Pretty soon the festival season will be upon us once again, and as many of you probably know, my wife Yoko and I are dedicated summer festival revelers, especially favoring those with fireworks. All we are waiting for is an end to rainy season!
By the end of June, the expected weather-permitting dates for most of the core festivals in Kansai will be set, and as usual I will be publishing an itinerary here. English Conversation students at the Smith's School of English in Kotoen スミス英会話 甲東園 are expecting this list soon. We are anticipating no cancelations this summer and as a result the list of festivals is likely to be long. We will focus on Hyogo, Kyoto, Osaka and Shiga Prefectures but will probably also include a few from Fukui Prefecture as well. Every year our personal favorite seems to be the Aug 16 Tsuruga Tohronagashi Festival and although we are most definitely open to having that exalted title challenged, we do expect that to happen again this year. We will therefore be including a number of worthwhile dates for Fukui Prefecture.


Summary: Shortly after takeoff, the pilot contacted the tower & advised of an engine fire. The flight was cleared to return but the aircraft crashed in the water approximately 5 miles west of the airport. In-flight fire for undetermined reasons.


text:
Raden Saleh
Artist (Indonesia)
16 K Artworks have been viewed 16,098 times.
5 Artworks have been added to favourites 5 times.
2 2 artworks.
7 7 followers.
Raden Saleh Sjarif Boestaman (1811 – 23 April 1880)[1][2] was an Indonesian Romantic painter of Arab-Javanese ethnicity who pioneered modern Indonesian art. He was considered to be the first modern artist from Indonesia (then Dutch East Indies), and his paintings corresponded with nineteenth-century romanticism which was popular in Europe at the time. He also expressed his cultural roots and inventiveness in his work.
Young Raden Saleh was first taught in Bogor by the Belgian artist A.J. Payen. Payen acknowledged the youth's talent, and persuaded the colonial government of the Netherlands to send Raden Saleh to the Netherlands to study art. He arrived in Europe in 1829 and began to study under Cornelius Kruseman and Andreas Schelfhout.
It was from Kruseman that Raden Saleh studied his skills in portraiture, and later was accepted at various European courts where he was assigned to do portraits. While in Europe, in 1836 Saleh became the first indigenous Indonesian to be initiated into Freemasonry. From 1839, he spent five years at the court of Ernest I, Duke of Saxe-Coburg and Gotha, who became an important patron.
From Schelfhout, Raden Saleh furthered his skills as a landscape painter. Raden Saleh visited several European cities, as well as Algiers. In The Hague, a lion tamer allowed Raden Saleh to study his lion, and from that his most famous painting of animal fights was created, which subsequently brought fame to the artist. Many of his paintings were exhibited at the Rijksmuseum in Amsterdam. Several of his paintings were destroyed when the Colonial Dutch pavilion in Paris was burnt in 1931.
Official Website www.raden-saleh.net/about-us.htm
Dimitra Valeonti Artist Representative (Greece)
Maria Chatzaki Artist (Greece)
Atiqur R Sumon Artist (United Kingdom)
Esraa Atef Artist (Jordan)
The Arrest of Pangeran Diponegoro
Raden Saleh (ID)
A Flood on Java 1876

redpajama_set_name: RedPajamaCommonCrawl


text:
Prost biopic to begin filming in August
F1 Fanatic Round-up
21st May 2017, 0:01 20th May 2017, 18:45 | Written by Keith Collantine
In the round-up: Filming for a biopic on the life of Alain Prost will begin in August.
Your daily digest of F1 news, views, features and more from hundreds of sites across the web:
Biopic of F1 champion Alain Prost heads to Cannes (Screen Daily)
"The 13-week shoot is due to kick off in late August at the historic Magny-Cours racetrack, the former home to Formula One racing in central France, for delivery in May 2018."
British Grand Prix at Silverstone in doubt over rising fees charged by F1 (The Guardian)
"I sincerely hope it won't be the end of grand prix racing at Silverstone but we've made clear to the Formula One management we can't live with the present contract beyond 2019."
I'm not in F1 to go to school - Stroll (Crash)
"The tyre is very hard to get working compared to some other years."
Brawn behind F1 Strategy Group attendance change (Motorsport)
"When it came to the idea of inviting those not involved in the group to attend as observers, Brawn presented it as a change that would happen, rather than one that was up for discussion and could be voted out."
Alonso's Indy attempt good for F1 - de Ferran (Racer)
"It's clearly fantastic for IndyCar, that's easy for everyone to see, but I think it's also great for Fernando and great for Formula 1 because he's already making new fans here in North America and these people will follow him wherever he goes."
McLaren plans further upgrade for Monaco (Autosport)
"In Spain we brought a new front wing, new bodywork, new floor, and new rear wing and it is correlating 95%."
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Contact F1 Fanatic
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Was fun treating my fans at Zandvoort at donuts! Hope you enjoyed it too 👍🏼 #JumboRacedagen pic.twitter.com/IB1m8IZMm2
— Max Verstappen (@Max33Verstappen) May 20, 2017
Find more official F1 accounts to follow in the F1 Twitter Directory
Does IndyCar's approach to broadcasting show the way for Formula One?
I recently cut off my cable and, here in the USA, there is no legal way for me to watch F1 online any more.
When I went to look for videos about Alonso practising and found that IndyCar had almost seven hours of video up almost as it happened, my jaw dropped. That IndyCar streams qualifying live is mind-blowing compared to F1's communications strategy.
I sure hope Liberty fixes this fast.
Lee (@Leejo)
There's still time to join in this weekend's Caption Competition here:
Caption Competition 129: Verstappen in the cockpit
From the forum
Tackle the latest question in the F1 Only Connect quiz
Happy birthday to Gv27, Kanyima, Thersqaured and Olivia Stephanie Ault!
If you want a birthday shout-out tell us when yours is via the contact form or adding to the list here.
On this day in F1
John Watson put his Brabham on pole position for the Monaco Grand Prix today in 1977
Posted on 21st May 2017, 0:01 20th May 2017, 18:45 Author Keith CollantineCategories F1 Fanatic round-upTags f1 fanatic round-up
63 comments on "Prost biopic to begin filming in August"
mfreire
21st May 2017, 0:11
There will have to be a massive make-up job to recreate Prost's massive nose. But seriously- a Prost biopic? Now that I am excited for.
And about the British GP- there has to be a way to come up with a new contract. The British GP is the second most important race on the calendar and if F1 loses that race that will be a sham of unprecedented proportions.
Ricky Johnson (@bamboo)
Theres a difference between no British Grand Prix and no Grand Prix at Silverstone. The issue we face at the moment is the latter.
Unprecedented is incorrect also. A Grand Prix (French word) hasn't been held in France since 2008. Life went on.
@bamboo, as things stand, Silverstone is the only circuit in the UK which has the necessary rating by the FIA to hold an F1 race – so cancelling a race at Silverstone is effectively equal to cancelling the British GP since there are no alternative venues.
I'm aware of that mate, but to say no Silverstone will mean no British GP is not true to an absolute degree. There are circuits all around the world which are Grade 1 capable, but are Grade 2 at present due to there being no need to maintain those standards given what races on them currently. Many of these have held F1 races in the past.
Donnington is one that comes to mind, and I would say they would have no issue getting that to a grade 1 standard if an attractive and non financial hemorrhaging F1 case was put to them.
That said, I'm sure Jonathan Palmer will be looking for revenge when his son is cut from F1, and will say no even if it makes sense.
bosyber (@bosyber)
You do recall that Donington is still working to recover from that massive debt, and the massive rework it was intended to finance to get an F1 bid that was part of a power play by Bernie to force Silverstone/BRDC to take the current contract right @bamboo?
Palmer is a business man, he will not want to hemmorage his own money to finance an F1 race – I don't think there is a realistic chance of another track taking on an F1 contract soon if Silverstone won't, the money just isn't there, especially when the government isn't going to put in money.
@bosyber, as you say, Donington have made clear that they have no interest in trying to bid for the British GP again after their attempts to upgrade the track to Grade 1 status put the circuit into administration and near complete financial collapse. The circuit has also been hit by the problems at the proposed Circuit of Wales – difficulties with raising funds for the Circuit of Wales meant that Donington, which was part of a joint bid for the MotoGP event, lost out on that event to Silverstone.
Asides from that, there is also the problem that the transport infrastructure for Donington Park is completely inadequate for holding the British GP. The original proposal to hold the British GP at Donington relied on a total ban on private transport to Donington Park, with all spectators having to travel in by bus from Nottingham, Leicester, Derby or a shuttle bus from the East Midlands Parkway station – a proposal considered dubious at best at the time.
@bamboo, as things stand, there are only three circuits in the UK which are classified as Grade 2 – Donington, Brands Hatch and Rockingham. As noted before, Donington is out of the question – as for Brands Hatch, the circuit is subjected to very strict noise emission regulations (whilst some fans seem to think that the current cars are too quiet, they would break the noise restrictions at Brands Hatch by a significant margin), which also means the circuit won't get planning permission to expand either.
Rockingham, perhaps, could be upgraded, but the circuit has really struggled to get any sort of major event at all – any other circuit in the UK, such as Snetterton, is Grade 3 and really only fit for club races and national events these days at best.
Yes, in theory you could, if you threw enough money at the problem, either upgrade an existing circuit to Grade 1 status or, at that point, create en entirely new circuit built to that standard in the first place. However, as @bosyber notes, in reality it is not economically viable.
I guess so. Having a British GP elsewhere in England would be alright. Hell, if I could have it my way I would rotate circuits for the British GP yearly (be at Silverstone one year, then go to Donington another year, a rebuilt, extended version of Brands another year and a rebuilt, extended Croft circuit another year, then back to the top of the rotation again.
The Monaco GP is still being run, so not having the French GP wasn't nearly as bad as not having a British or Italian GP's. Quite honestly the French GP lost a lot of its importance in the 1930's when Monaco started to gain prestige after only a few years of the event's existence.
Kgn11
It's interesting seeing how everyone including F1's media are so fascinated with Alonso' performance at the Indy, especially when you consider Alonso himself is no longer fascinated with F1.
… is no longer fascinated by Honda.
n0b0dy100
He's got a Honda engine behind him in that IndyCar though.
Why is it so hard to understand? Fernando Alonso is one of F1's greatest ever drivers. Whatever he chooses to do with have media attention.
22nd May 2017, 14:22
It's natural that everyone is interested in how FA does at Indy, and who says FA isn't interested in F1 anymore? And how do the two relate anyway? If FA was in fact disinterested in F1, which I doubt, does that mean people should therefore not be interested in his Indy appearance?
If Silverstone can't make good on an F1 contract, I fail to see how anywhere else can without some form of outside aid. Attendances are always high, ticket prices are too… realistically there's no space for them to increase revenues to meet the rising hosting fee.
Rather than the 'fan zone' stuff and positive words, I think what happens next with Silverstone will be our first real lesson in the way Liberty is going to run F1.
The reason indycar got "7hours" practice up for free is because no cablecompany is interested in buying content that gives them 1000 viewers. Alonso is a special case and cablecompanys cant just buy the Alonso practice sessions on demand.
GT Racer (@gt-racer)
Regarding COTD, Indycar only streams the stuff that isn't shown on TV in the US due to the same broadcaster exclusivity contracts that prevent F1 from live streaming anything.
Indycar streams practice as that isn't shown on TV & they produce it with a small team which is why it doesn't feature on-screen timing graphics & doesn't use all the available trackside or in-car cameras.
In terms of qualifying, For Indy only 1 hour (Of the scheduled 6) is scheduled to be streamed as the rest is available on TV or the ESPN3 app. The race also won't be available online legally.
For other races qualifying been streamed is dependent on if it's going to be shown on TV or not (NBC usually do, ESPN outside of Indy don't).
The Gasoline Alley stream ran all the way through qualifying and whilst it didn't show the track it did provide commentary and interviews with the drivers throughout. The IndyCar website also had live timing so between the two you're able to get a good idea of what is going on.
The race also won't be available online legally.
@gt-racer For the USA? It will for Europeans (that don't have a broadcaster), right?
@xtwl Buy the race on Espn online for 10 euro.
@Cat F1 also provide timing and commentary.
StefMeister (@stefmeister)
Sebastien Bourdais unfortunately seems like he's out of the Indy 500 with multiple fractures to his pelvis & a broken right hip after his big qualifying crash today.
https://twitter.com/IndyCar/status/866083196940595200
PeterG
Thats unfortunate :( After a great start to the year he's really had no luck the past few races.
That really was a massive hit though, for those that didn't see it-
https://www.youtube.com/watch?v=DzDpuD0iIt4
Horrifying. He's lucky to be alive after that.
schooner (@schooner)
It's really a shame. His car was looking good for the 500, and with those injuries he's probably out for the rest of the season. At the age of 38, I wouldn't even be surprised if this resulted in him calling it quits on his participation in the Indycar series. Maybe a quality seat in the WEC would be a good way for him to see out the next few years?
faulty (@faulty)
I hope the GTE pro seat bourdais has likely vacated now, this to jpm.
I'm sure Jenson is on the phone expressing interest!
I watched the qualifying, he was clearly fastest but he was loose, he had a full corner of opposite lock, caught it and speared into the wall at a 45º angle, had that been the concrete barrier, Bourdais would have been killed by the impact, so I'm not surprised he's out.
I reckon what's behind the blistering speed some teams showed; as everyone is full throttle for 4 laps, must be the mechanical set up, tyre pressures, camber and toe. Sato proudly eluded to his car "rotating" at the end of the corner, and not scrubbing speed, it's just incredible to think that even the second to last on the grid was full throttle all the way and yet far not only in Indy terms to the quickest.
@stefmeister I'm worried about Indy car's doctors. Hip and Pelvis are the same thing, the Pelvis is what is commonly referred to as the hip, and the hip is part of the Pelvis.
HEre you go Indy doctors.
Eoin (@eoin16)
@peartree you don't need to worry about the competence of the Indy Car doctors because you are very much mistaken. Your hips and pelvis are absolutely NOT the same thing and one is not a common reference for the other. You're hips are joints in your body much like your shoulders, your pelvis is not a joint. As someone who has had 4 hip surgeries (3 in the last year) trust me on this. Also, my pelvis has never been operated on.
22nd May 2017, 4:41
@eoin16 @johnmilk @pastaman http://teachmeanatomy.info/wp-content/uploads/The-Parts-of-the-Pelvic-Girdle-Hip-Bones-Sacrum-and-Coccyx.jpg
pastaman (@)
@peartree I read this one article on the internet, so I'm a doctor now.
Joao (@johnmilk)
http://www.hipandknee.com/wp-content/uploads/sites/13/2014/05/hip-anatomy.jpg
The hip is an articulation between the femoral head and a section of the pelvis called acetabulum. A hip fracture usually refers to a fracture in one of those bones. Sometimes due to impacts it is common for the femural head to punch through that socket.
A fractured pelvis isually refers to a lesion in the illiac crest. Even though it is made of a few bones, usually it is what they refer to. For example a fracture in the sacrum wouldn't be called a fractured pelvis.
Next time better search for a proper anotomy journal with fracture qualification.
I'm used to commenters pretending to know more than the drivers and teams, but I guess we can add doctors to the list now too!
Well, first, off, they're not "Indy Car Doctors", they're the trauma unit at IU Health Methodist Hospital, and they know significantly more about anatomy than your 4 color gif. Secondly, what they said was repeated by the IndyCar communications staff, and then repeated by journalists, so there's no chance of a miscommunication anywhere in there.
Oh, and Sebastien has already said he'll get back in the car as soon as possible.
He was flying out there! he could have eased off on the last two laps and would've still averaged enough to make the fast nine.
Alex McFarlane
That was a scary crash, almost a carbon copy of Gordon Smiley's violent fatal accident in 1982.
Makes you appreciate how far safety has come, even if it isn't always perfect.
Josh (@canadianjosh)
Fernando has a shot tomorrow. Wouldn't that be a story.
UNeedAFinn2Win (@uneedafinn2win)
He doesn't drink
oh, right. yes 😁
Phylyp (@phylyp)
Liberty needs to work with their broadcast partners across countries to ensure that streaming options are available – encourage the broadcast partners to provide a site where viewers can view the stream, with suitable monetization plan (e.g. practice is free for all, quali and race are paywalled for those who don't have an equivalent cable subscription, or better still, quali is free to bring eyeballs to the race). It needs to be sold to the broadcasters as a way of offering more content online, while still allowing them to offer a curated list of programmes on TV (e.g. keep the main race on TV & online, but keep added stuff like paddock walks and interviews online).
For instance, here in India, Star Sports is the broadcast partner of F1 (they syndicate a Channel 4 broadcast). The Star group of channels has an online streaming platform Hotstar that live streams all channels, and this includes quali and the race. Sadly in this case, the online platform does not get practice sessions on it, only quali/race, although they broadcast practice on TV. Nevertheless, its a start, and at INR 200 (£2.4) a month for a Hotstar subscription, it is a decent deal.
Sundar Srinivas Harish
The way they've handled the TV broadcast is stupid though. At least this year, as far as I've seen, live telecast is on Star Sports Select HD 2, but reruns are on SSS HD 1. But it is nice that the reruns are available for free on Hotstar.
Samurai (@royalz)
I have stopped paying subscribing starsports via the cable services as Hotstar is free for the jio subscribers. It's same with motogp as it's also free with Jio TV
*paying extra and subscribing
If the Silverstone directors have any analytical synapses – and we'll soon see if they do – they would trigger the escape clause today. Regardless of whether or not Liberty will reduce the hosting fee, and they won't at least not materially, Silverstone has a much bigger problem through 2026, which is that Lewis Hamilton is almost certainly going to leave F1 during that period. And if Silverstone thinks ticket revenues don't cover the sanction fee today, just wait until Lewis retired from F1; then they will really discover how far ticket revenue can fall short of the sanction fee.
Jose Bruna
Lack of free to air to coverage will kill the sport.i have been saying this for years and it is something Liberty need to sort out first before anything else
Why is there no news here… Fernando just qualified P3 at indy 500 yesterday. Now he'll be in the "fast 9" or whatever they call it, trying to get pole. :D just watched his laps on Youtube… YOUTUBE!
https://www.youtube.com/watch?v=oKIiv0VdhSA
Exciting, 370kph average speed, close to the walls. 2 Milion people watched his practice sessions on youtube. 2 Milion viewers is more than most F1 races get in UK.
Youtube > PayTV
@jureo, well apart from monetisation – I have to say, I really enjoyed Formula e when it wasn't on TV in Germany, as I could follow it fia the FIA formula e site – now I have to look for it. Found out recently that it has been on Eurosport, but now on DMAX – good I have that, but I only found the channel after the Monaco GP was done. It is annoying, and I just forgot about looking up where to watch it, just followed it occasionally via twitter. That just does not work. I'll enjoy it live when I go to the E-prix here in Berlin, but I more or less gave up following the season.
@bosyber
Same here in Sweden. First year they aired on the same channels as F1 which was great. Second it just dissapeared but i was able to follow it on free FIA streams. This year it airs on Eurosport so i payed extra to get those channels only to find out most of it is only shown on their webbased channels which apperently is an entierly different thing so i gave up. Im not gonna pay them anything more until they sort their mess out.
At least they put up the reruns on Youtube a week delayed so i will just have to stay spoilerfree.
Firstly, @jureo , Alonso qualified 7th yesterday, not 3rd. Secondly, at the time (UK time) when he did so, it was about the same time this goes live. Keith was commentating at the time (I heard him), so probably didn't have time to update the round up in the 1 minute available before publication.
Aha, see I have to go by Youtube news, hence my news was incorrect.
As for Keith, that is an understandable reason.
Todfod (@todfod)
@jureo
I'm surprised there isn't any mention of it on F1fanatic. It's quite a massive achievement by him to make it in to the top 9. Crazy to think that he took the McGarbage bin in F1 to P7 in Spain and then next weekend put another papaya colour car in to the top 7 in another racing series altogether.
I never doubted that Alonso would cut it with the cream of the crop in Indy.. and I'm pretty sure he's a strong contender for the win as well. Completely worth missing out on Monaco if you ask me.
Simon (@weeniebeenie)
I certainly don't want to lose a British GP but it's hard to feel sympathy for Silverstone, they were the ones who agreed to this contract where the fees raise each year. They knew this was coming.
@weeniebeenie As opposed to not hosting it at all?
Well that would have been up to Bernie or whoever was on the negotiating table, could they afford to lose the British GP? If the answer was no, Silverstone really shouldn't have put themselves into this position and agree the deal, they held all the chips with no other viable options. Donington went wrong with no chance of recovery, nothing else was possible. It was Silverstone or bust, and they must've known that. If Bernie was willing to let a British GP go, and it was this deal or bust, well then fair enough. They signed up with the devil what they felt they had to, but still, they did know this was coming from the day they signed it.
Stroll has something very Maldonado-ish about him. I think it's the fact that they both couldn't admit that they've put in poor performances… and that they like to completely ignore the fact that they need to learn and improve before anyone takes them seriously.
@todfod So I guess you didn't read the article then where he talks about learning.
Liberty won't let Silverstone go, how could they? They keep talking about making each race weekend a festival, well Silverstone is one venue that doesn't need any tweaking at all. It's what F1 should be about.
Fantastic news about Prost one of my favorite all time drivers. Can't wait, it should be very interesting. Also Ocon must be feeling very happy he is getting the approval from the Professor.
I'll never forget the scene from Sennas documentary when Prost ran up to the stewards like a little whining child so he could be "champion".
23rd May 2017, 2:34
If that is all you can remember about Prost then you really do not know racing. He was a lot more then that. He drove with the finesse of a computer something very few can do.
paulguitar
@canadianjosh
That's the problem with that film though. Much as I enjoyed it, it is painfully one-sided.
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                    url: 'JQGridHandler.ashx',
                    contentType: "application/json; charset=utf-8",
                    data: { USER_ID: $("#hdnUserId").val(), PERSON_ID: $("#PersonId").val(), USER_TYPE: $("#chkAdmin").is(":checked"),
                        USER_NAME: $("#txtUserName").val(), USER_PASSWORD: $("#txtPassword").val(),
                        USER_LOCK: $("#chkActive").is(":checked"), ActionPage: 'SecurityUser', Action: 'Update'
                    },
                    dataType: "json",
                    success: function (data) { }

                });
            }
            $("#btnAdd").click(function () {
                add();

             //$("#list").jqGrid("reloadGrid");

            });
            $("#btnUpdate").click(function () {
                update();
            });
        });

and html form For create jqGrid and popup panel

                       FullName

                        <input type="text" id="txtFullName" />

                        PersonId

                        <input type="text" id="PersonId" />

                        <input type="checkbox" id="chkAdmin" />IsAdmin?

                       UserName

                        <input type="text" id="txtUserName" />

                       Password

                        <input type="password" id="txtPassword" />

                        <input type="checkbox" id="chkActive" checked="checked" />IsActive

                        <input id="btnAdd" type="button" value="Add" />
                        <input id="btnUpdate" type="button" value="Edit" />

                        <input id="hdnUserId" type="hidden" />

i want when user click in btnAdd and record insert in database jqGrid data reload(I want refresh jqGrid data). but i get 2  errors
 Error: no element found
    Source File: http://localhost:1041/Clerance_New/JQGridHandler.ashx?PERSON_ID=1001&USER_TYPE=false&USER_NAME=tttt&USER_PASSWORD=tttt&USER_LOCK=true&ActionPage=SecurityUser&Action=Insert
    Line: 1

and
Error: uncaught exception: jqGrid - No such method: reloadGrid

and for reload in ?????? line not run server side code in handler, I do not know why.
please help me. thanks all

A: I am not sure why you wrote relatively complex code instead of usage standard form editing, but it should be sure some important reason.
The code
$("#list"). $("#list").jqGrid("reloadGrid");

is definitively wrong. The correct code you have commented for some reason
$("#list").trigger("reloadGrid", [{current: true}]);

Moreover it's important to place the call inside of success callback of the corresponding $.ajax request inside of add or update functions which you use.
UPDATED: I've seen now that you used loadonce: true option. It means that the data will be loaded from the server once. After the first loading the value of datatype will be changed to 'local'. The next reload of the grid will be done locally. If you need to reload the data one more time from the server you have to reset datatype to it's initial value ('json' in your case) and only then reload the grid. See the answer for details.

redpajama_set_name: RedPajamaStackExchange


text:
'Dracula Untold' Trailer Strikes a Deal with Satan
In theaters October 17, Dracula Untold was filmed in Belfast, giving the film a very convincing look. This version of the ultimate vampire deals with a [...]
What's That Creepin' Around the Corner? It's 'Hemlock Grove' Season Two
Remember the Emmy nominated Netflix original horror series, Hemlock Grove? Well, the show is back with a second season Friday, July 11 at 12:01 PM PT. I can barely believe [...]
Guillermo del Toro's "The Strain" is Headed to FX
This is welcome horror news. Variety announced FX has ordered a 13 episode run of The Strain. The series is based on del Toro's Dark Horse Comic title of the same name. [...]
"Night Watch" (2004) Movie Review
Written & Directed bv Timur Bekmambetov Starring: Konstantin Khabenskiy, Vladimir Menshov, Mariya Poroshina A fantasy-thriller set in present-day Moscow where the [...]
' Interview with the Vampire: The Vampire Chronicles' (1994) Movie Review
Directed by Neil Jordan Written by Anne Rice Starring: Brad Pitt, Tom Cruise, Antonio Banderas, Kirsten Dunst, and Christian Slater A vampire tells his epic life story: love, [...]
'Salem's Lot' (1979) Movie Review: Terror That Still Haunts Me 34 Years Later
Directed by Tobe Hooper Novel written by Stephen King – Screenplay by Paul Monash Starring: David Soul, James Mason, Lance Kerwin, Bonnie Bedelia, Reggie Nalder, and Fred [...]
"Supernatural" Season 9 "I Think I'm Gonna Like It Here" E901 Extended Promo
September 18, 2013 // 1 Comment
The ninth season of Supernatural premieres 10/8 on the CW and I could be none the happier. I've followed the Winchester brothers the previous eight seasons and feel [...]
True Blood "Radioactive" Season Finale Review
Just when you think there isn't a formerly cool show worse than Dexter, True Blood Season Six shook its tits into our lives. Maypoles? Wtf, True Blood. My biggest issue [...]
Next on the True Blood Season Six Finale: "Radioactive"!
Is it finale time already? Awesome. Now I can concentrate on Dexter, Newsroom, Ray Donovan, and the king of Sunday night shows: the untouchable Breaking Bad. Anyway, this [...]
"Byzantium" (2012) Movie Review: Moody & Compelling, Yet Somehow Super Boring?
Directed by Neil Jordan Written by Moira Buffini Starring: Saoirse Ronan, Gemma Arterton, and Caleb Landry Jones Residents of a coastal town learn, with deathly consequences, [...]
Great News for Fans of Terrible Television Shows!
Michael Lombardo, president, HBO Programming has announced that the whacky characters from True Blood will be back again next summer for a seventh season. Someone asked me [...]


As Chinese fakes go, this is as outrageous as it gets.
A factory in Wenzhou has been pumping out fake gold bars carrying the insignia of Australia's highly respected Perth Mint.
Like a knockoff Coach bag, the resemblance isn't perfect… but the kicker is that the bars — surprise, surprise — aren't made of gold. Or not much gold. "First, we did the silver plating, then the gold plating," a worker told an undercover reporter from Australia's Seven Network.
Gold at $1 an ounce!
The reporter paid A$300 for 300 bars. The real thing would have been worth A$510,000.


text:
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    Form.__entityName="org.shaolin.bmdp.workflow.form.SessionVarDefinitionTable";

    Form.init();
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        var o = this;
        var UIEntity = this;

        var constraint_result = this.Form.validate();
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        new UIMaster.ui.dialog({dialogType: UIMaster.ui.dialog.CONFIRM_DIALOG,message:WORKFLOW_COMFORMATION_MSG,messageType:UIMaster.ui.dialog.Warning,optionType:UIMaster.ui.dialog.YES_NO_OPTION,title:'',height:150,width:300,handler: function() {

        // cal ajax function.

        UIMaster.triggerServerEvent(UIMaster.getUIID(eventsource),event,UIMaster.getValue(eventsource),o.__entityName);

        }
        }).open();
    }/* Gen_Last:org_shaolin_bmdp_workflow_form_SessionVarDefinitionTable_invokeDynamicFunction */

redpajama_set_name: RedPajamaGithub


text:
Comparison of Characteristics Among Persons With and Without Hypertension in 918 Subjects Followed Up Prospectivelya
Data Relating Hypertension and the Risk of Incident MCIa
Data From General Estimating Equations Relating Hypertension to Change in Cognitive Scores With Time
Bischkopf JBusse AAngermeyer M Mild cognitive impairment: a review of prevalence, incidence, and outcome according to current approaches. Acta Psychiatr Scand 2002;106 (6) 403- 414PubMedGoogle ScholarCrossref
Petersen RCDoody RKurz A et al. Current concepts in mild cognitive impairment. Arch Neurol 2001;58 (12) 1985- 1992PubMedGoogle ScholarCrossref
Petersen RCStevens JCGanguli MTangalos EGCummings JLDeKosky ST Practice parameter: early detection of dementia: mild cognitive impairment (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56 (9) 1133- 1142PubMedGoogle ScholarCrossref
Larrieu SLetenneur LOrgogozo JM et al. Incidence and outcome of mild cognitive impairment in a population-based prospective cohort. Neurology 2002;59 (10) 1594- 1599PubMedGoogle ScholarCrossref
Petersen RCSmith GEWaring SCIvnik RJTangalos EGKokmen E Mild cognitive impairment: clinical characterization and outcome. Arch Neurol 1999;56 (3) 303- 308PubMedGoogle ScholarCrossref
Kivipelto MHelkala ELLaakso MP et al. Midlife vascular risk factors and Alzheimer's disease in later life: longitudinal, population based study. BMJ 2001;322 (7300) 1447- 1451PubMedGoogle ScholarCrossref
Launer LJRoss GWPetrovitch H et al. Midlife blood pressure and dementia: the Honolulu-Asia aging study. Neurobiol Aging 2000;21 (1) 49- 55PubMedGoogle ScholarCrossref
Guo ZViitanen MFratiglioni LWinblad B Low blood pressure and dementia in elderly people: the Kungsholmen project. BMJ 1996;312 (7034) 805- 808PubMedGoogle ScholarCrossref
Morris MCScherr PAHebert LE et al. The cross-sectional association between blood pressure and Alzheimer's disease in a biracial community population of older persons. J Gerontol A Biol Sci Med Sci 2000;55 (3) M130- M136PubMedGoogle ScholarCrossref
Qiu Cvon Strauss EFastbom JWinblad BFratiglioni L Low blood pressure and risk of dementia in the Kungsholmen project: a 6-year follow-up study. Arch Neurol 2003;60 (2) 223- 228PubMedGoogle ScholarCrossref
Di Bari MPahor MFranse LV et al. Dementia and disability outcomes in large hypertension trials: lessons learned from the Systolic Hypertension in the Elderly Program (SHEP) trial. Am J Epidemiol 2001;153 (1) 72- 78PubMedGoogle ScholarCrossref
Forette FSeux MLStaessen JA et al. Prevention of dementia in randomised double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial. Lancet 1998;352 (9137) 1347- 1351PubMedGoogle ScholarCrossref
Kalaria RN The role of cerebral ischemia in Alzheimer's disease. Neurobiol Aging 2000;21 (2) 321- 330PubMedGoogle ScholarCrossref
Vermeer SEPrins NDden Heijer THofman AKoudstaal PJBreteler MM Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med 2003;348 (13) 1215- 1222PubMedGoogle ScholarCrossref
Petrovitch HWhite LRIzmirilian G et al. Midlife blood pressure and neuritic plaques, neurofibrillary tangles, and brain weight at death: the HAAS. Neurobiol Aging 2000;21 (1) 57- 62PubMedGoogle ScholarCrossref
Sparks DLScheff SWLiu H et al. Increased density of senile plaques (SP), but not neurofibrillary tangles (NFT), in non-demented individuals with the apolipoprotein E4 allele: comparison to confirmed Alzheimer's disease patients. J Neurol Sci 1996;138 (1-2) 97- 104PubMedGoogle ScholarCrossref
Tang MXStern YMarder K et al. The APOE-ε4 allele and the risk of Alzheimer disease among African Americans, whites, and Hispanics. JAMA 1998;279 (10) 751- 755PubMedGoogle ScholarCrossref
Stern YAndrews HPittman J et al. Diagnosis of dementia in a heterogeneous population: development of a neuropsychological paradigm-based diagnosis of dementia and quantified correction for the effects of education. Arch Neurol 1992;49 (5) 453- 460PubMedGoogle ScholarCrossref
Pittman JAndrews HTatemichi T et al. Diagnosis of dementia in a heterogeneous population: a comparison of paradigm-based diagnosis and physician's diagnosis. Arch Neurol 1992;49 (5) 461- 467PubMedGoogle ScholarCrossref
Folstein MFFolstein SEMcHugh PR "Mini-Mental State": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12 (3) 189- 198PubMedGoogle ScholarCrossref
Kaplan EGoodglass HWeintraub S Boston Naming Test. Philadelphia, PA: Lea & Febiger; 1983
Benton A FAS Test. Victoria, BC: University of Victoria; 1967
Goodglass HKaplan E The Assessment of Aphasia and Related Disorders, 2. Philadelphia, PA: Lea & Febiger; 1983
Wechsler D Wechsler Adult Intelligence Scale–Revised. New York, NY: Psychological Corp; 1981
Mattis S Mental Status Examination for Organic Mental Syndrome in the Elderly Patient. New York, NY: Grune & Stratton; 1976
Rosen W The Rosen Drawing Test. Bronx, NY: Veterans Administration Medical Center; 1981
Benton A The Benton Visual Retention Test. New York, NY: Psychological Corp; 1955
Buschke HFuld PA Evaluating storage, retention, and retrieval in disordered memory and learning. Neurology 1974;24 (11) 1019- 1025PubMedGoogle ScholarCrossref
Golden RRTeresi JAGurland BJ Development of indicator scales for the Comprehensive Assessment and Referral Evaluation (CARE) interview schedule. J Gerontol 1984;39 (2) 138- 146PubMedGoogle ScholarCrossref
Gurland BGolden RRTeresi JAChallop J The SHORT-CARE: an efficient instrument for the assessment of depression, dementia and disability. J Gerontol 1984;39 (2) 166- 169PubMedGoogle ScholarCrossref
Blessed GTomlinson BERoth M The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. Br J Psychiatry 1968;114 (512) 797- 811PubMedGoogle ScholarCrossref
Stricks LPittman JJacobs DMSano MStern Y Normative data for a brief neuropsychological battery administered to English- and Spanish-speaking community-dwelling elders. J Int Neuropsychol Soc 1998;4 (4) 311- 318PubMedGoogle Scholar
American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994
Hughes CPBerg LDanziger WLCoben LAMartin RL A new clinical scale for the staging of dementia. Br J Psychiatry 1982;140566- 572PubMedGoogle ScholarCrossref
McKhann GDrachman DFolstein MKatzman RPrice DStadlan EM Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34 (7) 939- 944PubMedGoogle ScholarCrossref
Kleinbaum DKlipper LMuller K Applied Regression Analysis and Other Multivariable Methods. 2nd ed. Boston, MA: PWS-Kent; 1988
Hatano S Experience from a multicentre stroke register: a preliminary report. Bull World Health Organ 1976;54 (5) 541- 553PubMedGoogle Scholar
Hixson JEVernier DT Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. J Lipid Res 1990;31 (3) 545- 548PubMedGoogle Scholar
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Census of Population and Housing Summary Tape File 1: Technical Documentation [computer program]. Washington, DC: Bureau of Census; 1991
Skoog I The relationship between blood pressure and dementia: a review. Biomed Pharmacother 1997;51 (9) 367- 375PubMedGoogle ScholarCrossref
Luchsinger JAReitz CHonig LSTang MXShea SMayeux R Aggregation of vascular risk factors and risk of incident Alzheimer disease. Neurology 2005;65 (4) 545- 551PubMedGoogle ScholarCrossref
Lopez OLJagust WJDulberg C et al. Risk factors for mild cognitive impairment in the Cardiovascular Health Study Cognition Study: part 2. Arch Neurol 2003;60 (10) 1394- 1399PubMedGoogle ScholarCrossref
Solfrizzi VPanza FColacicco AM et al. Italian Longitudinal Study on Aging Working Group, Vascular risk factors, incidence of MCI, and rates of progression to dementia. Neurology 2004;63 (10) 1882- 1891PubMedGoogle ScholarCrossref
Tervo SKivipelto MHanninen T et al. Incidence and risk factors for mild cognitive impairment: a population-based three-year follow-up study of cognitively healthy elderly subjects. Dement Geriatr Cogn Disord 2004;17 (3) 196- 203PubMedGoogle ScholarCrossref
Petersen RC Mild cognitive impairment as a diagnostic entity. J Intern Med 2004;256 (3) 183- 194PubMedGoogle ScholarCrossref
Hu GSarti CJousilahti P et al. The impact of history of hypertension and type 2 diabetes at baseline on the incidence of stroke and stroke mortality. Stroke 2005;36 (12) 2538- 2543PubMedGoogle ScholarCrossref
Posner HBTang MXLuchsinger JLantigua RStern YMayeux R The relationship of hypertension in the elderly to AD, vascular dementia, and cognitive function. Neurology 2002;58 (8) 1175- 1181PubMedGoogle ScholarCrossref
DeCarli C The role of cerebrovascular disease in dementia. Neurologist 2003;9 (3) 123- 136PubMedGoogle ScholarCrossref
Luis CALoewenstein DAAcevedo ABarker WWDuara R Mild cognitive impairment: directions for future research. Neurology 2003;61 (4) 438- 444PubMedGoogle ScholarCrossref
Skoog ILernfelt BLandahl S et al. 15-Year longitudinal study of blood pressure and dementia. Lancet 1996;347 (9009) 1141- 1145PubMedGoogle ScholarCrossref
Farmer MEKittner SJAbbott RDWolz MMWolf PAWhite LR Longitudinally measured blood pressure, antihypertensive medication use, and cognitive performance: the Framingham Study. J Clin Epidemiol 1990;43 (5) 475- 480PubMedGoogle ScholarCrossref
Rothman KJ No adjustments are needed for multiple comparisons. Epidemiology 1990;1 (1) 43- 46PubMedGoogle ScholarCrossref
Vasan RSBeiser ASeshadri S et al. Residual lifetime risk for developing hypertension in middle-aged women and men: the Framingham Heart Study. JAMA 2002;287 (8) 1003- 1010PubMedGoogle ScholarCrossref
Dementia and Cognitive Impairment Hypertension Neurology
Reitz C, Tang M, Manly J, Mayeux R, Luchsinger JA. Hypertension and the Risk of Mild Cognitive Impairment. Arch Neurol. 2007;64(12):1734–1740. doi:10.1001/archneur.64.12.1734
Hypertension and the Risk of Mild Cognitive Impairment
Christiane Reitz, MD, PhD; Ming-Xin Tang, PhD; Jennifer Manly, PhD; et al Richard Mayeux, MD, MSc; José A. Luchsinger, MD, MPH
Author Affiliations: The Gertrude H. Sergievsky Center (Drs Reitz, Tang, Manly, Mayeux, and Luchsinger), the Taub Institute for Research on Alzheimer's Disease and the Aging Brain (Drs Manly, Mayeux, and Luchsinger), Departments of Neurology and Psychiatry (Dr Mayeux) and Medicine (Dr Luchsinger), Columbia University College of Physicians and Surgeons, and Departments of Biostatistics (Dr Tang) and Epidemiology (Dr Mayeux), Mailman School of Public Health, Columbia University, New York, New York.
Arch Neurol. 2007;64(12):1734-1740. doi:10.1001/archneur.64.12.1734
Objective To explore whether hypertension is associated with the risk of mild cognitive impairment (MCI), an intermediate stage of dementia, because there are conflicting data relating hypertension to the risk of Alzheimer disease.
Design and Setting Prospective community-based cohort study conducted in northern Manhattan. Multivariate proportional hazards regression analyses were used, relating hypertension to incident all-cause MCI, amnestic MCI, and nonamnestic MCI in 918 persons without prevalent MCI at baseline followed up for a mean of 4.7 years.
Results There were 334 cases of incident MCI, 160 cases of amnestic MCI, and 174 cases of nonamnestic MCI during 4337 person-years of follow-up. Hypertension was associated with an increased risk of all-cause MCI (hazard ratio, 1.40; 95% confidence interval, 1.06-1.77; P = .02) and nonamnestic MCI (hazard ratio, 1.70; 95% confidence interval, 1.13-2.42; P = .009) after adjusting for age and sex. Both associations were slightly attenuated in models additionally adjusting for stroke and other vascular risk factors. There was no association between hypertension and the risk of amnestic MCI (hazard ratio, 1.10; 95% confidence interval, 0.79-1.63; P = .49). Consistent with this association, hypertension was related with the slope of change in an executive ability score, but not with memory or language score. There was no effect modification of the association between hypertension and MCI by APOEε4 genotype or use of antihypertensive medication.
Conclusions A history of hypertension is related to a higher risk of MCI. The association seems to be stronger with the nonamnestic than the amnestic type of MCI in the elderly. These findings suggest that prevention and treatment of hypertension may have an important impact in lowering the risk of cognitive impairment.
Mild cognitive impairment (MCI) has attracted increasing interest during the past years, particularly as a means of identifying the early stages of Alzheimer disease (AD) as a target for treatment and prevention. Existing prevalence and incidence data are inconsistent because of different operational criteria, sampling, and assessment procedures.1 Studies using the criteria of Petersen et al2,3 for diagnosing MCI in clinical and epidemiological settings report an incidence rate of 9.9 per 1000 person-years for MCI among elderly persons without dementia4 and an annual conversion rate of 10% to 12% to AD in subjects with MCI, particularly amnestic MCI (AMCI), in contrast to a conversion rate of 1% to 2% in the healthy elderly population.5
There are inconclusive data relating hypertension, a modifiable vascular risk factor, to cognitive impairment and dementia. While most longitudinal studies6,7 reported an increased blood pressure before the onset of AD or vascular dementia, most cross-sectional studies8,9 or studies with a shorter follow-up10 observed associations between low blood pressure and dementia or no association between hypertension and cognitive impairment. We previously reported relationships between hypertension and vascular dementia but not AD. There are also conflicting data on the effect of antihypertensive treatment on cognition.11,12
The mechanisms underlying the associations between blood pressure and cognitive impairment or dementia remain unclear. High blood pressure levels may lead to white matter hyperintensities on magnetic resonance imaging or lacunar brain infarcts, which in turn may lead to cognitive impairment or dementia.13,14 More direct links between blood pressure and AD are suggested by autopsy studies15,16 reporting an increased frequency of neurofibrillary tangles and brain atrophy in hypertensive persons.
Our objective in the present longitudinal study was to determine whether hypertension is associated with the risk of incident MCI.
Subjects and setting
Participants were enrolled in a longitudinal cohort study by a random sampling of Medicare recipients 65 years or older residing in northern Manhattan (Washington Heights, Hamilton Heights, and Inwood). The sampling procedures have been described elsewhere.17 Each participant underwent an in-person interview of general health and function at study enrollment, followed by a standard assessment, including medical history, physical and neurological examination, and neuropsychological battery.18 Baseline data were collected from 1992 through 1994. Follow-up data were collected during evaluations at sequential intervals of approximately 18 months, performed from 1994 to 1996, 1996 to 1997, and 1997 to 1999. In this elderly population, some participants did not complete follow-up at all intervals because of refusal, relocation, or death. About half of participants were evaluated at the third follow-up visit. This study was approved by the institutional review board of Columbia-Presbyterian Medical Center.
The sample for this study comprised those participants who were without MCI or dementia at baseline, who had at least 1 follow-up interval, and who had complete information to ascertain MCI following the criteria of Petersen et al.2,5 Of the 1772 participants in whom a full neuropsychological examination was attempted, 339 (19.1%) were excluded because of prevalent dementia, 304 (17.2%) were excluded because of prevalent MCI, and 211 (11.9%) were excluded because of unavailability for follow-up. Thus, the final analytic sample included 918 individuals.
Compared with the original 1772 participants, the final sample without prevalent MCI and dementia and with prospective data was younger (mean [SD] age, 76.3 [6.1] vs 77.3 [6.8] years; P < .001) and had a similar distribution of women (69.4% for both) and African Americans (33.6% vs 32.6%), fewer Hispanics (43.9% vs 47.0%; P < .001), and more non-Hispanic whites (22.6% vs 20.4%; P = .008).
Data were available from medical, neurological, and neuropsychological evaluations.18,19 All participants underwent a standardized neuropsychological test battery that examined multiple domains in either English or Spanish.18 Orientation was evaluated using parts of the modified Mini-Mental State Examination.20 Language was assessed using the Boston Naming Test,21 the Controlled Word Association Test,22 category naming, and the complex ideational material and phrase repetition subtests from the Boston Diagnostic Aphasia Evaluation.23 Abstract reasoning was evaluated using the Wechsler Adult Intelligence Scale–Revised similarities subtest24 and the nonverbal identities and oddities subtest of the Mattis Dementia Rating Scale.25 Visuospatial ability was examined using the Rosen Drawing Test26 and a matching version of the Benton Visual Retention Test.27 Memory was evaluated using the multiple choice version of the Benton Visual Retention Test27 and the 7 subtests of the Selective Reminding Test28: total recall, long-term recall, long-term storage, continuous long-term storage, words recalled on last trial, delayed recall, and delayed recognition. Memory complaints were assessed using 11 items from the Disability and Functional Limitations Scale29,30 and the Blessed Functional Activities Scale.31 In addition, participants were asked if they had difficulties in general and in specific areas, such as names of persons or things. Participants were considered to have memory complaints if they indicated problems on 1 or more of these items. This neuropsychological test battery has established norms for the same community.32
Diagnosis of dementia and assignment of specific cause were done by consensus of neurologists, psychiatrists, and neuropsychologists based on baseline and follow-up information. The diagnosis of dementia was based on Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) criteria33 and required evidence of cognitive deficits on the neuropsychological test battery and evidence of impairment in social or occupational function (Clinical Dementia Rating of ≥1).34 Diagnosis of AD was based on the National Institute of Neurological and Communication Disorders and Stroke–Alzheimer's Disease and Related Disorders Association criteria.35
Definition of mci
The MCI criteria were retrospectively applied among individuals without dementia after the consensus conference. Persons considered for MCI were required to have the following: (1) a memory complaint, assessed as previously described; (2) objective impairment in at least 1 cognitive domain based on the average of the scores on the neuropsychological measures within that domain and a 1.5-SD cutoff using normative corrections for age, years of education, ethnicity, and sex; (3) essentially preserved activities of daily living (previously defined); and (4) no diagnosis of dementia at the consensus conference.
To cast the widest net to determine the prevalence of MCI and to determine which individuals were more likely to progress to dementia, the original criteria of Petersen et al,2 which focus on memory impairment, were expanded to include mutually exclusive subtypes based on cognitive features. The first subtype, AMCI without involvement of other cognitive domains, corresponds most closely to the original definition used by Petersen and colleagues. Memory impairment was defined as a score of less than 1.5 SDs below the demographically corrected mean on an average composite measure comprising the following learning and memory measures: (1) total recall from the Selective Reminding Test, (2) delayed free recall from the Selective Reminding Test, and (3) recognition from the Benton Visual Retention Test. Performance on composite scores from all other cognitive domains (executive, language, and visuospatial) was required to be within normal limits (score must be ≥1.5 SDs below the demographically corrected mean). Other MCI subtypes were classified that allowed for impairment in a single nonmemory domain if performance on composite scores from all other cognitive domains was within normal limits. Executive function MCI was assigned if impairment was demonstrated on an average composite measure comprising the following measures: (1) letter fluency, (2) category fluency, and (3) the Wechsler Adult Intelligence Scale–Revised similarities subtest. Language MCI was defined as isolated impairment on an average composite measure comprising (1) the Boston Naming Test, (2) the Boston Diagnostic Aphasia Examination repetition subtest, and (3) the Boston Diagnostic Aphasia Examination comprehension subtest. Visuospatial MCI was assigned if impairment was demonstrated on an average composite score comprising: (1) the Rosen Drawing Test and (2) the Benton Visual Retention Test matching subtest. Finally, we allowed for impairment in multiple cognitive domains in the absence of dementia. Multiple-cognitive-domains-with-memory-impairment MCI (MCI-MCDM) was diagnosed if there was objective impairment on the memory domain composite score and if there was impairment on at least 1 other cognitive domain. Multiple-cognitive-domains-without-memory-impairment MCI was assigned if there was impairment in 2 or more of the 3 nonmemory domains and if the memory domain composite score was within normal limits. Again, classification into the 6 subtypes was mutually exclusive. We used 3 out comes for these analyses: (1) all-cause MCI; (2) AMCI (including AMCI without involvement of other cognitive domains and MCI-MCDM); and (3) nonamnestic MCI (NAMCI). The rationale for this classification is that AMCI without involvement of other cognitive domains and MCI-MCDM equally predict the development of AD, and MCI-MCDM is thought to be a more advanced form of AMCI involving other cognitive domains.
Cognitive scores
A factor analysis was performed using data from the baseline assessment of the entire cohort with the 15 neuropsychological measures using a principal component analysis with varimax rotation and Kaiser normalization.36 This analysis yielded 3 factors: (1) a memory factor, for which the 7 subtests of the Selective Reminding Test were the main contributors28; (2) a visuospatial reasoning/cognitive factor (executive factor), for which visuospatial tests of reasoning were the main contributors (including the Rosen Drawing Test,26 matching and recognition components of the Benton Visual Retention Test,27 and the identities and oddities subtests of the Mattis Dementia Rating Scale25); and (3) a language factor, for which language measures were the main contributors (Boston Naming Test,21 Controlled Oral Word Association Test,22 and Wechsler Adult Intelligence Scale–Revised similarities subtest).24 Component scores for each subject at each visit were calculated by adding the loading weighted scores of the measures that contributed to each factor. We used the factor weights of the baseline factor scores and normalizing equations to calculate factor scores for the follow-up assessments.
Definition of hypertension and other covariates
At baseline, all participants were asked whether they had a history of hypertension any time during their life. If affirmative, they were asked whether they were under treatment and the specific type of treatment. Blood pressure was also recorded at each visit using a monitor (Dinamap Pro 100; Critikon Co, Tampa, Florida). The blood pressure cuff was placed on the right arm while the individual was seated, and a recording was obtained every 3 minutes over 9 minutes. The third measurement was recorded in the database. Values higher than 140 mm Hg (systolic) and 90 mm Hg (diastolic) were used as criteria for hypertension.
Stroke was defined according to the World Health Organization criteria.37 The presence of stroke was ascertained from an interview with participants and their informants. Persons with stroke were confirmed through their medical records, 85% of which included results of brain imaging. The remainder were confirmed by direct examination. Diabetes mellitus was defined as a history at any time during life. At baseline, all participants were asked whether they had a history of diabetes. If affirmed, they were asked whether they were under treatment and the specific type of medication. Heart disease was defined as a history of atrial fibrillation and other arrhythmias, myocardial infarction, congestive heart failure, or angina pectoris at any time during life. Assessment of all covariates was independent of cognitive assessment and diagnosis of cognitive impairment or dementia.
APOE GENOTYPING
APOE genotypes were determined as described by Hixson and Vernier,38 with slight modification. We classified persons as homozygous or heterozygous for the APOEε4 allele or as not having any APOEε4 allele.
Information on demographic characteristics and other potentially relevant factors was compared among individuals with and without a history of hypertension. χ2 Tests were used for categorical data, and analysis of variance was used for continuous variables. Multivariate Cox proportional hazards models were used to estimate the association of hypertension to incident all-cause MCI, AMCI, and NAMCI. Because the period between the follow-up assessments in this cohort is relatively short, the time-to-event variable was age at onset of MCI (ie, the age at the assessment at which the research diagnosis was made). Among individuals who did not develop MCI, those who developed dementia were censored at the dementia diagnosis and those who did not develop dementia, who died, or who were lost to follow-up owing to relocation before development of MCI were censored at their last evaluation. Information on covariates was obtained at baseline. We initially adjusted for sex and age, then we adjusted for sex, age, ethnic group, years of education, and APOEε4 genotype in a second model. In a third model, we adjusted for sex, age, ethnic group, years of education, APOEε4 genotype, stroke, diabetes, heart disease, and plasma low-density lipoprotein cholesterol level. The additional covariates in the third model are theoretically in the pathways linking hypertension and MCI. Thus, any attenuation of hazard ratios observed in this model should be interpreted as evidence of mediation and not of confounding. We checked the proportional hazards assumption that the effect of variables of interest is constant in time, by creating time-dependent variables that we then added to the model. When the variable tested added significant information (eg, proportional hazard assumption not satisfied), the model was adjusted for this variable. To explore the association between blood pressure levels and risk of MCI, we finally repeated all analyses using the continuous measure of blood pressure as the independent variable. We estimated the risk of conversion to dementia among persons with MCI using logistic regression. Generalized estimating equations39 were used to examine changes in neuropsychological domains over time, represented by cognitive scores, and compare them between persons with and without hypertension. The dependent variables were the cognitive scores, and the independent variables were hypertension and time (included as a continuous variable). Generalized estimating equation analyses yield coefficient values that represent associations between factor scores and variables included in the model. A significant coefficient for hypertension indicates a difference between 2 groups at baseline or at any subsequent interval. A positive value for the coefficient indicates that the group with a specific variable performed better than the group without that variable. A significant time coefficient would indicate a significant change in a score over the total duration of follow-up. A significant interaction term would indicate a difference in the rate of change in cognitive score between persons with and without hypertension. Data analysis was performed using 2 commercially available software programs (SPSS, version 13.0 [SPSS Inc, Chicago, Illinois], and SAS statistical software, version 9.1 for Windows [SAS Institute Inc, Cary, North Carolina]).
There were 334 cases of incident MCI, 160 cases of AMCI, and 174 cases of NAMCI during 4337 person-years of follow-up (incidence densities, 7.7, 3.7, and 4.0 cases, respectively, per 1000 person-years of observation). The mean ± SD age of the sample was 76.3 ± 6.1 years, and 69.4% were women; 22.6% were white, 33.6% were black, and 43.9% were Hispanic (percentages do not total 100 because of rounding). The mean (SD) years of education were 8.7 (4.6); 62.8% had hypertension, 21.3% had diabetes, and 30.4% had heart disease. Of the sample, 25.0% were homozygous or heterozygous for the APOEε4 allele, and use of antihypertensive medication was reported by 394 subjects (42.9%). Persons with hypertension were more often women, were less educated, and more often had a history of stroke, diabetes, or heart disease than were persons without hypertension (Table 1). Compared with persons without MCI, persons with AMCI were 6 times more likely (odds ratio, 6.0; 95% confidence interval, 4.0-8.9) to convert to dementia after adjustment for age, sex, years of education, ethnic group, and APOEε4 genotype. The odds ratio for persons with NAMCI was not statistically significant (odds ratio, 1.4; 95% confidence interval, 0.9-2.3).
Risk of incident mci
The mean (SD) age at onset of MCI was 80.7 (5.9) years. In multivariate analyses, hypertension was associated with an increased risk of all-cause MCI (P = .02) and NAMCI (P = .009) after adjusting for age and sex (Table 2). These associations remained stable in models additionally adjusting for years of education, ethnic group, and APOEε4 genotype, and were slightly attenuated in models additionally adjusting for stroke and other vascular risk factors, such as diabetes, low-density lipoprotein cholesterol level, smoking, or heart disease. The results did not change after adjusting for blood pressure measurements or use of antihypertensive medication. There was no relation between hypertension and the risk of AMCI (P = .49) in either model. There was no effect modification of the association between hypertension and MCI by APOEε4 genotype. Using blood pressure measurements instead of diagnosis of hypertension as the independent variable or restricting the analyses to persons with a longer follow-up (observation time is equal to the median follow-up of 3.9 years or longer) did not change the observed associations.
Hypertension and change in cognitive scores over time
We conducted generalized estimating equation analyses comparing slopes of cognitive score change between persons with and without hypertension (Table 3). All subjects had successive cognitive data in at least 2 intervals, 79% had at least 3 intervals, and 59% had 4 or more intervals. For the memory score, we found—after adjustment for age, sex, years of education, ethnic group, and APOEε4 genotype (model 2)—that it was not related to differences in hypertension status at baseline and declined with time. However, this decline was not different by hypertension status, indicated by the lack of significance of the interaction term. For the executive score, we found that it was not related to baseline hypertension and increased over time (indicated by a positive coefficient for time). However, this increase over time was lower for persons with hypertension, indicated by the significant negative interaction term for hypertension and time. We also found after adjustment for other vascular risk factors and stroke that the statistical significance for the interaction term was attenuated, which we interpret as evidence of mediation of vascular disease and stroke in the relation between hypertension and executive impairment. There was no relation between hypertension and changes in the language score.
In this longitudinal analysis of 918 persons, hypertension was associated with an increased risk of all-cause MCI that was mostly driven by an association with an increased risk of NAMCI after adjusting for age and sex. There was no relation between hypertension history and the risk of incident AMCI and there was no effect modification of the association between hypertension and any MCI subtype by APOEε4 genotype or use of antihypertensive medication. We also found that executive abilities increased over time, which we think was because of practice effects, but this increase was lower in persons with hypertension, consistent with the notion that hypertension increases the risk of impairment in executive abilities. Hypertension was not related to the change over time in memory and language abilities.
The mechanisms by which blood pressure affects the risk of cognitive impairment or dementia remain unclear. Hypertension may cause cognitive impairment through cerebrovascular disease. Hypertension is a risk factor for subcortical white matter lesions found commonly in AD.41 Hypertension may also contribute to a blood-brain barrier dysfunction, which has been suggested to be involved in the cause of AD.41 Other possible explanations for the association are shared risk factors, such as the formation of free oxygen radicals.41,42
Several studies have previously examined the relation of hypertension with MCI. In the Cardiovascular Health Study,43 persons with MCI had a higher prevalence of hypertension, but no distinction was made between persons with AMCI and NAMCI. White matter disease on magnetic resonance imaging, which could be considered an intermediary between hypertension and MCI, was also more prevalent in persons with MCI in this study. In the Italian Longitudinal Study of Aging, hypertension was related to a 44% higher risk of MCI that was close to statistical significance,44 but no distinction was made between AMCI and NAMCI. A study in Finland also found that hypertension was related to a higher risk of MCI,45 without distinction of MCI subtype. The main contribution of our study is the examination of this association in a multiethnic cohort in New York City, and the distinction between MCI subtypes.
In our study, hypertension was associated with a higher risk of all-cause MCI and NAMCI. Mild cognitive impairment has been described as an intermediate stage between normal cognition and dementia.2,46 There is evidence that NAMCI is related in particular to cerebrovascular disease and vascular cognitive impairment. Because hypertension is associated with a higher risk of cerebrovascular disease and vascular dementia,47,48 it seems reasonable that it is related to the risk of NAMCI in our study. Also, the relation of hypertension to NAMCI remained stable after adjusting for years of education, ethnic group, and APOEε4 genotype, and was attenuated after adjustment for stroke and vascular risk factors, indirectly suggesting that cerebrovascular disease may be mediating the relation between hypertension and NAMCI. These results suggest that hypertension is mainly related to an increased risk of nonamnestic forms of cognitive impairment,49 such as frontal-executive cognitive impairment.
There was no relation between hypertension and the risk of incident AMCI. Episodic memory deficits are a strong predictor of conversion to dementia, in particular AD.50 Consequently, the term amnestic MCI represents a subgroup with a high probability of conversion to dementia caused by AD.50 The association between hypertension and AD is unclear. A 15-year longitudinal study51 reported increased blood pressure 10 to 15 years before the onset of AD and vascular dementia. Others found it to be lower in older individuals with AD8 or did not find an association between hypertension and cognitive impairment.52
In the interpretation of these findings, it is of major importance to keep in mind that MCI is likely to be a clinically and pathologically heterogeneous syndrome, and that definitions of MCI and MCI subtypes rather represent diagnostic constructs than established diagnostic entities. The frequency of dementia in a group of individuals with cognitive impairment is the result of the definition of the disorder and the underlying pathological features. Thus, it is possible that a different definition of MCI or MCI subtypes would have led to different results.
There are alternative explanations for our observations. One is that hypertension is part of a preclinical syndrome of NAMCI or that persons with preclinical NAMCI reported hypertension while subjects who would not develop MCI did not; we tried to eliminate these possibilities by excluding persons with baseline MCI from the analyses and by repeating the analyses restricted to persons with a longer follow-up. Another potential explanation for our findings is chance because of multiple comparisons. However, the results are in line with the a priori hypothesis of an association of hypertension with NAMCI rather than AMCI when using the present MCI definition, and are mechanistically plausible. These facts make chance because of multiple comparisons an unlikely explanation for our findings.53 Another potential explanation is confounding. For example, if less education is related to hypertension, and persons with less education are more likely to be diagnosed as having MCI, then it is possible that the relation between hypertension and all-cause or NAMCI could be because of confounding by socioeconomic factors. We adjusted for years of education and ethnicity as markers of socioeconomic status to account for this possibility. However, it is possible that hypertension is related to other behaviors related to poor health that, in turn, may increase the risk of cognitive decline that we could not adjust for, and we cannot eliminate the possibility of lack of control for unknown confounders as a potential explanation for our findings.
The main limitation of our study is the lack of subclinical markers of hypertension, such as left ventricular hypertrophy by electrocardiogram or echocardiogram, and the use of self-reported history as our main measurement of hypertension. As shown in our sample, most elderly people will develop hypertension in their lifetime.54 Therefore, elderly cohorts may be too homogeneous to show differences in outcomes related to a history of hypertension. Our measurement of hypertension did not take into account severity or duration. Thus, it is possible that our results tend to underestimate the association between hypertension and MCI, and could bias our results to the finding of no association with AMCI. It is possible that studies in younger age groups with measures of hypertension burden in midlife could find stronger associations with risk of MCI than we report, including an association with AMCI. Also, this study was conducted in an elderly multiethnic community in an urban setting with a high prevalence of risk factors for morbidity and mortality, such as diabetes and hypertension. Persons who dropped out of the study during follow-up were mainly Hispanic and, at baseline, were older, were less educated, and had a higher prevalence of vascular risk factors than those who remained in the study. This could have resulted in an underestimation of the association between hypertension and MCI compared with the original cohort. Also, hypertension is related to higher cardiovascular mortality, and it is possible that some hypertensive persons would have demonstrated cognitive decline had they not died before inclusion in this cohort. Thus, there are important biases related to the sample of this study that should be taken into account in the interpretation and generalization of these findings. We did not have information on brain magnetic resonance imaging and measures of cerebrovascular disease. Thus, our stroke variable is likely an underestimation of the prevalence of cerebrovascular disease. We expected that the other vascular risk factor variables would be surrogate markers of cerebrovascular disease risk. Our ascertainment of MCI subtypes was based on neuropsychological criteria and would not have been affected by the availability of imaging data.
The main strength of our study is that it is a prospective cohort study designed for the diagnosis of cognitive impairment and dementia with standard criteria, and with complete clinical and neuropsychological evaluation at each interval, which permitted the ascertainment of different types of incident MCI.
Our findings support the hypothesis that hypertension increases the risk of incident MCI, especially NAMCI. Preventing and treating hypertension may have an important impact in lowering the risk of cognitive impairment.
Correspondence: José A. Luchsinger, MD, MPH, Division of General Medicine, Columbia University Medical Center, Presbyterian Hospital, 9 East-105, 630 W 168th St, New York, NY 10706 (jal94@columbia.edu).
Accepted for Publication: January 8, 2007.
Author Contributions:Study concept and design: Reitz, Mayeux, and Luchsinger. Acquisition of data: Manly, Mayeux, and Luchsinger. Analysis and interpretation of data: Reitz, Tang, Manly, Mayeux, and Luchsinger. Drafting of the manuscript: Reitz, Mayeux, and Luchsinger. Critical revision of the manuscript for important intellectual content: Tang, Manly, Mayeux, and Luchsinger. Statistical analysis: Reitz and Tang. Obtained funding: Manly, Mayeux, and Luchsinger. Administrative, technical, and material support: Manly and Mayeux. Study supervision: Manly and Luchsinger.
Financial Disclosure: None reported.
Funding/Support: This study was supported by grants PO1 AG07232, 1K08AG20856-01, and RR00645 from the National Institutes of Health; the Charles S. Robertson Memorial Gift for Research in Alzheimer's Disease; and the Blanchette Hooker Rockefeller Foundation.


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