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THE United States seems keener than most countries to celebrate the new millennium in style: maybe the nation is wealthy and optimistic enough that big parties seem apropos. Whatever the reason, come Dec. 31, there'll be an outpouring of music, dancing, laser shows and fireworks, along with time capsules enough to keep archaeologists busy until the next millennium.
Although one report has 60 percent of Americans staying home -- perhaps daunted by high prices and crowds, fearing the Y2K problems might complicate travel and A.T.M. withdrawals, and wondering whether maybe next year isn't the big transition after all -- from Lubec, Me., to San Diego, from Miami to Seattle, those who want to mark the moment they spin eastward into the year 2000 can find a civic gathering of kindred spirits -- reflective, hopeful, somber or exuberant.
Just about every town and city is celebrating in some way, many with nonalcoholic, family-oriented public festivals, with events that are either free or inexpensive. Of course, there will be plenty of Champagne flowing, too.
And, in case the moment passes too quickly, millennium events seem likely to span the entire year. Here are a handful of those end-of-the-year parties we'd hate to miss.
New York
New Year's Eve in Times Square will be the biggest party in the event's 95-year history, an ebb and flow of video broadcasts over 24 hours from around the globe on at least nine huge screens throughout the district, accompanied by a score of taped music from around the world, choreographed processional puppets, hundreds of costumed dancers and actors, tons of souvenir confetti and lots of special effects.
A new crystal ball will start its drop at 11:59 p.m. It is six feet in diameter -- a bit larger than any of its predecessors -- weighs 1,070 pounds and is covered with 504 Waterford crystal triangles. Its 600 multicolored halogen bulbs, 96 high-intensity strobe lights and 92 rotating pyramid mirrors should produce a dazzling light show.
A crowd of 1.5 million is expected, with more than a billion, perhaps, watching on television around the world.
The program is scheduled to begin at 6:30 a.m. on Dec. 31 to anticipate the arrival of the new year in the South Pacific at 7. Revelers will continue to celebrate with people around the world as each time zone greets the year 2000, until, finally, at 7 a.m. on Jan 1, Western Samoa moves into the 21st century. A major flourish will occur at 6 p.m. Friday, when midnight arrives in 41 countries in Africa and Europe, including a parade of a 741-foot banner of flags of those 41 nations.
Ten blocks south, about 25,000 paying guests are expected at the Jacob Javits Center for what is being billed as ''the party of the century,'' with performances by Aretha Franklin, Sting, Andrea Bocelli, the Duke Ellington Orchestra, Tom Jones, Kool and the Gang and others performing on four stages set up throughout the 22-acre center. There will also be dancing, drinks and food from top chefs. Tickets begin at $1,000 a person; (877) 313-3299 and (212) 644-8900, www .celebration2000.com.
Other options, for a price, include a four-hour dinner cruise on the Circle Line, (212) 563-3200; Act II of ''Die Fledermaus'' at the Metropolitan Opera, followed by dinner and dancing on the tiers of the opera house, (212) 362-6000; a black-tie party aboard the Intrepid, (212) 245-0072, and a five-kilometer midnight run through Central Park with the New York Road Runners Club, with fireworks over the south end of Central Park, (212) 860-4455.
More information on events is available from (800) 692-8474 and www.nycvisit.com, as well as the Times Square Business Improvement District, the organization producing the Times Square event, at the Times Square Visitors Center, Broadway between 46th and 47th Streets, and at www.timessquarebid.org.
The 24th annual First Night celebration in Boston will expand this year to three days of citywide festivities. Over three million people are expected at the alcohol-free event, to be centered around the Hynes Convention Center, City Hall, Boston Common and the waterfront. A $20 First Night button will cover a lot of territory.
Fireworks? In addition to the midnight finale over Boston Harbor on New Year's Eve, there will be a 7 p.m. (midnight Coordinated Universal Time, formerly Greenwich Mean Time) display over the Common, and more fireworks Saturday and Sunday at 7 p.m., over Boston Harbor. Throughout the three days, landmarks like the Custom House Tower and Boston Public Library will be transformed by lasers and other effects.
At City Hall, the plaza will be illuminated by 200 hand-carved ice candles, and two Jumbotron screens will broadcast the annual New Year's concert by the Boston Pops from Symphony Hall at 10:15 p.m. The conductor, Keith Lockhart, and Mayor Thomas M. Menino will lead an interactive countdown to midnight.
The Convention Center will be the site of drumming workshops and performances on Friday and Saturday, and the starting place of a ''Percussion Procession'' to Boston Common on Saturday afternoon. There will also be a family festival at the Hynes on Friday afternoon, with a Mardi Gras-style parade to the Common for the 7 p.m. kids countdown to New Year's at Greenwich. Dance parties with live music are scheduled for Friday and Saturday nights at the center.


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Final Week Spin
With the midterm elections now just days away, many campaigns and outside groups are making their final appeals. And, as has been the case all election season, some of the claims miss the mark.
A Project of the Annenberg Public Policy Center
With the midterm elections now just days away, many campaigns and outside groups are making their final appeals. And, as has been the case all election season, some of the claims miss the mark.
No shortage of tall tales in the midterm elections, from both parties.
The National Rifle Association implies Iowa Rep. Bruce Braley lied when he said he "never met Michael Bloomberg," but there's no evidence of that.
Longtime Iowa Sen. Tom Harkin is retiring, and Democratic Rep. Bruce Braley and Republican Iowa state Sen. Joni Ernst are each hoping to be the one to replace him.
In Iowa, a Republican ad claims that Democratic Senate nominee Bruce Braley "voted to raise taxes on every single Iowa taxpayer." That badly distorts Braley's clearly stated position.
A TV ad from Democrat Jim Mowrer claims Iowa Rep. Steve King "did vote to raise his own pay by $20,000 a year and take perks like free health care for life." That's a double whopper.
Democratic TV ads in Iowa have repeatedly misrepresented Republican Joni Ernst's position on Social Security, claiming she "would privatize Social Security" or that she has "proposed privatizing Social Security."
Democrats, Republicans spend nearly $50 million on TV ads that repeat old, scary Medicare claims.
Two ads from the conservative Crossroads organizations claim Democratic Senate candidates in Iowa and Michigan who oppose the Keystone XL pipeline are backed by an environmental activist who "stands to profit by blocking Keystone."
A veterans advocacy group is making false and misleading claims in a TV ad attacking U.S. Senate candidate Bruce Braley on his commitment to military veterans.
Q: Is Sen. Ted Cruz, who was born in Canada, eligible to be the U.S. president?
A: Most likely. The legal consensus is that Cruz qualifies because he was born to a U.S. citizen living abroad, making him a U.S. citizen at birth.

subset: commoncrawl


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Thursday, September 12, 2013
0 Comments | 1121 Views | Copyright: IANS
Taj Mohammed Rangrez created history by winning Rs. 1 crore in the seventh season of game show "Kaun Banega Maha Crorepati 2013" hosted by megastar Amitabh Bachchan. After the victory he says the people's perception about him had changed.
A history teacher, Rangrez said that people have now started calling him 'Crorepati Rangrez'.
"After my victory, after getting Rs. 1 crore on the show, people's perception towards me has changed. The way they look at me now is completely different from how they used to see me earlier," said Rangrez in a telephonic interaction from Fatehnagar, Udaipur, Rajasthan.
"When they see me they say 'It's the same guy, who is seen on newspapers these days.' They don't call me by my name, they use 'Crorepati Rangrez'," he added.
Rangrez, 42, is still in the celebration mode and says he still can't believe that he won a crore from the show, which is an Indian version of "Who Wants To Be A Millionaire".
"I still can't believe it. I never thought that I will win Rs.1 crore. I actually never thought that I will be able to reach Rs.6,40,000. Just entering the show and sitting on the hot seat with Amitabh Bachchan was enough for me," he said.
"When he said that I won Rs.1 crore, I started shivering. My wife was there with me on the show, she had tears in her eyes. It was all because of the cooperation by the Sony (channel) and KBC team. It's because of the wishes from my mother and sister," Rangrez added.
When asked how is he going to spend the amount, he said: "I first want to get my daughter treated from her partial vision impairment. Then, I want to buy a house. Also, I want to fund the marriage of two orphan girls. These three things are my priorities, rest will follow."
The episode featuring the first crorepati winner will air om September 15.
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OPINION: Beer is full of many delights. Before the taste there's a cheerful fizz as you pop the cap, the promising glug as you pour it into the glass and the aesthetic pleasure of colour and hue as well as the bead of rising bubbles. The head caps off the visual spectacle and is the reason why beer's always advertised in a tall, clear glass with a proud white head.
Tasting it is even better.
There is the smooth, mouth-filling pleasure provided by the malt, the nuances that yeast contributes, and the clean bitterness and aroma of hops. Many beers lean towards either malt or hops. Yakima Scarlet is designed to showcase the best of both.
It's brewed with six different types of English, Australian and Belgian malts, and was always going to share the characteristics of the beers that these regions produce. There is the smooth, nutty flavour of the English Bitter and the pleasing complexity of the Belgian ale. (Aussies, your beer underwhelms me. I would be happy to be proven wrong.)
The addition of five big American hop varieties could blow out this beer and make for an exercise in brewing indulgence.
Happily, this is not the case. The hops provide a counterpoint to the rich malt body, and the aroma is pleasing and subtle.
There is delicious late hop charge on the back of the tongue, which adds further satisfaction. If you had to put a style tag on this beer, you might call it a red ale because it is a glorious red colour.
However, brewer Joseph Wood of Liberty Brewing notes on the bottle that he isn't sure what style it is, although he does know that it is hoppy and it is red!
Yakima Scarlet is brewed by Liberty Brewing in New Plymouth. It is 6.9 per cent abv and should not be served too cold. It can be purchased from Fitzroy Liquorland. Warwick Foy
- Taranaki Daily News
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"Everybody I talked to -- they're disgusted. They're very upset with the way it's been handled. Seems like everyone wants to try and just ignore it, and I think that's sad."
Scott Jones
"I'm very upset that we lost somebody like him. We seem to have a lot of that going around."
Jason Varitek
"We're familiar with them. Both teams will be upset and ready to go. It will come down to who wants it more."
Dan Strojan
"I got upset with them at halftime because we weren't doing what we talked about. We were not attacking the zone. We were trying to attack it from outside, but whenever we got it inside, we were OK."
Dave Jones
"Of course they were upset after Saturday, but we had a good talk and now they are happy again. This is the game of their lives, so they have to be ready."
Nelson Rodrigues
"I came out and everybody was crying and upset. You talk about going from celebratory to just stoic all at once."
Beth Daniel
"Obviously, something upset him. Whether it was staged or something -- he seemed genuinely upset about it -- I don't know. He's as fired up and enthusiastic as any player out there."
Billy Donovan


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4/23/2015 Chandler, AZ Save This JobInternship - Material Planning Analyst Product Supply Cambridge, MA, United States Merrimack is a biopharmaceutical company discovering, developing and preparing to commercialize innovative medicines paired with companion diagnostics for the treatment of cancer. Merrimack
4/23/2015 Cambridge, MA Save This JobRequisition Number:710 Job Title:Level 1 RMM Analyst Area of Interest:Information Technology Position Type:Full Time - Permanent Shift: Location:Raleigh Office City:Raleigh State / Province:North Carolina Requirements: See Job Description Job Description: The qualified candidate
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With nakedness, body fluids and strange stuff aplenty, you may be anxious about giving birth – but there's no need for embarrassment. Here's why…
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VOICES Ideas and Insight From Explorers
Tag archives for cities
Video: President William J. Clinton Congratulates C40 on Reaching 10-Year Milestone
Editor's Note: 2015 marks the 10-year anniversary of C40 Cities Climate Leadership Group. To celebrate our 10 Years of Results, we will be featuring the voices of C40 principals, partners and other thought leaders throughout the year. 42nd President of the United States William J. Clinton, founder of the Clinton Foundation and prominent champion of climate initiatives, wishes C40…
Compact of Mayors gains further momentum at ICLEI World Congress
At the ICLEI World Congress in Seoul today, 35 leading cities, including Johannesburg, Paris and Seoul, announced their intent to comply with the Compact of Mayors – the global effort to cut greenhouse gas emissions, track progress and prepare for the impacts of climate change. The news gives further momentum to the burgeoning movement, which added 20 new cities at…
C40 Latin American Mayors Forum Showcases Region's Bold Climate Leadership
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Urban Growth: Mexico City over Time
In the above gif, we can watch forty years of Mexico City's built area expand, washing up against and around hills, lakebeds, and other obstacles. I'm very much drawn to this type of image in urban planning: evocative and based in fact, without telling the whole story up front. It requires intuition and imagination to…
Return Trip: On Leaving Cuautitlán and the Tren Suburbano
Infrastructure gives shape to the city, the same way a trellis gives shape to a vine. Along with natural and topographical features—primarily the hills and mountains that encircle the Valley of Mexico and the traces of the now-desiccated lakes—it's infrastructure that gives shape to the grey blob of urbanity that is Mexico City as photographed from a satellite. You can tell a lot about a city's development simply from looking at an unlabeled "photographic" view like that of Google Maps, as well as you can staring out the window of the Tren Suburbano as you ride home from a day in the city.
Cuautitlán: A Journal of Living in the Suburbs of Mexico City
About 18 miles from the Zocalo as the crow flies from the center of Mexico City, is my home for the month. A short, if convoluted ride on three of the city's metro lines (for about 30 cents) takes you to Buenavista Station. Dating to the 19th century, this was once the main inter-urban train station in…
The Nature Conservancy & C40 Release Urban Water Blueprint
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In Conversation: C40's Johanna Partin leads discussion with USDN and the Cities of London & Curitiba
For the second year in a row, C40 and the Urban Sustainability Directors Network (USDN) teamed up to bring a couple of international C40 cities to USDN's annual meeting, held last month in Houston. C40's Regional Director for North America, Johanna Partin, sat down with select participants to get their thoughts on the exchange. Johanna…
Watch Raccoons Escape Trash Can—Are Urban Animals Getting Smarter?
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Michael Waldrep: Understanding the Meaning of Sense of Place
Michael Waldrep will spend 9 months in Mexico City studying its stories, and specifically those of the sprawling reaches that envelope it. Certainly, the city has its historic center and its charming European-styled boulevards close by. But outside of its strictest boundary, the line that divides the Federal District from the surrounding State of Mexico, a 21st Century city, simultaneously typical of global development and unique to the specificities of Mexico, is being built. It includes the massive, quasi-legal, cinderblock districts of Ciudad Neza (1.1 million people, or nearly two Bostons) and Ecatepec (1.6 million people, or larger than Philadelphia)—the informal settlements that loom large in the mental image of the sprawling edges of Mexico City.
Mimi Onuoha: Charting the Intersections of the Physical and Online Worlds
The lives you lead are different, but not divorced. They stretch and meet at crucial intersections. You cruise websites and highways; you check into hotels and locations on mobile apps. You may like to eat a type of food and you may also "like" that food on Facebook, but those two actions do not necessarily mean the same thing.
Foodie Bees: Insects Head Downtown for Dinner
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A Retrofuturistic Train Journey to Explore America's New Frontiers
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Stop that Cow: When Ecuadoran Cities Organize to Protect Water Supplies
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Sex in the City: As Cities Grow, Are We Forgetting the Urban Poor?
Today, 3.9 billion of us live in cities. That's more than half the world's population. By 2050, two-thirds of us will live in urban areas. Today is World Population Day, and this week the United Nations Population Division released the latest version of its World Urbanization Prospects. The 2014 projections show continued population growth and…


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Dr. Van Doornum's work was supported by an NHMRC postgraduate scholarship.
Research Article
Screening for atherosclerosis in patients with rheumatoid arthritis: Comparison of two in vivo tests of vascular function
Article first published online: 10 JAN 2003
DOI: 10.1002/art.10735
Copyright © 2003 by the American College of Rheumatology
Additional Information
How to Cite
Van Doornum, S., McColl, G., Jenkins, A., Green, D. J. and Wicks, I. P. (2003), Screening for atherosclerosis in patients with rheumatoid arthritis: Comparison of two in vivo tests of vascular function. Arthritis & Rheumatism, 48: 72–80. doi: 10.1002/art.10735
Publication History
- Issue published online: 10 JAN 2003
- Article first published online: 10 JAN 2003
- Manuscript Accepted: 24 SEP 2002
- Manuscript Received: 24 JUN 2002
Funded by
- CVL (Pfizer) Research Grant
- Victor Hurley Trust
- Juvenile Diabetes Research Foundation
- The Arthritis Foundation of Australia
- Abstract
- Article
- References
- Cited By
Inflammation appears to play a central role in atherosclerosis, and endothelial damage mediated by systemic inflammation may contribute to the increased cardiovascular mortality in rheumatoid arthritis (RA). Brachial artery flow-mediated dilatation (FMD) and pulse wave analysis (PWA) are measures of vascular function. The aim of this study was to determine if FMD and PWA are abnormal in patients with RA.
Twenty-five RA patients and 25 matched healthy controls were studied. All were free of traditional cardiovascular risk factors. FMD was measured in all subjects. PWA was performed in 18 RA patients and 18 controls, with results expressed as large and small artery compliance (C1 and C2). Modified Sharp scores were calculated in 13 RA patients.
Results (mean ± SD) in RA patients and controls, respectively, were as follows: FMD 107.6 ± 4.6% versus 108.5 ± 4.1% (P = 0.49), C1 14.8 ± 2.8 ml/mm Hg × 10 versus 17.9 ± 3.1 ml/mm Hg × 10 (P = 0.0033), C2 4.5 ± 2.3 ml/mm Hg × 100 versus 7.7 ± 3.7 ml/mm Hg × 100 (P = 0.0039). There was an inverse correlation between C2 and modified Sharp scores in the RA patients (Spearman's rho −0.69, P = 0.0085).
FMD was normal in these RA patients, whereas arterial compliance was markedly reduced. PWA appears to be a more sensitive measure of vascular dysfunction than FMD in RA and may be the preferred surrogate marker of vascular dysfunction in longitudinal studies of RA patients. The inverse correlation between C2 and the modified Sharp score, a measure that reflects disease activity over time, supports the notion that chronic inflammation plays a role in RA-associated atherosclerosis.
Rheumatoid arthritis (RA) is associated with excess cardiovascular mortality, which is not explained by systemic vasculitis or traditional cardiovascular risk factors (1, 2). The role of more recently identified risk factors such as homocysteine and lipoprotein(a) in RA-associated vascular disease is unclear, although there have been reports of these occurring at elevated levels in RA patients (3–6). There is growing evidence that inflammation plays a role in the initiation and progression of atherosclerosis, the conversion of a stable to an unstable plaque, and the superimposed thrombosis which usually precipitates acute vascular events (7). For example, prospective epidemiologic studies in the general population have demonstrated a relationship between high-sensitivity C-reactive protein (hsCRP) levels and future risk of cardiovascular events (8, 9). Elevated concentrations of serum amyloid A, interleukin-6, and soluble intercellular adhesion molecule 1 have also been identified as risk markers for future cardiovascular events (10–12). The similarity between rheumatoid synovitis and atherosclerotic plaque has been noted (13), and most patients with RA have evidence of systemic inflammation in addition to articular disease.
It is reasonable, therefore, to postulate that the systemic inflammation associated with RA, acting either in isolation or in synergy with traditional and/or novel risk factors (1), could contribute to accelerated atherosclerosis in RA patients. In order to conduct further research into the prevalence and determinants of atherosclerosis in RA and to perform large-scale intervention studies, a surrogate marker of vascular function is needed. Ideally, such a test would be noninvasive and able to detect vascular disease at an early stage to allow effective intervention.
Maintenance of vascular homeostasis is largely dependent on the endothelial lining of blood vessels. Endothelial cells release vasoactive mediators (e.g., nitric oxide, endothelin 1) and express cell surface molecules (e.g., leukocyte adhesion molecules) which influence vascular tone, leukocyte adherence, platelet activation, coagulation, and smooth muscle proliferation (14). Endothelial dysfunction, characterized by reduced nitric oxide bioavailability, is an early stage of atherosclerosis. Several noninvasive tests of endothelial function are available. Flow-mediated dilatation (FMD) is an ultrasound-based technique which measures vasodilatation of the brachial artery in response to increased vessel wall shear stress (15). This vasodilatation is mediated by endothelial cell release of nitric oxide (16), and thus FMD is considered to be a measure of endothelium-dependent vasodilatation. FMD results correlate with findings obtained by invasive testing of coronary endothelial function (17) and with the extent and severity of coronary artery disease (CAD) (18). Impaired FMD has been demonstrated in subjects with vascular risk factors such as diabetes mellitus, smoking, hypertension, and hypercholesterolemia (15). FMD is also abnormal in inflammatory states including acute vaccine-induced systemic inflammation, systemic necrotizing vasculitis, and systemic lupus erythematosus (19–21).
In most studies of FMD, endothelium-independent vasodilatation (a measure of smooth muscle function) is also assessed by recording the vasodilator response to an exogenous nitric oxide donor such as sublingual glyceryl trinitrate (GTN) (22). Analysis of pooled data from 800 subjects who had participated in various studies of endothelial function demonstrated a significant relationship between GTN- and flow-mediated dilatation, independent of the effects of vessel size or traditional vascular risk factors (23). More recently, the dose-response curve for GTN-mediated vasodilatation has been examined in subjects with proven CAD and in healthy controls (24). Compared with controls, the CAD patients had significantly reduced GTN-mediated vasodilatation, with the greatest difference observed with lower doses of GTN (150–400 μg). This suggests that, in addition to endothelial dysfunction, atherosclerosis is associated with functional abnormalities of vascular smooth muscle cells (24).
Pulse wave analysis (PWA) is a technique in which large and small artery compliance (or elasticity) is estimated from analysis of the peripheral arterial waveform. The radial artery pulse wave is measured with a tonometer, and large and small artery compliance (C1 and C2, respectively) is calculated from the recorded waveform, using a modified Windkessel model (25). The modified Windkessel model is a mathematical depiction of the vasculature as a number of related components: capacitive compliance (C1 index), oscillatory or reflective compliance (C2 index), inductance, and resistance (systemic vascular resistance), measured during the diastolic decay portion of the cardiac cycle (25). This technique has been validated against invasive tests of arterial compliance (26), and reduced arterial compliance has been demonstrated in patients with hypertension, patients with diabetes, and smokers (27–29). Increased arterial stiffness as measured by pulse wave velocity has also been correlated with coronary atherosclerosis (30) and has been shown to predict coronary events and mortality in patients with hypertension (31, 32).
This study was undertaken to determine the relationship between RA-associated systemic inflammation and vascular function, using FMD and PWA. To reduce the confounding effects of known determinants of endothelial and vascular function, we studied young patients (ages ≤55 years) who did not have major cardiovascular risk factors. Brachial artery FMD was measured in 25 RA patients and 25 healthy controls, as well as in 10 individuals with multiple cardiovascular risk factors or proven cardiovascular disease. PWA was measured in a subgroup of 18 RA patients and 18 matched healthy controls.
Demographic characteristics of the study subjects.
We recruited 25 patients (6 men, 19 women; age range 26–55 years) with RA according to the criteria of the American College of Rheumatology (formerly, the American Rheumatism Association) (33) and 25 age- and sex-matched healthy controls. Exclusion criteria for both groups were known or suspected cardiovascular disease or the presence of 1 or more traditional cardiovascular risk factors. We defined traditional cardiovascular risk factors as cigarette smoking (in the previous 10 years), hypertension (systolic blood pressure >140 mm Hg or diastolic blood pressure >90 mm Hg), diabetes mellitus, hypercholesterolemia (total cholesterol >6.5 mmoles/liter or taking cholesterol-lowering medication), and a history of premature (in men, age ≤45 years; in women, age ≤55 years) CAD in a first-degree relative. We also recruited 10 subjects with either proven CAD or 2 or more traditional cardiovascular risk factors, to demonstrate the validity of FMD. The study was approved by the Institutional Ethics Committee, and written informed consent was obtained from all subjects. Demographic and clinical characteristics of the RA and healthy control groups are shown in Table 1.
Healthy controls (n = 25) | RA patients (n = 25) | P | |
| |||
Age, years | 44.8 ± 8.6 | 46.4 ± 8.0 | 0.51 |
Female, no. (%) | 19 (76) | 19 (76) | 1.00 |
Systolic blood pressure, mm Hg | 123 ± 9.2 | 125 ± 10.0 | 0.21 |
Diastolic blood pressure, mm Hg | 78 ± 7.9 | 80 ± 7.0 | 0.29 |
Mean arterial pressure, mm Hg | 93 ± 7.8 | 95 ± 7.7 | 0.28 |
Body mass index, kg/m2 | 25.2 ± 4.8 | 26.5 ± 4.8 | 0.32 |
Total cholesterol, mmoles/liter | 5.5 ± 0.8 | 5.3 ± 0.8 | 0.24 |
LDL cholesterol, mmoles/liter | 3.3 ± 1.2 | 2.9 ± 0.8 | 0.20 |
HDL cholesterol, mmoles/liter | 1.7 ± 0.6 | 1.7 ± 0.6 | 0.67 |
Triglycerides, mmoles/liter | 1.2 ± 0.4 | 1.5 ± 0.9 | 0.10 |
Fasting glucose, mmoles/liter | 5.2 ± 0.5 | 5.2 ± 0.6 | 0.60 |
Fasting insulin, mIU/liter, median (range) | 4.5 (1.6–18.5) | 7.4 (2.2–17.5) | 0.0008 |
Lipoprotein(a), gm/liter, median (range) | 0.07 (0.01–1.21) | 0.14 (0.01–0.88) | 0.44 |
Homocysteine, μmoles/liter, median (range) | 8.9 (5.4–12.4) | 9.0 (5.8–17.3) | 0.91 |
ESR, mm/hour, median (range) | 12 (1–48) | 19 (1–68) | 0.07 |
CRP, mg/liter, median (range) | 1 (1–12) | 4 (1–59) | 0.006 |
hsCRP, mg/liter, median (range) | 0.8 (0.18–14.4) | 3.43 (0.56–18.2) | 0.0002 |
Rheumatoid factor positive, no. (%) | – | 16 (64) | – |
Erosions present, no. (%) | – | 22 (88) | – |
Modified Sharp score, median (range)† | – | 58 (0–364) | – |
Duration of RA, years | – | 13.7 ± 9.0 | – |
No. of DMARDs ever used | – | 3.3 ± 1.9 | – |
Currently using DMARD, no. (%) | – | 24 (96) | – |
Currently using prednisolone, no. (%) | – | 9 (36) | – |
Currently using NSAID, no. (%) | – | 14 (56) | – |
Disease Activity Score | – | 4.6 ± 1.6 | – |
Baseline evaluation.
Venous blood was obtained from all subjects after they had been fasting. Measurement of erythrocyte sedimentation rate (ESR), rheumatoid factor, lipid levels (total, high-density lipoprotein, and low-density lipoprotein cholesterol, and triglycerides), lipoprotein(a), insulin, glucose, and homocysteine was performed by the Royal Melbourne Hospital Pathology Service. Serum hsCRP was measured by immunonephelometry (BN-II nephelometer; Dade-Behring, Marburg, Germany) (intraassay coefficient of variation 2.7%). Resting 12-lead electrocardiography (EKG) was performed on all subjects. Radiography of the hands and feet of the RA patients was performed to detect bone erosions, unless the presence of erosions had been documented previously. Radiographs obtained during the study were scored according to the modified Sharp method (34). Disease activity in the RA patients was measured using the Disease Activity Score (DAS), a validated composite score incorporating tender and swollen joint counts, ESR, and a patient global assessment of disease activity (100-mm visual analog scale) (35). A DAS of ≤1.6 indicates remission, while a value of ≥4.3 suggests active disease (35).
Vascular function testing.
Brachial artery FMD was performed in all RA patients, healthy controls, and positive controls (60 subjects in total). Eighteen of the RA patients and their matched healthy controls were available for PWA testing.
Brachial artery ultrasonography was performed by a trained investigator using the standard technique (15). It was administered in the morning, after the subject had fasted overnight. Nonsteroidal antiinflammatory drugs (NSAIDs) were withheld for 24 hours prior to study. No subject was taking aspirin, cardiac medication, or a lipid-lowering agent. Subjects rested supine in a quiet, temperature-controlled (22–24°C) room. Continuous EKG monitoring and regular blood pressure measurement were performed. An inflatable cuff was placed around the upper forearm. Studies of the left brachial artery were performed using high-resolution ultrasound (ATL HDI Ultramark 9; generously provided by Philips Medical Systems, Seattle, WA) with a 7–10-MHz linear array transducer. The left brachial artery was scanned in longitudinal section 2–15 cm above the elbow, and the transducer was fixed in position by a magnetic clamp. Focus, depth, and gain settings were set to optimize images of the lumen/arterial wall interface and remained unchanged throughout the study. A baseline scan was recorded for 2 minutes, followed by inflation of the cuff to 250 mm Hg for 5 minutes. The FMD scan commenced 30 seconds prior to release of the cuff and continued for 2 minutes after cuff deflation. Ten minutes later a second baseline scan was performed. A tablet of GTN (600 μg) was administered sublingually and recording continued for a further 5 minutes (the GTN scan).
The ultrasound images were recorded on Super-VHS videotape for subsequent analysis. All scans were analyzed by an investigator who was blinded to subject identity and disease status. Arterial diameter was measured from the intima–lumen interface of the near and far walls of the artery using ultrasonic calipers, coincident with the R-wave peaks on EKG. A minimum of 12 cardiac cycles were analyzed during the baseline and GTN scans. During the FMD scan, measurements were obtained at 5-second intervals following cuff deflation. FMD and GTN-mediated dilatation are expressed as the percentage change in artery diameter from baseline.
PWA was performed by a trained investigator using the standard technique (26). It was administered in the morning, after the subject had fasted overnight. A radial artery pressure sensor (tonometer) was placed over the radial artery at the right wrist and fixed in position. The position of the sensor was adjusted to optimize the radial artery waveform recording and remained in the same position throughout the study. The waveform was calibrated with a blood pressure cuff on the opposite arm and an internal calibration system. Thirty-second tracings of the radial artery waveform were digitized and waveform data were analyzed using a computerized modified Windkessel model (HDI) to derive estimations of large and small artery compliance (C1 and C2). The mean of 3 separate measurements was used in data analysis.
Reliability and validity.
Test–retest reliability of brachial artery FMD was assessed prior to institution of the formal study, by measuring FMD and GTN-mediated dilatation on 2 occasions, up to a week apart, in 11 volunteers. Between-test differences (mean ± SD) in FMD and GTN-induced dilatation were 1.5 ± 1.3% (intraclass correlation 0.79) and 3.1 ± 1.5% (intraclass correlation 0.88), respectively. Validity was demonstrated by measuring FMD and GTN-mediated dilatation under blinded conditions in 10 positive control subjects with either known CAD or ≥2 cardiovascular risk factors. Test–retest reliability of PWA was assessed prior to institution of the formal study, by measuring C1 and C2 on 2 occasions, up to a week apart, in 11 volunteers. Between-test differences (mean ± SD) in C1 and C2 were 2.8 ± 2.3 ml/mm Hg × 10 (intraclass correlation 0.74) and 1.0 ± 0.6 ml/mm Hg × 100 (intraclass correlation 0.95), respectively.
Statistical analysis.
Sample size calculations were performed based on the FMD component of the study. In previous studies of healthy subjects, reported mean FMD values have ranged from 106% to 112% (SD 3–6.5%), while in subjects with vascular risk factors such as cigarette smoking, hypertension, or hypercholesterolemia, mean FMD ranged from 100% to 106.5% (20, 36, 37). For the purpose of sample size calculations we estimated a mean ± SD FMD of 108 ± 4% in our healthy controls. Detection of a minimum reduction in mean FMD of 4% in RA patients compared with healthy controls, with power = 0.9 and α = 0.05, required 22 subjects per group. Results are expressed as the mean ± SD unless indicated otherwise. The RA and control groups were compared using the 2-sample (independent) t-test (for normally distributed data) and Wilcoxon's rank sum test (for skewed data). P values less than 0.05 were considered significant.
The RA and healthy control groups were well matched in terms of age, sex, blood pressure, lipid levels, and body mass index (BMI) (Table 1). The majority of RA patients had seropositive, erosive disease which was longstanding and had been treated aggressively with disease-modifying antirheumatic drugs (DMARDs) (Table 1). The mean DAS was 4.6, consistent with active disease despite DMARD treatment. The RA patients had a significantly higher median CRP level (4 mg/liter versus 1 mg/liter; P = 0.006), and median hsCRP level, (3.4 mg/liter versus 0.8 mg/liter; P = 0.0002) and a higher median ESR (19 mm/hour versus 12 mm/hour; P = 0.07) than the healthy controls (Table 1), reflecting active systemic inflammation. Fasting insulin levels were higher in the RA patients; however, the difference was not significant after correction for prednisolone usage. Fasting glucose, homocysteine, and lipoprotein(a) levels were similar in the RA and healthy control groups. Five of the female RA patients and 4 of the female healthy control subjects were postmenopausal. The positive control subjects were older (mean ± SD 60.3 ± 9.2 years) and had higher systolic blood pressure (150 ± 14.8 mm Hg) and BMI (33.3 ± 9.5 kg/m2) compared with the other 2 groups.
Flow-mediated dilatation.
FMD was significantly impaired in the positive controls compared with the healthy controls (mean ± SD 101.1 ± 3.9% and 108.5 ± 4.1%, respectively; P < 0.0001) (Figure 1 and Table 2). This result was expected and demonstrates the discriminative capability of this test under the experimental conditions used in this study. In contrast, FMD was normal in the RA patients (107.6 ± 4.6%), with no significant difference in percentage dilatation compared with the healthy controls (P = 0.49). GTN-mediated dilatation and baseline brachial artery diameter were similar in the RA and healthy control groups (Table 2). There was no significant correlation between FMD and ESR, CRP, DAS, disease duration, or Sharp score (data not shown).
Positive controls (n = 10) | Healthy controls (n = 25) | RA patients (n = 25) | |
| |||
Brachial artery diameter, mm | 3.4 ± 0.9 | 3.0 ± 0.5 | 2.9 ± 0.5 |
Flow-mediated dilatation, % | 101.1 ± 3.9† | 108.5 ± 4.1 | 107.6 ± 4.6 |
GTN-mediated dilatation, % | 120.5 ± 13.3 | 126.5 ± 7.3 | 129.2 ± 10.7 |
Pulse wave analysis.
Both C1 and C2 were significantly reduced in the RA patients compared with the healthy controls. C1 was 14.8 ± 2.8 ml/mm Hg × 10 in RA patients versus 17.9 ± 3.1 ml/mm Hg × 10 in healthy controls (P = 0.0033) (Figure 2 and Table 3), and C2 was 4.5 ± 2.3 ml/mm Hg × 100 in RA patients versus 7.7 ± 3.7 ml/mm Hg × 100 in healthy controls (P = 0.0039) (Figure 3 and Table 3). At the time of PWA testing the diastolic blood pressure was normal (≤90 mm Hg) in all subjects; however, mean diastolic blood pressure and mean arterial pressure were greater in the RA patients than in the healthy controls (78 mm Hg versus 73 mm Hg and 94 mm Hg versus 89 mm Hg, respectively; P = 0.042 and P = 0.053). The resting pulse rate was also greater in the RA patients (72 beats per minute versus 62 beats per minute; P = 0.0042). A modified Sharp score was available for 13 of the 18 RA patients who had PWA. In these patients there was a significant inverse correlation between C2 and Sharp score (Spearman's rho −0.69, P = 0.0085) (Figure 4). There was no significant correlation between PWA and ESR, CRP, hsCRP, DAS, disease duration, or FMD (data not shown).
Healthy controls (n = 18) | RA patients (n = 18) | P | |
| |||
Systolic blood pressure, mm Hg | 121 ± 11 | 126 ± 10 | 0.1 |
Diastolic blood pressure, mm Hg | 73 ± 5 | 78 ± 8 | 0.042 |
Mean arterial pressure, mm Hg | 89 ± 6.6 | 94 ± 8.7 | 0.053 |
Pulse rate, beats per minute | 62 ± 9.9 | 72 ± 9.3 | 0.0042 |
Height, cm | 169 ± 8.5 | 166 ± 8.6 | 0.22 |
Large artery compliance (C1), ml/mm Hg × 10 | 17.9 ± 3.1 | 14.8 ± 2.8 | 0.0033 |
Small artery compliance (C2), ml/mm Hg × 100 | 7.7 ± 3.7 | 4.5 ± 2.3 | 0.0039 |
Connective tissue diseases such as RA and systemic lupus erythematosus appear to be associated with accelerated atherosclerosis (1, 38). The mechanisms involved are not clear, but may include endothelial dysfunction mediated by systemic inflammation. Elucidation of these mechanisms may provide insight into the role of inflammation in atherosclerosis. The onset of RA generally occurs in early adulthood, and it is therefore especially important to explore potential markers for the early stages of atherosclerosis in this population. In the present study we explored 2 measures of vascular function, FMD and PWA, in young RA patients who did not have traditional cardiovascular risk factors. We first confirmed the reproducibility of FMD and PWA and demonstrated that FMD measurement performed as expected in patients with known cardiovascular disease. We then measured FMD and PWA in RA patients and age- and sex-matched controls who were carefully chosen to exclude the confounding influence of traditional cardiovascular risk factors. We found that both large and small artery compliance was reduced in the RA patients compared with the healthy controls. In contrast, FMD was normal in these RA patients. We believe this latter finding is accurate because we have demonstrated our ability to detect an abnormality in FMD if one is present, and our sample size calculation suggests that the study had adequate power to detect any meaningful difference.
A number of issues need to be considered when interpreting these results. The effect of treatment with antirheumatic medications on vascular function is unknown. In particular, NSAIDs could have a significant impact on endothelial function. The nonselective NSAIDs inhibit production of both prostacyclin (a vasodilator) and thromboxane A2 (a vasoconstrictor), whereas the cyclooxygenase-2 (COX-2)–specific inhibitors selectively inhibit prostacyclin alone (39). Fifty-six percent of the RA patients in this study were taking various selective and nonselective NSAIDs, the plasma half-lives of which range from 1.5 to 17 hours. Although NSAID treatment was discontinued in all patients at least 24 hours prior to vascular function testing, it is possible that washout of the drug was incomplete in some patients. In a study of healthy volunteers, however, Verma et al (40) demonstrated that 7 days of treatment with either naproxen (a nonselective NSAID) or rofecoxib (a selective COX-2 NSAID) did not alter endothelial function. Furthermore, we noted no difference in FMD or PWA between NSAID-treated and non–NSAID-treated patients. Hence, we believe it is unlikely that recent use of NSAIDs impacted significantly on our results.
The HDI PWA system used in this study, which derives arterial compliance from diastolic pulse contour analysis using the modified Windkessel model, is one of a number of different techniques to measure arterial compliance. The validity of the physiologic assumptions used in the Windkessel model has recently been debated (41). This issue is not fully resolved; however, the HDI system has been validated against invasive tests of arterial compliance (26), and reduced arterial compliance has been demonstrated in subjects with a variety of cardiovascular risk factors (27–29). Therefore, C1 and C2 may still be clinically useful as biomarkers of arterial dysfunction or disease (41).
In this study of vascular function in RA patients, FMD was preserved whereas large and small artery compliance was significantly reduced. How can these apparently discordant results obtained using 2 different measures of vascular function be explained? Not all subjects who participated in the FMD study were able to participate in PWA testing, and this could potentially have given rise to selection bias. However, the 18 RA patients who had PWA performed had lower mean blood pressure and cholesterol levels and higher mean FMD than the RA patients who did not undergo PWA. Although these differences were not statistically significant, the selected group presumably had better vascular function than the untested subjects, and hence any selection bias would favor the null hypothesis.
FMD and PWA are both dependent on nitric oxide bioavailability (16, 42) and therefore reflect endothelial cell function; however, the techniques have important differences. FMD is a stress test of dilatation in response to increased flow, whereas PWA measures resting arterial compliance and tone. FMD is mediated predominantly by endothelial release of nitric oxide, since the vasodilator response is almost completely blocked by treatment with nitric oxide synthase inhibitors (16). Therefore, the FMD response can be considered to be almost entirely dependent on endothelial cell function. McVeigh et al (43) reported that systemic infusion of L-NG-nitroarginine methyl ester, an inhibitor of nitric oxide synthesis, reduced small artery compliance in healthy male volunteers. Using a different method of pulse wave analysis, Wilkinson et al (42) demonstrated that infusion of L-NG-monomethyl arginine, an inhibitor of nitric oxide synthase, led to a dose-dependent increase in systemic arterial stiffness in healthy men. These data indicate that arterial stiffness is, in part, regulated by nitric oxide availability, and therefore PWA, at least in part, measures endothelial cell function. However the relative contribution of other factors, such as smooth muscle and connective tissue content of the artery wall, to PWA is unknown. The relationship between FMD and PWA has not been examined extensively, although correlation between the 2 measurements has been reported in a population of growth hormone–deficient subjects with abnormal endothelial function (44).
Perhaps PWA is a more sensitive measure of endothelial dysfunction than is FMD, detecting subtle reduction of vascular compliance before impaired endothelium-dependent vasodilatation becomes apparent. Alternatively, RA may cause specific vascular abnormalities, such as structural change in vessel walls or smooth muscle dysfunction, that are more readily detected by PWA than FMD. In this case one might expect GTN-mediated vasodilatation to be reduced in RA patients. We did not demonstrate a difference in GTN-mediated vasodilatation between RA patients and healthy subjects; however, the dose of 600 μg of GTN used in this study (chosen to obtain the maximal vasodilator response) may be too high to allow detection of this. Ideally, a dose-response curve for GTN-mediated dilatation should be performed to fully evaluate endothelium-independent vasodilatation.
Blood pressure, pulse rate, and height are known determinants of measured arterial stiffness (45). At the time of PWA measurement the RA patients had a higher mean diastolic blood pressure, mean arterial pressure, and resting pulse rate than the healthy controls, although the values remained within the normal range. Although the between-group differences in C1 and C2 persisted after correction for blood pressure (in an analysis of covariance model, in which mean arterial pressure, pulse rate, and height were included as covariants, a significant difference between groups was still evident [C1: F = 5.7, P = 0.023; C2: F = 5.9, P = 0.021]), this relative hypertension in the RA patients may be clinically important. Hypertension is an established and powerful risk factor for cardiovascular disease (46). Meta-analysis of multiple observational studies involving more than 420,000 untreated individuals projected that a 5–6 mm Hg average decrease in diastolic blood pressure would lead to a 25% reduction in coronary mortality (46). Many of the medications used to treat RA elevate blood pressure, including NSAIDs, glucocorticoids, and cyclosporine. Perhaps the excess cardiovascular risk in RA can be partially attributed to a slightly higher blood pressure in this population, even though it may remain within the normal range.
Increased resting heart rate has also been identified as an independent risk factor for cardiovascular and all-cause mortality in prospective population studies (47–50). The mechanism by which this operates is not known, but it may reflect physical fitness. Exercise capacity and activity status are established predictors of cardiovascular and overall mortality (51, 52), and RA may be associated with reduced exercise capacity due to joint inflammation and fatigue. The higher resting pulse rate in these RA patients may reflect reduced physical fitness, which in turn is associated with endothelial dysfunction.
If inflammation does indeed contribute to vascular disease, it could be due to the cumulative effect of chronic, low-grade inflammation, acute inflammation precipitating rupture of an unstable plaque, or a combination of the two. We found a significant inverse correlation between C2 and modified Sharp scores in the RA patients, whereas there was no correlation between arterial compliance and ESR, CRP, hsCRP, disease duration, or current DAS. These latter measures reflect RA disease activity at a single point in time, whereas the Sharp score reflects the degree of joint inflammation that has occurred over time (53). This relationship between cumulative disease activity and severity of arterial stiffness supports the notion that chronic inflammation plays a role in RA-associated atherosclerosis.
This is the first reported study of FMD and PWA in RA patients who were carefully screened to exclude an alternative explanation for abnormal vascular function. In our RA patients with moderate-to-severe arthritis and many years of systemic inflammation, FMD was preserved whereas large and small artery compliance was significantly reduced. Greater understanding of the determinants of arterial compliance may provide insights into the underlying mechanism(s) of accelerated atherosclerosis in RA. Blood pressure is a major determinant of arterial stiffness, and regular screening for and rigorous treatment of hypertension in patients with RA may be especially important. It may even be that the "safe" level of blood pressure in RA patients is lower than that for the general population. Reduced physical fitness may be a major contributor to the excess mortality in RA. Exercise training has been shown to be safe and beneficial in RA patients (54), and pursuit of regular exercise should be strongly encouraged in this group. The reduction in C2 in the RA patients correlated with the Sharp score, a measure that is known to reflect disease severity and activity over time (53). Further research is needed to determine whether optimal disease control with DMARDs preserves vascular function in RA. PWA appears superior to FMD in identifying asymptomatic vascular disease in RA patients, and investigators conducting intervention studies aimed at reducing vascular disease in RA should consider including PWA as an end point.
Longitudinal followup of a cohort of RA patients is needed to ascertain the extent to which increased arterial stiffness correlates with future cardiovascular events. In the meantime, our results highlight blood pressure, physical inactivity, and disease activity as potentially correctable causes of the increased cardiovascular burden in RA.
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- 40Cyclooxygenase-2 blockade does not impair endothelial vasodilator function in healthy volunteers: randomized evaluation of rofecoxib versus naproxen on endothelium-dependent vasodilatation. Circulation 2001; 104: 2879–82., , , , .
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- 42Inhibition of basal nitric oxide synthesis increases aortic augmentation index and pulse wave velocity in vivo. Br J Clin Pharmacol 2002; 53: 189–92., , , .
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- 44Effects of GH replacement on endothelial function and large-artery stiffness in GH-deficient adults: a randomized, double-blind, placebo-controlled study. Clin Endocrinol (Oxf) 2002; 56: 493–501., , , , , , et al.
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- 46Blood pressure, stroke, and coronary heart disease. 1. Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet 1990; 335: 765–74., , , , , , et al.
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Last updated Apr 4, 2013
Apr 4, 2013
Do NOT recommend. Hubby and I had been going there for years and it was always good. BUT went several weekends ago on a Saturday. He had the buffet and I ordered a scallop special since there was not much for me on the buffet as I don't eat meat. Our drinks were brought and he went and got a salad. He finished his salad and my food was not there yet, he was going to wait but I told him not to since it was close to the end of the buffet serving time. He went and got a plate of food and the waitress came and said my order went to the bar instead of the kitchen but it would be out soon. He finished his plate of food and my food still was not there. He was getting upset and that upset me. He normally has two plates of food from the buffet as the plates are small but he would not go and get any more. The waitress walked by again and he called her over and got more excuses and asked for the check as we were not going to wait any longer. Then the "manager?" (not sure as we were not told who she was) came over and as she arrived they ran out of the kitchen and put a plate in front of me. I could see that the scallops were not even fully cooked and didn't smell good and I surely was not going to eat them that way. They offered no discount or anything so (unfortunately) we asked them to pack it up, I figured I would finish cooking them at home and it wouldn't be a total waste. What a mistake that was. We do not live in Claremont and had a half hour ride home. The smell of those scallops was pretty bad. I put them in the fridge when we got home - another mistake. I had to air my jeep out with windows open for two days and the fridge had to be totally cleaned and dishes of baking soda put in and it still took a few days to get the smell out of it. If I had known they were actually BAD I never would have taken them home. We will NEVER go back there again.
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The Devil is in the...Dairy
By Tinka on June 02, 2013
I knew it would be, but still, the results were harsher than I expected. My youngest is so intolerant to dairy that he can't even have goat cheese, yogurt, milk which I had recently been relying on. Plus, they are both intolerant of almonds, so there goes the almond milk I use in all my baking, waffle making, etc and it also makes protein bar buying surprisingly difficult. My older one also needs to be off peanuts, eggs, and some other things that don't really matter for at least six months while their bodies heal from all the damage of ingesting gluten (and dairy) for years. Ah yes, the gluten~ I forgot to even mention that one, but that was a given also. The naturopath thinks my husband is probably also gluten intolerant b/c the kids' intolerances are so severe. He's finding out. Fun times at our house. Despite all my prepping for this, I am finding meal times exhausting during this transition period. I know it will get easier, my logical brain was fully prepared for a period of adjustment, some whining and frustration, and some uneaten foods that took a long time to prepare, but my emotional brain can't seem to keep my own level of frustration in check. When I look at the clock and realize it's close to a meal time I feel my cortisol levels rise and my mind starts speeding through options~ what can everyone eat so I have to make the least amount of separate meals that gives everyone balanced options and fairly happy and normal and not stressed out while meanwhile I'm stressing out before I even step foot into the kitchen...sigh. I know it will get easier, I really do~ I'm all set to start meal planning with input from every member of the family and to spend some extra time making food such as soups and casseroles that will last for a few days and will be good fall back food, but I don't feel like I can do that until I have all the bits of information assembled, namely my husband's and my own intolerances fully understood. We'll get there, I know. Of course I can say that calmly because it is 1:52PM and I don't have to make dinner for another 3+ hours...
On a different note, I read a very nice article today that spells out gluten intolerance quite well. For those who have to explain themselves all the time, or are just curious about it, this is a great (short) article to help make that explanation very clear and concise:http://www.mindbodygreen.com/0-9739/how-gluten-wreaks-havoc-on-your-gut.html.
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Brothers died in blaze after being 'locked' in bedroom
Wednesday 20 October 1993
The handles had been removed from the door which could only be opened from the outside by a pair of pliers, the hearing at Preston, Lancashire, was told.
Daniel Bamford, four, and his brother, Michael, two, were found in bed in each other's arms in the room at their Preston home in September. A cigarette lighter was also found in the room.
Attempts to revive them failed and they were dead on arrival at hospital. Their mother Maureen, 21, told the inquest that her sons were 'mischievous' like other children of their age and kept coming in and out of their bedroom. Her sister had taken the handles off the door, but 'you could get in using a pair of pliers', she said.
Mrs Bamford agreed with Howard McCann, the coroner, that the boys were 'effectively locked in'. Dr Edmund Tapp, a Home Office pathologist, said they died from smoke inhalation. The court also heard that a file was being sent to the Crown Prosecution Service.
Recording verdicts of accidental death, the coroner said the likely cause of the fire was one of the children setting fire to some toys. But a key factor was the bedroom door being locked.
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Forum - View topicViz Media Anime Solicitations Thread
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View previous topic :: View next topic | ||||||
Author | Message | |||||
Vata Raven Posts: 711 Location: TN |
Not if it's Viz themselves getting rid of old stock, since I'm sure they have a warehouse for their things before shipping them out. And with the new sets coming into print, I doubt anyone is going to want to buy the other sets at the high price. Though...not sure why they didn't just reprice them like they're doing with everything else. |
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Sheleigha Posts: 1488 |
It probably will be a thin pack >_> Makes me sad because it'll probably actually match The Final Act. Oh well, I already bought already the thicker packs. I wish I didn't lose the insert for S2 :/ Fell out apparently... Bugs me... | ||||||
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WTK Posts: 2494 |
via WBshop.com Box Type: VIVA 5 Disc 15mm Case | Details It should be similar to this below (ignore the color) |
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Rukiia Team Gurren Posts: 1798 Location: British Columbia, Canada |
Hmmm......I do like slimmer cases to help free up some shelf space. However, I am rather fond of my fat boxsets. Too bad it isn't a Blu-ray release as I would have definitely ordered it. I'll wait and see what the cover art looks like. | ||||||
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Sheleigha Posts: 1488 |
It still amazes me how back in the anime day of bricks, that those type of cases did not even exist. I'm staring at my MKR 2 economy box, where every little "door" only has 2 disks, and there are several doors. ... At least the thick Viz boxes look nice and presentable. | ||||||
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WTK Posts: 2494 |
More repackaged re-releases:
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WTK Posts: 2494 |
via TRSI...
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WTK Posts: 2494 |
via TRSI...
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Blood- It...it's not like I post for you or anything! Posts: 15941 Location: Toronto, Canada |
Cool. It's been a while since Viz has had a new release that I actually cared about. | ||||||
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classicalzawa Space Cowboy Posts: 5283 |
What in the hell kind of prices are those? They look like Walmart prices where everything ends in 88 cents instead of 99 cents. | ||||||
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jsc315 Posts: 925 |
Also why is set 2 more expensive for the same exact of episodes as well as special features. I hate when companies do this just to make you spend more since you already have the 1st half. Really makes me not want to support a company or buy anything when they price gouge a product just for the sake of it. |
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willag Moderator Posts: 3063 |
Um, I'm not certain where you're seeing set 2. The two that WTK have linked above are for DVD and blu-ray versions of set 1. |
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jsc315 Posts: 925 |
oops! I was tired. I retract my rant. Not sure what i was thining there |
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WTK Posts: 2494 |
Amazon.com has added the cover arts. Both formats now note episode 1 to 13 (instead of 12). |
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Kruszer Enjoying the time of EVE Posts: 7038 Location: Minnesota, USA |
Hah! So that's why everyone has the bigger versions on sale now for super cheap eh? Trying to get rid of old stock. |
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― The words "carnival" and "circus" have dual connotations. On the one hand, they are places of entertainment, words which make us think of swirling music and fantastic feats, glittering costumes and trained animals. On the other hand, the words can refer to a place where the rules of everyday life have b...
The Mike Toole Show - SNK-Hole
Mike dons his red trucker cap and takes a journey through all the various shlocky and unique OVAs based on old SNK fighting games.
― It took me ages to track it down. I'd been after this particular OVA for something like eight years, and for a long time, the hunt just didn't go well. First of all, the show wasn't a "true" OVA, it was an ONA that was briefly broadcast online, but region locked to Japa...