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Team outlooks are listed in predicted order of finish. Lineups and rotations are projections.
1 l Tampa Bay
2013 l 92-71, second place Last year in playoffs l 2013
Tampa's young rotation — average age: 25 — may prove to be the AL's best. And it could get better when 26-year Jeremy Hellickson returns from the disabled list in June. But the lineup lacks power and Grant Balfour's health concerns may one day have the Rays searching for a closer.
LF D. DeJesus
2B B. Zobrist
DH M. Joyce
3B E. Longoria
1B J. Loney
RF W. Myers
CF D. Jennings
C R. Hanigan
SS Y. Escobar
LH D. Price
RH A. Cobb
LH M. Moore
RH C. Archer
RH J. Odorizzi
RH G. Balfour
2 l Baltimore
2013 l 85-77, third place (tie)
Last year in playoffs l 2012
Which Chris Davis will the Orioles get? The one who had 37 homers and 93 runs batted in by the All-Star break, or the one who batted .216 down the stretch? Having Nelson Cruz hitting behind him may help. The rotation is solid, but Tommy Hunter is likely to be a work in progress as closer.
RF N. Markakis
LF D. Lough
CF A. Jones
1B C. Davis
DH N. Cruz
SS J.J. Hardy
C M. Wieters
3B R. Flaherty
2B J. Schoop
RH C. Tillman
RH U. Jimenez
LH W. Chen
RH M. Gonzalez
RH B. Norris
RH T. Hunter
3 l Boston
2013 l 97-65, first place
Last year in playoffs l 2013
David Ortiz carried Boston to a title last fall, but through 35 spring at-bats he was hitting .057. That may be an anomaly, lack of interest in spring training, or age — he's 38. But it won't matter if Jon Lester, Clay Buchholz and Jake Peavy pitch as well as they did in last season's second half, when they went 18-6 with a 3.13 ERA, including the postseason.
CF G. Sizemore
RF S. Victorino
2B D. Pedroia
DH D. Ortiz
1B M. Napoli
LF D. Nava
SS X. Bogaerts
C A. Pierzynski
3B W. Middlebrooks
LH J. Lester
RH J. Lackey
LH F. Doubront
RH J. Peavy
RH C. Buchholz
RH K. Uehara
4 l New York Yankees
2013 l 85-77, third place (tie)
Last year in playoffs l 2012
Only three men who played in the Yankees' 2013 opener will start on opening day this year. One, Jacoby Ellsbury, started for the other side last year. Derek Jeter will make his final opening-day start to begin a goodbye tour that probably won't end where his first full season did: in the World Series.
CF J. Ellsbury
SS D. Jeter
RF C. Beltran
C B. McCann
1B M. Teixeira
DH A. Soriano
3B K. Johnson
2B B. Roberts
LF B. Gardner
LH CC Sabathia
RH H. Kuroda
RH I. Nova
RH M. Tanaka
RH M. Pineda
RH D. Robertson
5 l Toronto
2013 l 74-88, fifth place
Last year in playoffs l 1993
The Blue Jays added $35.5 million in payroll before last season and still finished last. They may not do much better this year. Jose Bautista's slugging percentage has declined the last two years, Jose Reyes has a sore hamstring and no projected starter had an ERA below 4.15 last season.
SS J. Reyes*
RF J. Bautista
1B E. Encarnacion
DH A. Lind
CF C. Rasmus
LF M. Cabrera
3B B. Lawrie
C D. Navarro
2B R. Goins
RH R.A. Dickey
RH D. Hutchinson
LH M. Buehrle
RH B. Morrow
LH J.A. Happ*
RH C. Janssen
1 l Detroit
2013 l 93-69, first place
Last year in playoffs l 2013
No one will miss Prince Fielder more than Miguel Cabrera, who won consecutive MVP awards with Fielder hitting behind him. But the Tigers return four starters who won at least 13 games. The addition of Joe Nathan strengthens a bullpen that lost 25 games and saved just 39 in 2013.
LF R. Davis
RF T. Hunter
1B M. Cabrera
DH V. Martinez
2B I. Kinsler
CF A. Jackson
C. A. Avila
3B N. Castellanos
SS A. Gonzalez
RH J. Verlander
RH Anibal Sanchez
RH M. Scherzer
LH Drew Smyly
RH Rick Porcello
RH Joe Nathan
2 l Kansas City
2013 l 86-76, third place
Last year in playoffs l 1985
Seven Royals regulars weren't alive the last time Kansas City made the playoffs. But those 20-somethings could lead the Royals to a postseason appearance if the bullpen, which had an AL-best 2.55 ERA, pitches as it did last year, when the Royals won 31 one-run games.
RF N. Aoki
2B O. Infante
1B E. Hosmer
DH B. Butler
LF A. Gordon
C S. Perez
3B M. Moustakas
CF L. Cain
SS A. Escobar
RH J. Shields
LH J. Vargas
RH Y. Ventura
RH J. Guthrie
LH B. Chen
RH G. Holland
3 l Cleveland
2013 l 92-70, second place
Last year in playoffs l 2013
The Indians have lost 38 wins and 28 saves from a pitching staff that got them to the postseason. That depth will be difficult to replace, putting more pressure on an offense that was fourth in the league in runs despite no regulars hitting better than .284 and only one player with more than 20 home runs.
CF M. Bourn*
1B N. Swisher
2B J. Kipnis
3B C. Santana
LF M. Brantley
DH J. Giambi*
SS A. Cabrera
RF D. Murphy
C Y. Gomes
RH J. Masterson
RH C. Kluber
RH Z. McAllister
RH C. Carrasco
RH D. Salazar
RH J. Axford
4 l Minnesota
2013 l 66-96, fourth place
Last year in playoffs l 2010
With Joe Mauer moving from catcher to first base, newcomer Kurt Suzuki will be charged with sorting out a rotation that combined for a 33-55 record and 4.62 ERA last season. That would be an upgrade for the Twins, though, whose 2013 starters had an MLB-worst 5.26 ERA.
CF A. Hicks
2B B. Dozier
1B J. Mauer
LF J. Willingham
RF O. Arcia
3B T. Plouffe
DH J. Kubel
C K. Suzuki
SS P. Florimon
RH R. Nolasco
RH K. Correia
RH M. Pelfrey
RH P. Hughes
RH K. Gibson
LH G. Perkins
5 l Chicago White Sox
2013 l 63-99, fifth place
Last year in playoffs l 2008
Chicago will be competitive every fifth day — when Chris Sale pitches. The other days, not so much. Aside from the addition of Cuban defector Jose Abreu, the AL's lowest-scoring lineup remains largely intact, which is a problem since no one hit better than .284 last season and only Adam Dunn had more than 17 home runs.
CF A. Eaton
SS A. Ramirez
1B J. Abreu
DH A. Dunn
RF A. Garcia
LF D. Viciedo
3B C. Gillaspie
2B G. Beckham*
C T. Flowers
LH C. Sale
RH F. Paulino
LH J. Quintana
RH E. Johnson
LH J. Danks
RH N. Jones
1 l Texas
2013 l 91-72, second place
Last year in playoffs l 2012
Texas blew last-month division leads in each of the last two seasons, so Manager Ron Washington says, "We have to sustain at the end." Adding Shin-Soo Choo (107 runs) and Prince Fielder (25 home runs, 106 RBIs) should help, but a questionable rotation became more so with Yu Darvish's neck injury.
LF S. Choo
SS E. Andrus*
3B A. Beltre
1B P. Fielder
RF A. Rios
DH M. Moreland
C N. J.P. Arencibia
2B J. Wilson
CF L. Martin
RH Yu Darvish*
RH T. Scheppers
LH Martin Perez
LH J. Saunders
LH R. Ross
RH J. Soria
2 l Angels
2013 l 74-84, third place
Last year in playoffs l 2009
If Albert Pujols and Josh Hamilton bounce back, the Angels won't miss Mark Trumbo's 100 RBIs. If not, the heavy lifting is left to Mike Trout. The rotation has two proven starters, so the bullpen will have to be better than in 2013, when it blew more than a quarter of its save chances.
RF K. Calhoun
CF M. Trout
1B A. Pujols
LF J. Hamilton
3B D. Freese
DH R. Ibanez
2B H. Kendrick
C C. Iannetta/H. Conger
SS E. Aybar
RH J. Weaver
LH C.J. Wilson
LH H. Santiago
RH G. Richards
LH T. Skaggs
RH E. Frieri
3 l Oakland
2013 l 96-66, first place
Last year in playoffs l 2013
The Athletics return nearly the same lineup that finished third in the AL in homers and runs. They may have to do better this year, though, with the loss of Jarrod Parker (12-8, 3.97) weakening the rotation. Jim Johnson (101 saves the last two seasons) should bolster the bullpen.
CF C. Crisp
3B J. Donaldson
SS J. Lowrie
LF Y. Cespedes
1B B. Moss
RF J. Reddick
DH J. Jaso
C D. Norris
2B E. Sogard
RH S. Gray
LH S. Kazmir
RH J. Chavez
RH D. Straily
LH T. Milone
RH J. Johnson
4 l Seattle
2013 l 71-91, fourth place
Last year in playoffs l 2001
The $240-million signing of Robinson Cano puts the rebuilding Mariners on the clock. The core of Seattle's young, home-grown lineup becomes eligible for free agency in three years and it's unlikely the team will be able to keep them and pay Cano. Winning now is a priority.
CF A. Almonte
3B K. Seager
2B R. Cano
DH C. Hart
1B J. Smoak
LF D. Ackley
RF M. Saunders
SS B. Miller
C M. Zunino
RH F. Hernandez
RH E. Ramirez
LH J. Paxton
RH R. Elias
RH H. Iwakuma*
RH F. Rodney
5 l Houston
2013 l 51-111, fifth place
Last year in playoffs l 2005
The Astros had the youngest team in the majors last year and the addition of leadoff man Dexter Fowler, 28, won't change that. The worst-paid team in baseball might get cheaper as the Astros dip into their deep farm system, rarely a recipe for success. This could be another 100-loss season.
CF D. Fowler
LF R. Grossman
2B J. Altuve
C J. Castro
DH C. Carter
1B J.Guzman
3B M. Dominguez
RF L.J. Hoes
SS J. Villar
RH S. Feldman
RH J. Cosart
LH B. Oberholtzer
RH B. Peacock
LH L. D. Keuchel
RH C. Qualls
*May start season on the disabled list.


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Reno Chinati (Rapper From The Midwest) Performing Live At Sneakerpimps 2009 [Artist Submitted]
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Al Green
The silky vocals of Al Green are made from rugged soul meets Motown polish.
Whether Green is crooning to seduce, lament or celebrate, he holds nothing back. The raw power of his voice has carried him from decade to decade and genre to genre in a career that remains robust to this day.
With his incomparable voice, full of falsetto swoops and nuanced turns of phrase, Al Green rose to prominence in the Seventies.
One of the most gifted purveyors of soul music, Green has sold more than 20 million records. During 1972 and 1973, he placed six consecutive singles in the Top 10: "Let's Stay Together," "Look What You Done for Me," "I'm Still in Love With You," "You Ought to Be With Me," "Call Me" and "Here I Am (Come and Take Me)."
"Let's Stay Together" topped the pop chart for one week and the R&B charts for nine; it was also revived with great success by Tina Turner in 1984. In terms of popularity and artistry, Green was the top male soul singer in the world, voluntarily ending his reign with a move from secular to gospel music in 1979.
Beyond his chart-making abilities, Green set a new standard for soul music and essentially created a new kind of soul—one that combined the gritty, down-home sensibility of the Memphis based Stax-Volt sound with the polished, sweeter delivery of Motown. Over a fat, funky bottom, Green's subtle and inventive voice would soar into falsetto range with beguiling ease. His finest recordings showcase a penchant for jazzy filigree and soulful possession rivaled only by the likes of Marvin Gaye and Aretha Franklin. They also are the products of teamwork, as Green benefited immensely from a longstanding association with producer Willie Mitchell and the house band at Hi Records.
Green was born on an Arkansas farm in 1946 and grew up in Grand Rapids, Michigan. He sang gospel with the Greene Brothers, a family quartet, and belonged to the Creations and the Soul Mates in the Sixties. In 1967, Al Green and the Soul Mates had a Number Five R&B hit with "Back Up Train." In terms of influences, "I was raised on the sound of Sam Cooke and the Soul Stirrers," Green has said. A fateful crossing of paths between Green and Willie Mitchell in Texas, where both were performing, resulted in Green's signing to Memphis-based Hi Records in 1969. Mitchell produced Green's recordings and co-wrote material with him for the next eight years. It was a fruitful association that yielded high-quality albums (such as I'm Still in Love With You, 1972 and Call Me, 1973), as well as thirteen Top 40 hits that helped keep the sound of soul pure and alive in the Seventies.
Mitchell cut Green's groove-oriented records at his Royal Recording Studio, a converted movie theater in downtown Memphis. Essential components of Green and Mitchell's mix of silky ballads and bouncy funk included the Hi Records studio band: guitarist Mabon "Teenie" Hodges, bassist Leroy Hodges, keyboardist Charles Hodges and drummer Howard Grimes. In addition, drummer Al Jackson (of Booker T. and the M.G.'s) co-wrote and played on many of Green's biggest hits. Strings, horns and backup singers added to the intricate tapestry. But it was Green's light, skillful touch as a vocalist that made it all work so well.
Green's breakthrough came in 1971 with "Tired of Being Alone" (Number Seven R&B, Number Eleven pop). A slew of hits followed, keeping Green in the Top 40 (and often the Top 10) through 1976. His consistent quality and flawless phrasing prompted music critic Robert Christgau to pronounce him among "the half dozen prime geniuses of soul." His peak work as an R&B master is contained on a string of hit-filled albums released in the early Seventies: Al Green Gets Next to You (1971), I'm Still In Love With You (1972), Let's Stay Together (1972), Call Me (1973) and Livin' for You (1973).
With The Belle Album (1977), Green made an overt turn toward religious themes. The album was self-produced, as Mitchell amicably parted ways with Green over his turn to gospel. The 12th album of his career, it was "the most important release of my life," according to Green in his autobiography, Take Me to the River. He elaborated, "God had called me to a higher place, turned me away from earthly to heavenly love, and while it hurt to say it, I had to leave the sensual for the spiritual."
During the Eighties, Green recorded inspirational music for the Myrrh label while serving as pastor at a church he founded. The Nineties found him returning to his soul roots from time to time, yet to this day he remains primarily a singer and preacher of the gospel. On most Sundays, Green occupies the pulpit at Full Gospel Tabernacle Church on Hale Road in Memphis. The public is welcome to witness Green's sermons, which are no less full of fire and feeling than the flood of singles that set the standard for soul in the Seventies.


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The University of Minnesota announced that Gary Wilson is retiring as the Gophers women's cross country coach at the end of this 2012-13 season.
He will be replaced by Sarah Hesser, who is a a former Gophers runner and a current volunteer assistant on Wilson's staff.
The Gophers have seen Wilson built his team into a national power during his 28 years as head coach. Minnesota had a streak of five consecutive top-12 NCAA finishes from 2005-09 and has qualified for the national meet each of the past seven years.
Wilson was previously the head coach of the women's track team for 21 years; he has been an assistant on that staff since 2007.
As for the new girl, Hesser was a two-time cross country captain, senior track captain, and three-time Academic All-Big Ten honoree.


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It only takes a little looking around the web (even among professional web developers) to find the words "This site best viewed by…" emblazoned somewhere for all to see (as if it were something to be proud of.) A quick Google search shows several hundred million results. This particularly abhorrent practice is a major pet peeve of mine. It means that someone was too lazy to do their job properly and probably got paid for it anyway. That's just wrong.
There's also the implication that any site visitor not using the specific browser, browser version, or screen resolution listed as "acceptable" by this particular wannabe webmaster (or better yet, "webfailure") just deserves whatever garbage comes out on their screens. You'd think that no one else had ever heard the story of The Emperor's New Clothes.
I keep trying to imagine what day to day life would be like if this practice were adopted by any other industry. Can you imagine a television station that advertised the best brand of television on which to watch their broadcast and was unconcerned by the fact that their signal was blurry or unwatchable on any other brand? Can you imagine a sign outside your local grocery store that said, "This parking lot best used by Toyota Camrys, 1995 or later, 2-door, not 4-door." Tell me you wouldn't want to stick some massive, old RV across 14 of those parking spaces and dare anyone to say a word.
People, the time has come to end this practice once and for all! There have been efforts and all-out campaigns to do this before, but they've had very little success. I have a plan that I think could be pretty effective. I call it my "Many Happy Returns Plan." It goes like this:
- Everyone starts contacting the real owners of these sites and telling them to get their money back. It's clear that the person they paid to do this was either too incompetent to do it properly or too lazy to finish the job. They should get their money back to pay someone else who knows what the heck they're doing. It's only fair. I think that a few well-publicized lawsuits would end this particular trend in laziness.
It really comes down to this, the only time that you should see the words "This site best viewed by…" on a website is if they're followed by the words "…anyone in any browser they prefer." If you don't know how to do this, ask, search the web, learn, find out. Don't just stick some piece of garbage site up and charge a client for it. In the immortal words of Captain Jean-Luc Picard, "Make it so."


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'White Art in the Meat Food Business'
The above illustration comes from a 1944 pamphlet by Otto F. Fleiss titled White Art in the Meat Food Business: A Practical Handbook for Butcher, Pork Stores, Restaurants, Hotels and Delicatessens on How to Make Lasting and Transferable White Art Decorations out of Bacon Fat Back for Window Displays, Ornaments on Meat Food Cold Buffets and for Exhibits and Advertising Purposes. Enrich yourself with Personal Knowledge. [via Boing Boing]


text:
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Projects: Reclaimed Scaffold Board Storage Unit
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I have built a large Farmhouse cabinet for our kitchen using pocket holes of course. LOL. I used a 48" piano hinge for the 23"x57" door (an old window I found at the local antique shop).I want to add pistons or some other method to hold the window…Continue
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Do you have what it takes to be a successful Field Sales Consultant? Everest is hiring... across the Paisley area.
Everest? The double glazing people?
You got it. Though these days we offer a broad range of home fixture products: including doors, conservatories and windows. We've been going for over 50 years, and people remain at the heart of our business -- both customers and staff.
Right now we have some fantastic sales roles on offer...
What you'll be doing
As an Everest Field Sales Consultant you'll book and attend product design appointments in customers' homes; helping them realise their own vision using a creative consultative approach (with a little help from our bespoke design software).
Working with us, you'll quickly become an expert on our extensive range of windows, doors, conservatories and other home fixtures. You'll know the difference between double and triple glazing and the benefits of uPVC over aluminum, in no time (!).
And don't worry -- you won't be on your own drumming up business. Our marketing department spends a large amount of money on advertising every year, which creates an average of 2,500-3,000 weekly enquiries for our consultants to follow up on.
What we're looking for
You're customer-focused. You talk and listen. Sales experience is great, but you don't 'sell'
-- you find solutions to problems. You're a troubleshooter, committed to getting the best result for all concerned. Not just because it's your job; but because you care.
You have a positive outlook. Energy and confidence set great sales people apart from the mediocre. People are drawn to positivity. And let's be honest: we do business with people we like. You know how to handle rejection too: with a smile.
You're organised and professional. And because you'll be out in the field, you'll need to have a car and UK driving license too.
Ready to reap the rewards?
Our Field Sales Consultants earn between £40,000 and £60,000 per year (OTE) on average. Our top Sales Consultant earns £150,000. And so can you.
There are also outstanding rewards and incentives for those that meet their targets, including: a Premier League experience; Luxury holidays -- and much more.
We put a lot into training our staff, and because we're a national network there are stacks of progression opportunities right across the UK.
If you want to be part of a successful British enterprise that's built on trust, quality, and innovation, then...
Join The Best. Join Everest.
Apply now or request a call back.
We are an equal opportunities employer and do not discriminate on the grounds of 'Protected Characteristics' as defined under the Equality Act and other relevant UK legislation.
The number of jobs in each salary range for all:
We Love 9am
JOBSWORTH: £23,884 P.A.?Alexandria, Dunbartonshire
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We Love 9am
JOBSWORTH: £23,686 P.A.?Glasgow
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PeopleTree Recruitment
Up to £60,000 per annum OTE commission only
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Mana Resourcing Ltd
£32000 - £34000 per annum + £38,400 - £40,400 OTE ca…
Scotland, Glasgow
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Mana Resourcing
£32,000 per annum
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The Monarch series combines ultra-soft lumbar pillow support with unique "grip-rite" arm designfor easy transfer.
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Chandler's Medical Supply is a medical supply store in Hyattsville, Maryland. We carry a comprehensive range of medical supplies and equipment including diabetic shoes. We offer our customers quality medical equipment and medical supplies at very affordable rates 301-577-9001
Chandler's Medical Supply Inc.7425 Annapolis Rd.Hyattsville, Maryland 20784
Monday - Friday:10:00 AM to 6:00 PM
Saturday:10:00 AM to 4:00 PM
Closed on Holidays.Please call us at 301-577-9001 for questions


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Take note, NFL players of the world. If you (allegedly) decide to make casually harassing phone calls to a team employee and then (allegedly) send that same employee a photo of you naked from the waist down (SEXY), the NFL front office will NOT suspend you. Wednesday morning, FOX's Jay Glazer reported that Vikings QB and future empty shell of a man Brett Favrewould be fined for his incident with Jenn Sterger, but not suspended.
The league wanted to make a ruling before the end of the season, but did not want to do it on New Year's.
Yes, because New Year's would be ruined if I knew Brett Favre had to shell out a few grand for whipping out his junk on camera. Wednesday afternoon, the NFL announced that it had fined Favre $50,000 "for his failure to cooperate with the investigation in a forthcoming manner."
It's amazing that we had to wait until now for a judgment to come down on this stupid thing. The report about Favre surfaced on Deadspin all the way back in October, and the League spent nearly three months "investigating" the matter, which seems like an awful long time to investigate a man's nude photos of himself. I'm not saying the League office maybe has a thing for Favre, but he's certainly engendered the affections of thousands of middle-aged announcers the world over now, hasn't he?
And so this story comes to an end much like Favre's season will: It was a matter that garnered a great deal of attention, only to not have much substance to it.


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2) 薬剤師から第1類医薬品のご使用についてQpostをお送りいたします。
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Dear Customers, we are not liable for any lost of items, accidents, delays or other issues which are the responsibility of the shipping company. Please contact them for parcel related issues.Buyer choose Normal Mail as your shipping method means you have bound to agree and accepted the Terms & Conditions stated by Singpost Company. There will be NO Refund or Resend of any delayed or lost parcels by SingPost Normal Mail. It is the "SingPost Company" responsibilities to deliver your pacel and NOT Seller as we have SingPost Video Evidence Proof of all parcels. SingPost are the ones who handle your parcels delivery and Not the seller. With the latest technologies, all parcels have been captured by CCTV Cameras and Video Evidence Proof of all buyers parcel. (Video Evidence Proof will be submitted upon request)We always strongly recommend buyers to choose Registered Mail / Qxpress so we could keep track of your parcels with the delivery company for any issues.
Dear customer : Now is Festive period and Singpost might took longer timing for mailing delivery. We cant control over it ( as there are customer email us telling the customer service of q0010 that Singpost belong to us and q0010 want us to provide the evidence of it to prove we hold Singpost ( which is no true ) and hence hope all pucchase to be make and opt for Registered mailing to avoid unhappiness over non-receipt of parcels on time and giving us " not recomanded" Or " Netural " late delivery where it is not our fault at all. Normal mailing -- Delivery by singpost and will be the same as how you receive your normal bills. Mailing could took up to a month to reach as per our past experience and do not cream at us that your parcel did not reach on time . As you have agreed and understand and hence you have chosen normal . Regstered mailing will be delivery upon and traceable. For customer , select register mailing will be on time
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Good and best price..............
Have yet to use. No safety label.
Travel Adaptor it's very useful for traveling.
Looks OK. Delivery took quite a while.
Well packaged, received in good condition.
However seller distrusts buyer, that the latter 'refuses to confirm delivery' regardless s/he received the item(s).
There isn't any posted question about item.


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Green Projects for Students
The ultimate goal of making schools eco-friendly is to get the children involved in projects that help build a greener community. If the school uses renewable energy, recycles, and composts food waste, it demonstrates green living in action to children, parents, and people in the wider community.
A range of projects is the ideal so that everyone in the school — from the youngest and most academically minded to the oldest and most practically minded — can be engaged and involved. Some ideas include:
Dig a vegetable plot: Devote spare land on school grounds to a vegetable plot. Students can grow organic vegetables to use in the school cafeteria or to donate to local food banks. In the process of planting, monitoring, and caring for an organic garden, students learn about organic production, local and seasonal food, and the link between the land and what ends up on their plates.
If funding is an issue, seek sponsorship from the local community. Garden centers may be interested in providing tools, seeds, and expert advice, for example, or community organizations may provide funds to buy fencing to protect the garden from rabbits and other wildlife eager to sample the produce.
Visit the local landfill site and recycling facility: Taking children to a landfill to see the reality of waste management can have a big impact on their habits. Incorporate the following activities in the landfill visit to get children involved and thinking about waste management:Credit: PhotoDisc/Getty ImagesSeeing where trash ends up can serve as a wake-up call to children.
Ask them to identify things that could have been reused, repaired, or recycled.
Explain how long it takes various items they see to decompose.
Explain how toxic chemicals have to be prevented from getting into the ground and local water supplies.
Discuss the various other options for getting rid of and reducing the waste to a minimum in the first place.
From the landfill site, go to a local recycling facility if you can, and show the children what happens to the items sorted and processed there.
Plant trees: If the school has no land of its own on which to grow trees, find a local park or playground open to the project. Don't forget that part of the project is monitoring the growth and health of the trees, so choose a fast-growing species suitable for your environment.
Launch a green competition: Friendly competitions give children incentives to work, and green projects are an ideal opportunity to provide a little extra incentive for extra effort. The competition may be to find the students who come up with the best green project of the year or who write the best essays on a specific green issue, for example. Every aspect of the competition — including letting the kids and their parents know about it — should help to raise awareness about green living and green schools.
Prizes can come from you if you can afford them, or you may ask local green companies to donate either goods or funds for the prizes. It's best if the prizes contribute to green living, too.


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During clinical trials, people who have
multiple sclerosis (MS) participate in studies that
test new therapies for the disease. The therapies tested in clinical trials
have shown promise in laboratory and animal research, but they may not have
been shown to be safe and effective for humans yet. Each trial requires that a
person meet specific requirements (involving, for example, age, time since
diagnosis, and course of MS) in order to ensure that the results will be clear
enough to be useful.
Medicines being tested in clinical trials pass through four
Call the National
Multiple Sclerosis Society (1-800-FIGHT-MS, or 1-800-344-4867) or the Brain
Resources and Information Network of the National Institute of Neurological
Disorders and Stroke (1-800-352-9424) for information on clinical trials. Or
visit the National Institutes of Health clinical trials website at
www.ClinicalTrials.gov. Discuss with your doctor, nurse, or therapist the
possibility of participating in a trial. Current clinical trials involve
testing new medicines, higher doses of existing medicines, and combination
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Last Revised:
February 15, 2012
Healthwise Staff
Medical Review:
Adam Husney, MD - Family Medicine & Anne C. Poinier, MD - Internal Medicine & Barrie J. Hurwitz, MD - Neurology
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Glenn Beck's Scariest Meltdown Yet
It's worth remembering the fictional newsman of the moment, Howard "I'm mad as hell" Beale from Network, was actually mentally ill. Now Beale's closest modern analog is himself stumbling toward insanity.
It's never been clear to what extent Glenn Beck is actually unhinged, and to what extent his Fox News Channel antics are pure clowning. But it shouldn't matter much to the aspiring populist-demagogue-in-chief of our era: if he seems too far into the crazy side of the thin line between rage and psychosis, viewers will start to assume he really is mentally incompetent, and be less willing to take up pitchforks with him.
Which is why Beck probably shouldn't be pouring pretend gasoline on a hyperventillating volunteer (some Red Eye staffer, naturally), as he did tonight in a deranged imitation of Barack Obama, then following that up with maniacal screaming against "games" (uhh...) and in favor of "sanity" (HA!).
Beck may have run a disclaimer that the gas can was filled with water, and he may get all kinds of attention on various blogs (we'll plead guilty, preemptively here, to feeding the troll), but the disgruntled red-state housefraus who nod along to Beck's show in the early evening don't want to see a simulated lynching.
Or probably we're wrong, they'll eat this crap up, and Glenn Beck will fulfill his dream of being the Father Coughlin of our era. God help us (especially in getting a clear view of the train wreck).


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Yesterday, I described how Morgan Stanley was holding firm-wide conference calls to explain the Facebook disclosure scandal to its angry financial advisors and clients...and how, on at least one of those calls, my name had come up repeatedly.
The Facebook disclosure scandal, you will recall, is about how Morgan Stanley and the other IPO underwriters verbally relayed bad news to their big clients about Facebook having a crappy quarter...but didn't tell their financial advisors and individual clients about this.
As a result of this selective disclosure, in the days leading up to the Facebook IPO pricing, institutions had much better information about Facebook's current business than individuals did. And that may be one reason why the stock tanked after the IPO: Because there's nothing like finding out a company is having a lousy quarter to cause people to dump stock.
I also described how it has recently become a convention on Wall Street to blame me for everything. Bank of America blamed me for its cratering stock price last summer. Morgan Stanley is blaming me for the Facebook disclosure scandal. And so on.
(I am relieved to report that JP Morgan hasn't blamed me for its ~$5 billion trading loss yet. I've always thought that Jamie Dimon was a class act!)
The word I got yesterday was that Morgan Stanley was blaming the Facebook scandal on me because I have recently written articles about how outrageous it was that institutions were told about Facebook's lousy quarter and individuals weren't. In other words, because I had hyped up the scandal and gotten Morgan Stanley's clients all hot under the collar about it.
I tried to discuss this with Morgan Stanley yesterday, but their approach to dealing with me right now is to ignore my emails and calls. So I didn't get very far.
Instead, last night, I talked to someone familiar with Morgan Stanley's view of the situation.
And I discovered that the firm really is blaming the whole Facebook IPO disclosure scandal on me...and not just because of the recent articles I've been writing!
Explaining this story will require a lot of background, so grab a cup of coffee and settle in. Otherwise, the short version is this:
Morgan Stanley is saying that the regulations put in place after the research-banking scandal of the 1990s—in which I was Exhibit A—caused this new disclosure scandal.
The Origins Of The Ridiculous Rules That Just Hosed Morgan Stanley Clients
You will unfortunately no doubt recall that, a decade ago, I was a famous Wall Street analyst.
Specifically, I was one of the top-ranked Wall Street Internet analysts during the dotcom bubble. One of the reasons I was famous was that I had been very right about the Internet stocks for 3 or so years in the late 1990s, when some other analysts were wrong. But then, like a lot of other analysts, I made the mistake of trying to perfectly time the bursting of what looked like a bubble—and I waited too long to downgrade the stocks. And then I was disastrously wrong.
That was a searing lesson for me—one I will never forget. I had actually put a lot of money where my mouth was—on a handful of the top Internet stocks—and I lost most of that money. I also missed the chance to save my clients a lot of money by getting them out before the collapse. I will forever regret that.
(In my defense, it really wasn't just me who waited too long. Pretty much everyone waited too long. If you go back and read articles from the summer of 2000, you will find almost every big money manager quoted as saying the recent pullback in the NASDAQ was a fantastic buying opportunity. It wasn't until that fall, after I had downgraded the stocks, that the world ended.)
Anyway, part of every analyst's job in those days was to work with their firms' bankers to take companies public. Analysts were involved in evaluating IPO candidates, pitching IPO candidates, positioning IPOs, marketing IPOs, and then providing research on IPOs after the companies went public. This was a longstanding industry practice, one that had been around since long before I got into the industry. It had also been described frequently in the press: The top analysts were said to have to "wear two hats," banker and analyst, and have to help investors while also maintaining great relationships with companies. At some firms, analysts were even paid directly for banking deals, though that wasn't the case at my firm (Merrill Lynch).
This involvement of analysts in the IPO process, not surprisingly, occasionally created pressure and friction between bankers and analysts, as well as between analysts and companies. The banks made more money from banking than they did from trading, and there were many stories of analysts getting fired after annoying banking clients with negative reports. Companies, meanwhile, gave detailed information to friendly analysts and shut out negative analysts, so if you didn't maintain good relationships with companies, you often were unable to add much value for your investor clients. And this friction only increased as the bull market roared on, because negative analysts were not only annoying—they were also usually wrong.
After the market crashed, a new New York Attorney General named Eliot Spitzer decided to look into the research-banking conflict. And, thanks to my visibility, he started with me. My research team and I had had a penchant for writing really colorful emails to each other—I famously dissed a stock that we were covering that had collapsed as a "piece of junk"—and these emails provided spectacular ammunition. In the spring of 2002, Spitzer alleged that the reason I had been slow to downgrade the dotcom stocks was because of the banking conflict.
That latter conclusion was not, in fact, true. (My firm categorically denied that part of the allegations at the time). The reason I had been slow to downgrade the stocks was that, like thousands of other investors and analysts, I had thought that the bull market had longer to run.
But Spitzer was certainly right that the banking conflict had created friction and stress for us and that we had not wanted to recklessly damage the firm's banking business—or, for that matter, companies' businesses—by recklessly downgrading stocks. (After an 18-year bull market, downgrades were highly unusual).
After extending his investigation to many other firms, Spitzer forced an industry-wide settlement in which the involvement of research analysts in IPOs was pared back and the "Chinese Wall" between research and banking was strengthened.
This industry reform had several consequences, some of which were positive and some of which were negative.
On the positive side, the reforms removed some stress for analysts. Once analysts were no longer evaluated in part on banking business, they focused more on serving institutional investor clients and researching already public companies. And that's unequivocally a good thing.
On the negative side, it became harder for companies to go public...because it turned out that having analysts involved in the screening, positioning, and marketing of deals and then providing follow-on research coverage of small companies made the whole IPO process work better. So that, arguably, was a bad thing.
And that brings us to today...
When the Facebook IPO disclosure scandal was revealed a few days ago, Morgan Stanley immediately protested that it had followed all the rules.
And that may, in fact, be true.
The problem is that, as Facebook has illustrated, the rules themselves are grossly unfair.
The story that Morgan Stanley is telling people is that Spitzer's research reforms actually exacerbated the Facebook IPO disclosure problem, in the following ways.
Before Facebook, the assumption was that every communication from an underwriter's research analyst about an IPO candidate would be positive. Whatever the analyst had to say, in other words, could be construed as "hyping" the stock and making it easier to sell.
In their desire to protect unsophisticated investors from this "hyping" of IPOs, regulators decreed that underwriter research analysts would not be allowed to publish any research on an IPO—or publish anything in print—until a certain amount of time after the deal.
Back in the 1990s, this "quiet period" was 25 days. After the Spitzer reforms, it was lengthened to 40 days.
But, more importantly, the underwriter research analysts were still allowed to do three things to help the firm's big institutional investors:
- Talk to company management about the business
- Generate estimates for IPO companies with management's help
- Discuss these estimates and their opinions verbally with big institutional investors
The idea was that institutional investors would be sophisticated enough to evaluate the analysts' estimates and opinions, instead of just regarding them as "hype" and mindlessly placing orders.
In the view of the regulators, in other words, the institutions did not need to be "protected" from the enthusiasm of research analysts. So they could talk to the analysts and learn all they could from them (which in most cases was a lot). Individual investors, meanwhile, were assumed to be clueless and gullible and therefore in need of protection from analyst enthusiasm.
So now you can begin to see the irony of all this...
Most of the rules in the IPO process are designed to protect individual investors from getting too much good news about companies.
But the important news on the Facebook IPO was bad news.
When Facebook realized it was having a crappy second quarter, it called up the analysts at all the underwriters and told them to cut their estimates. And the analysts did as they were told. And then the analysts and their firms got on the phones with big institutional investors and told these investors about the crappy quarter and estimate cuts.
Meanwhile, the financial advisors and individual clients of the underwriters, who were thought to be in need of protection from good news, not bad news, were kept in the dark. Because that's what the regulators had wanted... to restrict communications from analysts to individual investors on IPOs, on the theory that anything analysts had to say about IPOs would be positive and, therefore, hype-y.
So that's the other way that Morgan Stanley is now blaming me for Facebook IPO disclosure scandal.
The research reforms that Spitzer's settlement brought about restricted the already limited level of communication between analysts and individual investors on IPOs. Because, after the dotcom bubble, it apparently never occurred to anyone that analysts would have anything negative to say.
So, in other words, we've just seen another vicious example of the Law of Unintended Consequences.
So, That's The Problem... What Is The Solution?
So, what's the answer?
Here's the answer:
We need to stop treating individual investors like babies.
We need to stop pretending that it can be smart and safe for individual investors to "play IPOs" and start being forthright about how investing in stocks is speculative and risky and that even expert analysts are often wrong.
We need to start educating the public about how hard it is even for the most well-trained and experienced professionals to consistently make money trading stocks. (Most pros lag index funds.)
And then, we need to make exactly the same information available to individuals as we do to institutions.
In this case, we can do this in one of two ways.
First, we can change our pre-IPO disclosure rules to match those in the UK. The analysts at the underwriters could write full research reports on the pre-IPO companies and then publish them BEFORE the IPO marketing process, thus sharing their insights and estimates with everyone.
If regulators are terrified that this might induce some innocent individual investors to start speculating, we should remind the regulators that the individuals are adults and, as such, should take responsibility for their own decisions.
Alternatively, we should eliminate analyst involvement in the IPO process entirely. No talks with company management, no phone calls with institutional investors, no estimates, no nothing.
Either of these solutions would be better than the current system.
Because, as the Facebook IPO just revealed, the current system is grossly unfair.
SEE ALSO: Morgan Stanley Is Holding A Firm-Wide Conference Call To Blame The Facebook IPO Scandal On... Me (I?)


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text: Turnaround Time Turnaround Times for Blood Bank Products and Services for Hospital Based Patients The following guidelines for expected response or turnaround time (TAT) have been determined by the Blood Bank staff and Medical Director. Circumstances that may cause deviation from these guidelines include, but are not limited to: patient identification problems, instrument malfunctions, shortage/availability of products, heavy workload, antibody problems or delay in transportation. The turnaround time is from the time the specimen is received in the Blood Bank. Guidelines for Typical Blood Bank Tests, Procedures and Services for Hospital Based Patients Procedure/Service Routine (minimum time) STAT (minimum time) Blood Type 30 minutes 15 minutes Type and Screen 2 hours 1 hour Type, Screen, and Crossmatch (negative antibody screen) 2 hours 1 hour Crossmatch (antibody screen negative) 20 minutes 10 minutes Antibody Identification 2 hours to 2 days (depending on complexity) ABORh (type) Specific (uncrossmatched blood) 30 minutes Group O (uncrossmatched blood) 15 minutes FP 30-45 minutes 30 minutes Platelets (available in-house) 1 hour 30 minutes Platelets (must order from blood supplier) 4 hours Minimum 2 hours Cryoprecipitate 30-45 minutes 30 minutes Guidelines for Special Circumstances and Pediatrics for Hospital Based Patients Note: For TATs for MTP/Trauma, please refer to MTP protocol 915.6149 and/or Blood Bank Policy BB.0230. Procedure/Service Routine (minimum time) STAT (minimum time) ABO, Rh, DAT 30 minutes 15 minutes RhIG Workup and Fetal Screen 2 hours 1 hour Antibody Titration 2 hours to 2 days Washing RBC's 1 hour (per unit) 45 minutes (per unit) Splitting or Dosing Products 30-45 minutes 25 minutes ECMO Setup 1.5 hours Exchange Transfusion 2 hours Return to top Blood Bank Orders Clot to Hold: Order if low likelihood of transfusion. Provides appropriately labeled blood sample tube to the Blood Bank. Sample is good for three days. Type and Screen: Order if low to moderate likelihood of transfusion. Provides blood type and antibody screen. If antibody is identified, the patient will get antigen negative blood available in case transfusion is ordered in the future. If antibody screen is negative, can crossmatch blood for patient in 20 minutes (routine) or 10 minutes (STAT). Sample is good for three days. Type and Crossmatch: Order if moderate to high likelihood of transfusion, or transfusion is imminent. Provides blood type and antibody screen. Actual units are tested and set aside for the patient. Units are kept ready for three days. Return to top


text: The world's favorite season is the spring. All things seem possible in May. — Edwin Way Teale It's finally Spring — a time when all things seem possible. It's a time to shed those winter doldrums and refocus energies on finding new ways to improve the overall health of our families. As dedicated parents, we […]Continue reading


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Please visit our Open House at 5 23651 132 AVE in Maple Ridge.
Open House on Saturday, December 15, 2018 12:00PM - 5:00PM Please use entrance off 133 Ave **$20,000 Christmas Decorating Allowance for limited time**
OPEN HOUSE SATURDAY & SUNDAY Noon-5 ONLY 4 HOMES LEFT in phase 3 at Myron's Muse. READY FOR IMMEDIATE OCCUPANCY! ***$20,000 CHRISTMAS DECORATING ALLOWANCE*** Finding a little corner of unspoilt countryside where the air is fresh yet the Town Centre is only a short drive away, is like finding a little piece of heaven on earth. Wonderful collection of 3 bedroom Townhomes offering a variety of spacious plans ranging from 1628 SF to 1680 SF w/family comfort & community in mind. In the kitchens, cabinetry, quartz countertops, undermount sink & stainless steel appliances are clean & modern, creating a space where the family & friends will naturally gravitate. All meas are approx. and may vary from existing floor plan.


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Cellular clues: the sustained dependability of a tireless heart relies ...on the performance of the trillions of chemical reactions occurring in its aggregate of cells every instant of its function.
The chemical chain of events that underlies the beating of these cells and of the heart as a whole is truly remarkable. First, there's the electrical impulse along the cell's membrane; then channels open in the cell membrane allowing sodium to flow into the cell. After that, more channels open and calcium enters and binds to a tiny structure near the membrane; then, much more calcium explodes out of that structure into the cell's inner fluid and combines with a myofilament protein called troponin. Troponin then changes shape to allow two other proteins, actin and myosin, to come together. The joined proteins slide past each other in such a way as to shorten the cell, pulling the ends of the cell inward--this is the actual contraction--and then the whole process reverses itself as the heart relaxes in preparation for the next beat.
During the past 30 years, scientists have made some intriguing discoveries about the process that changes an electrical impulse into a muscle contraction. These discoveries have led to novel hypotheses about aging and disease. Scientists have found that age-related changes in heart muscle cells (myocytes) help explain alterations in the heart as a whole. For instance, they've learned there are fewer myocytes to do the work as we age and those that remain enlarge, compromising their ability to pump blood efficiently. They've also discovered much about how these changes could interact with disease processes and found clues to how exercise affects the biochemistry of cells. Scientists have begun to question some of the long-held theories about the nature of the aging heart, including whether some myocytes can replicate and what role aging may have in this process. And they've learned a great deal more about the critical role calcium plays in the drama of the aging heart.
The Marvelous Calcium Pump
Scientists have long known that calcium--the mineral that helps keep your teeth and bones strong--also has an important job within your heart. Calcium entering the myocyte's inner fluid or cytosol binds with other contractile proteins to bring about contraction. Calcium leaving the cytosol allows the cell to relax. It's this constantly changing ebb and flow of calcium in and out of the cytosol of heart muscle cells that is the essence of the heart beat. (See How a Myocyte Contracts, page 23)
At the beginning of the calcium cycle--Which coincides with the heart filling with blood--calcium in the cytosol and surrounding the contractile filaments of each myocyte is at least 10,000 times lower than calcium levels in your blood and in other fluids between your cells, called the intercellular spaces. As the cycle progresses, pores (or channels) in cell membranes open and close, allowing various salts to flow in and out of the cell. This activity triggers momentary fluctuations in the positive and negative electrical charges across the cell's membrane. When these fluctuations reach a particular threshold, an electrical discharge occurs. This discharge, called the action potential, essentially flips a switch on the myocyte's membrane to open pores that allow a small amount of calcium to enter the cell.
This tiny bit of calcium binds to openings called calcium release channels on the sarcoplasmic reticulum, an organelle (a small cellular "organ") that serves as a storage bin for calcium. In response, the sarcoplasmic reticulum releases a large amount of its stored calcium into the cell. The calcium released from this storage compartment binds to the cell's myofilaments, causing them to tighten or shorten. As the myofilaments tighten, the myocyte compresses (shrinking in length and fattening in width). This process occurs almost simultaneously in every cell in the heart wall, causing them to contract and pump blood out of the heart.
In order for the heart to relax, the cycle winds down and calcium detaches from the myofilaments. A cellular mechanism kicks in and pumps most of the calcium back into the storage bins located in the sarcoplasmic reticulum. Any residual calcium is driven out of the cell through specialized exit calcium carriers located on the cell's membrane. These carriers are proteins that swap calcium inside the cell for sodium outside of it. Then the cycle restarts in preparation for the next heart beat.
If this system fails, and calcium cycling gets out of whack, chaos can ensue. The heart, for instance, can't relax and fill with blood properly and diastolic pressure in the heart increases. In addition, individual cells may fire off rapidly and independently, resulting in arrhythmias--variations from the normal heart beat rhythm--and fibrillation, which is a very rapid twitching of individual muscle fibers. In particular, older hearts are more susceptible to spontaneous calcium oscillations than younger hearts, and it takes fewer oscillations to bring about fibrillation. Fibrillation in the left ventricle leads quickly to acute heart failure and to death if not treated.
Heart failure occurs when the heart loses its ability to pump enough blood to meet the body's requirements. In particular, heart failure causes the heart to gradually lose its reserve pumping capacity and work less efficiently. Blood pressure and flow to body organs drops. The kidneys sense this and send out signals prompting retention of body fluid, which contributes to swelling. This can cause a backup of fluid into the lungs and body tissues triggering shortness of breath, swelling of the legs and feet, and other symptoms. As heart failure progresses the effects can become quite severe, and patients often lose the ability to perform even modest physical activity. Eventually, the heart's reduced pumping capacity may interfere with routine tasks, and individuals may become unable to care for themselves. Heart failure rises exponentially with advancing age, and studies of the calcium cycle in heart cells suggest a number of possible reasons.
When a Good Pump Goes Bad
Imagine sitting calmly in a living room chair when the smoke detector goes off. As you scramble to quickly get out of the house, your heart starts beating faster. A few moments later, after you discover it was a false alarm, you return to your comfortable chair, and your heart rate slows again. As this scenario suggests, your heart beat can vary from moment to moment. And your heart's ability to respond to these changes depends a lot on calcium. The more calcium your heart cells release from their intracellular storage bins, the greater the force of the heart's contractions. But how well these mechanisms work depends on how much calcium can be pumped from these storage bins between heart beats. In young hearts, these calcium pumps work quite well, but in older hearts these pumps are much less efficient.
After the heart beat, if you recall, most of the calcium returns to the storage bins in the sarcoplasmic reticulum and then awaits the next signal to do its job again. Scientists began taking a closer look at this mechanism when they learned that muscle from older hearts takes longer to relax than muscle from younger hearts. One of the prime suspects for this phenomenon was calcium. To test this idea, Dr. Lakatta and his colleagues at the NIA used a protein that binds to calcium and gives off a blue light to detect how much calcium is in a cell at any one time. When they injected this calcium-sensing protein into myocytes within heart muscle in laboratory dishes, the blue light showed that calcium levels, after a contraction, fell more slowly in older myocytes. Or, putting it in biologists' terms, the cytosolic calcium transit was longer. But why? Could the calcium be spending longer in the inner fluid because the sarcoplasmic reticulum wasn't removing it as quickly in older cells?
The answer was yes. In experiments, NIA scientists isolated the sarcoplasmic reticulum from the rest of the heart cell, placed it in a test tube, and then added calcium. The sarcoplasmic reticulum took up the calcium more slowly in samples from older animals than those from younger ones.
Subsequent studies confirmed that the sarcoplasmic reticulum--or more precisely, a protein on this organelle--removes calcium more slowly in older hearts. Researchers have found that older cells have lower amounts of this particular protein, often called the calcium pump protein because it removes the calcium in a series of repeated movements. In essence, the sarcoplasmic reticulum removes calcium from the inner fluid more slowly in older hearts because there are fewer pumps, and those that remain don't work as well because of communication breakdowns between the brain and the heart.
If these pumps aren't working properly or have shut down, the sarcoplasmic reticulum won't fill as well as it should with calcium, and there won't be enough calcium to fulfill the heart cells' needs, particularly during exercise or stress.
Once scientists learned about the pump protein, the next question was about that protein's gene. Proteins make up a huge category that includes enzymes, growth factors, hormones--almost all the substances that are responsible for the day-to-day functioning of living organisms. Proteins are produced by genes in the nucleus of every cell. Each protein has its own gene. Cells translate gene codes into proteins through a complex, multistep process called gene expression. Any alteration in this process can lead to changes in the end product, the protein.
In the case of the pump protein, the gene that produces it is only about half as active in older hearts as in younger hearts. The end result of all of these changes is a decline with age in the maximum strength of the heart beat during strenuous activity. Reduced calcium pumping also prolongs the time it takes for heart cells--and in turn, the heart as a whole--to return to a relaxed state. As a consequence, the heart can't fill with blood as readily as it once did and prepare for the next heart beat.
Like other changes, the longer calcium transient appears to be one way that the heart adjusts to age, or more specifically to the stiffer arteries that accompany aging. Unfortunately, like those other changes, this adjustment also has a cost.
"It makes sense from an engineering standpoint to have a longer contraction if you're pumping blood into stiffer vessels," Dr. Lakatta says. "The downside is that when you alter the dynamics of calcium, various stresses can more easily throw the calcium out of balance. One consequence of this is that an older person is more apt to feel short of breath during vigorous exercise."
Age Lengthens Action Potential
In addition to calcium transit, two other clusters of events in myocytes seem to be affected by age. One is the action potential. This is a transient alteration in the amounts of positive and negative charges on either side of the myocyte membrane. As mentioned earlier, the action potential triggers the opening of sodium and then calcium channels in the membrane.
The action potential is prolonged in older hearts and may contribute to the longer calcium transient. This occurs because as the heart ages, there are coordinated declines in both the activity and number of proteins involved in the action potential as well as the proteins that respond to its signals. A longer action potential generates a longer calcium transit, which in turn, produces a longer contraction. Each of these processes is controlled by specific proteins.
The prolonged action potential helps older hearts work well in most situations. It does this in two ways. First, pores on the myocyte's membrane stay open longer to allow more calcium to enter the cell between beats. Second, the proteins that carry calcium out of the cell and sodium back in work more slowly. The net result is that more calcium is available within the cell. These effects allow the weaker sarcoplasmic reticulum--which has fewer pumps--to load up on calcium in preparation for the next beat. But these adjustments, like so many other cardiovascular adaptations, may have a downside. For instance, in an aging heart the long action potential adaptation works well at slower heart rates. But during a rapid heart rate, the longer action potential contributes to calcium dysregulation of myocytes. As a result, the older heart doesn't respond as dynamically to the needs of the body as a young heart. So, a prolonged action potential is yet another possible reason that an older person usually can't do as much exercise as someone younger.
Contractile Proteins
The other mechanisms that change with age involve contractile proteins--actin, myosin, troponin, and others--that interact to shorten, or contract, the myocyte. These contractile proteins pass through a series of steps, triggered by calcium, which bring actin and myosin together into crossbridges. The crossbridges use energy released during the transaction to shorten the cell. With age, one part of the crossbridge alters--the part called the myosin heavy chain.
The myosin heavy chain can be produced in two slightly different forms, one dubbed alpha, the other beta. In experimental animals, the alpha myosin heavy chain decreases with age, while the beta increases. The same seems to be true in the human atrium. When the proportion of alpha myosin heavy chain is reduced in isolated cells, the contraction speed is slower.
Changes in the myosin heavy chain have been traced back to the genes involved--alpha is expressed less with age, beta more. The expression of these genes is regulated by proteins called transcription factors that start or regulate the first steps of cellular reproduction. One of the transcription factors for the myosin gene is the same as that for the sarcoplasmic reticulum pump, suggesting that there is a common aging link between the two cellular mechanisms. Studies in rodents suggest the activity of these factors declines with age. Because of these changes the expression of genes in the aging heart tends to go back to patterns of gene expression seen in the fetus.
These age-related changes in myosin and other contractile proteins, in conjunction with alterations in calcium transit and action potential, actually help the older heart work more efficiently. That's because slower and longer contractions don't use as much energy. Prolonged contractions also allow the older heart to eject blood into the arteries later in the heartbeat. This adaptation is good because it improves the blood flow through an older person's stiffer arteries.
Free Radical Damage
Myocytes produce free radicals, unstable oxygen molecules that can disrupt a cell's inner workings. As the heart ages, these free radicals can greatly alter how well the cellular calcium pumps on the sarcoplasmic reticulum work.
In myocytes, most free radicals are produced in tiny cellular organelles called mitochondria and by an enzyme in cell membranes called NADPH oxidase. Mitochondria convert oxygen and food into an energy-releasing molecule that powers most cellular processes. But during this process they also produce potentially harmful byproducts such as oxygen free radicals. A free radical can be produced by almost any molecule when it loses an electron from one or more of its atoms. In heart muscle cells, they are commonly created when mitochondria combine oxygen with hydrogen to form water. Free radicals can cause extensive damage to proteins,membranes, and DNA. As we age, mitochondria become less efficient, progressively generating less energy-releasing molecules and more free radicals.
In the aging heart, free radicals damage proteins, membranes, and calcium pumps on the sarcoplasmic reticulum that myocytes need to produce contractions. As a result of this cellular damage, myocytes can't process calcium as well. As calcium builds up in the cell, it can begin to contract erratically, causing an arrhythmia. If this arrhythmia spreads to other cells, it can eventually disrupt beating throughout the heart and lead to serious complications.
Nitric Oxide
Calcium isn't the only factor that helps the heart respond to the body's increased need for blood and oxygen during sustained exertion or times of stress. Nitric oxide, a potent chemical messenger that helps regulate blood flow in the arteries, also signals the heart to pump harder at critical times.
As we just learned, heart cells can increase their contraction force by releasing more calcium from the sacroplasmic reticulum. Once released from this cellular storage bin, calcium binds to troponin and other contractile proteins, which trigger the heart beat. The more calcium that binds to these contractile proteins, the greater the force of the contraction. But there's at least one other pathway, the Frank-Starling mechanism, that can increase the force of these contractions. This mechanism kicks in when increased blood flow into the heart stretches myocytes, signaling them to contract harder and produce more force. Normally, these two pathways work independently to tap the heart's reserve capacity. But if cell stretch is sustained for prolonged periods, the amount of calcium released into heart cells during contractions gradually increases. This suggests that some coordinating mechanism is operating to ensure that, even under duress, the heart continues to pump enough blood to the body. But what this link might be mystified scientists for many years.
Steven Sollott, MD and his colleagues at the NIA theorized that sustained cell stretch prompts an enzyme, nitric oxide synthase, to produce nitric oxide. Nitric oxide, in turn, binds to the calcium release channels in the sarcoplasmic reticulum and promotes the release of calcium into the cell.
To test this theory, the investigators conducted a series of experiments with adult rats and mice--mammals with cardiovascular systems similar to humans. Some rodents were genetically altered so they could not produce the enzyme that makes nitric oxide. Others were given drugs that blocked the production of the chemical messenger. In both cases, sustained cell stretch no longer triggered increased calcium release in heart cells. Previous studies have shown that nitric oxide levels may be diminished in heart failure and other cardiovascular diseases.
"Knowing that this nitric oxide mechanism exists and how it functions in the normal heart may help us understand what happens to it with age and disease," Dr. Sollott says. "This discovery offers scientists an opportunity to consider whether therapies that sustain or enhance the functioning of this mechanism might help aging hearts stay healthy and continue working properly."
New ideas are also emerging about two other phenomena that have puzzled gerontologists and cardiovascular scientists for decades. As heart cells get older, there are fewer of them to do the necessary work, and those that remain get bigger.
Bigger Heart Cells ...
To efficiently pump blood, the stiffness of the heart changes as it beats. When it is filling, the heart needs to be as relaxed as possible to allow blood to freely flow into it. When it contracts, it stiffens so that the pressure it exerts is greater than that found in the arteries. When this happens, blood is forced into the arteries with a minimal amount of effort. If there is a load mismatch--meaning the force differential between the heart and arteries isn't very good--the heart can't empty as well as it once did. As a result, the heart has to work harder to get blood into the arteries. If this occurs on a regular basis, some heart cells die, others enlarge, and the heart walls thicken.
This problem gradually increases as we get older. In some cases, the cells that remain enlarge up to 40 percent. The enlargement of these remaining myocytes seems to be the principal mechanism for the thickening of the heart walls--the hypertrophy--that occurs with normal aging.
Much evidence suggests that myocyte enlargement and the consequent thickening of the heart walls are ways that the heart adjusts to increased loads, especially from the growing stiffness of the arteries. Extra loads also may develop as the result of disease.
One reason cardiovascular researchers are so intrigued by myocyte enlargement is because of its possible links to disease. While enlargement seems to occur in response to aging and stiffening of the arteries, it is exaggerated by disease, such as coronary artery disease and high blood pressure. (However, enlargement occurs with high blood pressure at any age).
While myocyte enlargement seems to be one way that the heart adapts to increased loads, there is also evidence that at the oldest ages, it no longer adapts as much. Older animals, for instance, have less enlargement in response to heart overloads than younger animals. This failure or slowing of the adaptive response may explain why 80-year-olds are much more likely to experience heart failure following a heart attack than 60-year-olds.
These findings are yet another clue suggesting that specific age-associated changes in healthy hearts and blood vessels compromise their ability to respond to everyday stress and strain. In turn, these changes gradually lower the heart's resistance to certain cardiovascular conditions including left ventricular hypertrophy, atrial fibrillation, and congestive heart failure.
... But Fewer of Them
As we age, even the healthiest hearts lose cells. In a robust 70-year-old man without heart disease or high blood pressure, these age-related losses are estimated to account for up to a 30 percent reduction in the total number of myocytes in the heart. Although it's unclear whether this loss of heart cells is good or bad for the body as a whole, evidence suggests that loss of a significant number of heart cells may contribute to the decline in cardiovascular health in older people.
Cardiovascular scientists are exploring why some myocytes die while others continue to thrive. Injury, due to a lack of oxygen or ischemia, seems to be one of the prime killers. But studies suggest that programmed cell death--apoptosis--could be a significant factor as well.
Apoptosis is a process in which a cell orders itself to stop functioning, shrink, and ultimately dissolve. It has been observed in other cells in the body, where it may be a mechanism for adjusting to development or removing unwanted or potentially dangerous cells, such as cancer cells, from the body. At least one study suggests that apoptosis in the heart becomes more common with age. And other research has found that excessive apoptosis may contribute to decline in the aging cardiovascular system.
A number of molecular processes, such as increased free radical production, can activate a cell's apoptotic or self-destruct mechanism. In rodents, for instance, NIA grantee Christiaan Leewenburgh, PhD, of the University of Florida and his colleagues found that cytochrome c, a mitochrondial protein, becomes a signal for cell death if it "leaks" from the mitochondria. The hearts of older rats released greater amounts of that cell-death signal than did the hearts of younger rats. This difference may be partly responsible for the increase in heart cell death.
Cardiovascular scientists studying apoptosis are particularly interested in the role of a process called cardiac stretch. Myocytes are connected, so when one dies--for whatever reason--others must stretch to maintain the connections. As myocytes are stretched, they release chemical substances called growth factors, such as norepinephrine and angiotensin. These growth factors may not only help explain why these cells enlarge, but also why some of them die. In laboratory dishes, for instance, the same growth factors that regulate heart cell growth also trigger apoptosis in some myocytes. However, these and other growth factors may have an equally important role in a process that was once thought to be impossible: the replication and regeneration of heart cells.
The Untapped Promise of the Aging Heart
For decades it was believed that the heart had a set number of myocytes, and once one of these cells died, they couldn't be replaced. Because these cells were thought to be unable to divide, according to this view, their numbers progressively decreased with age and ultimately impaired heart function.
While this view was widely accepted, it was never proven. And now, compelling but controversial evidence raises new questions about its validity.
One of the first challenges to this dogma came in 2001 when scientists from New York Medical College in Valhalla, New York found large scale replication of heart muscle cells in two regions of the heart, and identified several other key indicators of cell regeneration. These scientists, led by NIA-grantee Piero Anversa, MD studied myocytes from the hearts of 13 patients, 4 to 12 days after their heart attacks, and from the hearts of 10 patients who did not have cardiovascular disease. Samples were obtained from the border zone near the site of the heart attack and from a more distant site from the damaged tissue.
By viewing these areas of the heart with a high resolution confocal microscope, the investigators were able to measure the expression of a protein found in the nucleus of dividing heart muscle cells. This protein is expressed during all phases of a cell's life cycle and is a strong indicator of ongoing cell division.
The scientists also obtained images of cell division and found other evidence of myocyte replication, including the formation of the mitotic spindle, and contractile ring, critical structural indicators of cell division. In comparison with normal hearts, the number of myocytes multiplying in diseased hearts was 70 times higher in the border zone and 24 times higher in the remote tissue.
But where were these new hearts cells coming from? Subsequent studies--in both animals and humans--suggested that, although most adult heart cells probably aren't able to replicate, a small core of adult stem cells might exist in the heart or in the bone marrow that are capable of replenishing and replacing damaged or dying myocytes. However, other scientists have had difficulty duplicating these results. So for now, the notion that adult stem cells can regenerate heart muscle remains a tantalizing, but unproven, possibility.
Some cardiologists theorize that adult stem cells in young hearts might be able to produce enough new myocytes to replace those that are naturally dying. In effect, these stem cells might help keep the total number of myocytes stable in the young heart. But mounting evidence suggests that even if these stem cells exist, their numbers decline with age. As a result, some scientists suspect there are fewer new heart cells to replace older ones which are dying in greater numbers due to age, injury, and other problems. So the deterioration of the older heart could be related, in part, to the inability of aging cardiac stem cells to replace dead and dying myocytes with new ones.
Gerontologists exploring this exciting new area of research have many questions, but few answers at this point. For instance, does the number of cardiac stem cells really decline with age? What role do growth factors play in regulating the activity of these cells? How are the changes in cardiac stem cells linked to other age-related alterations in the heart and arteries? Why are scientists having so much difficulty replicating the earlier findings? Are the myocytes in the heart of an 80-year-old basically the same ones present in his or her heart at birth or have the cells been gradually replaced over the years like the skin? And perhaps most importantly, if these stem cells exist, can anything be done to stimulate them to produce new myocytes that will counteract the effects of age in the older heart?
The key to answering this final question lies in learning more about stem cells and how they work. Investigators already know that stem cells have important characteristics that distinguish them from other types of cells. Unlike most cells in the body, such as skin or brain cells, which are dedicated to performing a specific function, stem cells are not specialists. But under certain physiologic or experimental conditions, they can be induced to become cells with special functions such as the beating cells of the heart muscle or the insulin-producing cells of the pancreas. Another unique characteristic of stem cells is their ability to renew themselves for long periods through cell division.
Scientists primarily work with two kinds of stem cells from animals and humans: embryonic stem cells and adult stem cells. Most of the basic science research discoveries on embryonic and adult stem cells come from research involving animals, particularly mice. Embryonic stem cells are derived from embryos. Specifically, embryonic stem cells are derived from embryos that develop from eggs that have been fertilized in vitro.
Adult stem cells typically generate the cell types of the tissue in which they reside. A blood-forming adult stem cell in the bone marrow, for example, normally produces many types of blood cells such as red blood cells, white blood cells, and platelets. Until recently, it had been thought that a blood-forming cell in the bone marrow--which is called a hematopoietic stem cell--could not give rise to the cells of a very different tissue, such as myocytes in the heart. However, a number of experiments over the last several years have raised the possibility that stem cells from one tissue may be able to make cell types of a completely different tissue, a phenomenon known as plasticity.
Because of this flexibility, stem cells hold enormous potential for cell replacement or tissue repair in heart disease and many other age-associated disorders. Gerontologists are seeking to find out if these cells will yield any practical interventions that might promote healthy aging.
"We've made substantial progress, but there is a lot more to be learned," according to Dr. Lakatta. "Finding ways to activate these cells and get them to where they are needed in the heart and ensuring that they develop into heart cells are significant challenges."
While daunting, these and other challenges are motivating gerontologists to investigate many new interventions that in the future could help keep aging hearts and arteries healthy.
As we age, for instance, pressure increases in the arteries, and this can affect the structure and function of the left ventricle. In fact, a growing number of scientists suspect that age-related changes in the blood vessels may actually instigate many of the transformations that occur in the older heart.
How a Myocyte Contracts
Action Potential
[1] Sodium (Na) channels open in membrane causing change in electrical charge.
[2] The causes surface membrane Calcium (Ca) channels to open, causing small Ca influx.
[3] Calcium binds to calcium releasing channel protein on sarcoplasmic reticulum.
[4] A large amount of calcium is released from sarcoplasmic reticulum.
[5] Calcium activates the contractile proteins. Cell contracts.
[6] Calcium disengages from the contractile proteins. Most is pumped back into the sarcoplasmic reticulum.
[7] Some calcium leaves the cell.
Cell relaxes and cycle renews.
Opposing Pressures: Heart Cavity Pressure vs. Aortic Pressure
[2] Aortic pressure, which increases as blood is pumped into it, impedes further ejection of blood from the heart.
[1] Heart cavity pressure, due to contraction of heart muscle cells within the wall, is exerted against blood.
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|Title Annotation:
|Aging Hearts & Arteries: A Scientific Quest
|Nuland, Sherwin
|Pamphlet by: National Institute on Aging
|Nov 1, 2007
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How Is It That A Random Comment On Reddit Leads To Your Friend Getting Tracked By The FBI?
from the that-doesn't-seem-right deptLast week, we wrote about the guy who found an FBI tracking device on his car. His friend then posted the pics to Reddit, leading the FBI to show up at the original guy's house, demanding the tracking device back. One odd part of the story is that in the discussion that ensued, the law enforcement agents showed the guy a post his friend (the one on Reddit) had made. This is how Wired described that part of the story:
Afifi retrieved the device from his apartment and handed it over, at which point the agents asked a series of questions -- did he know anyone who traveled to Yemen or was affiliated with overseas training? One of the agents produced a printout of a blog post that Afifi's friend Khaled allegedly wrote a couple of months ago. It had "something to do with a mall or a bomb," Afifi said. He hadn't seen it before and doesn't know the details of what it said. He found it hard to believe Khaled meant anything threatening by the post.Someone in our comments quickly pointed out that the "blog post" in question was actually a comment on Reddit that was in response to a discussion about silly security procedures, and the entire comment reads:
"He's a smart kid and is not affiliated with anything extreme and never says anything stupid like that," Afifi said. "I've known that guy my whole life."
bombing a mall seems so easy to do. i mean all you really need is a bomb, a regular outfit so you arent the crazy guy in a trench coat trying to blow up a mall and a shopping bag. i mean if terrorism were actually a legitimate threat, think about how many fucking malls would have blown up already.. you can put a bag in a million different places, there would be no way to foresee the next target, and really no way to prevent it unless CTU gets some intel at the last minute in which case every city but LA is fucked...so...yea...now i'm surely bugged : /I'm having trouble seeing how anyone could read that and think there's anything suspicious at all about it. But, as Bruce Schneier notes, what's really bizarre is how that comment doesn't just lead to the guy being tracked, but his friend having his movements tracked.
If they're doing this to someone so tangentially connected to a vaguely bothersome post on an obscure blog, just how many of us have tracking devices on our cars right now -- perhaps because of this blog?Schneier also wonders how many people are combing through the depths of sites like Reddit to totally misread comments out of context, and then using them to start surveilling someone's whereabouts.


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Modernist-looking Rovaniemi is the capital of Finnish Lapland and there's one reason for its fame
It's not its reindeer antler-style town layout. It's not its month-long midnight sun in summer or aurora borealis in winter. It's Santa. There are few better places on earth to meet the great man than here – and few other reasons to come this far north and experience weather this cold!
As you'd expect, Santa's hometown is a very special spot to pick up gifts and other Christmassy goodies. Meet the man himself, then explore his Christmas House shop at the Santa Claus Village (T�htikuja 2). Rovaniemi Tourist Information (Lordi's Square) also stocks locally made sweets, candles, Arctic dolls, ceramics and more. There are also several decades-old workshops in Rovaniemi. Try Lauri-tuotteet Oy (Pohjolankatu 25) for antler and wooden goods, Marttiini Knives (Vartiokatu 32) for beautifully crafted blades, and Taiga-Koru (Santa Claus Village) for gold jewellery.
Food & Drink
Rovaniemi boasts some truly unique eateries. For starters, the winter Igloo Restaurant at Snowland (Kajaanintie 1) serves steaming hot food on ice-sculpted tables under a snow-packed roof. Hilltop restaurant Sky Ounasvaara (Lapland Hotel Sky, Ounasvaara) is also one of north Finland's top restaurants, with a romantic atmosphere and spectacular views. Back in the town centre, tourist-friendly Restaurant Nili (Valtakatu 20) plays on the Lappish theme with reindeer hides, S�mi music and typical dishes on the menu. At the budget end, Kauppayhti� (Valtakatu) is a quirky little retro caf� with unfussy food and a young clientele.
Santa Claus Marathon
Rovaniemi's Santa Claus Marathon is not a race between red-clad and red-faced Santas, as the name suggests. This is actually a fairly standard marathon, though it starts at Santa's workshop watched over by the man in red, and passes over the Arctic Circle.
Men's 100m
The Men's 100m is a light-hearted romp through Rovaniemi's pedestrian heart on the first weekend of August. Young and old take part in the race, with varying degrees of seriousness, and plenty of amber refreshments to ease sore muscles.
Thousands of music fans descend on Rovaniemi for this two-day rock festival in the open air, making the most of the long hours of sunlight.
This week-long folklore festival celebrates Lappish S�mi culture, music and traditions as well as providing a stage for international performers.
Grand Opening of Christmas Season
It's Christmas time all year round in Rovaniemi, but the Santa-mania builds to a crescendo at the end of November, when the big man and his elves officially open the Christmas season at Santa Claus Village on the Arctic Circle.
The capital of Lapland, Rovaniemi has a wide choice of hotels. Santa's Hotel Santa Claus (Korkalonkatu 29) is a stylish four-star choice in the heart of town and isn't nearly so kitsch as the name implies. Santa Claus Holiday Village (T�htikuja 2), on the other hand, goes all out with sleigh bells and Christmas sparkle, and can arrange Santa himself to visit your cabin with gifts at any time of year. Skiers can glide right up to their cottage at mid-range Ounasvaaran Pirtit (Antinmukka 4) in the Ounasvaara Ski Centre, a short drive outside town, while budget accommodation is available at Santa's Hostel Rudolf (Koskikatu 41-43).


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The Segway company owner who died after a fall involving one of the two-wheeled transporters had just donated 1,000 Segways to be used by wounded American military troops, an advocacy agency official said Thursday.
Jimi Heselden was scheduled to be honored at a ceremony next week for the donation valued at $5 million. But Heselden, 62, the chairman of the British firm HESCO Bastion Ltd., plunged to his death Sept. 26 after riding an all-terrain Segway over a 30-foot cliff into the River Wharfe in England.
"We were so looking forward to thanking Jimi in person and are pained that we will not be able to do so," said Jerry Kerr, president and co-founder of Disability Rights Advocates for Technology, or DRAFT. "Jimi's tragic death is a staggering loss."
The organization sponsors the Segs4Vets program that provides Segways to help military veterans become mobile.
Forty-eight veterans, including many receiving treatment at the U.S. Army's Walter Reed Medical Center, are scheduled to receive the first of the Segways on Oct. 6. at the Marine Corps War Memorial. The program has distributed more than 500 Segways in the past five years to veterans of Iraq and Afghanistan who have sustained injuries limiting their ability to walk.
Kerr dismissed suggestions that Heselden's death raised new questions about the safety of Segways, and also warnings from a coincidental report released Monday that found rising numbers of Segway injuries reported at a Washington, D.C.,-area emergency room.
"The Segway is among the safest, if not the safest, mobility devices out there," said Kerr.
Heselden, who was chairman and creator of the British firm HESCO Bastion Ltd., bought the Segway company less than a year ago from U.S. inventor Dean Kamen. Company officials said there are no further details available about Heselden's death.


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Family rooms satisfy their multi-functional theme best by balancing the needs of every family member. To achieve that goal, make sure there's good lighting, kid-friendly furnishings and "zoned" areas for different activities.
Most often, family rooms are located adjacent to the kitchen - the hub of the household - or in a finished basement. They frequently double as a great room used for entertaining as well as an activity center and a place for adults to relax once the kids are tucked in for the night.
Setting Up Seating
For homeowners who entertain a lot, a multi-purpose room is an ideal space where guests can circulate and socialize with different groups. The room design may include different clusters of seating to allow one-on-one conversations as well as space for a larger group. A variety of seating options may include sofas, a small table with dining chairs and niche settings with soft seating and end tables.
In a large room, home decorators shouldn't skimp on the scale of their furniture pieces. Leaving large gaps in a basement family room that stretches across a long expanse of the home will make the room seem cavernous and uninviting, while big furnishings will command attention and create an unexpected coziness for a space so large.
Light and Warm
Bringing in natural light throughout the room without compromising privacy can be achieved with a variety of window treatments that fit different functions. Window shades are often better at reducing glare on large-screen TVs and computers, while softer window treatments can be coordinated with the overall decorating scheme.
Installing radiant floor heating in a family room ensures a comfortably warmed gathering place with just the flick of an electric switch. There is no duct system required, and radiant heat works well with a variety of flooring types.
Unity in Design
According to the Boston Globe magazine, furniture pieces in the same style can be spread throughout the room or homeowners can have a mix of furnishings that are pulled together in other ways.
"Unify the space with color, pattern, and texture," Boston interior designer Eric Roseff told the Globe. "Perhaps there are one or two accent colors that are consistent throughout the space, or you can go for an all-over monochromatic look or playfully mix patterns."
Once the uses of a family room are established, tying in art work and mementos can make it a room that is welcoming to both parents and youngsters as well as their guests.
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I'm just curious how some of the die hard comic fans feel about Superman in all his various interpretations, incarnations, and follies. I've always consider him to be a bit of a... well a dick, and well that's a more common thought than I expected:
I've rewatched the various films, both original and recuts (I probably prefer the Richard Donner Superman II, but the reuse of the first films plot device is rubbish and a real hideous mistake) and I have to say I don't mind them. Despite the crappy vision and story of returns, there's even some good points such as Kevin Spacey's Lex, and some of the imagery towards the end.
Smallville, Lois and Clarke and the early cartoon's kind of annoy me in that Superman loses some of his god like power. He seems to be crippled every couple of minutes and frankly this just ruins the character of Superman but on the plus side, plays up his alter-ego Clark Kent.
Anyway, I was reading that Christopher Nolan was working on a reboot for the franchise, which is interesting, but then I found out Zack Synder is directing:
http://www.slashfilm.com/2010/10/04/zac ... -superman/
Frankly, I think this is a mistake, and I'm not convinced that the story will be that good given its focus (reportedly) on other parts of Superman that personally I don't think the appeal lies in.
Just wondering, how does superman fit into the whole comic book world? Is he too powerful? Where does the interest lay? What is the balance between Clark Kent and Superman? Is Clark Kent just a skin or is superman the skin? He follows the opposite path to nearly all comic book characters in that Clark is the persona, where as Kal-El is the 'real' person. Do you have any hopes of this film being any good? Is the right person at the helm?


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My interest in genealogy started when I was a child. My dad's mom use to tell me that the family history book had been burned in a fire, but she knew we were related to Daniel Boone. I never forgot that, nor have I ever found the connection haha. Along with doing genealogy I spend a lot of my time doing photo restorations, namely for victims of Sandy through Care for Sandy, and also of family photos that I add to the books I write on our family history.
24 March 2012
Fearless Females - March 24 Inherited Traits
2 comments:
- Annmarie said...
Your blog is interesting and I'm nominating for the 'One Lovely Blog Award'. The award was started a little over two years ago at Works of Art by Sara and included the following rules.
Add the logo to your blog.
Link to the person from whom you received this award
Nominate 7 or more blogs
Leave a message on their blog, letting them know they are "One Lovely Blog"!
Blogging is still new to me, and I don't know how to put the logo on my blog, click on my link and you'll see the award. http://genealogymemorylane.blogspot.com/
- Amy Crooks said...
Thank you


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