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The Normal Town Council unanimously approved new rules for public comment Monday night, but not without resistance from its newest members.
Previously the town's ordinance allowed residents to notify staff that they'd like to speak during public comment up to two hours before the start of a meeting.
Council members voted to narrow that cutoff to 15 minutes. But for Council Members Karyn Smith and Stan Nord, the change didn't go far enough.
Smith proposed the town allow residents to give as little as 1 minute's notice to speak. That motion narrowly failed, 3-to-4, with Smith, Nord and Council Member Scott Preston voting yes.
Smith also proposed the town eliminate the requirement that residents' comments relate to a meeting agenda item; that motion failed too, 2-to-5, with only Smith and Nord voting yes.
Smith said the town denied her the opportunity to speak about the Trail East project under that provision early this year.
With the council choosing not to designate three buildings slated for demolition as historic sites, the proposal could move forward without the need for another council vote. Smith said that meant effectively preventing further comment on the project, despite changes to the proposed building's design.
She said she filed a complaint with the state's attorney general, and her case is currently awaiting review.
"I'm hoping that there will be a positive response from the attorney general, and rather than wait for that response, I'm asking that we proactively as a council strike this and make the council meetings open to the public to discuss whatever they desire," she said.
Nord supported both recommendations so as to "err on the side of giving the people an easier opportunity to talk with us," he said. "If we're going to err, let's err in favor of the people, always."
Smith isn't the only resident to lodge a complaint against the town's public comment policies: Craig Stimpert said he faced a similar situation in 2016. At the time the town imposed a 45-day waiting period on public speakers. After the attorney general's office ruled in his favor, the town dropped the rule in 2017.
Stimpert took issue Monday night with the so-called "germaine" rule, asking who defines what's relevant to the agenda. He also said while the 15-minute cutoff is an improvement, he didn't see why speakers couldn't just sign up on a sheet of paper at the meeting.
"I have personally witnessed council members showing up late to meetings, missing role call and the pledge, so I know some of you are not arriving 15 minutes prior to the start of each meeting," he said. "Why would you hold public comment speakers to a higher standard?"
Preston admitted he's been guilty of arriving late to meetings, and voted to support a 1-minute cutoff.
Mayor Chris Koos said he suggested the 15-minute requirement to give the town clerk enough time to record the speakers' information.
City Manager Pam Reece explained a 1-minute cutoff could present an administrative issue when a liquor commission meeting or special presentation precedes a council meeting.
"That just makes it very tight, so that would be the biggest concern. What about when we are all up here (on the dais) in advance of a 7 p.m. council meeting?" she said.
Council Member Kathleen Lorenz asked her colleagues not to make the perfect the enemy of the good.
"I think let's try this and let's get used to 15 minutes, and see how that works, and once we get really good at it cut it down to 10, or 5 if we think that some folks are at a disadvantage from that," she said.
Council Member Kevin McCarthy said the public has plenty of opportunities to make themselves heard, not just at council meetings.
"We're available by email, we're available by phone, I've met many people, including Mr. Stimpert who spoke tonight, at The Coffeehouse to listen to his input face-to-face," he said. "I got a better understanding of Mr. Stimpert's perspective of some of the concerns he had, and I know the rest of this council does the same."
Connect Transit
Nord and Smith also united in calls for Connect Transit to reconsider scheduled fare increases and the elimination of the Olive route, with Nord voting against the town's budgeted regular payment to the agency.
Smith said after examining the provisions of a 2012 memorandum of understanding with the City of Bloomington and Connect Transit, she believes the town could recall the agency's budget, prompting its board of trustees and newly formed working group to re-evaluate the changes.
Town Attorney Brian Day said he's currently in discussions with legal counsel from both the city and Connect Transit on the matter.
"Just looking at the overall purpose of the contract, the contract itself sets out the specific duties of the board, and one of those duties is to create, alter, or eliminate any routes," Day said. He added the memorandum doesn't require the board to seek approval to make those changes.
Reece said the route cut was a data-driven decision. In a 6-month period from fall 2018 to spring 2019, Connect Transit found the Olive route averaged zero daily riders at 12 of its 41 stops, she said. Another 15 stops averaged less than two daily riders.
And each of the three stops averaging a significant number of riders—the Walmart stop, the Orlando Avenue stop and the Fort Jesse Road stop near OSF Medical Group—are all covered by other routes, Reece said.
Smith said she suspects those numbers may not reflect the impact of eliminating the Olive route if the data was collected during winter months when bad weather negatively affects ridership.
Both Koos and Reece said the town is working with Connect Transit to find a time for General Manager Isaac Thorne to make a public presentation and take questions from the council.
The Connect Transit Board of Trustees will meet in the Town Council chambers at Uptown Station at 4:30 p.m. Tuesday to consider the recommendation of "Connect to the Future" working group members, among other matters.
Editor's Note: This story has been updated from its original version to clarify the three votes related to public comment.
People like you value experienced, knowledgeable and award-winning journalism that covers meaningful stories in Bloomington-Normal. To support more stories and interviews like this one, please consider making a contribution.


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subset: commoncrawl


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And must-reads are Kat's "Kat's Korner: Carole's back catalogue" and "Kat's Korner: Carole Touches the Sky and Soul."
The months are moving so fast. Soon it will be summer and it will be political convention time.
So let's take a moment to consider what PBS will offer by remembering what it offered in 2008.
In September 2008, Ava and C.I. offered "TV: More sexism, more self-promotion." From that piece:
That point was driven home best on Thursday when the boys decided to again explore women. It was interesting to see so many speaking about women and notice that not one person speaking was, in fact, a woman. You had the three male 'historians' (will get back to them), you had Jim Lehrer, David Brooks and Mark Shields as 'analysts' and you had a man from PEW research plus Ray Suarez. Eight voices discussing women -- eight voices and all of the male. Don't count on the increasingly inept watchdogs to call it out. They didn't do a damn thing when women were sidelined by PBS in Denver and they're not going to do a damn thing now.
Here are the 8 voices.
Not one woman. Will PBS try to get away with that crap this year?
"Iraq snapshot" (The Common Ills):


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A 5 year old boy cried on his first day to school, hoping his parents wouldn't make him stay. That same boy, at 17, showed great reserve as he put on a brave face on his last day at school, wishing he wouldn't have to leave. As Dickens so eloquently put,
"It was the best of times, it was the worst of times, it was the age of wisdom, it was the age of foolishness.."
Schola Nova is more than a school. My time there was spent in the company of amazing faculty and mentors, as well as life-long friends. We learned, we laughed, we lived. Schola Nova will always be home.
Batch: 2010-2011
(Baqir is currently in his final semester as a mechanical engineering undergraduate in NUST, Islamabad. With two months to graduate and his eyes on the horizon, he is ready to enter the professional world this coming June)


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>Here are the top 10 things you should know about the hotline:
- If your emergency is serious, activate local emergency medical services (EMS), or take the individual to the nearest medical facility. Medical professionals will be better able to stabilize the person and assess the patient's condition. Once EMS is activated, call DAN for additional assistance.
- When you call, be prepared to provide the following information:
- Each member of the DAN Medical staff has extensive credentials; they are paramedics (EMT-P), Emergency Medical Dispatchers (EMD), Dive Medical Technicians (DMT), Emergency Medical Technicians (EMT), Certified Hyperbaric Technicians (CHT) or physicians (MD) as well as dive instructors or dive leaders.
- Once the course of action is determined, DAN's medical staff may make an immediate recommendation or request to call you back after making arrangements with a local physician or facility, the appropriate TravelAssist contact or any number of DAN's network resources.
- If a call-back is necessary, please wait by the phone while arrangements are made. The resources may take 30 minutes or more to coordinate, as several elements and calls may be required to make the appropriate arrangements. The delay will not place the injured person in any greater danger, and DAN will call you as soon the arrangements are in order.
- The DAN Emergency Hotline also serves as your resource to activate the DAN TravelAssist membership benefit. When you are traveling more than 50 miles from home and need to access your TravelAssist benefits, including medical evacuation, call the DAN Emergency Hotline.
- The emergency hotline is not equipped to address inquiries regarding membership and insurance. All membership and insurance inquiries should be directed to the DAN Membership Specialists at +1-919-684-2948.
- The DAN Medical Information team adheres to strict standards of confidentiality. Your call and private information are both respected and protected.
- You can put a face to the DAN Medical Information team by participating in real-time webinars, watching the online video lecture series or stopping by the DAN booth at dive shows in your area.
- The hotline handles an average of 3,500 calls to the emergency line per year.
-Your name and the injured person's name
-Your location
-A call back number
-A description of the emergency or situation


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Under state law, any group that donates money for a specific political purpose must reveal its individual contributors. Federal law, in contrast, states that non-profit organizations do not have to disclose its funders. These conflicting laws allowed the people behind the money to filter the funds through the Arizona group, wiping it clean of any recognizable scuff marks.
It worked like a car wash.
The $11 million originated with Americans for Job Security, a Virginia nonprofit based in the same building as Karl Rove's Crossroad's media. Then it went to Center to Protect Patients' Rights, which multiple news reports have tied to oil tycoons Charles and David Koch. Then the money went to Americans for Responsible Leadership.
On Oct. 15, Americans for Responsible Leadership sent $11 million to Small Business Action Committee PAC, which supported Proposition 32 -- the measure that would have limited unions' ability to raise political funds -- and against Prop. 30 -- Gov. Jerry Brown's proposal to raise income and sales taxes. By that time, of course, the ties to the Koch Bros. and Rove were distant.
Fair Practices Political Commission, the state's campaign finance watchdog, called ARL out, declaring that the Arizona group had to reveal its funders. The California Supreme Court agreed with state authorities. ARL initially said it would appeal to the U.S. Supreme Court, but perhaps fearing an official audit, it eventually decided to disclose the two other groups from whom the money came.
Speculatively speaking, it's not hard to imagine the benefits of the convoluted white-wash: Policy endorsements from the Kochs and Rove would not have played well in Blue California, would have made some fence-sitters think, "wait a minute, isn't that the Bush guy and aren't those the ones spending millions of dollars to defeat Obama? I don't think I like those guys."
In one sense, though, the strategy did work: While the groups holding the money have been exposed, the individual donors remain anonymous.


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Welcome to the Pink History Lyrics site!
Here you will find all the lyrics to Pink's songs; from singles to album tracks, b-sides to live only songs. There will also be videos links to go with the songs.
How To Use This Site:
There is a drop down menu to all the different sections at the top of the page. However, not all of the lyrics are accessible from the drop down menu.
If you know a song that you are looking for, simply click on the album section at the top of the page, and there will be a track list, where you can click on the track title which will take you straight to the lyrics page of that song. Alternatively you can use the search option just under the header artwork.
All lyrics have been hand typed by Pink History for the album tracks, either from the lyrics in the album booklets, from listening to the tracks or from google searches, there may be some mistakes (even though I have checked over the pages a lot!), so if you notice anything wrong, please contact me using the contact information HERE. The 'B-sides, Unreleased….etc' section of the website was mostly used from lyrics websites, especially for the cover songs.
Sources of information:
- The booklets from Pink's albums
- Various lyric videos on youtube
- letssingit.com
- azlyrics.com
- Wikipedia
- As always, a big thanks goes to Operation Pinkies for the artwork on this site.


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Top ten recommendations to increase the speed and performance of Resharper 4.5.1 Follow
Fellow users,
I'm sorry but, I don't have the answer to this topic, but I am desperatly seeking it.
On my 10GB(Ram) HP quad core Xeon workstation, Resharper 4.5.1 is almost so slow as to be unusable from my perspective.
There are a great many options that may increase the performance of Resharper, although many come at the expense of
What I am strongly encouraging Jetbrains to do is to write a document: "Top Ten Things To Try To Accelerate Resharper",
for those of us with performance issues. The document should explain the tradeoffs of each recommendation.
This is not a knock on Resharper, or JetBrains, R# is an incredible product without (I.M.O.) any real competition,
but what I need is a short, clear, consise document helping me accelerate the performance of the product.
I search the FAQ for 'speed', 'performance', and 'faster[, but didn't find any such recommendations.
Thank you very much.
I would strongly encourage knowledgable users to submit their recommendations for speeding up
the user interface here too, as maybe that will have to be the basis for a Top Ten FAQ on
accelerating Resharper.
Hello Scott,
I don't have "10" recommendations. All I can say is, with your machine, R# should absolutely fly. I have a mere 4 GB dual core machine and I load HUGE VS projects with R# installed. I also use recourse intensive things such as " errors in solution"
I do have 3 recommendations:
- Do not use R# 4.5.1, it has some big performance problems which will hopefully be fixed soon by Jetbrains. Use R# 4.5.0 instead, which performs MUCH better
- Switch off R# unit testing. For some reasons, this seems to impact editor performance
- About every 3-4 hours, either restart Visual Studio or go to the Add-In Manager, turn off R#, go again to the Add-In Manager, turn on R# (it will reload all assemblies) => R# slows down gradually during a long editing session and will be much quicker after this operation.
Best regards,
Thank you for your feedback.
I am rather surprised and disappointed at the lack of feedback from JetBrains, for an otherwise excellent product,
this seems to be the only criticism I hear on the Internet.
Most of us, I believe would be happy to live with the state of things if we had a clear document outlining what to do
try to improve responsiveness. Without this, many (of us) will give up searching for the optimal configuration and
give up on R#, with such a document, I believe most of us (with performance issues), will agree R# can get bogged down,
but with the proper configuration (even limited), I would say, I cannot live (well, code) without it.
Please, JetBrains, write such a document, "The top ten things to do to keep R# running at top speed".
After having to deal with the slowness in any operations in my .aspx, .ascx, etc. (such as copying, pasting, typing, even saving a file... anything!) I would agree that 4.5.1 has some major performance issues in web files. Today it is driving me absolutely nuts.
Please sign in to leave a comment.


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Recently, someone shared a video on Facebook featuring a scene from the film Trainspotting 2 when one of the leading actors – Ewan McGregor was talking to another actress in the movie and explaining her the meaning of the 'Choose life' motto.
The 'Choose life' motto is a monologue speech of Ewan McGregor's character Renton depicted in the two episodes of Trainspotting. He was explaining the heroin addicts choice which is the 'liberating' life of the heroine over the choice of living as a slave in the modern consumer society. Good choice chaps! It takes you out you from the reality!
But on the serious note, what they are talking about as well is that you can literarily choose everything. You can, "Choose life. Choose a job. Choose a career. Choose a family. Choose history repeating itself. Choose a f*cking big television, choose rape jokes, sl*t shaming. Choose your future. Choose life!.."
So, guys choose your life. I mean, let's face it- life is unfair! We all have different start mainly, because of our family status. Some people are born rich, and they just need to follow what their parents say so that they could inherit all the sh*t loads of family money. Some people need to start from the bottom of the chain, to get where they want to be. So, in a certain way some people have an advantage, but for many things, we are equal at the end of the day. Especially, if talk about our intellectual and physical capabilities (again as every rule with some exceptions!).
I mean, for example, if you are a gifted footballer and your dad is David Beckham- yeah, it's probably a lot easier to find your way into the top-class football, considering that everyone knows who your dad is. But even if your dad is David Beckham, and you are an average footballer you will end up playing at an average level as well.
And on the other hand, if you are a gifted young kid with а excellent football talent you just need to choose to become a professional footballer and to chase that dream!
If you think, "Ohh…I so much want to be a doctor, an architect, an actor.." Well, do it! I know it is expensive, but there are different ways to get there. You would have to work and study hard, you might need to borrow money, but if you want precisely that career and you feel that you have the talent to do the job- go for it! Set your goals and start chasing them.
It's a cliché I know. But it's true! I haven't heard of a man who was well up for something and didn't achieve it. I mean with slight exceptions of course. I believe that some things are 'your thing'. But some things could come into your life, such as a new job, a new partner, a new town, and they are so not for you that never mind how hard you try to achieve something there, the universe will always bounce you back. Do you know why? Because, these things are not good for you, but they happened for a reason! They came into your life as a life lesson! But hey hey hey! That's an entirely new topic so that we won't go there now!
What I am trying to say is that if you firmly believe something is your thing and it is your thing (meant to be by the universe), well, my dear reader you will get it! You will f*cking get it. No, no, don't shake your head in disbelief- you will get it!
If you think that now is the time for a career change, then go for it! It's not late, never mind how old you are. If you think that you need to get a divorce and find a new partner, "Just do it!" as the Nike slogan says! If you are bored of the place where you live, just move somewhere else! It's hard I know. But it's not impossible.
I will bring another cliché from the book & film The Wolf of Wall Street, "The only thing standing between you and your goal is the bulls*it story you keep telling yourself as to why you can't achieve it…" Abso-fu**king-lutely true mate!
You will ask yourself, "But how could I know it's my thing?" Ohh c'mon, you know it from inside. You know, everything from the beginning, it's a pure gut feeling. I will give you an example with my ex-girlfriend. For our one year relationship broke up probably 4-5 times! The thing was that we were bouncing off each other all the time. And I wondered why, but I knew the answer from the beginning. We are just not compatible! We are just entirely different people, or maybe even similar in a specific, negative sense, but I knew it right from the start- she is not the one!
I hope that you know what I am on about while reading this post. We all have that guardian angel that whispers in our year and help us to shape our thoughts about our dream job, dream partner, or place to live, etc. If it's something realistic, keep pushing and chasing it even if it seems hard to achieve your goal. Choose your thing in this world and go and get it! And remember: God responds only to meaningful prayers.
p.s. Trainspotting is a fiction. You don't need to take heroin to get the liberating feeling! Just relax, calm down, take a breath and think about it. The answer is there, just bring it to the surface and choose life!


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Random.org has chosen our winners for YoBaby and Earth Mama Angel Baby!!
YoBaby - #7 ApachesPrincess
Congratulations to our winners! E-mail notifications have been sent. Each winner will have 48 hours to respond or we will have to choose another winner.
Thank you to everyone who entered!!
Wednesday, May 19, 2010
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Posts from May 2019
Men's Action Club BBQ
BBQ in West End of Atlanta on Saturday, May 11, from 9 a.m.
Great food!
Great food, great times We'd love to serve some delicious grilled food prepared by the men of the parish. Stay tuned for more information Mark your calendar!


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Educational Offerings
The Department of Anesthesiology has educational opportunities for medical students, residents, and fellows, as well as continuing education events for professional anesthesiologists and nurse anesthetists.
Our four year residency program comprises 60 interns and residents. Each year, we interview approximately 200 applicants to admit a Categorical class of twelve into our four year program with an integrated intern year. An additional four residents complete an internship elsewhere before coming to the University of Virginia for a three year Advanced program.
Dr. Julie Huffmyer, our Program Director, has been on the faculty of the University of Virginia since 2008. In 2011, she was appointed as Associate Program Director, and has been the Residency Program Director since 2016. She clinically practices cardiac thoracic anesthesiology and liver transplant anesthesia. She has been honored with numerous teaching awards and devotes her research efforts in the realm of education. Dr. Stephen Collins is the Associate Program Director and Chair of our Clinical Competency Committee. He has won numerous teaching awards and is a member of the UVA Academy of Distinguished Educators.
The Department has an accredited fellowship in Pain Medicine, Critical Care Medicine and unaccredited fellowships in Regional Anesthesia and in Anesthesia Education.
The Pain Medicine Fellowship, under the direction of Dr. Lynn Kohan, is a one year program with 6 fellows. The pain fellowship is part of the Office of Graduate Medical Education, and fellows are employees of the UVA Housestaff.
The Critical Care Medicine Fellowship, under the direction of Dr. Bhiken Naik, is a one year program with 2 fellows. The in-depth critical care training fellowship is part of the Office of Graduate Medical Education and fellows are employees of the UVA Housestaff.
The Regional Anesthesiology and Acute Pain Medicine newly accredited ACGME fellowship under the direction of Dr. Ashley Shilling, is a one year program with 2 fellows. This in-depth regional training fellowship is part of the Office of Graduate Medical Education at UVA and fellows are employees of the UVA Housestaff.
Our unaccredited fellowships are offered as Clinical Instructorship faculty positions. Typically, the fellow is assigned to general OR cases one day per week and devotes 4 days to the fellowship. Our fellows are employees of the UVA School of Medicine and hold the rank of Instructor. The Department has hired Clinical Instructors in recent years for advanced training in Regional, OB, Neuro, Quality, and Education Research.
A one year Fellowship in Simulation Education and Research is offered under the direct supervision of Dr. Keith Littlewood, Assistant Dean, Clinical Skills Education, Co-Director, Medical Simulation Center, Vice-Chair for Education, Department of Anesthesiology. Interested applicants are encouraged to contact Dr. Littlewood directly about this opportunity.
Medical Students
Third year medical students participate in the two week Peri-Operative Medicine Rotation. This Anesthesiology rotation is directed by Dr. Vaia Abatzis, Dr. John McNeil and Dr. Jessica Sheeran. Fourth year students may participate in the Anesthesiology elective for a maximum of four weeks, under the direction Dr. Peter Amato.
Continuing Medical Education
The Medical Simulation Center, under the direction of Dr. Keith Littlewood, offers full-day simulation workshops which fulfill the American Board of Anesthesiology requirements for Maintenance of Certification in Anesthesiology (MOCA).
The Regional Anesthesia Group offers a one- to two-day observational preceptorship for practicing clinicians at our outpatient surgical facility. Please contact Dr. Lee White for more information.
Anesthesiology Grand Rounds are held each Wednesday at 8 AM. These lectures by our faculty members and distinguished guests are certified for continuing medical education credits.


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My friend Brian Biggs, the former cartoonist, has a new book out, and his coauthor lives in DC.
Julie Segal-Walters' home page
Julie Segal Walters and Brian Biggs: All The Wonders, Episode 401
This Is Not a Normal Animal Book
Julie Segal-Walters (@J_S_Dub) and Brian Biggs (@mrbiggsdotcom), author and illustrator of This is Not a Normal Animal Book, stop by the podcast to talk about creating a metafiction book over animal classifications, incorporating the voices of a parent and a precocious child, and asking "what the heck is going on here?"
Episode Notes
Julie Segal-Walters' home page
Brian Biggs' home page
This is Not a Normal Animal Book Teachers Guide (Grades PreK-2) (Grades 3-6)
Story Storm (formerly PiBoIdMo – Picture Book Idea Month)


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TECH SUPPLIER May 2020 - Market Forecast - Doc # US46398120
Worldwide Communications Service Provider Operations and Monetization Solution Forecast, 2020–2024
By: Karl WhitelockResearch Vice President, Communications Service Provider Operations & Monetization
This IDC study shows that communications SPs are advancing their business IT and network operations systems to support new 5G-based services while continuing to reduce the cost of supporting existing customers tied to already-deployed network technology. The effects of COVID-19 on IT spend will be minimal through the remainder of 2020. IT spending will quicken in 2021, eventually exceeding previous forecast levels. The overall communications SP software solution market will grow from $27.9 billion in 2020 to $30.4 billion by 2024. A bulk of this spend will be from the North American and Asia/Pacific regions, while European spending will be at a slower pace as it wrestles with data security concerns and the role of regulation in technology evolution.
"Real-time data analysis, customer insight derived from that analysis, and agile systems capable of meeting rapidly changing business needs are the call of the day as 5G services start to take shape. Communications SPs now realize that in the 5G era, partner contributions — working with network technology capable of delivering far more than just a network connection — are rapidly becoming a strategic means for delivering end-to-end solutions to business challenges. This means a shift from just B2C services to also include B2B interactions," said Karl Whitelock, research vice president, Communications Service Provider Operations and Monetization. "Systems functionality, delivered via a cloud-native architecture, will be the key for monetizing new customer offerings."
Subscriptions Covered
Communications Service Provider Operations and Monetization
Regions Covered
Topics Covered
COVID-19, Networking and connectivity devices, Networking virtualization
List of Tables
List of Figures
Get More
When you purchase this document, the purchase price can be applied to the cost of an annual subscription, giving you access to more research for your investment.


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PHOTOS & VIDEO: Rep. Tulsi Gabbard Assesses Eroded Honoapiʻilani Highway, Hosts Roundtable with Maui DACA Recipients, Visits with Wailuku Residents & Businesses
Today on Maui, Congresswoman Tulsi Gabbard toured sections of Honoapiʻilani Highway in West Maui near Olowalu Reef that are deteriorating due to rising sea levels and erosion, creating a safety and environmental hazard. The highway is the only road in and out of West Maui, an area that is home to thousands of residents and Maui's largest tourist population. It is subject to frequent road closures due to car accidents, storms, high tides and more. The congresswoman discussed the state of the highway with the Maui Tomorrow Foundation and other community stakeholders and discussed solutions to maintain access, protect the shoreline, and keep residents safe going forward.
Later in the afternoon, the congresswoman met with a group of Maui residents who are recipients of Deferred Action for Childhood Arrivals (DACA). The program, initiated under Executive Order by President Obama in 2012, allows undocumented individuals who came to the United States as children and meet several guidelines to receive a renewable two-year period of "deferred action" or protection from deportation. Recent reports indicate that the program could be phased out by President Trump in the coming days. Members of the roundtable shared how DACA has empowered them to get their education, work, get a drivers' license and social security number, and more. They also shared their reality of living in fear before DACA came into existence. The congresswoman also provided the group with an update on legislation she's working on at the federal level to protect DACA recipients.
Following the roundtable, the congresswoman visited with local businesses in Wailuku and Kahului, and hosted a "pop-up" Congress on Your Corner outside of Wailuku Coffee Company to talk story with local residents and businesses. She will host another Congress on Your Corner tomorrow at 2:30pm at Waialua District Park on Oʻahu's North Shore.
B-roll video from today's visits can be downloaded here
Photos are available here for download


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Editorial Board-6
Yakimenko Stanislav, Professor, MD, Head of the Department of Eye Burns, Plastic Surgery, Keratoplasty and Keratoprosthesis in the Filatov Institute. He graduated from Ternopil Medical Institute. He is a winner of the Filatov Prize of Academy of Medical Sciences of the USSR. He is the author of 2 monographs, over 200 scientific papers, and 12 patents. Main activities are eye burns, keratoprosthesis, corneal transplantation, secondary glaucoma, plastic surgery, diseases of the lacrimal passages.
Recent Publications
1. Oleksiy Buznyk, Nataliya Pasyechnikova, M. Mirazul Islam, Stanislav Iakymenko, Per Fagerholm and May Griffith. Bioengineered Corneas Grafted as Alternatives to Human Donor Corneas in Three High-Risk Patients. Clinical and Translational Science. 2015 Oct; 8(5):558–562
2. Mohammad Mirazul Islam,Oleksiy Buznyk, Nataliya Pasyechnikova, Monika Ljunggren, Keith Meek, Philip Lewis,Sally Hayes, Stanislav Iakymenko, Jaywant Phopase, Emilio I. Alarcon, Kimberly Merrett, Wenguang Liu, Per Fagerholm and May Griffith. Biomimetic Collagen - Phosphorylcholine Hydrogels as Corneal Implants for High Risk Patients. Society for Biomaterials Annual Meeting and Exposition 2015, 15-17 April 2015: transactions. – Charlotte, NC, 2015.
3. M GRIFFITH, M ISLAM, S IAKYMENKO, N PASYECHNIKOVA and O BUZNYK. Next generation corneal implants as alternative to high risk donor transplantation. Acta Ophthalmologica. 2014; 92 (Sep). Issue Supplement: s253.
4. Oleksiy Buznyk, Nataliya Pasyechnikova, Stanislav Iakymenko, Mohammad Islam, May Griffith. Biosynthetic Corneal Substitutes with an Anti-Infective Peptide Release System. World Ophthalmology Congress, 2-6 April 2014 : e-abstract. Tokyo, 2014.
5. Iakimenko SA, Buznyk OI, Rymgayllo-Jankowska B. Amniotic membrane transplantation in treatment of persistent corneal ulceration after severe chemical and thermal eye injuries. Eur. J. Ophthalmol. 2013; 23(4): 496 - 503. doi: 10.5301/ejo.5000243.
6. Iakymenko S. Forty-five years of keratoprosthesis study and application at the Filatov Institute:a retrospective analysis of 1 060 cases. Int J Ophthalmol 2013;6(3):375-380,doi:10.3980/j.issn.2222-3959.2013.03.22
7. Pan HW,Iakymenko S,Xu JT,Hou GH,Sun BJ,Zheng AN. Implantation of Iakymenko keratoprosthesis in patients with severe ocular injury. Int J Ophthalmol 2012;5(2):167-171,doi:10.3980/j.issn.2222-3959.2012.02.108. Stanislav Iakymenko. Keratoprosthesis in the Filatov Institute: development, study, and results of application. DOI: 10.1007/s00717-014-0241-6
Participation in conferences
Austria, Vienna. EuropeanandAmericanSocietiesCongressofOphthalmology. 06.06.07-13.06.07
Poland, Krakow. International conference «Treatment of traumatic eye». 30.11-02.12.07
Russia, Saint Petersburg. «Traumatic eye» 22.09-29.09.08
Bulgaria, Sofia, Varna. Bulgarian conference of ophthalmologists. 02.10-09.10.08
Russian, Moscow. Fedorov memorial lectures-2009 and Russian scientific practical conference of young scientist with international participants 1-3.07.09
Russia, Moscow. IX Congress of Russian ophthalmologists. 16-19.06. 2010
Germany, Berlin. 22nd World Ophthalmology Congress. 5-9.06. 2010
France, Paris. World Glaucoma Congress. 29.06-07.07.2011
Glasgow, Great Britain. VIWorldGlaucomaCongress. 12-16.09.2012
Barcelona, Spain. European Congress of Reconstructive and Plastic Surgery. 19-21.09.2013
Salzburg, Austria. IX World Congress of Keratoprosthesis. 12.04.2014
Kishinev, Moldavia. BSOS XIII International Congress. 29.10-01.11.2015


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First prospective, multicenter trial evaluating safety and efficacy of sirolimus suggests drug could be an early therapy option for patients with autoimmune lymphoproliferative syndrome
The immunosuppressant sirolimus is an effective and safe steroid-sparing therapy for children and young adults with highly treatment-resistant autoimmune blood conditions, according to a study published online in Blood, the Journal of the American Society of Hematology (ASH). This treatment is particularly effective in children with autoimmune lymphoproliferative syndrome (ALPS), a chronic genetic disorder characterized by the buildup of white blood cells in the organs.
Patients with ALPS and other autoimmune disorders often have immune systems that destroy their body's own healthy blood cells. The resulting decrease in blood cells causes symptoms such as anemia, uncontrolled bleeding, and infection. Few effective and well-tolerated therapies exist to manage these chronic autoimmune issues. While standard immunosuppressive therapy with corticosteroids may help some patients, others are resistant, intolerant, or cannot successfully maintain healthy blood cell counts when they discontinue medication. Recently, investigators reported that sirolimus successfully resolved these autoimmune conditions in a small group of children with ALPS without causing adverse side effects.
"Patients with ALPS and other chronic autoimmune disorders have few long-term treatment options for managing harmful conditions related to reduced counts of red blood cells, platelets, or white blood cells," said senior study author David Teachey, MD, of the Children's Hospital of Philadelphia. "Corticosteroids are not a permanent solution, as they are often associated with long-term health effects, such as osteoporosis and higher risk of infection."
To improve disease management for patients with ALPS and similar autoimmune disorders, a research team led by Teachey and his colleague Karen Bride, MD, PhD, conducted a multicenter clinical trial evaluating sirolimus in 30 patients ranging from 5 to 19 years old. All study participants were either intolerant or resistant to corticosteroids. Patients received 2 mg/m2 to 2.5 mg/m2 per day of sirolimus in either liquid or tablet form for six months. After six months, those who benefited from the drug were allowed to continue treatment with continued follow-up appointments to monitor toxicities.
Researchers demonstrate that 11 of the 12 children with ALPS achieved normal blood cell counts within one to three months of starting sirolimus. The remaining patient achieved a complete response by 18 months. Additionally, all ALPS patients successfully weaned off steroids and discontinued all other medications within one week to one month after starting sirolimus. Patients remained on treatment for a median of 3.5 years. In addition, investigators observed that patients suffered few adverse side effects after a median follow-up of two years.
While the majority of study participants with similar autoimmune disorders also achieved complete response (8 of 12 patients), it did not occur until three months after start of treatment. Based on these findings, the authors propose use of sirolimus as early therapy for patients with these chronic treatment-resistant autoimmune blood conditions, especially for those with ALPS.
"This study demonstrates that sirolimus is an effective and safe alternative to steroids, providing children with an improved quality of life as they continue treatment into adulthood," said Dr. Teachey. "While further studies are needed, sirolimus should be considered an early therapy option for patients with autoimmune blood disorders requiring ongoing therapy."


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Toxoplasma gondii is an obligate intracellular parasite of clinical importance, especially in immunocompromised patients. Investigations into the immune response to the parasite found that T cells are the primary effector cells regulating gamma interferon (IFN-γ)-mediated host resistance. However, recent studies have revealed a critical role for the innate immune system in mediating host defense independently of the T cell responses to the parasite. This body of knowledge is put into perspective by the unifying theme that immunity to the protozoan parasite requires a strong IFN-γ host response. In the following review, we discuss the role of IFN-γ-producing cells and the signals that regulate IFN-γ production during T. gondii infection.
Toxoplasma gondii is an obligate intracellular protozoan parasite that infects at least a third of the world's population. Infection with the parasite is divided into a limited acute stage followed by a persistent chronic stage. In the chronic stage, T. gondii forms cysts, found mainly in brain and muscle tissues, which can persist for the lifetime of the host. The disease state, known as toxoplasmosis, generally occurs during the chronic stage after the host becomes immunocompromised, allowing the encysted T. gondii to reactivate. Toxoplasmosis is fatal if untreated, and yet treatments are ineffective at eliminating the encysted parasites, so patients are typically placed on antitoxoplasmosis drugs for as long as they are immunocompromised.
Basic research into the immune response to T. gondii established immunocompromised mouse models during the chronic stage of infection to model clinical observations. It was demonstrated that combined depletions of CD4+ and CD8+ T cells during chronic infection in mice resulted in parasite reactivation and host mortality (1). Additionally, SCID mice, which lack T cells, are susceptible during the transition from the acute to chronic stage of infection, which illustrates the requirement for T cell responses to control the infection.
While the adaptive response is ultimately required for host survival, components of the innate immune system determine initial susceptibility and the outcome of the infection independently of T cell-activation status (2). Mice deficient in myeloid differentiation factor 88 (MyD88), the downstream adaptor protein of most Toll-like receptors (TLRs), are extremely susceptible to T. gondii infection (3). Subsequently, it was shown in mice that MyD88-dependent responses to the parasite were primarily mediated by TLR11 (4), which recognizes a protein component of T. gondii known as profilin (4, 5). Innate responses through TLR11 via MyD88 result in the production of interleukin-12 (IL-12) and gamma interferon (IFN-γ) (3, 4). Dendritic cells (DCs) are the primary source of MyD88-dependent IL-12 (2, 6). However, IL-12 is not the only important effector for initiating the adaptive immune response; administration of IL-12 to MyD88-deficient mice does not rescue their acute susceptibility despite partially restoring Th1 responses (2, 7). These data suggest that there are additional MyD88-dependent factors necessary for full initiation of Th1 responses and host survival.
IFN-γ-PRODUCING CELLS: FROM T TO NK CELLS AND NEUTROPHILS
The cytokine IFN-γ is critical for survival during T. gondii infection. IFN-γ- or IFN-γ-receptor-deficient mice show extreme susceptibility to the parasite (1, 8–10) similar to that observed in MyD88-deficient mice. Additionally, it was shown that IL-12-deficient mice are extremely susceptible to T. gondii and that IL-12 enhances IFN-γ production (11, 12). While IL-12 is known to regulate IFN-γ, it has no protective role independent of IFN-γ-mediated pathogen resistance (9). These data established T. gondii as a model pathogen of Th1 immunity (13). A discussion of the individual cell types involved in producing this critical cytokine is fundamental to our understanding of host immunity to T. gondii.
T cells.Both CD4+ and CD8+ T cells seem to have an important synergistic role to play during T. gondii infection, because individual depletions of CD4+ or CD8+ T cells do not recapitulate the phenotype of double-depletion or T cell-deficient mice (1, 14). Mice lacking all T cells do not survive into the chronic stage of infection (15), and depletion of T cells in the chronic stage leads to reactivation of the disease state (1).
CD4+ T cells.The role of CD4+ T cells during intracellular infections is the production of IFN-γ. Adoptive transfer of immune CD4+ T cells into athymic nude mice during a T. gondii reactivation model partially rescues their survival (16). The importance of CD4+ T cells during infection is explained by the effector mechanisms induced by IFN-γ. It is known that IFN-γ made by CD4+ cells is needed to prime macrophages to produce potent antimicrobial responses (17). IFN-γ regulates inducible nitric oxide synthase (iNOS) expression, which is ultimately needed for control of the parasite, as iNOS-deficient mice succumb at 3 to 4 weeks postinfection (18). Production of nitric oxide interacts with diverse metabolic pathways, and, as a free radical, it is toxic to bacteria and intracellular parasites. Mouse macrophages can also use their respiratory burst to generate toxic reactive-oxygen species (ROS) in response to T. gondii, and this response is dependent on IFN-γ (19). Additionally, IFN-γ induces indoleamine 2,3-dioxygense (IDO), which is an enzyme that is involved in tryptophan catabolism and that degrades cellular tryptophan. T. gondii is a tryptophan auxotroph, and induction of IDO-1 inhibits parasite growth in human cells (20, 21). Recently, it was found that inhibiting both IDO-1 and IDO-2 during T. gondii infection in mice also results in increased parasite burden and increased susceptibility in the chronic phase of infection (22). There are additional IFN-γ-induced proteins in mice known as immunity-related GTPases (IRG); however, this large family of proteins is not represented in the human genome (23). The complex phenotypes of IRG knockout mice have been recently reviewed elsewhere (24). The importance for IFN-γ-mediated effector mechanisms is further illustrated by recent evidence that T. gondii actively inhibits IFN-γ signaling by inhibiting the turnover rate of its downstream transcription factor STAT1 in human cell lines (25). Removal of any one of the IFN-γ-induced mechanisms to control T. gondii leads to higher parasite burdens in mice, but acute survival is not impaired, in contrast to the extreme susceptibility of IFN-γ-deficient mice. However, in the absence of CD4+ T cells, an extended IL-12-dependent NK cell response is capable of producing adequate amounts of IFN-γ to allow survival (26). This survival depends on the NK cells helping to generate CD8+ T cell immunity to the parasite during the chronic phase of infection (26). Yet in the normal C57BL/6 model, IFN-γ is predominantly made by CD4+ T cells rather than by CD8+ T cells.
CD8+ T cells.CD8+ T cells have a complex role to play in control of T. gondii infection: they secrete IFN-γ and they can specifically kill infected cells. It has been shown by several groups that CD8+ T cells specific for parasite antigens can directly kill infected cells. For example, this can be illustrated with CD8+ T cells specific for an immunodominant T. gondii epitope, P30, which were found to be capable of killing both extracellular parasites and infected macrophages in vitro (27, 28). Additionally, CD8+ T cells generated from mice vaccinated with a temperature-sensitive mutant of T. gondii (ts-4) are cytotoxic in vitro for parasite-infected or antigen-pulsed cells in a major histocompatibility complex class I (MHC-I)-restricted manner (29). It is now established in mice that there are genetic variations in susceptibility to reactivation of T. gondii in the chronic stage of the infection: C57BL/6 mice, MHC-I H-2b haplotype, have the H-2Lnull allele and are susceptible to toxoplasmic encephalitis (TE), but BALB/c mice, MHC-I H-2d haplotype, have the H-2Ld allele and are genetically resistant to TE (30–32). This information explains why CD8+ T cells are the dominant T cell responders in BALB/c models but are minor players in C57BL/6 mouse models. A subsequent and perhaps unsurprising finding associated with this homozygosity of the MHC loci in inbred mice is that BALB/c mice have a corresponding TCR restriction, Vβ8 CD8+ cells, which are abundant in the brain of infected mice (33). Adoptive transfer experiments showed that Vβ8 CD8+ cells produced the most IFN-γ and were more protective than Vβ8 CD4+ cells in response to parasite infection, leading the authors to speculate that this restriction allows for the best recognition of T. gondii antigens presented via MHC-I H-2Ld on infected cells (33). CD8+ T cell responses to epitopes of several identified antigenic T. gondii proteins, including P30 (SAG1), GRA4, GRA6, and ROP7 in BALB/c mice (27, 28, 34, 35), GRA1, GRA7, and ROP2 in C3H mice (36–38), or Tgd057 in C57BL/6 mice (39), could potentially be generated, and while vaccination with one of these proteins, such as GRA1, provides some protection from lethal T. gondii challenge to a C3H mouse, this vaccination does not protect BALB/c or C57BL/6 mice despite generation of antigen-specific CD8+ T cells (40). Surprisingly, the exact T. gondii protein used for vaccination seems to be less important than the location of the epitope processed for antigen presentation within the original protein sequence (41), further illustrating that the specific MHC-I haplotype of the host, and consequent bias in peptide loading for antigen presentation, is critical for determining the contribution of CD8+ T cells to protection from the parasite.
While CD8+ T cells play an important role in BALB/c mice during the chronic stage of the infection, there is a considerable amount of conflicting literature as to whether this protection is mediated by secreted IFN-γ or by their direct cytolytic ability. For example, perforin-deficient mice lacking cytolytic ability survive acute T. gondii infection and have an unimpaired level of IFN-γ, but they have a higher cyst burden and slightly increased susceptibility at later time points of the infection. These results indicate that the cytolytic abilities of CD8+ T cells contribute to control of encysted parasites (42). In contrast, adoptive transfer of perforin-deficient CD8+ T cells was still effective at preventing TE in a chronic reactivation model utilizing sulfadiazine-treated athymic nude mice (43). Although adoptive transfer of perforin-deficient CD8+ T cells is effective at preventing TE, recent work supports the model of cytolytic cyst control, as transferred IFN-γ-deficient CD8+ T cells are able to greatly reduce cyst burden in a chronic reactivation model (44). The multifaceted effects of IFN-γ on the immune system make it difficult to separate the contribution of CD8+ T cell IFN-γ from that of other sources of this cytokine. IFN-γ itself increases expression of endothelial vascular cell adhesion molecule 1 (VCAM-1) to aid in recruitment of CD8+ T cells to the brain of chronically infected mice and thus enhances any effects of CD8+ T cells on immunity to T. gondii (45). It seems likely that both IFN-γ and cytolytic functions of CD8+ T cells are contributing to host resistance to pathogenesis (46).
NK cells.Early experiments into T. gondii infection during T cell deficiency revealed that NK cells were also a source of IFN-γ. Splenocytes from SCID mice were able to produce significant amounts of IFN-γ in response to the parasite (47, 48). In mice lacking CD8+ T cells, NK cells dramatically expand in numbers, produce IFN-γ, and mediate protection against T. gondii (48). Simultaneously, it was shown that NK cells are not directly cytotoxic for T. gondii-infected cells but that NK cell protection is mediated by IFN-γ (15, 48). IFN-γ from NK cells can be enhanced with the early administration of IL-12 during infection and this increases the survival of susceptible SCID mice (12); IL-12 is both required and sufficient for triggering IFN-γ production by NK cells (2). This IL-12 is produced by dendritic cells (DCs), which are discussed in more detail in a subsequent section.
The effect of DC-derived IL-12 on NK cell IFN-γ production triggers a positive-feedback loop that modulates the innate inflammatory environment. T. gondii-infected mice blocked for IFN-γ or depleted of NK cells demonstrate impaired maturation of DCs and inflammatory monocytes, increased numbers of resident macrophages, and decreased IL-12 production by DCs (49). The ability of monocytes to respond to IFN-γ priming is necessary for increased activation of monocytes and for IL-12 production by monocyte-derived DCs in response to T. gondii infection (49, 50). On the molecular level, it has been shown that IFN-γ enhances the production and transcription of IL-12 via induction of regulatory transcription factor 8 (IRF8), a major transcriptional factor regulating IL-12p40 and IL-12p35 transcription (50, 51). Together, these results indicate that NK cells are a critical effector component of the innate immune response—able to effectively prime monocytes and DCs for parasite recognition while mediating T cell-independent IFN-γ-dependent host protection from the parasite.
Neutrophils.An unforeseen player in the production of IFN-γ during toxoplasmosis is the neutrophil. Recent evidence illustrates that in both wild-type (WT) and TLR11-deficient mice, neutrophils are the dominant cell type responsible for early IFN-γ responses (52). The level of IFN-γ observed in each neutrophil is low compared to that of activated NK or T cells (52), and yet neutrophils are known to congregate in large numbers at the site of acute toxoplasma infection (49, 52–54). Depletion of neutrophils in TLR11-deficient mice resulted in acute mortality that can be delayed with injections of recombinant IFN-γ (52). These data revealed that neutrophil-derived IFN-γ is responsible for the partial survival of TLR11-deficient mice during the acute stage of the infection. In WT mice, both TLR11- and IL-12-dependent NK cell IFN-γ and TLR11-independent neutrophil IFN-γ are involved in resistance to T. gondii during the acute stage of the infection.
Neutrophils and their confusion with inflammatory monocytes.The consequences of IFN-γ production by neutrophils during T. gondii infection are both in agreement with and in contrast to previous data describing a role for neutrophils in host resistance to the parasite. Original studies on the importance of neutrophils were accomplished by utilizing the antibody Gr-1 to deplete neutrophils, and exacerbation of disease was observed (55, 56). The Gr-1 antibody recognizes two distinctly expressed but highly related surface receptors, Ly-6C and Ly-6G, which are expressed on both monocytes and neutrophils or on neutrophils alone, respectively (57). Conclusions about the importance of neutrophils drawn from experiments utilizing Gr-1 for depletion were confounded by simultaneous depletion of both monocytes and neutrophils. The individual roles these two cell types play during T. gondii infection began to be elucidated with chemokine and chemokine receptor knockout mice. CCR2- and MCP-1-deficient mice fail to recruit inflammatory monocytes, and the results are a loss of parasite control and acute susceptibility to T. gondii infection (58). These data suggest that inflammatory monocytes are essential for parasite elimination at the site of the infection. Yet both CCR2- and MCP-1-deficient mice have unimpaired IFN-γ levels in the serum and peritoneal lavage fluid (58). Furthermore, CD4+ T cells isolated from CCR2- and MCP-1-deficient mice produced similar amounts of IFN-γ in response to T. gondii antigens (58). These results indicate that IFN-γ production and generation of Th1 responses to the parasite are independent of the presence of inflammatory monocytes but that inflammatory monocyte effector mechanisms for parasite elimination are indispensable for the host protection. In contrast to CCR2- and MCP-deficient mice, CXCR2-deficient mice have impaired neutrophil recruitment during infection. CXCR2-deficient mice were found to harbor a higher parasite burden, but these mice did not display increased mortality during the acute stage of the infection (59). Unlike CCR2- and MCP-1-deficient mice, CXCR2-deficient mice did have dramatically reduced serum IFN-γ and T cell IFN-γ responses, implicating neutrophils as early players in influencing IFN-γ levels (59).
The recent availability of an antibody specific for Ly-6G (1A8) allowed further insight into the roles of neutrophils during infection. In an oral infection model, greater than 65% of WT mice treated with 1A8 survived infection, whereas CCR2-deficient mice and WT mice treated with Gr-1 succumb during the acute phase (60). The authors concluded that monocytes and not neutrophils were important for parasite control in part because administration of 1A8 had no effect on the percentage of monocyte recruitment to the site of infection. Interestingly, in a pathogen-free subcutaneous air pouch model, it has been shown that depletion of neutrophils significantly decreases the recruitment of inflammatory monocytes (61). In fact, neutropenia reduces monocyte recruitment in a number of models, as reviewed in reference 62. Thus, in the absence of neutrophils, there may be lower total numbers of inflammatory monocytes, and yet they could represent a percentage of the remaining cells in vivo similar to that seen with the nondepleted condition.
It is important to emphasize that the relative contributions of monocytes and neutrophils were largely examined in mice which have an intact TLR11 recognition system responsible for IL-12-dependent NK cell IFN-γ priming of inflammatory monocytes. But in the absence of inflammatory monocytes, such as in cases of CCR2 deficiency, MCP-1 deficiency, or depletion with anti-Gr-1, sufficient IFN-γ levels become irrelevant. TLR11-deficient mice still have significant amounts of IFN-γ present, initially provided by neutrophils, to prime monocytes, and these mice usually survive infection (4, 63). In the absence of both TLR11 and neutrophils, the early IFN-γ response is severely compromised and inflammatory monocyte recruitment may be reduced, resulting in acute susceptibility (Fig. 1).
The large variety of cell types capable of making IFN-γ illustrates the importance of this cytokine in immunity. The contribution of individual cell types to IFN-γ production is a complex subject, but the generation of conditional IFN-γ- or IFN-γ receptor-deficient mouse models may provide the opportunity to dissect this dilemma.
KNOWN AND UNKNOWN REGULATORS OF IFN-γ PRODUCTION: IL-12, IL-1β, AND TNF
DC IL-12 production is essential for IFN-γ production by NK cells.DCs are the major IL-12-producing cells in response to T. gondii infection. It was observed that IL-12 is initially produced by CD8α+ DCs upon exposure to T. gondii profilin in a TLR11- and MyD88-dependent manner (2, 4, 6). CD8α+ DCs produce large amounts of IL-12 but not other proinflammatory cytokines such as TNF and IL-1β (50). The explanation for this cytokine specificity was recently explained by the finding that TLR11 induction of IL-12 requires activation of the transcriptional factor IRF8 which is selectively expressed in naive CD8α+ DCs (50, 64). At the same time, recognition of T. gondii profilin by CD8α+ DCs fails to trigger substantial activation of NF-κB, which explains their relative lack of production of TNF and IL-1β (50), two cytokines regulated via the NF-κB-signaling pathway. After the initial recognition of the parasite and cytokine production, IFN-γ is produced early in infection by neutrophils and NK cells. Early IFN-γ production induces expression of IRF8 in macrophages and CD8α− DCs which enables them to respond to T. gondii infection, reinforcing the IL-12 response (50).
Impairment of parasite recognition in DCs, with DC-specific inactivation of MyD88 in mice, results in a delayed and reduced, but not abolished, IFN-γ response from NK cells, suggesting that additional sources of IL-12 also contribute during infection (2). Nevertheless, delayed NK cell IFN-γ production has a major impact on the outcome of the infection; mice with DC-specific inactivation of MyD88 are very susceptible to the parasitic infection, with a survival rate below 50% (2). Mice surviving infection with DC-specific inactivation of MyD88 have dramatically elevated cyst burdens during the chronic stages of the infection (2). Thus, even though NK cell IFN-γ production is largely initiated during the acute stage of the infection, it has long-term consequences seen weeks after initial T. gondii infection. It should be noted that this TLR11-dependent IL-12 response regulates IFN-γ production from NK cells (2, 15) and from effector CD8+ T cells (65) but is dispensable for neutrophil IFN-γ production (52). While much is known about TLR11-mediated immunity to T. gondii, these and other data suggest that TLR11 is not the entirety of the story for T. gondii recognition or regulation of cytokine production by immune cells.
TLR12 coordinates with TLR11 in parasite recognition.Pattern recognition receptors, such as TLRs, are innate immune receptors involved in recognizing conserved molecules present on bacteria, viruses, and parasites which are not expressed by the host cells. In mice, recognition of T. gondii profilin is mediated by TLR11, which directly binds profilin, forms a heterodimer with TLR12, and recruits the TLR adaptor protein MyD88 (4, 5, 50). Recent data suggest that TLR12 can function independently of TLR11 in plasmacytoid DCs (pDCs). pDCs are a specialized subset of DCs that produce large quantities of type 1 interferons. They are most often associated with viral infections but have also been shown to be involved in both bacterial and parasitic infections. pDCs were specifically observed to produce IL-12 and IFN-α in response to profilin, but in contrast to the TLR11 and TLR12 heterodimer complex that usually regulates IL-12 production, the TLR12 homodimer was sufficient (66). However, the conclusion by Koblansky et al. is inconsistent with an earlier analysis which found that pDCs fail to produce IL-12 or IFN-α in the absence of TLR11 (67); therefore, their further observations attributing NK cell IFN-γ to pDC IL-12 should be viewed with some skepticism. This discrepancy regarding the TLR dependence of pDC IL-12 needs to be clarified, as does the observed dependence of IFN-α on TLR12. Furthermore, how TLR12 can trigger cytokine production in the absence of TLR11 is a mystery because, in contrast to TLR11, TLR12 fails to biochemically interact with MyD88 (50).
Regulation and production of IL-1β and TNF.IL-1β is a powerful mediator of the inflammatory response. This cytokine is synthesized in a pro-form in response to TLR signals in a MyD88-dependent manner and then typically cleaved by caspase-1 and secreted in response to danger signals. Daily injections of IL-1β or TNF into T. gondii-infected BALB/c mice significantly prolong their survival, and administration of a single dose of IL-1β and TNF combined greatly enhances this survival (68). Furthermore, production of IFN-γ by SCID mouse splenocytes stimulated with IL-12 plus TNF was completely ablated by administering anti-IL-1β (69). As a pleotropic mediator of inflammation, IL-1β mediates its protective effects via multiple mechanisms, including enhancing expression of the TNF receptor, which may explain the synergistic effect of IL-1β and TNF (70). While TNF alone is unable to significantly increase the antiparasitic activity of macrophages, TNF synergizes with IFN-γ to enhance it (68). Additionally, both TNF and IL-1β are crucial regulators of neutrophil-derived IFN-γ, as blocking either TNF or IL-1β decreased the observed IFN-γ levels (52). IL-1R-deficient mice have almost no detectable neutrophil-derived IFN-γ, which is a stronger phenotype than blocking IL-1β and is in contrast to the resistance phenotype of caspase-1-deficient mice (52, 63). Possible explanations for the discrepancy between IL-1β blocking and IL-1R-deficient mice include incomplete blocking of IL-1β, the dominance of the TLR11 recognition system in IL-1R-deficient mice, and the fact that neutrophils are capable of caspase-1-independent IL-1β production (71). The dominant source of TNF and IL-1β is monocytes, but since neutrophils themselves are capable of making both of these cytokines, this may be an important feedback loop during the initial response (52). While it seems likely that TLRs are involved in the recognition system regulating TNF, it is possible that there is an unknown recognition system or danger signal(s) regulating IL-1β.
MyD88 dependence of host resistance independent of TLR11.A likely explanation for residual resistance to T. gondii infection in the absence of TLR11 is the cooperation of additional endosomal TLRs and IL-1β in activation of MyD88. In 3d mice, which lack functional UNC93B1—a chaperone protein that controls trafficking of TLRs from the endoplasmic reticulum to the endolysosome—resistance to T. gondii is lost because all endosomal TLRs, including TLR11, TLR12, TLR7, and TLR9, are incorrectly localized in these mice (50, 72–76). Interestingly, the severe acute susceptibility seen in 3d mice is nearly identical to that of MyD88-deficient mice, suggesting that there are additional UNC93B1- and MyD88-dependent TLRs involved (74, 75). TLR3-, TLR7-, or TLR9-deficient mice exhibit little to no phenotype during T. gondii infection (63, 74) even when the deficiencies are combined, as is the case of TLR3/TLR7/TLR9 triple deficiency (76). These data illustrate the dominant effect of TLR11/TLR12 profilin recognition in generating a Th1 immune response to the parasite in a mouse model. However, since humans do not have functional TLR11 or TLR12 (77), the importance of other TLRs must be considered. It has been found that TLR7 can recognize T. gondii RNA and that TLR9 can recognize many CpG motifs in T. gondii DNA (76), and a further discussion of these data, and other TLRs, has been recently reviewed (24). These additional intracellular TLRs likely contribute to the susceptibility of both MyD88 and 3d mice, as TLR3/TLR7/TLR9/TLR11 quadruple-deficient mice had almost no IL-12 or IFN-γ observed in the first week of infection (76).
Yet there is a striking difference between the survivability of 3d mice and MyD88-deficient mice during T. gondii infection in that administration of IL-12 to 3d mice rescues their survival but IL-12-treated MyD88-deficient mice are as susceptible to infection as nontreated mice despite partially restored Th1 responses (2, 7). This suggests that MyD88 is important beyond IL-12-dependent innate immune cell responses. At least some of this may be explained by the role of MyD88 in IL-1β production and neutrophil IFN-γ as discussed above. Additionally, MyD88 may be involved in the priming event in inflammasome activation. The inflammasome is a complex of proteins that assemble in response to intracellular danger signals, often mediated by proteins from the 'nucleotide-binding domain and leucine-rich repeat-containing gene family, with a pyrin domain' (NLRPs), capable of activating caspase proteins to cleave pro-IL-1β or pro-IL-18 into their mature forms for secretion. Before IL-1β and IL-18 can be cleaved, they need to be expressed, and priming through TLRs via MyD88 is one way to induce production of the pro-form of these cytokines. It was recently shown that T. gondii can activate NLRP1 (78, 79) and NLRP3 (79) inflammasome complexes to stimulate IL-1β or IL-18 cleavage and secretion. It is known that, in oral infection models of T. gondii, commensal bacteria can provide the ligands for TLR2, TLR4, and TLR9 stimulation (63). These bacterially derived TLR ligands could provide the priming signal necessary for successful inflammasome responses. However, T. gondii itself can also provide additional TLR ligands, as mentioned above, and these data are supported by the fact that LPS priming was not required in vitro for bone marrow-derived macrophages to produce IL-1β in response to T. gondii (79) and by the fact that T. gondii infection in germfree mice had a robust IL-1β response (78). These data indicate that MyD88 is necessary for a successful inflammasome response to T. gondii infection, although the precise signaling events leading to caspase activation upstream as well as downstream of MyD88 are not fully defined.
Additionally, experiments in conditional MyD88-deficient mice showed that removing MyD88 in T cells alone resulted in a dramatic abrogation of Th1 response to the parasite (80). Whether the mechanisms underlying T cell-intrinsic MyD88-dependent loss of IFN-γ in CD4+ T cells can be attributed to TLR- or IL-1-dependent activation of MyD88 remains to be identified. However, it is clear that the acute susceptibility of completely MyD88-deficient mice to T. gondii infection stems from multiple defects in activation of IFN-γ production by neutrophils and by NK and T cells: deficiency in IL-1β signaling impairs neutrophil IFN-γ production, DC-specific loss of TLR signaling results in deficient NK cell IFN-γ production, and T cell-intrinsic MyD88 deficiency abrogates Th1 responses to the parasite.
This review has given a broad overview of IFN-γ during T. gondii infection and serves to illustrate the blurring of the line between innate and adaptive responses: MyD88 is important for the IFN-γ immune responses from neutrophils and from NK and T cells (Fig. 2). Much is now known about the immune responses to T. gondii in murine models, including the dominance of TLR11-mediated recognition and IRGs. Humans lack these systems and yet have a robust immune response which includes the production of IFN-γ. Therefore, future work in the field will likely be focused on identification and clarification of the roles of innate sensors and resistance mechanisms important for T. gondii recognition in humans.
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.. Colorado State Senate President John Morse and one of his chief henchwomen , State Senator Angela Giron , were recalled tonight from office .
.. Even better , they were both replaced , I believe , with Republicans . Not sure on who yet . More on that later . Not sure on the partisan flip in the Colorado Senate , yet , but it should help , at least …
.. update — It changes the partisan layout to 18 to 17 , from 20 to 15 . One more seat changes hands (hopefully by recall , or in a by – election) , and the GOP grabs the Colorado Senate …
Related articles
- Outside money shows national interest in Colorado recall elections (denverpost.com)
- Tomorrow's Recall Vote For Gun Control-Supporting Colorado Senators Draws Strong Early Turnout (personalliberty.com)
- BREAKING: Anti-Gun Colorado Senator Concedes… He is RECALLED (capitalisminstitute.org)


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Field Hockey Camp
Event Description
Field Hockey
The Ursinus College Youth Field Hockey Camp is for all levels of experience for girls entering 1st through 8th grade. Campers will be grouped according to age and experience and will receive instruction from Head Coach Janelle Benner, the UC field hockey staff, and UC field hockey players. The camp will focus on teaching skills, basic field hockey concepts, and teamwork through a variety of games and drills. All field players must have a mouth guard, shin guards, and stick. Goalkeepers must be fully equipped. If you have any questions about equipment needs, please don't hesitate to contact Janelle Benner at email@example.com.
UC employees receive a $10 discount.
Location: Patterson


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Charles W. Fishburn, 61, of Dousman, WI passed away unexpectedly on Thursday, November 28, 2019 at his home.
Chuck was born on September 23, 1958 in Chicago, IL the son of Paul and Kathleen (Williams) Fishburn. Chuck was happiest when he was out in nature. He loved to hunt and fish. Chuck will be remembered by his family for his good heart and generosity. He will be missed.
He is survived by: his daughter, Erin; his siblings, John Paul (Cathy) Fishburn and Terry Goudie; and his cousins, Jim (Linda) Williams, Keith Schoenke, and Robin (Schoenke) Schutte. He is also survived by a number of nieces, nephews, other relatives and friends.
Chuck is preceded in death by his parents and a sister, Katherine Gunther.
A private family service will be held at a later date to honor Chuck's life.
Gibson Family Funeral Homes of Eagle & Palmyra, WI is serving the family. To place an online condolence please visit gibsonfuneral.com
To send flowers to the family or plant a tree in memory of Charles W. Fishburn, please visit our floral store.


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How many sessions will I need?
Some people need only one session, others may need counselling or hypnotherapy for many months. It always depends on the individual and we'll discuss this at your first session. It's important to have an end goal in sight so I usually offer a course of six sessions, with a progress review at the end. At this point, we can decide together whether to end there or continue your therapy. Your counselling will never be ended abruptly.


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The West Africa Fashion Week finale date scheduled to hold on the 9th December will see plethora of Nigerian celebrities making the list of awardees. These Nigerian celebrities will be amongst celebrities across West Africa whom were shortlisted for different awards in different categories.
They include Former Big Brother Naija housemate – Alex, model and fashionista – Denola Grey, Style Influencer – Noble Igwe and actress Juliet Ibrahim. Others are Tobe Onwumere and Aidi Aisien.
The West Africa Fashion Week is billed to hold in Lagos at the Atlantic Centre, Chevron Drive, Lekki Express way from the 7th to 9th December.


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It was a blast being able to be a part of a Christmas theme wedding shoot. The vendors were amazing and very creative!
Vendors: Photographer: Lady Rose Photography, LLC – Fine Art Portrait Artist
Venue: Tuscawilla Country Club
Bride/Groom: Brittany Shuff and Casey Shuff
Bridesmaids: Ashley BeLoat and Kayla 'blondi' Mcmullen
Gowns: Krustallos Couture Bridal – Custom Silk Gowns – Atelier
Jewelry: Yulisa: Chloe + Isabel by YuliNu
Floral: The Flower Studio
Cake: Bakers Cottage Cakes
Rentals: Orlando Wedding and Party Rentals
Vintage vehicle: VIP Wedding Transportation
Hair: Janie Tongue
Makeup: HAIRSTYLES & MAKEUP BY JACKIE
Stationary: Sign Brewery
Calligraphy: Dear Darling Studio
Tableware: The Vintage Dish – Timely Tableware


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Japanese Maple (2hr Paint & Sip)
Have fun creating your very own masterpiece painting with acrylic on a 40x50cm canvas without ever having painted before!
Our artists paint along with you demonstrating step-by-step from start-to-end how to paint the featured artwork while you enjoy the relaxing experience, sipping on a glass of your favourite beverage and socialising with friends.
It's all about Fun Art, not Fine Art!
And remember, we are a BYO studio, so bring along your favourite bottle or two of liquid creativity to enjoy while you paint and sip with us on the day.
You supply the wine and we'll provide all the art materials, glassware and good vibes. Leave the rest to us!
This is not your typical painting class!
Japanese Maple (2hr Paint & Sip) - BYO Food & Drink
Date and Time: Thu. 10 January 2019, 7:00 pm – 9:00 pm
Venue: Cork & Canvas, 206 Clarendon Street South Melbourne, Vic 3205
Cost: $50 Booking
Copyright © Australia-Japan Society of Victoria Inc. All rights reserved. PO Box 2128, Forest Hill, VIC 3131 T: +61 3 9028 2001


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Report: Secret Requests For Apple Data Jumped in 2015
Apple received more than 1250 secret government data requests in the second half of 2015, up from 750 in the first half.
Apple received more than 1250 secret government data requests in the second half of 2015, up from 750 in the first half.
Much has been said about Bill Campbell, but I wanted to add a little more since Bill meant a lot to me personally.
Adobe, however, warns users that uninstalling QuickTime on Windows could affect Creative Cloud.
Recycling bits and pieces from a library of electronic devices adds up.
Don't worry: Apple and the FBI still have plenty more iPhone unlocking cases to fight over.
Reports said the feds used Israeli firm Cellebrite to unlock the phone, but the Post dismissed those claims.
The agency reportedly briefed Sen. Dianne Feinstein, but Apple is not on its invite list.
We suspect Apple is working hard to patch the supposed exploit that the FBI has used to break into locked iPhones.
Should the FBI or other government agencies reveal bugs to tech companies or use them to their advantage?
Investigators have unlocked the San Bernadino killer's iPhone without Apple's help.
Apple isn't paranoid; the NSA has been known to intercept shipments to install snooping devices.
Apple's last event at its Cupertino campus saw the debut of smaller iPhone and iPad Pro models, plus software updates and more Apple Watch band options.
Now that ad blocking is going mainstream thanks to Apple, change is coming.
If you're an Australian Apple user, yesterday's iPhone 6s launch event was equal parts exciting and quietly disappointing.
After attending Build, I/O, and WWDC, what stood out the most to me was the effort that these companies are putting in to create intelligent systems that know as much as possible about you.


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Guangzhou's public transportation departments have taken precautions by inspecting all vehicles and checking passengers leaving and arriving in the city in response to the outbreak of novel coronavirus pneumonia (NCP), an official said at a press conference on February 11.
As of February 10, the authorities had examined about 5.44 million vehicles and checked the body temperature of about 41.8 million passengers. They have confirmed 1,688 people who have fever, and placed 209 people under quarantine for medical observation at designated hospitals.
Li Chaowen, deputy director of the Guangzhou Bureau of Transportation, said the inspection efforts to curb the spread of the virus have been reinforced since the city activated its first-level of public health emergency response. "Guangzhou has set up 222 temperature monitoring points from January 24, including 192 at intercity highways, 22 at national and provincial highways, and 8 at intracity roads," Li said. "Meanwhile, the government has urged transport companies to disinfect vehicles and parking places, inspect drivers and relevant staff, and suspend all regular traffic routes to Hubei province."
Wang Xiaodong, director of the traffic police detachment of the Guangzhou Bureau of Public Security, said all buses, metros, and taxies (including those hailed online) are disinfected every day, while drivers and passengers are required to have their body temperatures measured. The city's 826 bus lines are equipped with 14,000 hand-held thermometers, aiming to cover all stations and lines.
"Five disinfection centers have been established at Guangzhou Railway Station, Guangzhou East Railway Station, and Jixiang Road, offering free disinfection services for taxies and online hailed cars," Wang said.
All materials marked with "source: English.gz.gov.cn" on this website (including but not limited to text, photographs, audio and video materials) are the copyrighted property of Guangzhou International (the official website of Guangzhou Municipality). Without prior authorization from Guangzhou International, any media, website, organization or individual shall not transmit, interlink, distribute or republish such materials in any form. Any media and website authorized to republish such materials shall mark them with "source: Guangzhou International (English.gz.gov.cn)". Infringement of these copyrights will result in legal action.


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Greg DuPree
Frittatas are some of the most efficient vehicles for leftover vegetables. Here, we combine roasted butternut squash with quick-cooking kale for a fiber-rich breakfast duo. A touch of dairy lends custard-like creaminess to the egg mixture.
How to Make It
Step 1
Preheat broiler to high with oven rack in upper middle position.
Step 2
Heat an 8-inch ovenproof skillet over medium. Coat pan with cooking spray. Add kale and roasted butternut squash; cook 2 to 3 minutes.
Step 3
Whisk together eggs, yogurt, salt, and pepper. Add eggs to pan, and cook 2 minutes, stirring slowly and tilting the skillet a few times so runny parts hit the pan.
Step 4
Place pan under broiler; broil 1 minute or until eggs are almost set. Top frittata with avocado.


text: Valerie Plame is an undercover CIA agent turned author, and apparently she took the advice to write about what you know based on her debut novel Blowback and her spy main character Vanessa Pierson. In this story, Vanessa has one all-consuming goal, to catch the international arms dealer and terrorist known as Bhoot. This is a spy thriller, and it reads like one, filled with suspense, fast paced split second decision making by our heroine, and lots of intensity. The best part? Authenticity. I mean, these two kick ass ladies have the same initials for a reason.


text:
Jessica Sager
Miley Cyrus Smoking Weed Drove People to Quit Their Jobs
Miley Cyrus smoking weed is pretty annoying for everyone who realizes it's actually not that big of a deal, nor is it rebellious or unique or badass. But apparently Miley Cyrus' marijuana use still bothers some people, so much that they actually quit their own jobs over it. What happened?
Rumor: Beyonce + Jay Z to Open 2014 Grammys With 'Drunk in Love'
UPDATE: Check out Beyonce + Jay Z's Grammy performance here!
Beyonce and Jay Z will collaborate onstage at the 2014 Grammy Awards tomorrow night (Jan. 26), and now we know what hip-hop's power couple will perform! Well, maybe.
Beyonce and Jay Z will collaborate onstage at the 2014 Grammy Awards tomorrow night (Jan. 26), and now we know what hip-hop's power couple will perform! Well, maybe.
Adele Working With Phil Collins on New Record
We can't wait for the new Adele album, and neither can the rest of the world. Now we have more details on the privacy-loving star's new project. She'll be working with fellow Brit singer-songwriter Phil Collins!
Justin Bieber Leaves Miami for Los Angeles With Dad Jeremy Bieber [VIDEO]
Justin Bieber is finally leaving South Beach and heading home to Los Angeles after what's been, at best, a tumultuous stay in Miami. And rumor has it Biebs isn't looking forward to landing.
Justin Bieber May Not Have Been Drunk Nor Drag Racing After All
Beliebers, hold out hope! Justin Bieber may not have been drag racing nor driving under the influence after all ... maybe.
'Bachelor' Star Juan Pablo Galavis Is Really Confused by Homosexuality
'The Bachelor' is pretty much an hour-long lesson in humiliation and failed relationships, and this season is no different. But now the Bachelor himself, Juan Pablo Galavis, is humiliating himself with some really ignorant, borderline homophobic comments from an interview.
Justin Bieber Drugs: Reportedly Abusing Sizzurp + Urged to Go to Rehab
Sorry, Beliebers: If reports are to be believed, "Justin Bieber drugs" is about to start trending on your beloved Twitter feeds. In light of his egging fiasco, rumors have surfaced that the 'Beauty and a Beat' singer has been abusing drugs quite a bit -- especially sizzur…
Miley Cyrus + Britney Spears Deemed Too Hot for TV in France
Miley Cyrus and Britney Spears don't just have 'SMS (Bangerz)' in common. The pair now also share a ban from French television -- for being just way too sexy.
Bobbi Kristina Brown + Adopted Brother Nicholas Gordon Are Married
Bobbi Kristina Brown and Nicholas Gordon, her adopted brother, are officially married. Happiness and/or creepiness are both perfectly appropriate responses to this.
Former Teen Heartthrob David Cassidy Arrested for Drunk Driving for Third Time
Bad things come in threes, right? We bet David Cassidy agrees: This week, the onetime teen heartthrob was arrested on his third drunk driving charge. Yikes!


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The development strategy is an integral part of any organization, because it is thanks to it that we can:
1. Know where we are going, because there are clear goals set.
2. To involve all the sacraments in the club to move to a clear result.
3. Correctly direct the resources of the club and distribute responsibilities.
4. Assess our progress or regress.
5. Not to be divided into trifles.
♦ 150 active players;
♦ 10 teams of 15 people in each;
♦ 20 coaches (2 coaches per team);
♦ In the state of the club: an accountant, a clerk, a lawyer, a doctor, a revision commission;
♦ The formed parent committee, which helps to solve the problems of the club and actively participates in its development;
♦ Referee team;
♦ 10 partners providing regular sponsorship and players have individual sponsors;
♦ Regular participation in the championship of Ukraine;
♦ Permanent participation in foreign tournaments;
♦ Champions of Ukraine on the floorball;
♦ Club Fund, which will serve as a source of funding for players in the national team of Ukraine;
♦ Floorball is taught at a physical education school;
♦ Availability of office;
♦ Ownership of the club: boards, several gates, form;
♦ Functional school floorball league;
♦ Functional regular tournament in Uzhgorod.


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After a successful kick-off in Ho Chi Minh City, SCG Street Football 2018 continues its journey to Hanoi for the National Final. The tournament attracted 60 teams with nearly 400 players in Hanoi to play in the regional qualification round.
The best two teams in Hanoi will compete with the best teams in Ho Chi Minh in the Final in the capital's Old Quarter on October 7.
"With our passion for a better generation in Vietnam through sports, SCG is delighted to host SCG Street Football in both Hanoi and Ho Chi Minh City," said Mr. Chartchai Jadtanim, SCG's Country HR Director in Vietnam. "Street football is the starting point for many football stars, so we would like to see many more talent in Vietnam grow up from our street football tournament."
Aiming to excite football players and football fans alike, SCG Street Football 2018 not only features the competition but also brings interesting football mini games to spectators of all ages. Under the theme #fromstreettostar, the Kid Talent contest will find football talent under 14 years of age in Hanoi through unique challenges.
"This is the first time we've competed in such a street football tournament," said a member of FC Phui, one of teams. "The competition rules are quite unique, making teams play wholeheartedly and keep spectators interested until the final whistle. The atmosphere at the tournament is entertaining for everyone."
SCG Street Football 2018 is the second holding by SCG after the success of the first in Hanoi last year. The tournament has been expanded to Hanoi and Ho Chi Minh City this year, in a 3v3 format for players from 16 to 22. After the regional qualification rounds in Ho Chi Minh City (September 8) and Hanoi (September 29) to find the best four teams from both regions, the National Final will take place in Hanoi's Old Quarter on October 7.


text:
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Cooler temperatures have arrived in the wilderness north of Toronto and it's a great excuse to check out some fabulous indoor concerts. Here's just a partial list of live music performances happening in Almaguin, Loring-Restoule, Muskoka and Parry Sound this fall.
Algonquin Theatre Huntsville
Sharon & Bram: September 8
Séan McCann Sings: September 15
I & I with Meagan Ballantyne: September 22
The Everly Brothers Experience: October 4
Splash'n Boots Live: October 5
The John Fogerty/C C R Story!: October 6
Beatlemania Revisited: October 13
I & I with Nicole Lisa Craig: October 19
The Third Annual Rock and Roll Black Tie: October 20
A Musical Journey of Recovering & Thriving: November 3
Liona Boyd: November 7
All McCartney Live: November 10
The Travelling Milburys: November 17
Photo Credit: Algonquin Theatre
Brunswick Sports Grill & Pub Parry Sound
Check their Facebook Page for Weekend Live Music announcements
Charles W. Stockey Centre for the Performing Arts Parry Sound
Jim Cuddy: September 7
The Mudmen: September 14
Classic Albums Live presents Fleetwood Mac's Rumours: October 10
Brett Kissel: October 20
Terry Little's Autumn Fiddle Fest: October 27
Les Stroud / Survivor Man Live: November 2
Alan Doyle: November 7
Fred Penner: November 9
Wintersleep: November 10
The Slocan Ramblers: November 29
Photo Credit: Brett Kissel Facebook Page
The Country Gourmet Cafe & Gallery Parry Sound
The LYNNeS: September 21
Deerhurst Resort Huntsville
Brett Kissel: October 21
Serena Ryder at Girlfriends' Getaway Weekend: November 9-11
Etwell Concert Series Huntsville
MonkeyJunk: September 9
The Weber Brothers: September 16
Angel Forrest: September 30
Gravenhurst Opera House Gravenhurst
Oakland Stroke: September 29
Blazing Fiddles: September 30
Steve Hill: October 5
Motown Gold: A Live Musical Celebration of the Legendary Record Label: October 13
Orillia Silver Band Fall Harvest: October 28
Ensemble Vivant: November 9
Fred Penner Live!: November 10
The John Fogerty / CCR Story!: November 17
Metropolitan Silver Band: November 25
Photo Credit: Gravenhurst Opera House
The Griffin Gastropub Bracebridge
Enjoy live music every Thursday night and weekend acts as well
Highlander Brew Co. South River
Pam Millar & Sean Cotton: September 22
James Gray: November 17
The Kee to Bala Bala
The Wheat Kings: October 13
Stayin' Alive: October 13
The Landmark Pub Burk's Falls
Check their Facebook Page for Weekend Live Music announcements
Ms T's Grub Hub Burks Falls
Ms Ts Tuesday Tunes and Wing Night: September 18
Ms Ts Tuesday Tunes and Wing Night: October 2
Ms Ts Tuesday Tunes and Wing Night: October 16
The Oar & Paddle Gravenhurst
The Rough & Tumble: September 11
Grady Kelneck: September 12
Mitch Beube: September 18
Nicole Duquette: September 19
Sean Cotton: September 25
Mike Phillips: September 26
Papa John: October 2
Paul Noonan: October 3
Kenny Munshaw: October 9
Jamie Drake: October 10
Matt Allen: October 16
Mike Phillips: October 17
Sean Cotton: October 23
Papa John: October 24
Mitch Beube: October 30
Grady Kelneck: October 31
Photo Credit: Peter's Players
Peter's Players Gravenhurst
Coco Montoya: September 7
Peter's Players Fall Dinner Cruise: September 15
The Neil Young'uns: September 22
The Grapes of Wrath: October 6
The Electric Strawbs: October 13
Jill Barber: October 18
High South (trio): November 3
The Last Waltz – a Musical Celebration of The BAND: November 16
The Last Waltz – a Musical Celebration of The BAND: November 17
Rene M. Caisse Memorial Theatre Bracebridge
John McDermott Trio: October 17
Sawdust City Brewing Saloon Gravenhurst
Black Suit Devil: September 8
Law of Averages: September 15
If we've missed any great live music performances in the great Canadian wilderness just north of Toronto this fall, let us know at firstname.lastname@example.com.


text:
Bad Betty's Barbecue is a change of pace in sea of lariat ropes and spurs that have come to represent barbecue in the west. We are a true urban southern Barbecue experience in the heart of Montana. We have won many awards in the Barbecue competition world including first place at the Montana State Championship Cookoff in 2013 for both Ribs and Brisket. Bad Betty's Barbecue was named the best barbecue in the state of Montana in Thrillest Online Magazine's list of "The Best Barbecue Joint in Every State" in 2016.
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Nuclear Event – Hot Shutdown: Grand Gulf Nuclear Station, Mississippi
Technological Hazard – Nuclear Event
North America – USA | State of Mississippi, Claiborne County, Port Gibson, Grand Gulf Nuclear Station
Location: 32°00'24.0″N 91°02'54.0″W
Present Operational Age: ~30 years
Event: RPS ACTUATION – CRITICAL/HOT SHUTDOWN
Nuclear Event in USA on Tuesday, 29 March, 2016 at 11:23 [CDT]
"A Reactor Scram occurred at 1123 CDT on 03/29/2016 from 35% CTP [core thermal power]. The cause of the Scram appears to be a Turbine Generator trip. The station's procedures, '05-S-01-EP-2 RPV [Reactor Pressure Vessel] Control, 05-1-02-I-1 Reactor Scram ONEP [Off Normal Event Procedure] and 05-1-02-l-2 Turbine Generator Trip ONEP,' were entered to mitigate the transient with all systems responding as designed. No loss of offsite or ESF [engineered safety feature] power occurred. No ECCS [emergency core cooling systems] initiation signals were reached and no ESF or Diesel Generator initiations occurred. All control rods fully inserted. MSIVs [main steam isolation valves] remained open, no SRVs [safety relief valves] lifted, and no containment isolation signals were generated.
"Currently, reactor water level is being maintained by the Condensate and Feedwater System in normal band and reactor pressure and temperature are being maintained by the Reactor Water Cleanup System. The main condenser is available. There are no challenges to Primary or Secondary Containment at this time.
"The licensee has notified the NRC Resident Inspector."