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A Man Alone
Series: 'Deep Space Nine'
Episode Title: 'A Man Alone'
Episode Number: 103
Synopsis: "When an alien who was once incarcerated by Odo is killed in a holosuite, Odo becomes the prime suspect, but Kira and others suspect that he was framed. While they investigate, Keiko O'Brien opens a school for Bajoran and Federation children."
Original Airdate: January 17, 1993
Story By: Gerald Sanford, Michael Piller
Teleplay By: Michael Piller
Directed By: Paul Lynch
Guest Stars:
- Rosalind Chao as Keiko Ishikawa O'Brien
- Edward Laurence Albert as Zayra
- Max Grod�nchik as Rom
- Peter Vogt as Bajoran Man
- Aron Eisenberg as Nog
- Steven James Carver as Ibudan
- Tom Klunis as Old Man Ibudan
- Scott Trost as Bajoran Officer
- Patrick Cupo as Bajoran Man
- Kathryn Graf as Bajoran Woman
- Hana Hatae as Dabo Girl
- Diana Cignoni as Dabo Girl
- Majel Barrett Roddenberry as Computer Voice
- Judi Durand as Cardassian Computer Voice
- Michelle Erica Green - The Trek Nation
- div1701 - Fiver (Parody)
- Tim Lynch - Review - 6/10
- Jamahl Epsicokhan - Star Trek: Hypertext - 2/4
Prev: 'Past Prologue'
Can't get enough of 'A Man Alone?' Check out the following merchandise:Read the Review
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Next: 'Babel'
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My dear friend Susie is a crisp, courageous writer. Today, Elle.com published her essay about the heart-wrenching way our little Cal has factored into her family's life in the past year.
I cried in a bathroom stall at work as I read the first draft of this piece when Susie shared it with me. Feeling the weight of her friendship and longing made my heart hurt.
Her boldness and vulnerability are well worth reading.
(Love you, Susie.)

subset: commoncrawl


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The US Justice Department has charged a former government employee for allegedly trying to steal nuclear secrets through email attacks and sell them to China.
According to an indictment , Charles Eccleston allegedly attempted the "spear-phishing" attack in January targeting dozens of email accounts, which he believed would unleash a virus to collect sensitive information on nuclear weapons.
Eccleston, a former employee at the Department of Energy and the Nuclear Regulatory Commission, has lived in the Philippines since 2011 after being fired in 2010. Continue reading


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I recently acquired a copy of Princeton University Press's "Birds of Europe, Russia, China, and Japan" by Norman Arlott (copyright 2007), a two-volume illustrated checklist (7.5x5 inches, ~240 pages each, one for passerines and one for non-passerines). I have loved most of Princeton's line of bird books, but my review of this one may come across as a bit harsh.
First off, I'm not a fan of "illustrated checklists," whatever those are. Generally when I see that term, I picture a checklist with a single crummy representative photo per species. But that is not what you'll find here. Amazingly there isn't a single checklist to be found in either book. I don't
know what to make of that exactly, given the sub-genre to which these
books supposedly belong.
Basically we're dealing with a low-end field guide here. I will explain.
Here is the format: text on left page, plate on opposite page. See photo below:
This quote from the Introduction is telling: "I did not want to produce just a coloured checklist or the ultimate field guide..." So what we're left with is a hybrid of those two...except that there is no checklist, and the identification info is severely lacking.
The text is limited to just a few lines for most species, and most major field marks are excluded! Perhaps this is to avoid redundancy with the illustrations for the purpose of saving space, but the result is rather weak and uninformative text. Here is the description of Stilt Sandpiper: "In flight has inconspicuous white bar on upperwing and white rump, feet project well beyond tail." That's it! The remaining text describes the bird's call and preferred habitat.
Range maps are in a separate section at the end of the book - old Peterson style. That format has always driven me crazy, all the flipping back and forth...
I will say something positive though - the illustrations are of fairly high quality. They are, for the most part, detailed, accurate, and pleasing to the eye. The problem is that only adult plumages are illustrated. That's right...no juvenile shorebirds or immature gulls! Good luck identifying those groups with these books.
Unfortunately those illustrations that are included on each plate are often poorly organized. The images are crammed together with numbers to represent each species, and they are packed so tightly on some plates that you have to look closely to figure out which numbers refer to which illustrations. Too much work for too little information.
So, overall, I would not recommend this two-volume set to most birders. If you want a checklist, buy or print a two-page checklist for little/no cost (because you won't find one here!). If you want a field guide, invest in a comprehensive one. These hybrids just don't do it for me (that's something you won't hear me say often!).
To whom might this book be useful?
Perhaps for a beginning birder? I have heard it argued that simplicity is desired for beginning birders; that less can be more. But I generally disagree with this because I believe this leads to more misidentifications than anything. Withholding certain complicated information may be beneficial to the novice, but to leave out illustrations of immature birds is just making things more confusing IMO.
These books may work for a traveler to the region who does not plan on birding but still wants a small reference with basic ID information for whatever they see along the way. Their small size makes them easy to travel with.
Please read more reviews on these books before you judge them. I was surprised to see that the reviews on Amazon were generally favorable. So obviously they work for some folks, just not this one.
- Nick
Tuesday, June 18, 2013
Review: "Birds of Europe, Russia, China, and Japan" by Norman Arlott
Posted by Nick Bonomo at 7:42 PM
Labels: Book Reviews
3 comments:
I don't think these can work for anyone.ReplyDelete
- SulmaanJune 22, 2013 at 9:13 AM
Hi Nick, Thanks for the review. I was just wondering if there's a guide for the regions covered that might be more useful; having done some birding in China and Russia, I've been hoping to invest in one, but never really found anything quite satisfactory. Thoughts?ReplyDelete
Hope to see you out at Lighthouse Point in the fall.
Hey Sulmaan, nice to hear from you. Unfortunately I've not ventured to Asia at all, so I can't offer up any insights on other field guides. I'm sure that better options exist, but I'm just not aware. Perhaps start with a Google search, or head to Birdforum, and take it from there? Maybe some of our readers can suggest something for you?ReplyDelete
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Check out the Department of Workforce Development
Meet the Commissioner. CommissionerCommissioner Braun was appointed in 2014 to serve as Indiana's Commissioner of the Department of Workforce Development, which is tasked with building a highly skilled and educated Hoosier workforce that can compete in the global economy. Prior to graduating from Harvard University, Commissioner Braun was born and raised in Southern Indiana. After receiving a business degree, he immediately went to work for Price Waterhouse. Shortly after, he started his own technology consulting business that grew to over 750 employees across 13 offices nationwide. Both experiences have given…Read More


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Like lots of Americans last week, I boarded a Southwest flight from Indianapolis to Sanibel Island for a trip to warm sunshine and beaches. It was a full flight so there was the typical grumbling about no aisle seats or window seats from many of the passengers. Plus, we took off about 20 minutes behind schedule. First world problems, I know. But in 2 1/2 hours we landed in sunshine and balmy breezes.
Ahhhhh……Spring Break. After the horrible winter we had this year, it was even more of an anticipated trip than in recent past years.
We certainly enjoy the beaches, adult libations, shell collecting, and restaurants. But, for me, a perennial favorite shopping spot on the island is Gene's Books, a quirky small bookstore. It can't be any bigger than 3,000 sq ft, the size of a modern Barnes & Noble coffee area within their 80,000 sq ft store. But the serendipitous finds inside never fail to disappoint me. Books stacked floor to ceiling. Many no longer in print. It even has that musty library smell inside which is as intoxicating as Chanel #5 is for many genteel folks.
Anyway, I bought two books this trip for reading on the beach and lanai. One of the books was The Wright Brothers by David McCullough. I've read his other books, but never this one. The price was perfect–$8.95.
Cracking open the spine, his writings time warped my mind back into the early 1900's. For the next three days, I was engrossed in it. Like you, I always knew the surface details about how the brothers were the first to fly an airplane, blah, blah, blah. I've even had the pleasure of seeing their original flyer suspended from the Smithsonian Air Museum ceiling.
McCullough's deep research into their personal lives and the trials and tribulations from young boys until their deaths was inspiring. These men were true examples of:
- Perfect and absolute relentless focus.
- Precision, with the ability to monitor and review the smallest of details, lest their untested theories bring their deaths and family embarrassment.
- Perseverance, by suffering through hurricanes and mosquito infestations on the Outer Banks, ridicule by the experts at The Smithsonian (no shortage of irony here) and others attempting to steal their intellectual property like the infamous Alexander Graham Bell.
- Financial bootstrapping to generate cash for their 1903 flyer without any government or private grants.
- Society's failure to recognize, at the time, the magnitude of their miraculous achievement. Even an editor of the Associated Press was unimpressed with their 57 second flight.
Imagine what would have happened if they had given up, had thrown in the towel, had become distracted by other worldly desires?
The reason for such a soft discussion with you today, and thank you for your attention thus far by the way, is that sometimes we can feel like we're not making progress in our personal or professional lives.
We are now finished with the first quarter of 2019. Sometimes, it might feel like the whole world is against you or you should just quit and throw in the towel. It can be hard to recognize the small victories. Orville and Wilbur knew deep down in their souls what 57 seconds in the air like a soaring bird was going to bring their way. It was one small victory in a much longer journey, but they had the grit to keep after it.
So don't you dare quit.
If you're not hitting your rental property goals as a landlord, how can you refocus on smaller details to find out the problem? For the Wright Brothers, it was hiring a trusted mechanic named Charlie to operate their bicycle shop during their long trips to Kill Devil Hills and Kitty Hawk so they could focus exclusively on their experiments.
If you're not hitting your savings goals as a tenant to buy your next home or to get out of debt, how can you refocus? For the Wright Brothers, it was selling and repairing bicycles that generated enough profits to run their airplane experiments. The bicycle shop was just a means to an end for them.
If you're a business owner constantly battling staffing issues, which small one can you attack and remove first to gain momentum? For the Wright Brothers, it was befriending local folks at Kitty Hawk to help them build barns and living quarters.
As our Spring Break trip wound down to its inevitable conclusion, we arrived back at the airport for the flight home. I'll admit I was a little ashamed at how I can sometimes allow issues, frustrations or challenges to blow up in imaginary size compared to their actual relative scale. I sometimes let myself worry and wring my hands, instead of rolling up my sleeves and finding the solution.
We can keep trying.
We can keep learning.
And we can "Soar among the Heavens."


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I just wanted to document some thoughts on how I am feeling today about going "home". I have had people ask me how I'm feeling about going back for so long? Am I afraid I will not want to come back to Costa Rica? Will it be hard living out of suitcases for a month? Will it be hard to try to see everyone I want to see?
As for how long will be gone… It will be about a month. We will be traveling between Nashville, Paragould, Searcy and Memphis. I'm not really afraid about not wanting to come back to Costa Rica because where my husband and children are is where my home is. And at this point in our lives we need to be in Costa Rica. I think after living out of suitcases for a month we will be glad to be back in our own home.
I am a little bit anxious about trying to see everyone that we want to see and do everything we want to do in that time. People are busy and traveling as well so making definite plans can be difficult. I'm hoping to just be able to spend some time relaxing and appreciating all of the things that I took for granted before.
I imagine some long walks through target and visits to Chick-fil-A and our favorite restaurant OEC in Bartlett. I imagine all of the laughter that will be heard with all the cousins getting to see each other again. I imagine playing a lot of cards at the Cochran Christmas in Searcy.
I'm not looking forward to saying goodbye to friends and family again but at least I know that we are doing better than expected here and the kids are really thriving in school in Costa Rica. I have made some wonderful friends here and I will miss them and be ready to be reunited again. The kids and I are about to get on a plane so goodby for now!


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December 23, 2016
Peace on Earth, Goodwill to All
17 comments:
Merry Christmas to you!ReplyDeleteReplies
Thanks, Karen. Merry Christmas and blessings to you, too!Delete
Wish you a Merry Christmas and a Wonderful 2017 with lots of garden joy!ReplyDeleteReplies
Garden joy: That is something to look forward to! Blessings to you, as well! :)Delete
Merry Christmas to you too. May you and your have a great holiday together.ReplyDeleteReplies
Merry Christmas and Happy New Year, Lisa. Blessings to you and yours!Delete
Merry Christmas Beth.....wishing you and your family a blessed holiday and a very Happy New Year! We will hope....ReplyDeleteReplies
Happy Holidays, Donna. We must have hope--gardening should help. :)Delete
Thank you, Beth.ReplyDelete
Same to you!
And hope that 2017 is a great year for you and your garden!Replies
Happy Holidays, Aaron. And blessings to you and yours in the coming year!Delete
Thank you Beth. Happy Christmas to you and yours.ReplyDeleteReplies
Dear Chloris: I hope you had a Happy Christmas and all the best for the New Year!Delete
Beth - Merry Christmas! Thank you for all your beautiful postings, and may 2017 be full of blooms for all of us.ReplyDeleteReplies
Hi Pat: Yes, I hope both of our gardens will be full of healthy plants and beautiful blooms in the year ahead. :)Delete
Merry Christmas to you and your family, Beth!ReplyDeleteReplies
Holiday blessings to you and Judy and the entire family, Jason!Delete
Hope you had a joyous Christmas! I wish you Goodwill (Salvation Army, St.Vincent DePaul, insert name of thrift store here) as well!ReplyDelete
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Let's talk about Kill la Kill, Trigger's first full-length animated series. A warning: there will be SPOILERS in this post. Big, big spoilers. If you haven't seen the last episode, if god forbid you haven't seen any of Kill la Kill at all, TURN BACK WHILE YOU STILL CAN YOU FOOL
Okay, are we ready to talk Kill la Kill?
Let's talk Kill la Kill.
So after Ragyo's Wedding Dress of Death, a Nui-triggered Clothinstrumentality, a final Gurren Lagann-esque battle in space, what is Kill la Kill really about? Is it a family drama about two sisters born in horrible circumstances rising up to dethrone their tyrannical mother and avenge their father's death? Is it an extended homage to shonen manga of the 1970s-80s, especially the delinquent epics Sukeban Deka and Otokogumi? Is it an animated satire of old-school Go Nagai exploitation manga? A fetishistic and overly indulgent passion project that pretends to grant its heroines agency only to leer at their breasts? Is it feminist or misogynistic? An extended treatise on bondage? Anime's "savior" (whatever that means) or typical of all its worst excesses? Or (as the last episode makes clear, tied to the show's first ED) is it the story of two (or three) young women who fight so that one day they will be able to go out into the city on an honest-to-goodness date without the weight of crushing familial responsibility?
To be honest I would say that the last of those comes the closest to summing up the thematic core of Kill la Kill. From the very beginning, Ryuuko and Satsuki have been cursed to fulfill the roles granted to them by fate's blood-red threads. Ryuuko must wear Senketsu and challenge her mother because her father engineered her and her talking uniform to serve as humanity's last defense against his own wife. Satsuki dedicates her entire life from kindergarten on to overthrowing her mother, no matter the personal cost to her health or sanity. In the show's first ED, a homage to Sukeban Deka, Ryuuko wanders the city by herself staring at the clothes in shop windows. Every time it's a reminder that so long as Ryuuko must fight, she may wear no other clothes than Senketsu, just as Satsuki must wear Junketsu to overcome her mother even though her body is incompatible with it. At the same time, when Ryuuko sees the wedding dress on a stand it's an ever-present reminder that she, like Satsuki, is engaged to her fate (which she overcomes only by reclaiming her mother's kamui Shinra Koketsu, sewn in the shape of a traditional Japanese wedding dress.) In that light, Senketsu's death is sad, but inevitable – by passing on he frees Ryuuko to wear any kind of clothing she wants. At the end of the series, Ryuuko, Mako and Satsuki are all wearing clothes – but they're the clothes they want to wear, not Goku uniforms or kamui. They wear clothes on the outside but at heart, as Aikuro or Tsumugu might say, they are Nudist.
Of course, all of this ignores that Senketsu's final transformation is totally a reference to Daicon IV.
Wait, what's Daicon IV? Only the sequel to Daicon III, made by Hiroyuki Yamaga, Takami Akai and a little-known animator named Hideaki Anno for the eponymous Nihon SF Taikai conventions. Daicon IV was made by twelve people, working long nights while locked inside of a re-purposed studio building owned by a textile union. By all accounts it was a horrifying experience, one that gave those who participated nightmares for years after. But had Daicon III and IV not become successes, Gainax as we know it would not have existed. They even went on to reference it in their OVA FLCL, when Haruko rides on a guitar wearing a bunny suit and shouts "DAICON V!" So it's fitting that in the last episode of Trigger's first anime, finished literally hours before the deadline, when the main character powers up for the final time she's wearing a mash-up of Tengen Toppa Gurren Lagann and the bunny girl outfit. What is this, Daicon VI?!?
Here's why this matters: Kill la Kill's greatest strength (and its greatest weakness) is that director and writer Imaishi and Nakashima are deeply indebted to the classics. Every episode of the series is loaded with homages and visual gags, from the first episode's riffs on Ashita no Joe to the last episode's Clothinstrumentality being a clear (and perhaps inevitable) reference to End of Evangelion. Imaishi and Nakashima made it clear at the very beginning in interviews that the whole series started as a set of gender-swapped illustrations of characters from Otokogumi. Hell, according to some mashing together the names of Otokogumi's protagonist and his girlfriend gets you Ryuuko Matoi. The extent to which Imaishi and Nakashima try to fit in everything they can into their little project can verge on incoherency. Of course Kill la Kill has to have a tournament arc, what kind of shounen manga wouldn't have one? Who would even consider skipping over a school trip arc when the opportunity's right there? It's enough to make the viewer lament "All of this has already been done!" which is precisely the point. All of it has already been done, Trigger's just repurposing it in order to create an anything-goes universe in which all this pop-culture detritus from across the past few decades fits together logically. It's the same trick they pulled in their 2007 classic Gurren Lagann, though that show had a much higher budget and probably a tighter focus on its central character.
Seen in that light it's not hard to make a parallel between Trigger's struggle to make Kill la Kill and Ryuuko and Satsuki's struggle to defeat their mother and save the world. Ryuuko's a vagrant transfer student with only a ragged talking uniform for company, assisted by social rejects the Makanshokus and suave but borderline useless organization Nudist Beach; Satsuki's co-opting her mother's wealth in order to fund a private army to challenge the rule of clothing and save the human race. Meanwhile, Ragyo's corporation REVOCS (an anagram for the alien forces of COVERS) threatens to transmute the world not just into clothing, but into a vast sphere of inter-connected sameness, an Absolute Terror Field in which there is no room for individual self-expression. When Ryuuko flies into space to challenge her mother, she is wearing not a uniform slavishly produced over multiple weeks by a brainwashed army and a talented/armless couturier, but an amalgam of super-powered uniforms scraped together from her friends and family. Ryuuko starts the series as a loner, but at the end of it everyone has put their trust in her, even her sister and former rival. The end result takes a great deal of pain and suffering to engineer, but it's ultimately far more effective even than Ryuuko's combined scissor blades. It's Studio Trigger's Daicon IV.
In the end Kill la Kill is just like Senketsu's final transformation in that it's cobbled together from both countless anime and manga and from whatever resources Trigger could get their hands on. The final result is at times uneven, not as well animated as you would expect from someone as talented as Imaishi and his veteran crew of animators. Gurren Lagann is more polished, made as it was with the full weight of Gainax's funding and expertise. But there's a scrappy heart to Kill la Kill that I can't help but find endearing. Trigger came at this project with everything they had, and man it shows. The last episode of the series must have been hell to produce (according to Twitter most of the creative staff are taking a day off today) but they did it anyway, and they did it because despite the fact Trigger's next project will be one of those run-of-the-mill light novel adaptations all the other studios are doing, despite the fact that to be an animator in Japan pays just slightly better than working at a fast-food restaurant, they did it because they love it and because they wanted to make an impression in a field well into creative stagnation. It's that vein of seat-of-the-pants artistic creation coupled with unabashed love for fandom that defines old Gainax at its best, and I'm glad that they decided to carry the legacy on into the modern day.
In the end, Kill la Kill is this: love, sex, violence, animation, bondage, porn, the pursuit of freedom against seemingly impossible odds. It's been a wild ride and I'm glad that Trigger was allowed the opportunity to give the world a glimpse into their mad, mad head for twenty-four episodes. Until next time, don't lose your way, in your mind, we have to be as one…
- I promised a friend that I wouldn't neglect Gamagoori, so here's a picture of him destroying a giant condom with the power of his face.
- For another look at the last episode that goes into stuff I didn't even touch, go read ABCBTom's post over at the Hungry Bug Diner. tl;dr cut the bonds of matrimony with your scissors, polyamorous relationships are the way to go! (though it is interesting that Ryuuko absorbs, rather than cuts, Shinra Koketsu.)
- Additionally, Katriel (Kit) hit on a similar topic as I did but published it earlier and said it way more concisely than I could have managed. Check it out!
- Writing about this show's probably the most consistent blogging I've done recently, so. Thanks for reading! I hope you had as much fun watching this show as I did, and if you're one of those people who despises it than I hope these posts were at least somewhat entertaining. Either way I hope this show allows Trigger to make bigger and more successful projects in the future because they definitely deserve it.


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If you recognize that Obama failed to vigorously and immediately support the pro-freedom demonstrators in Iran, take a look at his attitude toward those suffering under the Castro dictatorship.
An extraordinary editorial ran in the liberal Washington Post on Thursday, June 25, about the indifference of the Obama White House to the plight of those who believe in freedom just 90 miles from our shores. The editorial, "A Dissident Deflected," told the story of how the Obama Administration wouldn't issue a statement recognizing the plight of five human rights activists in Cuba until the Post itself inquired about the matter.
The five leaders of Cuba's pro-democracy movement were recipients of the National Endowment for Democracy's 2009 Democracy Award. It was expected that they would not be allowed by the Castro regime to travel from Cuba to the U.S. to accept their award. But it wasn't expected, at least by the Post, that the Obama White House would seem unconcerned about their struggle for freedom.
The Post explained, "None were able to travel to Washington. They have been represented here by Bertha Antúnez, sister of Jorge Luis García Pérez. And Ms. Antúnez, an Afro-Cuban who was active in the Rosa Parks movement before she was forced into exile a year ago, has been snubbed by President Obama. Requests that he meet with her went unanswered. Only as the ceremony began did the White House issue a brief statement."
The paper said that "Mr. Obama's hastily drafted statement-issued after The Post inquired about his silence-said he wished 'to acknowledge and commend' the five dissidents 'and all the brave men and women who are standing up for the right of the Cuban people to freely determine their country's future.'"
The belated "Statement of President Obama on NED 2009 Democracy Award Recipients" consisted of one paragraph:
"I would like to take this opportunity to acknowledge and commend the National Endowment for Democracy's 2009 Democracy Award recipients Jorge Luis Garcia Perez, Jose Daniel Ferrer Garcia, Librado Linares, Ivan Hernandez Carrillo, and Iris Tamara Perez Aguilera and all the brave men and women who are standing up for the right of the Cuban people to freely determine their country's future. Like too many of their fellow citizens, four of these individuals have been unjustly jailed for defending the basic freedoms we all hold dear in the Americas. It is my sincere hope that all political prisoners who remain jailed, including three of today's award recipients, will be unconditionally released and allowed to fully participate in a democratic future in Cuba."
As important as the Post editorial was, Jack Otero of the Committee for Free Trade Unionism wrote a letter to the paper noting that the Post failed to highlight a leader of the Cuban independent labor movement by the name of Iván Hernández Carrillo, who is serving a 25-year prison term since his arrest in 2003. Otero said that Hernández Carrillo is imprisoned for the "crime" of organizing unions not beholden to the communist-controlled Cuban Labor Confederation. "The Post should have acknowledged that labor activists in Cuba also risk their lives for freedom," he said.
This takes on more interest because we recently discovered that a top official of the AFL-CIO, Karen Nussbaum, who spoke at a major "progressive" conference in Washington, D.C., is stonewalling questions about how she traveled to Cuba as a young radical and came away gushing about the Castro dictatorship. She went to Cuba on the Venceremos Brigades organized by Obama's political associate Bernardine Dohrn, then a member of the communist terrorist Weather Underground.
But the Post editorial raised questions about Obama's indifference toward Cuban freedom fighters in the context of his treatment of other Latin American Marxists.
The paper commented, "It's not that the president is too busy to concern himself with Latin American politics. The White House arranged for a Spanish journalist to ask a question at Tuesday's news conference; reporter Macarena Vidal pressed Mr. Obama on whether U.S. allies such as Chile and Colombia were doing enough to help with 'less democratic countries.' The president replied by heaping praise on visiting Chilean President Michele Bachelet, a socialist who has been promoting Cuba's readmission into the Organization of American States and who has gone out of her way to avoid offending Venezuelan strongman Hugo Chávez. 'Chile is leading by example,' Mr. Obama said, adding that its good relationship with Washington despite political differences 'points the way for other countries…where the democratic tradition is not as deeply embedded as we'd like it to be.'"
The Post said that the message from Obama to Chávez and the Castro brothers was that "We can work with you" while the message to Cuba's democratic opposition was "We don't have time for you."
This is an extraordinary indictment of Obama from the viewpoint of a liberal newspaper that now recognizes the far-left nature of the President's policies toward Latin America.
The paper then wondered if the brief Obama statement about the Cuban dissidents would be enough to satisfy the democratic forces opposed to the Communist dictatorship. "We suspect not," said the paper. "They, like the beleaguered pro-democracy movements of Venezuela and Nicaragua, are hoping that the American president will focus his policy on supporting them. Yet for now, Mr. Obama's diplomacy is clearly centered on their oppressors."
The sub-headline for the Post editorial was, "Why doesn't President Obama have time for Cuba's pro-democracy opposition?" Considering his failure to immediately and actively express support for the brave freedom fighters in Iran, the answer should be obvious by now. He doesn't believe in the freedom agenda.
Some of us knew this was coming and predicted it. Unlike most of the media, we had examined the influences behind Obama, such as Communist Frank Marshall Davis, his mentor and father-figure, and understood before the election that this was a candidate who viewed America and the American way of life as the main problems in the world. Obama is truly a revolutionary Marxist who sympathizes not with those being oppressed by anti-American governments but with the governments themselves.
Another example of this attitude can be seen in the U.N. conference that has been underway in New York, where the Obama Administration is facilitating the work of anti-American crackpot Miguel D'Escoto, the U.N. General Assembly President whose most notable distinctions include being suspended from his priestly duties because of his communist political activities and receiving the Lenin Peace Prize from the old Soviet Union.
By any objective measure, nothing good for America can come out of this conference. The main objective of D'Escoto and his ilk, including Hugo Chavez and the Castro brothers, is world government financed by global taxes. They have made it clear that the American people will have to pay the price because we have desecrated "Mother Earth," as D'Escoto called it.
The Washington Post editorial on Cuba only scratched the surface of the dangers we face from this White House. Ultimately, the question that has to be seriously addressed by the Post and other media is: What should we do about the fact that the President of the United States is allied with those forces that want to bury us?


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text: SB DX @ ARL $ARLD039 ARLD039 DX news ZCZC AE39 QST de W1AW DX Bulletin 39 ARLD039 From ARRL Headquarters Newington CT September 20, 2012 To all radio amateurs SB DX ARL ARLD039 ARLD039 DX news This week's bulletin was made possible with information provided by NC1L, The Weekly DX, the OPDX Bulletin, 425 DX News, The Daily DX, DXNL, Contest Corral from QST and the ARRL Contest Calendar and WA7BNM web sites. Thanks to all. CONWAY REEF, 3D2. A large group of operators will be QRV as 3D2C from September 24 to October 5. Activity will be on 160 to 2 meters, including 60 meters, using CW, SSB, RTTY, SSTV and PSK31. QSL via YT1AD. MONTENEGRO, 4O. Chab, YT7WA is QRV as 4O/YT7WA from the Village of Buljarice until September 23. Activity is on the HF bands using BPSK and QPSK. QSL to home call. ZANZIBAR, 5H. Harald, DL7VSN will be QRV as 5H1HS from September 23 to October 13. This includes being QRV as 5H1HS/3 during a short trip to Lazy Lagoon Island, no IOTA. QSL to home call. SENEGAL, 6V. Enrico, IK2FIL will be QRV as 6V7X from Le Calao from September 24 to October 4. Activity will be on the HF bands. This includes an entry in the upcoming CQ WW RTTY contest as a Single Op/Low Power entry. QSL via operator's instructions. WEST MALAYSIA, 9M2. Piju, 9M2PJU will be QRV as 9M2PJU/p from the Pertak dam in Kuala Kubu Bharu from September 22 to 24. Activity will be on 20 and 15 meters using CW. QSL direct to home call. FEDERAL REPUBLIC OF GERMANY, DA. A group of operators will be QRV as DM50ITA from Fehmarn Island, IOTA EU-128, from September 21 to 23. Activity will be on the HF and VHF bands using CW and SSB. QSL via bureau. SPAIN, EA. A group of operators are QRV as EG5INT from Columbretes Island, IOTA EU-069, until September 24. Activity is on all HF bands. QSL direct to EA5KA. AMERICAN SAMOA, KH8. Ron, N6XT and John, N7CQQ are QRV as KH8/home calls from Tutuila Island, IOTA OC-045, until October 1. Activity is on the HF bands. QSL direct to home calls. US VIRGIN ISLANDS, KP2. Jeff, K5WE is QRV as KP2/K5WE from St. Croix until September 26. Activity is on all HF bands using mainly CW and possibly some RTTY. QSL to home call. LEBANON, OD. John, OD5RW is again QRV on 80 to 10 meters, including 2 meters and 70 cm, using CW, SSB, RTTY, SSTV and a variety of other digital modes, including D-Star. QSL via K8NA. BELGIUM, ON. Special event station ON68POL is QRV until September 30 in remembrance of the liberation by the "Polar Bars" of the bridgehead of Rijkevorsel. QSL via bureau. CURACAO, PJ2. Jeoff, PD4JOF is QRV as PJ2/PD4JOF until September 29. QSL to home call. TURKEY, TA. Gab, HA3JB will be QRV as TA/HA3JB from September 22 to October 2. Activity will be on 80 to 10 meters using CW, SSB and various digital modes. This includes being an entry in the upcoming CQ WW RTTY contest. QSL to home call. ASIATIC RUSSIA, UA0. Valery, RA0SS/0 is QRV from Kunashir Island, IOTA AS-025, until the beginning of October. Activity is on 30 and 20 meters. QSL to home call. VANUATU, YJ. Rod, YJ8RN is QRV as YJ8RN/p from Loh Island, IOTA OC-110. Activity is mainly on 20 meters using SSB. His length of stay is unknown. QSL to home call. SOUTH SUDAN, Z8. Jim, K7QI and Diya, YI1DZ now hold calls Z81A and Z81D, respectively. Activity may be on 160 to 10 meters as conditions allow. QSL Z81A via K7GSE and Z81D via OM3JW. THIS WEEKEND ON THE RADIO. The NCCC Sprint CW Ladder, AGB NEMIGA Contest, DIG-PA Contest, FOC CW QSO Party, AGCW VHF/UHF CW Contest, BARTG Sprint 75 and the 222 MHz Fall Sprint are all on tap for this weekend. The SKCC CW Sprint and CWops Mini-CWT CW Test are scheduled for September 26. Please see September QST, page 79 and the ARRL and WA7BNM Contest websites for details. NNNN /EX


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The intensity of the sun is magnified by a concrete 'stone' patio, vinyl siding, and reflected heat from my windows. All windows reflect heat but because mine have been treated with a film to reduce the amount of heat entering the house, the amount of light, which plants receive as heat, is greater. On a 90 degree day like today, the plants in front of the window receive light at temps of 100 degrees or more. It's like being fried by a laser beam. Despite daily watering, the signs of heat stress are unmistakable: reduced growth, burned leaves, wilting.
I thought I had solved this problem last fall when I transplanted a squished 'Maraschino' salvia out of the garden and into a big pot on the patio. I thought the salvia would be tough enough to handle the Window of Death and I could watch hummingbirds feed on its nectar. As long as the temperature didn't rise much above 83, the salvia was happy. But it's June in Virginia and the temps this weekend are supposed to be over 100. Tired of being broiled every afternoon, the plants struck back and left their warning by the coffee pot.
1. Fantasy: Move the salvia to a more sheltered spot, buy another giant pot, a jumbo bag of potting soil, and a huge clump of ornamental grass. Reality: In addition to being expensive, positioning a stand of razor sharp grass so close to the door seemed hazardous, considering the sudden lock picking abilities of the salvia.
2. Fantasy: Buy a silk plant that looks like a giant clump of ornamental grass. Reality: In addition to looking hideous, it would probably spontaneously combust. Burning the house down is NOT a solution.
Gulping my espresso, I considered the extreme. It seemed crazy, but that is often my specialty. If I didn't act soon, my container garden, safety, and sanity would be at risk. I looked around nervously, tightened my belt, and crushed my paper cup into an angry ball. "I'm at a coffee shop in my bathrobe, for cryin' out loud!", I growled. Sanity was no longer an issue.
Armed with a hammer, an awl, and cup hooks, I pounded, screwed, and hung my weirdness out for all to see. Standing on the patio, surveying my work, I looked around and yelled, "I love my red salvia, globe thistle, and dahlias more than I love convention, tradition, or anything resembling normalcy." Birds chirped, bees buzzed, and fortunately, my neighbors weren't home.


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The Electric Association will once again be presenting the annual ChicaGO Safety & Sustainability Conference on Thursday, January 21st, 2016 at the Donald E. Stephens Convention Center in Rosemont, IL.
This year's conference features a great line-up of educational programs that will be of interest to all segments of the electrical and construction industries. Inspectors, planners, architects, contractors, engineers, and members of the construction community will get a sneak peek at the major changes coming to the 2017 National Electrical Code. Attendees will have many different tracks of seminars to choose from throughout the day, spanning an array of topics including: OSHA regulations and managing your company's safety plan, how to sell an energy efficient project, implementing renewable energies into your construction projects, the future of lighting technology, the Government's sustainability plans, and much more.
550+ Attendees are expected to attend in 2016!
- Building owners
- Facility Managers
- Electrical contractors, electricians, installers, project managers
- Architects, engineers, specifiers, designers
- Electrical and building inspectors
- Safety Managers and Professionals
- HVAC and Mechanical contractors
- Public sector planners: municipalities, schools, hospitals
- Energy professionals, consultants, utilities
- Industrial maintenance supervisors & personnel
Conference Details
- Date:
- Thursday, January 21, 2016
- Time:
- Workshops – 8am to 4pm
- Tradeshow – 11am to 6pm
- Networking Reception – 4pm to 6pm
- Location:
- Donald E. Stephens Convention Center
- 5555 North River Road, Rosemont, IL 60018
Join Steiner Electric, the Electric Association, and partnering organizations at Chicagoland's largest electrical construction conference of the year!


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15 Easy DIY Christmas Crafts and ProjectsThis post may contain affiliate links which won't change your price but will share some commission.
Need some homemade inspiration for the busiest season of the year? Here are 15 easy DIY Christmas crafts and projects for both the novice and expert.
When I started my series 31 Days to a Beautiful Home on October 1st I had no idea if I would finish on time, or even reach the finish line. Yet here I am!
If you've been following along I'm so grateful for you! These last 31 days have been a labor of love.
I've learned that I can reach beyond myself to achieve dreams that are just beyond my grasp.
I've also learned that sleep is highly overrated!
I can think of no better way to close out my series than with a roundup of my own favorite easy DIY Christmas crafts and ideas.
I've included projects for decorating, crafting and memory keeping, everything you need for the start of a beautiful holiday season.
This Simmering Homemade Potpourri is a perfect way to keep the house scented with the smells of the season.
Our Fence Board Christmas Tree was one of my DIY hubby's first fence board projects and is still a favorite.
Last year's fence board project was this Joy Christmas Sign.
I recently added this post and video on Mason Jar Labels, Tags and Printables which are perfect for the non crafter.
This No Mess Handmade Glitter Ornament post includes a surprise ingredient
I love this thrifty Christmas Rag Wreath and Ornament made out of fabric scraps and giveaway clothing.
You can see my home all decorated for Christmas last year with my 2013 Home Tour.
Decorating the table is one of my favorite projects and you'll see more fence board here with this Rustic Christmas Tablescape.
One of our favorite Christmas traditions is my Christmas Village and I've included a step by step tutorial to get you started.
Here's even more fence board goodness with this Rustic Christmas Centerpiece.
Are you without a mantel like me? No Mantel? No Problem! Find out all about my faux mantel!
Almost all of my home is filled with Thrifty Christmas Decor Ideas that I hope will inspire you to shop your own home.
I'm a scrapbooker at heart and love the memories included in this Christmas Ornaments Mini Scrapbook Album.
Like to give a homemade card but don't have any extra time? These 5 Minute Christmas Cards will help you think of new possibilities.
Finally, here are even more ideas for Christmas Cards with the Cricut diecutting machine for inspiration
Have you joined me for my 31 days series yet? You can find all my tips for creating a beautiful home here.
My hope is that my 31 Days to a Beautiful Home series will motivate and inspire you to spend just a bit of time creating a home you will love and embracing the life you have been given! Just click here to view all the posts.


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Amber & Austin's Wedding
A huge thank you to Eric and Jenn Photography for these amazing photos! Brownstone Reserve was the perfect setting for this blush and burgundy wedding that featured not only a beautiful bride and handsome groom but one pretty pug and tons of whimsical flowing flowers!
Want more pictures?
Check out our Instagram, and galleries on Facebook!


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About a third of the adult population is plagued by symptoms of insomnia, while 10 percent suffer from the actual disorder, but those figures can taper drastically with a simple fix, according to research published in the international journal SLEEP.
In the study, researchers from Northumbria University in England separated 40 adults with acute insomnia into two groups (each with nine males, 11 females). Both groups were asked to keep sleep diaries to record the duration and quality of sleep and complete the Insomnia Severity Index to measure the nature, severity, and impact of their insomnia seven days before one group received treatment.
10 Best Ways to Get Better Sleep >>>
The control group received no additional support, while the other received a one-hour one-on-one cognitive behavioral therapy session and a self-help pamphlet to read at home. In the therapy session, participants were introduced to the principle of sleep restriction; they were encouraged to spend only the time in bed required for sleep. They were coached to lie in bed for 15 minutes and if they couldn't fall asleep in that time frame, they were told to leave the bedroom. The idea is to associate the bedroom with sleep, not the stress and frustration that goes along with sleeplessness. Then, using their recorded sleep diaries, the lead researcher prescribed a time for each individual to go to bed and a time to rise to improve their sleep efficiency. The self-help pamphlet included information on how to recognize and act upon the symptoms of insomnia (called the "3D" approach): Detect (how to record their sleep diary), detach (how to control stimulus that could lead to disrupted sleep), and distract (instructions on how to use cognitive control and imagery to distract their mind.)
Within one month after treatment, 60 percent of participants reported improvements in their sleep quality. After three months, figures rose to 73 percent. As you might expect, 70 percent of those in the control group requested to be given the same treatment.
If you're suffering from acute phase insomnia, this could be the difference between a good night's sleep (every night) and the more dangerous side effects of insomnia like depression. If you don't want to go to therapy, give the "3D" steps from the pamphlet and sleep restriction a shot:
1. Detect: Learn how to record in a sleep diary so you can recognize patterns. Report the time you intended to wake up, the actual time you woke up, whether you woke up throughout the night or slept restfully, how you felt during the day, if you took any naps, etc. Try using this sleep diary from the Sleep Foundation.
2. Detach: Learn how to control stimulus that could lead to disrupted sleep. For example, use blackout curtains, cover any small light from television sets and wear a sleep mask to limit light disturbances; use ear plugs or listen to ambient noise to limit sound disturbances; and sleep with a fan or air conditioner (or sleep naked) to stay cool throughout the night since a raise in body temperature can disrupt your sleep.
3. Distract: Learn how to use cognitive control and imagery to distract your mind. Individuals with insomnia tend to worry and ruminate over problems, converting them into visuals as they lie in bed. Research shows verbally addressing these concerns before bed reduces its chance of appearing in your mind, disturbing sleep.
5 Reasons You Can't Sleep Properly >>>
For access to exclusive gear videos, celebrity interviews, and more, subscribe on YouTube!


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Agassi ousted by Grosjean
American appears rattled by Bill Clinton's presence at the French Open
PARIS - Former President Clinton showed up at the French Open to root for Andre Agassi, stayed for most of three sets and saw him win three games.
While Clinton had little to cheer about, Frenchman Sebastien Grosjean delighted the partisan Parisians in the capacity crowd with the match of his life yesterday to win 1-6, 6-1, 6-1, 6-3 and reach the semifinals.
The shocker ended Agassi's quest for a second successive Grand Slam championship and a second title at Roland Garros. He won the Australian Open in Januar the French in 1999.
"It's pretty disappointing at the moment," said a terse, sullen Agassi. "I played well. He played a lot better."
In truth, the third-seeded Agassi played poorly, particularly after Clinton arrived at the start of the second set. At times, Grosjean said, it appeared as if Agassi wasn't even trying - perhaps because he was so frustrated.
"It was strange because sometimes he hit the ball really hard, you know, like tanking," Grosjean said. "Maybe he was not really happy that the game wasn't like the first set."
And maybe - bizarre though it sounds - the seven-time Grand Slam champion was unnerved by Clinton's presence.
When the former president left briefly after the third set, Agassi won two of the next three games. Then Clinton returned, and Agassi double-faulted on the next point, double-faulted again on break point and struggled the rest of the way.
Agassi tried to dismiss the notion that Clinton distracted him.
"I didn't know he was there," said Agassi - a curious claim because the former president received a rousing ovation when he arrived and sat in the first row behind the baseline on Agassi's side. Even Grosjean took notice.
"I didn't realize that Bill Clinton was coming," the Frenchman said with a grin. "For me it was very good, because from then on I played very well."
The 10th-seeded Grosjean's opponent in the semifinals will be No. 13 Alex Corretja, who advanced by beating unseeded 19-year-old Roger Federer 7-5, 6-4, 7-5. The other match tomorrow pits top-seeded two-time champion Gustavo Kuerten against No. 4 Juan Carlos Ferrero.
Today, No. 4 Jennifer Capriati will play in her first French Open semifinal since 1990 when she faces top-seeded Martina Hingis. The other match will be a showdown between two Belgian teen-agers - No. 12 Kim Clijsters and No. 14 Justine Henin.
Last year, Agassi snubbed reporters after losing to Karol Kucera in the second round at Roland Garros. This time he showed for the mandatory postmatch news conference but shed little light on his implausible performance.
Before Clinton arrived, Agassi breezed through the first set in 22 minutes.
"He's a friend of mine, I like him," the former president said on his way into the stadium.
Faster than you can say "Hail to the Chief," the momentum turned. Agassi lost the next five points and 10 of the next 12 as the crowd began to chant Grosjean's name.
With a mustache, goatee and cap worn backward, the 23-year-old Marseille native looks like he should be working at a record shop in the Latin Quarter, rather than upsetting one of tennis' golden oldies.
But the 5-foot-9 Grosjean ranks among the quickest players on the tour and seemed to reach every ball. On one key point he dashed from the backhand corner to chase down a drop volle flip a forehand winner as he went skidding off the court, fist raised in jubilation.
"His speed puts a lot of pressure on you," Agassi said, "because you have to hit not just quality shots, but you have to hit a number of them."
While rushing Agassi into errors, Grosjean smacked winners from both sides, repeatedly dusting the lines. Once he hit two lines at once, ripping a backhand winner that skipped off the corner of the court.
He threw junk at Agassi, too.
"I tried to vary the pace because I know he doesn't like that," Grosjean said. "I tried to mix up my shots - long shots, short shots, slice shots."
The strategy eventually had Agassi cursing to himself, and he appeared to give up on the third set when the score reached 4-0. He framed an easy overhead, then double-faulted on set point.
As Grosjean closed in on the win in the fourth set, he kept looking to the sky, but it was Agassi who needed intervention. The Frenchman broke serve for the seventh and final time to lead 5-3, then closed out the upset with a 110-mph ace. The crowd erupted, with Clinton joining the applause.
"It was really great, great emotion," Grosjean said. "You don't want to leave the court."
When you win, that is. Agassi hastily headed for the exit as if chased by the cheers that weren't for him.


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- Primary research
- Open Access
- Published:
Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis
Cancer Cell International volume 11, Article number: 42 (2011)
6651 Accesses
16 Citations
1 Altmetric
Dysregulation of many apoptotic related genes and androgens are critical in the development, progression, and treatment of prostate cancer. The differential sensitivity of tumour cells to TRAIL-induced apoptosis can be mediated by the modulation of surface TRAIL receptor expression related to androgen concentration. Our previous results led to the hypothesis that downregulation of TRAIL-decoy receptor DcR2 expression following androgen deprivation would leave hormone sensitive normal prostate cells vulnerable to the cell death signal generated by TRAIL via its pro-apoptotic receptors. We tested this hypothesis under pathological conditions by exploring the regulation of TRAIL-induced apoptosis related to their death and decoy receptor expression, as also to hormonal concentrations in androgen-sensitive human prostate cancer, LNCaP, cells.
In contrast to androgen-insensitive PC3 cells, decoy (DcR2) and death (DR5) receptor protein expression was correlated with hormone concentrations and TRAIL-induced apoptosis in LNCaP cells. Silencing of androgen-sensitive DcR2 protein expression by siRNA led to a significant increase in TRAIL-mediated apoptosis related to androgen concentration in LNCaP cells.
The data support the hypothesis that hormone modulation of DcR2 expression regulates TRAIL-induced apoptosis in LNCaP cells, giving insight into cell death induction in apoptosis-resistant hormone-sensitive tumour cells from prostate cancer. TRAIL action and DcR2 expression modulation are potentially of clinical value in advanced tumour treatment.
Prostate cancer is the most commonly diagnosed malignancy in the male population and remains the second leading cause of cancer-related deaths in the developed world [1]. Inhibition of apoptosis is a critical pathophysiological factor that contributes to the onset and progression of prostate cancer, but the molecular mechanisms are not entirely understood. Therefore, insight into the mechanism(s) of the misregulation of apoptosis could be the basis for developing more effective therapeutic approaches to destroy apoptosis-resistant tumour cells, as found in prostate cancer [2].
Treatment with apoptosis-inducing ligands belonging to the Tumour Necrosis Factor-alpha (TNF-α) family could be an effective strategy for cancer treatment [3, 4]. The best characterized ligands, Fas ligand, TNF-α, and TNF-α-related apoptosis-inducing ligand (TRAIL, also known as Apo2L) [5, 6], are type II transmembrane proteins that can induce apoptosis in susceptible cells after binding to type I transmembrane receptors containing cytoplasmic "death domains". These interact with the downstream death domain-containing adapter proteins FADD or TRADD (for Fas- or TNFR-associated death domains, respectively), leading to activation of initiator caspases (e.g. caspase 8) and effector caspases (e.g. caspase 3) and apoptotic cell death [7]. Unfortunately, both TNF-α and Fas ligands have severe systemic cytotoxic effects, limiting their use as systemic agents [8]. Unlike TNF-α and FasL, TRAIL has been used effectively in systemic animal trials and has the unique feature of inducing apoptosis in cancer cells, whilst sparing normal cells [9, 10]. TRAIL may therefore be a promising candidate for cancer treatment.
Transcripts of TRAIL [5, 6] have been detected in many human tissues (e.g. spleen, thymus, prostate, and lung). To date, at least 4 type I transmembrane receptors have been identified, including DR4 (TRAIL-R1) [11], DR5 (TRAIL-R2) [12], DcR1 (TRAIL-R3) [13, 14] and DcR2 (TRAIL-R4) [15, 16]. Ligation of TRAIL with DR4 or DR5 induces trimerization of the receptor, which activates the apoptotic pathway. In contrast to DR4 and DR5, DcR1 and DcR2 act as decoy receptors for TRAIL. DcR1 is a glycosylphosphatidylinositol (GPI)-linked protein lacking an intracellular domain, and DcR2 contains a truncated death domain. They can prevent TRAIL-induced apoptosis, presumably by competing with DR4 and DR5 for binding to TRAIL [12, 14].
Because they can bind TRAIL but do not signal for apoptosis, DcR1 and DcR2 appear to serve as "decoys" that inhibit apoptosis by sequestering TRAIL from the death-inducing TRAIL receptors. Moreover, Clancy et al. [17] reported that inhibition of apoptosis depends on the formation of ligand-independent complexes between DR5 and DcR2 in primary human CD8+ T cells.
Finally, osteoprotegerin, a regulator of osteoclastogenesis, appears to be a soluble receptor for TRAIL [18]. The idea of targeting specific death receptors to induce apoptosis in tumours is attractive; thus it is particularly intriguing to explore how a complex family of death and decoy receptors modulates TRAIL function. Although DR4 and DR5 transcripts and TRAIL mRNA are expressed in many tissues, most normal cells are resistant to apoptosis induction by this ligand [9, 10]. Therefore DcR1 and DcR2 receptors may contribute to physiological resistance to TRAIL. In contrast, several tumour cell lines express DR4 and DR5, but little DcR1 and DcR2, suggesting that cancer cells are more sensitive to the TRAIL apoptotic signal. However, some tumour cells can acquire resistance to TRAIL-induced apoptosis by up-regulating decoy receptor expression [19]. Androgens are critically involved in the development, progression, and treatment of prostate cancer [20]. Currently, a major therapy for the treatment of localized and metastatic prostate cancer is androgen ablation, which induces extensive apoptosis of androgen-dependent prostate cancer cells, resulting in tumour regression and improved prognosis [21, 22]. Androgen deprivation by castration induces cell death in hormone-sensitive rat ventral prostate [23], and caspase-3 and -6 expression and activation are targeted by hormone action during this process [24]. The involvement of the death receptor pathway in ventral prostate apoptosis has been well studied [25–27]. We reported earlier that testosterone specifically controls DcR2 mRNA and protein expression in normal adult rat ventral prostate, and concluded that androgen withdrawal by reducing DcR2 expression might leave the cells vulnerable to the cell death signal generated by TRAIL via its functional receptors [28].
Although androgen regulation of human TRAIL receptor expression under pathological conditions has not been reported, we can hypothesize on the basis of our previous results that hormonal variations in DcR2 receptor expression levels are involved as inhibitor/inducer in TRAIL-induced apoptosis in prostate cancer cells. We have investigated the role of the decoy receptor DcR2 in apoptosis induction by TRAIL in human prostate cancer, using the androgen-sensitive cell line, LNCaP.
Initially the dose-dependent effects of androgen on TRAIL system expression showed that the hormone sensitivity of DcR2 and DR5 protein expression correlates with TRAIL-induced apoptosis. After silencing DcR2 protein expression with siRNA, we explored the consequences of the downregulation on TRAIL-induced apoptosis in LNCaP cells.
Sensitivity of LNCaP Cells to Androgen Concentration
The effect of androgen on TRAIL system expression in hormone-sensitive prostate cancer cells was examined using human hormone-sensitive LNCaP cells as a model. These cells gave a bell-shaped growth curve in response to increasing doses (1 pM-10 nM) of R1881 (Figure 1A). R1881 concentrations, in the pM range, induce cell proliferation, with a significant maximum at 0.1 nM (3H incorporation up 4.25-fold, P < 0.002, and cell number increased 1.9-fold compared with controls, P < 0.05), whereas doses in nM range impeded cell growth. DNA content was assessed by flowcytometry (Figure 1B). Under the best conditions of cell proliferation (0.1 nM R1881), there was less DNA fragmentation (P < 0.005) than at other concentrations (Figure 1C); and globally, compared with control cells, the absence of a significant increase in the DNA fragmentation percentage under all conditions indicated the absence of apoptosis. Incubation in 10 nM R1881 produced the highest level of cells in G0-G1 (+28%, P < 0.005) and the lowest level of cells in G2-M (-50%, P < 0.005) in comparison with controls (Figure 1D), confirming this concentration as inhibiting cell growth. In the positive control, etoposide, the increase in the DNA fragmentation percentage (Figure 1C) correlated with a decrease in the percentage of cells distributed in the 2 corresponding G0-G1 and G2-M stages (Figure 1D), compared with the DMSO control. Except in the positive control (etoposide), and in accordance with the absence of apoptosis under all other conditions, cleaved caspase-3 protein levels were unchanged (data not shown).
Androgen Action on TRAIL System Protein Expression in LNCaP Cells
To investigate the effect of androgen on TRAIL, DR4, DR5, DcR1 and DcR2 protein levels, hormone-sensitive LNCaP cells were cultured in increasing concentrations of R1881 (1 pM-10 nM). Ligand and receptors protein levels were measured by Western blot analysis (Figure 2). No significant variations were observed in TRAIL (present as a doublet), DR4 and DcR1 protein levels (Figure 2A), whereas DcR2 and DR5 levels were significantly increase in the nanomolar range compared to the control (1.6-fold, P = 0.002, and 5.6-fold, P = 0.003, respectively, at 1 nM; Figure 2B). All the samples were run and detected together, but some films were cut and pasted to remove spots from replicate cell protein extracts. A correlation was found between androgen concentration and DcR2 and DR5 protein expression that corroborated our previous results obtained in normal prostate (modulation of DcR2 expression [28]) and testis (modulation of DR4, DR5 and DcR2 expression [29]), another hormone-sensitive tissue.
There are no reports of androgen responsive elements in TRAIL receptor promoters. However, the following experiments show that DcR2 and DR5 expression can be regulated via the androgen receptor. LNCaP cells incubated simultaneously with R1881 and the specific androgen receptor antagonist, bicalutamide (25 μM), significantly abrogated the increase in DcR2 and DR5 protein expression due to 10 nM R1881 alone (Figure 3A and 3B). Similarly, the DcR2 and DR5 expression after R1881 incubation was not significantly modified in prostate cancer cells devoid of androgen receptors, such as PC3 cells (Figure 3C and 3D).
Androgen Regulates Apoptosis Induction by TRAIL in LNCaP cells
To investigate TRAIL-mediated cell death related to androgen concentration, LNCaP cells were cultured for 4 days in 0.1 nM or 10 nM R1881 before being treated with increasing TRAIL ligand concentrations from 10 ng to 1 μg for 24 and 48 h. Cell death was monitored by DAPI staining (Figure 4A). Androgen at 0.1 and 10 nM were chosen because they represented the best and the poorest cell growth conditions, respectively (Figure 1), and because of the variations in DcR2 and DR5 protein levels (Figure 2). In comparison with androgen-free conditions (Figure 4B), the percentage of fragmented nuclei in the presence of 0.1 nM R1881 increased significantly between 10 and 200 ng TRAIL per milliter (+28% and + 38% for TRAIL 100 ng and 200 ng, respectively; P < 0.005) to reach a plateau at 300-1000 ng/ml. TRAIL-induced apoptosis was not assessed at 10 nM R1881. Results obtained after 48 h treatment were slightly higher than after 24 h (data not shown). Consequently, the best TRAIL-induced apoptosis conditions for LNCaP cells were 100 ng of TRAIL over 24 h.
DcR2 Protein Expression is Correlated with TRAIL-Sensitivity in Prostate Cancer LNCaP Cells
We have reported a correlation between androgen status, apoptosis and DcR2 expression in rat prostate [28], and postulated that DcR2 decoy receptor expression may be directly related to TRAIL-induced apoptosis resistance in prostate cancer cells. If so, the downregulation of DcR2 protein expression could reverse resistance to TRAIL-induced cell death. Since DcR2 and DR5 protein expression in LNCaP cells is androgen sensitive (Figure 2), we tested the previous hypothesis by suppressing DcR2 gene expression using siRNA (Figure 5). Similarly, the role of DR5 was investigated to check its function and the efficiency of the silencing method. DcR2 (Figure 5A) and DR5 (Figure 5B) proteins were knocked down after transfection with the corresponding siRNAs, which were followed by 48 h incubation in 0.1 nM R1881 (-98% and -92%, respectively, in comparison with controls (untreated and si0 treated cells), P< 0.005). Protein silencing was less efficient after 96 h incubation than at 48 h because of the decrease in siRNA strands and exhaustion of the medium. No significant variations were observed in fragmented nuclei per thousand DAPI-stained cells treated with siDcR2 or siDR5 alone, or with the different transfection reagents (scrambled siRNAs/si0 and specific siRNAs, lipofectamine) (Figure 5C), indicating that there were not toxic materials present.
The 48 h silencing of the DcR2 Protein as described in Figure 5, followed by treatment with TRAIL as described in Figure 4, led to a significant increase in fragmented nuclei (2.13-fold, P < 0.002) in transfected LNCaP cells in comparison with untransfected control cells or scrambled siRNA transfected cells (Figure 6A). This was confirmed by a significant increase in caspase 3 activity in DcR2 siRNA transfected cells and treated with TRAIL (+26%, P < 0.005) in comparison with scrambled siRNA transfected or untransfected control cells with TRAIL, (Figure 6B). Silencing of the DR5 protein resulted as anticipated in a significant reduction in TRAIL-induced apoptosis in comparison with untransfected control cells and scrambled siRNA transfected cells (-54%, P < 0.002), and no significant variation in caspase 3 activity (Figure 6A and 6B, respectively).
LNCaP cells cultured in 10 nM R1881 showed no apoptosis without (Figure 1C) or with TRAIL peptide (Figure 4B), and an increase in DcR2 protein levels (Figure 2B). Silencing of DcR2 protein at 10 nM R1881 resulted in partial recovery of TRAIL-induced apoptosis in comparison with untransfected control cells and with scrambled siRNA transfected cells (3.1-fold and 3.8-fold, respectively, P < 0.005; Figure 7A), accompanied by a significant increase in caspase 3 activity in comparison with si0 transfected cells (+59%, P < 0.05; Figure 7B). This suggests that DcR2 upregulation rendered LNCaP cells more resistant to TRAIL-mediated apoptosis, whereas downregulation of DcR2 protein enhanced TRAIL-induced apoptosis.
In the pathological prostate, the physiological regulation of apoptosis by TRAIL in relation to death and decoy receptor expression and hormonal concentration is unknown. Our previous results [28] showed that androgen deprivation associated with an apoptotic process led to a decrease in DcR2 expression in normal adult rat hormone sensitive ventral prostate. The downregulation of DcR2 expression following androgen deprivation was thought to leave androgen sensitive cells vulnerable to the cell death signal induced by TRAIL via its pro-apoptotic receptors.
In the presence of R1881 at 1 pM-10 nM, the growth curve LNCaP cells was characteristically bell-shaped, with a peak at 0.1 nM [30, 31]. TRAIL, DR4 and DcR1 protein expressions were unaffected under these conditions, whereas DR5 and DcR2 protein expression increased over a nanomolar range. No androgen responsive elements have been reported in TRAIL-receptor promoters, but several experimental results suggest the genomic regulation of DR5 and DcR2 expression by androgens occurs in the same way as their inhibition by the anti-androgen, bicalutamid, and receptor expression remains unmodified in PC3 cells incubated with androgen. However, its regulation by an (as yet unidentified) androgen-dependent transcription factor is possible, and the increased DcR2 protein level in LNCaP cells may be due to its regulation by an (also as yet unidentified) androgen-dependent translational factor.
TRAIL-induced apoptosis of LNCaP cells is maximal at 0.1 nM R1881. Increases in DR5 and DcR2 receptor expression at R1881 concentrations of up to 0.1 nM may be related to the absence of TRAIL induced apoptosis in situations of poor cell proliferation. Silencing of hormone sensitive receptors with siRNA shows that, at 0.1 nM R1881, and when DcR2 protein expression is silenced by the corresponding siRNA, TRAIL-induced apoptosis is increased by a factor of 2 in comparison with the controls. In contrast and as expected, apoptosis could be reduced to half when DR5 is silenced, which may be due to pro-apoptotic receptor DR4 expression not being downregulated. DcR2 is therefore a regulator of TRAIL induced apoptosis in the best hormonal concentration for cell growth. Moreover, preliminary results show that the silencing of the DcR2 receptor results in a partial restoration of TRAIL induced apoptosis in otherwise resistant LNCaP cells cultured in 10 nM R1881. A partial restoration of TRAIL mediated apoptosis in 10 nM androgen may be due to poor cell growth involving an intracellular signalling and trafficking that is much slower than in the favourable growth conditions (0.1 nM) in vitro.
Rokhlin et al. [32] showed that the expression level of the DR4 and DR5 receptors in LNCaP incubated with fetal calf serum or 100 nM dihydrotestosterone was clearly superior to the control conditions without androgen, whereas the decoy receptor expression level was not given. Although these authors [33], like others [34], found resistance of LNCaP cells to TRAIL-induced apoptosis, interestingly they also showed that FADD and caspase 8 recruitment for TRAIL-DISC formation and cell death induced by the TRAIL ligand were androgen-related in LNCaP cells [32, 35]. These results along with ours support the hypothesis that LNCaP sensitivity to the TRAIL ligand is androgen-regulated, and related to the expression of its receptors (decoy and pro-apoptotic) and DISC formation [32, 35]. In contrast, no significant variations for DR4 expression were observed under our conditions with R1881 present under 10 nM, which may be due to differences in experimental conditions (androgen concentration, pH, media composition, temperature, timing of treatment, presence of PI3K/Akt pathway inhibitor, etc.). The relative contribution of each death receptor to apoptosis induction in cells expressing both receptors remains unknown [4]. In vitro, comparison of TRAIL-death receptors cell surface expression and TRAIL sensitivity of cancer cell lines did not show any consistent pattern, suggesting that TRAIL sensitivity may be dependent on a permissive environment for preferential signalling via TRAIL-DR4 or DR5 receptors expression controlled by other intracellular mechanisms in resistant cells [36, 37]. Our data indicates that androgens play a role in apoptosis sensitivity in LNCaP cells, and their resistance to TRAIL-induced apoptosis is more closely linked to the upregulation of the decoy receptor DcR2 expression than to downregulation of pro-apoptotic receptors.
Considering the context of the pathological and hormone-sensitive prostate, these results, like others [38], show that the resistance of such tissues to apoptosis is probably more closely linked to increased expression of apoptosis inhibitors than decreased expression of pro-apoptotic proteins. This hypothesis is strengthened by other data showing that the silencing of Bcl2, FLIP or IAPs (XIAP and survivine) by siRNAs sensitizes resistant melanoma cells to TRAIL-induced apoptosis [39]. In the same way, Sung et al. [40] reported that celastrol, a triterpene, enhanced TRAIL-induced apoptosis through the downregulation of cell survival proteins and upregulation of death receptors. Hesry et al. [41] showed that sensitivity to the TRAIL ligand is related to tumour progression (in LNCaP, DU 145, PC3 cells) and that TRAIL-induced cell death is only linked to the DR5 receptor, moreover they found DcR1 receptor expression to be undetectable, whereas DcR2 was significantly more abundant in tumour cells than non-neoplastic cells, and may thus contribute to the partial resistance to TRAIL found in some prostate tumour cells (e.g. LNCaP and DU 145). Interestingly, another study [42] reported that the combined treatment of prostate cancer cells (LNCaP and PC3) with TRAIL and chemotherapeutic agents overcame their resistance by triggering caspase activation; in the same way Sanlioglu et al. [43] indicated that DcR2 siRNA and adenovirus delivery of TRAIL dramatically affected the tumorigenic potential of prostate cancer LNCaP and DU 145 cells.
If androgen withdrawal in prostate cancer treatment decreases anti-apoptotic gene expression as DcR2 in androgen-dependent cells, this could induce apoptosis, resulting in prostate tumour reduction. Over the middle term and following androgen withdrawal [44], it is conceivable that androgen-independent cancer cells might arise as a subpopulation that has acquired the capacity to upregulate the expression of decoy receptors and perhaps other anti-apoptotic proteins, such as XIAP [45]; in this way they might escape anti-tumour surveillance by immune cells. Under these conditions, upregulation of anti-apoptotic proteins would be independent of androgen deprivation. Furthermore, the identification of drugs or experimental methods (downregulation by siRNAs) that decrease TRAIL decoy receptor expression for a long time after androgen ablation may prove to be useful therapeutically on their own, or in combination with other approaches (molecular/protein targets, cytotoxic agents, etc.) to induce apoptosis as treatment for prostate cancer and/or for otherwise resistant cancer cells.
The differential sensitivity of tumour cells to TRAIL-induced apoptosis may be mediated by the modulation of surface TRAIL receptor expression that could be related to the androgen concentration in prostate. Decoy (DcR2) and death (DR5) receptor protein expression is correlated with hormone concentrations and TRAIL-induced apoptosis in LNCaP cells. Silencing of androgen-sensitive DcR2 protein expression by siRNA leads to a significant increase in TRAIL-mediated apoptosis related to androgen concentration in LNCaP cells. The data support the view that hormone modulation of DcR2 expression is involved in regulating TRAIL-induced apoptosis in the androgen-sensitive prostate carcinoma cell line, LNCaP, and provides preliminary insight into cell death induction in apoptosis resistant hormone-sensitive prostate cancer cells. TRAIL action and DcR2 expression modulation are potential of clinical value for advanced tumour treatment when androgen-deprivation therapy fails, leading to recurrent tumour growth in a hormone-refractory manner.
Furthermore, the identification of drugs or experimental methods that enhance TRAIL-induced apoptosis through the downregulation of TRAIL decoy receptor or cell survival proteins expression may prove themselves to be therapeutically useful, or in combination with other therapeutic approaches to induce apoptosis as treatment for prostate cancer or for otherwise resistant cancer cells.
Materials and methods
Cell Culture
Human prostatic carcinoma cell lines, LNCaP and PC3, were obtained from the American Type Culture Collection (ATCC, Bethesda, MD). Cells were maintained in RPMI 1640 medium (Invitrogen, Cergy-Pontoise, France), supplemented with 7.5% fetal calf serum (FCS; Invitrogen), 2 mM L-Glutamine (Sigma, Isle d'Abeau, France), 20 μg/ml streptomycin, 20 U/ml penicillin (Invitrogen), and 50 U/ml Nystatin (Sigma). LNCaP and PC3 cells were used between passages 50-60 and 18-24, respectively. 17β-hydroxy-17-methyl-estra-4,9,11-trien-3-olone (R1881/testosterone analogue) was purchased from New England Nuclear (Boston, MA) and dissolved in ethanol. Bicalutamide (Casodex, [(2RS)-4'-cyano-3-(4-fluorophenylsulphonyl)-2-hydroxy-2-methyl-3'-trifluoromethyl propioanilide] was a gift from AstraZeneca (Alderly House, Cheshire, England); it was dissolved in 0.2% methanol.
Cell numeration, proliferation assay and treatment
LNCaP cells (5 × 104) were plated in triplicate per well in 24-well plates (Corning Incorporated, Corning, NY) in steroid-depleted media containing 2.5% charcoal-stripped FCS (HyClone, Logan, UT) for numeration. Cells of each well were counted in duplicate with a Coulter Z1 counter (Beckman Coulter, CA). For [3H]-thymidine incorporation, cells were plated in 12-well plates at 12 × 104 cells/well and incubated with 0.5 μCi/ml [3H]-thymidine (Du Pont-New England Nuclear, Les Ulis, France) in medium for 4 h before harvesting. Cells were washed twice with ice-cold PBS and DNA precipitated with 5% trichloracetic acid. The DNA precipitate was dissolved in 0.4 ml of 0.25 M NaOH and incorporated [3H]-thymidine was determined by liquid scintillation counting. Sampling at each time-point was in triplicate. For Western-blotting analysis, LNCaP cells were seeded in 10 cm disks (22 × 105 cells), with 3 disks per condition. Cells were allowed to attach for 24 h and treated with various concentrations of R1881 on day 0. All the cells, including the control cells, were cultured in the presence of the same ethanol concentration (0.001% being the highest concentration used).
Flowcytometric Analysis
Flowcytometry was used to assess the sub-G1 DNA population of cells undergoing apoptosis. LNCaP cells were seeded at 8 × 105 cells in 6-cm dishes. After 4 days of culture with or without R1881, cells were collected by trypsinization and fixed in 1% paraformaldehyde for 30 min at 4°C, then in 70% ethanol/30% PBS (phosphate buffer saline) for 2 h at -20°C. Fixed cells were washed with PBS, treated with 30 μg/ml Rnase A in PBS for 60 minutes at 37°C, and propidium iodide in PBS (10 μg/ml) was added. For positive controls, LNCaP were incubated with etoposide (Sigma) diluted with 0.03% DMSO (dimethyl sulfoxide; Sigma). Cell cycle profiles and distributions were determined using a BD Facscan flowcytometer (Becton Dickinson Biosciences, San Jose, CA). Cell cycle distribution was analyzed using Modfit LT software (Verity Software House, Topsham, ME).
Western-blot analysis
Cell protein extracts were prepared by direct addition of 5 volumes of cold lysis buffer, as previously described [40]. Protein concentration was determined using the Bicinchoninic acid assay reagent (Sigma, Isle d'Abeau, France), with bovine serum albumin as standard. Protein samples (15 μg/well) were resolved by 12% SDS-polyacrylamide gel electrophoresis and electroblotted as described earlier [46]. Nitrocellulose blots were treated and incubated with the following primary antibodies (Santa Cruz Biotechnology, Santa Cruz CA): rabbit polyclonal antibodies raised against human TRAIL or DR4 (1:1,000), goat polyclonal antibodies raised against human DcR1 or DcR2 (1:1,000) and secondary antibodies, horseradish peroxidase (HRP) conjugated goat anti-rabbit IgG (1:2000) or donkey anti-goat IgG (1:5,000) as previously reported [28]. The primary antibody anti-human DR5, obtained from AnaSpec, Incorporated (San Jose, CA), was used at a dilution of 1:1000. Protein loading was checked by reprobing the blot with a rabbit IgG anti-β-actin antibody (1/500) (Sigma). Bound antibodies were detected using the chemiluminescence Western blotting detection kit (Covalab). The Biomax MR films (Eastman Kodak Company, Rochester, NY) were scanned on a Gel doc 2000 apparatus (Biorad, Marnes-la-Coquette, France), and quantified with Quantity one Software Biorad.
Apoptosis assessment with 4', 6'-diamidino-2 phenylindole staining (DAPI)
LNCaP cells undergoing apoptosis were followed by chromatin condensation, nuclear shrinkage, and formation of apoptotic bodies, as visualized after DAPI staining [47]. Following various specific treatments, the medium was removed and cells fixed in ethanol/acetic acid (3:1, vol/vol) at room temperature for 10 min. Cells were washed with 0.9% NaCl and stained with 0.4 μg/ml DAPI in 0.9% NaCl at room temperature for 30 min and viewed by fluorescence microscopy.
si RNA
siRNAs (sense and antisense strands) were purchased from Ambion, Inc. (Austin, TX). The sense strand sequences were the following: DR5, 5'-GGACUAUAGCACUCACUGGtt-3'; DcR2, 5'-GGGUGUGGAUUACACCAUUtt-3'; siRNA control was a non-specific random scrambled sequence. In vitro transfections used lipofectamine reagent (Invitrogen, Cergy-Pontoise, France). Cells were cultured in 12-well plates, 1 ml/well of 2.5% charcoal-stripped FCS medium. They were allowed to attach for 24 h, the culture medium was then removed and replaced with serum-free RPMI (200 μl). Cells were treated with gene-specific siRNAs and control siRNAs (0.5 μg), plus reagent (2 μl), lipofectamine reagent (1 μl) and 50 μl of RPMI for 4 h at 37°C with 5% CO2 in air. Thereafter, 750 μl of 2.5% charcoal-stripped FCS-containing medium were added. Cells were collected or treated 48 h later with TRAIL peptide (PeproTech, Levallois Perret, France). The silencing of targeted proteins was estimated by Western-blot analysis with corresponding antibodies.
Colorimetric caspase-3 activity assay
The enzymatic activity of caspase-3 was assayed with a Caspase-3 Colorimetric Assay Kit (Alexis Biochemicals, Switzerland). To measure the activity of caspase-3, cell lysates were prepared after their respective treatments. After incubating 200 μg protein of cell lysate per sample in 100 μl of reaction buffer containing DEVD-pNA substrate (200 μM final concentration) at 37°C for 2 h in the dark, absorption was measured at 405 nm.
Statistical analysis
Statistical analysis were carried out by ANOVA and post-hoc Bonferroni/Dunn tests, except in Figure 3, where significant differences were obtained with the Student-Newman-Keuls post-test (StatView Software; SAS Institute Inc., Cary, NC). Differences were taken as statistically significant at P < 0.05. A representative experiment of each series is presented.
Data are expressed as the mean ± SD. Unless otherwise mentioned in the figure legends, the different analyses were performed 3 times with triplicate cultures, and investigated at least 3 times on cells at different passages. TRAIL-induced apoptosis experiments included 5 samples per treatment condition.
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The authors thank P. Contard and N. Riu-Muzet for their technical assistance.
This work has been funded by INSERM
Contract grant sponsor: Association pour la Recherche sur les Tumeurs de la Prostate (ARTP), Fondation pour la Recherche Médicale (FRM) and Association pour la Recherche contre le Cancer (ARC), fellowship to DV.
Contract grant sponsor: Ligue Contre Le Cancer: Comité de l'Ardèche & Comité de la Drôme, to RG.
The authors thank AstraZeneca (Alderly House, Cheshire, England) for their gift of bicalutamide.
The authors thank BioMedES Ltd (Leggat House Inverurie, Aberdeenshire, UK) for their assistance to improve the article.
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Competing interests
The authors declare that they have no competing interests.
Authors' contributions
DV performed cell treatments, Western blot analysis, experiments with siRNA, apoptosis assessment with DAPI, statistical analysis and construction of the figures.
MR carried out the caspase-3 activity assay and helped with cell culture. JC and CD performed cell cultures, numeration, proliferation assay and flowcytometric analyses. SY helped to carry out androgen cell treatment. AR and MD participated in the design of the study and discussed the results. MB participated in the design, in coordinating the study and discussed its findings. RG, as corresponding author, designed the protocol, helped to carry out experiments, helped to analyse the data during the study and wrote the manuscript. All authors read and approved the final manuscript.
David Vindrieux, Marie Réveiller contributed equally to this work.
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Vindrieux, D., Réveiller, M., Chantepie, J. et al. Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis. Cancer Cell Int 11, 42 (2011). https://doi.org/10.1186/1475-2867-11-42
DOI: https://doi.org/10.1186/1475-2867-11-42
- DcR2
- Prostate Cancer
- Apoptosis
- Androgen