Arts and entertainment events happening in Kent.
Calendars are published Wednesdays and Saturdays on a space-available basis. Items for the Wednesday edition must be submitted by noon the previous Thursday. Items for the Saturday edition must be submitted by noon the previous Tuesday.
Sococulture: For information about cultural events throughout South King County, visit www.sococulture.org.
Wings of Freedom Tour: 2-5 p.m. June 20; 10 a.m.-5 p.m. June 21-22. Ground tours available of Boeing B-17 Flying Fortress "Nine O Nine" WWII Heavy Bomber; Consolidated B-24 Liberator "Witchcraft" WWII Heavy Bomber; North American B-25 Mitchell WWII Medium Bomber; and P-51 Mustang. The Museum of Flight, 9404 E. Marginal Way S., Tukwila. www.collingsfoundation.org.
Musicians Emeritus Symphony Orchestra: 7:30 p.m. June 14. Cost: $10 donation. First Evangelical Presbyterian Church, 19800 108th Ave. S.E., Renton. MESO-orchestra@comcast.net.
The Singing Brawners: 4 p.m. June 15. Filipino couple Rita and Felix Brawner to perform traditional music. Cost: $20-$40. IKEA Performing Arts Center, 400 S. Second St., Renton. 253-288-3557.
Renton City Concert Band: 7:30 p.m. June 19. 70-piece band performs everything from Broadway to classics. Cost: $5-$7. IKEA Performing Arts Center, 400 S. Second St., Renton. 425-430-6700 or 425-430-6707.
Coulon Family Concert Series: 7 p.m. Wednesdays, June 25-Aug. 13. Free outdoors concerts. Performers: June 25, Renton City Concert Band; July 2, Duwamish Dixieland Jazz. Gene Coulon Memorial Beach Park, 1201 Lake Washington Blvd. N., Renton. 425-430-6700 or www.rentonwa.gov.
Cascade Lanes, Lounge and Casino: 9 p.m.-1 a.m. Nightly band performances, including: June 13-14, Kickstart; June 20-21, Knucklehead; June 27-28, Trix. Open to ages 21 and older. 17034 116th Ave. S.E., Renton.
Friday Night Jazz: 7 p.m. June 20, Hook Me Up Jazz Quartet; 7 p.m. June 27, Doug Ostgard Jazz Quartet. Baker Street Books, 32709 Railroad Ave., Black Diamond. 360-886-2131.
Gonzo's Bar and Grill: Ongoing: 9 p.m. Wednesdays, karaoke. Open to ages 21 and older. 15423 S.E. 272nd St., Suite 101, Kent. www.gonzosbarandgrill.com.
Interchange Bar & Grill: 9 p.m.-1 a.m., including: Thursdays and Saturdays, karaoke; Fridays, band performances; Sundays, free pool. Performers include: June 13, Cylas; June 20, Jet City Players; June 27, Knucklehead. Open to ages 21 and older. 8429 S. 228th St., Kent. 253-854-5650.
Pat's Bar and Grill: All performances 8 p.m.-midnight unless otherwise noted. Ongoing: 8 p.m. Thursdays, jam nights. 114 Railroad Ave. N., Kent. 253-852-7287 or www.patsbar.com.
Poppa's Pub: 9:30 p.m.-1:15 a.m. Saturdays, live music. 510 Washington Ave. N., Kent. 253-850-2812.
The Royal Bear Pub and Eatery: Performers: June 13, NRG; June 27-28, Black Dog. 35731 W. Valley Highway, Algona. 253-833-6686.
"I Do! I Do!": June 13-29. Cost: $15-$20. Renton Civic Theater, 507 S. Third St. 425-226-5529 or boxoffice@rentoncivictheater.org.
"Theseus and the Minotaur": 7 p.m. June 16. Musical presented by HOME Program. Cost: Free. IKEA Performing Arts Center, 400 S. Second St., Renton. 425-204-2521.
"The Complete Works of William Shakespeare (Abridged)": 8 p.m. Fridays-Saturdays and 2 p.m. Sundays through June 29. Three actors set out to perform all 37 of Shakespeare's plays in 97 minutes. Cost: $12-$15. Auburn Avenue Theater, 10 Auburn Ave. 253-929-6680 or www.experience-art.org.
Comedy Night at the Ave: 7:30 p.m. June 19. Performers: Key Lewis, Tony Boswell and Jack Mayberry. Recommended for ages 18 and older. Cost: $15-$20. Auburn Avenue Theater, 10 Auburn Ave. 253-931-3043 or www.auburnwa.gov/arts.
Skyway Park Bowl and Casino: 8:30 p.m. Thursdays, live stand up comedy. Headliners: June 12, Huck Flyn. 11819 Renton Ave. S., Seattle. 206-772-1220.
Petite Feet Performance: 2 and 3:30 p.m. June 14. Presented by Children's Dance Theater. Cost: $3-$5. Rainier Middle School, 30620 116th Ave. S.E., Auburn. 253-887-8937.
VCC Shopa Naida Kuchaipuda: 6:30 p.m. June 14. Cultural ballet performance features artists from India. Call for cost. IKEA Performing Arts Center, 400 S. Second St., Renton. 425-442-5886.
Southside Dance Force: 7 p.m. June 21; 2 p.m. June 22. Cost: $20 in advance; $25 at the door. IKEA Performing Arts Center, 400 S. Second St., Renton. 253-639-5829 or www.ssdanceforce.com.
Boots & Laces Square Dance Club: 7:30-10:30 p.m. the first and third Fridays of the month. Meridian Grange, 15422 S.E. 272nd St., Kent. 425-413-0084 or www.bootsandlaces.org.
Evening ballroom dance: 7:30-9:30 p.m. the second, third and some fourth Tuesdays of the month. Features live music by The Good Times Band. Open to all ages. Cost: $4. Kent Senior Activity Center, 600 E. Smith St., Kent. 253-856-5164.
Kings of Swing swing dance: 7:45-9:30 p.m. the first and last Tuesdays of the month. Open to all ages. Cost: $4. Kent Senior Activity Center, 600 E. Smith St., Kent. 253-856-5164.
Ring 'N Swing Square Dance: 1:15-3:15 p.m. Thursdays. Cost: $3. Kent Senior Activity Center, 600 E. Smith St., Kent. 253-856-5164.
Square dancing: 7:30-10:30 p.m. the second and fourth Saturdays of the month. Sponsored by Pi R Squares. Cost: $4. Meridian Grange, 15422 S.E. 272nd St., Kent. 425-432-0138 or www.pi-rsquares.org.
Swing dance classes: 3 and 4 p.m. Tuesdays through December. 3 p.m., Swing 1. No experience necessary. 4 p.m., Swing 2 (Lindy Hop). Must pass Swing 1 or have teacher's permission. Cost: $5 for students; $7 for non-students. Student Union Building at Highline Community College, 2400 S. 240th St., Des Moines. Des Moines. www.kevinbuster.com.
Tuesday Afternoon Dances: 1:15-2:15 p.m. Tuesdays. Free dances feature music styles ranging from ballroom to rock 'n roll. Kent Senior Activity Center, 600 E. Smith St., Kent. 253-856-5164.
Wagon Wheel Square Dance Club: Beginning lessons: 7:30-9:30 p.m. Tuesdays. First three lessons are free. Dances: 7:30-11 p.m. the first and third Saturdays of the month. Meridian Grange Hall, 15422 S.E. 272nd St., Kent. 206-915-1415.
Kent Historical Society Museum: Hours: Noon-4 p.m. Wednesdays-Saturdays. Admission: $1. Bereiter House, 855 E. Smith St., Kent. 253-854-4330.
Black Diamond Historical Society Museum: Hours: 9 a.m.-4 p.m. Thursdays; noon-3 p.m. Saturdays and Sundays. 32627 Railroad Ave., Black Diamond. 360-886-2142, museum@blackdiamondmuseum.org or www.blackdiamondmuseum.org.
Renton History Museum: Free tours: 11 a.m. the third Saturday of the month. Hours: 10 a.m.-4 p.m. Tuesdays-Saturdays. Closed on holidays. Admission: $3 for adults; $1 for children; free for ages 7 and younger and members. 235 Mill Ave. S. 425-255-2330 or www.rentonhistory.org.
Ryan House Museum: Hours: 1-4 p.m. Saturdays-Sundays and 7-9 p.m. the first Wednesday of the month through August. Closed on holidays. Cost: $1 for adults; 25 cents for children. 1228 Main St., Sumner. 253-299-5780.
White River Valley Museum: Exhibits: Through Aug. 10, "Crazy Quilts: Puzzle Patches and Fanciful Embroidery." Events: 1-3 p.m. June 14, "Quilt Restoration and Preservation" class and tour. Hours: Noon-4 p.m. Wednesdays-Sundays. Admission: $1-$2; free on Wednesdays. 918 H. St. S.E., Auburn. 253-288-7433 or www.wrvmuseum.org.
Hydroplane and Raceboat Museum: Hours: 10 a.m.-5 p.m. Tuesdays; 10 a.m.-10 p.m. Thursdays; 10 a.m.-4 p.m. Saturdays. Admission: $10 for adults; $5 for students and seniors; free for ages 4 and younger. 5917 S. 196th St., Kent. 206-764-9453.
Auburn City Hall Gallery: Exhibits: Through July 3, artwork by Anthony Huss and Cara Jennings, with artists reception 5:30-7 p.m. June 11. Hours: 8 a.m.-5 p.m. Mondays-Fridays. Admission: Free. Auburn City Hall, 25 W. Main St. 253-931-3043 or www.auburnwa.gov.
Centennial Center Gallery: Hours: 8 a.m.-5 p.m. Mondays-Fridays. 400 W. Gowe St., Kent. 253-856-5050, www.ci.kent.wa.us/arts.
Cheryl Sallee Gallery: Exhibits: Through June 27, Senior Artists' Exhibit. Hours: 8 a.m.-5 p.m. Mondays-Fridays. Admission: Free. Auburn Senior Activity Center, 808 Ninth St. S.E. 253-931-5043 or www.auburnwa.gov/arts.
New Earth Gallery: Hours: 11 a.m.-5 p.m. Tuesdays-Fridays; 10 a.m.-5 p.m. Saturdays. 213 W. Meeker St., Kent.
Seahurst Art Gallery: Events: 10 a.m.-5 p.m. June 14, open house. Exhibits: Through July, pottery by Don Schindler. Ongoing: Paintings by Nancy Bogni, Marianne Perkins and Cathy Woo. Hours: Noon-5 p.m. Wednesdays-Saturdays. 15210 10th Ave. S.W., Burien. 206-244-7844 or www.seahurstgallery.org.
Unexpected Productions 25th Anniversary Events: 6 p.m. June 13-midnight June 15, 54-Hour Improvathon; 8:30 p.m. June 16, Theatresports 25th Anniversary Show; June 17-22, International Festival of Improv. Call for cost. The Market Theater, 1428 Post Alley, Seattle. 206-587-2414 or www.UnexpectedProductions.org.
KPLU Listener Request Show: 7:30 p.m. June 14. Presented by Seattle Repertory Jazz Orchestra. Cost: $15-$36. Benaroya Hall, 200 University St., Seattle. 206-523-6159 or www.srjo.org.
"Busytown": Through June 15. Play brings Richard Scarry's "What do people do all day?" to life with music and puppetry. Recommended for ages 4 and older. Cost: $17-$33. Seattle Children's Theatre's Charlotte Martin Theatre, 201 Thomas St., Seattle Center. 206-441-3322 or www.sct.org.
Mighty Aphrodite: 12:30-5 p.m. June 15. Snacks and coffee will be available. Presented by Puget Sound Traditional Jazz Society. Cost: $8-$11. Ballard Elks Lodge, 6411 Seaview Ave. N.W., Seattle. 425-776-5072 or www.pstjs.org.
Theory of a Deadman: 8 p.m. June 17. Canadian band to perform. Cost: $15. Showbox SoDo, 1700 First Ave. S., Seattle. 206-628-0888 or www.ticketmaster.com.
"Recapturing the Banjo": 7 p.m. June 17. Otis Taylor and Band to perform songs from their latest album. Cost: $25-$30. The Triple Door, 216 Union St., Seattle. 206-838-4333 or www.thetripledoor.net.
Dimitriou's Jazz Alley: Performers: June 17-18, Esperanza Spalding; June 23-24, Maceo Parker. Call for cost. 2033 Sixth Ave., Seattle. 206-441-9729 or www.ticketmaster.com.
"A Marvelous Party—The Noel Coward Celebration": June 19-July 13. Comedic revue offers some of Coward's best-loved songs. ACT Theatre, 700 Union St., Seattle. 206-292-7676 or www.acttheatre.org.
Discover the Niña: 9 a.m.-6 p.m. June 19-24. Replica of Columbus' ship will dock in Seattle for self-guided tours. Cost: $3-$5; free for ages 4 and younger. Center for Wooden Boats, 1010 Valley St., Seattle. 787-421-0402 or www.thenina.com.
"Avenue Q": Through June 22. Call for cost. The Paramount Theatre, 911 Pine St., Seattle. 206-292-2787 or www.theparamount.com.
"Namaste Man": Through June 22. One-man show explores what it means to be an artist, and what it means to go home. Intiman Theatre, 201 Mercer St., Seattle. 206-269-1900 or www.intiman.org.
"Wait, Wait … Don't Tell Me!": 7:30 p.m. June 26. Join a live taping of NPR's oddly informative news quiz. Call for cost. The Paramount Theatre, 911 Pine St., Seattle. 206-292-2787 or www.theparamount.com.
Seattle Men's Chorus—"Comedy Tonight": June 27-28. Call for cost. McCaw Hall, 305 Harrison St., Seattle Center. 206-388-1400 or www.flyinghouse.org.
"Adventures in Mating": June 27-Aug. 9. Play offers a comedic choose-your-own-adventure about a first date. Theater Schmeater, 1500 Summit Ave., Seattle. 206-324-5801 or www.schmeater.org.
Seun Kuti & Egypt 80: 8 p.m. June 28. Cost: $25-$35. The Moore Theatre, 1932 Second Ave., Seattle. 206-628-0888 or www.themoore.com.
"All's Well That Ends Well": Through June 29. Presented by Seattle Shakespeare Company. Cost: $20-$34. Center House Theatre, 305 Harrison St., Seattle Center. 206-733-8222 or www.seattleshakespeare.org.


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Q: Unable to filter my dataset via where statement in sas I have the following dataset with 3 initial variables:

I have applied the following code to my data set to have months and quarter variables:
Data Example;
set Example;
month = put(date,monname8.);
quarter = QTR(date);
run;

I have then the following output(part of my table which have more than 30000 observations):

Then I want to filter for all observations with month = "June", I used the following code to do this :
Data Example;
set Example;
where month = "June";
run;

Then the output returns me a blank table with no observation at all:

I have tried with other variables such as country and quarter, they both works (returns me with the desired observations) with where statement. Only with the month variable it returns me with blank table.
Could anyone help me with this issue ?
Thank you!

A: First, check if there are not any blank spaces in your code (e.g. " June" instead of "June"). Second, make sure to avoid blank spaces before and after month names:
WHERE strip(month) = "June";

If neither of them work, make sure there is "June" in your data.

A: Use the -l alignment option in PUT otherwise it adds spaces for padding.
month = put(date, monname8.  -l);

redpajama_set_name: RedPajamaStackExchange


Dental veneers, also known as porcelain veneers, can make teeth appear flawless. While we often think of the cosmetic benefits of dental veneers, they are used to treat a variety of dental conditions, including chipped teeth, gaps, and discoloration. The team of dentists at the Cosmetic Dentistry Institute in Troy, Michigan, provides patients with dental veneers for a number of reasons.
Dental veneers are thin shells that are custom-crafted to fit over the surface of your tooth. Veneers can be made from porcelain or composite materials, and are firmly bonded to the tooth's surface for a flawless appearance that looks and feels natural.
A skilled cosmetic dentist who has experience with veneers will often choose porcelain as the material for veneers, as porcelain resists stains and looks more like natural teeth than other materials.
What Do Dental Veneers Treat?
Discoloration. When teeth have severe stains that cannot be removed with a professional whitening treatment, veneers can mask the discolored surface of the tooth.
Wear. When a tooth's enamel has been worn down from grinding or acidic erosion, dental veneers can restore its protective surface and appearance.
Chips. Porcelain veneers are an excellent solution for teeth that have severe chips or breaks that cannot be corrected with dental bonding.
Misalignment. If you want a straight smile but don't want to undergo time-consuming orthodontic treatment, dental veneers are your best option. By covering the surfaces of your teeth, the veneers can be shaped to create the straight smile you desire.
Irregular shapes. If the surface of your tooth naturally has ridges, craters, or other irregularities, dental veneers can provide a smooth, uniform appearance.
Gaps. Like misalignment, gaps between teeth can be corrected with orthodontics. However, if you'd like to see results sooner rather than later, porcelain veneers can provide an immediate solution.
One of the main advantages of dental veneers is that they provide immediate results - even if your teeth are chipped, cracked, or discolored, your smile can be transformed into one that is bright, smooth, and straight. However, the porcelain veneer process typically takes three visits to the dentist, over the course of several weeks.
During the first visit, your dentist will plan your treatment. You'll be able to share your desired results, and possibly view computerized representations of what your teeth will look like with veneers. Your dentist will determine if veneers are right for you, and if they will successfully accomplish all of your goals.
Your teeth will be prepped for your veneers during your second visit. Your dentist will remove some enamel from the surface of the tooth so it can accommodate your veneers. An impression will then be made of your teeth, which will be sent to a laboratory and used to craft your veneers. Depending on your situation, you may be fitted with temporary veneers in the meantime.
During your final visit, often about two weeks later, your dental veneers will be bonded to the surface of your teeth with a special adhesive. Once your dental veneers have been placed, your dentist will ensure that the shape and color integrates seamlessly with your existing teeth. You'll be free to enjoy your brand new smile!
If you have teeth that are chipped, worn, or discolored, there's a solution! To learn more about how dental veneers can transform your smile, contact the Cosmetic Dentistry Institute today.


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Argentinian Football Legend Maradona Successfully Undergoes Knee Surgery After Quitting as Dorados Coach
Latestly 25 July 2019
The former coach of the Argentine national team quit his job at Mexican second division outfit Dorados last month for health reasons after just nine months in charge.
Buenos Aires, July 25: Former Argentina World Cup winning captain Diego Maradona underwent a successful knee operation at a clinic in Buenos Aires on Wednesday, his lawyer revealed. The former coach of the Argentine national team quit his job at Mexican second division outfit Dorados last month for health reasons after just nine months in charge. His lawyer, Matias Morla revealed then that Maradona needed to undergo surgery on his knee and shoulder. Diego Maradona Health Scare During Argentina vs Nigeria Match! Football Legend Flashes Middle Finger, Goes Overboard During 2018 FIFA Tie; Watch Video.
Also Read | Former Argentine President Fernando de la Rua Passes Away at 81
"Everything went perfectly," said Morla on his Twitter account, in reference to the operation on Maradona's right knee. Maradona's appointment at Dorados in September had been a surprise, despite his inglorious coaching history since leaving the national team post following the 2010 World Cup.
It caused much amusement too amongst skeptics as Dorados are based in the western state of Sinaloa, which is best known for its powerful drug cartel that used to be run by notorious kingpin Joaquin "El Chapo" Guzman, who was earlier this month jailed for life in the United States.
Also Read | Boris Becker Goes Bankrupt: From Diego Maradona to Mike Tyson, Here's a Look at Sports Personalities Gone From 'Riches-to-Rags'
Maradona, 58, has had his problems in the past with substance abuse, including cocaine. He came tantalizingly close to taking Dorados up to the Mexican top flight before resigning. Diego Maradona Smokes Cigar Watching Argentina vs Iceland, 2018 FIFA World Cup Match From 'Smoke-Free' Stands (Watch Video).
Maradona previously underwent a successful operation on his left shoulder in 2017 in Dubai, while he was coaching second division Emirati side Fujairah.
The former Barcelona and Napoli star forward is perhaps best known for guiding his country to victory at the 1986 World Cup in Mexico.
Along the way, Maradona scored the infamous 'Hand of God' goal against England in the quarter-finals, as well as another wonderful individual strike widely considered the best World Cup goal of all time.
India vs New Zealand | India Are the Best But New Zealand Back in Familiar Conditions: Ross Taylor
ICC U19 World Cup 2020: Team India's Full Schedule, Venue, Timings at U19 World Cup in South Africa
Morales announces candidates for MAS party in Bolivia's elections
Australian Open 2020: Roger Federer results and form ahead of second-round match with Filip Krajinovic
Australian Open 2020 Day Two Live Score Updates: Sharapova exits; Nadal, Pliskova advance
Ishant Sharma Has an Ankle Tear, Doubtful for NZ Test Series

redpajama_set_name: RedPajamaCommonCrawl


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DealBook | With Gupta's Arrest, Insider Inquiry Goes Beyond Wall St.
Hedge Funds | Legal/Regulatory
With Gupta's Arrest, Insider Inquiry Goes Beyond Wall St.
By Azam Ahmed
October 26, 2011 8:37 am October 26, 2011 8:37 am
Douglas Healey for The New York TimesRajat Gupta at his home in Westport, Conn., on Wednesday morning.
8:46 p.m. | Updated
Rajat K. Gupta, a former director at Goldman Sachs and Procter & Gamble, pleaded not guilty Wednesday to insider trading charges, setting the stage for a courtroom battle that will extend the government's broad crackdown on Wall Street to the corporate boardroom.
On Wednesday, a federal grand jury in Manhattan charged Mr. Gupta, 62, with one count of conspiracy to commit securities fraud and five counts of securities fraud. He is accused of sharing corporate secrets about Goldman and Procter & Gamble with Raj Rajaratnam, the co-founder of the Galleon Group who was sentenced to 11 years in prison earlier this month for insider trading.
The details of the indictment, many of which came out during Mr. Rajaratnam's trial and a previous action by the Securities and Exchange Commission, could prove explosive; he is the first executive from the upper echelons of corporate America to be implicated in the far-reaching scandal.
Complete Coverage: Galleon Investigation
The Challenges of Prosecuting Rajat Gupta
The grand jury indictment
The S.E.C.'s civil complaint
"Rajat Gupta was entrusted by some of the premier institutions of American business to sit inside their boardrooms, among their executives and directors, and receive their confidential information so that he could give advice and counsel for the benefit of their shareholders," Preet Bharara, the United States attorney in Manhattan, said in a statement. "As alleged, he broke that trust and instead became the illegal eyes and ears in the boardroom for his friend and business associate, Raj Rajaratnam, who reaped enormous profits from Mr. Gupta's breach of duty."
A stoic Mr. Gupta, wearing a navy blue suit and red tie, pleaded not guilty to all charges. He is set to be released on a $10 million bond, secured by his home in Westport, Conn., and will turn over his passport.
"The facts in this case demonstrate that Mr. Gupta is innocent of any of these charges and that he has always acted with honesty and integrity," Gary P. Naftalis, a lawyer for Mr. Gupta, said in a statement.
Judge Jed S. Rakoff, a federal judge in Manhattan, has been assigned to the case, set for trial on April 9, 2012. He ruled on a matter between Mr. Gupta and the S.E.C. this summer.
The government has taken aggressive action against insider trading. In the last two years, the government has charged 56 people with swapping illegal tips, including Mr. Gupta; of those, 51 have pleaded guilty or have been convicted.
With Mr. Gupta, the campaign has moved beyond financial professionals. As the head of McKinsey & Company, the prominent consulting firm, Mr. Gupta advised some of the world's most influential people, rubbing elbows with the chief executive of General Electric, Jeffrey R. Immelt, and the former President Bill Clinton.
Mr. Gupta's case has been tricky for the government. Although his name came up repeatedly at Mr. Rajaratnam's trial, both in testimony and in secretly recorded phone conversations, the Justice Department never brought charges against him.
The S.E.C. filed an administrative action against Mr. Gupta. In response, he filed a separate lawsuit, asking to move the case to federal court, where it would be heard by a jury.
Judge Rakoff allowed Mr. Gupta's suit to move forward in July, saying the S.E.C. took a "cavalier approach" in approving the administrative proceeding. The agency later dropped the matter, but reserved the right to refile.
On Wednesday, the S.E.C. filed a civil complaint against Mr. Gupta and Mr. Rajaratnam, claiming an "extensive insider trading scheme." It mirrored the agency's earlier action against Mr. Gupta.
"Gupta was honored with the highest trust of leading public companies, and he betrayed that trust by disclosing their most sensitive and valuable secrets to the disadvantage of investors, shareholders, and fellow directors," Robert S. Khuzami, director of the S.E.C.'s division of enforcement, said in a statement.
According to the indictment, Mr. Gupta gave Mr. Rajaratnam advance word of Warren E. Buffett's $5 billion investment in Goldman during the financial crisis. After hanging up from a special board meeting in September 2008, Mr. Gupta called Mr. Rajaratnam within 16 seconds, prosecutors said. Moments later, Mr. Rajaratnam purchased shares in Goldman, ultimately netting about $840,000, according to the indictment.
The next month, Mr. Gupta ostensibly informed Mr. Rajaratnam that Goldman would report an unexpected quarterly loss. Acting on the tip the next day, Mr. Rajaratnam, sold off shares in the company, saving millions of dollars, the indictment stated.
Mr. Gupta is also accused of tipping Mr. Rajaratnam about Procter & Gamble's quarterly sales projections, which were going to be weaker than predicted. Mr. Rajaratnam promptly bet against the company's stock, the indictment says.
The government has said that Mr. Gupta was eager to deepen his personal and financial ties with the billionaire hedge fund manager, which predate the alleged tips. From 2003 to 2005, Mr. Gupta had money in at least two of Mr. Rajaratnam's hedge funds, an investment valued at about $2.5 million by March 2005, according to the indictment.
The two men also started several financial ventures together, including Voyager Capital Partners, financed with $10 million from Mr. Gupta and $40 million from Mr. Rajaratnam. The investment fund allocated some money to Galleon hedge funds, including ones managed by Mr. Rajaratnam.
"There were legitimate reasons for any communications between Mr. Gupta and Mr. Rajaratnam," Mr. Naftalis, Mr. Gupta's lawyer, said in a statement. "Mr. Gupta lost his entire investment in the fund at the time of the events in question, negating any motive to deviate from a lifetime of probity and distinguished service."
In past Galleon-related trials, the government relied heavily on the use of wiretaps and recordings to make its case. But prosecutors may not have the same breadth of evidence this time, since the Goldman discussions between Mr. Rajaratnam and Mr. Gupta were not taped. Instead, the government has conversations between Mr. Rajaratnam and his employees.
In one call played during Mr. Rajaratnam's trial, the hedge fund manager told someone: "I heard yesterday from somebody who's on the board of Goldman Sachs that they are going to lose $2 per share." In a different call, Mr. Rajaratnam said, "I got a call saying something good is going to happen to Goldman."
That could present a challenge. The judge could disallow the calls as hearsay, meaning they would be deemed too unreliable to pass court muster.
U.S. v. Rajat K. Gupta
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U.S. Expected to Charge Executive Tied to Galleon Case
Morning Take-Out


Type I interferons (IFN-Is) serve as mediators of antiviral innate immunity and also regulate adaptive immune responses. The molecular mechanism that regulates virus-induced IFN-I production, particularly in tissue-resident immune cells, is incompletely understood.
Here we identified the E3 ubiquitin ligase Peli1 as a negative regulator of IFN-I induction in microglia, innate immune cells of the central nervous system (CNS). Peli1 deficiency profoundly promoted IFN-β expression in microglia in response to in vitro stimulation by toll-like receptor (TLR) ligands or a CNS-tropic virus, the vascular stomatitis virus (VSV). Upon intranasal infection with VSV, the Peli1-deficient mice displayed heightened in vivo IFN-I responses in the CNS, coupled with reduced brain viral titer and increased survival rate.
These results establish Peli1 as an innate immune regulator in the CNS that modulates the threshold of IFN-I responses against viral infections.
Type I interferons (IFN-Is) provide one of the body's primary defense systems against viral infections. The high susceptibility of type I IFN receptor (IFNAR)-deficient mice to infection by a variety of viruses provides strong evidence for the major role of the IFN system in anti-viral innate immunity . In addition, IFN-Is also play an important role in modulating the development of adaptive immune responses . Induction of IFN-Is is mediated by pattern-recognition receptors (PRRs), such as the toll-like receptors (TLRs) and the cytoplasmic RIG-I-like receptors (RLRs). The PRRs can efficiently detect viral infections through recognition of molecular patterns associated with viral genomes and replication products [3–5]. The TLR family is composed of members that signal through two major adaptors, MyD88 and TRIF. The TRIF-dependent TLRs, TLR3 and TLR4, as well as the RLRs stimulate Ifnb gene expression via activation of two homologous kinases, TBK1 and IKKε. These kinases in turn phosphorylate the transcription factor IRF-3, which causes IRF-3 dimerization and translocation to the nucleus, where it mediates the transactivation of the Ifnb gene [6, 7].
Although IFN-I induction has been extensively studied using macrophages and dendritic cells, IFN-Is are also produced by tissue resident cells and play a tissue-specific role in mediating antiviral innate immunity and regulating immune homeostasis [2, 8]. In particular, the microglia are resident macrophages of the central nervous system (CNS) that are important for immune responses against infections in the CNS [9, 10]. These cells, which seed the parenchyma of the CNS early during embryonic development, express various PRRs, including the TLRs and RLRs, and become rapidly activated upon detection of infections and tissue damage [11–13]. In addition to mediating antiviral innate immunity, IFN-Is play an important role in regulating other types of immune responses, thereby exerting pathogenic or protective roles in the CNS . Thus, the production of IFN-Is is subject to both positive and negative mechanisms of regulation.
Despite the extensive studies on the core components of the IFN-I induction pathway, the regulatory factors are still poorly defined. We have recently shown that the E3 ubiquitin ligase Peli1 (also called Pellino1) is required for TLR-stimulated proinflammatory cytokine expression in microglia, although its role in regulating IFN-I expression has remained unclear . Unlike peripheral macrophages, which express both Peli1 and its homologs, Peli2 and Peli3, microglia predominantly express Peli1 . We found in the present study that in contrast to its positive role in regulating proinflammatory cytokine induction, Peli1 is a potent negative regulator of IFN-I induction by TLR ligands and viruses. In response to intranasal infection by a neurotropic virus, vascular stomatitis virus (VSV), the Peli1-deficient mice expressed elevated levels of IFNα and IFN-β in the microglia of CNS, coupled with reduced brain viral titer and increased rate of mouse survival. These findings establish Peli1 as a negative regulator of IFN-I induction and antiviral innate immunity in the CNS.
To investigate the role of Peli1 in regulating IFN-I induction, we prepared primary BMDM and microglia from Peli1-KO mice and wildtype (WT) control mice. In contrast to the BMDMs expressing an E3 ligase-defective Peli1 mutant , the Peli1-KO BMDMs did not show significant reduction in LPS-stimulated IFN-β induction (Fig. 1a). On the other hand, the Peli1 deficiency reduced the induction of several proinflammatory cytokine genes, likely due to the role of Peli1 in mediating TRIF-dependent NF-κB activation . Since BMDMs express different Peli family members at comparably levels , Peli1 might have functional redundancy with the other members. We thus examined the role of Peli1 in IFN-β regulation in microglia, in which Peli1 represents the predominant Peli family member . As we previously reported , the Peli1 deficiency in microglia profoundly inhibited the induction of several proinflammatory cytokines by LPS and other TLR ligands (Fig. 1b, c). To our surprise, the loss of Peli1 in microglia resulted a striking upregulation of IFN-β induction stimulated by LPS as well as by several other TLR ligands (Fig. 1b, c). These results suggest that Peli1 functions as a negative regulator of IFN-β induction in microglia.
To delineate the molecular mechanism by which Peli1 negatively regulates IFN-β induction, we examined the effect of Peli1 deficiency on the activation of two major IFN-stimulating kinases, TBK1 and IKKε, based on their phosphorylation. Stimulation of WT microglia by LPS led to the phosphorylation of both TBK1 and IKKε (Fig. 1d). Moreover, the Peli1 deficiency substantially enhanced the LPS-stimulated TBK1/IKKε phosphorylation. These results suggest that Peli1 negatively regulates TLR-mediated IFN-I induction through inhibition of signaling events involved in the activation of TBK1 and IKKε.
To examine the in vivo role of Peli1 in regulating IFN-I induction, we stereotaxically injected LPS into cerebrospinal fluid (CSF) and examined the IFN-I induction in the mouse brain. We found that injection of LPS stimulated the expression of Peli1 in the brain (Fig. 2a). Consistent with our previous work , the LPS-stimulated induction of several proinflammatory cytokines was significantly decreased in the brain of Peli1-KO mice, as compared to that of the WT mice. In contrast, the Peli1 deficiency substantially enhanced the Ifnb gene induction following the LPS injection (Fig. 2b). Similarly, ELISA also revealed an elevated level of IFN-β protein in the whole brain homogenization of the LPS-injected Peli1-deficient mice (Fig. 2c). These results are consistent with the in vitro studies using the Peli1-deficient microglia (Fig. 1b) and further establish an in vivo role for Peli1 in negatively regulating IFN-β production in the brain.
Microglia serve as a major type of CNS-resident cells that respond to viral infections [18–20]. To investigate the role of Peli1 in regulating antiviral immune responses in microglia, we employed VSV, a virus known to infect microglia and CNS [21, 22]. Infection of microglia with VSV led to the induction of both IFN-Is and proinflammatory cytokines. Furthermore, Peli1 deficiency in microglia significantly enhanced the induction of Ifna and Ifnb genes and concomitantly inhibited the induction of the Il6 and Tnf genes (Fig. 3a). To examine the functional role of Peli1 in mediating anti-VSV host defense, we infected the Peli1-deficient and WT microglia with VSV-GFP, which allows quantification of the infected cells by flow cytometry based GFP expression. Consistent with their hyper-production of IFN-Is, the Peli1-KO microglia were substantially more resistant to VSV infection, as evidenced by the much lower level of VSV-infected cells (Fig. 3b). These results suggest that Peli1 negatively regulate anti-VSV immune responses in microglia.
To examine the in vivo role of Peli1 in regulating antiviral function, we challenged the Peli1-KO and WT control mice with VSV through intranasal injection, a route that is known to lead to CNS infection [21, 23]. Compared with the WT control mice, the Peli1-KO mice were remarkably more resistant to VSV infection, as revealed by the much improved survival rate (Fig. 4a). This phenotype of the Peli1-KO mice was associated with significantly enhanced expression of IFN-Is in the brain (Fig. 4b), and remarkably lower VSV titer in the homogenates of the olfactory bulb (OB) and brain (Fig. 4c, d).
To identify the neural cell linage that is responsible for the production of IFN-Is against virus infection, we infected WT and Peli1-KO mice with VSV-GFP through intracranial injection, and then isolated different type of neural cells by FACS sorting for QPCR analysis. The microglia isolated from VSV-GFP-infected Peli1-KO mice expressed a significantly higher level of Ifna and Ifnb than the microglia derived from the VSV-GFP-infected WT mice (Fig. 5a). In contrast, neither astrocytes nor neurons, isolated from the VSV-GFP-infected WT and Peli1-KO mice, had significant differences in IFN-I expression (Fig. 5b, c). We also found that the Peli1-KO microglia exhibited significantly reduced GFP expression compared to the WT microglia, suggesting augmented anti-VSV function of the Peli1-KO microglia (Fig. 5d, e). This result was consistent with that obtained with the in vitro microglial infection model (Fig. 3b). Taken together, these data suggest that Peli1 negatively regulates CNS host defense against VSV infection through suppressing IFN-I production in microglia.
In the present study, we identified the E3 ubiquitin ligase Peli1 as a pivotal negative regulator of IFN-I induction in microglia of the CNS. The Peli1 deficiency profoundly promoted the induction of IFN-Is in microglia in response to stimulation by the ligands of TRIF-dependent TLRs, poly(I:C) and LPS, or infection by the RNA virus VSV. The hyper-production of IFN-Is by the Peli1-deficient microglia was associated with enhanced protection against VSV infection. The Peli1-KO mice were also more resistant to intranasal infection with VSV, coupled with heightened production of IFN-Is in the CNS.
The microglia-specific role of Peli1 in negatively regulating IFN-I expression is at least partially due to its cell-specific expression. We have previously shown that Peli1 deficiency has no appreciable effect on the induction of IFN-Is in peripheral innate immune cells and MEFs . Interestingly, however, a Peli1 knockin study demonstrates that IFN-β induction is attenuated in myeloid cells and MEFs expressing a Peli1 mutant lacking E3 ligase activity . It is currently unclear whether this discrepancy is due to cell-type specific functions of Peli1 or the differences between expression of a Peli1 mutant and complete ablation of Peli1. One possibility is that the E3-defective Peli1 may exert an active role by binding to, and modulate the function of, other Peli family members. In this regard, Peli3 serves as a negative regulator of IFN-I induction by TLR3 and viruses . Future studies will examine whether the mutant form of Peli1 is able to bind Peli3 and promote the negative role of Peli3 in IFN-I regulation. Notwithstanding, our present study identified Peli1 as a negative regulator of IFN-I induction in microglia in response to TLR stimulation and VSV infection. In these CNS resident macrophages, Peli1 is the predominant Peli family member , which allows us to investigate Peli1 function without a major influence from other Peli family members. Our findings suggest that Peli1 and Peli3 share similar functions in the regulation of IFN-I induction, which is consistent with the high level of structural homology between these two Peli family members.
Although how precisely Peli1 negatively regulates IFN-I induction in microglia remains to be further investigated, our present study suggests that Peli1 controls a signaling step that mediates activation of the protein kinases TBK1 and IKKε. Peli1-deficient microglia were hyperresponsive to LPS stimulation in the activation of both TBK1 and IKKε. Previous studies have identified TRAF3 a central mediator of IFN-I induction by both TLR ligands and viruses [25, 26]. Notably, we have previously shown that the Peli1 deficiency causes accumulation of TRAF3 in microglia following TLR stimulation . It is thus possible that the accumulated TRAF3 expression in Peli1-deficient microglia may contribute to the enhanced activation of TBK1 and IKKε and hyper-induction of IFN-Is. This possibility will be examined in future studies.
The findings of the present study establish Peli1 as a negative regulator of IFN-I induction in microglia and an important modulator of antiviral immune responses in the CNS.
Peli1-deficient mice (on the C57BL/6 × 129/Sv background) have been described. Peli1 +/− heterozygous mice were bred to generate age-matched Peli1 −/− (Peli1-KO) and Peli1 +/+ (WT) mice. Green fluorescence protein (GFP) transgenic (C57BL/6-Tg(CAG-EGFP)10sb/J) mice were from The Jackson Laboratory. Mice were maintained in a specific pathogen-free facility, and all animal experiments were in accordance with protocols approved by the Institutional Animal Care and Use Committee of the University of Texas MD Anderson Cancer Center.
Antibodies for TBK1 and phospho-TBK1 were purchased from Cell Signaling Technology Inc. The anti-IKKε and anti-phospho-IKKε antibodies were from Santa Cruz and Millipore, respectively. LPS (derived from Escherichia coli strain 0127:B8) was from Sigma-Aldrich, poly(I:C) was from Amersham, CpG (1668) was from TIB Molbio, Pam3CSK4 was from Alexis Biochemicals, and R-837 was from Invivogen.
We slowly injected PBS, LPS or VSV-GFP into the cerebrospinal fluid (CSF) (AP, −0.4 mm; ML, −0.8 mm; and DV, −2.5 mm) of Peli1-KO or wild-type control mice as described previously .
WT and Peli1-KO mice (8-weeks-old) were lethally irradiated (950 rads) and reconstituted with mononuclear BM cells (1 × 107) from the GFP transgenic mice. After 8 weeks, the chimeric mice were immunized for EAE induction as described previously .
Cell suspensions were subjected to flow cytometry analyses as previously described using a LSRII flow cytometer .
VSV (Indiana strain) and VSV expressing GFP (VSV-GFP) were provided by Glen Barber. For infections, 1 × 107 pfu of VSV in 30 μl of endotoxin-free PBS was administered in drops (~5 ml/drop) to isofluorane-anesthetized 8–12 week-old mice, with PBS-only as control. Thereafter, mice were monitored daily for disease symptoms and mortality. In some experiment, mice were sacrificed 24 h after virus infection, the brain were collected for RNA extraction or for preparation of neural cells by using Neural Tissue Dissociation Kit (Miltenyi Biotech). The isolated neural cells were subjected for flow cytometric analysis or for FACS sorting of microglia (CD11b+), astrocyte (GLAST-1+), and neuron (CD11b−CD31−GLAST1−O4−) by using the Neuron isolation kit from Miltenyi Biotec.
For quantification of infectious VSV in organs, mice were anesthetized with pentobarbital (150 mg/kg). Organs were snap-frozen in liquid nitrogen, weighed, pestle/tube-homogenized in 1 ml of PBS per brain or lung or 0.1 ml per pair of olfactory bulbs, and virus was titered in 10-fold serial dilutions on BHK21 cells by plaque assay. Results are expressed as plaque-forming units (pfu) per gram of tissue.
Mixed glial cultures were prepared from 1- to 2-day-old mice. In brief, after removing the meninges, brains were dissociated by 0.25 % trypsin, and were filtered with a 40-μm mesh. Cells were cultured in DMEM supplemented with 10 % heat-inactivated fetal calf serum, 100 U/ml penicillin, and 100 mg/ml streptomycin. The culture medium was changed after 24 h and then every 3 days. Two weeks later, microglia were obtained by intensive washing and shaking the culture (250 rpm) for 1 h at 37 °C. The purity of the microglia was >97 % as determined by flow cytometry to measure the percentage of CD11b+ cells.
Real-time quantitative RT-PCR (qPCR) was performed as described using gene-specific primer sets (Table 1). Gene expression was assessed in triplicate and normalized to a reference gene, Actb.
Primary microglia were stimulated with 100 ng/ml LPS for the indicated time period and lysed in RIPA buffer. The whole cell extract were separated via 8.25 % SDS-PAGE, transferred to PVDF membranes, blocked and subject to IB analysis.
One-way ANOVA, where applicable, was performed to determine whether an overall statistically significant change existed before the Student's t-test to analyze the difference between any two groups. Data are presented as means ± SD. A P-value less than 0.05 is considered statistically significant.
We thank G Barber for the VSV. We also thank the personnel from the NIH/NCI-supported resources (flow cytometry, animal facility, and histology core facilities) under award number P30CA016672 at The MD Anderson Cancer Center. This research was supported by grants from the US National Institutes of Health (AI057555 and AI104519).
YZ designed and performed the experiments, prepared the Figures, and wrote the manuscript; JJ, QZ, HH, and XC contributed to the performance of the experiments, and S-CS supervised the work and wrote and edited the manuscript. All authors read and approved the final manuscript.


The number of homes for sale that are described as "fixer-uppers" is on the rise – which is good news if you're a homeowner that hopes to sell your house "as is" or a buyer looking for a project. The analysis, done by Zillow, found that, over the past five years, there's been a 12 percent increase in the number of homes on the market that'll require some extra love from their new owners. They also found that the trend is more pronounced on the higher end of the market, with a 35 percent increase in the number of "fixer-uppers" among the top third of homes for sale compared to a 3 percent increase among more affordably priced homes. So why are more homes being listed "as is"? Simply put, the increase is due to low inventory. With fewer houses for sale, homeowners in many markets feel more comfortable listing their homes without having done every repair and renovation because buyers have fewer choices. Svenja Gudell, Zillow's chief economist, says there are also more older homes out there. "Sellers are in the driver's seat, with the freedom to list their home for sale 'as-is' without worrying about price cuts or the home sitting on the market," Gudell said. "And without sufficient new construction, the housing stock has aged, so home buyers are finding more and more homes on the market in need of a little TLC." More here.


text:
<?php

/**
 * This file is part of the Haringo library.
 *
 * @author Łukasz Makuch <kontakt@lukaszmakuch.pl>
 * @license MIT http://opensource.org/licenses/MIT
 */

namespace lukaszmakuch\Haringo\ClassSource\Impl;

use lukaszmakuch\Haringo\ClassSource\FullClassPathSource;

/**
 * Holds key from the map of class path sources.
 *
 * @author Łukasz Makuch <kontakt@lukaszmakuch.pl>
 */
class ClassPathFromMap implements FullClassPathSource
{
    private $keyFromMap;

    /**
     * @param String $keyFromMap key from the map
     */
    public function __construct($keyFromMap)
    {
        $this->keyFromMap = $keyFromMap;
    }

    /**
     * @return string key from the map
     */
    public function getKeyFromMap()
    {
        return $this->keyFromMap;
    }
}

redpajama_set_name: RedPajamaGithub


The Adventurers meet from noon until 2:00 on the 2nd Wednesday of the month (September-June) for lunch and a program in the Christian Fellowship Center. Programs include speakers, musical programs, and slide shows of interest to all. Cost for lunch is $10 and reservations should be made at least the Monday before.


Motorcycle racing is a sport also known as Moto racing or Bike racing. This sport involves motorcycles racing against each other on a pre-decided circuit. The circuit can be tarmac-based or off-road. The international body for the sanctioning of motorcycle racing is the FIM. Although most nations have their own governing bodies to manage the sport at their level, other independent governing bodies also exist, which operate on both national and international levels.
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text:
Q: Is the variant direct image mathematically significant? Preimages have the property that for an arbitrary function $f : X \rightarrow Y$ and all $B \subseteq Y$ it holds that $$f^{-1}(B^c)=[f^{-1}(B)]^c.$$
However, the analogous statement for direct images is false. Thus, we have two definitions of direct image; the usual one, and a variant. $$f_*(A) = \{b \mid \exists a \in X : a \in A \,\wedge\, f(a)=b\}$$
$$f_\diamond(A) = \{b \mid \forall a \in X : a \in A \,\vee\, f(a) \neq b\}$$
Now I think (though I have not proved it) that, for all functions $f$, it holds that $f_* = f_\diamond$ iff $f$ is an injection bijection. Note also that, under these definitions, we have $$f_*(A^c) = [f_\diamond(A)]^c, \quad f_\diamond(A^c)=[f_*(A)]^c.$$
Here's another observation. If $X$ and $Y$ are topological spaces, then we have that $f_*$ preserves openness iff $f_\diamond$ preserves closedness, and vice versa.
Okay, but does $f_\diamond$ have any real mathematical significance? Like, does it show up naturally in any interesting theorems etc.? If so, what's the standard terminology/notation, and where can I learn more?

Addendum. Two related maps are $f_\cap(A) := f_*(A) \cap f_\diamond(A)$ and $f_\cup(A) := f_*(A) \cup f_\diamond(A).$ If anyone knows where I can learn more, please leave a comment! Note that all four concepts coincide in the case of bijections.

A: The variant direct image is universal quantification. So if you think universal quantification is significant...
To explain, let $X, Y$ be sets and let $f : X \times Y \to Y$ be the projection onto the second coordinate. If $\varphi(x, y)$ is any proposition involving variables $x \in X, y \in Y$, then it cuts out a subset of $X \times Y$ (namely the subset for which $\varphi(x, y)$ is true). The corresponding direct and variant direct image subsets in $Y$ are precisely the subsets of $Y$ cut out by the existentially and universally quantified statements $\exists x : \varphi(x, y)$ and $\forall x : \varphi(x, y)$ respectively.

Much more generally, let $F : C \to C'$ be a functor between two categories and let $D$ be another category. Then $F$ induces a functor $D^{C'} \to D^C$ between functor categories. A left adjoint to this functor, if it exists, is called left Kan extension along $F$, and a right adjoint is called right Kan extension.
Now let $C, C'$ be sets regarded as discrete categories (categories with only identity morphisms), and let $D = \{ 0 \to 1 \}$ be the category with two objects $0, 1$ and a single non-identity morphism $0 \to 1$. $D$ is a poset, and so are the functor categories $D^C, D^{C'}$, which are naturally identified with the poset of subsets of $C, C'$ under inclusion. If $F : C \to C'$ is a functor (so just a map of sets), the induced functor $D^{C'} \to D^C$ is the usual preimage functor, the usual direct image is the left Kan extension along $F$, and the variant direct image functor is the right Kan extension along $F$.
Left and right Kan extension are ubiquitous in mathematics; Mac Lane famously said that they subsume all the other fundamental concepts in category theory. So it is a little hard to give examples because there are so many. This example is the simplest example I know.


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Books in the Freezer Favorites
Curated list from the Books in the Freezer podcast full of stories that are sure to send a chill down your spine.
Playlist Tags: genre: Horror audience: bookish podcast fans mood: scary
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By William Peter Blatty
Narrated by: William Peter Blatty & Eliana Shaskan
#17 in Bestselling Horror Audiobooks
"What an excellent day for an exorcism..."
Originally published in 1971, The Exorcist remains one of the most controversial novels ever written. A literary phenomenon soon after its release, it spent fifty-seven weeks on the New York Times bestseller list, seventeen consecutively at number one. Inspired by the shockingly true story of a child's...
Bookseller Pick
By Josh Malerman
Narrated by: Cassandra Campbell
Length: 9 hours 8 minutes
"Imagine something so terrifying, one glimpse and a person is impulsively driven to commit deadly violence, to oneself and others? Suddenly forced into a world of darkness, covered windows and blindfolds, Malorie must survive for the sake of her unborn child. Finding herself amongst a group of survivors, led by the knowledgeable Tom, Malorie soon learns the threat may not only be outside, but, living inside their house. While switching between the past and present, Josh Malerman's debut novel is a thriller from start to finish. Flash forward to five years later, Malorie is desperate to make a twenty mile journey downriver, blindfolded with the four-year olds, boy and girl. Will their wits and trained ears guide them to salvation or will they encounter the horrific threat that has annihilated most of mankind? Extremely creepy...especially if you are afraid of the dark, like myself!"
Kristin, McLean & Eakin Booksellers
Mongrels
By Stephen Graham Jones
Narrated by: Chris Patton & Jonathan Yen
Length: 9 hours 41 minutes
Nominated for both the Shirley Jackson and Bram Stoker Awards, and a Best of 2016 selection of Tor.com and Book Riot, acclaimed horror writer Stephen Graham Jones' Mongrels goes beyond your typical werewolf story to show a young boy, mired in poverty and always on the run, coming-of-age in a world that fears him and hates his family...but may...
The Cabin at the End of the World
By Paul Tremblay
Narrated by: Amy Landon
"Wen and her dads are taking a break from everything by visiting a remote cabin for vacation. Wen is studying grasshoppers in their yard when a man comes up and warns her that she and her dads are going to have to make a decision. And that's about all I can tell you without spoiling the story. This book was so creepy, in a very good way. I'd classify this as horror, but very realistic."
Jennifer Jones, Bookmiser
The Dark Descent of Elizabeth Frankenstein
By Kiersten White
Narrated by: Katharine Lee McEwan
"Elizabeth Lavena's life has never been easy. But when she embarks on a journey to find Victor Frankenstein it's about to get a lot darker. Clever, creepy, and enthralling this re-imagining is a beautiful homage for the 200th anniversary of Mary Shelley's classic tale."
Hanna Fischer, Rediscovered Books
By Grady Hendrix
Narrated by: Bahni Turpin
"I don't know about everyone else, but I, for one, am really excited that vampires are making a comeback. I think they're such a fun trope in pretty much every genre, and this was no exception. True to the Grady Hendrix style, this book was the perfect campy, slightly off-kilter, and moderately gory suburban horror story I didn't know I needed."
Kendall, Brilliant Books Audio
By Courtney Summers
Narrated by: Dan Bittner, Fred Berman, Gabra Zackman & Rebecca Soler
"Engrossing, thrilling and original. The story alternates between a podcast format and Sadie's voice. Sadie is a compelling protagonist - strong, determined and on a mission. Fantastic listen!"
Jennifer, East City Bookshop
Into the Drowning Deep
By Mira Grant
Narrated by: Christine Lakin
"In Into the Drowning Deep, Mira Grant has conjured up scary mermaids living in the depths of the Pacific Ocean. An expedition sets out to learn if mermaids truly exist and to uncover the fate of a previous expedition. The new crew is being recorded for a documentary, with the hope it will prove mermaids are real and clear the network of wrongdoing. Both Tory, whose sister was killed on the first expedition, and Jillian, who has been teaching about mermaids for years, are going out on the state-of-the-art ship; however, that ship has one major flaw. You will not look at The Little Mermaid the same way again!"
Jason Kennedy, Boswell Book Company
The Dead House
By Dawn Kurtagich
Narrated by: Charlotte Parry
Debut author Dawn Kurtagich is dead on in this terrifying psychological thriller!
Over two decades have passed since the fire at Elmbridge High, an inferno that took the lives of five teenagers. Not much was known about the events leading up to the tragedy - only that one student, Carly Johnson, vanished without a trace...
...until a diary is... Read more »
By Stephen King
Narrated by: Stephen King
Set in the fictional town of Castle Rock, Maine
Master storyteller Stephen King presents the classic #1 New York Times bestseller about a mysterious store than can sell you whatever you desire—but not without exacting a terrible price in return.
The town of Castle Rock, Maine has seen its fair share of oddities over the years, but nothing is as... Read more »
I Call Upon Thee
By Ania Ahlborn
Narrated by: Madeleine Lambert
Maggie Olsen had a pretty ordinary childhood-swimming and sleepovers, movie nights and dad jokes. But then there were the other things...the darker things...the shadow that followed her home from the cemetery and settled into the corners of her home, refusing to let her grow up in peace. Now, after three years of being away from the place she's...
By Victor LaValle
Narrated by: Victor LaValle
"[This] haunting tale weaves a mesmerizing web around fatherhood, racism, horrific anxieties and even To Kill a Mockingbird. And the backdrop for this rich phantasmagoria? The boroughs of New York."—The New York Times
Winner of an American Book Award, a Locus Award for Best Horror Novel, a British Fantasy Award for Best Horror Novel, a World... Read more »
You Should Have Left
By Daniel Kehlmann
Narrated by: Robertson Dean
From the internationally best-selling author of Measuring the World and F, an eerie and supernatural tale of a writer's emotional collapse
"It is fitting that I'm beginning a new notebook up here. New surroundings and new ideas, a new beginning. Fresh air."
This passage is from the first entry of a journal kept by the narrator of Daniel Kehlmann's... Read more »
FantasticLand
By Mike Bockoven
Narrated by: Angela Dawe & Luke Daniels
Since the 1970s, FantasticLand has been the theme park where "Fun is Guaranteed!" But when a hurricane ravages the Florida coast and isolates the park, the employees find it anything but fun. Five weeks later, the authorities who rescue the survivors encounter a scene of horror. Photos soon emerge online of heads on spikes outside of rides and... Read more »


With weather warming up, more people are on the streets. Traveling by foot might be a wiser and healthier option, but it's not always safer.
Seventy-thousand pedestrians are injured — and more than 4,000 die — in automobile collisions every year. While this is only a slither of the vehicle-accident total, it's a disproportionate amount: Eleven percent of transport (disregarding miles traveled) happens by foot, but pedestrians are involved in 13 percent of vehicle-related fatalities (Source: National Highway Traffic Safety Administration (NHTSA) Traffic Safety Facts) .
Although drivers are legally responsible for controlling their vehicle at all times, the majority of pedestrian accidents are caused by pedestrian actions. Sunny days — where more people are outside– rack in 90 percent of incidents. Age is also a factor – seniors over 65 and children under 15 account for a combined 27 percent of fatalities and 34 percent of injuries. (Source: NHTSA Traffic Safety Facts ).
The vast majority of pedestrian accidents happen in the road with two-thirds occurring on city streets. A bike riding on the sidewalk can hit pedestrians or force them onto the road.
Intersections are a hotspot for pedestrian accidents. Using signaled crosswalks dramatically reduces the risk. Clearly marked pedestrian pathways are vital at or near parking lots because drivers are less likely to see people when they're focused on parking.
The no-texting rule isn't only for drivers. A recent study by NYU Langone Medical Center on New York City pedestrian accidents found eight percent accidents occurred while the victim was using electronics including cellphones, and music devices. The study also found a substantial number of accidents occurred from passengers exiting vehicles on the roadway side.
Nearly 50 percent of all pedestrian accidents happen on the weekends and 70 percent happen at night. (Source: Insurance Institute for Highway Safety (IIHS))After the sun goes down, bright and lightly colored clothes are easier to spot– critical in less populated stretches with poor street lighting. Pocket flashlights are also a good idea for night-prowling.
As cities draw more and more people, multi-lane, high-speed roadways are increasingly necessary to move traffic to and from the freeway. Unfortunately, these sites are also hazardous to the densely populated areas they serve, where walking is commonplace and bus stops are plentiful.
Some of these accidents are also caused by poorly marked construction zones. One way to help signal drivers is by using lots of road cones and other hazard markings.
According to a 2010 report by University of North Carolina's Highway Safety Research Center, the majority of urban pedestrian accidents happen in these roadways.
This article is very helpful for a report I'm doing on the causes of pedestrian deaths! Thank you soo much this helped me a bunch!
Interesting statistic about dark clothes, makes a lot more sense then you would think than at first glance.


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The focal point of the NSON-DK project is how the future massive offshore wind power and the associated offshore grid development will affect the Danish power system in the transition towards a future sustainable energy system. NSON-DK is a Danish part of the North Sea Offshore and Storage Network (NSON) project framework, which has emerged from the European Energy Research Alliance (EERA) as a pioneer project framework joining nationally funded research according to the European Commission's Berlin model.
- How will the offshore wind power development affect the variability and uncertainty of variable renewable generation in the Danish power system and neighboring systems?
- How will this increased variability and uncertainty from the offshore wind power development together with onshore renewable generation development influence the balancing and need for reserves in the Danish power system?
- How will the offshore wind power and offshore grid development influence the electricity markets in future systems with large scale energy storage and coordination of the electricity system with other energy systems (mainly heat and transport)?
- How will the scale and architecture of the offshore grid development influence the adequacy and security of supply in the Danish power system?
- Which polity instruments should be applied to support an effective and cost-efficient transition of the Danish power system combining the offshore development with energy storage and coordination between energy systems?
Impacts of offshore grid developments in the North Sea region on market values by 2050: How will offshore wind farms and transmission lines pay?


text:
Cheng Xueqi (程學啟, 1828-1864) est un général de la révolte des Taiping qui rejoignit la dynastie Qing en 1861 en même temps que Ding Ruchang. Il est un éminent fonctionnaire han et officier militaire de la fin des Qing. Il organise l' qui combat les Taiping, restaure la stabilité des Qing avec d'autres personnalités de premier plan, telles que Li Hongzhang et Zeng Guofan, commande la défense de Shanghai avec succès. L'empereur Tongzhi le considère comme « intelligent et brave ».

Il est promu lieutenant-général en  et défend Shanghai lors de la , et crée la première troupe de fusiliers chinois en . Il reconquis les villes de Taicang, Kunshan, Wujiang, est promu capitaine-général en , et créé la première troupe chinoise de canons modernes. Il est décoré avec avoir reconquis 20 villes de la province du Jiangsu et défendu Shanghai deux fois en deux ans.

En 1864, après un mois de siège de la ville de Jiaxing, Cheng Xuechi décide de conquérir la ville au plus vite. En utilisant des centaines de kilos d'explosifs, il ouvre une brèche dans les murailles. Il ordonne alors à ses troupes de charger immédiatement vers la brèche. Mais tandis qu'il prend la tête de cette charge, il reçoit une balle à la tête. Il est dit qu'il continua la charge même après avoir été touché. Il meurt cependant de ses blessures une semaine plus tard en exprimant sa joie de retrouver sa femme et ses fils dans l'autre vie (sa famille avait été tuée quatre ans plus tôt par les rebelles taiping. Lorsque l'empereur Tongzhi apprend sa mort, il se met à pleurer.

Voir aussi
 Ébauche d'une histoire des Qing
 Massacre de Suzhou

Liens externes

Naissance en 1828
Décès en 1864
Général chinois du XIXe siècle
Transfuge chinois

redpajama_set_name: RedPajamaWikipedia


Dr. Winston majored in biochemistry at the University of Colorado-Boulder and then attended medical school at the University of Minnesota where she was AOA. She also went on to complete a four year Combined Internal Medicine – Pediatrics Residency at The Warren Alpert Medical School at Brown University. After her residency, she worked as a Clinical Research Fellow at the Miriam Hospital Immunology Center and completed a Clinical Fellowship in Pediatric Infectious Disease at Hasbro and Women & Infants Hospitals. She has authored a number of papers and has received numerous awards. Dr. Winston has experience working in the African countries of Kenya, Rwanda and Mali.


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