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KDHE leader voices concerns over flood of EPA regulations
A steady stream of proposed regulations from the Environmental Protection Agency could be a burden for Kansas.
"We are in a period of time where the EPA is coming out with new regulation proposals almost weekly, sometimes it seems like it's daily," said John Mitchell, director of the environment division at the Kansas Department of Health and Environment.
Mitchell discussed those regulations and how they could impact the state as part of his opening remarks Wednesday at the Kansas Environmental Conference in Topeka.
"States are in a position of reduced resources in way of staff and funding, but these new proposals that have come out generally are required to be implemented in a short period of time. That is a challenge for the staff," Mitchell said after his remarks.
In particular, Mitchell is concerned about proposed regulations surrounding air and water quality.
Among the biggest question marks is the possibility of the EPA raising the standards for ozone pollutants, which cause smog. If new standards are adopted, some Kansas cities such as Wichita could be at risk for not meeting the federal agency's standards and would be required to implement a plan to reduce ozone levels.
Kansas also is among the six Midwest states targeted in the Cross-State Air Pollution Rule, which the EPA finalized in July. The new rule requires these states to reduce their nitrogen oxide emissions during the summertime when ozone levels are at their highest. Kansas is also among the 27 states that have to work with power plants to reduce harmful emissions such as mercury, nitrogen oxide and sulfur dioxide.
Phase one of those regulations goes into effect next January and phase two in 2014. While states in the eastern part of the country have had programs in place to prevent cross-state air pollution, those west of the Mississippi have not, Mitchell said.
"The rule is requiring us to really think hard and work with (electric utility) companies in Kansas and figure out how we stay in compliance with new regulations. It's a real challenge," Mitchell said.
The EPA is also focusing on nutrient reduction, mainly for nitrogen and phosphorus levels. The nutrients come from wastewater treatment plants as well as water runoff and groundwater that contains fertilizer.
While the EPA is pushing to set a specific limit for nutrients, Mitchell said the reduction needs to be a shared effort among stakeholders.
High nutrients have become a concern because of the prevalence of large blue green algae blooms in reservoirs and ponds throughout the state. These algae blooms have made people sick and caused animals to die. Mitchell urged the state to take a leadership role in the problem.
"We do need to address nutrient reduction in surface water. We need to do that working together or someone from the federal level is going to do it for us," Mitchell said.
By Christine Metz
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With the 2013 college football kickoff just two weeks away, head coaches and coordinators across the country have had time to create game plans geared to defeat upcoming opponents on both sides of the ball.
But some players are more difficult to account for than others, so Todd McShay put together a ranking of the top 10 matchup nightmares in college football -- the guys who require the most attention because of their ability to single-handedly take over a game.
To read the 10 toughest matchups in college football, click here.

subset: commoncrawl


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Album Rating: 1.0the whole thing feels so dumb, lazy and poorly considered (and to me atleast, exploitative). i get that they're just "fun beats to enjoy" but the arrogance on display during that facttv interview really rubbed me the wrong way. the people claiming this as innovative or intelligent in any way have lost the bloody plot.
Album Rating: 3.5That Foals video is great
Album Rating: 4.0Shame that mix they put out was dreadful
Album Rating: 3.5I was wondering whether we'd seen a Dev review for this.
Album Rating: 4.0I wonder how many 4.5s there are because of the needle drop. I might enjoy this a lot more once I listen to it on my speakers. Currently I am stuck with headphones.
Album Rating: 4.0Gosh, I get all of my music from Fantano
Album Rating: 4.0"The internet's busiest music nerd"
Album Rating: 4.0
"The internet's busiest music nerd"
Album Rating: 4.0 | Sound OffTwitter hashtags and Trill shit
Album Rating: 4.0Already been sorted man
Album Rating: 3.0this is fun, not really my thing though.
I want a DVD version of this with just Lunice dancing the whole time
Really didn't know it was pronounced 'subtract'. My mate asked me what I was listening to the other day, and I was like "sbtrchhhtht" which I realise now makes me a bellend
Only Deviant can write an exceptionally long review on 16 minutes of music!
This is an ability I sometimes wish I had, and I'm sometimes glad I don't. Regardless, awesome read as always. :]
Album Rating: 4.0I started off with a two paragraph max threshold in mind. That didn't hold
Great read though man, I'm gonna check this out tonight
Album Rating: 4.0Do you think anyone will rap over these beats?
Album Rating: 4.0Idk, maybe the success of this will make them stay their hand
Album Rating: 4.5BNM
Album Rating: 4.5 | Sound OffThis is too good, listened to this so much the last few days
Bands: A B C D E F G H I J K L M N O P Q R S T U V W X Y Z


text:
Disrupting the Borg is expensive and time consuming!
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Daily Archives: November 3, 2012
Obama Looking Forward To Getting The Election Over With
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Posted in Uncategorized 14 Comments
Racism Is The Essential Element Of The Obama Campaign
"If you're thinking about voting for Mitt Romney, I would like to make this one plea: black people know who you are and they will come after you" – Bill Maher Bill Maher Warns Romney Supporters: 'Black People Know Who … Continue reading
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Candidates Define Themselves In The Closing Days
Romney wants his supporters to vote for "love of country." Obama wants his supporters to vote for "revenge" against successful Americans
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UK Faces Drought Catastrophe
I am watching the Chelsea/Swansea match being played in freezing cold rain, and remembered that a global warming induced drought threatens to wreck the UK. April 17, 2012 Parts of England face drought 'catastrophe'
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Team climate moron tells us that warmer temperatures lead to more storms – which explains why there are many more storms in winter than summer, and why the most severe storms occur in the Arctic. Warm places like Honolulu and … Continue reading
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wikiHow to Improve Video Streaming
Three Methods:Improving Your Internet ConnectionSpeeding Up Your Computer and SoftwareOptimizing Your Router for Video StreamingCommunity Q&A
These days, watching a movie is as easy as a few clicks of a button. That is, until the film freezes and buffers just as the creepy slug monster sneaks up on the camp counselor. It's often difficult to tell what is responsible for the slowdown. If making improvements to your internet setup, computer usage, and router settings all have no effect, consider a different internet service plan or a different provider altogether.
Improving Your Internet Connection
1Use Ethernet to get a computer online. A wired connection is usually faster than WiFi. Try connecting your computer to the router with an Ethernet cable and you may notice improvements.
- This option is not usually available for mobile devices.
2Get close to your WiFi signal. If you cannot use ethernet, connect to a WiFi signal, as this is much faster than a standard mobile phone's data connection. Move to the same room as the wireless router, or purchase a WiFi range extender to boost the signal across your home.
- See the section on optimizing your router below to further maximize your WiFi signal.
3Turn off competing devices. If you are on a network sharing an Internet connection, disconnect all devices from the network while they are not in use. Additional computers and mobile devices can slow down a video stream considerably.
4Contact your ISP. Call your Internet Service Provider and ask them to analyze your connection for potential problems. Sometimes, the provider can fix an issue on its end that was slowing down your internet. If you have exceeded your data cap for the month, your ISP may be "throttling" your connection, making it much slower until the next billing cycle.
- Upgrading your internet service package is also an option, or switching to a different ISP.
Speeding Up Your Computer and Software
1Close all programs you are not using. If other intensive applications are open, your computer or mobile device may not be able to stream video as quickly as your internet connection would allow. Video games and programs that use the internet can be especially processor-heavy, even if you are not actively using them.
- The rest of this section is focused on computers. If you are using a mobile device, skip down to the router optimization section instead.
2Investigate your computer's memory use. On Windows, open "Task Manager" by pressing Ctrl Alt Delete. On Mac, go to Applications → Utilities → Activity Monitor. Either way, look at the list of processes and decide which ones to close carefully, following these guidelines:
- If you recognize the name of an application, and are not using it, stop it by clicking End Process or Quit Process.
- If you don't recognize the name of a process, leave it alone. If unfamiliar processes are using a large amount of "Memory" or "%CPU," try restarting your computer or scanning for viruses.
3Get rid of viruses. Some malicious viruses force your computer to use its processing power for another person. Download antivirus software if you do not have any installed, and scan your computer for viruses using that software.
4Disable hardware acceleration on older computers. Turning off hardware acceleration will allow your video playback application to set the resource requirements, instead of using your computer's predefined settings. This is a good idea if your computer struggles to handle modern websites and videos, but is not necessary on more powerful devices.
- On a Windows computer, click this link and follow the instructions that match your operating system.
- On a Mac, disable this setting on the Flash player or other video player by right-clicking, command-clicking, or "two-finger clicking" the video itself to bring up the options menu.
5Clear your browser's cache. Go to your browser's preferences and find the cache settings. Clear the cache, or increase the amount of space your browser can use to store information.
- See these instructions for more specific information by browser.
Optimizing Your Router for Video Streaming
1Access your router settings. Access your wireless router settings by typing in your router's IP address, listed here for most common router brands.
2Log in to your router settings. Enter the username and password you selected for your router, or the default password for your brand of router. Once you have accessed the settings, continue reading to optimize your network for video streaming.
3Turn on QoS or WMM. Each company that makes routers organizes its settings a little differently. You may find a link directly to "QoS" or "Quality of Service," or you may need to click through other menus until you notice a QoS setting. Turn this setting to "On" to prioritize video streaming and other high-intensity network usage. On some newer routers, you can turn on the "WMM" setting instead for a similar result.[1]
4Try enabling Burst ACK if possible. If your router has ACK settings, they are likely in the same menu as the QoS settings. Changing your ACK setting to "Burst ACK" may increase your video streaming speed, but it can cause dropped connections, shorter range, or other problems over some connections. Take note of the default setting (typically "Immediate ACK") so you can reverse this change if you notice these problems.
5Upgrade your router. If your wireless router is old, replacing it with a newer model may be a good idea. For best results, purchase a router with the 802.11n standard (and not "802.11n draft") for the best signal, or the newer 802.11ac standard.[4]
- Check that the router's results match its advertising by visiting the WiFi Alliance website and searching for the product name in the upper right search bar. If the product is listed, it has been certified.
Community Q&A
- If video streaming is unusually slow, pause it and wait for it to buffer, or download the video instead if a download link is provided.
- If YouTube will only buffer a small section at a time, change this option using the YouTube Center add-on.
- Keeping your browser or video-streaming app updated is also a good idea.
- Be careful when using the Task Manager or anti-virus software to quit programs. If you don't know what an application or process does, do not shut it off.
Sources and Citations
- ↑ http://www.pcmag.com/article2/0,2817,2399897,00.asp
- ↑ http://kb.netgear.com/app/answers/detail/a_id/23853/~/how-do-i-optimize-video-streaming-performance-with-downstream-quality-of
- ↑ http://www.howtogeek.com/75660/the-beginners-guide-to-qos-on-your-router/
- ↑ http://www.pcmag.com/article2/0,2817,2347539,00.asp
Article Info
Categories: Website Application Instructions
In other languages:
Italiano: Migliorare lo Streaming dei Video, Español: mejorar el streaming de video, Deutsch: Video Streaming verbessern, Português: Assistir Vídeos Online Mais Rapidamente, Français: améliorer la qualité d'une vidéo en streaming, Русский: улучшить потоковое видео, Bahasa Indonesia: Memperbaiki Pengaliran Video, Nederlands: Het streamen van video verbeteren, العربية: تحسين بث الفيديو
Thanks to all authors for creating a page that has been read 1,038,421 times.


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We're happy to share this interview between George R. R. Martin and Bernard Cornwell, whose new book, Death of Kings, goes on sale today.
GRRM: It has long been my contention that the historical novel and the epic fantasy are sisters under the skin, that the two genres have much in common. My series owes a lot to the work of J.R.R. Tolkien and the other great fantasists who came before me, but I've also read and enjoyed the work of historical novelists. Who were your own influences? Was historical fiction always your great passion? Did you ever read fantasy?
BC: You're right - fantasy and historical novels are twins - and I've never been fond of the label 'fantasy' which is too broad a brush and has a fey quality. It seems to me you write historical novels in an invented world which is grounded in historical reality (if the books are set in the future then 'fantasy' magically becomes sci-fi). So I've been influenced by all three: fantasy, sci-fi and historical novels, though the largest influence has to be C.S. Forester's Hornblower books.
GRRM: A familiar theme in a lot of epic fantasy is the conflict between good and evil. The villains are often Dark Lords of various ilks, with demonic henchmen and hordes of twisted, malformed underlings clad in black. The heroes are noble, brave, chaste, and very fair to look upon. Yes, Tolkien made something grand and glorious from that, but in the hands of lesser writers, well ... let's just say that sort of fantasy has lost its interest for me. It is the grey characters who interest me the most. Those are the sort I prefer to write about... and read about. It seems to me that you share that affinity. What is it about flawed characters that makes them more interesting than conventional heroes?
BC: Maybe all our heroes are reflections of ourselves? I'm not claiming to be Richard Sharpe (God forbid), but I'm sure parts of my personality leaked into him (he's very grumpy in the morning). And perhaps flawed characters are more interesting because they are forced to make a choice . . . a conventionally good character will always do the moral, right thing. Boring. Sharpe often does the right thing, but usually for the wrong reasons, and that's much more interesting!
GRRM: When Tolkien began writing The Lord of the Rings, it was intended as a sequel to The Hobbit. "The tale grew in the telling," he said later, when LOTR had grown into the trilogy we know today. That's a line I have often had occasion to quote over the years, as my own Song of Ice and Fire swelled from the three books I had originally sold to the seven books (five published, two more to write) I'm now producing. Much of your own work has taken the form of multi-part series. Are your tales too 'growing in the telling,' or do you know how long your journeys will take before you set out? Did you know how many books Uhtred's story would require, when you first sat down to write about him?
BC: No idea! I don't even know what will happen in the next chapter, let alone the next book, and have no idea how many books there might be in a series. E.L. Doctorow said something I like which is that writing a novel is a bit like driving down an unfamiliar country road at night and you can only see as far ahead as your somewhat feeble headlamps show. I write into the darkness. I guess the joy of reading a book is to find out what happens, and for me that's the joy of writing one too!
Comments (30)
This is awesome. Two of my favorite authors! Thanks for making this interview happen.
Posted by: Mike in Seattle | Wednesday January 18, 2012 at 7:23 PM
This interview was a pleasure to read. As an avid reader of both authors, I always found their writing to be so complimentary of one another. Especially with GRRM and his style of Fantasy having such strong roots in reality. I hope to see a reciprocal interview in the near future!
Posted by: Scruggy | Thursday January 19, 2012 at 5:52 AM
This interview was a pleasure to read! I especially liked the discussion about the 'grey' characters...they too interest me the most :). Thanks for sharing this interview!
Posted by: The Lit Bitch | Thursday January 19, 2012 at 6:22 AM
Awesome my 2 absolute favorite authors! Can't wait for the new books.
Posted by: Bobby Winebrinner | Thursday January 19, 2012 at 12:50 PM
This is by far the greatest thing that has ever happened
Posted by: Rossome | Thursday January 19, 2012 at 2:49 PM
I am knee deep in the "Death of Kings". I've dreamed about doing a series on Uhtred...hope it happens!
Posted by: Ron Newcomb | Thursday January 19, 2012 at 5:07 PM
This was an awesome article. Neat to see that Martin has authors that he deeply admires even though he is a giant in the field as well.
Posted by: Dan Bracewell | Thursday January 19, 2012 at 5:33 PM
I really like this interview as you seemed to have a personal relationship, to an extent, with this author. I would love to read an interview by you with Diana Gabaldon. She's my favorite author, and you are my second. It would be so awesome! Um...thanks ahead of time for even thinking on my suggestion!
Posted by: Can you Interview Diana Gabaldon Next! | Friday January 20, 2012 at 10:58 AM
Great interview!!! I love the work from both authors!!! Wonderful books. I have been reading BC for years. I always feel as if I am part of the past. Now reading the Game of Thrones and I agree. I miss Ned Stark. Really enjoy both authors books! Keep getting into trouble because I can't put them down. Looking forward to more.
Posted by: Kim | Friday January 20, 2012 at 1:23 PM
Great interview. My two favorite authors of all time. (And Bernard's right about Ned!)
Posted by: Adam K | Friday January 20, 2012 at 6:53 PM
Two of my favorite Authors !!! Enjoyed reading this article and enjoy your books even more can't put them down. I think the whole family has finished the newest of what we call the Game of Thrones Series :-) I read Redcoat and the perspective blew me away. Keep it up fellas take your time and we will be waiting.
Posted by: Oakheart | Saturday January 21, 2012 at 7:15 AM
Wow! This is incredible! I got to read a conversation between my two favorite authors! I feel like I should be ashamed of myself for eavesdropping!
Posted by: Dean | Saturday January 21, 2012 at 7:23 AM
I love both of these great writers, cant wait to read the next game of thrones book and the next death of kings. Keep on writing gentlemen, i will allways buy your books
Posted by: Gabriele | Sunday January 22, 2012 at 9:00 AM
Holy crap. Such a fanboy dream come true. I discovered Cornwell through GRRM's recommendations on his site years ago and soon afterwards I devoured The Last Kingdom. GRRM has great taste.
Posted by: CJScribbler | Tuesday January 24, 2012 at 5:51 AM
My favorite authors in one interview, can it get any better? Thanks so much for this glimpse. So glad Bernard is writing just one more Thomas of Hookton tale!
Posted by: Ann | Thursday January 26, 2012 at 12:50 PM
I especially enjoyed Bernard's comments about writing grey characters. I've always greatly preferred conflicted protagonists and multi-faceted antagonists to Dudley Do-Right protagonists and Batman style, one-note antagonists.
He did this so well with Richard Sharpe and his main nemesis Obadiah Hakeswill, who were then masterfully brought to life by Sean Bean and Pete Postlethwaite. Pete, in particular, had this wonderful ability to be both menacing and vulnerable at the same time.
I do hope Bernard will write another Sharpe novel some time so
Posted by: Tracy Smith | Thursday January 26, 2012 at 1:31 PM
I've found this interview to be very interesting. I'm the most avid reader I know, and these are two of my favorite authors. what I love about them is how there novels connect with history ; which is on my checklist when looking for a new series to read. So thanks for the informative interview.
Posted by: Micah Bonewell | Thursday January 26, 2012 at 2:37 PM
I have long been a reader of the great Mr Cornwell, having the full collection of Richard Sharpes adventures, which have all been read multiple times. I was enthralled by my introduction to 'A Song of ice and fire' just before my son wrote a preview article in his magazine of the tv series. He has since gifted me the whole collection, I'm currently in a world that could only truly exist in a book. Both writers have an amazing talent of drawing you into that world. At times feeling exhausted, like i have fought the battles myself. Please keep up the amazing work.
Posted by: Kev Roberts | Thursday January 26, 2012 at 3:11 PM
Imagining the voices...
Posted by: Mateus | Thursday January 26, 2012 at 5:58 PM
I love both of these authors novells and it's very interesting to see them talking to each other.
And I'm even more pleased to see that Mr. Cornwell intends to continue on Uthred, as this is my favourite series from him.
Posted by: gerhard | Friday January 27, 2012 at 12:44 AM
Great to know that there's more Uthred coming as well as Hookton. I have almost read every book written by BC and have enjoyed them all. Have just got into Song of Ice and Fire and am into book 4. I hope GRRM can up the pace of writing a little as I hear it might be a long wait for book 6.
Posted by: Calvin | Friday January 27, 2012 at 1:58 AM
A good interview, though I must admit I am very disappointed in the last question and Mr Cornwell's reply. I am an avid fan of his books, but I have felt the last few (Azincourt, The Fort, the entire Uhtred saga) have fallen well below the standard that was published before, almost to the extent that he is writing for the paycheck.
The Uhtred series especially is now beginning to bore me, Uhtred appears to be single-handedly killing off the Danish warlords; I know that he has similarites to Derval from the Warlord Chronicles, but in my opinion Derval has more character than Uhtred will ever have. Uhtred even comes across as something of a Mary Sue character, especially as Mr Cornwell has stated many times that his ancestors owned Uhtred's lost castle referenced in the novels.
As for the Hookton books... how many more books about archers is he going to release?
Sorry if this seems a rant, but I do like Bernard Cornwell and immensely enjoyed the Sharpe series, the Warlord Chronicles, the Starbuck Chronicles, but his latest offerings are nowhere near the same standard.
Posted by: James | Friday January 27, 2012 at 2:18 AM
I love that Bernard thought Ned Stark should have lived, he must have read a song of fire and ice as regular read not a critic/writer.
Posted by: paul | Friday January 27, 2012 at 8:04 AM
Loved the interview, 2 of my favourite authors. Just need Conn Iggulden and ill be in literary heaven!
As for Uhtred become televised that would be amazing, they were the first books i read of Bernards and i was hooked. Glad to hear that there are more coming!
Posted by: david lugton | Friday January 27, 2012 at 3:43 PM
I've lost my taste for BC. Sorry, but tired of his anti-Christian nature. He could have been different from nearly every other Brit and moved off of that same pattern so many times, opening up so many new possibilities with plots and characters. But no, the same predictable nature remains throughout all his works. I still love the Hookton series and the Warlord Chronicles moved me in such a profound way. Saxon chronicles start off decent but Uhtred starts to grate on me after some time as he quickly becomes an uninteresting brute. He doesn't hold a candle to Derfel's story. But I'm not motivated these days to take up another title by him.
Posted by: Josef | Saturday January 28, 2012 at 10:47 AM


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Leaves allow you to extend your table without compromising the look or style. Choose between creating a large table for a big party or a smaller table for an intimate gathering. These options allow you to create a dining room ideal for any occasion.
Paula's Table features large scale turned posts to anchor its top. The rectangular table top extends from 76 inches long to 112 inches with the use of two 18-inch leaves. With the sophisticated style of this formal dining table and the generous space it provides for diners, it makes a great setting for large gathering and special occasion meals in your home.Complete the table with your choice of coordinating side chairs and arm chairs.
The Paula Deen Home Paula's Rectangular Leg Table by Paula Deen at Morris Home in the Dayton, Cincinnati, Columbus, Ohio area. Product availability may vary. Contact us for the most current availability on this product.
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The Paula Deen Home collection is a great option if you are looking for Transitional
Cottage furniture in the Dayton, Cincinnati, Columbus, Ohio area.
These images are representative of this group as a whole and may differ from this item.
Browse other items in the Paula Deen Home collection from Morris Home in the Dayton, Cincinnati, Columbus, Ohio area.
This item has been tagged as: Table, Dining Tables, Table Set, Dining Table Set, Pub Table, Counter Height Table, Bar Table, Pub Table Set, Counter Height Table Set, Bar Table Set, Dining Room Furniture, Entertaining Furniture, Furniture Sets, Game Table Set, Gaming Tables, Office Furniture, Conference Tables, Meeting Tables, Serving Tables, Kitchen Table, Kitchen Table Set, Bistro Table, Bistro Table Sets, Pedestal Table, Leg Table, Dining Room Tables, Food Table, Table with Leaves, Leaf Table, Dinner Table, Dinette, Dinette Set, Extension Dining Table, Extendable Table
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text:
Brand New, never been lived in Independent 3 Bedroom Villa!!!
This villa is available now- Please call Laura on- 0509189494 to arrange a viewing.
I also have 3, 4 & 5 Bed Villas Available for RENT & SALE
Actual photos of Villa.
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There is also Blossom Nursery, Bbq areas, tennis courts, playgrounds and community pools and mosque. Soon to be opened Fitness First.
About Us-
Belleview Real Estate Broker was established in 2003. We are a specialist agency registered in the Emirate of Dubai.Our specialist leasing service is tailored to meet both the Land Lord and tenant requirements in terms of onsite support, comprehensive documentation following RERA guidelines, proper follow ups with both land lord and Tenant as well as optional turn-key solutions including furnishing, interiors and other move in assistance. Our business growth has been a result of regular referrals which we have found to be the key to success in this niche area. For us, client referrals are the ultimate testimonial. With our expertise, experience and professionalism we look forward to serving your real estate requirements.


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Palin is given protection from McAdoo man
JUNEAU, Alaska (AP) - Sarah Palin has been granted a restraining order against a McAdoo man accused of stalking and threatening her.
Alaska Magistrate Judge Colleen Ray issued a 20-day protective order Monday against 18-year-old Shawn R. Christy, finding probable cause to believe he had stalked the former governor.
Palin and her attorney claimed Christy had made implied threats through phone and written messages, including making references to gun, allegedly telling Palin to watch her back and saying he was buying a one-way ticket to Alaska and sending a receipt for a gun purchase.
Christy was ordered to have no contact with Palin's family and to stay a mile away from her home.
A message left for Christy at his home in McAdoo, wasn't immediately returned.
The Mat-Su Valley Frontiersman first reported the case.


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FAQ for Guardians
Common Questions from Guardians of LGBTQA Individuals
Why did our family member have to tell us?
When a person decides to come out to their loved ones, they are expressing a desire to be open and honest. They may feel the need to be honest and open to the people they love, are close to, and care about. It can be a very difficult admission for someone to make, and support is needed. Understanding from the people that mean the most to them is vital. Some guardians may initially feel it would be better if they did not know. These are natural feelings.
Please explore the Coming Out section of the LGBTQA WebCenter for more information about what Coming Out is like for someone and what someone may be experiencing. We also encourage you to watch the free short documentary Leading with Love to see what the Coming Out process was like for other parents. The Parents Project, Our Daughters and Sons: Questions and Answers for LGBT Youth and Adults, and Out Proud Families are also excellent resources for guardians with LGBTQ children.
Is this just a phase?
Homosexuality is not a phase or something a person chooses to be. Hopefully you are able to take time and be thankful that your loved one feels close enough to you that they know your love for them will not fade. It is important to remember that nothing about someone is different after they tell you about their sexuality. They are still the same person whom you have known for their whole lives.
It is true some people do experiment with their sexuality, but someone who has reached the point to come out to you has thought for a long time about their sexuality. This is something that someone has take time to think about, and they are now ready to include you in this significant part of their life.
Why did they take so long to tell us?
It is normal for guardians to feel guilty or worried because their loved one has gone through so much on their own before sharing information about their sexuality. Sometimes it can take and individual years to come to the realization that they may be gay, lesbian, bisexual, or transgender.
Guardians may interpret this as being a lack of trust or lack of love. It can also be painful to realize that you didn't know your loved one as well as you thought. Remember how hard it may have been for your loved one to come to terms with his or her sexuality.
It is common to feel disappointed because your loved one did not tell you this information sooner, but remember what picture our society paints. Your loved one may have not known your feelings on sexuality or maybe they knew too well your feelings on this subject.
Why is our loved one gay?
It is common for guardians to feel that their loved one's sexuality is somehow their fault. This is not true. It is not really known for what makes and individual homosexual, bisexual or transgender, but it is known is sexual identity has nothing to do with the way and individual has been brought up. Gay, lesbian, bisexual, and transgender individuals come from all backgrounds. No one is at fault for having a loved one that identifies as LGBTQ.
Why am I uncomfortable with my loved one's sexuality or gender?
Uncomfortable emotions with anything that is different from the norm and different from what may have been planned are natural and common. Mapping out a loved one's future unknowingly happens to most guardians. It is easy to believe that your loved one's future is drastically going to be change when they come out.
It is also common to believe that now a loved one will have to live a life of secrecy and not get married and not have grandchildren. Some guardians may believe that their child can not possibly be happy being heterosexual.
All of these struggles are common. All LGBTQ individuals have the potential to find happiness just as heterosexuals do. They can still be happy, successful, have a lifetime partner, and even have children.
Take time to research more information about LGBTQA culture and identity. The LGBTQA Web Center is ripe with information that will prove valuable in your research.
Why must our loved one flaunt their sexuality?
They are being themselves. Showing and receiving affection from someone you love is very important for a person's well being.
In fact many LGBTQ people are more likely not to show affection in public because of the negativity that it may bring. Sometimes when our loved one comes out they may change the way they dress or cut their hair. These changes may be a shock to you. They are just feeling free to be who they are now they have come out.
Should we tell extended family and friends?
Coming out for a lesbian, gay, bisexual or transgender person can be very difficult. Coming out for a guardian can be very difficult as well. Before you tell family or friends please ask your loved one's permission. You will be discussing their personal sexuality and it is important to keep in mind how private this matter can be to some individuals.
Will my child be ostracized, have trouble keeping a job, or even be physically attacked?
Unfortunately there is no clear answer. This can happen to some people, but not everybody and not all the time. There are some individuals that these issues may arise with and others are lucky to never experience these items. While overall society has still got a long way to go, you may be surprised that people in general are far more accepting of LGBTQ people.
Gay rights groups are working all the time to help to fight discrimination in schools and work places. They also have fought to change laws against homosexuals and their rights.
To find out more about these groups, check out the National Resources page of the LGBTQA WebCenter.
Will my loved one get AIDS?
It is important to share safe sex practices with your loved one regardless of sexual orientation. If they practice safe sex by always using a condom, water based lubricant and also does not share needles, they greatly minimize any risk associated with contracting HIV/AIDS.
It is also valuable to remember that HIV is not a gay disease; Everyone is at risk. All individuals should be educated in how to prevent being infected with HIV. Prevention is the best solution as there is no cure.
Will my child become a pedophile?
It is a common serotype the pedophilia is synonymous with the LGBTQ community. This is not true. Pedophilia and other forms of child abuse mainly happen in the child's home environment and are most often perpetrated by a family member or close friend of the family.


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Over the past 80 years, physiological research has moved progressively in a reductionist direction, providing mechanistic information on a smaller and smaller scale. This trend has culminated in the present focus on "molecular physiology," which deals with the function of single molecules responsible for cellular function. There is a need to assemble the information from the molecular level into models that explain physiological function at cellular, tissue, organ, and whole organism levels. Such integration is the major focus of an approach called "systems biology." The genome sequencing projects provide a basis for a new kind of systems biology called "data-rich" systems biology that is based on large-scale data acquisition methods including protein mass spectrometry, DNA microarrays, and deep sequencing of nucleic acids. These techniques allow investigators to measure thousands of variables simultaneously in response to an external stimulus. My laboratory is applying such an approach to the question: "How does the peptide hormone vasopressin regulate water permeability in the renal collecting duct?" We are using protein mass spectrometry to identify and quantify the phosphoproteome of collecting duct cells. The response to vasopressin, presented in the form of a network model, includes a general downregulation of proline-directed kinases (MAP kinases and cyclin-dependent kinases) and upregulation of basophilic kinases (ACG kinases and calmodulin-dependent kinases). Further progress depends on characterization and localization of candidate protein kinases in these families. The ultimate goal is to use multivariate statistical techniques and differential equations to obtain predictive models describing vasopressin signaling in the renal collecting duct.
- aquaporin-2
- signaling networks
- collecting duct
- phosphoproteomics
- mass spectrometry
- Nedd4-2
Vasopressin Action in the Kidney
The most distal segments of the renal tubule, the connecting tubules and collecting ducts, have variable water permeability that is controlled in response to the peptide hormone vasopressin, allowing water excretion to vary physiologically (46). These renal tubule segments express three molecular water channels called "aquaporins" (57). These are aquaporin-2 (AQP2), aquaporin-3 (AQP3) and aquaporin-4 (AQP4). AQP2 is present in the apical plasma membrane and in endosomes (6, 20, 56). The latter two aquaporins are seen chiefly in the basolateral plasma membrane (16, 71). Although there is evidence for regulation of the basolateral water channels by vasopressin (15, 16), it seems clear that the regulation of water permeability of the collecting duct epithelium is mediated largely through vasopressin's effects on AQP2 (57).
There are at least two modes of water permeability regulation in the kidney corresponding to two processes that control the amount of active AQP2 in the apical plasma membrane. The first mode is "short-term regulation" occurring over a period of 5–30 min as a result of the regulation of trafficking of AQP2-containing membrane vesicles to and from the apical plasma membrane in response to vasopressin (55). The second mode is "long-term regulation" occurring over a period of hours to days as a result of regulation of whole cell AQP2 abundance by vasopressin (13, 28, 56). Both modes depend on the binding of vasopressin to V2-type vasopressin receptors (gene symbol: Avpr2)1 present in the basolateral membrane. The downstream signaling events that are pertinent to the two modes of regulation are, however, largely undiscovered. In this review, I discuss application of systems biology techniques to the discovery of the signaling processes that are triggered by V2 receptor occupation in the renal collecting duct.
Reductionist Versus Integrative Approaches to Biology
Over the past 80 years, research in the field of physiology (and biological study in general) has proceeded in a reductionist direction, dealing with smaller and smaller structural levels (Fig. 1). Taking renal physiology as an example, in the 1930s, whole animal or whole person studies were the major sources of information employing clearance techniques. This allowed information to be gleaned about the three major processes determining excretion, namely glomerular filtration, secretion, and reabsorption (69). The rise of micropuncture (21) and the isolated perfused tubule technique (7) during the 1960s changed the focus of renal physiology to a tissue level, providing information about each of the nephron segments or about the glomerulus. Application of these techniques together with biochemically based techniques such as transport measurements in isolated brush border vesicles (54) provided a wealth of detail about transport mechanisms. This knowledge paved the way for the next major era in renal physiology in the 1980s and 90s, during which cDNAs for many of the important renal transporters were cloned and sequenced. This development switched the emphasis from a tissue and cellular level down to a molecular level. Success in cloning many of these cDNAs was greatly abetted by the development of the Xenopus oocyte expression system (12). This expression cloning approach allowed cDNA pools and ultimately single cDNAs to be selected on the basis of functional assays that were designed utilizing the findings of isolated perfused tubule experiments, micropuncture experiments, and isolated brush-border vesicle experiments done in the preceding decades. Thus by the mid- to late 1990s renal physiologists had obtained the primary structure of the proteins that mediate the most important transport processes along the nephron. The cDNAs could then be expressed in cultured cell lines or in Xenopus oocytes and studied, either in native form or mutated form, to gain a greater understanding of the relationship between protein structure and function. Thus, by the end of the 20th century there had been a spectacular expansion of information about transport in the kidney based on a progression of knowledge from reductionist approaches.2
Because of the drive toward reductionism in physiology, we have achieved a high level of understanding of structure and function of many of the individual proteins that mediate important physiological processes including transport along the renal tubule. However, knowledge of molecular structure and function does not necessarily imply a mastery over the physiological knowledge needed to understand disease processes in humans. Most human disease is not easily explained as an effect of a single dysfunctional gene and protein, but rather often represents complex phenomena that depend on nonlinear integration of the functional properties of many proteins. Even so-called "monogenic" diseases have polygenic consequences. Likewise, normal physiological phenomena at the organism or organ level can rarely be understood from knowledge about a single protein. Therefore, there is a need to develop methods to integrate information about the molecular functions of individual proteins and their molecular interactions to create predictive models of cellular, tissue, organ, and whole organism function (Fig. 1). The ultimate goal is to understand disease processes and to discover how to treat them. Thus, there is a need for integration, i.e., learning how many small pieces can assemble into larger ones to create complex emergent behavior. This integration process has been referred to as "systems biology."
Systems Biology and Physiology
Data-poor systems biology.
Systems biology is not a new approach. Starting in the 1960s and 70s with the advent of mainframe computers, various investigators used differential equation-based mathematical modeling to integrate data from the literature. The differential equations were constructed to represent physical principles such as mass balance, energy balance, and various laws that represent the relationships between driving forces and movements of various substances, e.g., nonequilibrium thermodynamics (42). Typically, data from a myriad of sources were used in parameter estimation in these models, a labor intensive process that could only be done manually, assigning one parameter at a time. This type of systems biology has been referred to by Westerhoff and Palsson (74) as "data-poor" systems biology. Despite its laborious nature, this approach has been very productive. For example, models of the kidney concentrating mechanism (75) have been useful in generating hypotheses that could be tested experimentally (26). My own mathematical modeling of the kidney medulla [done as part of my PhD dissertation (44)] led to the conclusion that a specialized urea transport mechanism was required in the inner medullary portion of the collecting duct to explain the observed cortico-medullary urea gradient. This observation from mathematical modeling stimulated a series of studies using isolated perfused inner medullary collecting ducts that ultimately demonstrated the predicted transporter (10, 11, 45, 65), eventually leading to the cloning of corresponding cDNAs (41, 68, 76) and gene knockouts of collecting duct urea transporters in mice (17, 18).
Data-rich systems biology.
With the advent of genome sequencing projects for various animals, plants, and microorganisms at the beginning of the current century, systems biology has moved to a so-called "data-rich" format (74). As a result of these sequencing projects, we can now limit our view to a finite set of protein-coding genes (approximately 21,000 in humans, mice, and rats) when looking for protein species that may explain a particular physiological phenotype. This translates to a finite set of molecular hypotheses. More importantly, the genome sequence information has made possible a set of technologies that are capable of providing genome- or proteome-wide read-outs of physiological experiments. These large-scale data acquisition techniques include protein mass spectrometry (58), hybridization-based expression microarrays (3), and deep sequencing of nucleic acids (27). Each of these modalities allows the experimenter to identify the cellular responses to physiological stimuli comprehensively across the entire proteome, transcriptome, or epi-genome. Such experimental approaches are becoming relatively straightforward and can be readily applied to a variety of physiological problems at the cellular level.
To some extent such experiments can be interpreted through direct perusal of the data. For example, a protein mass spectrometry study of renal inner medullary collecting duct cells isolated from rat kidneys showed that vasopressin changes the phosphorylation of the aquaporin-2 water channel at four sites near the carboxyl terminus of the protein (30, 34), a finding that has spawned numerous follow-up studies both within our own laboratory and in others. Additional studies revealed the presence of three vasopressin-regulated phosphorylation sites in the vasopressin-regulated urea transporter UT-A (5).
However, most of the information present in large-scale data sets from these technologies cannot be so easily interpreted, and requires computational approaches aimed at achieving large-scale data integration to create models describing the interactions among the relevant proteins. In a particular physiological experiment involving a given physiological perturbation, the large-scale integration task often consists of two major elements: 1) analysis of the responding proteins, transcripts, or genes within a data set to determine how the responding entities are related to one another functionally; and 2) analysis of the responding proteins, transcripts, or genes to determine their relationships to information that has been obtained in previous studies. The latter analysis typically results in the generation of a so-called "network" consisting of "nodes" and "edges" (Fig. 2). For a protein network, the nodes represent individual proteins and the edges are the relationships between proteins. A pair of nodes and edges that connect them can be viewed as a grammatical sentence known as a "triplet," where one node is the subject, the edge is the verb, and the other node is the direct object. In the example shown in Fig. 2, the sentence represented is "Protein kinase A catalytic subunit phosphorylates aquaporin-2." Large numbers of triplets can be merged into directed graphs like that shown in Fig. 3 depicting the vasopressin-signaling network for the renal inner medullary collecting duct based on phosphoproteomic studies (33).
To carry out large-scale data integration needed for generation of network models, databases of triplets (also known as "protein interactions") can be gleaned from the general literature to identify possible interactions between nodes of the physiological system under study. There is a major effort within systems biology to develop computer-based text mining algorithms that can extract appropriate information (i.e., triplets) from the literature to create these databases (29). Lacking full success in this area, a number of databases have been constructed chiefly through manual curation. These include two commercially available databases within Ingenuity Pathway Analysis and Metacore software suites. These approaches and others like them are useful in organizing large data sets but continue to have significant limitations with regard to the ability to construct causal models (43, 53, 67). Consequently, the network models that can be produced with today's technologies fall short of having the predictive power of differential equation-based models. Nevertheless, network models like that shown in Fig. 3 provide a useful way to consolidate and visualize the findings of large-scale experiments.
Using Mass Spectrometry to Construct a Vasopressin-Signaling Network for the Renal Collecting Duct
My laboratory is using systems biology approaches to identify the vasopressin-signaling network responsible for regulation of water permeability in the renal collecting duct. The studies use liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) to identify and quantify thousands of phosphorylation sites in native inner medullary collecting ducts isolated from rat kidneys (5, 33, 34) and in cultured mouse mpkCCD(clone 11) cells (62). Figure 4 shows a general scheme describing how LC-MS/MS can be used to identify thousands of peptides in a given biological sample. Application of the method to identification and quantification of phosphopeptides has been the subject of several reviews (31, 32, 59, 61).
The studies aim to identify a signaling network (Fig. 5) linking the input (a change in the concentration of vasopressin in the extracellular environment) to a key output (a change in the amount of active aquaporin-2 in the apical plasma membrane). The signaling network to be identified (yellow box) is the set of proteins in the collecting duct cell that link the input to the output, carrying information via a sequence of biochemical changes in the cell. We can identify two subtasks (Fig. 5, bottom): 1) identification of the protein components of the system, i.e., the proteins expressed in collecting duct cells including their posttranslational modifications; and 2) determination of how these components interact.
Identification of system components.
The former subtask is the easiest of the two. Application of standard transcriptomics (from microarray studies or RNA-seq) and proteomics analysis has identified most of the gene products expressed in native inner medullary collecting duct cells and in mpkCCD(clone 11) cells. This information has been placed on publicly accessible databases described by Huling et al. (37) and available at http://helixweb.nih.gov/ESBL/Database/ or https://intramural.nhlbi.nih.gov/labs/LKEM_G/LKEM/Pages/--TranscriptomicandProteomicDatabases.aspx. Collecting duct cells appear to express approximately 8,000 out of the 21,000 protein coding genes in the genome, and the user can easily identify by searching these databases whether a given protein or a related protein is expressed in these cells. Indeed, these databases can be interrogated online in a variety of ways or the entire database can be downloaded by the user.
Databases enumerating phosphorylation sites that have been identified in collecting duct proteins (as well as proteins in other renal tubule segments) are available at the same URLs listed in the previous paragraph. In general, these phosphorylation sites are modifications of the side-chains of serines, threonines, or tyrosines through covalent attachment of a phosphate group. The phosphate addition produces characteristic changes in the mass-to-charge ratio of peptides that can be recognized by the mass spectrometer. The databases have been derived from a number of LC-MS/MS-based studies profiling phosphorylation sites observed in collecting duct cells (5, 33, 34, 36, 62, 79) and other kidney cells (19, 23).
Protein phosphorylation databases provide useful tools for the study of cell signaling. However, other types of posttranslational modifications are important in cell signaling (including glycosylation, acetylation, methylation, S-nitrosylation, SUMO-ylation, and ubiquitylation) and their identification could provide key information regarding the nature of vasopressin action in the collecting duct. However, protein phosphorylation plays a preeminent role in vasopressin signaling and so has drawn most of our attention.
Determination of how system components interact.
The second subtask described below (Fig. 5, bottom) requires that LC-MS/MS be adapted to allow quantification of proteins and phosphorylation sites. The quantification techniques available include label-free methods and labeling approaches such as Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC) and isobaric Tags for Relative and Absolute Quantitation (iTRAQ). The technical details of these approaches have been reviewed previously (8, 58, 59) and are beyond the scope of this paper. We used quantitative phosphoproteomics methodologies to determine what phosphorylation sites undergo changes in abundance in response to vasopressin (using the V2 vasopressin-receptor selective analog dDAVP) both in suspensions of native inner medullary collecting ducts (4, 33, 34, 36) and in cultured collecting duct mpkCCD cells (62). The proteins that bear the changes can then be considered elements (nodes) in the vasopressin signaling network (Fig. 3), although they are not necessarily involved in regulation of aquaporin-2 or water permeability. Indeed, elements of Fig. 3 point to potential roles of vasopressin in processes that may be unrelated to regulation of transport. For example, a set of proteins that contain vasopressin-regulated phosphorylation sites are involved in regulation of programmed cell death or apoptosis (Fig. 3, turquoise background: Bad, Bok, Pak2, Bcl2l14, and Tp53bp). The direction of these phosphorylation changes suggested the hypothesis that vasopressin inhibits apoptosis, which was confirmed by direct experiments (33). Other regions of Fig. 3 are enriched for proteins in the Wnt signaling pathway (green background: Ctnnb1, Lrrfip1, Lrrfip2, Csnk1e, Tnik, and Phkb), and pathways involved in the regulation of various MAP kinases (pink background) including p38 (Mapk14) and Jnk2 (Mapk9). The phosphorylation changes seen for p38 and Jnk2 are consistent with inactivation of these kinases by vasopressin as seen previously for additional MAP kinases, viz. Erk1 and Erk2 (60). Finally, the results showed changes in phosphorylation of two proteins involved in regulation of protein degradation, namely Nedd4-2 (Nedd4l) and Ankyrin repeat and SOCS box protein 4 (Asb4). Nedd4-2 is a well-characterized ubiquitin E3 ligase in the renal collecting duct that is involved in the regulation of the epithelial sodium channel ENaC (70). Since, the inner medullary collecting duct exhibits little or no sodium transport activity (64) and only very low levels of ENaC expression (25), we speculate that Nedd4-2 may be involved in regulation of water or urea transport in this segment. In general, it can be assumed that a subset of the vasopressin-induced phosphorylation events depicted in Fig. 3 play roles in the regulation of aquaporin-2. The identification of these phosphorylation changes will require additional studies using systems techniques (described in the remainder of this review) to dissect different pathways within the overall network.
Identification of Protein Kinases Responsible for Regulated Phosphorylation in the Collecting Duct
The phosphoproteomics studies discussed in the last section identified a large number of phosphorylation sites in the collecting duct that exhibit altered abundance in response to vasopressin. These sites and their associated proteins represent nodes in the vasopressin signaling network (Fig. 3). The edges drawn in Fig. 3 are tentatively identified based on our reading of the literature and did not employ any of the available databases for automatic generation of a network architecture. Hence further studies are needed to assemble these nodes into a causal network that can explain how vasopressin regulates aquaporin-2 location and expression in the renal collecting duct. The general question under consideration is therefore how to draw the correct edges representing causal interactions between nodes. One way to address this is to identify the protein kinases and protein phosphatases involved in regulating the level of phosphorylation at each of the regulated sites. Our current focus is on the protein kinases.
Approximately 518 protein kinases are expressed in mammalian genomes (49). Only a fraction of these protein kinases are expressed in renal collecting duct cells. Collecting duct kinases have been identified in transcriptomic profiling experiments using Affymetrix expression arrays. This approach has provided a comprehensive list of genes expressed in native inner medullary collecting duct cells (73) and in mpkCCD cells (77). Among the genes expressed in both cell types are those that code for 154 protein kinases (Fig. 6). Thus, through transcriptomic profiling we have reduced the list of protein kinases that are candidates for roles in vasopressin signaling by 70% (from 518 to 154). These kinases can be classified into distinct families based on sequence similarities (Fig. 6). In the following, we discuss a strategy for narrowing down the list of protein kinases to the few that are likely involved in vasopressin signaling.
It is widely accepted that prediction of what protein kinases phosphorylate particular protein targets depends on two types of constraints (48): 1) linear target motif specificity based on the amino acid sequence just upstream and downstream from the phosphorylation site in the target protein; and 2) requirement for physical propinquity of the kinases and their prospective targets in the same subcellular compartment.
Linear target motif specificity.
A phosphoproteomic study by Rinschen et al. (62) provided key information that narrows the possible kinases involved in vasopressin signaling to fewer than the 154 protein kinases specified in Fig. 6. This study identified 273 phosphorylation sites that were increased and 254 phosphorylation sites that were decreased in response to dDAVP exposure across the mpkCCD cell proteome. When the sequences surrounding the sites that were increased were analyzed together it was found that there was a predominance of basic amino acids (lysines and arginines) upstream from the phosphorylated amino acid. Such sites are compatible with the conclusion that vasopressin activates so-called "basophilic" protein kinases. Basophilic kinases include those from the AGC protein kinase family (AGC in Fig. 6) and those from the calmodulin-activated kinase family (CAMK in Fig. 6). This narrows the potential kinases that are activated by vasopressin to the 40 kinases from the two families that are expressed in collecting ducts. In contrast, when the sequences surrounding the 254 phosphorylation sites that were decreased by vasopressin were analyzed, a predominance of sites with a proline in the amino acid following the phosphorylated amino acid was found. This consensus is compatible with the conclusion that vasopressin reduces the activity of so-called "proline-directed" protein kinases, which include those from the MAP kinase family and cyclin-dependent kinase families (CMGC in Fig. 6). Only 20 of these are expressed in native inner medullary collecting duct cells and mpkCCD cells. From these considerations, we have narrowed the number of protein kinases that are likely to be involved in vasopressin signaling by more than 88% (from the 518 present in the genome to 60). Some of these kinases are already present in the vasopressin signaling network (Fig. 3) since they are phosphorylation targets (e.g., Camkk2, Mylk, Prkar1a, Phkb, Tnik, Pak2, Mapk9, and Mapk14).
Thus, it is practical to classify protein kinases within general families based on the linear sequence surrounding their target phosphorylation sites. The question remains whether the sequence surrounding a particular phosphorylation site is ever specific enough to identify a single protein kinase that is responsible for a phosphorylation event without additional information. For example, the sequence R-R-X-pS-X (where pS indicates a phosphorylated serine) is often cited as evidence of involvement of one of the protein kinase A isoforms in the phosphorylation event. A number of experimental approaches have been used to identify target sequence preferences for specific protein kinases: 1) curation of sequences of known substrates of a given kinase from multiple literature studies (2); 2) in vitro phosphorylation of peptide arrays (38, 72); and 3) use of mass spectrometry to identify phosphopeptides from native tissues that are phosphorylated as a result of in vitro incubation with recombinant, active protein kinases (14). Many of the consensus sequences reported in the literature are summarized in a database called HPRD (Human Protein Reference Database; 22). A useful compendium of protein kinase sequence preferences derived from peptide array studies has been published as the NetPhorest Kinase Motif Atlas (52). Some data from mass spectrometry-based kinase substrate profiling (14) is shown in Fig. 7 listing target sequence preferences for three basophilic protein kinases expressed in collecting ducts {protein kinase A catalytic subunit α [Prkaca], death-associated protein kinase 1 [Dapk1], and Ca2+/calmodulin-dependent protein kinase II-δ [Camk2d] as well as two proline-directed protein kinases [mitogen-activated protein kinase p38α (Mapk14) and glycogen synthase kinase-3β (Gsk3b)]}. Comparing the first two basophilic kinases, protein kinase A (catalytic-α) and death-associated protein kinase 1, it can be seen that both have a preference for basic amino acids in positions −2 and −3 relative to the phosphorylated serine. Thus, a target sequence R-R-X-pS-X would be compatible with phosphorylation by either of these two kinases, and it may be necessary to rely on the amino acids downstream from the phosphorylation site to discriminate the two. In contrast, the preference for basic amino acids in Ca2+/calmodulin-dependent protein kinase II-δ is shifted upstream to the −3 and −4 position, overlapping the sequence preference reported for Akt and related kinases (22, 52). In general, examination of the data of Douglass et al. (10) together with the NetPhorest Kinase Motif Atlas, and the HPRD, indicates that there may be too much overlap between target sequence preferences to expect to be able to reliably assign the specific protein kinases responsible for a given phosphorylation event solely from sequence data. A comparison of the target sequence preferences for the two proline-directed kinases in Fig. 7 leads to a similar conclusion. Consequently, other approaches must be taken to reliably assign edges to the nascent vasopressin-signaling network depicted in Fig. 3.
Requirement for physical propinquity of the kinases and their prospective targets.
It is self-evident that a given kinase can only phosphorylate a target protein if the two come into physical contact. Thus the requirement for colocalization is a useful constraint that can be used to rule out certain kinases that would otherwise be considered candidates for phosphorylation of a given protein based on linear sequence preference (Fig. 3). The subcellular localization of the kinases and substrates can be addressed by a variety of approaches including 1) biochemical separation of subcellular fractions (63, 78) followed by either immunoblotting or mass spectrometry of the fractions to identify the protein amounts in the fractions; and 2) microscopy-based techniques including confocal immunofluorescence and immuno-electron microscopy. It is important to remember that many protein kinases are regulated through processes that involve translocation of the protein from the cytosol to a membrane-bound state (9), so that the colocalization of enzyme and substrate needs to be sought under conditions compatible with activation of the kinase. Many kinases "find" their targets by mutually binding to the same multiprotein complex. Examples include Gsk3β and β-catenin in the canonical Wnt pathway (51), protein kinase A and various substrates via AKAP family proteins (50), and the protein kinases in MAP kinase cascades through the aid of scaffold proteins (47). Hence, it may be practical to identify kinase substrates in a given cell type by immunoprecipitating the kinase under conditions in which the associated proteins are likely to remain bound and then identifying them by mass spectrometry. An important requirement for most of these approaches is the availability of high-quality antibodies or the ability to generate them. With this requirement in mind, we have produced an online antibody-design software application called NHLBI-AbDesigner (http://helixweb.nih.gov/AbDesigner/). This tool allows the user to identify regions of the protein that are predicted to be relatively immunogenic. These peptide sequences can be synthesized, linked to a carrier protein, and used to immunize rabbits or mice.
Identification of Protein Kinase Networks Using Multivariate Statistical Analysis and Protein Kinase Inhibitors
Above, I have proposed that two types of information are key to narrowing down the possible network configurations that could explain the input-output behavior of the collecting duct in its response to vasopressin: 1) determination of the target sequence specificities of every kinase expressed in collecting duct cells; and 2) determination of the subcellular locations of each kinase relative to all potential targets. Thus, once all this information has been collected, hypothetical network models can be proposed. How can these hypothetical models be tested? Two sets of tools will allow us to do the critical hypothesis testing experiments: 1) extensive collections of drugs developed as protein kinase inhibitors; and 2) a set of data analysis techniques that are classified under the general moniker of "multivariate statistical approaches." I deal briefly with these in the following.
Protein kinase inhibitors.
Because protein kinases have long been viewed as druggable targets chiefly for therapy of malignancies, there exists a wide range of agents that can inhibit protein kinases, many with at least moderate selectivity. Since phospho-specific antibodies are available for many of the vasopressin-regulated phosphorylation sites that we have found in our mass spectrometry-based studies, it will be practical to screen protein kinase inhibitor compounds for their abilities to alter phosphorylation in collecting duct cells. For example, drugs that have been identified to alter aquaporin-2 phosphorylation at any of its four carboxyl-terminal sites can provide useful tools to probe the entire network if the drugs exhibit at least a degree of selectivity. Many of these agents have been characterized before, giving clues to which kinases they may inhibit. However, such agents can be useful even if their kinase targets are not known, or are diverse, if used in experiments involving multivariate statistical analyses.
Multivariate statistical analysis.
The simple idea is that phosphorylation events that correlate highly across a variety of perturbations are likely to be functionally related. They may for example be downstream from the same protein kinase or may be elements present in a cascade of enzymatic reactions. Conversely, phosphorylation events that correlate poorly across a variety of perturbations can be expected to be more distant in the overall signaling network. Based on this concept, experiments can be done in which proteome-wide phosphoproteomic read-outs are obtained for a battery of protein kinase inhibitor molecules at a variety of concentrations. One can then identify the phosphorylation sites that correlate most closely with sites known to be involved in regulation of water transport, e.g., the four phosphorylation sites at the COOH-terminal tail of aquaporin-2 that are believed to be involved in water channel trafficking (34, 35) or serine 552 of β-catenin which is thought to be involved in the regulation of the expression of the Aqp2 gene (66). There exist standard statistical methods for identifying correlations in large data sets, e.g., partial least squares analysis (24, 39, 40). Such approaches identify underlying relationships that allow the network to be partitioned into modules or subdomains that can be investigated experimentally. Ultimately, so-called "structural equation modeling" (1) can be employed to provide a means to map the data into directed graphs and to optimize the fit between the derived network structure and the data.
Here I have described the use of systems biology tools to carry out integrative study of physiological systems at a cellular level. I have illustrated the approaches with data from my own studies focusing on the question, "How does the peptide hormone vasopressin regulate water permeability in renal collecting duct cells?" These studies have exploited phosphoproteomics methodologies to reveal phosphorylation events within the cell that are triggered by vasopressin. Based on the results, we have begun to assemble vasopressin-modulated phosphoproteins into functional networks that may explain the regulation of the water channel aquaporin-2. In addition to phosphoproteins that are involved in transport regulation, the studies have revealed phosphoproteins that point to other processes in collecting duct cells that appear to be regulated by vasopressin. The studies have generated extensive lists of proteins and phosphorylation sites identified in collecting duct cells that have been placed online in the form of user-accessible databases that can be interrogated in various ways.
Both the old-style data-poor approach using differential equations to describe complex systems and the new-style data-rich approach using multivariate statistical analysis and graph theory to create relational models can be exploited to investigate physiological systems at the cellular level. Ultimately, the two types of modeling can be used together in hybrid structures to integrate large-scale experimental data with information from the literature. The ultimate goal of modeling is to expose missing information and thus to guide further experimental work. Thus, although the integrative approach described has been touted over the traditional reductionist approaches in this review, in reality the most effective overall method of attack is to use both reductionist and integrative approaches, presumably via cross-laboratory cooperation and collaboration.
No conflicts of interest, financial or otherwise, are declared by the author.
M.A.K. conception and design of the research; analyzed the data; prepared the figures; drafted the manuscript; edited and revised the manuscript; approved the final version of the manuscript.
This work was funded by the Division of Intramural Research of the National Heart, Lung, and Blood Institute (Project ZO1-HL001285 to M. A. Knepper).
↵1 Official gene symbols are indicated by italics throughout.
↵2 One of the interesting by-products of this trend toward reductionism has been the loss of clear boundaries among traditional biological fields. Thus, by the end of the 20th century, physiological researchers were typically using the same methodologies as other biologists including biological chemists, pharmacologists, or cell biologists, often publishing in the same journals. Thus the trend toward reductionism in physiology may have had the unintended consequence of undermining the traditional field of physiology and perhaps, in some cases, the very existence of physiology departments in US medical schools.
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text:
Lowndes County Health Department
About Lowndes County Health Department507 Montgomery Highway
Hayneville, AL 36040
Phone: (334) 548-2564
Fax: (334) 548-2566
Service Area for Lowndes County Health Department
We don't have the exact service area for Lowndes County Health Department. Based on the average area most agencies cover, the agency is very likely to provide services to the area in green and less likely to provide services further outside this area. Be sure to contact the agency to make sure they provide services in your area.
Other Nearby Home Health Care Agencies


text:
October 10, 2013
Picking a Great Names speaker is always a tough decision. Hamilton can secure a well-known person to speak, but name recognition does not guarantee the quality of the speech. With Hillary Clinton, the Sacerdote Great Names series was spot on, reigning in a talk that is sure to go down in Hamilton history.
Several Hamilton students agreed that this Great Names speech would be just another waste of money. What is the point of bringing in a big name if he or she will just give a generic speech targeted at an audience primarily of college students? We all expected to hear a few words on how we were the future of this country, and the value of a college education. There would be no real substance to the speech, nothing we had not heard before.
Instead, Clinton gave one of the more personable talks in my recent memory. She praised Hamilton's liberal arts background and its commitment to need-blind admissions. She highlighted the work of several Hamilton students and alumni, showing that she actually cared about this school. She pointed out the community service projects that Jorett Joseph '15 and Nick Solano '14 have taken on, showing she had done her research.
Clinton also touched on key issues that Americans all over the country are wondering about. Before the question and answer period, she spoke on the elephant in the room: the government shutdown. While I did not agree with some of her ideas, the fact that she brought this up showed her courage to take issues head-on. Several politicians in her position would have dodged this topic altogether, knowing its recent occurrence would exclude it from the questions, which were just selected days in advance.
Clinton spent a valuable amount of time answering numerous questions. She provided insight on the Arab spring, economic statecraft and health-care. Her experience in the field added a unique opinion on some of the key issues that Americans face everyday.
She also gave meaningful answers to more general questions about her career and the challenges she faced. Rather than taking the stereotypical politician's move of dodging the tough questions, Clinton addressed most of them directly, showing respect for the members of the Hamilton community that put time and thought into them. She provided thoughtful answers and spent more time responding to questions than speaking.
Unfortunately, I have only been at Hamilton for two Great Names speeches and do not have many standards for comparison. Shirin Ebadi and Bernard Kouchner gave the other Great Names lectures I attended.
While Kouchner's speech was interesting, it lacked the connection and coherence of Clinton's. Ebadi showed a lot of passion for human rights in the Arab world, but the bulk of her speech was lost in translation.
Hillary Clinton's talk was one of the best I have heard in my time at Hamilton. Now, the Great Names committee faces a challenge: bringing another speaker as knowledgeable, thoughtful and personable as Clinton to the Hill.
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text:
Can priests of Mishakal not take a life? In the Reign of Istar Michael is talking to Mishakal and the goddess says to him, "But by killing this man, Michael, you do break my vows."
Can priests of Mishakal not take a life? In the Reign of Istar Michael is talking to Mishakal and the goddess says to him, "But by killing this man, Michael, you do break my vows."
1) She is ordered to accept the action. An example would be the cataclysm, where a LOT of people died. I don't think Mishakal would be happy with millions dying with an asteroid strike, but I think the deal with all the gods means it's going to happen. However, In Taladas, she did create a secret cult to stave off the pain and suffering of so many people.
2) The needs of the many outweigh the need of the many. I doubt it, but if the killing a person and harvesting his blood to cure thousands of people from a deadly disease..... maybe?
3) If the pain and suffering of an incurable disease is so great that a person would like to die, maybe Mishakal would be in favor of mercy killings, and the right to die. But it's quite a long step. I tend to say no, because in a world where the afterlife is real, the pain and suffering in this incarnation of life "builds character." In my mind, Mishakal's desire to heal the suffering from death and disease stems from a belief that everyone deserves a second chance, and everyone should be given as much chances to redeem the irredeemable. A key example would be Elistan. You would think that the spread of the church of Paladine under Elistan is a good think, and keeping him from dying would further the church. But Elistan still dies. Perhaps he fulfilled his destiny, did good works, and so dies with the blessing of Mishakal.
Also, with the Elistan example, his death paves the way for Crysania to take over. That would be an example of reason #1.
So, I would say, ask any doctor on why he could renounce his Hippocratic Oath and help/allow people to die. I would think you could draw on that for more reasons Mishakal could possible accept one of her own taking a life. Hope that helps.
Last edited by Weldon Chen; 05-08-2017 at 12:19 AM.
Formerly from Wikipedia, circa 2006-7,
A fanwank is [...] an attempt by fans of a work of fiction to explain or justify plot holes or continuity errors, often through convoluted contrivances...
What's not clear from the book is whether taking a life breaks the vows, or doing so under that exact circumstance would. His intention was for what he thought was a righteous cause, so I tend to think Mishakal meant killing breaks the priest's vows.
In the Age of Mortals Mishakal is definitely more militant. I think taking a life in cold blood would break her vows.
-Dragonlance Nexus Social Media Manager-
GM - ICRP: Star Wars - Dawn of Defiance
Could it be his specific vows to Mishakal?
Seriously; what's the point of being a minotaur if you're not going to skewer something, anything, on those beautiful horns....
I can't recall the name, but there was a prestige class in HOotS that was in essence a cleric of Mishakal that had pledged a vow on non-violence and earned increased healing powers and advantages against the undead. From a narrative point of view kind of makes sense to have clerics from different parts of Krynn, like the Khur Mishakites, with a more liberal aptitude towards violence to protect others, and more civilized or less militant races and nations which have no tolerance towards it.
I had to check my Holy Orders of the Stars to find the Pacifism feature:
"Pacifist: A 1st level, the healing hand has sworn an oath
of nonviolent action. Although this oath does not prevent
her from defending herself or her charges from enemies,
she is forbidden to take a life or cause the death of another.
For the purposes of this oath, the following creatures are
exempt: constructs, elementals, oozes, plants, undead,
and vermin. A healing hand that willingly or accidentally
breaks this oath suffers the consequences(...)"


text:
For zoos, how to keep the visitors separated from the wild animals is an evolving science of its own, with the goal being to protect people even if they find their way past the primary barrier.
On Monday, president of the Pittsburgh Zoo and PPG Aquarium said the zoo where a 2-year-old boy was fatally mauled by African wild dogs over the weekend met or exceeded all safety standards for animals and visitors. Zoo president Barbara Baker said the tragedy is proof that no exhibit is "fail-proof."
The boy's mother had put him on a wooden railing at the edge of a viewing deck before he fell late Sunday morning. He bounced out of netting below before dropping more than 10 feet into the dogs' enclosure.
African wild dogs, also known as painted wolves, are social animals and skilled hunters. And if visitors come to a zoo with a well-designed habitat, it's almost like seeing them in the wild.
"A habitat like this gives an idea how wild dogs live," said John Lewis, LA Zoo director.
Lewis said many considerations go into habitat design, but the crux is safety.
Whether a better barrier system could have prevented the Pittsburgh tragedy will be the subject of investigation, but over the decades, zoos have moved increasingly to multiple barrier systems, like ones at the LA Zoo.
In recent years at the LA Zoo, an orangutan and a chimp have managed to escape their enclosures briefly, but there were no injuries.
"Big part of our business is protecting the public but also the animals as well," Lewis said.
Older habitats often relied on being at a lower level than the viewing point, but that tended to tempt people to peer over the barrier, so that type of design has fallen out of favor.
Associated Press contributed to this report.


text:
27 November 2012
Today we are about to witness a bill that will be introduced to bar legislators from making sexist remarks during parliamentary proceedings.
This conscientization strategy includes a punitive element and is hoped to increase sensitivity to gender-insensitive remarks and behavior.
It's just rather alarming to note the need to specify sexism as offensive behavior instead of expecting MPs to know better.
Nonetheless, it is a positive step forward and is hoped to draw attention to the unacceptabiity of offensive behavior.
But in meeting such objectives, I believe that we must view policies in a more holistic manner.
As such, I applaud YB Teo Nie Ching's initiative as it brings home the plight of mothers in Malaysia.
In 2009 I gave birth to little Harith. The very same year I made an application to parliament for a breast-feeding room – for the use of all nursing mothers working in parliament.
Unfortunately, the room was not equipped with a crèche nor the necessary parliamentary standing orders that allow children in the vicinity of parliament.
I believe the first step is for all governments – state and federal – to set up a breast-feeding room fully equipped with a crèche to accommodate nursing mothers. Such showcase of political will goes a long way in sending a message that our government is one that is mother-friendly and concerned with nurturing the child.
Nurul Izzah Anwar
Member of Parliament for Lembah Pantai
Vice President of Keadilan


text:
Hi my friend now has a brick! He updated to 4.2e then downgraded to 3.2e
then used and update pack wannis 4.1 I think now bricked.
I was looking for a solution on the web could this
with some software reprogram a NAND dump to the tsop?
Wii PAL 4.2e
The Wii has a RVL-001(EUR) model number and is produced for the European market. The copyright year is 2006.
NOW with softmod thanks guys!
Ipsa scientia potestas est.
Warning: Piracy is NOT supported. Word your questions carefully.


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