text:
Message boards :
The Lounge :
BOINC Pentathlon 2015
(Message 61438)
Posted 7 Apr 2015 by pschoefer
Once again, SETI.Germany invites all BOINC teams to the BOINC Pentathlon. For the sixth time, the winner is battled out in five disciplines at five projects between May 5 and May 19.
After the introduction of Marathon and Sprint in the last couple of years, there will be a new discipline in this year, again. Details will be announced prior to the beginning of the Pentathlon, for now I can reveal that it will run for at least five days at a CPU project.
Each team that wants to participate has to sign up using the registration form at http://www.seti-germany.de/boinc_pentathlon/anmeldung.php until April 27. The teams may suggest one GPU project and three CPU projects, please see this page for details.
All information is available on the Pentathlon page at http://www.seti-germany.de/boinc_pentathlon/22_en_Welcome.html, while you can find the answers to many questions in our FAQ.
Looking forward to seeing you at the Pentathlon! :)
Message boards :
The Lounge :
BOINC Pentathlon 2014
(Message 53525)
Posted 5 Apr 2014 by pschoefer
For the fifth time, SETI.Germany invites all BOINC teams to the BOINC Pentathlon, a competition inspired by the Pentathlon in ancient Greece. Between May 5 and May 19, five disciplines at five different BOINC projects are held to find the overall winner.
Each team that wants to participate has to sign up using the registration form at http://www.seti-germany.de/boinc_pentathlon/anmeldung.php. Registration is open until April 27.
For all but the Marathon discipline, the teams may suggest their favorite project when signing up. A list of possible projects is available at http://www.seti-germany.de/boinc_pentathlon/25_en_Disciplines.html, you may suggest other projects as long as you think they are able to handle the increased load. Note that projects that were part of last year's Pentathlon are excluded for this year.
For more information including the full rules, please visit the BOINC Pentathlon page at http://www.seti-germany.de/boinc_pentathlon/22_en_Welcome.html.
Please spread the word and gauge the interest within your team. Looking forward to seeing you at the Pentathlon! :)
Message boards :
News :
BOINC 7.0 released to public
(Message 43347)
Posted 9 Apr 2012 by pschoefer
There's also a massive work fetch bug. Was this version tested before releasing it to public?
Message boards :
BOINC client :
massive work fetch bug in 7.0.25
(Message 43342)
Posted 9 Apr 2012 by pschoefer
Just switched to the new recommended version... and it's definitely nothing I would recommend. ;)
My system: i7 980X + ATI HD 5850 + NVIDIA GTX 470
Active projects:
- PrimeGrid (only on NVIDIA)
- Collatz Conjecture (only on ATI, so ATI is currently idle because of downtime)
- WUProp@Home
- EDGeS@Home (CPU; Resource Share 0, because I used it as backup project during last PrimeGrid Challenge and did not change it back afterwards)
Work buffer settings:
While PG on NVIDIA and WUProp (nci) run nicely, the client keeps requesting EDGeS work for CPU and ATI... of course, it can't get work for ATI there, but it gets one more CPU WU on each request. 320 WUs and counting, about 12 hours of work according to BOINC's own estimation... that's 0.5 days, way more than 0.01 days.
At least I did a backup before the update, so I can switch back to 6.12.34 for now.
Message boards :
BOINC client :
Connected Frac = -1.000000
(Message 12087)
Posted 15 Aug 2007 by pschoefer
I will test another project, as soon as I can access it again, to see if it is a problem with the host and/or PrimeGrid's server-update.
Works well with ABC@home, so it is a PrimeGrid problem. I'll ask over there again.
Message boards :
BOINC client :
Connected Frac = -1.000000
(Message 12050)
Posted 13 Aug 2007 by pschoefer
The connected frac should have nothing to do with anything. It is suposed to measure how often you are connected to the internet, but it has never worked properly on *nix and is not reliable on windows. So as far as I know it is ignored. The other time stats may have a bearing on your problem though.
The other time stats are normal, and since this is the only difference to my other hosts, I thought this might be the problem.
OK, this host is running WinXP on a RAM Disk, while the other ones are on Win2k, but before last week it worked well...
I will test another project, as soon as I can access it again, to see if it is a problem with the host and/or PrimeGrid's server-update.
Message boards :
BOINC client :
Connected Frac = -1.000000
(Message 12046)
Posted 13 Aug 2007 by pschoefer
Hi all!
Last week my C2D, which is running with BOINCpe, started to get only one WU per request, although much more work is requested and I did not change the preferences. There are two projects attached: Pirates@Home and PrimeGrid.
Here's a part from the logfile:
06.08.2007 10:03:48|PrimeGrid|Sending scheduler request: To fetch work 06.08.2007 10:03:48|PrimeGrid|Requesting 325679 seconds of new work 06.08.2007 10:03:53|PrimeGrid|Scheduler RPC succeeded [server version 511] 06.08.2007 10:03:53|PrimeGrid|Deferring communication for 7 sec 06.08.2007 10:03:53|PrimeGrid|Reason: requested by project 06.08.2007 10:03:55|PrimeGrid|[file_xfer] Started download of file llrTPS_7055979 06.08.2007 10:03:56|PrimeGrid|[file_xfer] Finished download of file llrTPS_7055979 06.08.2007 10:03:56|PrimeGrid|[file_xfer] Throughput 425 bytes/sec 06.08.2007 10:04:03|PrimeGrid|Sending scheduler request: To fetch work 06.08.2007 10:04:03|PrimeGrid|Requesting 325041 seconds of new work 06.08.2007 10:04:08|PrimeGrid|Scheduler RPC succeeded [server version 511] 06.08.2007 10:04:08|PrimeGrid|Deferring communication for 7 sec 06.08.2007 10:04:08|PrimeGrid|Reason: requested by project 06.08.2007 10:04:10|PrimeGrid|[file_xfer] Started download of file llrTPS_7054620 06.08.2007 10:04:11|PrimeGrid|[file_xfer] Finished download of file llrTPS_7054620 06.08.2007 10:04:11|PrimeGrid|[file_xfer] Throughput 512 bytes/sec
...and so on...
At that time I was using BOINC 5.8.15, I updated to 5.10.13 at first, now 5.10.18, but still the same behaviour (my other host's are running fine and getting lots of PG-WUs per request). I also tried different prefs, but nothing changed.
Today I discovered <connected_frac>-1.000000</connected_frac> in the client_state.xml. Because this is the only difference form my other host's (there it is 0), I think that this is the reason.
I tried to manually set it to different values from 0 to 1 (client closed before that), but after restarting the client, it was -1 again.
Message boards :
BOINC Manager :
Where have all the messages gone...?
(Message 11884)
Posted 30 Jul 2007 by pschoefer
After reading some old BOINC logs of mine, I find some useful messages missing in newer versions of BOINC.
Since 5.8.x we have two times "starting task" (I still don't see any sense in that), "resuming task", "restarting task" and "computation finished". But while switching from one task to another one, there used to be the following message:
2006-09-12 15:52:03 [SETI@home Beta Test] Pausing task 01my06aa.17871.305.972158.3.126_0 (left in memory)
Next examples:
2006-10-18 09:44:06 [---] Using earliest-deadline-first scheduling because computer is overcommitted.
2006-10-18 09:44:06 [---] Suspending work fetch because computer is overcommitted.
2006-10-18 12:46:24 [---] Resuming round-robin CPU scheduling.
2006-11-25 18:03:15 [---] Allowing work fetch again.
OK, the EDF scheduling has become more complicated with 5.8.x, but it would be great, if there was at least a message when work fetch is suspended/allowed.
And last but not least (and -unfortunately- NOT missing ;)) something about the error messages. I think it was in some of the 5.8 versions... Error messages where easy to see, as they were displayed in red. Now you might not see some error messages, because all messages are black. :|
Message boards :
The Lounge :
Really, who likes the new BOINC logo?
(Message 11840)
Posted 28 Jul 2007 by pschoefer
At first sight I did not like the logo, but now I start loving it. :D
The old logo was just some kind of ink blot with the letters BOINC on it.
Now you can interprete those blue arms as seperated things (e.g. computers), which unify into one whole thing (i.e. the orange circle). That's exactly, what BOINC is! :)
Message boards :
BOINC Manager :
Problems with 5.8.15
(Message 9618)
Posted 16 Apr 2007 by pschoefer
If you click Retry or Update project or similar, it enables network again for 5 minutes. I'm tired of asking for that stupid "feature" to be removed.
It's really a useless feature that should be removed. I had the following problem with it: After all Workunits were crunched I set all projects on "no new tasks", enabled network communication, reported the WUs and disabled network again. Then I allowed the projects to fetch work again, and lots of WUs were downloaded, although network communication was DISABLED.
Message boards :
BOINC Manager :
Problems with 5.8.15
(Message 9371)
Posted 5 Apr 2007 by pschoefer
The problem with two instances of Internet Explorer 6 is still there in BOINC 5.8.16 :(
Yes, of course. But it could have been that the libCurl-problem was fixed and the new solution was built in in BOINC 5.8.16 ...
btw: Is there any overview of the changes between the 5.8.x releases, like the one of 5.4.x?
Message boards :
BOINC Manager :
Problems with 5.8.15
(Message 9360)
Posted 5 Apr 2007 by pschoefer
The problem with two instances of Internet Explorer 6 is still there in BOINC 5.8.16 :(
Message boards :
BOINC client :
Trouble with router
(Message 9060)
Posted 24 Mar 2007 by pschoefer
I don't know if you can believe it, but I could not at the first sight...
I made a firmware update (manually, because the router didn't find the new version automatically), and it works now.
Thanks for your support, although I finally solved the problem on my own.
Message boards :
BOINC Manager :
Trojan boinc installation by rogue member
(Message 9016)
Posted 23 Mar 2007 by pschoefer
Anyone else find David Braun at Predictor@Home's response to this matter puzzling? I have to say I did.
We reopened the discussion. It cannot be that the oldest BOINC project supports abusing!
Message boards :
BOINC Manager :
graphically blind
(Message 8987)
Posted 22 Mar 2007 by pschoefer
Are you not able to start the graphics via the BOINC manager, too, or is only the screensaver not working? Which projects are you running?
To give you a piece of advice: Forget about the graphics, they're just eating performance.
Message boards :
BOINC client :
Trouble with router
(Message 8837)
Posted 17 Mar 2007 by pschoefer
Remember this is all outgoing.
Are there any ports needed for incoming connections? I spoke to an expert from Netgear today at Cebit, and he could only imagine that BOINC needed some ports forwarded.
Message boards :
BOINC Manager :
Trojan boinc installation by rogue member
(Message 8770)
Posted 15 Mar 2007 by pschoefer
What a shame!
Wate is the featured volunteer of the day!
Message boards :
BOINC client :
Trouble with router
(Message 8606)
Posted 7 Mar 2007 by pschoefer
Let's not forget port 443 please, though few projects use it.
Do you know, which projects use that port?
As mentioned before, I can contact SETI, SETI-Beta, and the account manager BAM!, while ABC, LHC, QMC, Einstein, PrimeGrid, Predictor, Spinhenge are unreachable.
Message boards :
BOINC Manager :
Boinc Manager suggestions
(Message 8575)
Posted 6 Mar 2007 by pschoefer
To extend your list:
But since it was built-in in a former version, I don't think it'd be a big problem to build it in again.
Message boards :
BOINC Manager :
North American Daylight Saving Time change
(Message 8574)
Posted 6 Mar 2007 by pschoefer
It certainly does save energy, as most people who have the choice don't get up at daybreak and do stay up late enough to need electric lighting. Summer Time reduces the number of hours in the evening when electric light is required.
But most people have no choice when to get up, so they need electric light in the morning, exspecially at the begin and the end of DST. Take me for an example: I have to get up at 6 AM CET. In march, when the sun rises earlier, our European DST starts, so I have to get up at 6 AM CEST = 5 AM CET. At that time it's still dark outside, so I need light.
Everyone, who likes the DST, can get up earlier on his/her own and go to bed an hour earlier, too, without a clock showing one hour later. But those, who dislike the DST, have not this choice in most cases.
btw: The 3/4 of the French population voted against the DST, but they're forced to accept it.
Copyright © 2017 University of California. Permission is granted to copy, distribute and/or modify this document under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation.


text:
Man arrested after van with kid in it is stolen
LAKE FOREST – A 21-year-old man was arrested on suspision of stealing a van with a 15-year-old asleep inside, police said.
The incident was reported to police at 12:25 a.m. on Sunday after a 16-year-old left the van for a short time while it was parked in the 23700 block of Rockfield Boulevard near the Quality Inn Suites, Lt. Roland Chacon said.
Chacon said that the 16-year-old girl reported that a man got inside the van and drove away. While at an intersection, the 15-year-old jumped from the van and returned to the hotel.
Deputies searched the area and found the man on foot shortly after the incident occurred, Chacon said. The man was identified as Brian Gutierrez Montes and he was arrested on suspicion of vehicle theft and kidnapping, Chacon said.
The teens were returned to the custody of their parents. The van was also recovered in Irvine, about half a mile away, Chacon said.
Montes was taken to Orange County jail where he is being held in lieu of $100,000 bail. His occupation, according to arrest records, is a mechanic.
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subset: commoncrawl


text:
Category:Peckett and Sons locomotives
From Wikimedia Commons, the free media repository
English: Locomotives manufactured by Peckett and Sons.
This category has only the following subcategory.
- ► Peckett and Sons steam locomotives (21 C, 56 F)
Media in category "Peckett and Sons locomotives"
The following 3 files are in this category, out of 3 total.


text:
TAWLA is joining hands with the rest of the World to commemorate the International Girl Child Day celebrated worldwide every 11th October. The theme for this year's International Day of the Girl Child is based on the seventeen Sustainable Development Goals. The slogan is: Girls' Progress equals Goals' Progress: What Counts for Girls.
It is estimated that there is 1.1 billion girls worldwide who are central to achieving the 2030 Sustainable Development Agenda. Therefore in the realization of this year's theme, TAWLA is committed and further pledges to continue providing legal empowerment to end discrimination and harmful practices like early marriages and violence against girls.
TAWLA believe that investing in girls will empower them to be able to build their dreams for their future lives.
"Let us all work hard to make sure we count all girls, because all girls count." (Ban Ki-moon-UN Secretary–General: 2016)
As a vibrant leading human rights women organization, TAWLA embark on road safety agenda. TAWLA leads the Road Safety coalition of CSO's and key stakeholders. The purpose of this project is to contribute to the improvement of road safety legal and policy environment by addressing gaps in the road safety legislation that link directly to current high rate of road accidents in the country.
Additionally, TAWLA has engaged itself with several media houses in advocating for the improved road safety legal and policy environment. For instance, TAWLA's Executive Director Ms. Tike Mwambipile together with other Coalition members participated in one Television program namely, "This Week in Perspective" at TBC 1 TV Station (hosted by one Adam Simbe) to discuss the current road safety situation in the Tanzania. Ms. Mwambipile spoke generally on the existing road safety legislation and the need to have the proposed amendments for better improvement of road safety situation in the country.
Apart from the above activities, TAWLA has conducted a two days capacity building meeting with road safety stakeholders aimed at; capacity building and sensitization of officials from relevant Ministries by aligning gaps in the existing laws and policies on road safety; creating champions who will help to promote an improved road safety legal environment with increased political will.
Saba Saba exhibition
Welcome to our pavilion at Saba Saba grounds - Dar es Salaam from 1st July to 7th July, 2016 to familiarize more on women and children rights
African Child Day
African Child day is celebrated every year on the 16th June, to honor the courage of students who marched for their right to education in 1976 in Soweto – South Africa. Nearly ten thousand black students protested as a way to demonstrate their disapproval of the Black Education Act, which was segregating students based on their race.
Currently, the Day of the African Child is an opportunity to raise awareness for the ongoing need to improve access to education for children across Africa.
Unfortunately, for a variety of reasons a large number of children in Africa still do not have access to education. Poverty, child marriage, discrimination and exploitation are major reasons for why many children do not attend schools.
Yet, as we all know, education is a powerful tool for human development. Education is the foundation for a better life for the children themselves and for prosperous African societies.
As we commemorate the African Child day this year, let us unite our efforts and "let's help children to realize their rights and say no to issues affecting their lives in a negative way"


text:
Lent begins soon! Celebrate the Easter season with our free Lent & Easter devotions.
God's guidance is promised to those who genuinely desire it and seek it.
Ps 25:4-5; Jas 1:5 See also Ex 33:12-16; Job 6:24; Ps 5:8; Ps 27:11; Ps 31:3; Ps 61:1-2; Ps 86:11; Ps 143:8
Ps 43:3 See also Ps 16:7-8; Ps 73:23-24; Ps 119:35,105,133; Jn 10:3-4,27
Pr 3:5-6 See also 2Ch 6:26-27; Ps 25:9; Ps 139:23-24; Isa 57:15,18-19; Jer 50:4-5; Eze 20:1-3,30-31
Mt 26:39 pp Mk 14:35-36 pp Lk 22:42 See also Nu 14:8-9; Ps 32:8-9; Isa 48:17-18; Ro 12:1-2
Lk 12:11-12 See also Ps 143:10; Jn 16:13; Ac 10:19-20; Ac 13:2; Ac 16:6-7; Gal 5:18; 1Jn 2:26-27
Ps 119:105,133 See also Ps 19:8; Isa 8:19-20; Ac 17:11; 2Pe 1:19
The pillar of cloud and the pillar of fire Ex 13:21-22 See also Ex 14:19-20; Ne 9:19
The Urim and the Thummin Ex 28:29-30; Nu 27:21
The casting of lots 1Sa 14:36-42; Pr 16:33; Jnh 1:7; Ac 1:26
Dreams and visions Mt 2:19-20; Ac 9:10-11 See also Ge 40:5-8; Joel 2:28; Ac 10:3-6; Ac 11:5-9
Angels Ac 8:26 See also Ac 5:19
Starting your free trial of Bible Gateway Plus is easy. You're already logged in with your Bible Gateway account. The next step is to enter your payment information. Your credit card won't be charged until the trial period is over. You can cancel anytime during the trial period.
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Try Bible Gateway Plus, a brand-new service that lets you experience Bible Gateway free of banner ads! It also gives you instant access to over 40 Bible study and inspirational devotional books, including the NIV Study Bible. With Bible Gateway Plus, you can experience and understand God's Word in life-changing new ways, without the distraction of ads. Try it free for 30 days—you can cancel at any time. Following your 30-day free trial, Bible Gateway Plus is only $3.99/month.
Three easy steps to start your free trial subscription to Bible Gateway Plus.


text: Alston Photos Alston Old Photos Old Maps Memories of Alston Photo Books Nearby Places Displaying all 11 Photos Sort & display options Sort by Default Sort by Most Popular Sort by Oldest Sort by Newest Sort by Description Sort by Memories Shared Sort by Recently Added Show Image References Show Landscape Images Show Portrait Images New Alston, Tyne Bridge c.1955 Ref. A290015M Alston, Kirkhaugh Church c.1955 Ref. A290029 Alston, Market Cross c.1955 Ref. A290012 Alston, Front Street c.1955 Ref. A290011 Alston, Market Cross c.1960 Ref. A290055 Alston, Market Square 1952 Ref. A290014 Alston, Cross Fell c.1960 Ref. A290040 Alston, From Tower Hill c.1955 Ref. A290018 Alston, Gossip Gate c.1955 Ref. A290016 Alston, Physic Hall c.1960 Ref. A290034 Alston, Tyne Bridge c.1955 Ref. A290015 Displaying all 11 Photos


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Hostelworld anbefaler
Vi elsker dette vandrerhjemmet! Vi gir tommelen opp for gjennomgående gode kundekarakterer og utmerkede kvalitetsvurderinger.
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text:
Designed with gaskets and multicolored lids, this glass canister set is perfect for storing coffee, sugar, tea and pasta.
A-line silhouette offers generous sweep and is very comfortable. 34″ length provides great coverage. Button on/off hood can be removed with ease and can zip up or be left open. Constructed of soft, washable anti-pill polyester fleece.
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text:
Brad Landon Denham
Brad Landon Denham passed away Tuesday, Feb. 19, 2013, at his residence in Morgan City at the age of 36. He was employed with Gulf Coast Broadband in Morgan City.
He attended Nicholls State University and LSU. He was a member of Blackwater United Methodist Church in Central.
There will be a visitation at Blackwater United Methodist Church in Central on Friday, Feb. 22, 2013, from 10 a.m. until the memorial service at 11 a.m., conducted by Michi Head and Marie Williams.
Survived by his wife, Casey Batiste Denham; father and stepmother, Duane C. and Dodie Denham; mother and stepfather, Donna Forbes and Ed Meyer; one daughter, Brittany L. Denham; four sisters, Tara Shaffer, Terry Little, Sarah Rogillio and Callie Tranchina; three brothers, Todd Denham, Jonathan Meyer and Alexander Meyer; maternal grandmother, Margie Forbes; and numerous nieces, nephews, aunts and uncles.
He is preceded in death by his maternal grandfather, O.T. "Dude" Forbes; and paternal grandparents, Charles and Bertha Denham.
Please make memorial donations to a charity of your choice.
Seale Funeral Home in Central is in charge of arrangements. Please visit the online registry book at www.sealefuneral.com.
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SOD Blitz 2016 Results & Map
SOD Blitz Training Sessions and Community Meetings
Updated Recommendations for SOD Management and Treatment
SOD Blitz Spring 2016 Training Video, Instructions, and PowerPoint
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Sudden Oak Death – SOD – Symptoms Guide
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Disclaimer: Between 10/2015-2/2016 the risk assessment function of SODmap mobile may not have functioned properly with Apple iOS 8 and above. The current version of SODmap Mobile is functioning properly.
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The University of Tampa Press extends the educational mission of the University through the publication of works of scholarship, creativity, and regional interest. Its publications disseminate the fruits of learning to a wide audience of serious readers both within and beyond the academic institution.
New and Selected Stories by Peter Meinke, with drawings by Jeanne Clark Meinke.
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Poems by Patrica Hooper
Patricia Hooper's new collection of poetry is the latest winner of our Anita Claire Scharf Award. The judges wrote that it is "a collection that quite literally lifts off!
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Poems by Michelle Boisseau
Michelle Boisseau received the latest Tampa Review Prize for Poetry for this new collection that the judges praised for making "graceful and unexpected leaps from personal to mythic, tender to satiric, and tragic to comic in poems that elude predictability and command attention."
Tampa Review 51/52 invites us to consider the ways that artistic forms and disciplines can overlap and interact as artists seek to realize their distinctive visions and share them with others, crossing disciplinary boundaries to give voice to thought and feeling.


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We have recently reported that tumour necrosis factor-α (TNF-α) increases oxidative stress and apoptosis in cardiomyocytes by upregulating p38 mitogen-activated protein (MAP) kinase (MAPK) phosphorylation. Interleukin-10 (IL-10) blocked these effects of TNF-α by upregulating extracellular signal-regulated kinase 1/2 (ERK 1/2) MAPK phosphorylation. However, the precise site of this IL-10 action is still unknown, and this is investigated in the present study.
Cardiomyocytes isolated from adult Sprague–Dawley rats were exposed to TNF-α (10 ng/mL), IL-10 (10 ng/mL), and IL-10+TNF-α (ratio 1) for 4 h. Hydrogen peroxide and antioxidant trolox were used as positive controls. Exposure to TNF-α resulted in an increase in the production of reactive oxygen species, the number of apoptotic cells, caspase-3 activation, and poly-ADP ribose polymerase (PARP) cleavage. Increased oxidative stress by using hydrogen peroxide also caused apoptosis. The changes due to TNF-α were associated with an increase in the inhibitor of κB kinase (IKK) and nuclear factor kappa-B (NFκB) phosphorylation. IL-10 by itself had no effect, but it prevented the above mentioned TNF-α-induced changes. Trolox also mitigated TNF-α induced changes. Pre-exposure of cells to an IKK inhibitor (PS-1145) prevented TNF-α-induced caspase-3 and PARP cleavage. Inhibition of ERK 1/2 MAPK with PD98059 attenuated the protective role of IL-10 against TNF-α-induced activation of IKK and NFκB as well as cardiomyocyte apoptosis.
The present study shows that TNF-α-induced activation of the NFκB pathway plays a critical role in cardiomyocyte apoptosis. IL-10 prevents TNF-α-induced NFκB activation and pro-apoptotic changes in cardiomyocytes by inhibiting IKK phosphorylation through the activation of ERK 1/2 MAPK.
Tumour necrosis factor-α (TNF-α), a pro-inflammatory cytokine, is elevated in many pathogenic conditions including cardiovascular injury and disease states.1–3 The anti-inflammatory cytokine interleukin-10 (IL-10) inhibits the production of various pro-inflammatory cytokines including TNF-α.4 IL-10 has also been shown to act as an antagonist to TNF-α by inhibiting TNF-α-induced oxidative stress.5,6 Sustained long-term over-expression of TNF-α provokes the induction of cardiomyocyte apoptosis,7 which contributes to the pathophysiology of several heart diseases, including dilated cardiomyopathy, myocardial infarction, and heart failure.8,9 Surprisingly, anti-TNF-α therapy had no benefit or even had harmful effects in patients with heart failure.10,11 Thus there is a need to study how TNF-α influences downstream cell-signalling pathways leading to cardiomyocyte apoptosis and how IL-10 mitigates the harmful effects of TNF-α. Identification of the intermediary steps involved in the TNF-α-induced cardiomyocyte apoptosis can offer potential therapeutic targets to abrogate TNF-α-induced cardiovascular diseases.
Nuclear factor kappa-B (NFκB) is a transcription factor that regulates gene transcription of many pro-inflammatory cytokines.12 Thus suppression of NFκB activity can be a potential mechanism for regulating inflammatory responses. Several studies have identified NFκB as the key regulator of TNF-α gene activation.13 The NFκB family of transcription factors exists in the cytoplasm of unstimulated cells as homo- or heterodimers complexed with the inhibitory-κB (IκB) proteins. On stimulation, phosphorylation of IκB by inhibitory-κB kinase (IKK) triggers its degradation and the activation of NFκB. The activation and translocation of NFκB to the nucleus is followed by transcription of various pro-inflammatory genes including TNF-α.14,15 The anti-inflammatory actions of IL-10 inhibit the production of pro-inflammatory cytokines in human monocytes through the suppression of NFκB activation.16 In rat alveolar macrophages and lung tissue, it has been reported that IL-10 and IL-13 inhibit nuclear localization of NFκB by preserving the expression of IκB protein.17
In a recent study, we have reported that TNF-α induces cardiomyocyte apoptosis by upregulating p38 phosphorylation. IL-10 prevented this effect of TNF-α by upregulating extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation.6 However, the precise site of action of ERK 1/2 in the TNF-α signalling pathway is still unknown. The current study investigated (i) the role of NFκB pathway in TNF-α-induced cardiomyocyte apoptosis, and (ii) how IL-10 regulated the NFκB pathway to suppress TNF-α-induced-cardiomyocyte apoptosis.
Materials and methods
The investigation conforms to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85-23, revised 1996). All animal-experiment protocols were approved by the University of Manitoba Animal Care Committee following the guidelines established by the Canadian Council on Animal Care.
Cardiomyocyte isolation
Cardiomyocytes were isolated from normal adult male Sprague–Dawley rats (250–300 g) using a previously described procedure.5 Hearts were excised and mounted on a modified Langendorff perfusion apparatus. The perfusate (modified Krebs buffer) contained 110 mM NaCl, 2.6 mM KCl, 1.2 mM KH2PO4, 1.2 mM MgSO4, 25 mM NaHCO3, and 11 mM Glucose (pH 7.4). The Ca2+ free perfusion was then switched to recirculating mode with the buffer containing 25 µM calcium, 0.1% w/v collagenase, and 0.25% w/v bovine serum albumin, for 20 min. The collagenase-digested ventricles were chopped into small pieces and gently passed through pipettes with progressively smaller tip diameters and with an increasing concentration of CaCl2. The suspension was filtered through a nylon mesh (200 µM) and was allowed to settle for 10 min. The supernatant was discarded and the cell pellet was resuspended in medium M199 containing CaCl2 (1.8 mM). Cardiomyocytes (1 × 105 per dish) were plated on 4% serum-coated polystyrene tissue culture dishes. Plated cells were incubated in serum-free culture medium M199 supplemented with antibiotics (streptomycin/penicillin, 100 µg/mL) at 37°C under a 5% CO2−95% air atmosphere. Two hours after plating, the culture medium was changed to remove unattached dead cells, and the viable cardiomyocytes were incubated overnight.
Treatment of cardiomyocytes
After initial incubation of 24 h, >90% of cardiomyocytes were viable and these cells were treated with one of the following: H2O2 (100 µM), TNF-α (10 ng/mL), IL-10 (10 ng/mL), and combination of IL-10 + TNF-α (ratio 1) for 4 h. This dose and treatment protocol is based on our earlier studies.6 To investigate the involvement of oxidative stress in TNF-α-induced changes in NFκB pathway and caspase-3 activation, cells were treated with 20 µmol/L of trolox (a water-soluble antioxidant) for 30 min and then incubated with the combination of trolox and TNF-α (10 ng/mL) for 4 h. In order to study the physiological role of NFκB pathway and ERK 1/2 MAPK (mitogen-activated protein kinase) in the TNF-α and IL-10 regulation of cardiomyocyte apoptosis, cells were pre-treated with 25 µM of PS-1145 (IKK inhibitor) or 25 µM of PD-98059 (ERK inhibitor) or with vehicle solution (DMSO at a concentration of 0.1%) for 15 min.
The concentration and time of exposure for PS-1145 were chosen following the completion of a separate pilot study (data not shown), and for PD-98059, they were chosen from our previous study.6
Measurement of reactive oxygen species
The level of oxidative stress was monitored by the measurement of reactive oxygen species (ROS).18 Cardiomyocytes from different treatment groups in the culture dishes were washed with phosphate-buffered saline (PBS) and incubated with 10 µM solution of fluorescent probe, 5-(6)-chloromethyl-2′7′-dihydroflourescein diacetate probe (DCFDA) (Molecular Probes, Eugene, Oregon, USA) at 37°C for 30 min in a humidified chamber. Fluorescent images of 100 cells from multiple fields per dish were recorded with the Olympus BX 51 fluorescent microscope. From each perfused heart, at least 10 dishes (35 mm × 10 mm) were prepared; the study was done in duplicate for each treatment group. Fluorescence intensity was measured using digital image-processing software (Image Pro Plus). Experiment was repeated six times (n = 6) and statistical analysis was done.
Western blot analysis
Phosphorylated and total IKKα, IKKβ, and NFκB levels, as well as caspase-3 and poly-ADP ribose polymerase (PARP) cleavage were measured by western blotting using specific antibody kits (Cell Signaling Technology). Whole-cell protein extracts prepared from control and treated cardiomyocytes in different groups were suspended in PBS containing protease inhibitor cocktail. The protein samples (30 µg) were then subjected to 12% SDS–PAGE and transferred to PVDF (Roche Diagnostics, USA) membrane. Proteins bound to the membrane were detected with BM chemiluminiscence blotting substrate (POD) kit (Roche Diagnostics, USA). Bands were visualized with Fluor S-MultiImager MAX System (Bio-Rad Laboratories, Canada) and quantified by image analysis software (Quantity One, Bio-Rad Laboratories, Canada).
Caspase-3 and PARP cleavage were studied by western blotting (as described earlier), and caspase-3 activity was measured by fluorescence spectrophotometric assay using the fluoro-chrome 7-amino-4-methyl coumarin (AMC) and substrate DEVD-AMC, provided in the CaspACE™ assay system (Promega Corp., Madison, WI, USA). The assay was performed in 96-well polystyrene plate (Becton Dickinson, USA). From each sample, 100 µg of protein was added to the reaction wells, together with 32 µL of caspase assay buffer, 2 µL DMSO, 10 µL of dithiothreitol, and 2 µL of DEVD-AMC substrate (dissolved in DMSO). The reaction mixture was incubated at 30°C for 60 min and thereafter analysed for AMC fluorescence in a plate reader (Spectra Max Gemini) at excitation and emission wavelengths of 360 and 460 nm, respectively. The fluorescence data given in the figures were corrected by subtracting background values.
Cardiomyocyte apoptosis was also studied after staining the cells with Hoescht 33258. For this, the cardiomyocytes from different groups in culture dishes were washed three times with PBS and incubated with Hoescht 33258 (1 µg/mL) for 10 min in a humidified chamber, protected from light, at 37°C. After staining, the culture plates were examined using fluorescent microscope (Olympus BX 51). Cardiomyocytes were observed for apoptosis. A total of six different fields per dish were counted to quantify the number of cells containing fragmented nuclei. From each perfused heart, at least 10 dishes (35 mm × 10 mm) were prepared; the study was done in duplicate for each treatment group. Experiment was repeated four times (n = 4) and statistical analysis was done.
Protein and statistical analysis
Total protein concentration was determined using bovine serum albumin as a standard.19 Data are expressed as the mean ± SEM. Groups were compared by one-way ANOVA, and Bonferroni's test was performed to identify differences between groups. A value of P < 0.05 was considered significant.
Oxidative stress studies
The production of intracellular reactive oxygen species (ROS) was significantly increased in TNF-α-exposed cardiomyocytes. By itself, IL-10 treatment of the cardiomyocytes did not show any effect on ROS levels (Figure 1A). However, TNF-α-induced increase in ROS production was significantly mitigated by IL-10 treatment. Exposure to H2O2 (positive control) significantly increased the ROS production in cardiomyocytes as measured in terms of green fluorescence intensity (Figure 1A).
Cardiomyocyte apoptosis
Cardiomyocyte apoptosis was studied by fluorescent microscopy after staining the cells with Hoescht 33258. In the control group, the cells were rod-shaped, binucleated, and the nuclei had normal appearance (Figure 1B). Exposure to TNF-α resulted in nuclear fragmentation and the number of apoptotic cells significantly increased. Treatment with IL-10 alone did not show any significant change, whereas TNF-α-induced increase in nuclear fragmentation in cardiomyocytes was significantly prevented by IL-10 treatment. Hydrogen peroxide treatment also increased the number of apoptotic cells (Figure 1B).
Cardiomyocyte apoptosis was also studied in terms of caspase-3 activation and PARP cleavage. The caspase family of aspartate-specific cysteine proteases is the central executor of apoptosis. The activation of caspase-3 by proteolytic processing of pro-caspase-3 into 17 and 12 kDa subunits serves as an early marker of apoptosis in various cell types. The 17 kDa-cleaved caspase-3 fragment was detected in TNF-α-exposed cardiomyocytes (Figure 2A). Treatment with IL-10 prevented the TNF-α-induced fragmentation of caspase-3. Whereas IL-10 treatment alone did not show any effect on caspase-3 activation (Figure 2A). To confirm the activation of caspase-3, we monitored the cleavage of its substrate, the nuclear enzyme PARP. In TNF-α-treated groups, caspase-3-induced proteolysis of 116 kDa-native PARP molecule was detected in immunoblots as 89 kDa fragment. Treatment with IL-10 prevented the TNF-α-induced cleavage of PARP, whereas IL-10 alone did not show any effect. Antioxidant trolox also prevented the TNF-α-induced caspase-3 activation and PARP cleavage. Trolox by itself had no effect (Figure 2A).
Caspase-3 activity in fluorescence spectrophotometric assay was increased by 107% in TNF-α-exposed cardiomyocytes. There was no difference between control- and IL-10-treated cells with respect to caspase-3 activity. However, the TNF-α-induced increase in caspase-3 activity was completely mitigated by IL-10 treatment. Antioxidant trolox also prevented the TNF-α-induced increase in caspase-3 activity. Trolox by itself had no effect on the baseline caspase-3 activity (Figure 2B).
Phosphorylation of IKKα, IKKβ, and NFκB
Phosphorylation of IKKα, IKKβ, and NFκB was examined in the cardiomyocytes exposed to TNF-α (10 ng/mL), IL-10 (10 ng/mL), and IL-10 + TNF-α (ratio 1). Exposure to TNF-α caused a significant increase (P < 0.001) in IKKα, IKKβ, and NFκB phosporylation compared with the respective control group. Treatment with IL-10 alone did not cause any change in these parameters, whereas TNF-α-induced increase in IKKα, IKKβ, and NFκB phosphorylation was prevented by IL-10 treatment (Figure 3). Antioxidant trolox was used to study the role of TNF-α-induced oxidative stress in the activation of IKKα, IKKβ, and NFκB in cardiomyocytes. Trolox completely prevented the TNF-α-induced changes in these three parameters. Trolox by itself had no effect (Figure 3).
Inhibition of NFκB pathway
There are several pharmacological approaches to study the role of NFκB pathway in cell signalling. These include repression of NFκB transactivation potential and stabilization of inhibitory kappa-B (IkB), and more recently, inhibition of upstream IKK has also been used.20 In order to study the role of NFκB pathway in TNF-α-induced cardiomyocyte apoptosis, we measured the caspase-3 activation and PARP cleavage after inhibiting IKK with PS-1145. To check whether PS-1145 actually inhibited TNF-α-induced IKK phosphorylation, cells were pre-incubated with PS-1145 (25 µM) for 15 min followed by treatment with TNF-α (10 ng/mL) for 4 h and measurement of IKK phosphorylation. Treatment with PS-1145 significantly inhibited TNF-α-induced IKKα and IKKβ phosphorylation (Figure 4A–C). In the presence of IKK inhibitior, TNF-α exposure did not cause cardiomyocyte apoptosis, as no change was observed in caspase-3 activation and PARP cleavage (Figure 5A and B). IL-10 treatment alone as well as along with TNF-α did not show any change in caspase-3 activity and PARP cleavage (Figure 5A and B). When the cells were treated with PS-1145 alone, we did not observe any effect on caspase-3 activation as well as PARP cleavage (data not shown).
Inhibition of ERK MAPK
We have previously reported that IL-10 prevented TNF-α-induced cardiomyocyte apoptosis by up-regulating ERK 1/2 phosphorylation.6 In this study, to investigate the involvement of ERK 1/2 MAPK in IL-10 modulation of TNF-α-induced NFκB pathway and caspase-3 activation in cardiomyocytes, we pre-treated the cells for 15 min with PD-98059 (ERK inhibitor) and then studied the effects of TNF-α and IL-10 treatment on caspase-3 activation, PARP cleavage, and IKK as well as NFκB activation. TNF-α-induced increase in caspase-3 activity and PARP cleavage were not blocked by IL-10 in ERK-inhibited cardiomyocytes (Figure 6). Furthermore, IL-10 treatment was not able to prevent TNF-α-induced increase in IKKα, IKKβ, and NFκB phosphorylation in cardiomyocytes pre-treated with PD-98059 (Figure 7). Treatment with the inhibitor alone did not show any effect on IKK, NFκB, caspase-3, and PARP (data not shown).
We have recently reported that IL-10 prevented TNF-α-induced oxidative stress and apoptosis in cardiomyocytes by upregulating ERK 1/2 MAPK phosphorylation.6 The present study examines some of the intermediary steps downstream to TNF-α and IL-10 receptor activation and upstream to the induction of cardiomyocyte apoptosis (Figure 8). Our data show that TNF-α-induced oxidative stress in cardiomyocytes leads to apoptosis by an activation of NFκB pathway. IL-10 prevented the TNF-α-induced apoptosis by downregulating the IKK phosphorylation and in turn NFκB activation. Furthermore, data in this study show that this effect is mediated by IL-10-induced activation of ERK 1/2 MAPK.
Direct exposure of cardiomyocytes to TNF-α caused an increase in oxidative stress as indicated by an increase in ROS signal. In this regard, it has been shown that TNF-α-induced oxidative stress alters redox homeostasis by impairing the membrane permeability, mitochondrial function, and hence cardiac function.21 TNF-α has been shown to increase the oxidative stress in the failing heart in the patients with dilated cardiomyopathy.22 It has also been reported that TNF-α blockade decreases oxidative stress and sympathoexcitation in heart failure in rats.23 Exogenous administration of IL-10 has been shown to protect against TNF-α-induced oxidative stress in other situations. In this regard, IL-10 treatment decreases the severity of acute pancreatitis by attenuating the TNF-α-induced oxidative stress.24 It has been reported that TNF-α-induced increase in ROS production and oxidative stress in cardiomyocytes lead to apoptosis.25 Since cardiomyocytes are terminally differentiated, any loss of cells due to cell death can have critical functional consequences.26,27 Thus, cardiomyocyte apoptosis is implicated in the pathogenesis of heart failure of numerous aetiologies, including myocarditis, ischaemia/reperfusion injury, chronic pressure overload, and congestive heart failure.9,28,29 In the present study, TNF-α caused a significant increase in apoptosis as confirmed by an increase in the caspase-3 activation and PARP cleavage, which is also associated with an increase in the number of apoptotic nuclei.
The pro-apoptotic role of TNF-α has been extensively investigated in a variety of in vitro and in vivo models.16,30,31 Binding of TNF-α to its cell-surface receptors triggers apoptotic signalling through caspase-3 activation and causes apoptosis. Caspase-3 has been identified as a key protease in the execution of apoptosis.32 It is activated by several pathways: one possible route being the release of mitochondrial cytochrome c, formation of apoptosome, and activation of caspase-9, which in turn activates effector caspase-3.33 TNF-α-induced cardiomyocyte apoptosis in the present study was significantly decreased by IL-10 treatment. Pro-apoptotic effects of TNF-α have been shown to be modulated by IL-10 treatment in various cell types. In this regard, in human articular chondrocytes, IL-10 upregulated bcl-2 expression and downregulated TNF-α-induced caspase-3 activity.34 We have recently shown that TNF-α-induced increase in the ratio of pro- and anti-apoptotic (Bax/Bcl-xl) proteins in cardiomyocytes was prevented by IL-10 treatment.6
The NFκB pathway is a key component of the cellular response to a variety of extracellular stimuli. The uniqueness in the response through this pathway to different stimuli may reside in the extent of phosphorylation as well as involvement of other co-factors not well understood at this time. In the current study, we have shown that TNF-α exposure leads to a significant increase in NFκB phosphorylation. It has been shown that TNF-α is responsible for the activation of NFκB pathway in human prostate carcinoma PC-3 cells.35 It is also reported that TNF-α-induced ROS generation leads to apoptosis in human breast MCF-7 cells through the activation of NFκB.36 The major mechanism of NFκB activation involves up-regulation of inhibitor kappa B kinase (IKK), which leads to the degradation of IkB and in turn translocation of NFκB to the nucleus and its activation.37 In the present study, TNF-α exposure leads to a significant increase in IKK phosphorylation. Furthermore, when the cardiomyocytes were pre-exposed to PS-1145, a specific IKK inhibitor, TNF-α-induced increase in cardiomyocyte apoptosis was blocked, as no activation of caspase-3 and PARP cleavage was observed, which implies that NFκB pathway is responsible for TNF-α-induced cardiomyocyte apoptosis. PS-1145 itself had no effect on caspase-3 activation and PARP cleavage.
The present study also shows that IL-10 prevents TNF-α-induced activation of NFκB in cardiomyocytes. In this context, it has been reported that IL-10 inhibits NFκB activation in human monocytes to suppress the synthesis of various pro-inflammatory cytokines.16 This action of IL-10 on NFκB pathway in the monocytes involves the blockade of the release of IκB from the NFκB complex. It has also been shown in human monocytic cell lines THP-1 and U937 that TNF-α-induced phosphorylation of IKK is blocked by IL-10 treatment.38 The present study demonstrates that cardiomyocytes also show a similar interplay between TNF-α and IL-10 with respect to IKK phosphorylation and NFκB activation. Although IL-10 has been found to inhibit the NFκB activation in various cell types, no concrete molecular mechanism has been elucidated so far. Data obtained in the present study suggest the sequence of events shown in Figure 8. Inhibition of ERK 1/2 with PD98059 upregulated IKK phosphorylation, thereby blocking the protective role of IL-10 against TNF-α-induced activation of NFκB pathway and cardiomyocyte apoptosis. Thus, in TNF-α-challenged cardiomyocytes, IL-10 treatment activates the cell-survival pathway by upregulating the ERK 1/2 MAPK, thereby inhibiting the NFκB activation. It should also be noted that ERK 1/2 activation has been reported as the mechanism for cell survival during the activation of different death receptors such as Fas receptor, TNF-R1, and TRAIL-R.39
In conclusion, this study provides the evidence that TNF-α-induced cardiomyocyte apoptosis is mediated by the activation of NFκB pathway. IL-10 is able to mitigate TNF-α-induced NFκB activation and cardiomyocyte apoptosis via the upregulation of ERK 1/2 MAPK and the downregulation of IKK phosphorylation.
Conflict of interest: none declared.
This study was supported by an operating grant from the Canadian Institute of Health Research. P.K.S. is the holder of the Naranjan S. Dhalla Chair in Cardiovascular Research supported by the St Boniface Hospital & Research Foundation. R.C.A. is the recipient of Rudy Falk Clinician Scientist Award. S.D. was supported by a Postdoctoral Fellowship from Manitoba Health Research Council and CIHR/HSFC IMPACT Strategic Training Program Grant in Pulmonary and Cardiovascular Research.


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This is the first batch of delicious Clynelish single malt from That Boutique-y Whisky Company. It's got a lovely flavour, typical of the house style, though with a good dose of sherry thrown in for good measure.
The label depicts a trio of cats, inspired by the grammatically inept felines of the internet. In this instance, a mother cat is scolding a ginger tom (Clynelish), telling him she'd prefer him to be more like his older brother (Brora). This is a reference to the fact that, in the whisky world, Clynelish is often (unfairly) made to play second fiddle to the now-silent, nearby distillery Brora...
This is a release of 197 bottles.
'That Boutique-y Whisky Company' bottles single malts, single grains, bourbons, blended malts and blends from a variety of renowned distilleries. These whiskies are adorned with cultish graphic-novel-style labels.
Nose: Ginger and hints of sea salt. A little overripe grape, orange peel and spice. Dried apricots.
Palate: Coastal, oily mouth-feel with notes of fruit to the fore, particularly cantaloupe melon. A touch of apricot, with a development of sherry, figs and spice.
Finish: Spiced finish. Very fruity now, with gorgeously intense spice notes.
Overall: A fruity, coastal whisky from Clynelish with a lovely sherry flavour.
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Publisher's Description+
From 2 Creative Monsters LLC: My Best Friends Facebook Edition let's you know who comments or like your posts on Facebook the most!- You must have an Facebook account to use this app.
What's new in this version:
We've addressed several bugs and improved stability in this release.** If you like this app, please consider review our app. It only take a minute **
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- HOTTTTTHere's ForteBowie's second new track of the day, "Paid Programming."2,297 Views 3 Comments Feb 2, 2015 at 06:48pm
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This list is made up of items like Sierra Nicole McCormick and Jane Lynch
If you are wondering, "Who are the actors from Monk?" or "Who starred on Monk?" then this list will help you answer those questions.
In most cases you can click on the names of these popular Monk actors and actresses to find out more information about them. If you're looking for a particular Monk actor or actress, then type their name into the "search" bar to find them directly.
- 1
Alona Tal Supernatural, Veronica Mars, Cult
- 2
Bitty Schram Monk
- 3
Jason Gray-Stanford Monk, Taken, Extreme Dinosaurs
- 4
Melora Hardin The Office, Monk, Dirty Dancing
- 5
Stanley Kamel Monk
- 6
Brad Garrett Everybody Loves Raymond, The Transformers, Justice League
- 7
Ted Levine Monk, The Bridge, Crime Story
- 8
Tony Shalhoub Monk, Wings, We Are Men
- 9
Traylor Howard Monk, Two Guys and a Girl, Boston Common
- 10
Brianna Brown Devious Maids, Robbery Homicide Division, Lost at Home
- 11
Brooke Adams Nero Wolfe, Lace, O.K. Crackerby
- 12
Casper Van Dien Shark Attack, Titans, The Veteran
- 13
Craig T. Nelson Parenthood, Coach, The District
- 14
Donald Trump Retrosexual: The '80s, Be Good Johnny Weir, Donald J. Trump's Fabulous ...
- 15
Eric Stonestreet Modern Family, Scare Tactics, This Might Hurt
- 16
Felicia Day Eureka, Dr. Horrible's Sing-Along Blog, The Guild
- 17
Heather Tom Rizzoli & Isles, The Young and the Restless, The Bold and the ...
- 18
Héctor Elizondo Last Man Standing, Chicago Hope, The Pirates of Dark Water
- 19
Howie Mandel Muppet Babies, St. Elsewhere, Bobby's World
- 20
Jane Lynch Glee, Two and a Half Men, Married... with Children
- 21
Jason Alexander Seinfeld, Franklin & Bash, Duckman
- 22
Jeffrey Dean Morgan Supernatural, Magic City, Extreme
- 23
Jeffrey Donovan Burn Notice, Touching Evil, The Beat
- 24
Jonathan Lipnicki The Jeff Foxworthy Show, Meego
- 25
Julie Bowen Modern Family, Boston Legal, Justice League
- 26
Kane Ritchotte
- 27
Kevin Nealon Saturday Night Live, Weeds, Crank Yankers
- 28
Krista Allen Married... with Children, Baywatch, What About Brian
- 29
Lola Glaudini Criminal Minds, Blue Bloods, The Good Guys
- 30
Marguerite Moreau Shameless, Life as We Know It, Firestarter: Rekindled
- 31
Mini Anden Fashion House, MyNetworkTV telenovelas, Sweden's Next Top Model
- 32
Moon Bloodgood Burn Notice, Falling Skies, Journeyman
- 33
Nick Offerman Parks and Recreation, Robbery Homicide Division, Good Morning^! Miami
- 34
Odette Annable House, Life on Mars, Breaking In
- 35
Sarah Silverman Bob's Burgers, Mr. Show with Bob and David, Greg the Bunny
- 36
Sierra Nicole McCormick A.N.T. Farm, Romantically Challenged
- 37
Stanley Tucci Conspiracy, Murder One, 3 lbs
- 38
Sunny Mabrey Memphis Beat, Final Approach
- 39
Tim Curry Darkwing Duck, It, Aaahh!!! Real Monsters


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Center of Innovation
At the MIT ORC, our vibrant community of scholars and researchers work collaboratively to connect data to decisions in order to solve problems effectively—and impact the world positively.
At the MIT ORC, we highly value research and the important role it plays in operations research and analytics. That's why our students are actively engaged in research from the start.Read More
Global Impact
Our impact can be felt around the world in areas ranging from finance to education to health care. We create mathematical models to help individuals and organizations make smarter decisions—and to improve society as a whole.Read More
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The MIT ORC is made up of a supportive community of creative and talented students and faculty who work together to positively impact the world.Read More
Analytics is the science of using data to build models that lead to decisions that add value to institutions, companies, and individuals.
Novel Algorithm Can Improve Outlook for Type 2 Diabetics
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Thanks to smartphones, millions of people now hold the ability to text, tweet, post, and ping in the palm of the
Putting data in the hands of doctors
Regina Barzilay is working with MIT students and medical doctors in an ambitious bid to revolutionize cancer car
Facilitating the Search for Partners on Matching Platforms: Restricting Agent Actions
2/23/2017 | 4:15pm | E51-335
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Comodo Internet Security 3.13.121240 | 38.72 Mb
Comodo claim that their firewall is unique in that it passes all known leak tests to ensure the integrity of data entering and exiting your system. Comodo has put firewall through all kinds of sophisticated tests to ensure its firewall powerful enough to ward off these attacks with default settings. No other firewall has had to work this hard.
* PC Magazine Online's Editor's Choice
* Secures against internal and external attacks
* Blocks internet access to malicious Trojan programs
* Safeguards your Personal data against theft
* Delivers total end-point security for Personal Computers and Networks
* IMPROVED! AV engine now includes more advanced detection techniques
* IMPROVED! Windows XP 64 registry protection has been hardened
* FIXED! Defense+ does not handle object names properly
* FIXED! Defense+ does not protect against registry key ACL modifications
Información (Cómo descargar - NUEVO: Ver Enlaces de Descarga actualizados al 2017):


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This model features three columns which include a two glass door cabinet, two lateral file drawers, one pull-out drawer, along with a full length coat closet.
jazzyexpo.com Executive Office Furniture headquarters, showroom, and warehouse is located in North San Diego at 1332 Rocky Point Dr, Oceanside, California 92056 SEE MAP Telephone (760)727-1190 email
Copyright © 2004-2016 jazzyexpo.com, a division of Starship Worldwide LLC, a California manufacturer of executive office furniture. All rights reserved.


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Perfecting the Shot: Photographing Babies & Toddlers
Lesson 1: Introductionwith Tamara Lackey
About CoursePortrait photography with babies and toddlers might be one of the most challenging subjects you'll ever face. Capturing cute expressions or perfect poses requires just the right balance of patience and persistence. Leading lifestyle and portrait photographer, Tamara Lackey walks you through easy, but useful tips on how to catch those "keeper" shots. You'll follow Tamara, along with two different families in multiple locations, as she teaches her time-tested techniques that are sure to help you respond to shifting moods, feelings and expressions from your smallest of subjects.
- Lesson 1: Introduction 02:35
- Lesson 2: Choosing Clothing 08:11
- Lesson 3: Setting Up the Room 02:56
- Lesson 4: Scouting Outdoor Locations 03:49
- Lesson 5: Bedroom Shoot: Part 1 12:05
- Lesson 6: Bedroom Shoot: Part 2 03:48
- Lesson 7: Bedroom Shoot: Part 3 08:30
- Lesson 8: Outdoor Shoot 09:47
- Lesson 9: Lily: Part 1 06:55
- Lesson 10: Lily: Part 2 10:23
- Lesson 11: Lily: Part 3 05:17
- Lesson 12: Lily: Part 4 07:58
No course objectives yet
No materials available for this course
Tamara Lackey
Tamara Lackey is a renowned portrait photographer and Nikon USA Ambassador whose lifestyle photography, from children's portraits to celebrity portraits, has appeared in dozens of media outlets, including O - The Oprah Magazine, Men's Journal, Vogue, Nikon World, The Martha Stewart Show and The Today Show. The recipient of the 2014 WPPI Adorama Inspire Award, Tamara speaks at a range of venues, from delivering presentations on the Google Stage to speaking at international photography and lifestyle conventions to delivering private workshops around the globe. Tamara has co-produced and hosted a number of live broadcasts and her web series, reDefine Show, is a mix of inspiring stories of top-tier creative artists who make it work with detailed walkthroughs of her photography. The author of four books, her latest are Envisioning Family and The Posing Playbook, and her edutainment media set, "Capturing Life Through (Better) Photography" won the Booklist Editors' Choice Award. Most recently, she was the subject of a 5-part web series Nikon produced about photographing portraits, entitled Nikon Behind The Scenes. For the last eleven years, Tamara has run a busy, associate-based studio focused on portrait, commercial and editorial work. She and her husband, three children, and three dogs all live together in Chapel Hill, North Carolina.
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SkagenSkagen Gitte Orange/White Analog Watch
Rs 7995
SizeFree Size
Flaunt accessories that stand out easily, like this orange coloured analog watch by Skagen. Designed for urbane women, this watch with a leather strap and a round dial will stay in its perfect condition for years to come. It is also water resistant upto 10m and so, can survive through accidental splashes of water. Furthermore, it comes with 2-year warranty.
- MovementQuartz
- Dial ShapeRound
- Dial ColorWhite
- Strap ColorOrange
- Strap MaterialLeather
- Water Resistance10 M
- Product warranty2 Year
- Additional InformationThis Style Is A Factory Surplus Item And May Have Cosmetic Issues, Which Are Not Covered By The Manufacturers Warranty.
- Model NumberSKW2135
- Model StatsMeasurements in the image refer to the case size.
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Meadowlake Ranch
Sand Springs, OK 74063
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South Milford weather map
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Forecast summary
Regional forecast for Yorkshire & Humber
Cloudy with periods of rain and strong winds.
This Evening and Tonight:
Cloud will increase with outbreaks of rain spreading across the region. Rain will be occasionally heavy over the Pennines with widespread hill fog. Chilly over hills at first, becoming milder later. Southwesterly winds will become strong and gusty. Minimum Temperature 3 °C.
Mainly cloudy with periods of heavy rain, mainly over Pennines, and strong gusty winds. Lighter, intermittent rain later with winds moderating. Occasionally bright in the east. Becoming dry overnight. Maximum Temperature 11 °C.
Outlook for Sunday to Tuesday:
Dry start to Sunday, then showery rain and strong winds for a time. Occasionally bright or sunny with sometimes brisk winds and increasingly wintry showers on Monday and Tuesday.
Updated at: 1350 on Fri 24 Feb 2017
UK forecast for the next 5 days
Cold and bright. Turning wet and windy in the north-west.
It will be a cold and bright start with patchy frost and the risk of ice. England and Wales will remain fine and cold with lighter winds, but across western Scotland and Northern Ireland it will become wet and windy.
Unsettled weather will arrive overnight with gales in the north-west and persistent rain across western Scotland and north-west England. Further south it will be drier but cloudy. Mild for all.
Wet and windy weather will spread southwards, with persistent rain on western upslopes of England and Wales. Little rain will reach the east and the north-west will turn drier. Mild.
Outlook for Sunday to Tuesday:
Staying unsettled over the next few days with spells of wet and windy weather for many. Turning colder next week with sunshine and blustery showers, these wintry on the hills.
Updated at: 0156 on Fri 24 Feb 2017
Outlook for the UK over the next 6-30 days
UK Outlook for Wednesday 1 Mar 2017 to Friday 10 Mar 2017:
An unsettled picture is likely at the start of March, as further weather systems affect the UK from the Atlantic. Frontal systems will cross the UK, bringing cloudy and wet weather at times, with some snow over northern hills. It will be rather cold at times in the north, with temperatures closer to average in the south. The changeable Atlantic influence is expected to remain in place through early March, with strong winds and rain at times and possibly gales. Temperatures will be around normal, and possibly a little above average in the south. In between frontal systems, there is likely to be some spells of drier and brighter weather with some showers and patchy overnight frosts.
Updated at: 1221 on Fri 24 Feb 2017
UK Outlook for Saturday 11 Mar 2017 to Saturday 25 Mar 2017:
For the rest of March signals are weak and confidence is low. It will probably be rather unsettled with spells of wet and windy weather at first, interspersed with brighter and showery conditions with some snow possible across the north of the UK. There should, however, also be some drier and brighter spells, where we may see some local frost and fog at times overnight. Temperatures are expected to be slightly above normal for the time of year. However, there remains the possibility of seeing a more prolonged cold spell, with an increased chance of snow in places. This is more likely later in the period.
Updated at: 1219 on Fri 24 Feb 2017
Location Details
South Milford
Location: 53.77805, -1.24274
Altitude: 12.0 m above mean sea level