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2014 Winter Olympics, Bobby Orr, Chicago Blackhawks, Drew Doughty, Duncan Keith, Los Angeles Kings, Montreal Canadiens, Nicklas Lidstrom, P.K. Subban, Paul Coffey, Steve Yzerman, Tampa Bay Lightning
Say you've won the Norris Trophy as the National Hockey League's best defenseman, lead your team in scoring as a defenseman, and are sixth among the league's blue-liners in goals and assists.
Is that enough to earn a free round trip ticket to Sochi, Russia to represent your country at the 2014 Winter Olympics? Maybe not, if you're Montreal Canadiens defenseman P.K. Subban.
One of the biggest questions heading into Hockey Canada's January 7 announcement of its Olympic team is will Subban, the reigning Norris Trophy winner, make the cut?
"It would be silly not for a Norris Trophy winner to be on the team. I don't even know why that's a debate," said Cyril Bollers, president and head coach of Skillz Hockey, a Toronto-based program and team that's produced a bevvy of minority NHL and major junior hockey players. "You've won a prestigious trophy and you're the best defenseman in the whole entire league, why would there be a debate for you not to be on the Olympic team?"
But questions about whether Subban will make it to Sochi have been brewing since October when media reports indicated that he appeared to be a long shot to play on an Olympics squad assembled by Tampa Bay Lightning General Manager Steve Yzerman and guided by Detroit Red Wings Head Coach Mike Babcock.
Babcock added fuel to the debate last month when offered what seemed to be read-the-tea-leaves comments about Subban's game and his chances of making Team Canada.
"The great thing about playing on the Olympic team is you've got to be a 200-footer," Babcock told The Toronto Star. "You've got to do it in both ends of the rink consistently and the coach has to trust you."
"What I mean by that is, you don't put people on the ice you don't trust, so you have to be dependable," Babcock continued. "So that's the No. 1 priority. I mean, there's skating, elite hockey sense, but you've got to be a trustworthy player – whether you're a goaltender, defenseman, a center. That's what we told (the players) at camp, I don't think it's different for anybody."
Babcock's comments were vaguely similar to the rationale given by Subban's detractors for why he should be excluded from the Canadian squad.
Subban's a high-risk, high-reward defenseman whose defensive deficiencies would be exposed on the larger international ice surface that the games will be played on in Sochi, his critics say.
He takes too many penalties, he's too flamboyant and too cocky for a team-oriented sport, they add. Besides, Team Canada will have enough offensive firepower from the blue line with the likes of Chicago Blackhawks' Duncan Keith, the Los Angeles Kings' Drew Doughty, and Shea Weber of the Nashville Predators.
The "Whither P.K." drama reached reached such a fever pitch in Canada that The Province newspaper of British Columbia wrote a scathing editorial last month headlined "With P.K. Subban, What Are They Thinking?"
"Some say that the hockey establishment's snubbing of Subban is related to his strong personality and to the fact that he is black," the op-ed piece said. "He plays the game on his terms and won't conform to the code of expected behavior. If that's the case, it's the establishment and not Subban that should adapt."
"Subban is one among the greatest defensemen in the world," the editorial concluded. "He's exciting to watch, has real joy for the game and is a terrific, entertaining personality. Leaving him off Team Canada would be unthinkable."
Subban has taken all the Olympics talk in stride.
"Obviously, just like most of the Canadian players in the league, I'd love to have that opportunity to represent my country," Subban said on Sirius XM's "Hockey Night in Canada Radio" in November. "There's a ton of players to pick from. The reality is that in Canada we're so good we could send maybe even two teams over if we had to. I don't think there are too many people who would want to be in Steve Yzerman's position right now because there are so many great players to pick from, but I'm confident he'll make the right decision in selecting a team, for sure."
Putting together a hockey team to compete in the high-pressure Olympic tournament isn't as simple as putting together an NHL All-Star team, said Darren Lowe, head coach of the University of Toronto's Varsity Blues men's hockey team.
Yzerman and Babcock must put together a team of players who fill specific roles and Subban could become a victim of numbers because of that, according to Lowe, who was the first black skater to play hockey for Canada in the 1984 Winter Olympics.
Adding to the roster anxiety is the fact that the Olympics is happening outside of North America and away from NHL-sized rinks. Team Canada and Team USA have performed poorly on the larger international ice surfaces used in Europe and elsewhere. Hockey Canada and USA Hockey are looking at players who they think have the skating skills and hockey sense to thrive on the 200 ft. long by 100 ft. wide international ice.
"He seems to have a very good offensive game, that's without question," Lowe said of Subban. "Based on how many offensive or power play guys they're going to select for the team, and how many guys they're going to have as shut-down guys, there becomes a debate. There are obvious guys who are going to make the team and then there are those who are that sort of in-between who are good at something. But how many guys will they have who are good at whatever he's good at? That's the only reason why I would think there'd be a debate."
Subban's advocates scoff at the claim that he's a potential liability on big ice by reminding people that he played junior hockey for the Ontario Hockey League's Belleville Bulls. They play their home games on a international-sized rink
Remember, they say, that Subban helped power Canada to Gold Medals at the 2008 International Ice Hockey Federation World Junior Championship – a tournament played on big ice in the Czech Republic – and the 2009 IIHF Junior World Championship that was played on NHL-size ice in Ottawa.
They debunk the Subban is penalty-prone argument by pointing out that he had 41 penalty minutes as of Dec. 31, 2013, only one minute more than the Kings' Doughty.
John Paris, Jr., the first black hockey head coach to win a professional league championship, said the criticisms of Subban should actually be considered compliments.
"We go back to the best of them all, who was Bobby Orr by far," Paris, Jr., told me recently. "Some of the most ridiculous comments we heard about him were 'He can't play defense, he can't do this, he can't do that.' Bobby Orr did everything that was physically and mentally possible for a defenseman to do – the best one ever to put on a pair of skates. But they found a way to criticize him enormously. Doug Harvey was the same thing, Paul Coffey was the same thing. Nicklas Lidstrom, for a while they gave him a difficult time. Good hockey players are always subject to a little bit of controversy. Subban is in the same category. Being an extraordinary athlete, it's normal they're going to criticize."
But Bollers believes the criticism aimed at Subban has a certain edge to it.
"I think the issue is if you watched when P.K. first entered the league he brought that sort of swagger, the low-fives and all that sort of stuff, and I guess the NHL wasn't ready for that," he told me recently. "At times he's very confident about in how he plays and his ability and sometimes that rubs people the wrong way."
It rubbed "Hockey Night in Canada" commentator Don Cherry rougher and tighter than one of his starched, high-collared shirts. The man with the flamboyant wardrobe wasn't a fan of the player with the flamboyant game.
But Cherry has been one of Subban's biggest boosters as the Team Canada roster announcement nears. So has Edmonton Oilers great Wayne Gretzky.
"I keep hearing a doubt that he's going to be on Team Canada," Cherry said on a recent "Coach's Corner" segment during a "Hockey Night in Canada" telecast in December. "What are they, nuts?"
Cherry took it a step on "Hockey Night in Canada Radio" a few days later.
"But if they let him go, he could turn it on with that big ice surface, and that cannon (of a shot) he's got from the point," Cherry said. "I don't understand how they can think about (not choosing him). I'm not knocking the guys that they've got, but good gravy. He's supposed to be the best defenseman, you think he'd be there somewhere."


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BP is the latest corporation under attack by the White House, but polls show the public thinks BP is handling the oil spill about as well as the government is. What's the message about the President's brand of populism? Also, the Supreme Court upholds anti-terror law, and the Tea Party movement and conservatism -- American style.
Banner image: President Barack Obama and Adm. Thad Allen meet with local leaders during a visit June 4, 2010 in Grand Isle, Louisiana. Photo: Win McNamee/Getty Images

subset: commoncrawl


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In 1998 F. Dean Lueking was teaching at the Lutheran seminary in Bratislava, Slovakia.
This article appeared in the Christian Century, May 7, 1997 p. 447, copyright by the Christian Century Foundation and used by permission. Current articles and subscription information can be found at www.christiancentury.org. This material was prepared for Religion Online by Ted & Winnie Brock.
Now that Pentecost has come, the primal divine command to have dominion over creation requires the church to get on with good stewardship of the earth. We do so not to the neglect of the gospel, but because we believe it and act upon it.
. . . the whole creation has been groaning in travail together until now . . . but the Spirit intercedes for us with sighs too deep for words . . .
In Romans 8, St. Paul's witness leads into the mysterious depths of the Paraclete's ceaseless intercession for the church and all creation. Like a woman in labor, both church and creation long for the new life to arrive. How do we begin to understand a truth of this scope?
Recently I was on an island in Lake Michigan. In a house nestled in dense woods, my reverie on the vast sweep of Romans 8 was interrupted by a bat zooming around the room. Instinctively I reached for a tennis racket to zap this black-winged thing commonly regarded as rabid, a blood sucker and a hair nester. I missed with the tennis racket but secured it with a waste basket and delivered it out the door into the nighttime sky
Here was an unexpected moment of exegesis. This tiny creature, part of the whole creation in travail, was guided away from my lethal swats by its sonar. Much of our scientific mastery of echolocation is learned from bats. Their astounding capacity to delay ovulation from fall until spring holds clues about human fertility. Their arteries remain cholesterol-free even though they eat their weight in fatty insects. We humans are the problem for bats and for the rest of creation as it awaits liberation for which the Spirit intercedes, works and groans with sighs too deep for words.
Here is potent Pentecost truth for the church. As Christians, our motive for earth care is the Holy Spirit's prayer and restorative work on behalf of the earth that supports us, the air we breathe, the water essential for life. Grace embraces nature, as Joseph Sittler kept teaching us. Human sin -- our sin, my sin and the tennis-racket solution for bats -- all spill over to the massive despoiling of nature.
The pleading of the Spirit intensifies as leaky tankers spew millions of gallons of oil into ocean waters. The Spirit's groaning must be heard above the clang of 2.5 million cans and bottles tossed out every hour, each aluminum can taking 500 years to decompose. In the U.S. alone, we produce enough garbage every day to fill the New Orleans Superdome to the roof twice -- and half of it is recyclable. A cigarette flicked out of a car window sets a forest ablaze and thousands of acres of precious timber go up in smoke. On and on it goes. By a measure and at a pace that would have stunned St. Paul, the whole creation groans and travails.
It is the will of God to put his mighty arm under the fractured, threatened creation -- not just to preserve it from rapacious humans, but to set it free and us with it. This is the saving plan of God already at work in the gospel of the death and resurrection of Jesus Christ our Lord. Foolish as it may seem, the risen Lord, through the Spirit, sustains those who are weary, indeed a whole creation that is weary.
The scope of the Spirit's work is as wide as the universe, yet not so cosmic that it cannot find a home in every heart where the gospel word opens the way. The miracle of Pentecost, with its testimony to the Spirit's calling, gathering, enlightening and sanctifying people, creates a partnership between church and creation. Now that Pentecost has come, the primal divine command to have dominion over creation requires the church to get on with good stewardship of the earth. We do so not to the neglect of the gospel, but because we believe it and act upon it.
As those baptized into the new creation, we can reclaim St. Francis of Assisi's vocabulary in speaking of brother earth and sister fire. Psalm 65 sings of fields, meadows, sky, mountains and the fecundity of God's good earth, teaching us to rejoice over it and praise God for it. Ironically, the Puritans who came to the New World saw the land as a howling wilderuess; it was from those they called "pagan primitives" that they learned to husband its resources. Too often since, the vast richness of our land has been the target of unconscionable greed rather than God's gift for which we are accountable.
Our calling is to join the Spirit in caring for the creation and praying for faithfulness in a world that both serves and threatens creation with technology. Our view of Spirit-filled people must include Millard Fuller, founder of Habitat for Humanity, and the 1,300 congregations who join the Spirit's pleading for decent housing for the impoverished urban poor. Charismatics include not only those gifted with tongues, prophecy and healing, but Nobel laureate Norman Borlaug, whose teaching of viable methods of food production in the Third World has spared many from starvation. Arthur Simon, founder of Bread for the World, is another partner with the Spirit. This network of Christians continues to plead, advocate and lobby Congress for butter instead of guns.
The ranks of those who respond to the Spirit's sighs are never overcrowded, but because it is God the Holy Spirit who silently, ceaselessly works, there is hope. Gerard Manley Hopkins speaks of that hope in his poem "God's Grandeur":
And for all this, nature is never spent;
There lives the dearest freshness, deep down things;
And though the last lights off the black West went
Oh, morning, at the brown brink eastward, springs --
Because the Holy Ghost over thebent
World broods with warm breast and with ah! bright wings.


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I have been stuck on Reverend Alvah Russel Rutan for quite some time. He is my husband's 3rd great grandfather. He born in New Jersey 7 Mar 1821 and he died 12 Mar 1877. I loose him and his family in the 1870 census, then I have an 1876 map that shows where his farm is, and then a will dated 10 March 1877 (the will brings up many questions for another post). I have no idea who his parents are.
Alvah is most notably known for his involvement in the Fishing Creek Confederacy he was arrested at least twice in 1864 before being sent to trial for draft resistance.
The image above is Alvah's Individual Information screen and you can see in his Events/Facts the two times he was arrested, his trial, when he was sent to prison, and when he was released from prison(where the green arrows are). You can also see that I have an Event/Fact called note; I use the note Event/Fact to keep all of my information together where I can easily see it in Alvah's timeline.
If anyone knows anything about Alvah Rutan please let me know.


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Fully changed...
to become just like Jesus!
Our 'training of trainers' spiritual transformation programme has been designed to help church pastors and leaders to better understand and put into action God's plan for the lives of all Christian believers. Transformed International aptly describes the process that God initiated in our lives from the point of spiritual re-birth, a process that will only be complete either when we die or when Jesus returns. The end result of this spiritual transformation is to be fully changed to become just like Jesus!
For many in Africa, it is the first opportunity to have any meaningful Christian training
Over the past 10 years…
Since the introduction of this Spiritual Transformation training programme, at least 3,000 African church pastors and leaders have passed through the training. The aim has always been for these leaders to then take the teaching and their personal testimonies of transformation back to their own families, churches and congregations. God only knows how many tens of thousands of Christian believers are now living with a greater understanding and outworking of God's plan for their lives.
Will you support us?
At least 3,000 African church pastors and leaders have passed through the training.
Will you support us to enable many more lives to be transformed?
Will you support us to enable many more lives to be transformed?
What is the Spiritual
Transformation training
This intensive training programme takes 7-8 full days to complete, culminating in the awarding of certificates for those who have successfully completed the course. For many village pastors this may be their first opportunity to have any meaningful Christian training and with a certificate to back it up! Even for those who have completed diplomas and degrees in theology, the testimony of many has been that they have never encountered such life-transforming teaching before!
Can you help?
Could you, your church or business help by sponsoring a Spiritual Transformation Programme?
Frequently asked questions
What are the key topics covered under the training?
The key topics covered under the Spiritual Transformation training programme include:
- Understanding the times we are living in
- The importance and means of spiritual transformation
- Obstacles to spiritual transformation
- Transformation in marriage and family life
- How to keep in the process of transformation
- What it means to be Christian disciples and disciple-makers
How much does it cost to sponsor a course?
Each Spiritual Transformation leadership training programme lasts for 7-8 days. Resources given out to the pastors and leaders during the training include:
- A student training manual
- A teacher's training manual and certificate (at the end of the training)
- Lunch provided for the duration of the programme
These training resources cost just UK£13.50 per person. For one of our African national teams to organise and hold a full Spiritual Transformation training event for 25-30 church pastors and leaders costs around UK£500 (This includes travel, local accommodation and food for the trainers).
Stay updated
Simply enter your email below to receive news and project updates from Transformed International.
We keep your data private and do no share it with any third party. You can edit your email preferences at any time by clicking the link on the bottom of our emails. For more information, please read our privacy policy. View our privacy policy


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What is a Medicare Advantage Special Needs Plan?
Medicare is a health insurance program run by the federal government. It is also known as original Medicare. It provides medical and health-related services to:
- People age 65 and older.
- People of any age who are qualified as disabled.
- People of any age who have kidney disease that requires dialysis or a transplant.
- People of any age who have amyotrophic lateral sclerosis (ALs) (also known as Lou Gehrig's disease).
Medicare is made up of four parts: Part A, Part B, Part C, and Part D.
Part A is hospital coverage. It helps cover the costs of being in the hospital as an inpatient, as well as long-term hospitalization. Most people automatically get Part A at no monthly cost.
Part B is medical coverage. It helps cover your doctor visits and outpatient care as well as some preventive services that help maintain your health. Medicare Part B has a monthly premium. Once you meet a certain amount of spending, known as your deductible, Part B generally covers about 80% of your costs for Medicare-approved services.
Part C is also known as a Medicare Advantage plan. Part C is provided by plans like AmeriHealth Caritas VIP Care (HMO-SNP) that have been approved by Medicare and have contracts with the Center for Medicare & Medicaid Services (CMS) to cover medical and hospitalization care for their members. They can also offer extra benefits that original Medicare doesn't cover such as hearing, dental, and vision services.
Part D is prescription drug coverage. Like Part C, it is also provided by private companies like AmeriHealth Caritas VIP Care that have a contract with CMS. It is designed to lower the amount that you pay for your prescription drugs. You can purchase a Part D plan to go with original Medicare, or prescription drug coverage may be included with a Medicare Advantage plan.
What are Medicare Special Needs Plans?
Medicare Special Needs plans (also known as SNPs) are Medicare Advantage plans that are designed for people who have special needs. A dual-eligible SNP, like AmeriHealth Caritas VIP Care, is a Medicare Advantage plan specifically for people who are both Medicare and Medicaid beneficiaries.
How do I enroll in Medicare?
You are automatically enrolled in Medicare when you turn 65 if you receive Social Security or Railroad Retirement payments. If you're receiving Social Security benefits or Railroad Retirement Board benefits, you'll receive information in the mail three months before your 65th birthday, explaining your options.
If you are not yet receiving Social Security payments, then you will have to contact Social Security to enroll. You can call the Social Security Administration at 1-800-772-1213 (TTY 1-800-325-0778), visit the Social Security Administration website, or apply at your local Social Security office. It's a good idea to do this well before your birthday so you can start receiving benefits as soon as you're eligible.
When can I enroll in Medicare?
Medicare limits the times when most beneficiaries can add, change, or drop coverage (known as election or enrollment periods). Generally, beneficiaries who receive both Medicaid and Medicare can add, change, or drop coverage only once during each of the following:
- January 1 – March 31
- April 1 – June 30
- July 1 – September 30
- October 15 – December 7: You may request to add, change, or drop coverage, but the change won't go into effect until January 1 of the following year.
What is a Health Maintenance Organization (HMO)?
An HMO is a type of health plan that uses a network of different health care providers — doctors, dentists, nurse practitioners, pharmacies, and hospitals — to treat members.
Enroll now: Call us at 1-800-858-1487 (TTY 711) or enroll online.
8 a.m. to 8 p.m., seven days a week.
AmeriHealth Caritas VIP Care has been approved by the National Committee for Quality Assurance (NCQA) to operate as a Special Needs Plan (SNP) until 12/31/2024 based on a review of AmeriHealth Caritas VIP Care Model of Care.


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For sale... new and collectable vinyl.
Vinyl is listed alphabetically - click the links and get digging. We have 1000's more records yet to be listed, please ask if you can't find what you want. We take pre-sale orders. Please email.
Well also sell turntables and a range of accessories, including cartridges and phono pre-amps.
To buy please email a list giving your name and full mailing address. You will be sent an invoice shortly after. Payment is by PayPal or cheque/postal order (UK only). We sell worldwide.
We also sell through the Discogs website. Discogs is the worlds leading website for cataloguing and selling vinyl.
Please note: Artists are listed alphabetically by first name i.e. Albert King is in the A's. Details on postage are here. Vinyl is graded by the Goldmine Standard.
For sale... Rega RP1 Turntables...
We're excited to be able to offer a new range of high quality turntables. The Rega RP1 is available in the Standard and Performace packages, together with the Union Flag Model. These superb turntables have drawn 5 star reviews across the world. Details here.
Recently added...
Here's what's new at Plectrum HQ...
Marrs Plectrum Records (C) - 2023 all rights reserved
Open Mon to Fri by appointment only - Book now!
Buying, Selling and Trading Vinyl Records
07884 357021
387 Fulbridge Road, Peterborough, PE4 6SF.


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Subscribe to the Glazov Gang's YouTube Channel.
Please donate through our Pay Pal account to help The Glazov Gang keep going. Thank you!
In this new Jamie Glazov Moment, Jamie focuses on: The Left's Manhattan Massacre, unveiling how the utopian dream fuels Islam's killing machine.
Don't miss it!
And make sure to watch our special edition with John Guandolo, a former FBI agent, combat veteran Marine, and now the president of Understanding the Threat. John discusses McMaster's Firing of Higgins: Crippling America in the Face of Jihad, where he reveals how the National Security Adviser is in the enemy camp:
Subscribe to our YouTube Channel and to Jamie Glazov Productions. Also LIKE us on Facebook and LIKE Jamie's FB Fan Page.


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Surprise Thunderstorms Last Night
About 2:00 am I woke up to thunder so of course I had to get up and go watch. It looked very promising for a good storm with a constant flashing in the distance with fairly frequent flashes close by. It looked like it had already rained a bit. It was actually nice outside on the porch.. Cool but humid but I'm adjusted to the humidity now.
Things calmed down.. with still lots of lightning in the distance. I went and looked at the radar and saw that a small cell had formed and a northwest to southeast line of storms was exploding to the west. The line was severe thunderstorm warned and they mentioned lots of cloud to ground lightning.. I guess that explained the flashing in the distance.
We were under a warning also so I stayed up. There was occasional nearby lightning with some moderate rain. I saw the solid line of storms so I figured I'd wait and it would get better. Now the rain is pretty much just drizzle with some nearby lightning with some light breezes. First there were some warm breezes from the east or so it seemed then it switched to a cool breeze from the west and the lightning was becoming more distant. I went and looked at the radar. The line had become a really nice east west solid looking line with a time break right over us! Usually that happens with storms moving from west to east here but not ones from the southwest. oh well.. Maybe next time. It was a bit of a disappointment but still a nice little unexpected surprise.


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Mrs. Hausner's ELL Blog
Lindbergh Schools Home Page
Google Sign-in
SIS- Check Grades, Lunch Account
Wednesday, August 22, 2012
Open House
Welcome back! Both middle schools will have open house on Thursday, August 30 from 6:30 to 8. I hope to see everyone there. I will be at Truman from 6:30 to 7 and at Sperreng from 7:30 to 8. If you can not make it to open house but would like to visit with me, you can call or email to set up a meeting. I can be reached at email@example.com or 729-2400 ext. 2316 (Sperreng), ext 7031 (Truman).
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Las Gavias Grand 2-Bedroom condo
Las Gavias Grand, the latest residential beach front tower from Pronova Developments, was designed by a world-class architectural firm with notable clients such as Ritz Carlton and Four Seasons. Each condominium floor plan at Las Gavias Grand is exceptional, but the 2-bedroom / 2 Bathroom corner residence is its crown jewel with every window and sliding tempered glass door providing an unobstructed ocean view. This particular condominium located on the 10th level, is impeccably decorated with tasteful one-of-a-kind furnishings which the sellers will include with its purchase. Extraordinarily large, private oceanfront terraces (1893 sq. ft. total area), 12 ft. ceilings, granite counter tops, stainless steel appliances, washer and dryer in its separate laundry area, porcelain flooring throughout. Expansive green areas, Fitness Center, Community Salon, majestic infinity pool, Business Center, Covered parking, 24 hour...view the listing
hotel in Sabalo Country
This property is priced at $29,000,000 Mexican pesos calculated at 13 * 1. Exchange rate is variable. This succesfull hotel in a prime commercial location on Camaron Sabalo near the Marina Mazatlan is a unique opportunity. Across the street, the old Camino Real hotel will soon be remodelled under new ownership, which will cause a surge in property values all around, with a very positive impact on this one. – 9 Two bedroom, one bath, living, dinning and kitchen units. – 8 One bedroom one bath, living, dinning and kitchen units. – 3 Hotel type rooms – 3 Commercial locals – 1 Suite with three bedrooms, Two bathrooms, living, dinning, kitchen and service room (Perfect for an owner operator). Highlights ▪With minimal investment, this property can be returned to its turnkey operation with daily, weekly, and monthly rentals with very attractive margins, or ▪The owners regretably must sell this property, and an opportunity like this, in this prime area, will be hard to come by again; a savy investor will not pass this up! ▪It can be developed into a B&B type operation in the PRIME tourist and snowbird location in Mazatlan. Features ▪ Ocean View Extra Features ▪ Controlled Access ▪ Lobby ▪ Storage Lot Features ▪ Corner Lot ▪ Courtyard ▪ Swimming Pool ▪ Trees / Shrubs Type: Commercial Garage: 8-Stalls Size: 1,946 sq. m. Lot Type:...view the listing
Plaza Balboa
GREAT COMMERCIAL LOCAL FOR SALE in GOLDEN ZONE. LOCATED ON THE 2nd FLOOR WITH 4 PRIVATE SPACES, 1 BATHROOM AND CAR PARKING SPACE. Price: $70,000 USDview the listing


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A preliminary hearing was continued last Thursday for Zachary Fraley, the Homer High School student charged with first-degree terroristic threatening, a felony, for allegedly placing a bomb-like device at the high school that caused an evacuation May 16.
Fraley, 18, appeared before Judge Margaret Murphy at the Homer Courthouse with about a dozen family and friends supporting him. Fraley had been released on $1,000 bail at his first hearing on May 17. His Soldotna lawyer, Kenneth Cole, entered a plea of not guilty on his behalf then. Under court rules for felony charges, the grand jury must deliver an indictment within 20 days for a defendant not in custody unless a preliminary hearing is held.
Appearing telephonically, Cole said he was still waiting for discovery, that is, more information on the case. Cole said the state has made an offer and he and his client needed time to review it. Cole and the prosecutor, assistant district attorney Amanda Browning, did not discuss in court the terms of a plea deal. Cole and Browning also did not return phone calls requesting more information on the possible deal.
Cole agreed to waive rules requiring an indictment and to continue the preliminary hearing to 3:30 p.m. June 27. Cole also agreed to suspend the calendar in regard to speedy trial rules.
The evacuation happened about 8:55 a.m. May 16 after Homer High School Principal Allan Gee found a suspicious device that appeared to be a bomb in the B-wing stairwell. Following Kenai Peninsula Borough School District protocols, Gee ordered an evacuation of the school. The building was safely evacuated and students and staff returned to class after Homer Police cleared the building. Police inspected the suspicious device and determined it was not dangerous.
In a letter sent to parents at the end of the school year, Gee said after the evacuation a teacher aide said she had found the device and, thinking it was a science experiment, picked it up and moved it to a corner of the stairwell. She didn't think it was a bomb.
In a photo released by Homer Police of the suspicious device, the fake bomb is made of a can about 6-inches tall with what appears to be a battery taped to it.
At a court hearing May 17, Gee said Fraley admitted that he had put the fake bomb in the stairwell. Fraley said he and another student, a 16-year-old boy, had been playing pranks on each other. Police arrested Fraley and the boy, and the boy was referred to the Alaska Division of Juvenile Justice, where proceedings are confidential.
Fraley was charged under a section of the statute that defines first-degree terroristic threatening "as knowingly sent or delivered a bacteriological, biological, chemical or radiological substance or an imitation bacteriological, biological, chemical or radiological substance and as a result caused evacuation of a building, public place or area, business premises, or mode of public transportation."


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Numero Uno
These can be boosted in closed sessions with friends, most can be done with 2 players, with a few requiring 4. It has been confirmed by some gamers now that doing races solo does not count towards this achievement.
Here is a list of the awards which are required. (These must be wins, ties do not count)
- Win a Deathmatch
- Win a Team Deathmatch Requires 3 or more players. (Rank 6 gives access to the Supply TDM at Cypress Flats, which is 3-6. UPDATE: You can do TDM with 2 people by starting a regular deathmatch that requires 2 people, then switch it to TDM.)
- Win a Land Race
- Win an Air Race
- Win a Sea Race
- Win a GTA Race (To do a GTA Race, the host of the race must switch it from a standard race to GTA)
- Win a Rally Race (The host of the race must select Rally as the race type) Requires more than 2 players
- Win at Arm Wrestling
- Win at Darts
- Win a round of Golf (Can be set to 1 hole)
- Win at Tennis (Can be a single Set)
- Complete all Waves of Survival (It unlocked after completing it, regardless of deaths.)
- Win any challenge at the Shooting Range (Some people claim all three challenges are required, whereas others claim only the one, it may be safer to do all three)
Game Types which aren't covered by the Victory Awards which are also required include:
- Parachuting
Some people have only had their achievements unlock after completing a mission, so the completion of any mission may be needed too.
Survival tips
- It helps to use a map where you and your team can hold position. The Boneyard has a big building with two entrances and is a good choice for four players, with two on each entrance.
-Another good map is Processed, you can hide in the middle hanger behind the sandbags, with two other players behind the small cabin inside there. Be careful as some enemies climb over the fence, but aside that, it is an easier map.
-If you have leveled up enough, you can call in Merryweather support. Backup helicopters, ammo drops, mercenaries and airstrikes can turn things around if you are struggling.


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Istanbul Mehmet Traditional 16" China Pang Cymbal
The Traditional Series Cymbals are ideally suited for pretty much every style of music imaginable. The authentic concept of these fully lathed cymbals has proven its value through the years. These chinas provide low pitched trashy crash sounds and they will do great in any given situation.
- 16"


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The recognition and correct interpretation of cutaneous signs of diseases that primarily affect the bronchopulmonary system may aid the clinician in diagnosis and assessment of prognosis. This article reviews selected pulmonary diseases with distinctive cutaneous findings.
The distinctive blue or purple skin discoloration of cyanosis indicates the presence of at least 5 g/dL of desaturated hemoglobin. Severely anemic patients (regardless of the degree of desaturation) are, therefore, unable to manifest cyanosis. Cyanosis may be classified as central or peripheral, referring to the etiology of the hemoglobin desaturation, not to the observed anatomic location of the cyanosis. Central cyanosis is often a manifestation of congenital heart disease characterized by right-to-left pulmonary shunts. Central cyanosis typically involves the entire body but may be best appreciated on warm areas of the body (eg, tongue, oral mucosa, conjunctiva, skin). Peripheral cyanosis is a manifestation of diminished tissue perfusion with resultant increased local oxygen extraction leading to high levels of desaturated hemoglobin. Shock, heart failure, and peripheral vascular disease are common causes.
Clubbing describes the bulbous, clublike deformation of the distal portion of the fingers and toes resulting from connective-tissue proliferation (see the image below). The condition was first described by Hippocrates[1] ; an alternate term is Hippocratic fingers.
Clubbing may be hereditary (ie, primary hypertrophic osteoarthropathy, which is discussed in the next section), but, more often, it is acquired and is associated with a number of infectious, inflammatory, neoplastic, and vascular disorders. Although it may occur with several lung diseases (ie, lung cancer, tuberculosis, lung abscess, bronchiectasis, cystic fibrosis, idiopathic pulmonary fibrosis),[2] clubbing is a distinctly unusual finding in chronic obstructive pulmonary disease and its presence should prompt the clinician to search for other causes (particularly lung cancer).[3, 4]
The pathogenesis of clubbing has not been definitively determined. One promising hypothesis suggests that platelet-derived cytokines may play a central role.[5] This hypothesis proposes that diseases that disrupt the pulmonary circulation and allow right-to-left shunting of blood prevent the normal fragmentation of megakaryocytes in the pulmonary vasculature. If the megakaryocytes gain access to the systemic circulation, then lodge in the microvasculature of the digits, platelet-derived growth factor and/or vascular endothelial growth factor are released.[6, 7] These cytokines may induce a cascade of events (eg, increased vascular permeability, increased smooth muscle cell and fibroblast production, monocyte and neutrophil chemotaxis) that ultimately results in clubbing. A wide variety of malignant tumors, including lung cancer tumor, are also known to produce vascular endothelial growth factor.
Histologic findings may correspond to the duration and severity of disease. Early findings include dermal fibroplasia. Later, mucoid degeneration of the ground substances occurs. Severe long-standing clubbing is characterized by interstitial edema and infiltration by plasma cells and lymphocytes. Connective-tissue proliferation and interstitial edema result in a characteristic spongy quality to the proximal nail fold—as if the nail were floating in the nail bed.
Clinical examination findings may correlate with the severity of clubbing. The earliest finding may be the Schamroth sign, first described by a South African physician when he developed clubbing secondary to infective endocarditis.[8] In healthy individuals, a rhombus is observed when the dorsal surfaces of the right and left second fingers are placed against each other with the distal interphalangeal (DIP) joints and distal aspect of the nails touching. An absence of this rhombus is consistent with clubbing. The accuracy of this sign has not been examined.
The phalangeal depth ratio (see the image below) appears to be the simplest, validated bedside test.[9] If the depth of the finger at the proximal nail fold equals or exceeds that of the DIP joint (a ratio greater than or equal to 1), clubbing may be diagnosed.
Clubbed fingers also exhibit changes in nail-fold angles. Lovibond first observed that in healthy individuals, the nail exits the nail bed at an angle of approximately 160°.[10] The Lovibond (also called profile) angle approaches 180° in persons with clubbing.[9] The hyponychial angle is formed by a line joining the dorsal surface of the DIP joint with the dorsal surface of the proximal nail fold and a line joining the dorsal surface of the proximal nail fold with the hyponychium (thickened skin under the distal end of the nail).[11] A normal hyponychial angle is approximately 180°; mean values of approximately 195° have been obtained in children with clubbing secondary to cystic fibrosis.[9]
Although breast and prostate cancer are more prevalent in women and men, respectively, lung cancer remains the leading cause of cancer death in both sexes. Cutaneous, subcutaneous, or superficial lymph node metastases are relatively uncommon events in the pathobiology of lung cancer. However, these metastases may be encountered in clinical practice because of the relatively high prevalence of lung cancer.
Some variability exists in the reported rates of cutaneous metastases in lung cancer. One study of 1000 patients with unresectable lung cancer reported that 12% had a skin metastasis; an additional 4.8% had superficial lymph node involvement.[12] Based on data from a large tumor registry, another study reported 2.6% of patients with metastatic lung cancer were noted to have a skin metastasis.[13] Most studies report cutaneous metastases in 2-8% of cases of lung cancer. Only in rare instances does a skin nodule lead to the diagnosis of lung cancer.[13, 14, 15]
The most common sites for cutaneous metastases are the chest and abdominal wall, neck, and scalp. The cutaneous nodules are usually solitary and fast growing and mobile, painless, and firm (sometimes described as "rock hard"). Superficial lymph nodes are also typically firm and may be fixed to the adjacent skin. They are most often supraclavicular (mimicking the Virchow node seen in gastrointestinal malignancy) or in the anterior cervical lymph node chains, ipsilateral to the primary tumor (see the image below). Adenocarcinomas appear to have the greatest propensity to metastasize to the skin.[12, 13, 16]
Importantly, a simple punch biopsy of a suggestive skin nodule may readily establish the diagnosis, as well as offering important prognostic information and obviating the need for additional staging procedures. Additionally, monitoring changes in the size of skin lesions is a simple way to monitor response to chemotherapy.
Clubbing associated with periostitis and arthritis is termed hypertrophic osteoarthropathy (HOA). HOA was described independently by E. von Bamberger in 1889 and Pierre Marie in 1890. HOA includes 2 distinctive clinical conditions.
Primary HOA, also termed pachydermoperiostosis, is an autosomal dominant condition usually diagnosed in the second decade (typically around puberty), characterized by coarsening of the facial features as a result of sebaceous hyperplasia, cutis verticis gyrata, hyperhidrosis (especially of palms and soles), and severe seborrhea.[17] Arthritis is notably absent in persons with pachydermoperiostosis.
Secondary HOA is most frequently associated with lung cancer.[18] Symptoms of HOA commonly precede the diagnosis of underlying lung cancer by several months.[19, 16] HOA is more frequently associated with non–small cell lung cancer, particularly squamous cell carcinoma and adenocarcinoma.[20, 21, 22] Other conditions less frequently associated with secondary HOA include lung abscess, mesothelioma, primary biliary cirrhosis, ulcerative colitis, and Hodgkin disease.
Patients often report bone or joint pain. Periostitis typically affects the distal portions of the long bones of the leg or forearm, and bony tenderness is found in these areas during the physical examination.[19, 23]
Patients who present with acute polyarthritis may initially be misdiagnosed with rheumatoid arthritis (RA). Similar to RA, the knees, ankles, and wrists are most often affected. In contrast to RA, the rheumatoid factor is rarely positive and synovial joint fluid is noninflammatory (ie, < 500 leukocytes/µL, with few neutrophils and a low protein concentration).
Plain radiographs of symptomatic bones reveal periostitis in persons with well-established disease. However, early in the disease course, plain radiograph findings may be normal (approximately 50% of bone is resorbed when changes become evident on plain radiographs). Because it relies on increased osteoblast activity, radionucleotide bone scanning is a more sensitive modality to detect periostitis in the early stages, but it lacks specificity.
The differential diagnosis of HOA includes clubbing, pachydermoperiostosis, thyroid acropachy, and acromegaly. Thyroid acropachy is seen in approximately 1% of patients with Graves disease and is usually accompanied by exophthalmos and pretibial myxedema. Patients with thyroid acropachy also may have clubbing and periostitis, although the periostitis is usually limited to the hands and feet, and the joints are spared.
Acromegaly is a result of a growth hormone excess and results in enlargement of the hands and feet in all patients. Overgrowth of bone and cartilage results in thick, blunted digits (without clubbing). Arthritis may occur but is due to degeneration of joints; radiographs reveal increased soft tissue along with tufting of the distal phalanges.
Symptoms of HOA may respond dramatically to treatment of the underlying neoplasm, particularly if curative resection is possible. Partial symptomatic relief of pain related to periostitis or arthritis may be achieved with aspirin or nonsteroidal anti-inflammatory drugs.[24]
The superior vena cava (SVC) arises from the confluence of the right and left brachiocephalic veins. It travels approximately 7 cm before emptying the venous drainage of the upper body (ie, head, neck, arms, chest) into the right atrium. SVC syndrome occurs when blood flow through the SVC is impeded, either by extrinsic compression or intraluminal narrowing.
A 1992 review underscores the importance of observing and interpreting the dermatologic findings in this condition.[25] Many patients with this syndrome were initially diagnosed by dermatologists after referral for evaluation of a rash on the upper chest. Malignant neoplasm is by far the most common cause. Thrombosis of the SVC is encountered more frequently in critically ill, hospitalized patients in association with intravascular devices (eg, central venous catheters, pulmonary artery catheters, pacemakers).
Lung cancer is the most common cause of SVC syndrome. Because of the tendency to arise centrally (near the SVC), small cell carcinoma is the most common histology. Lymphomas, specifically the non-Hodgkin variety, are the next most common etiology. Other, much less common etiologies for SVC syndrome include mediastinal fibrosis, most commonly secondary to histoplasmosis, and retrosternal goiter.
Markedly dilated veins or venules (often in vertical parallel clusters on the chest above the level of the heart) constitute the earliest cutaneous finding in SVC syndrome (see the image below).[25] These result from increased collateral flow through the subcutaneous vessels of the chest wall. The engorged vessels shrink or disappear with relief of the obstruction of blood flow. Other signs that may result from the venous congestion include hoarseness, facial edema, plethora of the head and neck, conjunctival suffusion, and proptosis.
Although malignancy-related SVC syndrome was previously viewed as an oncologic emergency that required immediate radiation treatment, even before tissue diagnosis, now recognized is that most patients do not require emergent radiotherapy.[26] In fact, radiotherapy prior to biopsy may make histologic diagnosis and subsequent treatment decisions difficult.[27] Exceptions include patients with life-threatening laryngeal or cerebral edema or tracheal compression resulting in respiratory compromise.
Initial conservative management, including elevation of the head of the bed and supplemental oxygen, often provides symptomatic improvement and allows sufficient time to obtain a tissue diagnosis. Diuretics and corticosteroids are often used, but their efficacy is not well established. Anticoagulants and thrombolytics may be used in the setting of intravascular thrombosis (but may cause intracranial hemorrhage in patients with malignancy-related SVC syndrome and brain metastases). Intraluminal stenting can also be considered for patients who require rapid symptomatic improvement.
Sarcoidosis is a multisystem granulomatous disease of unknown etiology.[28] Almost all patients have involvement of the respiratory tract at some point during the disease course. Patients often present with dyspnea, nonproductive cough, and pleuritic chest pain. Nonspecific symptoms, such as fatigue, malaise, anorexia, weight loss, and low-grade fevers, are also common.[29]
The disease is often first suspected when bilateral hilar adenopathy without parenchymal disease is discovered on a chest radiograph (see the image below), particularly in an asymptomatic patient.[30, 31]
Chest radiographs may also show diffuse parenchymal disease with or without hilar adenopathy. The pattern of parenchymal disease is typically interstitial but also may be nodular. Pleural effusions are uncommon. Importantly, radiographic findings may not correlate with clinical findings. Pulmonary function testing typically reveals a restrictive pattern of disease with reduced lung volumes and decreased diffusion capacity.
Cutaneous involvement occurs in approximately a quarter to one third of patients but seldom is the sole manifestation of disease.[32] The presence of cutaneous sarcoidosis should prompt physicians to undertake a thorough evaluation.[33]
Cutaneous manifestations are described as either specific (histologically revealing typical noncaseating granulomas) or nonspecific.[34]
Many theories have been proposed for the etiology of sarcoidosis, but none is universally accepted. Antigen exposure in genetically predisposed individuals is widely believed to be the common pathophysiologic pathway. Many believe that Mycobacterium subspecies are the causative agents, but definitive evidence is lacking. Although sarcoidosis may affect persons in any racial or ethnic group, it is more common in African Americans, Scandinavian populations, and Irish populations.
The pathologic hallmark of the disease is the noncaseating granuloma.[28] Granulomas in the skin have the same histologic appearance as granulomas in the lung parenchyma. In patients with specific cutaneous manifestations, a skin biopsy may obviate the need for more invasive and expensive procedures. Other laboratory test results (eg, elevated serum angiotensin-converting enzyme levels, hypercalcemia, hypercalciuria) may be suggestive of sarcoidosis, but it is a diagnosis of exclusion.
Maculopapular sarcoidosis is the most common specific cutaneous manifestation of sarcoidosis.[34] Lesions are red/brown-to-purple dermal papules and are typically seen on the face or extensor surfaces of the arms or legs. Papular sarcoidosis is usually associated with the acute forms of sarcoidosis and suggests a good overall prognosis.[35]
Lupus pernio is the most characteristic lesion of sarcoidosis and is often seen in older African American women. Lesions are violaceous, indurated plaques on the face and nose (see the image below) that resemble those seen in persons with chilblains (hence the name pernio). The cosmetic effects of lupus pernio may be particularly distressing to patients and may prompt them to seek medical attention. Unfortunately, patients with lupus pernio tend to have a more indolent disease course with a poorer overall prognosis than those with papular sarcoidosis.[35] Systemic disease manifestations, including pulmonary fibrosis specifically affecting the upper respiratory tract, chronic uveitis, and bone cysts, are also more common.
Subcutaneous nodules (Darier-Roussy sarcoid) may occur at any time during the disease course but most often are a manifestation of late-stage, chronic sarcoidosis. The subcutaneous nodules are firm, mobile, nontender, red/brown to purple, and 0.5-2 cm in diameter; they usually occur on the extremities and trunk and are often symmetrical.[36] They do not offer any clue to the prognosis.[35]
Cutaneous plaques may be round or oval, annular or arciform, and red/brown to purple (see the image below). The dermal infiltrates may be strikingly thick and tend to occur on the trunk and limbs. Plaques are a common manifestation of sarcoidosis and are associated with persistent pulmonary disease and more severe systemic involvement.[36, 35]
Preexisting well-healed scars from prior trauma or surgery may become red or purple and indurated as they are infiltrated with granulomas. Scar sarcoidosis can be confused with keloids. They may be seen in the acute phase, along with erythema nodosum (EN), but more often is associated with chronic disease.[35] Erythema nodosum is generally associated with a good prognosis.[36]
EN lesions are poorly circumscribed, tender, reddish nodules that resemble bruises and are located in the anterior tibial region. EN is associated with a number of conditions, mostly infectious. A 1998 retrospective study found sarcoidosis to be the second most common identifiable etiology for EN (streptococcal infections were the most common).[37] The lesions tend to erupt in crops and often occur in young white females. Sarcoidosis-related EN in combination with fever and uveitis is termed Lofgren syndrome. The prognosis of Lofgren syndrome is good; greater than 80% of patients experience spontaneous resolution of symptoms in less than 2 years.[35]
Cardiac involvement occurs in only 5-10% of patients but is associated with a poor prognosis. Most patients have rhythm or conduction disturbances noted on electrocardiograms. Anterior uveitis usually manifests as photophobia and blurred vision. Approximately 5% of patients have nervous system involvement; unilateral cranial nerve VII palsy is the most common manifestation. Liver infiltration is relatively common but is usually not clinically important. Liver function tests usually exhibit a cholestatic pattern (ie, elevated alkaline phosphatase levels and mild elevations of serum transaminase levels).
Corticosteroids remain the mainstay of treatment for sarcoidosis and are generally reserved for patients with symptomatic pulmonary disease, hypercalcemia, uveitis, and neurologic or cardiac involvement. Severe, disfiguring cutaneous involvement may rarely require systemic corticosteroid therapy. Many other agents have been used in the treatment of cutaneous sarcoid (eg, topical corticosteroids, antimalarials, thalidomide, allopurinol, methotrexate) but none has been well studied.[35]
Wegener granulomatosis is a systemic vasculitis of unknown etiology that may affect any organ but most commonly involves the upper and lower respiratory tracts and the kidneys. Cutaneous manifestations are relatively common but usually not diagnostic.
Histopathologic findings fall into 4 distinct categories: (1) necrotizing vasculitis, (2) granulomatous vasculitis, (3) lymphomatoid vasculitis, or (4) necrotizing palisading granuloma.[38, 39, 40] Skin findings are noted in approximately 10% of patients at presentation and develop in approximately 50% throughout the course of disease.[41, 42, 43] Purpuric lesions, specifically palpable purpura, are the most common and are usually found on the lower extremities. The second most frequent skin finding is necrotic ulcers, also typically found on the lower extremities. These lesions may be mistaken for pyoderma gangrenosum, but they lack the classic heaped-up border. Other cutaneous findings include subcutaneous nodules, papules, petechiae, and hemorrhagic bullae.
Up to 60% of patients may have oral mucosal disease; nonspecific oropharyngeal ulceration is most common. A rare and unusual gingivitis is considered pathognomonic of Wegener granulomatosis and is described as gingival hyperplasia with red petechiae and a friable granular appearance. Patients report pain and bleeding from the gums. Some evidence suggests that patients with cutaneous lesions have a higher incidence of renal involvement and that this may serve as an important prognostic indicator.
The classic clinical triad of findings in Wegener granulomatosis is upper respiratory tract involvement, lower respiratory tract involvement, and renal disease.[41, 42, 43] Ear, nose, and throat involvement is present in more than 70% of patients at presentation, and lung involvement is present in approximately 50% of patients. Ear, nose, and throat findings include sinusitis, epistaxis, nasal septal perforation or saddle nose, or otitis.
Pulmonary disease may manifest as a nonproductive cough with or without hemoptysis and dyspnea. Less commonly, patients present with diffuse alveolar hemorrhage and renal failure; diagnostic confusion may arise in such cases (ie, Goodpasture syndrome vs Wegener granulomatosis). The finding of antineutrophil cytoplasmic antibodies (ANCAs) with diffuse cytoplasmic staining rather than antiglomerular basement (anti-GBM) antibodies is useful to distinguish these between the 2 entities.
Two types of ANCAs may be identified by immunofluorescence or enzyme immunoassay.[44] The diffuse cytoplasmic form of ANCA (c-ANCA) is characterized by granular staining with interlobular accentuation and is commonly detected in patients with Wegener granulomatosis. In most cases, the identified antigen is serine proteinase 3 (PR3). The test has a sensitivity of approximately 90% during active disease. Titers of cytoplasmic ANCA may correlate with disease activity (and may disappear in remission), but this correlation is not absolute.[44]
The perinuclear ANCA (p-ANCA) staining pattern is associated with antibodies that bind primarily to myeloperoxidase. The perinuclear ANCA pattern is less disease specific and may be seen in association with many different vasculitides, including polyarteritis nodosa (PAN), Churg-Strauss syndrome, microscopic polyarteritis, and Wegener granulomatosis.
The classic chest radiographic finding in Wegener granulomatosis is multiple, bilateral cavitary nodules, but less distinct parenchymal infiltrates or nodules are also commonly observed (see the image below).
Bronchoscopy is frequently performed and may reveal tracheobronchial stenosis, focal or diffuse hemorrhage, or inflammatory or ulcerative lesions. Biopsy samples of these lesions usually show an inflammatory infiltrate but rarely reveal vasculitis. The presence of renal disease defines classic or generalized Wegener granulomatosis; the absence of renal involvement (ie, upper and/or lower involvement) is termed limited Wegener granulomatosis, but many of these patients eventually develop renal disease.
Initial therapy often involves the combination of corticosteroids and cyclophosphamide and has dramatically improved long-term survival.[43] Untreated disease typically progresses rapidly and is nearly uniformly fatal (approximately 90% mortality rate at 2 y). Most patients can expect complete remission of their disease with treatment, although relapses are common.
Churg-Strauss syndrome is a rare multisystem disorder that primarily affects the lungs, peripheral nervous system, and skin. Churg and Strauss' initial description of the syndrome in 1951 required histologic criteria to establish the diagnosis. Clinical and laboratory criteria have been more difficult to establish. Asthma, peripheral blood eosinophilia, and extrapulmonary vasculitis affecting 2 or more organs are cardinal clinical manifestations of Churg-Strauss syndrome.[45, 46]
The disease typically begins as allergic rhinitis in a patient without a prior atopic history. Mild asthma, a nearly invariable part of the clinical picture, then develops and progressively worsens. Cardiac disease, although less frequent than reactive airway disease, accounts for a substantial percentage of mortality. Cardiomyopathy results from endocardial and myocardial infiltration with granulomas or coronary arteritis.
Mononeuritis multiplex, similar to that seen with PAN, may be seen in as many as 70% of patients and usually involves the peroneal nerve with resultant foot drop. Another feature shared with PAN is gastrointestinal disease. As many as 60% of patients may have abdominal pain, which most often results from mesenteric ischemia secondary to mesenteric vasculitis.
Chest radiographs typically reveal characteristic bilateral, patchy, and nonsegmental fleeting infiltrates.[47] Other less common intrathoracic manifestations include pleural and pericardial effusions.
Laboratory findings include striking peripheral eosinophilia, usually more than 1.5 X 109 cells/L. Eosinophilia is also common in patients with asthma; however, the magnitude is greater in patients with the Churg-Strauss syndrome. Eosinophils are the dominant cell in pleural or pericardial effusions. Other laboratory findings may include a positive perinuclear ANCA serology and elevated immunoglobulin E levels.
As many as 70% of patients with Churg-Strauss syndrome have cutaneous manifestations.[48] A variety of lesions may be seen, the most common of which are palpable purpura, subcutaneous nodules, urticarial rashes, and livedo reticularis.
Palpable purpura usually involves the lower extremities and is common but nonspecific. Biopsy of these lesions reveals leukocytoclastic vasculitis. The most distinctive lesions are tender subcutaneous nodules occurring on the limbs and scalp, or, less frequently, on the trunk. Biopsies of these lesions reveal an eosinophilic granuloma, characterized by a necrotic core surrounded by densely packed eosinophils.
Most patients with Churg-Strauss syndrome respond well to high-dosage corticosteroids. For those who do not, alternate therapies include azathioprine, cyclophosphamide, and intravenous immunoglobulin (IVIG).
Relapsing polychondritis is a rare multisystem disorder of unknown etiology.[49, 50] The disease is characterized by recurrent, and typically progressive, bouts of inflammation of cartilaginous structures. The diagnosis is based on clinical findings (ie, no diagnostic test is available). Relapsing polychondritis predominantly affects whites in the fifth and sixth decades of life. A number of associated conditions have been reported, including several systemic vasculitides (ie, Wegener granulomatosis, PAN, Churg-Strauss syndrome), collagen-vascular diseases (ie, RA, systemic lupus erythematosus, reactive arthritis [Reiter syndrome], scleroderma, Sjögren syndrome), hematologic diseases (ie, leukemia, lymphoma), thyroid disease, ulcerative colitis, primary biliary cirrhosis, and diabetes.
External ear pain and inflammation is a frequent presentation and an almost universal finding at some point during the disease course. Patients are routinely misdiagnosed with an infectious process (ie, auricular cellulitis). Physical examination offers an important clue—because only the cartilaginous portion of the external ear is affected in persons with relapsing polychondritis, the ear lobe is spared (see the image below). Other cutaneous findings include leukocytoclastic vasculitis, EN, and erythema multiforme.
Most features of the disease share the common pathophysiologic pathway of cartilaginous inflammation. Saddle-nose deformity may occur as a result of destruction of the cartilage in the nasal septum (see the image below). A nonerosive nondeforming arthritis affecting both large and small peripheral joints occurs in as many as 85% of patients. Ocular inflammation is extremely common and may affect any part of the eye.
Destruction of cartilage in the laryngotracheal tree occurs in half to two thirds of patients and is the most feared disease manifestation. Respiratory distress results from destruction of the cartilaginous tracheal rings and subsequent tracheobronchial collapse or from inflammation of cartilaginous tissue and subsequent tracheal edema. Some patients may develop recurrent pneumonia because of insufficient clearance of secretions. Aortic root dilatation and subsequent aortic valve regurgitation is a less common, but potentially morbid, intrathoracic manifestation.
A variety of immunosuppressive therapies have been used, but because of its rarity, clinical trial data are not available to guide treatment. In general, disease extent and severity are used to determine the intensity of treatment. Laryngeal, tracheal and bronchial involvement may result in stenosis or collapse and may require surgical intervention (resection and/or reconstruction) or placement of endotracheal or endobronchial tubes or stents.[51, 52]
Pulmonary arteriovenous malformations (PAVMs) are abnormal communications between pulmonary arteries and pulmonary veins. Most PAVMs are congenital. Approximately 70% of patients with a PAVM have hereditary hemorrhagic telangiectasia (HHT), also termed Osler-Weber-Rendu syndrome; conversely, 15-35% of persons with HHT develop PAVM.[53] HHT is associated with a mutation in the endoglin (HHT type 1) or ALK1 (HHT type 2) gene; the phenotypic expression of these 2 mutations is indistinguishable.[54]
PAVMs are typically multiple, bilateral, and located in the lower lobes. HHT affects multiple organ systems, including the skin, mucosal membranes, lungs, brain, and gastrointestinal tract. Recurrent epistaxis is frequently the earliest symptom and occurs in nearly all patients. Other extrapulmonary manifestations include notoriously difficult to manage gastrointestinal hemorrhages from arteriovenous malformations and central nervous system complications (eg, stroke, brain abscess) caused by paradoxical embolization through the PAVM.
Pulmonary symptoms of PAVM result from the right-to-left shunting of blood. Patients may report fatigue, dyspnea, and platypnea (dyspnea worsens while upright and improves when supine). Although less common, hemoptysis may be the first symptom to prompt a patient to seek medical attention.
Physical examination may reveal nonspecific signs (eg, clubbing, cyanosis, occasional pulmonary bruit). Orthodeoxia (ie, decreased oxygenation while upright and improved when supine) is the physical examination correlate of platypnea and is the result of gravitational redistribution of blood flow to the lung bases (thus through the lower lobe PAVM) while the patient is upright.[55] Chest radiographs may reveal oval or round, homogeneous, nodular lesions several millimeters to several centimeters in diameter in the lung bases.
A clinical diagnosis of HHT can be suggested by examination of the skin. Telangiectasias of the face, hands, feet, chest, lips, tongue, and oral, nasal, and conjunctival mucosa become apparent in the second and third decades (see the image below). Lesions typically range from one to several millimeters in diameter, but they may grow much larger. Three-dimensional reconstructions of serial sections of skin biopsy specimens have established these lesions to be arteriovenous malformations.
The treatment of PAVMs consists of surgical resection or obliteration of the shunt by catheter embolization with coils (see the image below). A large or enlarging PAVM, pulmonary symptoms or signs (dyspnea or hypoxia), or paradoxical emboli are suggested indications for treatment.[54]
Synthesized by hepatocytes, alpha-1 antitrypsin is the principal serum protease inhibitor. A single amino acid substitution results in a profound structural alteration of the enzyme, preventing its release from hepatocytes. Although perceived as a rare disease, the prevalence of alpha-1 antitrypsin deficiency may be as high as 1 case per 3000 persons in the United States.[56]
The major organ systems affected by alpha-1 antitrypsin deficiency are the lungs, liver, and skin. The clinical manifestations are the result of unchecked proteinase activity that damages the parenchyma of these organs. Emphysema is the primary pulmonary manifestation of alpha-1 antitrypsin deficiency. Patients with alpha-1 antitrypsin deficiency develop severe fixed airflow obstruction at an early age, usually before age 50 years. Cigarette smoking greatly accelerates the progression of disease. Alpha-1 antitrypsin deficiency–associated emphysema occurs predominantly in the lung bases, as opposed to the upper lobe predominance seen in smoking-induced emphysema. Diagnostic testing includes quantitative (ie, determination of plasma alpha-1-antitrypsin levels) and qualitative (commonly referred to as phenotyping) studies.
Approximately 10% of children with the ZZ phenotype develop clinically significant liver disease; adults with cirrhosis of unknown etiology are occasionally found to express this phenotype.
Recurrent ulcerative, necrotizing panniculitis is a rare extrapulmonary manifestation alpha-1 antitrypsin deficiency.[57, 58] The panniculitis is often preceded by trauma and is often mistaken for bacterial cellulitis. Crops of painful, red or violaceous, subcutaneous nodules occur on the trunk and proximal extremities. The nodules subsequently ulcerate and spontaneously drain a clear-to-yellow serosanguineous fluid, which may be oily as a result of liquefaction of fat.
Biopsy specimens reveal lymphohistiocytic infiltrate with areas of acute neutrophilic panniculitis. Culture results for bacteria, fungi, and mycobacteria are routinely negative.
Intravenous infusions of purified alpha-1 antitrypsin, corticosteroids, dapsone, and doxycycline have been used to treat alpha-1 antitrypsin–related panniculitis.
Multiple and extensive cutaneous symptoms have been reported in cases of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although COVID-19 largely manifests as a respiratory illness, dermatologic sequalae are common. One study estimates that 6% of all patients with COVID present with cutaneous symptoms.[59]
Ghafoor et al found that maculopapular, morbilliform, and/or erythematous rash was the most common cutaneous symptom associated with COVID-19 infection. Urticaria and retiform purpura were the next most frequent signs. Skin infections and vesicular/pustular exanthem were also seen in a significant number of patients.[60]
The literature differs on the most common site for COVID skin manifestations. Some authors maintain the trunk is the most frequent location, while others assert that the acral regions of the lower extremities, specifically the feet and toes, are the most common site. Certainly, perniosis (chilblains) of the feet and toes (so-called "COVID toes") is a prevalent symptom in COVID infections.[61] This particular symptom has noted to be most common in pediatric patients and is associated with a milder clinical course.[62, 63]
Cytokine storm, including an inflammatory response to the spike (S) protein of SARS-CoV-2, vitamin D deficiency, angiotensin-converting enzyme 2 (ACE2) receptor activation, androgen levels, and psychological stress have all been proposed as mechanisms for the cutaneous sequalae present in many COVID infections.[64]
In SARS-CoV-2 infection, a type II transmembrane serine protease (TMPRSS2) enzyme activates the ACE2 receptor subsequent to the attachment of the S protein to ACE2. This binding and TMPRSS2 activation results in S protein activation and allows viral entry into the host cell through receptor-mediated endocytosis. Androgen receptors both promote and increase TMPRSS2 gene expression, and there is no other known regulatory mechanism for TMPRSS2. This relationship explains the less symptomatic course of COVID often seen in children who would have low relative expression of androgen receptors.[64]
Fat embolism syndrome is a systemic disease that follows trauma and fractures of the long bones or pelvis. Fat embolism (without systemic manifestations) may also occur in association with hemoglobinopathies (sickle cell anemia), pancreatitis, bone marrow transplantation, and sepsis, and it may occur as a surgical complication of total hip and knee arthroplasty.
The classic triad of findings in persons with fat embolism syndrome includes respiratory distress, altered mental status, and thrombocytopenia, typically occurring within 24-72 hours of long bone or pelvic fracture. The classic cutaneous manifestation (occurring in approximately one third to one half of patients) is an evanescent petechial eruption on nondependent portions of the body (ie, upper chest, neck, axillae, conjunctivae).[65] The finding is frequently overlooked but may be a key to diagnosis; it resolves in 5-7 days. Subsequent respiratory decompensation may range from mild hypoxemia to respiratory failure requiring intubation. Chest radiographs frequently show progressive, diffuse bilateral interstitial and alveolar infiltrates that are described as a "snowstorm pattern." Neurologic manifestations vary widely but typically are reversible upon resolution of the respiratory component.
The pathophysiology of respiratory compromise is uncertain, but theories include direct mechanical occlusion of the pulmonary capillaries by fat droplets released from the bone marrow or from the biochemical toxicity of these droplets once they are hydrolyzed to free fatty acids by lipases.[66]
Distinguishing between fat embolism (the presence of fat globules in peripheral circulation) and fat embolism syndrome (a systemic disorder that may be life threatening) is critical. Fat embolism occurs in as many as 90% of patients with long bone fractures; fat embolism syndrome is much less common (estimated rate of 1-2%).
The mortality rate for patients with fat embolism syndrome is substantial (approximately 5-10%), and therapy is primarily supportive. Prognosis is primarily dependent upon the degree of respiratory compromise.
First described in 1964 by Samman and White, yellow nail syndrome consists of the triad of yellow slow-growing nails, lymphedema, and pleural effusions.[67] The pathogenesis is unknown, but Samman and White postulated lymphatic impairment as the cause. One study suggests that a functional, rather than structural, lymphatic abnormality may be responsible.[68]
Yellow (occasionally green) nail discoloration is the most obvious clue to diagnosis. The nails are characteristically thick and dystrophic with onycholysis, transverse ridging on an otherwise smooth surface, and loss of the cuticle. Women with yellow nail syndrome often color their nails with polish. The growth rate of fingernails is less than 0.5 mm/wk (approximately half the normal rate).
Lymphedema typically involves the lower extremities to a greater extent than the upper extremities and is symmetrical and nonpitting.
Pleural effusion is the classic pulmonary manifestation of yellow nail syndrome and usually the last in the triad to develop. The exudative effusions are characterized by a high concentration of protein (>3 g/dL) and lactate dehydrogenase (>200 IU/L), with fewer than 1000 leukocytes/µL, mostly lymphocytes. Effusions may be unilateral or bilateral and often recur after initial drainage. Other respiratory manifestations include bronchiectasis, recurrent pneumonias, bronchitis, and sinusitis.
Treatment of pleural effusions may warrant pleurodesis (ie, instillation of a sclerosing agent into the pleural space), pleuroperitoneal shunts, or pleurectomy.[69]
Named after Arthur Birt, Georgina Hogg, and James Dubé in 1977, Birt-Hogg-Dubé syndrome is characterized by pneumothorax and lung cysts, benign skin tumors, and kidney tumors.[70]
It is a rare autosomal dominant condition caused by mutations in the FLCN gene, which normally provides instructions for making a protein called folliculin. Although the exact function is unknown, researchers believe that the FLCN gene is responsible for restraining cell growth and division. Hence, a mutation of the gene leads to the formation of tumors. However, the cause of the cyst and pneumothorax formation in the lung is not yet understood.
According to the Birt-Hogg-Dubé foundation (BHD Foundation), every patient presents differently, even among members of the same family. The condition is characterized by skin lesions, renal tumors, and lung cysts or pneumothorax. It is estimated that 90% of patients have skin lesions, 90% have lung cysts, 25% have a collapsed lung, and 33% have kidney cancer.
The most frequent skin features include fibrofolliculomas, trichodiscomas, and acrochordons. The cutaneous lesions are frequently on the face, neck, and upper torso and are described as multiple, pale-yellow, slightly raised, dome-shaped papules measuring 2-4 mm in diameter.[71]
Diagnosis is suspected with the presence of multiple skin fibrofolliculomas, with at least one histologically confirmed. Differential diagnosis includes tuberous sclerosis. However, identification of the FLCN germline mutations is most supportive of the diagnosis. Even with this mutation, the manifestations can vary among all patients.
Other features include spontaneous pneumothorax, lung cyst(s), and renal tumors. The renal tumors are most frequently diagnosed at an early age, are bilateral, or are multifocal. They are often a hybrid pattern with chromophobe and oncocytoma features. These manifestations in a patient or the patient's relatives can be diagnostic.
Testing for the mutation can lead to early diagnosis in family members. It is important to recognize the kidney tumors early and perform annual MRI scans of the kidney. Smoking cessation is recommended to prevention of pneumothorax.[72]


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SAP Business One B1 HANA multiple Tenant Installation
Dear community,
to give a short answer to the question "How to setup SAP Business One in a HANA multipe tenant DB environment": not to setup 🙁
As far as my testing has shown to me: currently, SBO4HANA does not support being installed in a multiple tenant HANA DB.
I have done a "regular" setup with a single DB HANA System, installing SBO and got it as expected to work without any issue.
Afterwards, I converted the HANA system to a multiple tenant DB system. Proceeding like this has the advantage that in the remaining HANA tenant DB, where SBO has been installed, the HANA scriptserver as well as the HANA nameserver are still present.
And the port for accessing SQL will remain as it has been.
So no problem to connect after converting to the existing SBO DB's, except an error when starting FIORI menu (instead of main menu an error "not authorized") but other style menu worked fine, same with using menu bar.
So now trying to get SBO working in the 2nd and new tenant DB:
– for every new tenant DB, a new port range is used, starting with 3xx41 – 3xx43 for the first new created tenant DB, 3xx44 – 3xx46 for the second tenant DB and so on.
– SQL server in my new tenant DB is reachable using port 30041
– Successfully adding a new DB Instance <Server>:30041 in SLD: DB instances and Companies
– Starting SBO: choose company: I can select between "old" HANA DB instance <Server>:30015 and new <Server>:30041 🙂
– unfortunately, with selection of port 30041 an error occurs in status bar. Button "Create new Company is inactive.
OK, I don't mind, no problem to copy company DB from old instance 30015 into new instance 30041.
Starting SBO, selecting 30041 instance: no DB 🙁
OK, same with SBOCOMMON, and SLDDATA: starting SBO, selecting 30041 instance: no DB 🙁
Reason: the SAP Server installation on Linux is asking to specify a DB server with port nr – so it is binded to one port, and can not handle two ports.
Of course I have tried to install SBO Server Linux part on a second Linux server and connect it to the 2nd HANA tenant DB: unfortunately, in the new tenant DB nameserver and scriptserver are missing and I could not get them installed.
So my final conclusion: no way to use multiple tenant DB's in HANA environment with SAP Business One:
– SBO Server does not work with two DB instances in same HANA system
– setup new SBO Server for a new tenant DB not possible; nameserver and scriptserver missing.
Sorry not to have good news about that point; I would be very happy if someone could show me that I am wrong 🙂
kind regards to all


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How to remove grease stains from headrests and armrests
Porous smooth leather (aniline) darkens over time especially in areas that come in regular contact with skin and other body parts. This continued contact causes body oils from skin and hair to transfer onto the leather and penetrate the leather surface. When the leather is new, the oils and fats are absorbed by the leather but over time with more use of the same areas the accumulation becomes a very visible stain.
In most cases, such stains cannot be removed by general cleaning. As professionals, we have methods to absorb the penetrated fats and to refresh and renew the leather colour. However, sometimes following repairs the area will not look like new. However, in some cases our technicians have only been contacted when the problem has extremely worsened and it is only possible to aesthetically improve the damaged area.
Our recommendation for DIY solution (as good as possible):
Clean the darkened area very carefully with COLOURLOCK Leather Cleaning Spirit. Take some Cleaning Sprit on a clean soft cloth and wipe fast over the surface without wetting too much. Allow it to dry before re-applying. This ensures you avoid getting borders or edges. This process dissolves the penetrated fats a little bit. Continue the treatment with COLOURLOCK Grease Absorber Spray. Spray the product onto the darkened area and allow it to dry completely. The product contains solvents that dissolves and absorbs the fats and pull it out of the leather. The contents of the spray dry into a white powder but as it pulls out the grease, it turns into a yellowish powder. This remaining powder can simply be brushed off or vacuumed. Repeat the process until the powder stops turning yellow or until no further improvement can be achieved.
In most cases, such areas remain darker or lighter in comparison to the rest of the unaffected area. As the fats have damaged the surface over the years. These areas will need to be adjusted with COLOURLOCK Leather Fresh. Therefore, the leather colour must be more or less of one tone and the leather shouldn't be too porous. Leather Fresh seals the surface and reduces the risk of a repetition of such stains.
We recommend protecting the unaffected areas COLOURLOCK Aniline Protector as it contains oils, UV-filters and antioxidants to prevent from aging. Don't apply the protector in areas that were darkened and have been treated. This helps to avoid new stains as the protector contains oils. But the rest of the leather should be treated to keep the leather soft and to avoid aging damages. Especially areas that are exposed to sunlight must always be protected.
Heavily damaged. DIY solution may not give the best result and may have to be treated professionally.


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What is worship?
The next few newsletter articles will tackle the subject of "worship." For now, let's start with what was heard at a popular local Christian church not very far away . . .
"when you go to a Justin Timberlake concert…you are worshipping: showing love, admiration, affection…Lucas Oil stadium…same thing…the question isn't whether but what you will worship?"
"your church experience will only be as good as what you bring to it"
"you were made to worship…you were made to love and show admiration and affection"
"God is worthy of the WOW that is already in your heart"
"aim the WOW in your heart toward the one that is only worthy of it"
"you are already worshipping so direct it to Him"
"aim your worship…to God"
"life is hard and challenging….worship your way through it"
The underlying premise of this "sermon" is that true worship is standing, dancing, clapping, praising, exactly how you see done at a concert or football game. The pastor even went so far as to say that God commands such worship and that humans beings are created to do just that.
Let's start with John 6:28-29, Then they asked him, "What must we do to do the works God requires?" Jesus answered, "The work of God is this: to believe in the one he has sent."
The highest form of worship is FAITH. Not what you do or how you do it, but belief in Jesus Christ, the Son of God, crucified and risen for your sins and the sins of the whole world.
The local pastor went on to claim that "you were made to worship" and that you are doing just that at a Colts game or Justin Timberlake concert. Since this is worship, you merely need to "aim your worship at God." This is also false on many levels:
- Man is spiritually dead in his trespasses and sin. He is not made to worship, he is so infected by sin that even Jesus says in John 8:44 You are of your father the devil, and your will is to do your father's desires.There are many passages that speak to our inability to worship God or that we can control or aim anything. Here is another from 1 Corinthians 2:14 The natural person does not accept the things of the Spirit of God, for they are folly to him, and he is not able to understand them because they are spiritually discerned.
- Many Christians assume that the word "worship" is the same as the word "praise." This is why many churches, even Lutheran, have a "Praise Service" or a "Praise Team". The first word for worship that occurs in Genesis actually means "bow down." This is quite different from the definition of worship I shared above. Bowing down is quiet and reverent and submissive. I suggest we start a "Bowing Service" and a "Bowing Team"! Just joking.
- God commands that we only worship Him, so if what we do at a Colts game or Timberlake concert is the same thing, then following the logic from this popular local Christian church, it would be sinful according to Scripture! Consider these passages where God commands worship of Him only: Luke 4:8 And Jesus answered him, "It is written, "'You shall worship the Lord your God, and him only shall you serve.'" Deuteronomy 6:13 It is the Lord your God you shall fear. Him you shall serve and by his name you shall swear.
So we see that the definition of "worship" from this big box church is incorrect, from Scripture. Furthermore, how do you deal with sin in your life? This church falsely tells you to "worship your way through it". This puts ALL the work on you!
Our Divine Services as Lutheran-Christians focus on two things: humbling ourselves before the almighty God with reverence and awe, but an awe that bows down before Him, which is so different from the way the world worships. We don't worship God like we do the Colts or Timberlake, because we have nothing to offer Him. We are sinners. Thus, the Divine Service is not about us coming to God, but rather God coming to us. Forgiving us. Which reminds me, Jesus commands (mandates) the Apostles' and the church that follows them John 20:19-23, On the evening of that day, the first day of the week, the doors being locked where the disciples were for fear of the Jews, Jesus came and stood among them and said to them, "Peace be with you." When he had said this, he showed them his hands and his side. Then the disciples were glad when they saw the Lord. Jesus said to them again, "Peace be with you. As the Father has sent me, even so I am sending you." And when he had said this, he breathed on them and said to them, "Receive the Holy Spirit. If you forgive the sins of any, they are forgiven them; if you withhold forgiveness from any, it is withheld."
I watched the entire service of this local church. Never once did I hear the pastors speak these life-giving words of Jesus: I FORGIVE YOU. Why don't they do that? Jesus commands it.
Luke 24:46-47 Jesus said to them, "Thus it is written, that the Christ should suffer and on the third day rise from the dead, and that repentance for the forgiveness of sins should be proclaimed in his name to all nations, beginning from Jerusalem.
Forgiveness of sins was mentioned once or twice, but it was not the main thing in the "sermon". They never mentioned the Gospel in terms of what Jesus did by living a perfect life, dying a death as the once for all sacrifice upon the cross, and rising to new life in His resurrection. This church is trying to get you and others to believe a false gospel, that you can and should worship God in a certain way. This is all Law. I am saddened to hear such drivel and fear for those who may be led astray.
And if we are going to talk about what God commands, what about Jesus also commanding the Lord's Supper? We do it every Sunday. And not just because He commands (mandates) it, but because we also need it and desire what He forgives: forgiveness of sins, life and salvation. I did not see nor hear this emphasis at this local church. Luke 22:19-20 And he took bread, and when he had given thanks, he broke it and gave it to them, saying, "This is my body, which is given for you. Do this in remembrance of me." And likewise the cup after they had eaten, saying, "This cup that is poured out for you is the new covenant in my blood.
Lastly, disciples are NOT made by teaching them to worship or aiming their worship at the right person or place. Hear again the words of Jesus, Matthew 28:18-20, And Jesus came and said to them, "All authority in heaven and on earth has been given to me. Go therefore and make disciples of all nations, baptizing them in the name of the Father and of the Son and of the Holy Spirit, teaching them to observe all that I have commanded you. And behold, I am with you always, to the end of the age."
Disciples are made first by baptizing, not worshipping. Which is one of the reasons we baptize our infants. They, as sinners, receive God's grace and mercy. They do nothing, He does everything. Then we teach. We catechize. I did not hear this emphasis from Scripture, at this local and popular "Christian" church. They are preaching a false gospel and twisting God's word to appeal to you and others, leading them away from the gifts of Christ.
The crux of this first newsletter article on worship is this: we have nothing to offer Him, but He gives everything to us through Jesus Christ, through His Word, through His Sacraments. It is not sinful to celebrate at a Colts game or Timberlake concert. True worship is faith and quiet submission, which should bring to mind the story of Mary and Martha. Martha is busy working and doing things for Jesus. Mary is sitting quietly, at Jesus' feet, listening, learning and receiving. Jesus commends Mary's faith and actions, not Martha's. Let us first receive His gifts of Word and Sacrament and then get busy with all that needs to be done this side of heaven. How we worship, what we say and do, does matter. More to come in the next newsletter article.
Forgiveness of sins, life and salvation are freely yours through Jesus Christ your Savior!
Peace be with you,
Pr. Mackay


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There are very few things that are more discouraging than being rejected for a promotion. You may feel you're ready to move up the ladder, but you watch others get promotions while you're passed over.
Believe it or not, the reasons are often pretty simple. It's not some complicated plot that involves Vladimir Putin or the CIA. It often comes down to this:
- You're like a bull in a china shop. You not only gossip and complain loudly enough to be heard by anyone with a half-mile radius, but you make inappropriate comments and swear like a sailor on shore leave. Obnoxious and bratty behavior that could net you a reality show isn't the professional attitude that is appreciated by bosses. If you embarrass, offend or anger co-workers with your demeanor, you can bet the boss doesn't want you carrying your offensiveness into a leadership position.
- You can't go anywhere without your GPS. If you can't take the next step in a project without clear guidance from your supervisor or a trail of bread crumbs from team members, then you're not showing the boss that you're capable of taking on a new challenges if promoted. Standing around dithering while you wait on instructions reveals you as someone who needs to be constantly supervised, and that's not a recipe for a promotion.
- "Huffy" is your middle name. Do you take feedback well, or get huffy and pout or gripe about any criticism? You've got to develop thicker skin the higher you go on the career ladder, so an inability to accept feedback professionally could be sending the message you're immature and not ready to play with the big kids.
- You're never late for happy hour. There's nothing wrong with enjoying your time off after work, but you can't expect the boss to consider you for a promotion when you hit the door at 5 p.m. like a bullet, racing out to your car to get to happy hour or yoga class. Try lingering a bit after quitting time to show the boss that something else is not always more important than your job.
- You don't speak up. Bosses are not mind readers. If you want a promotion, ask for it. Then, give all the reasons why you'd be great for the job.
- You don't have the right skills. It's surprising how many people ask for a promotion when they have no real idea of what the job entails. Do your homework so that you know the specific skills or certifications you need to fulfill the job duties. Then, take stock of what soft skills you have to offer. Perhaps you're adept at soothing angry customers or you're good at rallying diverse team members around a common goal. A combination of skills are critical for getting a promotion because any boss wants to feel like she's getting a well-rounded person who won't require a lot of hand-holding.
- You never make a good suggestion. Sure, you thought your idea of putting a slushie machine in the breakroom was brilliant, but how exactly does that help the boss or the company? Those who want to be promoted have to show that (read more here)


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BIOSDECODESection: Maintenance Commands (8)
Updated: February 2007
Index Return to Main Contents
NAMEbiosdecode - BIOS information decoder
SYNOPSISbiosdecode [OPTIONS]
DESCRIPTIONbiosdecode parses the BIOS memory and prints information about all structures (or entry points) it knows of. Currently known entry point types are:
- •
SMBIOS (System Management BIOS)
Use dmidecode for a more detailed output.
- •
DMI (Desktop Management Interface, a legacy version of SMBIOS)
Use dmidecode for a more detailed output.
- •
- •
- PNP (Plug and Play)
- •
- ACPI (Advanced Configuration and Power Interface)
- •
- BIOS32 (BIOS32 Service Directory)
- •
- PIR (PCI IRQ Routing)
- •
32OS (BIOS32 Extension, Compaq-specific)
See ownership for a Compaq ownership tag retrieval tool.
- •
- SNY (Sony-specific, not decoded)
- •
VPD (Vital Product Data, IBM-specific)
Use vpddecode for a more detailed output.
- •
FJKEYINF (Application Panel, Fujitsu-specific)
biosdecode started its life as a part of dmidecode but as more entry point types were added, it was moved to a different program.
- -d, --dev-mem FILE
- Read memory from device FILE (default: /dev/mem)
- -h, --help
- Display usage information and exit
- -V, --version
Display the version and exit
BUGSMost of the time, biosdecode prints too much information (you don't really care about addresses) or not enough (because it doesn't follow pointers and has no lookup tables).
AUTHORSAlan Cox, Jean Delvare
SEE ALSOdmidecode(8), mem(4), ownership(8), vpddecode(8)
This document was created by man2html, using the manual pages.
Time: 04:45:58 GMT, September 16, 2022