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Everyone who knew Jim Hayward knew he would be strong. Six-foot-4, 280 pounds, he was an imposing man, and in uniform he seemed to be bigger, taller. They knew he would fight the cancer for as long as he could — more than eight years — before it would take him.
His last day was Christmas Day last week, after a long, devastating battle. His memorial service will be on Friday.
"He was a very kind, very gentle man," said Weld County Sheriff John Cooke. "You couldn't help but like Jim."
That personality, as a sheriff's deputy, is what brought him through cases that others may not have been able to solve. When he was a jail investigator, the story was that he could get the needed information out of any prisoner.
"He solved a lot of old homicides while he was working the jail," Cooke said. "He'd get a prisoner to talk, then work on solving the case. He even solved one longtime homicide for another law agency."
But then the cancer hit. In 2004, the tumors began forming inside his brain, and within the next few years, nine tumors had to be removed. It was a rare form of cancer, Malignant Meningioma, and it took a toll, both on Hayward's physical condition, but also on his and his wife Stephanie's livelihood. Despite insurance, the medical procedures to remove the tumors were expensive, of course, and his medication cost $500 per month.
In an auction at their Greeley home, they had to sell Jim's special collections: coins, stamps, antique toys. He said then it was hard to part with the collections, but it had to be done. Friends inside and outside the sheriff's office went to the Hayward home that day to help move and arrange for the auction.
A little more than a year ago, they had to get out from under their house payment in Greeley, and Stephanie said they were able to sell the house on the day they moved from Greeley. They sold most of their belongings at an auction and moved to Ann Arbor, Mich., to be closer to family.
In Ann Arbor, Jim continued the fight. One of the leading cancer hospitals in America was there to help Jim, but the hospital wasn't in their insurance network. "The insurance company was really good," Stephanie said. "They made Jim a special case and took care of many of the high expenses."
There were more tumors, more hospitalization, radiation treatments, operations, and a heart attack. And big, strong Jim Hayward began to slip.
Last August, he went into the hospital to stay. They placed him in a hospice palliative care unit to care for him, to keep him comfortable, but he was also "DNR" — Do Not Resuscitate. He almost died in August, Stephanie said, then near Thanksgiving, and finally, his last breaths came on Christmas Day. "For that, Christmas Day will always be extra special for us," said his wife.
Jim had a son in Kansas from another marriage, and when Jim and Stephanie got married, he adopted her daughter. It was at that adult daughter's home where they were staying in Ann Arbor.
According to one of his working friends, retired Weld County Sheriff's Commander Bill Spalding, there were many unforgettable moments with Hayward.
"He was a tremendous Nebraska fan," Spalding said, "and kept a Barbie Doll in a Nebraska cheerleaders' outfit in his office. On the week of a Colorado-Nebraska game, the cheerleader doll was kidnapped, and he received ransom notes along with photos of "Colorado" Ken and "Nebraska" Barbie in unusual positions. It took him a couple of weeks to get her back."
If Hayward or Spalding would leave town for a training session in another city, the one who was left back in Greeley would call the other guy's hotel room at 3 a.m. "To tell him that his wake-up call was coming in a few hours," Spalding said, laughing.
Spalding was also highly impressed with Hayward's interrogation of suspects. "Somehow, he was able to get through to the suspects when no one else could," Spalding said. "He just knew how to handle them."
Indicative of Hayward's many friends, Heath Carroll of the Carroll-Lewellen Funeral Home in Longmont put together a memorial service without charge to the family.
Weld County Criminologist Jan Lemay summed up his feelings for Hayward, placing his Christmas death into the right light: "He went to have a birthday party with Jesus."
Mike Peters is a retired Tribune staff writer. He can be reached at email@example.com.


text:
Top Definition
A thunderclap is the sound of a scrotum slapping against the body when going balls-deep
I went balls-deep with Deedra last night. So you gave her the ol' thunderclap
dodane przez TSUAOJAP kwiecień 15, 2010
Trending Now
Can you define these popular missing words?
When a man is a.) naked or b.) wearing clothing that is non-constraining on the crotchal region, and he begins pelvic thrusting with such violent determination that his scroat (scrotum) begins to repeatedly smack audibly againnt his chode/taint/chonch.
Honey, stop that! Your thunder clap so goddamn loud it's going to wake the neighbors again.
dodane przez Masterclapper październik 19, 2006
The act of thrusting ones waist back and forth causing a man's scrotum to to slap the gootch creating a clapping noise.
*At the Superbowl*
Boy: "Shit bro, my hands are full."
Friend: "You can always Thunder Clap"
Boy: "If I must." (clapclapclap)
Boy: "Shit bro, my hands are full."
Friend: "You can always Thunder Clap"
Boy: "If I must." (clapclapclap)
dodane przez thunderclappingpro marzec 21, 2011
Clapping in the air with a sliding motion. With one hand raised first, with the second to meet it half way, clapping, with the second hand left extended. Repeat back and forth.
Look at that guy, he knows how to thunder clap!!
dodane przez Setrock październik 29, 2004
The name given to the slapping sound produced during the act of sexual intercourse in the famed doggy style position when a males testicles, which are especially loose and/or saggy due to heat or over stimulation, smack against the back of the females thigh and produce a slapping sound reminiscent of a soft clap of the hands.
Man 1 "Nigga i was bangin my girl the other night doggy style and my balls were so loose that the sound of the thunderclap was proper so loud that i went deaf in my left ear."
Man 2 "Shit nigga you best calm down on swingin dem testiclots around."
Man 1 "Word."
Man 2 "Shit nigga you best calm down on swingin dem testiclots around."
Man 1 "Word."
dodane przez Ninja Mc Stealth Kill sierpień 23, 2009
To dominate (punking) something or someone in a very epic and irreversible manner.
Yo JT, you need to establish your dominance and thunder clap the first no body you see.
dodane przez Jono86 styczeń 05, 2014
A scientific term used to describe an advanced stage of Chlamydia, in which the genitals are covered with blistery and often puss filled pustules that pop like thunder. Often resembling the face of a pizza delivery boy.
I knew that girl was slutty, but I didn't realize how slutty until I heard her thunderclaps from across the room!
dodane przez Walker Thundercox wrzesień 20, 2011

subset: commoncrawl


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Former state representative seeks to challenge Johnson for Congress
July 18, 2013
LISBON — Announcing she is running on concerns for jobs and education, Marietta resident Jennifer Garrison is the first to announce she will run against 6th District U.S. Rep. Bill Johnson in 2014....
Other than government jobs, government can't create jobs. This is all a new candidate promises. Environmental regulations, good or bad have had a drastic effect on local jobs and Obamas war on coal is one of the major job killers. On the other hand the government can kill jobs with legislation. The folks that voted for Obamacare are the ones that have lead to a continuing lack of jobs. Even the President has admitted it is a drag on the economy. This bill has to be thrown out and something that really will lower health care cost needs to be done. Instead of working through this issue everyone seems to be trying to find loopholes to avoid it, and now we are all faced with higher insurance costs. Heath care insurance is not health care. We need to make that distinction. We need representatives that are willing to fight for the working people of this country and right now that does not appear to be the democrats.
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If I wouldn't know better I would swear she took that script right out of Obama's handbook.
Stofit....excellent post!
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Ok this is my silly question, for anyoone who was following skating during that time:
Why did RUS only had 2 entries in Men for the Nagano Olympics?.
1997 Worlds results were Yagudin 3rd and Kulik 5th. 3+5 = 8 so three should go next year. Don't know when did the "13" rule started to apply but I understand previously to that it was three spots for a country that medals and Yagudin took bronze, so what gives???
Thanks in Advance
IIRC, it's because Urmanov withdrew with injury during 1997 Worlds. Under the (ridiculous) rules at the time, his withdraw counted as "skater didn't make it to the free skate." They counted it as Russia having three skaters at those Worlds, with one of them doing so terribly they lost a spot at the Olympics. That, of course, is not the reality, but that's what the rulebook counted it as.
In 1997, the new system for determining slots took into account all entered skaters' results.
Russia had three entries at 1997 Worlds. Alexei Urmanov withdrew before the freeskate, which gave him 18(?) points, along with 3+5 for Yagudin and Kulik. That total entitled Russia to two spots for 1998 Olympics and Worlds.
After that occurrence specifically -- injury withdrawal by the reigning Olympic champion and winner of the short program at 1997 Worlds costing the strongest men's team at the time a spot at the next year's Olympics -- the rules were changed for 1999 and following to take into account only the top 2 entries in a team of 3, and not to give points(?) to skaters who withdraw midcompetition. IIRC the total for 2 skaters was also changed from 23 to 28(?) to keep 2 slots for the following year.
Thanks a lot Gkelly and Sandpiper! That was bugging me for a while..
And damn that Urmi withdrawal was reaaally unfortunate for him. NOt only did it cost him a World title (he rocked the SP!) but also a place on the olympics. such a shame
Yeah, it was really unfortunate, what happened to Urmanov. That was his best chance to win a World title, with Elvis Stojko placing fourth after the SP. How sad that he competed for many years even after winning Olympic gold (which I respect), but never got on the Worlds podium again.
Well, he reinjured himself during the off season and ended up not competing at all again until more than a year later at Goodwill Games in summer 1998.
So if there had been a third men's spot available for Russia, it would have gone to Plushenko or possibly Abt.
All of which was even more unfortunate for Urmanov.
Yeah, third spot in Nagano couldn't have gone to him anyway (I'm guessing, even with two spots, they would've given Yagudin's spot to Urmanov had he been fit to compete). I speak more about how he never won Worlds, which was really a shame. At his best, he actually had the technical arsenal to compete with Stojko and Kulik.
Stupid qestion? But I'm perplexed as to why this season's Scale of Value still list base points for single jumps on their charts when they've revised the rules so that 'Jumps with less than 1.5 revs in both Short and Free programs of Seniors/Juniors will have no value'. Are the base values remaining for the sake of Novices and under?
Another stupid question.
Obviously there's no reason (and even risky) for ice dancers to even attempt jumps elements, but I'm wondering if they can do them if they tried, maybe even do them just for fun during practices. If so, has anyone ever seen any of them do them? (just thinking how awesome it'll be to see someone like Meryl or Charlie do a loop, an Axel or others)
Charlie White did both singles and ice dance until the 2005-2006 season (That was the year he and Meryl won Nationals at the junior level and the bronze medal at Junior Worlds). Here's a video: https://www.youtube.com/watch?v=n6f3ow-4au8
Another example is Vanessa Crone. I think after she ended her partnership with Paul Portier she competed as a singles skater.
Last edited by Mrs. P; 07-06-2014 at 10:11 PM.
IIRC, Virtue and Moir both have performed jumps for a show as well. Again, don't remember details --maybe CSOI??? -- and do not have a link.
Wow, thank you Mrs. P for the link and the quick response! Just like I thought, awesome to see Charlie jumping !!
Thank you, also, to golden411 for the quick response! Now Scott and Tessa jumping is also something I'd love to see.
I suppose it makes sense that ice dancers with their superb skating skills can do jumps if they try.
I think this question may not be ok to ask on this forum and if it is delete away and I apologize. But I am just so curious ...... are Tara and Evan a couple?


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Cullen Greentaner, Ardell Lash expert, spends hours each day applying eyelash wefts to clients. Greentaner has learned that the new Color Effects Lashes can enhance a look to make the eyes pop more than ever. Available in Wine, Blue, Plum, Greentaner says the best shade for a brown eyed client is blue, and for the blue or green eyed client, wine or plum.
When asked for the one most important tip for applying lashes...he had an immediate answer: "It's the adhesive. You really don't need that much. I see make up artists overdoing it all the time. You just need a thin line."
Learn more from Greentaner in this short video.


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Agreed. Our near future is certain... elite talent willing to give it their all to retain their status as 'top-dog' after two 2nd round and one 1st round exit. Long-term future, lots of you seem to doubt our organization. We have been going strong for 20 years now, and yes every good thing comes to an end, but why would you think now? There's no real concrete evidence IMO. We went from 02 to 08 with nothing, and I bet the same crap was being spewed about Detroit's dynasty 'about to fall' then!
First of all I think the long-term outlook of a team always matters to potential FA's. Second, there is reason to think it might be now.
1. The numbers: The numbers of all our 'core' or 'star' players are and have been falling in past years save for Filpulla.
2. IMO, there are no prospects with real star potential to replace these guys that are getting older and watching their production fall. I think Smith is the closest thing to that and even he could be a bust. And even if he makes something of himself, is it going to be Nik Lidstrom something? Not likely.
3. It all starts and stops with Lidstrom for me. I think his retirement (be it this year or the next) is going to be the beginning of the end of our twenty year run. It always seems to me that when Nik goes, we go. He's the leader of this team without question and it's going to be hard to compensate for the loss of him.
Edited by centcougar07, 27 May 2012 - 03:23 AM.


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Corbett seems set on making pension reform top priority
January 24, 2013
Gov. Corbett hasn't let up on his top priority for this year....
Probably most are covered by union contracts that only allow lay offs based on seniority. Others are covered by Civil Service rules that are probably similar. Only a small percentage, mostly management, could be subject to lay offs in such a manner. And I really don't believe it would happen if it could. Who could they get to fill those positions knowing that they would be booted before they became eligible for a pension?
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mike, thanks for the legal explanation. That is something I wasn't familiar with actually. I would agree to a system that would make changes that would affect new hires and let the 'current employees' ride our their benefits. Here is one question I would have with that however, does that make employees a target to layoffs? Aka avoiding the benefits/pension all together?
Because if so, that's not fair either.
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Zippie-""legal contracts" have been broken by the government before"
I don't know if they have or not, but what I do know is that the pensions, which are a matter of law, not contract negotiations, have been ruled a legal contract by the PA Supreme Court that can't be changed or broken once in force.
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From what I've read and heard, the PS Supreme Court has ruled that you can't change the plan for those currently in the system. I've also heard it said that it's those who are vested (and it depends on when you were hires as to how many years you needed to be vested since it recently changed).
I am glad to finally see the SG recognize those in the system who have given service to the people of the Commonwealth and have based their retirement planning on what they were told they were getting in return for their service and the money taken each payday from their checks.
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That is why legal, moral, and ethical are not synonyms.
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"legal contracts" have been broken by the government before
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.......These people worked decades with one understanding of what their retirement plan would look like. That can't be changed at the last minute........
What about us who worked/are working in the private sector and saw our retirements fall like lead ballons during the stock market crash?
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Elimination going forward for new employees makes more sense to me. That said, give this guy credit for at least addressing the fact times have changed and the word 'pension' hasnt existed in non-union workers i the private sector for a decade.
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Here's the problem. These people have a legal contract with the state that says upon your retirement your benefit will be calculated using this formula # x % x $ = . You can't simply change the formula, it's a binding legal agreement. If you took out a 30 year fixed-rate mortgage from your bank and signed the contract, I bet you'd be getting a lawyer when midway through the term the decided that the interest rate should be raised because they need more money. It's not right and it's not legal (imho). Harrisburg has created this problem with a decade of underfunding and now they are trying to deflect the blame and cover their collective arses.
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I agree with the mentioned changes, but I'm curious, what determines the 'cut off' for employees near retirement? Pension changes are NEEDED. But I also agree that it's not fair to make changes to the pensions of those who've worked for years and are very close to retirement, so would say 5 years be reasonable? Anyone within 5 years of retirement would not be affected by pension changes? I think that's fair and then change it for everyone else. Because $41 Billion is insane.
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Stream SP men Finland
today 17.10 Finland
Eastern Great Lakes starts Oct. 5 through Oct 9th in Ann Arbor, MI
Results will be found here:
The USFS page for the event
North Atlantics also run Oct 5 through Oct 9th in Hackensack, NJ
Results will be found here:
The USFS page for the event
There will be non-qualifying competitions run concurrently at both sites.
Ice Network will put up On Demand Videos at some point.
Katia Shpilband, Igor's daughter, won Eastern Great Lakes in the Junior Ladies Division.
3 Regionals done, 6 to go - my compilation of all U.S. qualifiers to Sectionals, plus byes, so far: http://unseenskaters.wordpress.com/sectionals/
I've also compiled links for all 9 Regionals as well as the Top Ten total scores from the first 3 Regionals (NWP, EGL, NA) for the higher level ladies and men here: http://unseenskaters.wordpress.com/regionals/
Here are the Start orders/Results pages for the 3 Regionals this week.
New England Regional: http://www.usfigureskating.org/leade...1/results.html
Bye to Eastern Sectional in Sr.: Stephen Carriere (won Easterns last year), Harrison Choate (2nd JGP).
Yasmin Siraj won Easterns last year but has elected to compete - if she places in the top 4, the top 5 Sr. ladies will advance to Easterns (rule 2472).
Upper Great Lakes Regional: http://www.usfigureskating.org/leade...3/results.html
Jason Brown elected to skate Sr. Men SP & FS exhibitions on Saturday. He landed 7 triples+3A< in his FS, 149.09; landed 3A<<, 3Lz3T, 3F in SP, 65.45; 214.54 total score.
Other current JGP competitors at UGL are Kiri Baga (Sr. Ladies) and Barbie Long (Jr. Ladies).
Southwest Pacific Regional: http://www.usfigureskating.org/leade...2/results.html
Bye to Pacific Coast Sectional: Courtney Hicks in Sr. (2nd JGP), Shotaro Omori in Jr. (2nd JGP).
Senior Men's event (Mon.-Tue.): Jonathan Cassar, Scott Dyer, Andrew Gonzales, Sean Rabbitt, Philip Warren - all 5 will advance to Pacific Coast Sectionals due to the fill-up rule.
Vanessa Lam (Sr. Ladies) is a current season JGP competitor at SWP.
Among those competing Junior are 2012 Novice Men's champ Vincent Zhou and Novice bronze medalists Spencer Howe and Amanda Gelb.
Byes through this week's Regionals and Sectionals next month to Nationals: Gracie Gold (UGL), Mirai Nagasu, Leah Keiser, Richard Dornbush (all SWP).
Last edited by Sylvia; 10-14-2012 at 10:19 AM.
Vanessa Lam won Sr Ladies at SWP with 113.44 in the FS. 6 Triples , a little trouble on the 3LO landing. Total score of 168.05, no edge calls in both programs was a big achievement!


text:
Systemwide Events Calendar
Fashion Society Car WashNovember 9, 9:00am - 1:00am
Honolulu Campus, Dillingham Boulevard Administration parking lot (across Costco)
Fundraiser for Fashion Society at Honolulu Community College Spring Fashion Show.
Ticket Information
Starting at $7.00
Event Sponsor
Fashion Technology, Honolulu Campus
More Information
845-9203, car wash (PDF)
|Saturday, November 9
|The Wellness Center - Fitness Class Schedule
Maui Campus, Pilina Bldg., Wellness Center
|Fashion Society Car Wash
Honolulu Campus, Dillingham Boulevard Administration parking lot (across Costco)
|Pay-Per-View Showing of UH Football vs. Navy
Manoa Campus, Campus Center 2nd Floor
|UH Jazz Ensembles
Manoa Campus, Orvis Auditorium
- Highlighted dates have scheduled events.
- Select the date to view all events for that day.
Ongoing Events
- The Wonder of Learning: the Hundred Languages of Children Exhibit
- Course Reserves Deadlines and Information
- Red Hat System Administration I
- EWC Arts Exhibition: Bollywood & Beyond: Costume in Indian Film
- Kalaupapa -- A Source of Light, Constant and Never-Fading
- Trip Around the Island
- Convergence: Glitch_Click_Thunk, Featuring Mark Amerika
- Trip Around the Island exhibit
- Waikiki Parc Features Ashley Huang


text:
Top Definition
To divine future events or gain perspective on current events in far off location using a crystal ball.
The old witch scried a horde of plunderers en route to the village. scry
de drodawg 5 août 2007
Trending Now
Can you define these popular missing words?
a verb. To scream and cry simultaneously; rage; basically, to lose your shit.
de E Dub 28 mars 2015
1. very cool, rad, wicked, unbelievable, skillful, praise-worthy.
Background: indie/alternative slang
Background: indie/alternative slang
Was that you shreading? Your guitar playing is hella scry!
de The Turp 7 juillet 2004


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From the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Municipal and Provincial Archives of Vienna, University of Vienna, Vienna, Austria; and University College London, London, United Kingdom.
Note: An earlier version of these analyses was included in Dr. Zegers's Academisch Proefschrift at the University of Amsterdam in 2008.
Acknowledgment: The authors thank Mag. Martha El Hadidi, Wienbibliothek im Rathaus, Vienna, Austria, for providing several missing pages of Verzeichnis der Verstorbenen and Anton Neumayr, MD, PhD, professor of gastroenterology, Vienna, for assistance with the translation and interpretation of the original names of diseases. They also thank Johan W.G. Tielen, MD, gastroenterologist, Gouda, the Netherlands; Jos G.U. Ridderbeks MD, general practioner, Ulestraten, the Netherlands; Peter Speelman, MD, PhD, professor of infectious disease, and Ray T. Krediet, MD, PhD, professor of nephrology, Amsterdam, the Netherlands; L.P. (Berto) Roegholt, MD, PhD, internist, Middelburg, the Netherlands; and Martin Hohenegger, MD, PhD, professor of pharmacology, Vienna, for fruitful discussions of Mozart's possible cause of death. Finally, they thank Josephine M.E. Tusveld, MD, Utrecht, the Netherlands, for her support in preparing this manuscript.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Richard H.C. Zegers, MD, PhD, Department of Ophthalmology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands; e-mail, firstname.lastname@example.com.
Current Author Addresses: Dr. Zegers: Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands.
Dr. Weigl: Municipal and Provincial Archives of Vienna, MA 8, Rathaus, 1082 Vienna, Austria.
Dr. Steptoe: Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom.
The early death of the composer Wolfgang Amadeus Mozart on 5 December 1791 has fascinated the world for more than 2 centuries. It has been suggested that his final illness was caused by poisoning, renal failure, Henoch–Schönlein purpura, trichinosis, and many other conditions. The official daily register of deaths in Mozart's Vienna was evaluated to provide an epidemiologic framework into which the observations of contemporary witnesses of his death can be integrated. All recorded deaths in Vienna during November and December 1791 and January 1792 were analyzed, together with the corresponding periods in 1790 to 1791 and 1792 to 1793. The deaths of 5011 adults (3442 men, 1569 women) were recorded over these periods. The mean ages of death were 45.5 years (SD, 18.5) for men and 54.5 years (SD, 19.9) for women. Tuberculosis and related conditions accounted for the highest number of deaths; cachexia and malnutrition ranked second, and edema was the third most common cause. According to eyewitness accounts, the hallmark of Mozart's final disease was severe edema. Deaths from edema were markedly increased among younger men in the weeks surrounding Mozart's death compared with the previous and following years. This minor epidemic may have originated in the military hospital. Our analysis is consistent with Mozart's last illness and death being due to a streptococcal infection leading to an acute nephritic syndrome caused by poststreptococcal glomerulonephritis. Scarlet fever, which represents the same underlying disease from an etiologic perspective, is a less likely possibility.
Top. Deaths among men and women in the fall and winter of 1790–1791, 1791–1792, and 1792–1793. Error bars represent SEs. Bottom. Deaths among civilians and soldiers in the fall and winter of 1790–1791, 1791–1792, and 1792–1793. Error bars represent SEs.
A. Total deaths. B. Deaths from tuberculosis and related diseases. C. Deaths from gastrointestinal inflammatory diseases. D. Deaths from fever and inflammatory conditions.
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Only few composers in history have earned any fame from their medical history investigated by several experts. Besides Georg Friedrich Handel and Maurice Ravel it is for rare composers to have numerous pathographies but Mozart, with about 100 articles on Medline, is one of them. However no autopsy was performed and there is no medical documentation preserved that would be acceptable by current scientific standards, so it is almost impossible to perform a proper pathography. Although most commonly noted in medical literature, Tourette's syndrome in not only neurological disorder Mozart suffered from during his life (1). Davies and Bett reported on lapses of consciousness but also convulsions. Mozart did probably faint occasionally, but probably out of his sloppy lifestyle, overworking, alcohol consumption or occasional malnutrition, however there is no evidence he suffered from epilepsy. Mozart's immobility as sign of muscular paralysis assuming postinfectious polyradiculoneuritis was discussed by Davies (2). Complete immobility, severe weakness and preserved consciousness during his final illness may support that theory but pain, absence of paresthesiae and generalized excessive swelling of limbs and body suggest other conditions.
Many authors have supported the kidney disease theory for Mozart's final and fatal illness - taking in account his fatigue, depressive tendencies, headaches, syncopes, anorexia, insomnia, increasing weakness, nausea, vomiting and peculiar metallic taste in his mouth, all as signs of uraemia and renal failure, thereby Karhausen suggested diagnosis of uraemic and hypertensive encephalopathy (3). It was described that Mozart's sudden deterioration 2 hours before death included possible convulsions, delirium, coma, face turned to wall, cheek puffed out so Davies reads those symptoms (consciousness impairment, paralysis, conjugate gaze and facial nerve palsy) suggesting massive brain hemorrhage as a consequence of vasculitis in Schoenlein Henoch syndrome (4). Nevertheless there is no evidence that Mozart showed any signs of focal neurological deficit during his final illness. In such manner Baroni unconvincingly suggested stroke as terminal cause of Mozart's death (5). Theory about Mozart's multiple congenital malformation syndrome including his famous left ear malformation, polycystic kidney as onset of subsequent renal failure and intracranial arterial aneurysm (malformation) that caused fatal subarachnoidal hemorrhage is inconsequent since the clinical course of his final illness rule out that possibility. Puech explained that the linear fracture in the temporoparietal region oriented anteriorly and downwards, without displacement, was found on the skull owned by the Mozarteum in Salzburg and attributed to Mozart and he reasoned chronic extradural hematoma with headaches, fainting, vomiting, chronic weakness and exhaustion (6). Further on Drake suggested chronic subdural hematoma which could be consistent with described skull fracture, several falls in 1789 and 1790 and weakness, headache and fainting Mozart experienced in 1790 and 1791 (7). Both authors failed to work out the substantial question: is the Mozarteum skull Mozart's skull at all? Even DNA analysis performed 2006, on 250th anniversary of Mozart's birth, did not solve that mystery.
1. Ashoori A, Jankovic J. Mozart's movements and behaviour: a case of Tourette's syndrome? J Neurol Neurosurg Psychiatry. 2007 Nov;78(11):1171- 5.
2. Davies PJ. Mozart's death: a rebuttal of Karhausen. Further evidence for Schönlein-Henoch syndrome. J R Soc Med. 1991 Dec;84(12):737-40.
3. Karhausen LR. Contra Davies: Mozart's terminal illness. J R Soc Med. 1991 Dec;84(12):734-6.
4. Davies JP. Mozart's illnesses and death. J R Soc Med. 1983 Sep;76(9):776-85.
5. Baroni CD. The pathobiography and death of Wolfgang Amadeus Mozart: from legend to reality. Hum Pathol. 1997 May;28(5):519-21.
6. Puech B, Puech PF, Dhellemmes P, Pellerin P, Lepoutre F, Tichy G. Did Mozart have a chronic extradural haematoma? Injury. 1989 Nov;20(6):327-30.
7. Drake ME Jr. Mozart's chronic subdural hematoma. Neurology. 1993 Nov;43(11):2400-3.
None declared
The BBC
have the following comment on Mozart's Death - Murder, Accident or Disease?
A couple of investigators have surprisingly broken from the norm of attributing Mozart's death to murder and strange ailments by announcing that Mozart died from complications arising from accidents. The first to push this story was French anthropologist Pierre-Francoise Puech, who claimed to have positively identified a skull at Salzburg's Mozarteum to be that of Mozart. Puech drew attention to a fracture in the skull, claiming that it had been sustained from one of Mozart's many falls in 1791, and that it had caused a chronic bruising that had eventually put Mozart in a coma and killed him. The skull was supposed to have been rescued by a gravedigger named Joseph Rothmayer during the reorganisation of the composer's grave, who later gave it to the Salzburg Mozarteum.
Three years later, the American physician Niles E. Drake concurred with Puech's theory in an article that was published in the journal BioScience. This theory would indeed help explain why Mozart was depressed and dizzy not long before his death. The obvious problem with this theory is that there is still no consensus as to whether the skull actually belonged to Mozart. Rothmayer had allegedly wrapped wire around the neck of Mozart's corpse before burying it, and had retrieved the skull ten years later when it was exhumed. Research had concluded that the skull belonged to a 20-40 year old South German male who suffered a developmental abnormality called premature synopsis of the metopic suture (PSMS). This abnormality is characterised by the bone of the forehead developing in two halves, and the failure of the metopic suture to close after birth, resulting in a broad midface and a small, abnormally-shaped skull.
As Mozart's portraits depicted a straight, vertical forehead, bulbous nose, prominent cheekbones and upper lip, and prominent brow arches, it was supposed that the skull did indeed belong to him. Further research involving the superimposition of a photograph of the cranium of the skull on portraits of Mozart painted between 1778 and 1788 indicated conformity with all side proportions of the head. However, Nova Scotian neurologist Professor TJ Murray, who founded the Dalhousie Society for the History of Medicine, denied that the skull was that of Mozart as seen in portraits. Walter Brauneis, archivist of the Office for the Preservation of Historical Monuments in Austria, undertook to carry out his own research by locating official medical records concerning Mozart's death. Surprisingly he found a doctor's description of the body, which noted that Mozart (the dentist's worst nightmare!) had only seven teeth remaining in his mouth (the rest having rotted or fallen out)!
When the Mozarteum skull was re-examined, it was found to have four more teeth than had been recorded by the doctor. Puech supporters countered that the doctor probably counted only the healthy teeth. Puech Pierre Francois (email@example.com)add: The only way to be sure just whose skull was to perform DNA analysis on the skull; unfortunately, all of Mozart's children died childless, and his parents' grave has been disturbed and was not able to give an answer. DNA analysis of the "Mozart" skull confirmed that it was masculine, or it was on the simple assetion that the skull dimention where feminine that the Mozarteum rejected the forensic anthropological studies that gives a positive identification. There is no more objections to the identification of the skull. PS for the supposed wrong number of teeth, a simple photo give evidence that the 4 incicives crowns are broken off and there presence can or can't be counted.
I would like to point out that having treated or examined over 200 cases of Rheumatic Heart Disease with collegues at the American University of Beirut Medical Center, it is difficult to conceive that beta hemolytic Streptococci infection causing post stretococcal glomerulonephritis would from an epidemiologic point of view affect only Mozart, without other members of the household, his spouse Constanza,or his children, as was shown by our studies. Beta Hemlytic Streptococcus infects more than one member of a household. The majority of our patients studied after the fact, developed Acute Rheumatic fever and later Rheumatic Heart Disease as a consequence of acute Beta Hemolytic, Streptococcal Tonsillitis infection. Minority of patients came down with Acute Glonerulonephritis. Although certainly Mozart's fatal symptoms do suggest genralized edema secondary to renal failure and its complications as noted by Drs Richard H.C.Zegers and colleagues (1).
1. Richard H.C. Zegers, Andreas Weigl, and Andrew Steptoe The Death of Wolfgang Amadeus Mozart: An Epidemiologic Perspective Ann Intern Med 2009; 151: 274-278
Precisions: The mandible was lost and the skull has 15 teeth. If Mozart's maxillary had 11 teeth, as counted after the time of death (per a medical certificate discovered by Walter Brauneis), it is because the crowns of the four upper incisors are broken off. Two children of Mozart survived and 4 died in infancy. The younger son surviving, Franz X. Wolfgang, died on 29 July 1844 in Karlsbad where he was buried. His tomb, the only one known for the children, was moved ten years later to a different cemetery of the town. It has been reported that the body is now missing (1,2).
1. Puech PF, Puech B, Tichy G. Identification of the cranium of W.A. Mozart. Forensic Sci Int. 1989 April-May;41(1-2):101-102.
2. Dr. Walther Parson, 2006. Army helps DNA scientists unravel Mozart mystery. Accessed at http://www.scienceblog.com/cms/army_helps_dna_scientists_unravel_mozart_mystery_9713
In 1988 H.C. Robbins Landon in Mozart's Last Year:1791, discussed all the evidence and subsequent discussions by scholars about Mozart's fatal illness which included pretty much the same conclusions as Zegers et al. Volkmar Braunbehrens in 1986, Mozart in Vienna, (translation 1989), covered the same ground extensively. I've never seen anyone consider one of the acute leukemias as a likely cause for his illness. We all know another half century would pass before this was recognized as a pathological entity, but it seems a possible, even likely, candidate. Comment would be welcomed.
To the Editor:
The work undertaken to discover the reason Mozart died so young was truly prodigious, but I wish to draw your attention to an article entitled "New Thouts on Mozart's Terminal Illness" in the Dalhousie Review in 1993. I came to the same conclusion, that Mozart's anasarca was a result of renal failure, but there was no evidence of acute illness or fever preceding his demise. A survey of causes of death at the time could not have produced evidence that led to Mozart, but renal failure is a sure possibility, as the earlier paper also claimed.
1. Ehrlich, George E.: New Thoughts on Mozart's Terminal Illness, in: Dalhousie Review 73 (1993), No. 2, Halifax, Summer 1993, S. 241-245
The proposal that Mozart died from acute post-streptococcal glomerulonephritis (APSG) (1) following streptococcal pharyngitis fails to explain several features of his disease. It does not account for the two components, pyrexia and skin rash, inherent in the diagnosis of "miliary fever" that Mozart's highly respected physician, Thomas Closset, listed as the cause of death(2). Fever is rare in adult APSG (0-10%) (3-5), and skin rash is not a feature of the disease, except for residual pyoderma when the preceding streptococcal infection is cutaneous, not pharyngeal. The authors assert that the omission of a skin rash in the family's accounts of Mozart's illness suggests that it was a late manifestation noted only by those attending his death. Yet, Sophie Haibel, his sister- in-law, saw him on his last day of life and mentioned no dermatologic problems in her account (2). More plausible explanations about the absence of a rash in the family's recollections are: 1) they had forgotten about this finding in the three decades that had elapsed between Mozart's death and their testimony; 2) the eruption was subtle or transient and seen only by his doctors; or 3) not realizing its diagnostic import, they simply omitted mentioning what seemed inconsequential in an illness dominated by massive edema and pain.
The authors' explanation for that pain is unsatisfactory. Attempting to support their diagnosis of APSG, the authors assert, without any documentary justification, that Mozart had back pain. The accounts indicate a different type and location of the discomfort. Dr. Guldener, who examined the body after death and was knowledgeable about Mozart's clinical course said that he had a "rheumatic and inflammatory fever." Sophie Haibel stated that his "arms and limbs were much inflamed and swollen (2)." The terms "rheumatic" and "inflamed" suggest musculoskeletal pain accompanied by such features as erythema, tenderness, and warmth. APSG cannot explain rheumatic inflammation of the arms and legs.
Another problem with APSG is that Dr. Guldener asserted that the disease causing Mozart's death had a considerable mortality rate (2). APSG is nearly always self-limited, and, even if untreated, is rarely lethal. The rate of death or uremia requiring dialysis in epidemics exclusively or primarily affecting adults is <10%. (3,4) The only disease that satisfactorily explains all the features Mozart's illness is trichinosis (2). Once clinicians recognized this infection in the 19th Century, they recorded mortality rates as high as 19% and 30% in epidemics.
1.Zegers RHC, Weigl A, Steptoe A: The death of Wolfgang Amadeus Mozart: an epidemiologic perspective. Ann Intern Med 2009;151:274-8.
2. Hirschmann JV. What killed Mozart? Arch Intern Med 2001;161:1381-9.
3. Stetson CA, Rammelkamp CH, Krause RM, Kohen RJ, Perry WD: Epidemic acute nephritis: studies on etiology, natural history and prevention. Medicine (Baltimore). 1955 Dec;34:431-50.
4. Balter S, Benin A, Pinto SWL, et al: Epidemic nephritis in Nova Serrana, Brazil. Lancet 2000;355:1776-80.
5. Lien JWK, Mathew TH, Meadows R: Acute poststreptococcal glomerulonephritis in adults: a long term study. Q J Med. 1979 Jan;48(189):99-111.
I appreciate the comments of Dr Hirschmann, but have to notice that he brings up some incorrect issues that are presented as accomplished facts. First he states that the official diagnosis of Mozart's death was listed by Mozart's physician Closset and uses his own article as a reference (1). Unfortunately there is no documentary justification for this assumption. In fact, the diagnosis of "miliary fever" might has not been given by a physician at all, as Maximilian Stoll "" of whom Closset was a faithful scholar "" already had demonstrated that fever and a rash were not a disease entity, but represented symptoms (2). We simply do not know who introduced the official diagnosis and hence cannot estimate the significance of this piece of information.
The same applies to the localisation of the pain. Naturally, being present day physicians, we think of musculoskeletal pain when the term "rheumatic" and "inflamed" are involved, but Sophie Haibel could have thought of something completely different, like Mozart for example did when he described a "rheumatic pain of the head" in one of his letters (3). Also for physicians, the term "rheumatic" was not specified in those days, since this term can be found in many diseases like "rheumatic pain of the head", "rheuma of the breast", "rheumatic biliary fever", and "rheumatic stroke" (2). Guldener's diagnosis is an unspecified one, just like miliary fever. Dr Hirschmann states even himself that "inflammation" and "rheumatism" are somewhat non-specific terms (4).
What should be considered in reading our article on Mozart's death is that we studied the causes of death and this is exactly what our finding of a minor epidemic of edema represents: the number of people that died from edema, might as a consequence of an acute poststreptococcal glomerulonephritis (APSG). This can imply that many more suffered from APSG, but only the people that died as result from this cause were registered and hence included in our study. As a consequence, the self- limiting cases were not reported; and percentages of fever, death, or uremia requiring dialysis in epidemics do not make sense in this discussion as we know nothing about the total number of people affected by APSG around Mozart's time of death. Furthermore, since we are talking about Europe in the 18th century, it would seem more reasonable to compare this case to the present day situation in developing countries rather than compare it to the epidemiology and "˜natural' course of APSG nowadays in Europe and the United States. Studies from developing countries question whether the outcome is always benign; and APSG remains a cause of morbidity and mortality in developing countries and among impoverished populations (5).
I feel our hypothesis provides a fine epidemiological reconstruction of what might could have happened to this great composer.
1. Hirschmann JV. What killed Mozart? Arch Intern Med. 2001; 161: 1381-9.
2. Bär C. Mozart. Krankheit "" Tod "" Begräbnis. Schriftenreihe der Internationalen Stiftung Mozarteum Salzburg. Kassel: Bärenreiter; 1972.
3. Bauer WA, Deutsch OE. Mozart. Briefe und Aufzeichnungen. Gesamtausgabe. Band V: 1787-1857. Kassel: Bärenreiter; 1971.
4. Hirschmann JV. In reply. Trichinellosis is unlikely to be responsible for Mozart's death. Arch Intern Med. 2002; 162: 946-7.
5. Ahn SY, Ingulli E. Acute poststreptococcal glomerulonephritis: an update. Curr Opin Pediatr. 2008; 20: 157-62.
TO THE EDITOR: Zegers and colleagues are to be congratulated for adding an important piece to the puzzle concerning the etiology of Mozart's final illness (1). Their contribution is to have corroborated a statement made by Dr. Eduard Vincent Guldener von Lobe at the time of the composer's death that: "A great number of the inhabitants of Vienna were at this time laboring under the same complaint, and the number of cases which terminated fatally, like that of Mozart's, was considerable." (2) In effect, their findings confirm that Mozart died of an epidemic disorder. Unfortunately, they do not identify the specific disorder responsible for the epidemic . Nevertheless, given the clinical characteristics of Mozart's illness, an acute glomerulonephritis is, by far, the most likely diagnosis for the reasons enumerated by Zegers et al in their paper.
In considering possible etiologies of both Mozart's death and the epidemic of which it was a part, Zegers et al conclude that post- streptococcal glomerulonephritis is the best diagnosis. Although not specifically stated, the variety of post-streptococcal glomerulonephritis they appear to favor is the classical one caused by Lancefield group A, Streptococcus pyogenes . It produces generalized edema as one of its most striking and consistent features . Fever, which Mozart also seems to have had, is less common, developing only in approximately half of the cases. Muscle and joint pains, which Mozart might or might not have had, are not prominent in cases of classical post-streptococcal glomerulonephritis. The disorder occasionally occurs in epidemics, but is a disease primarily of children between the ages of 2 and 10 years. Fewer than 10 percent of cases are older than 30 years of age. Moreover, classical post- streptococcal glomerulonephritis is typically an acute, but reversible disorder from which patients normally recover fully within 2 to 4 weeks (3). Thus, classical post-streptococcal glomerulonephritis leaves much to be desired as the cause of the epidemic that took Mozart's life. There is, however, another form of post-streptococcal glomerulonephritis - - one that affects adults, sometimes with fatal consequences "" that is a better fit. This variety of acute glomerulonephritis is caused by streptococci belonging to a different Lancefield group -- group C. The particular species of streptococcus responsible for such epidemics is Streptococcus equi. It primarily attacks horses, causing strangles, a highly contagious infection characterized by fever, lymphadenitis and abscesses of the head and neck (4). It also infects cows. In the rare instances in which human outbreaks occur, generally as a result of the consumption of milk or milk products contaminated with S. equi, fever, headache and muscle aches are initial manifestations of the illness, followed in a week or so, by bloody urine, kidney failure and anasarca. Rash is uncommon. In outbreaks of the disorder, over ninety percent of the victims have been adults. One in fifty has died. One in twenty patients has required renal dialysis and, presumably, would have died in Mozart's time because of the lack of such treatment (4). Thus, epidemic, acute post-streptococcal glomerulonephritis caused by S.equi "" contaminated milk or cheese is, in many respects, the best explanation for Mozart's terminal illness (5). It would explain Mozart's edema, his fever, his pain and also the epidemic nature of his illness, so cleverly documented in the recent investigation by Zegers and colleagues.
1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: An epidemiologic Perspective. Ann Intern Med 2009, 151: 274-8.
2. Robbins Landon HC. 1791: Mozart's Last Year. New York: Thames and Hudson, 1999; p. 175.
3. Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med 1998; 339: 888-99.
4. Balter S, Bennin A, Pinto SWL, et al. Epidemic nephritis in Nova Serrana, Brazil. Lancet 2000; 355: 1776-80.
5. Mackowiak PA. Post Mortem. Solving History's Great Medical Mysteries. Philadelphia: ACP Press, 2007:p. 173-202.
To the Editor: The article by Zegers and colleagues speculating on the cause of death of Wolfang Amadeus Mozart on 5 December, 1791 is of considerable historical interest (1). After reviewing the death records in the 2 months proximate to Mozart's death compared to those from the preceding and following years together with eyewitness accounts of his symptoms, the authors concluded he died of an acute nephritic syndrome due to post-streptococcal glomerulonephritis. It appears there was an epidemic of mortality among younger men during the period surrounding Mozart's death compared with the years before and after his death. This suggested that an infectious agent may have been transmitted in December 1791. Also, Mozart's most prominent symptom prior to his death was edema.
In light of the credible epidemiologic and clinical evidence that his death may have been caused by acute post-streptococcal glomerulonephritis (AGN), it is curious that the authors dismissed the skin lesions, which were described as a "white eruption." These skin lesions could have been impetigo caused by infection with a nephritogenic strain of Group A streptococcus. It would be of interest to know how many of the other excess deaths in the young men during November 1791-January, 1792 were listed as "Hitziges Frieselfieber" and also were accompanied by a white eruption? Post-streptococcal acute glomerulonephritis (AGN) can result from infections of either the skin or throat with nephritigenic Group A streptococci (2, 3). However, epidemics of AGN following skin infections with Group A streptococci are generally much more common in summer than in winter in countries with temperate climates (4-6). Nevertheless, the post -hoc diagnosis of glomerulonephritis from Group A streptococcal infection postulated by the authors certainly seems reasonable.
1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfang Amadeus Mozart: An epidemiologic perspective. Ann Intern Med 2009; 151:224-228.
2. Stollerman GH. Rheumatogenic and nephritogenic streptococci. Circulation 1971; 43:915-921
3. Dillon HC Jr. Post-streptococcal glomerulonephritis following pyoderma. Rev Infect Dis 1979; 1: 935-945.
4. Bisno AL, Pearce IA, Well HP et al. Contrasting epidemiology of acute rheumatic fever and acute glomerulonephritis. Nature of the antecedent streptococcal infection. N Engl J Med 1970; 283:561-565.
5. Nelson KE, Bisno AI, Waytz P, Brunt J, Moses VK, Haque R. Epidemiology and natural history of streptococcal pyoderma: an endemic disease of the rural southern United States. Am J Epidemiol 1976; 103:270 -283.
6. Meekin GE, Martin DR. Autumn- the season for post-streptococcal acute glomerulonephritis in New Zealand. NZ Med J 1984; 97:226-9.
Dear Editor, In their article, Zegers et al. (1) examine the circumstances of Mozart's death from an epidemiological perspective and come to the interesting conclusion that the great composer died of post-streptococcal glomerulonephritis (PSGN).
Even though PSGN can appear in epidemics, the sporadic form is more frequent. PSGN is usually a childhood disease with an incidence peak between the ages of 2 and 14 years. Outbreaks might affect family members in a significantly greater percentage compared with the general population. Subclinical disease is four to five times as common as clinically evident nephritis. Overall, the prognosis is good, with permanent renal failure being very uncommon (1-3%).
To our view, PSGN seems less likely in the case of the Mozart's death, taking into account the following facts: (i) an acute disease led him to be confined in bed for 2 weeks until the very end, whereas in PSGN there is an asymptomatic interval of 10 days between acute pharyngitis and the manifestations of nephritis (2), (ii) there was no testimony of hematuria or tea-colored urine, the worrisome tell-tale symptom of PSGN that would probably have been documented by Mozart's attending physician, and (iii) the illness had an unrelenting clinical course with a fatal outcome.
We agree that an acute illness with the cardinal features of fever and generalized edema clearly raises suspicion of acute glomerulonephritis. However, we think a more plausible alternative explanation needs to be considered: a Hantavirus-associated infection caused Mozart's illness.
The group of Hanta viruses is endemic in Europe and can lead to epidemic outbreaks. The human hemorrhagic fever with renal syndrome epidemiology follows the local rodent cycle (which is the host), meaning that human cases occur in the same rhythm as the rodent cycles. Austria, the home country of Mozart, experiences the co-circulation of two or three hantavirus serotypes, Puumala (PUUV), Dobrava (DOBV) and Saaremaa (SAAV) (3). The clinical presentation is characterized by the acute onset of fever accompanied by backache, abdominal pain, chills, myalgia, malaise, and bradycardia. Photophobia, pharynx enanthema, and a diffuse reddening of the face are also observed. The clinical manifestation can be differentiated into five chronological phases: the febrile phase lasting 3 -7 days, ending up with the appearance of severe proteinuria, the hypotonic phase with the appearance of hemorrhages and a possible petechial rash, associated with shock in most severe cases, the oliguric phase associated with acute renal failure and often combined with hypertension due to simultaneous hypervolemia, the diuretic phase, indicating a good case prognosis and the convalescence phase with complete recovery of renal function in most cases.
Renal involvement is characterized by acute renal failure as a result of interstitial hemorrhage and interstitial infiltrates (4). Severe cases show a case fatality rate which may exceed 10% (5).
Notwithstanding the gaps in the description of Mozart's illness, we conclude that a Hantavirus infection can explain most of the already discussed symptoms and signs of his illness, including the contemporary minor epidemic in deaths of young adults highlighted by Zegers et al.
1. Zegers RH, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: an epidemiologic perspective. Ann Intern Med. 2009;151(4):274-8. [PMID: 19687494]
2. Tejani A, Ingulli E. Poststreptococcal glomerulonephritis. Current clinical and pathologic concepts. Nephron. 1990;55(1):1-5. PMID: [2191230]
3. Heyman P, Vaheri A; ENIVD Members. Situation of hantavirus infections and haemorrhagic fever with renal syndrome in European countries as of December 2006.Euro Surveill. 2008;13(28). pii: 18925. [PMID: 18761927]
4. Muranyi W, Bahr U, Zeier M, van der Woude FJ. Hantavirus infection. J Am Soc Nephrol 2005;16:3669""3679. [PMID: 16267154]
5. Faulde M, Sobe D, Kimmig P, Scharninghausen J. Renal failure and hantavirus infection in Europe. Nephrol Dial Transplant. 2000;15(6):751-3. [PMID: 10831620]
Zegers and others present interesting information about the death of Mozart. Could Thrombotic thrombocytopenic purpura (TTP) be the cause of his death? Out of the five diagnostic features of TTP (pentad), Mozart had at least 3; fluctuating neurologic symptoms, fever and possible renal failure. The other two criteria for the diagnosis of TTP are thrombocytopenia and microangiopathic hemolytic anemia, discernable only by a laboratory examination. The etiology of TTP could be idiopathic or secondary to infections such as E. coli. The fact that there were several deaths associated with edema also supports this speculation. Infections such as E. coli might have been common in this pre-antibiotic era, leading to several clusters of cases. An unknown viral illness capable of triggering TTP is also a possibility as suggested by Zegers' data.
Zegers and colleagues (1) recently presented an "epidemiologic perspective" on the death of Wolfgang Amadeus Mozart. This paper calls for some comments. 1. The authors' basic assumption that "according to the eywitness accounts, the hallmark of Mozart's final disease was severe edema" is unwarranted and wide off the mark (2). What did the eywitnesses actually state? None of them mentions the prsence of sever edema (3). Sophie Haibel, Mozart's sister in law, who attended his last illness, merely reported that "his arms and limbs were much inflamed and swollen (4)." Moreover, neither "severe edema" nor even "edema" were mentioned by Guldener von Lobes, even though he saw Mozart's body after his death and wrote that "he made a careful inspection of the cadaver and saw nothing unusual (5)." To be sure, Sophie Haibel attricuted Mozart's "almost complete inability to move" to his swelling (6). But Benedikt Schack (1758 -1826), a tenor and close friend of Mozart, who attended his last illness said that his "weakness was such, that he was obliged to be drawn forward whenever he required to sit up in bed (4)." This suggests that weakness besides swelling of the extremities may have explained Mozart's inability to move.
Further more, according to the four death notifications (7), Mozart died of Hitziges Frieselfieber (heated miliary fever), a diagnosis made by Dr. Closset. Incidentally, there were two brothers, Thomas and Nikolaus Closset: both were physicians and the original sources never mention Dr. Closset's first name, so that we do not know which was which. Be that as it may, Thomas Closset in his 1783 treatise on Faulfieber (putrid fevers) (8) described a condition which helps us to figure out a picture of what Mozart's illness was like. Edema was not part of its manifestations. Actually Hitziges Frieselfieber implied a diagnosis of hitziges Fieber (heated fever) and an additional sign: the Friesel (rash). Death assigned to miliary fever (Friesel, hitziges and galliges Fieber) corresponded to 14% of all causes of death, and, between 21 and 40 years of age, it referred to every third death, i. e. "a common clinical condition comparable to influenza or pnuemonia (9,10)." Guldener von Lobes in two written documents went beyond this merely descriptive label, and proposed a diagnosis of Rheumatische Entzungsfieber (Inflammatory rheumatic fever). On this score, Mathias Edler von Sallaba (1764-1797), who visited Mozart during his last illness and wrote an Historia Morborum published in 1791, described what he called rheuma inflammatorium, a blanket diagnosis that conflated musculoarticular conditions with a mixed bag of disorders which attacked the brain, lung (pluerisy) and instestine (enteritis) (11). There was no necessary connotation implying arthritis. Lord byron, Emperor Leopold II and King Gustave XII of Sweden, supposedly died from rheumatic inflammatory fever. But again, neither was edema nor severe edema listed in the manifestatations of this condition.
2. In light of this, what is the epidemiological evidence? Mortality tables set up by Ignaz von Lucca (1746-1799) have been reprinted in fac simile for the International Mozarteum Foundation by Car Bar (4). According to the death statistics, there were 858 adult deathls in Viennna in November and 874 in December 1791, i.e. a death rate which was 17% higher than the death rate observed in the two previous months. There was a corresponding 14% increase during the same period of the previous year in 1790. If one makes a seasonal adjustment, there is not much of an epidemic. But what were then the death rates for specific diseases? These rates are available for Vienna in 1791. Car Bar writes that if one looks at the registers of death in the months of November and December 1791, Mozart was the only case of Hitziges Frieselfieber. In a span of six months, there was only one other recorded instance of this same cause of death besides that of Mozart: two cases in six months comparred with six from gangrene in one month alone cannot be described as an epidemic! According to von Lucca, during the months of Novemeber nad December 1791, the death certificates showed 636 cases of stroke (Schlag), 440 of putrid fever (Faulfieber), 149 of smallpox (Pocken) and 64 miscellaneious diseases (zufallig). Yet one has to assume that the death certificates were not entered in a very consistent way: thus, the deaths attributable to the alleged epidemic which killed Mozart must have been spread over different diagnostic categories instead of being assigned to a single disease entity. In view of the available clinical evidence, Carl Bar identified a list of death certificates among the months of Nov and Dec 1791, which would be compatible with the diagnosis attributed to Mozart, inasmuch as the put forward different clinical aspects of a similar condition. Again, not much for an epidemic of a sever emematous condition!
3. Then beyond this, Zegers and colleagues underplay the importance of venesections. The brothers Closset, both physicians, were pupils of professort Stoll, the medical head of Vienna's general hospital. It is now generally admitted following Car Bar, that Mozart may have bled two or three times during his last two weeks, thereby losing roughly two liters of blood. Moreover, the documents pertaining to Mozart's estate include a document listing Mozart's unpaid bills. This includes a bill amounting to 9 silver florins for bloodlettings made a home, though the fee could be larger when the practitiioner was called at night or on emergency. In addition the outstanding debt owed to the pharmacist amounted to 139 florins and 30 Kronen. This could have included various prescriptions made by Closset such as sudorifics, saline beverages and emetics in addition to time-honored procedures such as enemas.
4. What's more, Zegers and colleagues rule out the hypothesis that Mozart could have been poisoned. However, during the last months of his life and his final illness, Mozart was treated by Closset and Sallaba: potential iatrogenic poisoning (12)included mercury chloride, used for its diuretic properties, calomel (mercurous choloride) used as a purgative, arsenic, as well as anitmony salts used for the treatment of febrile conditions. Finally, during the summer and fall of 1791, when Constanze spent much time taking a cure in Baden, Mozart stayed in Vinenna and often put up at an inn: wine was then quite often adulterated with various forms of lead compounds such as lead oxide, ceruse, or metallic lead (13). Even though such iatrogenic or accidental poisonings cannot by themselves explain Mozart's death, they were probably contributing causes.
5. Besides sever edema, Zegers and Colleages mention several other undocumented signs and symptoms such as pain of unknown localisation and back pain. Nether was pain, nor backache mentioned by the eyewitnesses such as Sophie Haibel or Constance Mozart; neither were they brought up by Nissen, in his biography of Mozart. To be sure, Rochlitz claims that Mozart last illness was painful but he was not an eyewitness and his writings are considered to be a very unreliable source and are now excluded from use as authentic sources.
To sum it up then, Mozart died from an acute, feverish, unspecified, infectious condition, compounded by heavily aggressive medical treatment. It was not characterised by severe edema, but rather by a mere sweling of the extremities, severe weakness, vomiting, fever, hyperacousia, dysgeusia, stench and a skin rash evolving into a brief coma preceding death. One hundred eighteen causes of death have been attributed to Mozart up to this publication by Zegers and colleagues, and it does not seem that this paper is shoring up any additional line of diagnosis.
1. Zegers, RHC, Weigh, A., Steptoe, A. The death of Wolfgang Amadeus Mozart; an epiedmioligic perspective. Ann Intern Med 2009; 151: 274-278.
2. Karhausen, L. Mozart's terminal illness: unravelling the clinical evidence. J. Med Biography. 2001; 9:34-48.
3. Karl Thomas Mozart, Wolfgang's son, wrote in 1824 that his father's body showed "a generalised edema (una gonfiezza generale) a few days before his death" but cannot rely on this statement since he was only seven years of age when his father died!
4. Medici, N & Hughes, R. A Mozart Pilgrimage, London, 1951, p. 214-215.
5. Deutsch, OE. Mozart: die Dokumente seines Leben. Barenreiter Kassel. 1961, p. 450.
6. B. Schak in Holmes, E. The Llife of Mozart. 1845, London. Chapman and Hill, p. 347.
7. Carpani, G. Lettera del sig. Carpani in defesa del M. Salieri calumniato dell' avvelanamento del M. Mozzard. Bibliotheca italiana s sia giornale di letteratura, science ed arti. 1825; 35: 262-276.
8. This includes the death certificate, the notification in the register of deaths record office of Sankt Stephan Cathedral, the notification of Sankt Stephan Parish book of accounts, and the death certificate signed by Dr. Franz Bierner, physician in charge of infectious diseases.
9. Kisskalt, K. Die Sterblichkeit im 18. Jahrhundert. Zeitschrift fur Hygiene und Infektionskrankheiten. 1921; 93: 438-511.
10. Peller, S. Zum Kentnnis des stadlichen Mortalitat im 18. Jarhrhundert mit besonderer Berkucksichtigung des Sauglings -und Tuberkulosesterblichkeit (Wien zur Zeit des ersten Volkszahlung) Zeitschrift fut Hygiene und Infektionskrankheiten. 1920; 90: 227-262.
11. Fuhrmann, R. Frieselfiber und aderlass. Mitteilungen der Internationale Stifttung Mozarteum. 1989; 37: 83-136.
Zegers, Wiegl, and Steptoe discovered a significant increase in the number of young soldiers dying in Vienna from edema and related illnesses during the months surrounding Mozart's dealth (1). This increase occurred in the midst of a Russian-Turkish war, in which the Austrians had joined the Russians. The Austrian armies occupied Moldavia and Walachia, where the Austrian emperor contracted a deadly illness amidst his troops. His successor ended the war with the Peac of Sistowa in August 1791, whereupon the Austrian army withdrew. The soldiers in Vienna presumably came from those battlefields. Their renal disease seems identical with the 'trench nephritis' or Feldnephritis' of "Flanders Fields.'
In World War II thousands of patients on the German Eastern front suffered from Feldnephritis, which could clearly be differentiated from postsreptococcal glomerulonephritis (2). There was no preceding infectin, a causative agent was never found, and after 1947 the illness was gone. From epidemic transmissions an incubation period of 3-4 weeks was calculated. Acute massive edema was the first and dominant symptom, in contrast with little or no urine abnormalities. A diet of hunger and thirst reduced the acute mortality to less than 1%. The outcome was better than that of poststreptococcal glomerulonephritis: 82% as against 30% cured with little or no rest symptoms (2). The kidneys showed a diffuse exsudative and proliferative glomerulonephritis (3,4), as in poststreptococcal glomerulonephritis, but this is an aspecific reaction on immune complexes.
Zegers, Weigl and Steptoe seem to have detected the first documented outbreak of Feldnephritis. It is sad to learn that Mozart may have died of this epidemic, whereas a simple diet could have saved his life.
1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: An edpidemiologic perspective. Ann Intern Med. 2009; 151: 274-278, W 96-97.
2. Sarre H. Nierenkrankheiten. 2er Auflage. Stuttgart: Thieme; 1959: 291-323.
3. Allen A. The Kidney. New York: Grune and Stratton; 1951: 116-118.
4. Staemler M. Die Kriegs -oder Feldnephritis. In: Kaufmann E, Staemler M, eds. Lehrbuch der speziellen pathologischen Anatomie. II. Bd, 1. Tiel. Berlin: Walter de Gruyter & Co; 1957: 623-624.
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YOUNGSTOWN -The Potters put forth a strong showing.
The East Liverpool boys' and girls' swim teams competed at the Salem Small School Invitational Saturday at Youngstown State University.
Scoring was not made available for the meet.
Article Photos
East Liverpool's Kelsey Diddle swims during the Salem Small School Invitational Saturday at Youngstown State University. (Photo courtesy pottersportsonline.com)
"The kids swam well," East Liverpool head coach Tim?Diddle said. "We had been off since Dec. 18. Our last meet was down at Edison.
"The kids swam well for being off that long without any competition."
Matt Campbell was the lone Potter to finish first in a race. Campbell finished first in the 50 free style with a time of 24.41.
"He was our only winner on either side," Diddle said. "We had swimmers set multiple new best times, but they weren't school records.
"Everything is going good so far this season. I hope it keeps going well."
There were 21 boys' teams and 22 girls' teams at the meet.
"The girls are right where I thought they would be," Diddle said. "The boys are ahead of where I?thought they would be."
East Liverpool's next meet is Monday in a tri-meet with Barnesville at Wheeling Park.
"The kids competed well today," Diddle said. "Youngstown State has a very-nice pool up there by the way."


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Women's Tennis Defeats Toledo in MAC Tournament
DEKALB, Ill. - The No. 9 Ball State University women's tennis team captured a 4-3 victory over No. 8 Toledo, Thursday afternoon at the Mid-American Conference Tournament.
The Cardinals fell early on in doubles action on court one after Courtney Wild and Ashlyn Rang fell 8-1 to Kelsey Anonsen and Lexy Pitt. Ball State's No. 2 doubles tandem of Paola Rodriguez and Sarah Hebble found themselves down 6-1 but fought back winning five straight games to tie the match 6-6. Toledo would then go up 7-7 but then scored two straight games to win the doubles point for the Cardinals and the match 9-7.
Ball State headed into singles play up 2-0 after Toledo had to default its match at the No. 6 spot. The Rockets then took the 3-2 edge over the Cardinals after posting victories on courts two, three and five. Hebble came back in the third set at No. 4 singles after being down 6-5 and won in the tie breaker 7-6 (2) over Pitt. Wild then beat Anonsen in straight sets on court one, 7-5, 7-5, given Ball State the victory.
The No. 9 Ball State women's tennis team will face No. 1 Miami, Friday at host Northern Illinois with the match beginning at 11 a.m. (EST).
2012 Mid‐American Conference Women's Tennis Championship
No. 9 Ball State (7‐15) def. No. 8 Toledo (9‐13), 4‐3
Thursday, April 26, 2012 | NIU West Tennis Courts | DeKalb, Ill.
1 ‐‐ Kelsey Anonsen/Lexy Pitt (UT) def. Courtney Wild/Ashlyn Rang (BSU), 8‐1
2 ‐‐ Paola Rodriguez/Sarah Hebble (BSU) def. Pia Rygh/Amanda Border (UT), 9‐7
3 ‐‐Dena Boulieris/Lauren Pickrel (BSU) def. UT by default
1 ‐‐ Courtney Wild (BSU) def. Kelsey Anonsen (UT), 7‐5, 7‐5
2 ‐‐Pia Rygh (UT) def. Kristel Sanders (BSU), 6‐1, 6‐4
3 ‐‐Chrissy Coffman (UT) def. Kylee Johnson (BSU), 6-3, 6-2
4 ‐‐ Sarah Hebble (BSU) def. Lexy Pitt (UT),4-6, 6-1, 7-6 (2)
5 ‐‐Amanda Border (UT) def. Ashlyn Rang BSU), 7‐5, 6‐0
6 ‐‐Lauren Pickrel (BSU) def. UT by default


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LORETTO - While the Bishop Guilfoyle Catholic girls' basketball team came out strong offensively against Portage in Friday's District 6 Class A championship game, its early defensive effort may have been more effective.
The Lady Marauders held the Lady Mustangs to just four first-quarter points, holding Portage's 6-foot-1 forward, and leading scorer, Olivia McCabe scoreless in the frame, as they won their seventh straight district championship game, 61-36, at St. Francis University's DeGol Arena.
"[Olivia] McCabe is a great player," Bishop Guilfoyle coach Mark Moschella said. "Our kids aren't very tall, but they're smart. They make up for their lack of size with knowing where to be on the court."
Article Photos
Mirror photo by Gary M.Baranec
The BG girls celebrate their seventh straight district title at St. Francis.
BG's Kayla Bates battles two Portage players for a rebound.
McCabe, averaging 16.9 points per game, was limited to just two first-half points, and six total.
Katie Nolan led Portage with 10 points, while Emily Chobany added nine.
"BG is a great defensive team," Portage coach Lance Hudak said. "They were making it a point to make [McCabe] work. They were defending her hard in first half."
It wasn't just McCabe that was defended well, either. Guilfoyle (24-2) held Portage (22-3) to just 17 first half points, leaving the Lady Mustangs staring at a 23-point deficit, 40-17, that proved too be too much.
In fact, the Lady Mustangs never had a lead in the game, and its first quarter deficit, 18-4, was as close as it would be the rest of the night.
"They made us pay in the first half," Hudak said. "If you give them just a step or two, they bury their shots."
And the Lady Marauders did.
It was the senior duo of Brittany Boslet and Halee Adams that led the way for Guilfoyle, as the two combined for 16 of the Lady Marauder's 18 first quarter points and 31 of Guilfoyle's 40 at the half.
Boslet finished with 19 points, including 14 in the first half to help build the Lady Marauders' lead.
"I just felt it tonight," Boslet said. "I wanted it so bad for our team. We've been together for so long and I do anything to help out."
Teammate Halee Adams had a game-high 23 points for Guilfoyle, and Boslet was fast to compliment her.
"[Adams] is a great leader," Boslet said. "She's so consistent and has never stopped fighting."
Although the Lady Marauders possess plenty of district and state playoff experience, Moschella credits his players' attitudes for their continued success.
"[The experience] could have helped us get off to a good start," Moschella said. "But I attribute more of [their success] to work ethic and discipline that these girls have on and off court."
Despite the loss, Portage will advance to the state playoffs, as the Lady Mustangs will play next Saturday against District 5's third seed.
"We're going to rest up this weekend," Hudak said. "It's a brand new season. That's the thing about having the great season we've had. We're being rewarded for it."
Bishop Guilfoyle will also open its state playoffs next Saturday, as it will face District 9's 4-seed at a District 6 site.
Adams echoed Boslet's feelings about the togetherness of the senior group.
"[The win] feels amazing because we've grown up together," Adams said. "We just want to go as far as we can."
PORTAGE (36): Chobany 3 0-2 9, Zatek 2 1-2 7, Ramus 1 0-0 2, O. McCabe 3 0-0 6, E. McCabe 1 0-0 2, Nolan 4 0-0 10, Wozniak 0 0-0 0, Jubina 0 0-0 0, Baker 0 0-0 0, Crum 0 0-0 0. Totals-14 1-4 36.
BISHOP GUILFOYLE (61): Boslet 8 0-0 19, Bates 3 2-2 8, H. Adams 8 6-9 23, Stessney 0 2-2 2, Ehredt 1 2-2 4, Miller 1 0-0 2, Craig 1 0-0 3, Luciano 0 0-0 0, E. Adams 0 0-0 0, Irvin 0 0-0 0, McGhee 0 0-0 0. Totals-22 12-15 61.
Portage 4 13 11 8-36
Bishop Guilfoyle 18 22 14 7-61
3-point goals: Portage 7 (Chobany 3, Zatek 2, Nolan 2); Bishop Guilfoyle 5 (Boslet 3, H. Adams 1, Craig 1).
Team records: Portage (22-3); Bishop Guilfoyle (24-2).
Officials: Tona Williams, Dan Gales, Jeff Fisher.


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Buck is a documentary about legendary horse trainer Dan "Buck" Brannaman, the modern day horse whisperer and inspiration for both the book and film alike. His horsemanship skills are legendary because he can train a horse to do just about anything in nearly ten minutes without touching the horse.
His natural abilities and skills on are display and he tours the country giving seminars on how train troubled horses. He helps cowboys with their colts and he helps professional equestrian riders perfect their dressage. You have to see it to believe it. The only disappointing part is that there is one horse in the film that could not be helped and the owner decided to euthanize it.
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Beta LT Hybrid Jacket
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By: MadiMack on October 1, 2012 - 3:51pm - Add new comment
It's officially October!
By: MadiMack on September 24, 2012 - 7:52pm - Add new comment
Over the past six months, I've uttered the phrase "You have been Spotted!" more times than I could possibly count.
The city of St. Augustine has an almost endless list of events throughout the year. I've had the pleasure of covering many of these exciting events for Spotted.
From the concerts, to the festivals, to the banquets — I've met incredible people and heard remarkable stories.


text:
LC-MS Gains Favor Due To the...
Expanding Use of NGS Has Largely...
Quadruple Helices Appear To Have Role...
Wall Street Decline Takes Its Toll...
Screening more than 300,000 small molecules, scientists have identified a way to 'turn off' the defect behind myotonic dystrophy type 1.
Writing in Nature Communications, investigators from The Scripps Research Institute (TSRI) in Jupiter, FL, identify small molecules that inhibit a critical RNA-protein complex in the disease.
Narrowing the hundreds of thousands of targets down into those that bound RNA or protein, or had unknown function, the team zeroed in on RNA-binding compounds, which in their human muscle tissue studies appeared to cause signs of disease remission.
"This is the first example I know of at all where someone can literally turn on and off a disease," TSRI's Matthew Disney, Ph.D., said in a statement. "This easy approach is an entirely new way to turn a genetic defect off or on."
Dr. Disney added that his team's finding lays a foundation for future investigations of myotonic dystrophy at the molecular level. The RNA-binding small molecules, he noted, are not ready for clinical use just yet.
"In complex diseases, there are always unanticipated mechanisms," he said. "Now that we can reverse the disease at will, we can study those aspects of it."
The team's next steps are to better learn how to control RNA splicing using small molecules, which could have implications for other diseases, from sickle-cell to cancer.
"Induction and reversal of myotonic dystrophy type 1 pre-mRNA splicing defects by small molecules" was published June 28 in Nature Communications.
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STEUBENVILLE - Two of the more storied wrestling programs in the Ohio Valley met on the mat Wednesday night.
In the end, the Beavers were unable to take down top-seeded Big Red as Steubenville came away with a 46-21 victory over Beaver Local in the Ohio Division II State Dual Meet semifinals at the Crimson Center.
Beaver Local advanced to the semifinals by defeating No. 2 seed Tri-Valley, 42-26, in the quarterfinals. Big Red defeated Cambridge, 54-21.
Article Photos
Beaver Local's Morley Marsden wrestles against Tri-Valley on Wednesday. (Photo by Aaron?Petchal)
"We wrestled tough," Beaver Local coach Jordan Williams said. "We wrestled well against Tri-Valley. We had some kids banged up, and they gutted it out and got some tough wins. I'm happy about that.
"We beat the No. 2 seed which is nice. It is nice beating these good teams.
"I was happy with our effort in both matches. We wrestled tough. We got after it. I'm proud of the kids. They pushed themselves. They are working hard. They are listening to the coaching the coaches are giving them. This will help us going into the rest of our season, and we have got some big things ahead for our team."
Big Red will now compete in the Region 12 final at 6 p.m. on Wednesday. The winner of that match will advance to the state quarterfinals.
"It is always good to wrestle duals against two pretty good teams from the OVAC in Cambridge and Beaver Local," Steubenville coach Mike Blackburn said. "We knew we had to do this to set up a regional final match against Claymont and a shot at the state dual meet championship.
"We just wrestled a tough dual against Claymont. Hopefully, this sets up an historic dual Wednesday."
The Beavers won nine of the 14 weight classes against the Scotties, but Beaver Local won just five against Big Red.
Despite winning five matches and losing by 25 points, the match between the two OVAC rivals was closer than the final resulted indicated.
Beaver Local led 18-17, but were done in by four big results in Big Red's favor. Not counting those four weight classes, Big Red was out in front 22-21.
Unfortunately for the Beavers, Big Red made the most of those four weight classes as the victors recorded 24 points to gain the upper hand in a big way.
"We knew going in there was going to be a couple of matches that had to go our way," Williams said. "We lost at 132 pounds in a battle. If we would have been able to win those matches, it would have made a big difference in the match.
"Our kids wrestled hard. They did a good job keeping off of their backs, and they were able to secure some team points for us."
Individually for the Beavers, Josh Henderson (113), Jason Keyes (120), Daniel Hasson (145/138), Josh Barber (152/145) and Cody Martsolf (285) all won two matches on the night.
Henderson pinned Tri-Valley's Robby Kaplisky in 1:11 before gaining a victory via forfeit against Big Red.
Keyes and Martsolf each won both of his matches by decision.
Keyes defeated Tri-Valley's Slade Tyson, 8-5, before defeating Big Red's Dakota Goff, 9-5.
Martsolf defeated the Scotties' Tyler Edwards-Frick by a score of 4-3, and he defeated Big Red's Ryan Wood, 3-2.
Hasson got a forfeit victory against the Scotties at 145 before defeating Big Red's Jacob McKitrick by a score of 6-5. Hasson trailed 3-0 in the third period before rallying for the win.
Barber defeated Tri-Valley's Matt Fellows by decision by a score of, 13-11, at 152, and then at 145 he earned a victory via forfeit against Big Red.
Also for Beaver Local, Ron Foster (132), Morley Marsden (160), Daniel Lattanzio (170) and Cody Green (220) all won one match on the night.
Foster, Marsden and Lattanzio all won via pinfall. Green won by decision.
Foster pinned Tri-Valley's William Kaufman in 34 seconds. Marsden pinned the Scotties' Ethan Atkinson in 1:00. Lattanzio pinned Tri-Valley's Dylan Marple in 1:46.
Green defeated the Scotties' Winston Spiker by a score of 8-3.
Big Red's Greg Moray defeated Green by injury default. Green was injured during the match, and he had to be attended to by the trainer. After a few tense minutes, Green was able to get up and walk off the mat. Moray was out in front 7-0 when the match was stopped.
With the split, Beaver Local ends it dual meet season with a record of 11-3.
Beaver Local will be competing at the EOWL Tournament Friday and Saturday at Boardman.


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I am supporting Mary Hetherington to continue her fine work with our Airport District Board. Her commitment to the needs of our community and airport has been demonstrated quite effectively during her current term. I appreciate the open space land acquisition and noise reduction in our neighborhood. Cast your vote for Mary Hetherington and her fellow board members to continue excellent representation and service in Truckee!
Lydia Sparksworthy


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Top Definition
Angry. You normally say it while you're rubbing your chin annoyingly. It makes the angry person angrier.
Oooh, chissy! You know my team has been pumped up ever since their shock loss to your team.
av Jamie Mackenzie 30. mai 2007
Trending Now
Can you define these popular missing words?
the opposite of a chode ie. a long and very thin penis
mo said zach has a chissy
av crandall marlman 1. august 2008
Opposite to the chode, a chissy is a penis that is elongated and abnormally skinny, as to the point where it would be equivalent to 4 twizzlers melted together in single-file.
"Patrick, pick your chissy up in front of the ladies."
av BabyDave 13. september 2006


text:
Finally! We've been waiting all summer long for Kenny Chesney's No Shoes Nation tour to make its way to New York – okay, New Jersey – and the time has arrived.
On Thursday, the singer took the "no shoes" part of his tour name seriously, shedding his footwear in Bangor, Maine, as pictured.
So, as PEOPLE gets ready to make our annual pilgrimage for what will undoubtedly be a day of great music, check out this playlist full of old and new Chesney hits that have been getting us in the mood.
While we couldn't pick one favorite song if we tried, when the cold beer is flowing and the mercury rising, "Summertime," "Beer In Mexico" and "Got A Little Crazy" hit the spot – just as listening to "Back Where I Come From," "There Goes My Life" and "Don't Blink" remind us to live in the moment.
We could go on and on about the songs that make us "Feel Like A Rock Star" and keep us "Young," but we'd be here all day.
So, for now, sit back, pop a cold one and enjoy these 29 Chesney tunes.
Kenny Chesney: The PEOPLE Playlist
Jill Trunnell


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dcdonnie4:The more costeffective army can win vs a more expensive (better unit) because they can just keep throwing them at the other player.
in supremacy the funnest civ i think is sioux too. rifle riders + wakina +tepee and warchief = Taunt 21 also its fun to get tanshuke in peoples town then back on stealth before they know what happened
for treaty i think aztecs, theyre stuff is just so cool. occasionly i have beat people with my start army of 100+ overpop with firepit on attack dance + natives from the map i'm actually on +30 zapotec+30 maya
kittychix:If you know your behaviour or language is going to result in a ban, and continue with the actions anyway...you are heading in a direction of less then temporary action.
funniest civ are: dutch... astec, with stealth jag and oto/india
knight_br:Optimal explanation .. very succinctly
LordStefanIII: Unkown_Genius:Leave it to Age.Comm to get a thread twenty miles off topic.:)Or turn into a flame war.
Unkown_Genius:Leave it to Age.Comm to get a thread twenty miles off topic.
sioux are fun ive never figured out their eco though aswell as aztech but i do love iro ima start using em in nr
pocahontas_:To sum up Sioux eco= extremely lame lol but you'll never run out of resources with them unless your using them wrong. Sioux can cut wood the fastest out of the civs though so that is really nice on a heavy wood map, other then that there a slow on resources
Actually sioux are excellent hunters. With an extra age 2 hunting card and the wise woman age up, they gather from herds very fast. The problem is that they have only one mill card and 0 plantation cards. That is one of the reasons i have always though sioux should have an infinite bison shipment. The wise woman going to age 5 gives you a 40% bonus to hunting. Im not sure, so correct me if im wrong, but i think they have the fastest or one of the fastest gathering speeds from hunts with all cards.
its also funny to see your musks making forts everywhere as russia 21
then you get to see enemy get heart attacks :P


text:
Windows, NT Object Manager
- Posted: Jun 03, 2005 at 3:24PM
- 7 comments
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I'd agree that the OM receives very little attention(wrongfully so). But the "LPC facility" receives barely any. Microsoft barely acknowledges its existence. Please have a video on that....I'd really like to hear something about it other than "It's there"
PS- really good job on the videos so far. they are really enjoyable.
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