hip Size:
Lucky Number:
Lucky Stone:
Lucky Color:
Best Match for Marriage:
Facebook Profile/Page:
Instagram Profile:
Wikipedia Profile:
IMDB Profile:
View more / View fewer Facts of Toni Braxton
If you break your knee, you have therapy on your knee, and it's the same for your heart
I'll probably be 80 years old and still performing. Music is like fashion, it changes. But some things will always be the same
I take an active role in my imaging and how I look.
Relationship Statistics of Toni Braxton
What is Toni Braxton marital status ? (single, married, in relation or divorce):
How many children does Toni Braxton have ? (name):
Two (Denim Cole Braxton-Lewis & Diezel Ky Braxton-Lewis)
Is Toni Braxton having any relationship affair ?:
Is Toni Braxton lesbian ?:
More about the relationship
Toni Braxton is currently single. She has called off her engagement with rapper Birdman in Jan 2019. She was in a relationship with Birdman (a.k.a Baby) since April 2016. They had exchanged rings in Feb 2018.
Talking about past affairs, Toni was married to Keri Lewis on April 21, 2001. They stayed together from 2001 to 2013. As things didn't work out long and they got divorced. The couple gave birth to two children together named, Denim Cole Braxton-Lewis & Diezel Ky Braxton-Lewis.
Moreover, she had been into multiple relationships before her marriage with Keri. Toni dated Shemar Moore from 1994 to 1995. Similarly, she also dated Curtis Martin, Franklin Beverly, and Eddie Murphy.
1 Who is Toni Braxton?
2 Age(51 years), Parents, Siblings, Family, Ethnicity, Nationality
3 Toni Braxton: Education, School/College University
4 Toni Braxton: Professional Life and Career
5 Toni Braxton: Awards, Nominations
6 Toni Braxton: Salary and Net Worth
7 Toni Braxton: Rumors and Controversy/Scandal
8 Body Measurements: Height, Weight, Body Size
9 Social Media: Facebook, Instagram, Twitter, etc.
Who is Toni Braxton?
Maryland-born Toni Braxton is a singer. She is extremely talented when it comes to acting too. Multi-talented Toni is a pianist and a record producer. Additionally, she is also popular as a television personality and philanthropist too. Toni is an incredible personality and a well-known R&B icon. She is 3 times Grammy award-winning artist.
Presently, she is a prominent figure in the media as one of the outstanding voices of her generation. Her debut album sold more than 10 million copies worldwide.
Age(51 years), Parents, Siblings, Family, Ethnicity, Nationality
Toni was born in Severn in the state of Maryland. Born on October 7, 1967. She possesses American nationality and her ethnicity is African-American.
Her birth name is Toni Michelle Braxton. She was born to parents, Michael Conrad Braxton(father) and Evelyn Jackson(mother). Her father was a Methodist Clergyman and her mother was an Opera singer. Her parents were pretty strict about religion. Consequently, she grew up in a religious family. She started singing in the church choir from a young age.
Toni Braxton: Education, School/College University
As per her education, she attended Bowie State University. She thought of getting a teaching degree from there. But she left the college to pursue her singing career.
Toni Braxton: Professional Life and Career
Toni sang from a young age. She quit college to pursue her singing career professionally. William E. Pettaway, Jr. discovered her after he found her singing in a fuel station. This changed her life. Although her first single with her sisters were not successful, she moved on positively. She kept on working hard. Consequently, her debut studio self-titled album made a huge breakthrough in her career.
The album sold more than 10 million copies worldwide. Similarly, Toni Braxton went on to release other albums like, "Secrets", The Heat", "Snowflakes", and "Libra" in later years. Furthermore, she released more albums like, "Pulse", "Love, Marriage & Divorce (with Babyface) part 1 & 2" until now.
As per TV career, she has appeared in multiple shows till now. She appeared in reality TV series, "Braxton Family Values" since 2001 to present. Discussing her film career, she debuted in a film named, "Kingdom Come".Similarly, he did other films like, "The Oogieloves in the Big Balloon Adventure", "Twist of Faith", and so on.
Toni Braxton: Awards, Nominations
This talented singer has received many awards and nominations. she has won awards like Favorite Soul/R&B New Artist (1994, 1997, 2001), Favorite Soul/R&B Album (1997), Best International Pop/Rock Female Artist (1998), and more. Toni was also nominated for Best International Female (1997), Favorite Pop/Rock Female Artist (1998), etc.
Toni Braxton: Salary and Net Worth
She has a net worth of $10 million but her salary is not revealed yet.
Toni Braxton: Rumors and Controversy/Scandal
Toni dragged herself into controversy back in the past. Consequently, she made headlines in all the media forms. She stated in her memoir that her son's autism was God punishing her for abortion and using acne vaccine. Presently, there are no rumors that surround her personal or professional life.
Body Measurements: Height, Weight, Body Size
Toni Braxton has a height of 5 feet 2 inches. Her body weighs 54kg. She has black hair and dark brown eyes. Furthermore, her bra size is 34B, shoe size is 7US and dress size is 4US. Besides these, her body measurement is 34-26-34 inches.
Social Media: Facebook, Instagram, Twitter, etc.
Toni Braxton is active on Facebook, Instagram, and Twitter. She has more than 3.7 million followers on Facebook, 2.9 million followers on Instagram and 1.7 million followers on Twitter.
Also know more about the early life, career, net worth, relationships, and controversies of other singers including Niykee Heaton, Jasmine Guy, Rhashan Stone, Melveen Leed, and Wally Kurth.
Tags : Actress Philanthropist Pianist Record producer Singer Songwriter TV Personality
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Related Posts on Toni Braxton
Toni Braxton has lost her engagement ring and has pleaded her fans to help her in recovering it!
American singer-songwriter Toni Braxton celebrates her 51st birthday amidst wishes from her fans and friends!
Stokley speaks about the reaction of the Mint Condition about Keri Lewis tying knot with Toni Braxton!
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redpajama_set_name: RedPajamaCommonCrawl


The ever-reliable Heyman center hosts two favorites this spring, Bruno Latour and Peter Sloterdijk. See more on their site or below.
Globalization: Which Globe? Which Politics?
No Tickets, no reservations required.
Click here for Peter Sloterdijk's webpage.


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UHS Mock Trial Team Wins County Finals
Chaitanya Kotra, Staff Writer
The Mock Trial team celebrates their county competition win over Valencia High School via a Zoom call.
The UHS Mock Trial team placed first in Orange County, after defeating Valencia High School in the county finals round.
This is the second time that the UHS Mock Trial team has won the county finals, the first time being in 2017.
The county championship took place on Thursday, February 25, against Valencia High School. The team competed in eight rounds from February 2 to 25 and were undefeated by the end of the county season. The competition was held by the Orange County Constitutional Rights Foundation virtually on Zoom in adherence with coronavirus safety guidelines.
Senior Cheyenne Hwang, the president of the Mock Trial team, described the excitement surrounding the championship round.
"The match was equally nerve-wracking and exciting. The other team, Valencia High School, was also impressive, but ultimately our team's cohesion and overall strength won us the championships," Hwang said. "Uni's team hasn't won [county] since I was a freshman 3 years ago, so it was nice to win back the title in my final year."
Sophomore Ryan Alavi, playing a witness on the team, agreed that it was an exciting competition, and recalled the many hours of practice that the team as a whole had invested in the months before.
"Winning was the best feeling ever because all our hard work paid off," Alavi said. "Our hours of practice all came together and it was amazing."
Junior Scott Burke, one of the prosecution attorneys, described the gratification that came from winning the final round against Valencia High School.
"The match was a close one; we faced Valencia who had beaten several hard-hitting teams to make it to the championship round," Burke said. "With victory came the satisfaction that the many hours spent practicing had paid off."
Junior Simona Forster expressed how much she enjoyed being part of the team, describing their growth and success.
"I have been on the team since my freshman year, and it's been amazing to see how our team has learned and grown so much over the past few years," Forster said. "Lots of practice and feedback from our awesome attorney coaches and alumni coaches was definitely the key to our victory. We have been practicing every week since the summer."
On the days they were competing, the team spent hours on Zoom preparing, competing, and reflecting on the trial.
"Trial days were long— on Tuesdays and Thursdays in February we got on a pre-competition call at 3:30, trial started at 5, and then we were on a debrief call until 9 PM some nights," Forster said. "I felt that all of the time and energy we put into Mock Trial showed in our presentation and propelled us to victory."
The amount of time and effort is something that the team collectively believes was a major contributor to their victory at the championship. As restrictive as this year's circumstances may have been, the new virtual format of the Mock Trial team's practices and meetings allowed for them to meet more frequently and consistently, especially with the postponement of the competition by several months.
"With our competition happening in February, rather than its usual time in the fall, our team had much more time to practice than we would during a normal season," Burke said. "Additionally, with the implementation of Zoom, we were able to schedule meetings with team members and coaches more frequently and conveniently, adding to our ability to prepare as a team. I am sure the extra time we put into practicing this year contributed to our county victory."
Sophomore Karina Pandurangadu, a prosecution attorney on the team, emphasized the importance of their confidence as a team, and how it ultimately contributed to their victory along with their many hours of practice.
"The match was, above all, fun. There were some questionable calls but we were confident throughout the trial," Pandurangadu said. "The victory felt like all the hard work we had put in since the summer had finally paid off. We've put in hours of work every week since July, the practice on both the team level and individual level helped us prepare for unpredictable situations and allowed us to win major arguments."
Hwang also believed that the overall support and cooperation amongst the team played a major part in their victory.
"What won us our victory was all of the practice and preparation we had been putting in all year, in addition to the collaborative and supportive environment we had on the team," Hwang said.
As the county champions, the Uni Mock Trial team represented Orange County at the California Mock Trial State Championship, held on Zoom from March 18-21, but did not place in the top eight teams.
chaitanya kotra
Cheyenne Hwang
karina pandurangadu
orange county constitutional rights foundation
Orange County Mock Trial
ryan alavi
simona forster
UHS Mock Trial
valencia high school
Chaitanya Kotra, Sports Section Editor
Hi, I'm Chaitanya Kotra! I'm a senior and one of the sports section editors this year. I'm looking forward to getting involved with yet another aspect...


It is at this park that Lee Soo-yeon's (Lee Je-hoon) gets a phone call from his airport colleagues that Han Yeo-reum (Chae Soo-bin) is hurt in episode 22 of Where Stars Land / Fox Bride Star (여우각시별) (SBS, 2018). Shocked by the news, he drops his cellphone and sitting in his wheelchair has difficulties to reach it.
This is one of Kim Shin (Gong Yoo) and Ji Eun-tak (Kim Go-eun) places to meet up in Goblin/Guardian: The Lonely and Great God (쓸쓸하고 찬란하神 – 도깨비) (tvN, 2016-17). In episode 4, a tipsy Shin talks a bit more about himself as he would have a done with a sober mind and also tells Eun-tak that she is his first and last bride. In episode 13, Eun-tak summons him here because she has missed him.
Also seen in episode 21 of Still 17 / Thirty But Seventeen / 30 But 17 (서른이지만 열일곱입니다) (SBS, 2018).
Cheongna Lake Park [청라호수공원] or Incheon Cheongna Central Lake Park/Cheongnajung-ang Waterside Park [청라중앙호수공원] is a public park located in Incheon's neighborhood Gyeongseo [Gyeongseo-dong/경서동] in the Seo District [Seo-gu/서구]. Opened in 2015, it is part of the development project 'Cheongna International City [청라국제도시]' and is understood as its leisure and recreational hub. One of the attractions of this park is its musical fountain [청라호수공원 음악분수].


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Call of Duty: Modern Warfare 3 takes US$775 million in five days
By Wei-Meng Lee on 18 November 2011 6:16pm - No Comments
As if it hasn't trumpeted its success enough, Activision announced today that Call of Duty: Modern Warfare 3 has shattered all previous five-day entertainment records — including movie, book and video game sales — by grossing US$775 million (S$1 billion) in the five days since the game's launch.
"Call of Duty has become the first entertainment property in history to set five-day launch records for three consecutive years across all forms of entertainment," said Robert Kotick, CEO of the game's publisher Activision Blizzard. "Life-to-date retail sales for the Call of Duty franchise have exceeded $6 billion worldwide."
I'm not sure how valid comparison between video games and other entertainment mediums are — a game like Modern Warfare 3 costs way more per unit and entertain longer than movies and books, and have a much longer pre-launch hype and marketing period — but it does show how big a juggernaut the Call of Duty franchise has become.
To underscore that, Activision also included some multiplayer statistics provided by Microsoft's Xbox LIVE service:
More than 7.0 million multiplayer hours were logged by the end of launch day
More than 3.3 million unique gamers played Call of Duty: Modern Warfare 3 in one day on November 8
A new record for concurrent players on Xbox LIVE with 1.4 million simultaneous users on November 8.
Pretty amazing numbers, and that's only from the Xbox 360, leaving PlayStation 3 and PC stats out of the picture. Now, if only Activision will move on from the Modern Warfare series/theme and introduce a new storyline and a new game engine…
We previously reported that the record concurrent players on Xbox LIVE was 3.3 million. Activision has since revised that figure to 1.4 million and we have corrected the mistake.
« Previous Story AFA11 photo post: Game and other cosplay Next Story » Minecraft comes out of beta; version 1.0 released
Two is just right for Modern Warfare 2 co-op
Modern Warfare 3 vs Battlefield 3: aka Steam vs Origin
More Modern Warfare 2 controversy
Is Modern Warfare 2 also a 3rd person shooter?
Call of Duty : World at War multiplayer demo released.


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Return the cosine of the parameter

### Declaration
```glsl
float cos(float angle)
vec2 cos(vec2 angle)
vec3 cos(vec3 angle)
vec4 cos(vec4 angle)
```

### Parameters
```angle``` specify the quantity, in radians, of which to return the cosine.

### Description
```cos()``` returns the trigonometric sine of angle.

### See Also
[acos](index.html#acos.md), [sin](index.html#sin.md), [asin](index.html#asin.md), [tan](index.html#tan.md), [atan](index.html#atan.md), [Chapter 05: Shaping Functions](../05/)

redpajama_set_name: RedPajamaGithub


# Count how many words are in a string.
# Count how many lines are in a string.
# Return the length of a string in chars.
string="$(min_string_length "$string" $number " ")"
| grep -o "^$(min_string_length "." $number ".")"
# Print an ANSI "unbold" escape string.
# Print an ANSI "bold" escape string.
# Format a URL appropriately.
# Return the video ID of a result_line.
# Return the URL of a result-line.
# Return the title of a result-line.
# Return the duration of a result-line.
# Return the channel of a result-line.
echo "$format_title | $format_duration | $url"
echo "$format_duration |  $format_uploaded |  $format_channel  |  $url"
# Get the title of a playlist, from HTML.
# Get the video-count of a playlist, from HTML.
# Get the view-count of a playlist, from HTML.
# Get the uploaded date of a playlist, from HTML.
# Get the author name of a playlist, from HTML.
# Get the author URL of a playlist, from HTML.
# Get the description of a YT video, from HTML.
# Get the views of a YT video, from HTML.
# Get the uploader's name of a YT video, from HTML.
# Get the title of a video, from HTML.
echo "usage: yt playlist --list [-UIcsmb] url/id"
echo "usage: yt playlist --search [-UIcsmb] search_query"
echo "usage: yt playlist views url/id"
echo "usage: yt playlist author [-Un] url/id"
echo "usage: yt playlist date url/id"
echo "usage: yt playlist title url/id"
query="$(echo "$query" | sed 's/ /+/g')"
if echo "$1" | grep "youtube" > /dev/null; then URL="$1"
echo "$(playlist_author_name "$html") | $(playlist_author_url "$html")"
echo "usage: yt video search [-UIcsmb] query"
echo "usage: yt video desc url/id"
echo "usage: yt video views url/id"
echo "usage: yt video author [-Un] url/id"
echo "$(video_author_name "$html") | $(video_author_url "$html")"


Vintage shower Glass Cabinet. Classic shower furnishings comes with a excellent personality to your room. Select this light green little nook cabinet. Merely studying this, people will know the shower is owned by people who understand room design and style very well. The basket in this cabinet will be able to enable you to be more organized.
You may also must consider classic minimalist structure. A whole lot of people think that a modern and minimalist design wouldbe perfect for the little dressing table cupboard. It's right, but just for the vanity without any prime. A traditional minimalist would make the mens shower shoes more cosmetic. Overly modern design can create your shower resemble a hardware store. At this time, it is suggested for you to decide on a shower vanity compared to coloration. Let's imagine that you own a light and neutral colour shower, the brownish or even black vanity using tops will probably be more decorative.
The Disadvantages of mens shower shoes. Recessed shower medicine cabinet costs you more because it takes carpenter, plumber, and electrician if you need to modify the path of one's wires and pipes. The very front mirror of recessed shower medicine cabinet is some inches farther in relation to wall mounted shower drug cupboard.
Other Classification of Vanities Cupboards. The opposite of classification of dressing table cabinets are filling together with the modern day shower vanities, conventional shower vanities, along with modern shower dressing table. It is my hope that this guide will grant you the clue to detect the appropriate of this dressing cabinet predicated on what you need. So, let us begin to get an appearance for that mens shower shoes!


text:
Genetic diagnosis by whole exome capture and massively parallel DNA sequencing
Murim Choi, Ute I. Scholl, Weizhen Ji, Tiewen Liu, Irina R. Tikhonova, Paul Zumbo, Ahmet Nayir, Ayșin Bakkaloğlu, Seza Özen, Sami Sanjad, Carol Nelson-Williams, Anita Farhi, Shrikant Mane, and Richard P. Lifton
PNAS November 10, 2009 106 (45) 19096-19101; https://doi.org/10.1073/pnas.0910672106
Murim Choi
Ute I. Scholl
Weizhen Ji
Tiewen Liu
Irina R. Tikhonova
Paul Zumbo
Ahmet Nayir
Ayșin Bakkaloğlu
Seza Özen
Sami Sanjad
Carol Nelson-Williams
Anita Farhi
Shrikant Mane
Richard P. Lifton
For correspondence: richard.lifton@yale.edu
Contributed by Richard P. Lifton, September 17, 2009 (received for review September 8, 2009)
Protein coding genes constitute only approximately 1% of the human genome but harbor 85% of the mutations with large effects on disease-related traits. Therefore, efficient strategies for selectively sequencing complete coding regions (i.e., "whole exome") have the potential to contribute to the understanding of rare and common human diseases. Here we report a method for whole-exome sequencing coupling Roche/NimbleGen whole exome arrays to the Illumina DNA sequencing platform. We demonstrate the ability to capture approximately 95% of the targeted coding sequences with high sensitivity and specificity for detection of homozygous and heterozygous variants. We illustrate the utility of this approach by making an unanticipated genetic diagnosis of congenital chloride diarrhea in a patient referred with a suspected diagnosis of Bartter syndrome, a renal salt-wasting disease. The molecular diagnosis was based on the finding of a homozygous missense D652N mutation at a position in SLC26A3 (the known congenital chloride diarrhea locus) that is virtually completely conserved in orthologues and paralogues from invertebrates to humans, and clinical follow-up confirmed the diagnosis. To our knowledge, whole-exome (or genome) sequencing has not previously been used to make a genetic diagnosis. Five additional patients suspected to have Bartter syndrome but who did not have mutations in known genes for this disease had homozygous deleterious mutations in SLC26A3. These results demonstrate the clinical utility of whole-exome sequencing and have implications for disease gene discovery and clinical diagnosis.
congenital chloride diarrhea
whole-exome sequencing
personal genomes
Genetic variation plays a major role in both Mendelian and non-Mendelian diseases. Among the approximately 2,600 Mendelian diseases that have been solved, the overwhelming majority are caused by rare mutations that affect the function of individual proteins; at individual Mendelian loci, approximately 85% of the disease-causing mutations can typically be found in the coding region or in canonical splice sites (1). For complex traits, genome-wide association studies have identified more than 250 common variants associated with risk alleles that contribute to a wide range of diseases (2, 3). To date, most of these impart small effects on disease risk (e.g., odds ratio of 1.2); moreover, even when extremely large studies have been performed, the vast majority of the genetic contribution to disease risk remain unexplained (4–6). These findings suggest that individually rare variants with relatively large effect may account for a large fraction of this missing trait variance. Indeed, studies addressing this question have documented the presence of individually rare variants with relatively large effect (7, 8). Consistent with the Mendelian model, coding variants have proven to be prevalent sources of such rare variants.
These considerations motivate implementation of robust approaches to sequencing complete coding regions of genomes (i.e., the "exome"). This has the potential to play a major role in disease gene discovery and also in clinical use for establishing a genetic diagnosis. As coding regions constitute only approximately 1% of the human genome, this is a potentially efficient strategy for identification of rare functional mutations, the more so given that our current ability to interpret the functional consequences of sequence variation outside coding regions is highly limited. The utility of this approach has been demonstrated in cancer, in which PCR amplification of individual exons has led to identification of new somatic mutations with large effect (9); nonetheless, PCR amplification of each coding sequence is cumbersome. Methods of enriching targeted genomic segments by hybridization have been used for 30 years (10), and have recently been extended to the whole exome scale (11), although their utility has been limited by the large amounts of genomic DNA required and by coupling to sequence platforms of modest throughput. Key considerations in this process will be cost effectiveness and completeness of the information obtained.
We report the adoption of whole-exome capture on single arrays on the Roche/NimbleGen platform to the Illumina sequencing platform. We illustrate the utility of this approach by identification of a rare mutation in a patient that led to an unexpected clinical diagnosis.
Coupling of NimbleGen Whole-Exome Capture to Illumina Sequencing.
The Roche/NimbleGen whole-exome array capture protocols were developed for DNA sequencing on the 454 platform (11); because the cost of sequencing on the Illumina platform is potentially considerably lower, we adapted hybrid capture using the NimbleGen 2.1M Human Exome Array to the Illumina DNA sequencing platform (see Methods). These arrays tile oligonucleotides from approximately 180,000 exons of 18,673 protein-coding genes and 551 micro-RNAs and comprise 34.0 Mb of genomic sequence. Resulting sequence data were processed using an automated pipeline: quality filtered sequence reads were aligned to the reference human genome (hg18) using Maq software (12). Single nucleotide variants (SNVs) were detected using Samtools (13) and further filtered (see Methods). For heterozygote calls we required at least 10× coverage by reads with different start sites, base call with Phred-like (14) quality scores greater than 45, and the probability of the frequency of major and minor alleles deviating from the binomial distribution of at least 10−7. Rare SNVs that cluster within 1 kb were tagged and evaluated for mapping errors. SNVs were annotated for effect on the encoded protein and for conservation by comparison versus sequences of 43 vertebrate species (15) and orthologues in fly and worm (see Methods).
Major changes in the protocol included shortening the length of the genomic DNA used for hybridization from 250 to 150 bases, which significantly increased the percentage of sequenced bases mapping to targeted bases (from 29% to 37%). We varied stringency by increasing the wash temperature from 47.5 °C to 53.5 °C. The higher stringency increased the percentage of on-target bases to 56%, but reduced breadth of coverage: at mean 30× per base coverage, the percentage of bases read fewer than 10 times increased from 7% to 23%.
In our current protocol, we captured and sequenced samples from 5 Caucasian subjects to a mean depth of 44×; these samples were also genotyped on the Illumina 370K SNP platform. The targeted bases constituted approximately 37% of all bases read (Table 1). An additional 12% of bases were within 100 base pairs of targeted sequences. The distribution of reads across all targeted bases is shown in Fig. 1A, which demonstrates that nearly all targeted bases are captured. Poorly captured bases, however, are correlated across different capture experiments, with approximately 352 kb (1.0%) read fewer than 10 times in each capture experiment. These underrepresented bases are predominantly from segments with exceptionally high G-C composition [supporting information (SI) Fig. S1]. We have captured 10 additional samples with this protocol with similar enrichment. With a single lane of Illumina sequencing using 75 base paired-end sequence using Illumina pipeline v. 1.4, we were able to produce an approximate mean 30× per-base coverage of the targeted bases, with 93% of targeted bases read at least 10 times; at 60× coverage with 2 lanes, 97% were read at least 10 times.
Summary statistics for whole exome capture on samples from 5 subjects
Coverage of targeted bases, error rate, and sensitivity to detect variants in whole-exome capture data. (A) Distribution of per-base read coverage among 5 capture experiments. A small fraction of targeted bases are poorly captured across all experiments. (B) The per-base error rate in this data set is shown as a function of read position. (C) Subject GIT 264–1 was sequenced to a mean depth of 99×. The sensitivity to detect homozygous (solid line) or heterozygous (dashed line) variants as mean depth of whole-exome sequence coverage increases from 0 to 100× is shown. Sensitivity to detect heterozygous variants increases from 81% to 90% to 95% as mean coverage is increased from 20× to 30× and 40×, and plateaus at 98%. (D) Sensitivity of detection of heterozygous variants at exact per-base coverage. Sensitivity is approximately 80% at 10× coverage, and approaches 100% at or greater than 20× per-base coverage.
To assess the effect of coverage depth on sensitivity to detect sequence variants, one of these samples, GIT 264–1, was further sequenced to a mean depth of 99× and the genotype calls at known SNP positions were compared versus the results obtained with genotype calls on the Illumina 370K chip. At this depth of mean coverage, the sensitivity of exome sequencing for detecting homozygous and heterozygous variants was 99.8% and 98.2%, respectively (Fig. 1C). Sensitivity increased steeply as coverage increased from 5× to 20×, then more gradually thereafter, reaching a final plateau at approximately 50×. At any mean depth of coverage, there is a range of coverage at each base, and the ability to call heterozygous bases varies with the exact read coverage. Thus, the sensitivity to detect heterozygous variants with 10 reads is 78.6%, but increases to 95.2% at 20× and approximately 100% at 30× and greater (Fig. 1D). The overall per-base error rate for this sample was 0.75%, with error rate increasing approximately 10-fold from base 20 to base 75 (Fig. 1B).
Among the 5 test samples, we found a mean of 20,356 exomic variations from the reference sequence per subject (Table 1). An average of 1,055 per exome are not previously reported to our knowledge [i.e., not in the reference genome or 4 individual published genomes (16–19)] and were classified as novel. The small fraction of novel variants is consistent with a very high specificity for variant detection. These variants included a mean per exome of 12,372 coding SNVs (cSNVs; 642 novel), of which there were 5,341 missense variants (368 novel), 32 premature termination codons (7 novel), 81 canonical splice site variants (7 novel), and 6,815 synonymous substitutions (240 novel). Among the novel missense variants, 147 per exome introduce substitutions that are highly conserved among vertebrates, and among these, 40 are at positions that are also conserved in Drosophila melanogaster and/or Caenorhabditis elegans. Of the previously unreported exomic variants, 166 were shared among 2 or more subjects.
In subjects such as GIT 264–1 who are the product of consanguineous union (as described later), large segments of the genome are homozygous by descent; in these segments, all variations from the major allele can be considered errors, and heterozygous calls in such segments provide a further estimate of specificity (a small fraction of these could be bona fide de novo mutations). In this subject, 462 Mb of the genome were homozygous by descent as determined by genotyping (defined as segments of ≥100 consecutive SNPs spanning ≥1 Mb with ≥98% homozygosity; Table S1), including 5.3 Mb of the exome, comprising 2,459 genes. In these homozygous segments there was 1 heterozygous call at 99× coverage. This leads to an estimated false heterozygote discovery rate of 6 per exome and specificity for heterozygous calls of 99.9%. The specificity remains 99.9% at mean coverage of 30×. Interestingly, the false-positive call is present in the SNP database, so if one considers only novel variants in these calculations, specificity would be 100% at both levels of coverage.
These findings demonstrate a protocol of sufficient sensitivity and specificity to be highly useful for detecting rare sequence variants across the whole exome.
Case Report, Subject GIT 264–1.
Subject GIT 264–1, a Turkish male, presented at age 5 months for evaluation of failure to thrive and dehydration. The history was notable for premature birth at 30 weeks and parental consanguinity, with 2 spontaneous abortions and death of a premature sibling on day 4; the parents were healthy (Fig. 2). Blood pressure was 90/55 mmHg and laboratory evaluation was notable for serum K+ level of 2.8 mmol/L, HCO3− level of 36 mmol/L; plasma renin activity and serum aldosterone levels were markedly elevated (Table 2). Despite volume depletion, his diapers were noted to be wet. The differential diagnosis of the admitting physician and consultants was broad, including a renal defect such as Bartter syndrome; however, a neurologic defect or an infectious process was not excluded. A venous blood sample was obtained and genomic DNA was prepared.
Kindred GIT 264. The affected subject is indicated by the arrow, and the pedigree structure demonstrates parental consanguinity. A presumably affected sister died 4 d after premature birth (gray symbol), and there were 2 other spontaneous abortions (small triangles, disease status unknown). The parents and other relatives were free from clinical syndromes like that seen in the index case. For simplification, the mother's 10 siblings and the father's 8 siblings are not depicted in the pedigree.
Clinical data of patients with mutations in SLC26A3
Molecular Genetic Analysis.
From the history, it was inferred that the patient likely had a recessive genetic trait. Genome-wide SNP genotyping was performed as described earlier. To search for copy number variants, the SNP data were interrogated by using a likelihood ratio-based copy number variant detection algorithm (see Methods). Within the homozygous-by-descent segments, 20 homozygous deletions were identified. All these were previously reported in the Database of Genomic Variants (20); none of these alter protein coding sequences (Table S2). No homozygous duplications were identified. Interestingly, none of the known loci for Bartter syndrome were within segments of homozygosity.
Analysis of Whole-Exome Sequence of Subject GIT 264–1.
Given the diagnostic uncertainty, this patient's genomic DNA was subjected to whole-exome sequencing as described earlier. A total of 143 million reads passed quality assessment and 95.0% aligned to the human reference sequence; 38.4% of the total bases mapped to the targeted bases with mean coverage of 99×. At this depth of coverage, 99.3% of the bases were read at least 5 times and 98.4% of the bases were read at least 10 times (Table S3).
Mutation in SLC26A3.
We anticipated finding a homozygous disease-causing mutation within a segment that is homozygous by consanguineous descent. We consequently sought novel and rare mutations that alter the encoded protein within the 5.3M base pairs and 2,495 genes in these segments. We identified 2,405 homozygous variations, including 1,493 homozygous cSNVs, from the reference sequence in these segments. These cSNVs included 668 non-synonymous substitutions (29 of which were novel), 791 synonymous coding variants (16 novel), 12 canonical splice site variants (0 novel) and 19 coding region indels (0 novel; Table S4). There were 3 premature termination codons in these segments (0 novel). The remaining 931 variants were in introns, UTRs, or intergenic regions. All of the novel missense variants were confirmed by Sanger sequencing of PCR-amplified segments, confirming the high specificity for detection of rare variation.
Substitutions at positions that are completely conserved from invertebrates to humans are highly likely to disrupt normal protein function (8), and we ranked the novel missense variants by conservation scores to identify the most likely functional mutations using the phyloP conservation score (Table S4). Ten of the homozygous variants were at highly conserved positions (i.e., score ≥2).
Among the novel homozygous mutations at extremely conserved positions, one strongly stood out: a single-base substitution that introduced a missense variant in SLC26A3 (Fig. 3). This mutation was identified in 172 of 173 reads covering this base; reads of this base had divergent start and end points and were read from both strands; the remaining read of this base was neither WT nor this mutant (Fig. 3A). The identity and homozygosity of this mutation was confirmed by PCR amplification and direct Sanger sequencing (Fig. 3B). This mutation introduces a D652N substitution at a position that is completely conserved among all invertebrates and vertebrates studied (Fig. 3C). This residue is also identical in 8 of 9 human paralogues (Fig. 3D); the only exception, SLC26A11, has glutamate rather than aspartate at the corresponding position. This mutation is noteworthy because SLC26A3 encodes an epithelial Cl−/HCO3− exchanger comprising 764 aa (Fig. 3E); recessive loss of function mutations in this gene are known to cause congenital chloride-losing diarrhea [CLD; i.e., OMIM 214700 (21)] in humans and mice (22). The D652N mutation lies in a β-pleated sheet in the STAS domain (Sulfate Transporters and bacterial Anti-Sigma factor antagonists) of the protein (Fig. 3E), which is known to be required for both the activity and biosynthesis/stability of the transporter. Indeed, other mutations at conserved positions in the STAS domain have been shown to cause congenital chloride diarrhea (23). This mutation was absent among 190 control chromosomes. We identified no other compelling homozygous or heterozygous candidates for disease-causing mutations outside homozygous chromosome segments.
Homozygous missense mutation at highly conserved position in SLC26A3 in GIT 264–1. (A) Top: Reference sequence of aa 636–668 of SLC26A3 and the corresponding DNA sequences are shown. Below: Independent Illumina DNA sequence reads from GIT 264–1 are shown. Forward and reverse reads are shown in capital and lowercase letters, respectively. The results demonstrate a homozygous missense mutation, D652N. (B) Sanger sequence of codons 651–653 of SLC26A3 in a WT subject and GIT 264–1 are shown and confirm the D652N mutation. The mutated residue is indicated by an asterisk, and the encoded amino acids are shown in single-letter code. (C) Conservation of D652 across species. The amino acid sequence of segment 648–656 of human SLC26A3 is shown and compared to the corresponding sequence of 6 (of 39) vertebrates and identified in D. melanogaster paralogue and C. elegans orthologue. Positions identical to Homo sapiens (H.s.) are highlighted in yellow. D652 is completely conserved among all species examined. M.m., Mus musculus; O.c., Oryctolagus cuniculus; B.t., Bos taurus; G.g., Gallus gallus; X.l., Xenopus laevis; D.r., Danio rerio; D.m., D. melanogaster; C.e., C. elegans. (D) The sequence of the same segment of human SLC26A3 is compared to 9 paralogues of the human SLC26A gene family (SLC26A1-A11; SLC26A10 is a pseudogene). (E) Structure of SLC26A3. The protein has 12 transmembrane domains and a C-terminal STAS domain (highlighted in blue). The D652N mutation (red circle) lies in the STAS domain.
Our genetic findings strongly suggested that this patient had congenital chloride diarrhea; the clinical findings of volume depletion, hypokalemia, and metabolic alkalosis are all consistent with this diagnosis. This prompted clinical follow-up with the referring physician to determine whether the volume loss was from renal or gastrointestinal sources. Follow-up revealed that the patient indeed had diarrhea that occurred every 1 to 2 h, which had been persistent. Urinary electrolyte measurements with the patient volume replete did not reveal hypercalciuria or other features of Bartter syndrome (urinary Ca2+:Cre ratio, 0.0076 mg:mg), indicating a primary diagnosis of CLD.
Additional Patients with SLC26A3 Mutations.
These findings led us to consider whether additional subjects referred with a presumptive diagnosis of Bartter syndrome might instead have CLD caused by mutation in SLC26A3. This mistaken diagnosis is particularly likely at the acute presentation: after volume and electrolyte resuscitation, urinary electrolyte levels can be appropriately high (when in balance, net intake and output are equal) but mistakenly interpreted as inappropriate, and volume loss from the urinary tract versus the gastrointestinal tract may not be immediately discriminated in infants.
We consequently screened 39 subjects referred with a suspected diagnosis of Bartter syndrome in whom mutations in NKCC2, ROMK, ClC-Kb, and Barttin had not been identified. We found 5 additional patients who had homozygous mutations in SLC26A3 (Table 2 and Fig. 4). These mutations included 2 unrelated subjects with a G187X premature termination codon, one with a frameshift mutation at codon 454 resulting in premature termination at codon 458, one with the same D652N mutation found in the index case, and one with a Y520C mutation (Y520 is completely conserved among all vertebrates and invertebrates studied; Fig. 4F). All these mutations are considered novel except for the G187X mutation, which is a known founder mutation for congenital chloride diarrhea in Saudi Arabia (24). None of these mutations were found in sequencing of 190 control chromosomes from unrelated Caucasian subjects. All these patients had hypokalemia, metabolic alkalosis, and evidence of salt wasting. Follow-up with the referring physicians in 3 cases documented that volume depletion was caused by gastrointestinal losses from watery diarrhea and not renal losses; in 2 cases, high stool chloride level was documented (GIT 366–1, 112 mM; GIT 409–1, 148 mM; value should be >90 mM in CLD), a finding that is pathognomonic for congenital chloride diarrhea. In each of the 2 remaining cases, the patient was not available for further evaluation.
Additional patients with SLC26A3 mutations. Sanger sequence traces of WT and 5 subjects with homozygous mutations in SLC26A3 are shown. These include two subjects with premature termination at codon 187 (A and B); a frameshift at codon 454 resulting from a single base deletion that leads to termination at codon 458 (C); a second patient with the D652N mutation (D); and a patient with a Y520C mutation (E). (F) Conservation of Y520 across species: Y520 is conserved among all orthologues and paralogues examined.
Our results demonstrate the utility of whole-exome sequencing, coupling sequence capture on the NimbleGen platform and sequencing on the Illumina platform, for identification of rare variants and disease-causing mutations. The protocol used provided sufficient enrichment to drastically reduce the amount of DNA sequencing required to identify sequence variation in coding regions. Virtually all the targeted bases can be captured by using the current protocol albeit with varying efficiencies, and additional efforts might further balance the coverage of poorly sequenced bases. We estimate that exon capture reduces the cost of detection of exonic mutations by a factor of 10 to 20 compared with whole-genome sequencing, depending on the sensitivity pursued. Using the current protocol, 2 lanes of capture sequence can produce approximately 60× read depth per base, resulting in detection of approximately 97.2% of the heterozygous bases; it is expected that, among the approximate average of 402 protein-altering rare variants per exome, there will be a very small number of false-positive variants. Increased reads per lane are expected to occur in the near future, likely permitting virtually complete capture of variation in a single lane of sequence, and further improvements in base calling will likely occur as well, resulting in improvements in both sensitivity and specificity.
During preparation of this manuscript, a related paper was published that demonstrated development of a different platform for whole-exome capture and sequencing on the Illumina instrument (25). The targeted exons were similar, both based on the consensus coding sequence database. The overall results are similar, with both platforms showing high sensitivity and specificity. We anticipate that it will be useful to have multiple platforms available for performing whole-exome analyses.
We have demonstrated the utility of this platform by making an unexpected genetic diagnosis in a patient with an undiagnosed illness; to our knowledge, this has not been previously reported. The diagnosis of congenital chloride diarrhea was not considered in the referral differential diagnosis, but after identification of mutation in SLC26A3 suggested the diagnosis, it was confirmed by follow-up clinical evaluation. This example provides proof of concept of the use of whole-exome sequencing as a clinical tool in evaluation of patients with undiagnosed genetic illnesses. These findings further underscore the ability to parse large quantities of sequence data to produce clinically useful information that combines clues from the clinical condition in conjunction with the genetic data to arrive at a correct diagnosis. We can envision a future in which such information will become part of the routine clinical evaluation of patients with suspected genetic diseases in whom the diagnosis is uncertain.
In addition to clinical genetics, we anticipate applications for whole-exome sequencing that include discovery of genes and alleles contributing to Mendelian and complex traits, and to somatic mutations in cancers. For dominant traits, we expect that many whose causes have not yet been identified are explained by alleles that have been difficult to map by linkage analysis. Likely explanations include traits with reduced penetrance, traits that show substantial locus heterogeneity, and alleles that impair reproductive fitness sufficiently that many affected subjects harbor de novo mutations. The finding of independent de novo mutations in the same gene among a small number of affected subjects would constitute compelling evidence of disease causation. Similarly, with locus heterogeneity, identification of a significant excess in the number of independent mutations in the same gene versus that expected by chance will constitute evidence that a disease gene has been identified. Mapping data that constrain the location of the disease locus, animal models that produce similar phenotypes, and compelling biology can all contribute to identification of such loci; however, in the absence of such information, inference from the large number of variants in a single subject will be challenging.
For recessive traits, affected subjects arising from consanguineous union contain substantial mapping information: in this setting, the disease locus is expected to be homozygous within a segment that is homozygous by descent from a recent ancestor. For first cousins, this constrains the search on average to approximately 10% of the exome. Detection of homozygous novel variants in these segments is highly efficient at even low levels of per-base coverage (e.g., 5×); these considerations simplify the problem as there are very few (approximately 29) rare homozygous protein-altering variants in these segments. As described earlier, the finding of an excess of independent mutations in the same locus will provide compelling evidence that a disease locus has been identified, and KO animal models may be particularly helpful as recessive mutations so typically impart loss of function.
Finally, for complex traits, sequencing large numbers of cases/controls or subjects at the tails of a quantitative distribution will enable identification of genes preferentially harboring an excess of rare functional mutations at one end of the distribution. The sample sizes required to identify such loci are expected to be large for alleles that have odds ratios of disease of 2 to 3 (26–28). Such studies can be achieved either by whole-exome sequencing of all subjects or by sequencing the exome of a subset of subjects followed by selective sequencing of the most promising genes in follow-up studies. It is of course likely that non-coding sequences will harbor some rare variants with relatively large effect that would be missed by selective sequencing of coding regions.
At present, the sequence of each new individual identifies approximately 402 novel variants introducing changes in the encoded protein. Recognition of functional mutations among these poses a challenge. Investigation of consanguineous kindreds for recessive traits can reduce the search complexity by an order of magnitude. Mutations that introduce truncations of the encoded protein, or that occur at highly conserved positions, are more likely to have functional effects and can be prioritized. In addition, as databases are filled with exome sequences of large numbers of subjects, the ability to distinguish low-frequency alleles descendent from ancient ancestors from de novo or extremely rare mutations recently introduced into the population will markedly improve, permitting focusing attention on this smaller set of alleles. We anticipate that whole-exome sequencing will make broad contributions to understanding the genes and pathways that contribute to rare and common human diseases, as well as clinical practice.
Human Subjects.
The study protocol was approved by the Yale Human Investigation Committee. Consent for participation was obtained in accordance with institutional review board standards. Patients were referred for studies of Bartter syndrome, and consanguineous kindred subjects in whom no mutation in genes causing Bartter syndrome had been identified were chosen for further analysis. Genomic DNA was prepared from venous blood by standard procedures.
Targeted Sequence Capture.
Genomic DNA was captured on a NimbleGen 2.1M human exome array following the manufacturer's protocols (Roche/NimbleGen) with modifications at the W. M. Keck Facility at Yale University. DNA was sheared by sonication and adaptors were ligated to the resulting fragments. The adaptor-ligated templates were fractionated by agarose gel electrophoresis and fragments of the desired size were excised. Extracted DNA was amplified by ligation-mediated PCR, purified, and hybridized to the capture array at 42.0 °C using the manufacturer's buffer. The array was washed twice at 47.5 °C and 3 more times at room temperature using the manufacturer's buffers. Bound genomic DNA was eluted using 125 mM NaOH for 10 min at room temperature, purified, and amplified by ligation-mediated PCR. The resulting fragments were purified and subjected to DNA sequencing on the Illumina platform. Captured and non-captured amplified samples were subjected to quantitative PCR to measure the relative fold enrichment of the targeted sequence.
Sequencing.
Captured libraries were sequenced on the Illumina genome analyzer as single-end 50-, 74-, and 75-bp reads, or 75-bp paired-end reads, following the manufacturer's protocols. Image analysis and base calling was performed by Illumina pipeline versions 1.3 and 1.4 with default parameters.
Sequence reads were mapped to the reference genome (hg18) using the Maq program (12). Reads outside the targeted sequences were discarded and statistics on coverage were collected from the remaining reads using perl scripts. For indel detection, BWA was used to allow gapped alignment to the reference genome (29). SAMtools was used to call targeted bases, and any base call that deviates from reference base was regarded as a potential variation (13). Additional filters were applied as described in the SI text. Identified variants were annotated based on novelty, impact on the encoded protein, conservation, and expression using an automated pipeline (SI Text).
Genotyping and Identification of Loss-of-Heterozygosity Intervals.
Samples were genotyped on the Illumina HumanCNV370-Duo BeadChips. Sample processing and labeling were performed following the manufacturer's protocols. Plink v. 1.06 was used to identify homozygous intervals from subject GIT 264–1. A sliding window of 50 SNPs was used on the tag SNPs and included no more than one possible heterozygous genotype. Resulting intervals have to meet the limit of at least 100 SNPs and 1 Mb in size.
Copy Number Variation Prediction Algorithm.
To predict possible deletion or duplication events in the genome, LogR and B allele frequency data were extracted from SNP array and normalized to the larger sample pool to remove sample-specific noise. Based on the empirical distribution of LogR and B allele frequency values from the validated deletion and duplication SNPs, for a given SNP, the likelihoods of being 0, 1, 2, and 3 or more copies were calculated, respectively. If more than one SNP supporting deletion or duplication arose consecutively and the likelihood ratio of the SNPs exceeded threshold, they were called a deletion or duplication.
DNA Sequencing.
The ExonPrimer script (http://ihg2.helmholtz-muenchen.de/ihg/ExonPrimer.html) was used to generate primers for amplification of SLC26A3 coding exons using as a template genomic DNA of patients or controls (Table S5). Products were analyzed via gel electrophoresis, and amplicons sequenced using the forward or reverse primers. Disease-causing mutations were confirmed by at least 2 independent sequences from different primers.
Orthologues and Paralogues.
Full-length orthologous and paralogous protein sequences from vertebrate and invertebrate species and human paralogous protein sequences were extracted from GenBank. Orthologues were confirmed based on database identity of annotation. If an orthologue could not be identified, the closest paralogue (i.e., top "hit" of a BLAST search of the respective proteome) was studied. Protein sequences were aligned using the ClustalW algorithm. GenBank accession numbers are listed in the SI Text.
We thank the patients studied and their families for their irreplaceable contribution to this study. We thank Tom Albert of Roche NimbleGen, Ali Gharavi, Lynn Boyden, George Farr, Murat Gunel, and Matt State for helpful discussions. Supported in part by the Leducq Transatlantic Network in Hypertension, a National Center for Research Resources High End Instrumentation grant and the Yale National Institutes of Health O'Brien Center for Kidney Research.
1To whom correspondence should be addressed. E-mail: richard.lifton{at}yale.edu
Author contributions: M.C., U.I.S., S.M., and R.P.L. designed research; M.C., U.I.S., W.J., T.L., I.R.T., P.Z., A.N., A.B., S.Ö., S.S., C.N.-W., A.F., S.M., and R.P.L. performed research; M.C., U.I.S., W.J., and R.P.L. analyzed data; and M.C., U.I.S., W.J., and R.P.L. wrote the paper.
This article contains supporting information online at www.pnas.org/cgi/content/full/0910672106/DCSupplemental.
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(2006) slc26a3 (dra)-deficient mice display chloride-losing diarrhea, enhanced colonic proliferation, and distinct up-regulation of ion transporters in the colon. J Biol Chem 281:37962–37971.
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(2008) Congenital chloride-losing diarrhea causing mutations in the STAS domain result in misfolding and mistrafficking of SLC26A3. J Biol Chem 283:8711–8722.
(1998) Clustering of private mutations in the congenital chloride diarrhea/down-regulated in adenoma gene. Hum Mutat 11:321–327.
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You are going to email the following Genetic diagnosis by whole exome capture and massively parallel DNA sequencing
Murim Choi, Ute I. Scholl, Weizhen Ji, Tiewen Liu, Irina R. Tikhonova, Paul Zumbo, Ahmet Nayir, Ayșin Bakkaloğlu, Seza Özen, Sami Sanjad, Carol Nelson-Williams, Anita Farhi, Shrikant Mane, Richard P. Lifton
Proceedings of the National Academy of Sciences Nov 2009, 106 (45) 19096-19101; DOI: 10.1073/pnas.0910672106
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text:
Spilobotys snelleni är en fjärilsart som beskrevs av M.Gaede 1914. Spilobotys snelleni ingår i släktet Spilobotys och familjen nattflyn. Inga underarter finns listade i Catalogue of Life.

Källor

Nattflyn
snelleni

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Their Ad is a scam.
Leaders in category of worst mobile operators.
Facing network problem, Worst network.
Airtel 4G promised at a speed of lower than 2G.
CONNING IN NAME OF AUTO RENEW.
Worst network. Airtel is charging more than the plan we selected that is the reason where airtel has more that 95000 cr as revenue. Airtel employee him self confisted that airtel network is giving fake information and bluffing customers. so please go with airtel network.


text:
Game 10 Recap
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Team Observations
--One thing I don't understand is that we came out with a rather stagnant offense right from the start in the first quarter. Zach needs to get many, many touches but haven't we proved by now that you cannot just enter the ball from a standstill to Zach and wait until he gets double teamed? All night the lesson was the same: cut and penetrate, we score either off the dribble or through the dish. Stand and post and we get swamped, throw up a desperation shot, or turn the ball over. And it's not like this is the first time we've talked about this. So why, for the first three minutes of the game (when theoretically we should be running the coached game plan), are we all standing still?
--It was not a bad first quarter at all defensively. We stayed in front of our men and for the most part didn't let their key guys get off. That, however, was soon to change...
--We didn't control the boards as much as I had hoped.
--We really didn't draw fouls as much as we needed because Boston was penetrating and we were not.
--Boston also predictably torched us from deep because we did not rotate out. In fact the defense tonight was pretty horrible after the first quarter. (It's like we said, "Whew! Didn't get blown out in the first! It's Miller Time!) And what was the #1 rule of defense for this game? "Do not leave Wally Szczerbiak in order to help." He scored 19 on 60% shooting. That was the straw that broke the camel's back.
--After the camel's back snapped, we just lost it entirely. Not only was there no hustle or mental commitment, there was just no team out there. It's not even a matter of talking about what went technically wrong at that point. We just got run out of the gym altogether. This is the first real sign of "give up" we've seen this year.
Individual Observations
--Zach's stats say 23 and 12, which looks pretty good. He did do a decent job defensive rebounding and drawing fouls. But Zach was not into this game. He missed a bunch of pretty decent shots, he made some abhorrent passes, and the (admittedly biased) Boston broadcast crew accused him of loafing. I'm not sure I'd use the "L" word exactly but at least part of the night's frustration came from him not being in it and part of the giving up came from him checking out early. I have not pinned much of anything on Zach this year because he's been pretty active in all the games we've played, but he does shoulder some of the responsibility tonight.
--I think Aldridge got a little caught up in the starting thing. He did remember to score. In fact he did an excellent job with the ball in his hands, and what's more making himself available for nifty point guard passes. A+ for that. But for most of the game he forgot to do what got him there, which was rebound with intensity. I like the elegant Aldridge, but we really need more of the gritty Aldridge too.
--Jarrett Jack went up and down in this game. For parts of the game he was penetrating, scoring, and dishing like the second coming of Sergio. Not coincidentally, those were the parts of the game where we made our runs. For other parts he was much less aggressive. During those parts we saw more jumpers from the team, less movement, and more turnovers. Despite 8 assists Jack had 5 turnovers all on his own. I like Jack's game but he should only play for as much of the game as he can provide that attacking energy, because the passive Jack isn't that good for us.
--It's a shame Travis Outlaw got into foul trouble because he was having a really nice game for us and probably could have made a difference out there. The newly found point guard passing ability is helping his game a lot.
--The stats say Juan Dixon had a nice game (5-9, 11 points, 3 assists, 2 boards) so why didn't I notice him?
--Ime Udoka also had a really good stat line (6-13, 2-4 from deep, 14 points, 6 rebounds, 4 assists, 1 turnover) but I was hoping for a little more on the defensive end against Pierce I guess. That's probably expecting way too much of Ime though. I'm not sure he should get 13 shots a game but if he can deliver comparable stats with every 30 minutes he gets he'll be fine.
Now for the ripping...
--Sergio returned to earth. 2 assists, 3 turnovers. I don't mind the latter too much because a couple of them just weren't his fault. If people had been ready to catch his passes it would have been 4 assists, 1 turnover. My beef is with his 0-6 shooting. The shots weren't that hard either. If you can't hit a layup you can't play no matter how good of a passer you are. On the upside, his defense wasn't that terrible tonight.
--Stephen Graham must have thought we put him in to win the game by himself. There was a fair amount of 1-on-1 going on for him. The results were no made shots, no rebounds, no assists, 1 turnover, 1 free throw, 1 point, and three fouls in 10 minutes. Wah-wah-waaaaaaah.
--Martell picked up 4 fouls in 19 minutes. Can't do that. And nobody's getting the ball to the weak side on offense anymore either. You better start running him off of screens and curls again pretty soon.
--Note to Jamaal Magloire: You are a rebounder. Your job is rebounding. We are one of the worst rebounding clubs in the league so you know nobody else on our team is taking them away from you. Here's your stats from the last few games:
vs. Lakers 11 rebounds...win.
vs. Hornets 6 rebounds (in 17 minutes)...win.
vs. Mavericks 1 rebound...loss.
vs. Timberwolves 2 rebounds...loss.
vs. Cavaliers 3 rebounds...loss.
vs. Celtics 1 rebound...loss.
If you do not rebound, you cannot play, because if you do not rebound you do not help us. End of story.
--The refs had an inconsistent night tonight at both ends. This didn't cause us to lose, it's just annoying.
--Speaking of annoying, please, please, PLEASE tell me when we play Boston again on January 1st NBA League Pass will show the Portland broadcast feed. I say this every year, but time passes and I forget and somehow I am always surprised anew: Tommy Heinson is the pits as an analyst. Short example: Sergio Rodriguez hits a wet spot on the floor and his feet slide out from under him...somehow this is brilliant defense on the part of the Celtics. Had something similar happened to Boston the story would have been the opposite. I understand that team-paid crews root for the teams that pay them. Lord knows ours do more than I'd like. But sheesh, at least Mike Rice comes across like he knows you shouldn't believe everything he says. Heinson is like on another planet or something...


Dropkick Murphys St. Patrick's pre-sale. UK tour with Souls.
Dropkick Murphys are happy to announce that once again we will be playing in our hometown of Boston for St Patrick's Day in 2005. These shows have become an institution and we hope to make next year's event bigger and better than ever.
The shows will be on Thursday 17th, Friday 18th, Saturday 19th & Sunday 20th March. And for the first time we will be offering tickets for sale through our website before they go on sale to the general public.
All the people who are on our mailing list will be sent out the information Tuesday November 30th on how to buy these early bird tickets. A week later on December 7th the tickets will go on sale to everyone else.
We have also worked out a special deal for the people who do buy tickets through our website so that you will get a reduced rate on the service charges. There will only be a limited number of tickets at this special rate so you will need to be quick. To get tickets head href='http://images-staging.musictoday.com/stores/dropkickmurphys112904a.asp' target='_blank'>HERE after 4.00pm EST today!
We hope to be able to offer this service to you for more of our shows in the future so it's worthwhile to get onto the mailing list now. Stay tuned for more information about door times, ticket outlets and support bands and happy thanksgiving!
We are very happy to announce that our good friends the Bouncing Souls will be joining us on our UK tour in March 2005, opening act is the Godawfuls. These show are going to be awesome, tickets are on sale now through various outlets - please click here for more details.


Receiving a cancer diagnosis can be a life-altering, stressful event for patients and their families. Day-to-day tasks seem less important as priorities shift to accepting the diagnosis and deciding the next steps in the treatment plan. Choosing where to receive treatment is nearly as important as what treatment plan to pursue.
Every cancer is unique. Treatment options, survival rates and complexity vary with each type of cancer. Take time to ask questions, understand your treatment options and the risks and potential outcomes of each choice. Key to these discussions is the best location for your treatment.
How many cases of my type of cancer have you treated in the last year?
How many of these cases have been treated in this facility?
How many times has this therapy been performed here?
How should I expect to feel during and after treatment?
What is the purpose of this therapy?
What will my quality of life be with this option?
Some types of cancer, such as breast, colon, prostate and skin cancer, are often discovered through routine screening exams ordered by primary care physicians. In most cases, a patient facing a cancer diagnosis will need a referral to a specialist or for follow-up testing. Family medicine physicians can coordinate these referrals. Many will make appointments with specialists for patients to ensure timely follow-up care.
Patients and their families may feel overwhelmed by the cancer treatment process, the steps to take or how to seek assistance. A patient navigator or nurse navigator can provide support for cancer patients and their families by managing the tasks and issues associated with cancer treatment. Usually a free service provided by certain cancer centers, the primary goal of a cancer nurse navigator is to ensure that patients receive quality diagnostic, therapeutic and support services on a timely basis.
Thomas Kayal, MD, colorectal surgeon and Troy Sukkarieh, MD, urologic surgeon with the new DaVinci robot at CentraState Medical Center in Freehold, NJ.
Some patients or their family members believe the only options for comprehensive cancer care are at facilities in New York City or Philadelphia. Bigger isn't always better. If you have considered a treatment center outside of your geographic area, be sure to meet with local specialists as well to compare facilities and treatment plans. If each specialist recommends the same course of treatment, it may make sense to choose a local cancer treatment center for convenience and continuity of care.
Treatment may require multiple visits with multiple specialists, which can be stressful, costly, time consuming and physically exhausting, especially for patients undergoing chemotherapy or radiation therapy. Most suburban cancer specialists trained at the same facilities as the specialists who practice in a major city. Choosing a local facility means you'll not only have the convenience of being close to home, but you'll also have access to seasoned, highly-skilled physicians and cutting-edge cancer treatments, like robotic surgery, video-assisted thoracic surgery, targeted proton therapy and promising clinical trials.
No matter where you choose to have treatment, it's important that your local physicians are involved in that process. At large facilities, communication between physicians can break down. Continuity of care from primary care physician to oncologist to surgeon and back to primary care physician is paramount, because it's often the primary care physician who treats the side effects of cancer treatment. It's important to choose a facility that supports and emphasizes open communication among providers – and patients.
Every cancer diagnosis is serious. Patients and their caregivers should thoroughly research and review their options and include family physicians in these discussions. Ask your physician questions if you don't understand the information that you've been given. Be well informed about your diagnosis, fully understand your treatment options and, perhaps more importantly, be sure to understand the expected outcomes of your treatment.
Locally, the Statesir Cancer Center at CentraState Medical Center delivers comprehensive treatment and support services to help patients and their families. With a team of skilled primary care physicians, leading cancer specialists and compassionate nurse navigators, patients can experience a unified support system. If you or a loved one have received a diagnosis and need information, patients can speak to someone at (855) 411-CANCER.


You will be helping this little teen fairy with her preparations making sure she gets as pretty as can be. In order to do that, you'll have to take her through a multi-stage makeover which will include a nice facial, a wonderful makeup session and will end with a great dress-up session and the selection of some beautiful accessories.
Start things off with a facial treatment that will make your fairy feel spoiled and special. Use the very best cleansers, exfoliants and moisturizers that will give her skin an extra touch of beauty. Once you've completed the facial, you can then move on to the makeup part of the routine. Remember you're doing a fairy's makeover, so no amount of glitz and sparkle is too much! Next, on to the dress-up session, where you can mix and match a wide variety fanciful fairy outfits. You even get to choose a beautiful set of fairy wings, so let your imagination run wild! Don't forget to pick the appropriate hairstyle and some wonderful accessories – and you're all set!


text:
Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 10, No. 2, 2011, pp. 211-218 Bioline Code: pr11029
Tropical Journal of Pharmaceutical Research, Vol. 10, No. 2, 2011, pp. 211-218
en Phytochemical and Antibacterial Evaluations of the Stem Bark of Newbouldia laevis against Isolates from Infected Wounds and Eyes
Akerele, JO; Ayinde, BA & Ngiagah, J
Purpose: To examine the phytochemical constituents and verify the ethnomedical claim of Newbouldia laevis (P.Beauv.) Seeman ex Bureau Bignoniaceae in treating septic wounds and eye problems.
Methods: Applying standard methods, the phytochemical constituents of the stem bark were examined while the antibacterial potentials of the methanol extract of the stem bark and its organic solvent fractions were tested on clinical bacterial isolates from infected wounds and eyes using the agar -well diffusion method. Ciprofloxacin and gentamicin were used as standard controls. The time-kill kinetics of the methanol stem bark extract and ciprofloxacin were determined using isolates of Staphyloccocus aureus .
Results: Phytochemical screening of the stem bark revealed the presence of flavonoids, tannins, saponins and alkaloids with no traces of cyanogenic glycosides. The 65 bacterial pathogens isolated included Proteus mirabilis (26.0 %) and Pseudomonas aeurginosa (17.4 %) from non-diabetic patients' wounds; Staphylococcus aureus (32.0 %) and Escherichia coli (16.0%) from diabetic patients' wounds; Staphylococcus aureus (35.3%) and Pseudomonas aeruginosa (35.3 %) from infected eyes. The chloroform fraction was observed to be more active on Gram-negative organisms while the aqueous fraction was more active on Gram-positive organisms. Time-kill kinetics of Staphylococcus aureus showed that the extract was bactericidal (99.9 % killing) at MIC and 2 x MIC after 24 and 3 hours, respectively.
Conclusion: The study has established that the stem bark of Newbouldia laevis has antibacterial activities against bacterial isolates from infected wounds and eyes as claimed in ethnomedicinal practice.
Newbouldia laevis, Antibacterial, Phytochemical, Wound isolates, Eye isolates
© Copyright 2011 Tropical Journal of Pharmaceutical Research.
Alternative site location: http://www.tjpr.org


Enter into a distant future, where the rise and fall of countless civilizations have left Earth in a rough state. By playing, you must explore the Ninth World, discover other castoffs, and make new friends and enemies along the way.
Torment: Tides of Numenera is a successful Kickstarter story. The game was crowd-funded in the first six hours of the project's launch back in March 2013. Torment: Tides of Numenera is a single-player role-playing video game that continued the theme of its predecessor Planescape: Torment. It was developed by inXile Entertainment and it is available in February 2017 for Microsoft Windows, OS X, Linux, Xbox One, and PlayStation 4.
In Torment: Tides of Numenera, the players are on their own when it comes to an important decision, such as what does one life matter? The game emphasizes on text and dialogue rather than on sheer combat.
In the game, the player plays as the "Last Castoff", a person who was once a vessel for an immortal being called the Changing God. With the Changing God being out of the body, the player is left to shape his own existence. To put a further depth into this, right in the character creation the player can shape both his stats and his in-game personality. Being a game that focuses on text and dialogue, whichever answer the player chooses will guide his character's personality and it will decide how people react to the character.
The world of Numenera is set in a distant future where the Earth is in a medieval stat as a result of the rise and fall of countless civilizations. The current age in the world is called the Ninth World. The scholars believe that the previous eight ages were destroyed or disappeared for unknown reasons. The Ninth World was left with nothing but ruins and various artifacts behind. The artifacts are an actual piece of science and technology of the past civilizations. Many of these aren't even functional, but the ones that are, are believed to be objects of magic.
The developers inXile Entertainment have put extra time and effort to create backstories for minor characters even though some of them have little to no relevance to the greater plot.
The main villain in the game is "The Sorrow". He seeks to destroy the Changing God and every one of his previous creations. As one of his creations, Last Castoff is also targeted by The Sorrow. His journey is all about finding their master before he is undone. In order to do that, Last Castoff must explore the Ninth World, find friends and battle enemies along the way. While exploring, the Last Castoff finds artifacts that let him take control over another castoff and experience different worlds through them. With these travels, the Last Castoff will find answers the previously asked question: What does one life matter?
Torment: Tides of Numenera is a brilliant successor to the Planescape: Torment RPG. The game appeals to all fans of classic computer RPGs. The game's textual and dialogue based gameplay are the reasons why most players find it very exciting.


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A Personal Assistive Technology Consultation is the first ray of hope! It includes an in-depth ½ -hour telephone interview followed-up within a week by a professional 1-page description of potential worksite solutions for your medical condition.
The Personal Assistive Technology Consultation is the first ray of hope for a skilled tradesman with a disability because it gives realistic ideas for ways to keep working. In a discouraging world that tells workers to just 'go on disability', this is a breath of fresh air. Workers compensation cases or insurance claims can use the consultation and written description as a pre-assessment list of potential accommodations.
The Personal Assistive Technology Consultation is the first step in completing an onsite Worksite Assistive Technology Assessment. If you choose to schedule a full Worksite Assistive Technology Assessment after your Personal Assistive Technology Consultation, you will receive a $100 discount.
The Personal Assistive Technology Consultation interview will ask questions regarding the worker's job site. Are the floors level and smooth, or are there ruts , mud or clutter to walk through? Does the worker climb ladders? What hand tools are commonly used? Is the work site well lighted and ventilated? Questions such as these help the Assistive Technology Professional to understand the challenges of the work environment.
The interview also provides information regarding the worker's physical abilities. How high can you lift your knee? Can you twist your back to look behind a vehicle while driving? Do you have full grip strength on both hands? If a worker has an occupational or physical therapy evaluation or a functional capacity assessment, that information will allow the Assistive Technology Professional to describe potential solutions within those abilities.
The Personal Assistive Technology Consultation 1-page description will help the worker see the possibilities and realities of working with a physical limitation. It will help workers start thinking in terms of solutions and progress towards returning to work instead of focusing on all the obstacles. The description will list desired improvements in order of priority. Addressing issues one at a time according to a plan makes the accessibility project appear doable.
Read our blogs to better understand Assistive Technology Assessments and Assistive Technology Professional certification, or visit the South Carolina Assistive Technology Program website http://www.sc.edu/scatp/assessment.html.


text:
Q: How to fetch images from folder? I have a folder named as images.  I just want to fetch those images from the folder and show them randomly on web page.  When the user refreshes the page, the image should change.
Thank you.

A: An idea could be:

*

*you fetch all the images names frome the images folder

*you randomly pick one

*you visualize that one

so you can go like this
<?
    $dir = '/my_directory_location';
    $files = scandir($dir);
    $rand_img = array_rand($files, 2);
    $imcolumn = "
";
?>

<?= $imcolumn ?>

A: <?php

  $folder = "templates/images/";

  $search = glob($folder."/*");
  shuffle($search);

  foreach ($search as $image) {
    print "
";
  }

?>

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