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JWPL is a language independent, database-driven, high performance Wikipedia API that provides structured access to information nuggets like redirects, categories, articles, and link structure. It contains a Mediawiki Markup parser that can be used to further analyze the contents of a Wikipedia page or standalone with other text, TimeMachine, which reconstructs a snapshot of Wikipedia from a specific date, or multiple snapshots from a time span, and RevisionMachine, which offers efficient access to the history of articles using a dedicated storage format which decreases storage space by 98%. This enables random access to the whole revision history without requiring several terabytes of storage for a single Wikipedia dump.
|Wikipedia API revisions edit history JWPL converter Parser MediaWiki
|Operating Systems
|Platform Independent
|Java 1.6+ hibernate
Release Notes: This release contains major changes in the JWPL API. However, some of the changes are still ongoing, i.e. the switch from the JWPL parser to the SWEBLE parser. Hence the minor release. Nevertheless, the JWPL should be stable. The JWPL parser has been moved to its own module. Projects using the parser have to add it as an additional dependency. Individual bugfixes and enhancements can be seen in the individual module changelogs.
Release Notes: This release fixes a bug in the API which prevented fetching inlink IDs. Several improvements to hibernate session handling have been made.
Release Notes: JWPL Core now depends on Hibernate 4.0.0-final. The PageIterator can now iterate over a predefined list of pages. All components of the RevisionMachine are now able to produce datafiles in addition to SQL dumps. A severe error in the DiffTool has been fixed that caused exceptions when creating a new revision dump.
A Fluent OpenStack client API for Java.
A TWiki appliance that is easy to use and lightweight.


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Hey everyone! I'm a goofy footed surfer and im having MAJOR problems taking the wave to the left, im perfectly fine going right but every time i try to take it left i wipe out almost immediately... Any advice for me? i just wanna be able to ride em both ways when its necessary. Thanks in advance! Btw, anyone on the georgia coast notice unusually better waves today? Lol because Tybee doesnt usually get clean 3-5+.
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Problems going left

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"It was like living at a time when Beethoven and Mozart were alive.Ugg Slippers Kids This coat, as I'm sure all the coats from parajumpers are ridiculously warm.Ugg Classic Cardy" Raskin's former student Bill Atkinson sided with Jobs." The move was only three miles to the south, to a former apricot orchard in Los Altos that had been turned into a subdivision of cookie-cutter tract homes. These are the boots to wear walking in snow. "My dad would drive me in the morning and pick me up in the evening."He nodded his head toward the outer corridor. ugg sale women " Terrell was impressed enough to hand Jobs and Woz his card.Ugg Brand Boots "My dad would drive me in the morning and pick me up in the evening. There is no heal support like authentic Uggs, so the conterfeits slouch when warn, the shape is different from the front seam to the toes (barely noticeable, but it IS different) the height of the SHORT boots are slightly off and the lining of the counterfeit is not as plush or thick." Kay pushed the vision of a small personal computer, dubbed the "Dynabook," that would be easy enough for children to use. Boasting signature Twinface sheepskin, luxurious natural wool, and added foam for all-day wearability, this cuffable boot delivers the ultimate in warmth and comfort. "I started pointing them out everywhere until he was completely convinced.Ugg Boots Sale Free ShippingSizing On Ugg Boots' It was all laid out—the tones, the frequencies.
It wears off when he's not around, but it makes it hard to have realistic schedules. Ugg Slippers Kids An independent developer came up with the first spreadsheet and personal finance program for personal computers, VisiCalc, and for a while it was available only on the Apple II, turning the computer into something that businesses and families could justify buying.Ugg Australia Boots On Sale Free Shipping Boasting signature Twinface sheepskin, luxurious natural wool, and added foam for all-day wearability, this cuffable boot delivers the ultimate in warmth and comfort.S. She would go to his office, shut the door, and gently lecture him. In hopes of attracting more male consumers, UGG started an ad campaign with New England Patriots quarterback Tom Brady in 2012. [Ugg Slippers Kids] "So he's pointing the gun right at my stomach, and he says, 'Hand it over, brother.
But Telemachus as he lay covered with a woollen fleece kept thinking all night through of his intended voyage of the counsel that Minerva had given him.Ugg Boots Sale Free Shipping In the meantime I will go to Ithaca, to put heart into Ulysses' son Telemachus; I will embolden him to call the Achaeans in assembly, and speak out to the suitors of his mother Penelope, who persist in eating up any number of his sheep and oxen; I will also conduct him to Sparta and to Pylos, to see if he can hear anything about the return of his dear father — for this will make people speak well of him." The Jobses' house and the others in their neighborhood were built by the real estate developer Joseph Eichler, whose company spawned more than eleven thousand homes in various California subdivisions between 1950 and 1974. And yet somehow these attitudes seemed to weave together rather than conflict. "Neighborhood kids used to come over and we would toss them in it and it was great fun," said Kottke, "but then Chrisann brought home some cats who peed in the foam, and then we had to get rid of it. [Ugg Slippers Kids] "There were holy men all around.
"Chrisann would get into this kind of victim mode, when she would say that Steve and I were ganging up on her," Kottke recalled. ugg sale women " Midway through the summer, Jobs was almost killed when his red Fiat caught fire. Jobs immediately called Wozniak at HP. So the Xerox folks huddled privately and decided to open the kimono a bit more, but only slowly. [ugg sale women] When they were within he took her spear and set it in the spear — stand against a strong bearing-post along with the many other spears of his unhappy father, and he conducted her to a richly decorated seat under which he threw a cloth of damask.


text: Grace Lord was a Silostophan who, along with many of her people, was enslaved by the Christmas Corporation to work as elves. They were kept drugged so they would obey the managing director, S. Claus. The Fourth Doctor and Adric met Grace when they were captured by Mr Claus. She helped them start a rebellion of the slaves. (PROSE: Planet of the Elves)


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Samsung Galaxy Nexus is expected to come with the much anticipated Android 4.0 Ice cream sandwich where as Motorola Droid Razr makes use of the older Android 2.3 Gingerbread as of now. As far as the design of both the smartphones are concerned. Both come with extremely slim and sleek design which makes both the products extremely attractive and portable. It seems that Samsung has a slight edge with this better performing operating system as of now. Galaxy Nexus weighs around 135 grams where as Droid Razr is much lighter at 127 grams. Galaxy Nexus has a thickness of 8.9mm where as Droid Razr is a slim model with 7.1 mm which gives Motorola a slight edge over its rival.
Galaxy Nexus comes with a 4.65 inches display with a screen resolution of 1280*780 pixels where as Motorola Droid Razr has a 4.3 inch LED display with a screen resolution of 960*540 pixels which gives Samsung smartphone a clear edge. Both the products possess simultaneous hardware features that include 1.2 GHz T1 OMAP dual cores Processor which is further enhanced by the presence of a PowerVR SGX 540 GPU processor. The two Smartphones comes with 16GB of internal storage capacity. Where as Galaxy Nexus also has an option of 32GB of internal storage. Both make use of 1GB of RAM. Both the smartphones comes with the presence of a microSD card slot which plays the role of memory expandable card.
Motorola Droid Razr make use of an 8 mega pixel camera with 1080p of high definition video recording where as Galaxy Nexus comes with a 5 mega pixel camera that also provides high definition video recording of 1080p. Motorola Droid Razr comes with LTE as well as Bluetooth connectivity. Where as Samsung Galaxy Nexus comes with HSPA+ connectivity as well as Bluetooth connectivity. Both the smartphones comes with 802.11 b/ g/ n Wi-Fi connectivity also. Galaxy Nexus comes with 1750mAh of removable lithium ion battery that comes with a considerable talk time as well as stand by time where as Droid Razr comes with 1800mAh battery that has the capability of providing up to 12.5 hours of talk time.
The expected price in India of Droid Razr is Rs.12, 000 where as the expected price in India tag of Galaxy Nexus is Rs.13, 000.


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The 6-9 Lauderdale will be a junior this season. He returns after leading Solon to a 25-1 record and a berth in a Division I regional final. Only a 53-52 loss to Mansfield Senior prevented Solon from reaching the state final four.
Lauderdale earned first-team All-Ohio and Northeast Lakes District player of the year honors after averaging 17.5 points, 13 rebounds and 4.8 blocks per game.
"I feel a repeat coming," Lauderdale said. "We lost one of our best shooters in Jordan Krantz. But we have some people to pick up that slack.
"Right now, I'm just getting acquainted with my teammates," Lauderdale said. "We have a couple of people moving in and some guys moving up to the varsity. I think we can be pretty good."
Recruiting experts have taken notice of Lauderdale. He is ranked as the state's third-best junior-to-be by Ohio High magazine, falling in just behind the North College Hill duo of O.J. Mayo and Billy Walker. Lauderdale is also ranked as the nation's 40th-best junior-to-be by ScoutHoops.com.
"I don't pay attention to that," Lauderdale said. "People come to me every day and say I'm good and talk about where I'm ranked and all that. I don't pay attention to any of that. I just play basketball."
Lauderdale works hard to get the ball in the post, but he is also a high-effort guy on the glass. At the team camp, he routinely skied to finish plays around the rim.
"I always try to work hard," Lauderdale said. "Respect everybody but fear nobody. I just play basketball."
As far as the college level, Lauderdale said, "I'm trying to work on my outside game. I think about the NBA. I look at T-Mac (Tracy McGrady). He's 6-8 and playing the two-guard in the NBA. I'm 6-9. If I'm 6-9, I would be a small post in the NBA. That's why I know I have to work on my jump shot. I think I have my post game down."
Lauderdale also plays for the Cleveland Titans AAU team.
"I know we will be playing at nationals in Orlando in July," he said. "I don't know about individual camps and where I might be going. I've been invited to everything."
In terms of colleges, Lauderdale listed a top five of Ohio State, Syracuse, North Carolina, Illinois and Michigan State.
"The schools I have spoken with have offered, like O-State and Syracuse," he said. "I've gotten a lot of letters from a lot of places, including Kentucky and Duke."
Lauderdale said OSU coach Thad Matta and his staff offered him a scholarship shortly after coming to Columbus last July – that would have been after Lauderdale's freshman year at Solon.
"Right then, it was overwhelming," Lauderdale said. "I wasn't expecting anything. I was only going to be a sophomore. I've seen them develop very quickly here. I think O-State will be pretty good in a couple of years.
"They picked up (Dayton Dunbar's) Daequan (Cook) and also my good friend (and AAU teammate) David Lighty. I see them winning a national championship. I'd like to be a part of that, of course."
OSU's recruitment of Indiana 7-foot center Greg Oden, the nation's top senior-to-be, may impact Lauderdale.
"If he comes here, he would be the five probably," Lauderdale said. "I know they also have (a verbal from) B.J. Mullens. Maybe he would play the four. I could play the three if I come here, but then you have David and Daequan, so I don't know exactly where I would be."
Regarding Syracuse, Lauderdale said, "I like the coaching staff. One of my friends told me they have an excellent communications program. That's what I'm thinking about majoring in right now. I just like the gym and everything. It's huge in the (Carrier Dome). I fell in love with that the first time I played on it."
Lauderdale lists a 3.0 GPA.


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Newcastle have sprung a surprise on the final day of the window by reportedly giving 23 year-old Haris Vuckic a new contract and he has been loaned out to Wigan Athletic in League One.
Well, that's according to the Daily Record in Scotland, and Sky Sports are also reporting the same story – and if it's true it's a bit of a surprise.
Haris Vuckic – while at Rangers earlier this year
Keith Downie of Sky Sports tweeted this from the Benton Training grounds – so he probably has inside information on this.
We understand Haris Vuckic is close to signing a contract extension at #NUFC and going out on a season-long loan to Wigan Athletic.
— Keith Downie (@SkySports_Keith) September 1, 2015
Vuckic has been at Newcastle since January of 2009, when he was signed from Domzale with great fanfare, and he had great potential.
But probably because a number of long term injuries, he has never fulfilled the enormous promise he showed as a teenager.
When he was signed six and a half years ago, Domzale held a press conference to announce the then 16 year-old was leaving, and let's just say he was one of the best players in Europe at his age at that time.
We had thought with one year left on his current contract, the once capped Slovenian International would be sold this summer, but it looks like Newcastle are giving Haris the chance.
It's similar to what the club did with Sammy Ameobi, who got a new contract of two years, and was sent off to Cardiff City on loan for the season.
It looks like Steve McClaren has seen enough of the central midfielder to think he may still be a good player and we suppose he gets a chance to prove that at Wigan.
There's no mention of how many years the contract has been extended by – but we'd be surprised if it was than a one year extension – so his contract will run out in 2017.
This looks like a safety first move by Newcastle, who seem to be giving Haris another season to prove he should be staying on Tyneside long term.
It's not yet official of course.
Haris Vuckic has played 19 times with one goal for Newcastle, and while at loan at Cardiff, Rotherham and Rangers, he has made another 46 first team appearances with 14 goals, with 9 of those coming while north of the border earlier this year.
What do you think?
Comments welcome.


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Rationale: Genomic loci are associated with FEV1 or the ratio of FEV1 to FVC in population samples, but their association with chronic obstructive pulmonary disease (COPD) has not yet been proven, nor have their combined effects on lung function and COPD been studied.
Objectives: To test association with COPD of variants at five loci (TNS1, GSTCD, HTR4, AGER, and THSD4) and to evaluate joint effects on lung function and COPD of these single-nucleotide polymorphisms (SNPs), and variants at the previously reported locus near HHIP.
Methods: By sampling from 12 population-based studies (n = 31,422), we obtained genotype data on 3,284 COPD case subjects and 17,538 control subjects for sentinel SNPs in TNS1, GSTCD, HTR4, AGER, and THSD4. In 24,648 individuals (including 2,890 COPD case subjects and 13,862 control subjects), we additionally obtained genotypes for rs12504628 near HHIP. Each allele associated with lung function decline at these six SNPs contributed to a risk score. We studied the association of the risk score to lung function and COPD.
Measurements and Main Results: Association with COPD was significant for three loci (TNS1, GSTCD, and HTR4) and the previously reported HHIP locus, and suggestive and directionally consistent for AGER and TSHD4. Compared with the baseline group (7 risk alleles), carrying 10–12 risk alleles was associated with a reduction in FEV1 (β = –72.21 ml, P = 3.90 × 10−4) and FEV1/FVC (β = –1.53%, P = 6.35 × 10−6), and with COPD (odds ratio = 1.63, P = 1.46 × 10−5).
Conclusions: Variants in TNS1, GSTCD, and HTR4 are associated with COPD. Our highest risk score category was associated with a 1.6-fold higher COPD risk than the population average score.
Genome-wide association studies have reported novel loci for lung function, but the association of these loci with chronic obstructive pulmonary disease (COPD) has not yet been tested, and their effects in combination have not yet been documented.
We show associations between COPD and polymorphisms in HTR4, GSTCD, and TNS1. Using a six-SNP (single-nucleotide polymorphism) risk score, incorporating variants in HTR4, GSTCD, TNS1, AGER, THSD4, and near HHIP, the highest risk category (~5% of Europeans) is associated with a 1.6- fold risk of COPD compared with a common baseline group.
Chronic obstructive pulmonary disease (COPD), characterized by airflow limitation that is not fully reversible, affects approximately 210 million people worldwide (1) and is among the leading causes of death in developed and developing countries (2, 3). Tobacco smoking is a potent cause of COPD, but not all smokers develop COPD and genetic determinants are also important (4). Identification of the genetic determinants of COPD could provide insight into molecular pathways that may be amenable to improved preventive and treatment strategies. A further potential utility of newly identified genetic associations is to predict disease risk. Current evidence available from common complex diseases where family history may be used, such as type 2 diabetes, suggests that tens of genetic variants with individually modest effects may provide similar but not necessarily substantially improved disease risk prediction over existing scores that incorporate family history (5, 6)
Genetic variants in SERPINA1 that cause α1-antitrypsin deficiency have long been known to affect COPD risk. Although there had been limited success in identifying additional susceptibility loci for COPD until 2009 (7), more recent genome-wide association (GWA) studies have shown associations between genetic loci and lung function measures that underpin the diagnosis of COPD (8–10). Two of these studies have investigated genome-wide association with lung function in large sample sizes (>20,000 subjects), focusing exclusively on quantitative lung function measures (8, 9). Since the advent of dense GWA genotyping platforms, the only loci convincingly associated with COPD have been HHIP (10, 11), which to date remains the strongest signal, CHRNA3/5 (11), and FAM13A (12).
We hypothesized that genetic variants associated with FEV1 and FEV1/FVC would be associated with COPD. In a study of 20,288 individuals with GWA data and follow-up of top signals in a further 54,276 individuals (SpiroMeta Consortium), we previously identified five novel loci showing association (P < 5 × 10−8) with FEV1 or FEV1/FVC: in TNS1 at 2q35, in GSTCD at 4q24, in HTR4 at 5q33, in AGER at 6p21, and in THSD4 at 15q23 (9).
In this article, based on the five loci reported by the SpiroMeta Consortium (9), we further investigate the clinical relevance of these loci. First, we test association of the sentinel single-nucleotide polymorphism (SNP) at each locus with COPD. Second, we investigate the combined effect of the risk alleles at all five novel loci described previously (TNS1, GSTCD, HTR4, AGER, and THSD4) and the previous association at 4q31 (near HHIP) (10) on lung function and COPD risk.
Some of the results of these studies have been previously reported in the form of abstracts (13, 14).
Figure 1 shows the study populations and loci included in the study design. The study population consisted of 31,422 individuals over the age of 40 years from 12 population-based studies. These studies included the European Prospective Investigation into Cancer and Nutrition obese cases cohort (EPIC-obese case subjects) and population cohort (EPIC population-based), Generation Scotland: Scottish Family Health Study (GS:SFHS), Cooperative Health Research in the Region of Augsburg (KORA F4), Adult-onset Asthma and Nitric Oxide (ADONIX) Study, Busselton Health Study (BHS), British Regional Heart Study (BRHS), British Women's Heart and Health Study (BWHHS), Gedling Study (Gedling), Hertfordshire Cohort Study (HCS), Finnish Health 2000 Survey (Health 2000), Nottingham Smokers Study (Nottingham Smokers), and Medical Research Council National Survey of Health and Development (NSHD, or British 1946 Birth Cohort).
FEV1 and the ratio of FEV1 to FVC were measured in each study, using the spirometry methods detailed in the online supplement. The percent predicted FEV1 was calculated according to previously described prediction equations (15, 16). Individuals with percent predicted FEV1 less than 80% and FEV1/FVC less than 0.7 (Global Initiative for Chronic Obstructive Lung Disease [GOLD] stages 2–4) were classified as COPD case subjects (17). Individuals with FEV1 greater than 80% predicted and FEV1/FVC greater than 0.7 were classified as control subjects. To minimize potential misclassification of COPD case subjects and control subjects, individuals not falling in either category (GOLD stage 1) were excluded from the analyses of COPD risk. We also excluded related individuals from the case–control analyses.
Genotyping was undertaken for a sentinel SNP at each of the following loci: TNS1 (rs2571445), GSTCD (rs10516526), HTR4 (rs3995090), AGER (rs2070600), and THSD4 (rs12899618). Standard quality control approaches were used. To incorporate the previously reported locus near HHIP into the analyses, rs12504628 was genotyped in studies that employed KASPar genotyping (KBioscience, Hoddesdon, Herts, UK) and available in silico data for rs12504628 were used for EPIC, Health 2000, and a subset of BHS (footnote † in Table 1).
Each SNP genotype was coded 0, 1, or 2, corresponding to the number of copies of the coded allele. The effect estimates were oriented to the forward strand of the National Center for Biotechnology Information (NCBI) build 36 reference sequence of the human genome, using the alphabetically higher allele as the coded allele. For each of the five SNPs reported by the SpiroMeta Consortium (9), logistic regression was used within each study population to test association of the SNP with COPD. Adjustments for additional covariates were not used for this analysis given that the percent predicted FEV1 (used to define COPD) includes adjustments for age, sex, and height (18). We defined Bonferroni-corrected statistical significance as P less than 0.01, to account for the testing of the five independent SNPs. After quality checks of the study population level data, pooled effect size estimates and their standard errors were computed across all studies, using an inverse variance weighting. Although previously shown to be associated with COPD and therefore not the focus of our analysis, for completeness we present the associations with rs12504628 (near HHIP).
The studies and loci included in study 2 are shown in Figure 1. We included the subset of studies that were genotyped for all six SNPs and that were not in the set of GWA data that led to the discovery of these loci (9). This restriction was to avoid cumulative biases resulting from individual SNP estimates of association that tend to be biased away from the null in "hits" from genome-wide discovery sets (winner's curse bias) (19). The phenotyping and genotyping of these studies were undertaken as described for study 1.
To derive an unweighted risk allele score theoretically ranging from 0 to 12, each allele previously associated with reduced FEV1 or FEV1/FVC (9) contributed one to the risk score. The risk alleles for the six loci were as follows: A for rs2571445 (TNS1), A for rs10516526 (GSTCD), T for rs12504628 (HHIP), A for rs3995090 (HTR4), C for rs2070600 (AGER), and A for rs12899618 (THSD4). We categorized the risk scores into five groups; 0–4, 5–6, 7 (median number of risk alleles, baseline group), 8–9, and 10–12 risk alleles.
We performed linear regressions of FEV1 and FEV1/FVC onto age, age squared, sex, and height to obtain residual phenotypes. Linear regressions were undertaken with each residual phenotype as the outcome variable, and an intercept and four indicator variables (for the four nonbaseline risk allele groups) as the explanatory variables to test for association. After quality checks of study level data, we computed pooled estimates using an inverse variance weighting.
Individuals were classified as COPD case subjects (GOLD stages 2–4) or control subjects on the basis of the criteria described previously for study 1. To test the association of the unweighted risk allele score with COPD we used logistic regression with COPD as the outcome, an intercept, and the four indicator variables. Study level estimates were pooled after quality checks using an inverse variance weighting.
The characteristics of the study participants are shown in Table 1. For the individual SNP associations with COPD a total of 3,284 individuals were classified as COPD case subjects (percent predicted FEV1 < 80% and FEV1/FVC < 0.7) and 17,538 individuals as control subjects (FEV1 > 80% predicted and FEV1/FVC > 0.7). Of the variants at the five loci shown to be associated with lung function (9), variants at three loci showed significant association with COPD: rs2571445 in TNS1 (odds ratio [OR] per A allele, 1.10; 95% confidence interval [CI], 1.03–1.16; P = 1.89 × 10−3) (Figures 2 and and3),3), rs10516526 in GSTCD (OR per A allele, 1.24; 95% CI, 1.10–1.40; P = 3.75 × 10−4) (Figures 2 and and3),3), and rs3995090 in HTR4 (OR per A allele, 1.12; 95% CI, 1.05–1.18; P = 1.79 × 10−4) (Figures 2 and and3).3). The associations with COPD were in the direction expected, given the reported direction of these allelic effects on lung function (Figure 2) (9). The point estimates of the effects on COPD for the sentinel SNPs in AGER (rs2070600) and in THSD4 (rs12899618) were of the magnitude and direction expected, but did not reach statistical significance. Although it was not a primary aim of our study to investigate the association between COPD and the locus near HHIP at 4q31 (an association reported by several studies [10, 11, 20]), we were also able to test this in a subset of our data (2,890 case subjects and 13,862 control subjects) for which the rs12504628 genotype was available. We confirmed the association between the 4q31 locus and COPD: OR per rs12504628 T allele, 1.19 (95% CI, 1.12–1.27) and P = 4.55 × 10−8. We tested for heterogeneity of effect sizes across the studies for each SNP; a chi-squared heterogeneity test was not statistically significant (P > 0.10) for any of the six SNPs.
As expected, a much higher proportion were ever-smokers among COPD case subjects (72%) than among control subjects (49%). This raises the possibility that these variants could influence COPD risk via an effect on smoking behavior. Therefore we explored whether the effects on COPD risk could be mediated via smoking. First, we examined the effects of an additional pack-years adjustment in smokers in a subset of our data with pack-years available and obtained similar results to those without adjustment for pack-years (see Figure E1 in the online supplement). Second, we assessed the association between these SNPs and two smoking behavior phenotypes in the Oxford-GlaxoSmithKline (Ox-GSK) consortium data set (21). As shown in Table E1, none of the SNPs showed even nominal association (P < 0.05) in 18,598 ever-smokers versus 15,041 never-smokers and none of the SNPs showed nominal association with the number of cigarettes smoked per day (n = 15,574). This evidence strongly suggests that the effects of these variants on lung function and COPD risk are not mediated via tobacco addiction.
The characteristics of the study participants are shown in Table 1. In all, 15,883 individuals were included in the analyses of FEV1 and FEV1/FVC (Table 1). A trend in lung function (FEV1 and FEV1/FVC) was shown across risk allele categories (Figure 4). Notably, compared with the baseline group of seven risk alleles, carrying 10–12 risk alleles was associated with a reduction in FEV1 (coefficient –72.21 ml [95% CI, –112.12 to –32.30 ml]; P = 3.90 × 10−4) and a reduction in FEV1/FVC (coefficient –1.53% [95% CI, –2.20% to –0.87%]; P = 6.35 × 10−6). Approximately 5% of the study population carried 10–12 risk alleles and 28% of the study population carried seven risk alleles. The magnitude of decline in FEV1 compared with the baseline group is equivalent to the physiological average ageing decline in lung function over approximately four years in a nonsmoking population (22).
To assess the joint effects of the risk alleles on COPD, data from nondiscovery cohorts (Figure 1) with genotype data available on all six SNPs were used. This included 2,252 COPD case subjects (percent predicted FEV1 < 80% and FEV1/FVC < 0.7) and 8,952 control subjects (FEV1 > 80% predicted and FEV1/FVC > 0.7) as shown in Figure 1 and Table 1. Again, a clear trend in COPD risk across the categories was observed (Figure 4). Compared with a baseline of seven risk alleles, carrying 10 to 12 risk alleles was associated with an increased risk of COPD (OR, 1.63; 95% CI, 1.31–2.03; P = 1.46 × 10−5) (Figure 4).
In a study of the set of novel variants we reported to be associated with lung function (9), we show significant association with COPD for three of the five loci—in HTR4, GSTCD, and TNS1—emphasizing the clinical relevance of these loci to respiratory disease. We also confirm the association between the 4q31 locus near HHIP and COPD, and show expected direction and magnitude of effect (although nonsignificant) for the two remaining of the five lung function loci studied. In addition, we provide an estimate of the combined effect sizes of these loci on lung function and COPD in studies independent of the data used to discover these associations. We show that the highest number of risk alleles (10–12 risk alleles, 5% of our population) is associated with a 1.6-fold elevation of COPD risk, compared with a common baseline group of individuals with 7 risk alleles (28% of our population).
The loci associated with COPD may provide important insights into the pathways underlying the development of COPD. The sentinel SNP at the 4q24 locus (rs10516526) is intronic in GSTCD, which encodes a glutathione S-transferase, C-terminal domain–containing protein. This protein may be involved in cellular detoxification, catalyzing conjugation of glutathione to products of oxidative stress (23), and in regulating the synthesis of prostaglandins and leukotrienes (23). GSTCD also shows homology with chloride intracellular channels and could therefore influence lung function via other molecular pathways (9). A second locus associated with COPD was localized to TNS1 at 2q35, where the sentinel variant was a nonsynonymous coding SNP. Tensin-1 is an actin-binding protein with SH2 (Src homology-2) domains, possibly involved in signal transduction (24) and cell migration (25). At 5q33, the sentinel variant was an intronic SNP (rs3995090) in HTR4 encoding the 5-hydroxytryptamine receptor-4 (HTR4), which is expressed in neurons and airway epithelial type II cells, where it may regulate cytokine responses (26). In contrast, the sentinel SNP at 4q31 reported in our study (rs1250468) and that reported in previous studies (rs13147758, r2 = 0.97 with rs1250468) (10, 11), lies in an intergenic region upstream of HHIP. The hedgehog (Hh) gene family encodes signaling molecules involved in regulating lung morphogenesis (27), although this locus has been previously associated with height (28), implicating a role in skeletal growth and development.
Although we did not demonstrate a statistically significant association between COPD and two loci, the estimated effects were in the expected direction. These included a nonsynonymous coding SNP (rs2070600) in AGER, within a gene-rich region of the major histocompatibility complex (6q21), and an intronic SNP (rs12899618) in TSHD4 (15q23). AGER is a strong candidate as it is highly expressed in the lung (29) and altered AGER expression has been noted in COPD lung tissue (30) and in subjects with idiopathic pulmonary fibrosis (31). Similarly the gene product of THSD4 shows homology with the thrombospondin family of extracellular calcium-binding proteins implicated in wound healing, inflammation, and angiogenesis (32) and could also be a good candidate for COPD development. Of the five new loci (9) we examined, the loci showing association with COPD in our data showed strongest association with FEV1 (HTR4, GSTCD, and TNS1), whereas the two loci that did not show a significant association with COPD (AGER and THSD4) showed association with FEV1/FVC, but without a strong association with FEV1. A simpler explanation for these different findings may be limited statistical power to detect the modest effects of these common genetic variants on a binary outcome.
The effect sizes of the SNPs at the three loci associated with COPD (HTR4, GSTCD, and TNS1) and the locus previously reported (HHIP) are modest, in the range 1.10–1.24 per copy of the risk allele at each locus. For the previously reported 4q31 locus near HHIP, we estimate an odds ratio of 1.19 (95% CI, 1.12–1.27) for COPD. Although larger effect sizes have been described, for example, an odds ratio for COPD equivalent to approximately 1.4 for the risk allele A at rs13118928 in the U.S. National Emphysema Treatment Trial/Normative Ageing Study and Bergen populations (11); the Rotterdam Study (20) and Framingham Heart Study (10) described odds ratios of 1.25 and 1.10 for this allele. Although the differences in the effect size estimates for the 4q31 locus could be attributable to differences in study characteristics, such as age, these differences could be explained in part by winner's curse bias (19), in which the effect size is generally overestimated in the study that first detects the association at the stringent levels of significance required in GWA studies. Additional evidence from independent populations, such as that provided from our study, can be important in establishing effect size estimates that are likely to be unaffected by such biases.
Most of the constituent studies did not measure postbronchodilation spirometry, and therefore our analysis was limited to prebronchodilation spirometry measures. In the Nottingham Smokers Study, in which both pre- and postbronchodilation spirometry were measured, the positive predictive value of prebronchodilation-defined COPD for diagnosis of postbroncholidation-defined COPD was 98% (Table E2). In all association tests reported in this article, we excluded individuals with GOLD stage 1 COPD from both case subjects and control subjects. As has been shown previously (33), the use of prebroncholidation spirometry to diagnose COPD when GOLD stage 1 COPD case subjects are included would lead to substantial misclassification (e.g., in the Nottingham Smokers Study the positive predictive value would decline to 89%; Table E3). Demonstration of airflow obstruction with postbronchodilator spirometry is required to make a formal diagnosis of COPD. Patients with partly or fully reversible airflow obstruction may have fundamentally different pathological processes contributing to airflow obstruction. One potential bias is that there may be some cases with misclassification of either an asthma diagnosis or the COPD diagnosis. In addition, both asthma and COPD are common diagnoses and may coexist in the same individuals. The associations with lung function that we show were found in the general population and if the SNP effects are specific to asthma and not present in COPD, then the inclusion of patients with asthma could overestimate the contribution of the SNPs to COPD. However, we examined the effects of exclusion of patients with known asthma from the case subjects in a subset of the data with asthma diagnosis available and this did not alter the findings substantially (Figure E2). In addition, within the Nottingham Smokers Study, for which we have in-depth phenotype data and know that individuals with asthma and never-smokers with airflow obstruction have been specifically excluded, we found similar effect estimates. The effect size estimates in Nottingham Smokers were also consistent with effects on COPD for our sentinel SNPs in HTR4, GSTCD, and TNS1 (Figure 3).
Various criteria have been proposed for the classification of COPD. Our main analysis was based on GOLD criteria (17). As misclassification is particularly likely to occur when there is poor separation of criteria for case subjects and control subjects, we excluded from our analyses altogether any individuals with mild COPD (stage 1 GOLD criteria: FEV1/FVC < 70% but FEV1 ≥ 80% predicted).
Our conclusions were not materially altered by classifying cases instead on the basis of lower limit of normal equations (18) (Figure E3). Misclassification could also occur as a consequence of spirometry measurement error, and this too would tend to lead to underestimation of the effects of the SNPs studied. An important limitation of our study is that the misclassification and smoking exposure cannot be fully addressed, using these cohorts, because postbronchodilator spirometry and quantification of tobacco smoke exposure is not captured in several of our cohorts. Further studies of patients with COPD with more detailed smoking exposure measurements and more extensive respiratory phenotyping should provide further insight into the precise effects of these SNPs on COPD risk and COPD progression.
We focused on the study of SNPs in six loci: TNS1, GSTCD, HHIP, HTR4, AGER, and THSD4. Further studies will be required to investigate the potential association with COPD of SNPs in the regions of GPR126, ADAM19, PTCH, and PID1 (additional regions described by the Cohorts for Heart and Aging Research in Genomic Epidemiology [CHARGE] Consortium) (8). The addition of these SNPs, the sentinel SNP from FAM13A (associated with COPD and lung function [8, 12]), CHRNA3/5 (11), and other new loci from ongoing powerful genome-wide association studies to the risk score we constructed would be expected to improve the discrimination of such a score for prediction of COPD. With some exceptions, such as the major histocompatibility region, genome-wide association studies have been successful in localizing association signals (34, 35), but further research is likely to lead to improved resolution of association signals and possibly to detection of multiple independent causal variants at each of these loci. The simple risk score we present here would need to be adapted to incorporate an appropriate weighting as the score incorporates more SNPs, with a greater range of effect sizes. However, for the limited number of SNPs we examined, the inclusion of a weighting (based on the allelic effect size estimate) did not materially alter our findings. We also constructed risk scores in a subset of the data, measuring the effect on COPD per risk allele in all individuals and in ever-smokers only; the odds ratios were 1.14 and 1.13, respectively, suggesting that the effect of these loci on COPD is similar in the general population and in ever-smokers only. As more complete risk scores are constructed, it will be important to investigate their predictive potential in subgroups stratified by smoking status, and to examine whether such a score can improve on risk prediction from conventional risk factors alone (including age, sex, smoking status, history of asthma, and family history, where available).
Our study demonstrates that some loci underlying lung function are associated with COPD, and provides a proof of concept that investigation of genetic determinants of lung function can be a successful strategy to discover molecular pathways underlying COPD. Pathways involving HTR4, GSTCD, and TNS1 are strong candidates for potential interventions to prevent or alleviate COPD. We show, in studies unaffected by winner's curse bias, that the highest risk category of a six-SNP risk score is associated with a 1.6-fold risk of COPD compared with a common baseline group of seven risk alleles. It is not yet known whether these SNPs could contribute to a clinically useful strategy for prediction and intervention to prevent COPD, although the high absolute risk of COPD in smokers would suggest that the clinical and public health impact of such an approach is worthy of investigation as more loci are discovered and incorporated into risk scores.
The SpiroMeta Consortium acknowledges ENGAGE (Engaging ICT cooperation between Europe and the Asia-Pacific region).
Supported/partially supported through the European Community's Seventh Framework Programme (FP7/2007-2013), ENGAGE project, grant agreement HEALTH-F4-2007-201413. Complete information concerning funding may be found before the beginning of the References.
Complete information concerning author contributions may be found before the beginning of the References.
This article has an online supplement, which is available from this issue's table of contents at www.atsjournals.org
Originally Published in Press as DOI: 10.1164/rccm.201102-0192OC on June 16, 2011
Author Contributions
ADONIX: investigators—Åsa Torinsson Naluai, Fredrik Nyberg, Anna-Carin Olin, Santosh Dahgam; contributions—project conception, design, and management: A.-C.O.; phenotype collection and data management: A.-C.O.; genotyping: A.T.N., F.N.; data analysis: A.T.N., F.N., A.-C.O, S.D. BHS: investigators—Gemma Cadby, Jennie Hui, Alan L. James, Lyle J. Palmer; contributions—project conception, design, and management: A.L.J., L.J.P.; phenotype collection and data management: G.C., A.L.J., L.J.P.; data analysis: G.C., J. Hui, L.J.P.; BRHS: investigators—Aroon D. Hingorani, Richard W. Morris, S. Goya Wannamethee, Peter H. Whincup; contributions—phenotype collection and data management: R.W.M., S.G.W., P.H.W.; genotyping: A.D.H., R.W.M., P.H.W.; data analysis: R.W.M. BWHHS: investigators—George Davey Smith, Shah Ebrahim, Debbie A. Lawlor, Peter H. Whincup; contributions—phenotype collection and data management: G.D.S., S.E., D.A.L., P.H.W.; data analysis: D.A.L. EPIC: investigators—Inês Barroso, Ruth J. F. Loos, Nicholas J. Wareham, Jing Hua Zhao. contributions—project conception, design, and management: I.B., R.J.F.L., N.J.W., J.H.Z.; phenotype collection and data management: N.J.W.; genotyping: I.B., R.J.F.L., N.J.W., J.H.Z.; data analysis: R.J.F.L., J.H.Z. Gedling: investigators—John R. Britton, Tricia M. McKeever, Ian D. Pavord; contributions—phenotype collection and data management: J.R.B., T.M.M., I.D.P.; data analysis: M.O., M.D.T. GS:SFHS: investigators—Cathy Jackson, Shona Kerr, Anna Dominiczak, Blair Smith; contributions—project conception, design, and management: C.J., A.D., S.K., B.S.; phenotype collection and data management: C.J., B.S., A.D.; genotyping: S.K. HCS: investigators—Cyrus Cooper, Elaine Dennison, John W. Holloway, Seif Shaheen; contributions—project conception, design, and management: C.C., E.D., J.W.H.; phenotype collection and data management: C.C., E.D., S.S.; genotyping: C.C., E.D., J.W.H.; data analysis: J.W.H., S.S. Health 2000: investigators—Markku Heliövaara, Mika Kähönen, Samuli Ripatti, Ida Surakka; contributions—project conception, design, and management: M.H., M.K.; phenotype collection and data management: M.H., M.K.; genotyping: S.R., I. Surakka; data analysis: M.K., S.R., I. Surakka. KORA F4: investigators—Eva Albrecht, Stefan Karrasch, Joachim Heinrich, Holger Schulz; contributions—project conception, design, and management: S.K., J. Heinrich, H.S.; phenotype collection and data management: S.K., J. Heinrich, H.S.; data analysis: E.A. Nottingham Smokers: investigators—John D. Blakey, Ian P. Hall, Ma'en Obeidat, Ian Sayers; contributions—project conception, design, and management: I.P.H., M.O., I. Sayers; phenotype collection and data management: J.D.B., I.P.H., M.O., I. Sayers; genotyping: I.P.H.; data analysis: M.O., I. Sayers, M.D.T. NSHD: investigators—The "NSHD Respiratory Study Team" team members involved were as follows: Zaina Al-Kanaani, Anna Hansell, Rebecca Hardy, Diana Kuh, Andrew Wong; contributions—phenotype collection and data management: R.H., D.K., A.W.; genotyping: D.K., A.W.; data analysis: Z.A.-K., A.H., R.H., A.W. Ox-GSK: investigators—Jason Z. Liu, Jonathan Marchini; contributions—project conception, design, and management: J.M.; data analysis: J.Z.L.
Manuscript Conception, Design, and Management: I.P.H., M.S.A., M.D.T.
Data Analysis and Bioinformatics: P.R.B., I.P.H., T.J., M.O., E.R. I.S., M.S.A., M.D.T., L.V.W.
Writing the Manuscript: I.P.H., M.S.A., M.D.T.
Cohort Funding
ADONIX: The ADONIX Study was funded by the Swedish Research Council for Worklife and Social Research (FAS), grants 2001-0263, 2003-0139, Swedish Heart and Lung Foundation grant 20050561 and a collaborative research grant from AstraZeneca. BHS: The Busselton Health Study acknowledges the generous support for the 1994/5 follow-up study from Healthway, Western Australia. The Busselton Health Study is supported by The Great Wine Estates of the Margaret River region of Western Australia. The BHS gratefully acknowledges the assistance of the Western Australian DNA Bank (NHMRC Enabling Facility) with DNA samples and the support provided by the Western Australian Genetic Epidemiology Resource (NHMRC Enabling Facility) for this study. BRHS: Blood collection and spirometric measures were performed in 1998–2000 as part of a field study funded by the British Heart Foundation (grant PG/97012). DNA was extracted by Geneservice Limited. A.D.H. has a British Heart Foundation Senior Research Fellowship (FS05/125). BWHHS: The British Women's Heart and Health Study (BWHHS) is funded by the U.K. Department of Health Policy Research Program and the British Heart Foundation. A separate British Heart Foundation project grant (PG/06/154/22043) funded cotinine assays. EPIC: The EPIC Norfolk Study is funded by Cancer Research UK and the Medical Research Council. I.B. acknowledges funding from the Wellcome Trust (077016/Z/05/Z) and from the U.K. NIHR Cambridge Biomedical Research Centre. Gedling: The Nottingham Gedling cohort collection was funded by Asthma UK and the British Lung Foundation. GS:SFHS: The Generation Scotland: Scottish Family Health Study is funded by the Chief Scientist Office, part of the Scottish Government Health Directorate (http://www.sehd.scot.nhs.uk/cso), grant reference number CZD/16/6. Genotyping was conducted by the Genetics Core at the Wellcome Trust Clinical Research Facility, University of Edinburgh, Western General Hospital, Edinburgh, UK. HCS: The Hertfordshire Cohort Study DNA collection was funded by the Medical Research Council, Arthritis Research Campaign, and International Osteoporosis Foundation. Health 2000: This study was financially supported by the Medical Research Fund of the Tampere University Hospital. KORA F4: The KORA Augsburg studies were financed by the Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany and supported by grants from the German Federal Ministry of Education and Research (BMBF) in the context of the German National Genome Research Network (NGFN-2 and NGFN-plus). Our research was supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ. Nottingham Smokers: The Nottingham Smokers cohort collection was funded by the University of Nottingham. NSHD: The Medical Research Council National Survey of Health and Development (NSHD, also known as the British 1946 Birth Cohort) is funded by the Medical Research Council. The MRC Unit for Lifelong Health and Ageing is responsible for NSHD. Z.A.-K., R.H., D.K., and A.W. are all affiliated with the MRC National Survey of Health and Development, MRC Unit for Lifelong Health and Ageing, London, UK except A.H., who is affiliated with the MRC-HPA Centre for Environment and Health, Imperial College London. Z.A.-K. has a studentship funded by Department of Health Air Pollution PRP Grant Ref. No. 0020029. Ox-GSK: GlaxoSmithKline (GSK), a pharmaceuticals company that is interested in developing therapies for lung disease and new cessation therapies for smoking, funded a postdoctoral fellowship for J.Z.L. at Oxford University. GSK also funded the collection, characterization, and, in some cases, the genotyping and genotype data preparation for several of the cohorts used in this study. A. Roses and P. Matthews played crucial roles in establishing and funding the Medical Genetics activities at GSK.
Author Disclosure: I.S. received a sponsored grant from Pfizer. I.P.H. is a board member of the MRC Clinical Training Panel and has received lecture fees from Pfizer. M.A.S., L.W., E.R., M.O., P.B., T.J., J.Z., E.A., A.D., S.K., B.S., G.C., J.H., L.J.P., A.H., S.W., P.W., S.E., G.S., I.B., R.L., N.W., C.C., E.D., S.S., J.L., J.M., S.D., Å.N., A.C.O., S.K., J.H., H.S., T.M.M., I.P., M.H., S.R., I.S., J.B., M.K., J.B., F.N., J.H., D.L., R.M., A.L.J., C.M.J., and M.T. do not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Showing Results: Most Recent
This review is from: MSI H110M PRO-D LGA 1151 Intel H110 SATA 6Gb/s USB 3.1 Micro ATX Intel Motherboard
Pros: Anything present on this board (e.g. port or slot) performs as well as that same port or slot on a higher-end board. My article describing this board on Tom's Hardware should be published soon. Inexpensive.
Cons: This board is sparse. A lot of things simply aren't there, like an M.2 slot, and there's only a DVI video connector. If you load the software, you can get 7.1 audio out of it, but you have to use both front and rear audio jacks so your wiring will likely be messy. Limited tweaking and no overclocking. Only two RAM slots.
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This review is from: 400LM CREE Q5 LED ZOOMABLE Cap Hat Light Torch Headlamp Headlight Hiking Fishing
Pros: Bright, excellent battery life. Grip on a cap is strong.
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This review is from: F15038-A 5Pcs Portable USB LED Lamp Bendable Foldable Mini Light Eye-protection for Reading Notebook Laptop PC Power Bank
Pros: Light is very bright, but doesn't glare; easily enough for reading. No bluish cast. Stalk holds position if not bent too much.
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Other Thoughts: Appears to be an excellent prepping/camping item. Plugged into a power bank, it should last a very long time. I will order more of them. A 15%-20% DOA rate isn't good, but these are still cheap enough to be worthwhile.READ FULL REVIEW


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|Home > Darcio
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Darcio [dar-cio] as a name for boys is of French derivation, and the meaning of the name Darcio is "dark". Darcio is an alternate form of Darcel (French): variation of the surnames Darcy.
ASSOCIATED WITH dark
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Which version is better?with its source form and related boy names. Darcy is the only popular related form of Darcio (OUTSIDE TOP 2000). This form of Darcio was popular as a birth name 5 decades ago. (TOP BABY NAMES, 2015)
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Darcio is pronounced similarly to Darcey, Darsey, Darsy and Dorsie. Other suggested similar names are Curcio, Dacio, Darach, Darbie, Darek, Darias, Daric, Darick, Darin▼, Dario▲, Darion▼, Darious, Darius▼, Darko, Darrick▼, Darrin▼, Darrion▼, Darriq, Darrius▼, Darro, Darvin, Darwin, Decio, Deric, Derik, Deriq, Derrik, Dirck, Draco, Drago, Marcio, Marco, Mario and Narciso. These names tend to be more commonly used than Darcio.See names in meaning and etymology.


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A boy put his hand into a jar of filberts and grasped as many as his fist could possibly hold.
Four decades ago, Richard Nixon grasped sooner than most the huge potential of China.
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My voice had some effect upon her, for she grasped the stick to which she was clinging.
The cartoonists of the Civil War do not seem to have grasped this idea.
mid-14c., "to reach for, feel around," possibly a metathesis of grapsen, from Old English *græpsan "to touch, feel," from Proto-Germanic *grap-, *grab- (cf. East Frisian grapsen "to grasp," Middle Dutch grapen "to seize, grasp," Old English grapian "to touch, feel, grope"), from PIE root *ghrebh- (see grab). Sense of "seize" first recorded mid-16c. Figurative use from c.1600; of intellectual matters from 1680s. Related: Grasped; grasping. The noun is from 1560s.


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text: You are here: Home > Course > Accompaniments > Dips / Sauces > Hot Garlic Sauce Hot Garlic Sauceby Tarla Dalal 15 Jun 2014 You are not signed in. Please sign in to access your cookbooksExisting members click here to sign inNew visitors click here to sign up Please sign in to create shopping lists! 5/5 stars 100% LIKED IT 7 REVIEWS ALL GOOD Added to 87 cookbooks This recipe has been viewed 50468 times A spicy dip with a predominant garlic flavour, and a dash of tang with the addition of ketchup. Add your private note Hot Garlic Sauce recipe - How to make Hot Garlic Sauce Tags Quick Dips & SaucesDips / Sauces Perparation Time : 5 mins. Cooking Time: 2 mins.   Total Time: 7 mins     Makes Approx.1 cup. Show me for servings Ingredients 3/4 cup tomato ketchup6 whole dry kashmiri red chillies6 large cloves garlic (lehsun)4 tsp oil a pinch of salt Method Pound the chillies, garlic and salt in a mortar and pestle to a coarse paste. Heat the oil in a pan till it is very hot. Take it off the flame, add the prepared chilli-garlic passte and stir for 10 to 20 seconds. Add the tomato ketchup and mix well.Cool and use as required. Other Related Recipes Accompaniments Cheese and Vegetable Sticks Corn Chips Fried Mozzarella Sticks Nutrient values per servingEnergy220 calProtein1.8 gCarbohydrates7.1 gFiber3.4 gFat20.4 gCholesterol0 mgVitamin A875 mcgVitamin B10.2 mgVitamin B20.1 mgVitamin B30.8 mgVitamin C53.5 mgFolic Acid59.4 mcgCalcium95 mgIron1.3 mgMagnesium0 mgPhosphorus0 mgSodium25.5 mgPotassium289.1 mgZinc0 mg RECIPE SOURCE : Snacks Under 10 Minutes


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The Official EWN Foodie Hangout and Recipe Exchange
by, 06-10-2014 at 04:48 PM (3176 Views)
The joy of flanking
Flank steaks are usually my steak of choice in the summer months because, in addition to being a cheaper cut of meat, they're just so damn much fun to play with. A lot of people think because it's an inexpensive steak option that must mean that it's a lesser steak in terms of flavor. BULLSHIT. These things are like friggin' flavor sponges, and you'll never grow tired of experimenting with your marinades. That sort of versatility is invaluable, trust me. Regardless of whether you're doing Asian or Southwestern, it's super simple to just establish your framework with the flavor profile of your meat and then build around.
If you don't like your meat a little bloody, then a flank cut probably isn't going to be for you- fuck, if you don't like a little blood, meat-eating period probably isn't for you, but that's better left for another discussion- as it's imperative that the flank be served rare, otherwise things get tough and chewy and then that smaller price tag starts making a little more sense.
Also, and I can't stress this enough: COOKED MEAT SHOULD ALWAYS BE PROPERLY RESTED. ALWAYS. Your steak needs time to reabsorb all of those delicious juices. 10 to 15 minutes should do it. And if you tent your meat immediately after removing from the grill, you won't have to worry about it getting cold.
Is there anything sexier than freshly-carved meat piled on a wooden cutting surface?
Marinade recipes coming up...
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15 Books to Empower Tween Girls
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At long last, the Star Wars story of the mysterious Sith Lord Darth Plagueis and his apprentice, Darth Sidious, is revealed!
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|Message view
|« Date » · « Thread »
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|Rodney Waldhoff <rwaldh...@apache.org>
|Re: [DBCP] Idle time on connection not reset when working with connection?
|Tue, 11 Mar 2003 23:57:55 GMT
Within [pool] (and hence [dbcp]), an object is considered "active" when it has been borrowed (in dbcp, via getConnection or prepareStatement) but not yet returned (in dbcp, via close). An object is considered "idle" when it is not "active" (i.e., after it has been returned to the pool but before it has been borrowed again.) Hence a long running transaction will not be impacted by idle object eviction. The "AbandonedObjectPool" has different (orthogonal) semantics, dealing with how long an active object has been active, I think by design. On Tue, 11 Mar 2003, Mario Ivankovits wrote: > Am i right, when i have found out, that the idle-time on the connection > is only set on "activate" (pop from pool) and not when using the > connection? > > Shouldnt it be set when creating statements, operation on resultset > (next, getters, setters, ...) > > Else long running transaction might fail due to "abandone" the > connection. --------------------------------------------------------------------- To unsubscribe, e-mail: email@example.com For additional commands, e-mail: firstname.lastname@example.com
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|"Tako Schotanus" <quinte...@gmail.com>
|Re: Questions regarding nt:file and nt:folders
|Tue, 07 Aug 2007 22:42:24 GMT
On 8/7/07, qcfireball <email@example.com> wrote: > > > I hope this provides you some clarity. > > In reply to Bob's question (his text omitted for brevity): > Here are 2 scenarios involving files. One involves a single file, the > other > an arbitrary number of files. The format of the text is: > node-type|node-name, with children underneath, indented: > > nt:file|<arbitrary name> > nt:resource|jcr:content > (p) jcr:encoding=... > (p) jcr:mimeType=... > (p) jcr:data=0x...... (binary content) > (p) jcr:lastModified=... > > nt:folder|<arbitrary name> > nt:file|<arbitrary name #1> > nt:resource|jcr:content > (p) jcr:encoding=... > (p) jcr:mimeType=... > (p) jcr:data=0x...... (binary content) > (p) jcr:lastModified=... > nt:file|<arbitrary name #2> > nt:resource|jcr:content > (p) jcr:encoding=... > (p) jcr:mimeType=... > (p) jcr:data=0x...... (binary content) > (p) jcr:lastModified=... > > It seems to me, what you want to version is the nt:resource, NOT the > nt:file. I am not sure what function or responsibility the nt:file node > provides, but as you know, the actual content resides in the nt:resource. > It seems reasonable that you would want to version the ACTUAL item that is > varying, not the node that contains it. You have mentioned this in your > post. Mentioned elsewhere, I cannot find it right now, David mentions > that > in his own use of the JCR, he rarely (if ever) extends nt:file, but > regularly extends nt:resource. Unless of course you want to keep track of folder and file renames. I would be inclined to have an implicit trust in his statement on this. > Maybe naive, maybe not. So, it would seem that an extension of > nt:resource > would be preferable. > > > I have a couple additional questions to this issue of files/folders. > > 1) why the additional level of indirection with nt:file? If this is > analogous to a filesystem, the file IS the file. What is the benefit of > nt:file and nt:resource existing as separate entities? I imagine the reason is "content re-use", an nt:resource is an anonymous item that could possibly belong to an nt:file and several nt:linkedFile nodes. 2) What is involved in creating an extended nt:resource node type? Is there > a document discussing how to do this? Or would I be able to figure this > out > by inspecting the source code? I think it's nothing more than registering a new node type, like this for example: [foo:i8nResource] > nt:resource - jcr:language (STRING) 3) Because I know I will be asked, if extending nt:resource is a frequent > occurence, why is there not a "stock" version that would allow some > additional capabilities, such as extra arbitrarily named/typed properties? > In the new world of development where Enterprises want to use more "off > the > shelf" software and less custom written software, why would this not be a > part of the spec? Some folks, perhaps in our Enterprise, would view this > as > a deficiency rather than a benefit, due to the possibility of breakage as > updates occur. I have no idea, sorry. Cheers, -Tako
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text:
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Hi there,
I was wonderig if it would be possible to add more then one Administrator password within the same IP subnet? Some of our laptops in the network aren't in Active Directory and require a local admin password wich is different then on all the AD computers.
When I try to "add" one with the same IP range it overwrites the previously configured authentication method.
Thanks in advance....
2 Replies
Mar 31, 2008 at 4:30 UTC
The only way you can do this is to break up the scan range. For instance, lets say the devices on 192.168.1.1-100 have the password PASSWORD01, 192.168.101-215 have the password PASSWORD02 and 192.168.216-254 have the password PASSWORD01. You would set your range up as follows:
192.168.1 -100,216 -254 for one scan range
192.168.1.101 -215 for the second range
Let me know if that answers your question or if it doesn't make sense.
Apr 1, 2008 at 2:40 UTC
It does makes sense and I already noticed that. Unfortunately I was hoping for a "better" solution since I cannot break up the IP range. Some workstations in our building aren't in the domain so I don't hare authentication on those machines but I do want them to show properly in SpiceWorks.
This discussion has been inactive for over a year.
You may get a better answer to your question by starting a new discussion.


text:
|Message view
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|"James Dyer (Commented) (JIRA)" <j...@apache.org>
|[jira] [Commented] (SOLR-3029) Poor json formatting of spelling collation info
|Thu, 29 Mar 2012 15:02:27 GMT
[ https://issues.apache.org/jira/browse/SOLR-3029?page=com.atlassian.jira.plugin.system.issuetabpanels:comment-tabpanel&focusedCommentId=13241289#comment-13241289 ] James Dyer commented on SOLR-3029: ---------------------------------- Yonik, I can answer some of your questions. I do agree the spellcheck response format leaves something to be desired and maybe 4.0 is a good time to break backwards and improve it. {quote} Unless order is really important, "suggestions" should be a map {quote} I don't see why order would matter here, although some users might like to see the corrections listed in the order they appeared in the query. {quote} same for "collation" {quote} The collations are ranked, so order is important. {quote} and "misspellingsAndCorrections" {quote} The order shouldn't matter unless users are picky about the corrections being presented in the order they occur in the query. {quote} why is "collation" inside "suggestions" along with other words? should this be one level higher? {quote} This always confused me too. I agree it should be one level higher. {quote} why isn't this giving me multiple collations {quote} This is a bug. See SOLR-2853. {quote} why aren't multiple suggestions returned in misspellingsAndCorrections? (and what's the purpose ...?) {quote} This is nested with the Collation and gives details, for that particular collation, which misspelled word got which replacement. This makes it easy for clients to generate messages like "no results found for abcdefgq ... Showing abcdefgx instead!" You can suppress this information by not specifying "spellcheck.collateExtendedResults=true". For users (like me) who are interested in the collations only and don't care about individual-word corrections, it would be nice if we could suppress the first section of the response entirely. {quote} I briefly tried distributed search... {quote} DistributedSpellCheckComponentTest is supposed to detect problems like this but maybe something is going on and there is a bug this test isn't catching? For what its worth you had voiced some misgivings about the JSON format when the multiple-collations feature was added. At that time I supplied a quick patch to address your concerns. I'm not sure if that patch fixes the problem described here. See SOLR-2010 and your comment from Oct 16, 2010 and the (now outdated, never committed) patch I supplied on Oct 20. The patch on this issue causes multiple test failures although I didn't look into them. > Poor json formatting of spelling collation info > ----------------------------------------------- > > Key: SOLR-3029 > URL: https://issues.apache.org/jira/browse/SOLR-3029 > Project: Solr > Issue Type: Bug > Components: spellchecker > Affects Versions: 4.0 > Reporter: Antony Stubbs > Priority: Blocker > Attachments: SOLR-3029.patch > > > {noformat} > "spellcheck": { > "suggestions": [ > "dalllas", > { > <snip> > { > "word": "canallas", > "freq": 1 > } > ] > }, > "correctlySpelled", > false, > "collation", > "dallas" > ] > } > {noformat} > The correctlySpelled and collation key/values are stored as consecutive elements in an array - quite odd. Is there a reason isn't not a key/value map like most things? -- This message is automatically generated by JIRA. If you think it was sent incorrectly, please contact your JIRA administrators: https://issues.apache.org/jira/secure/ContactAdministrators!default.jspa For more information on JIRA, see: http://www.atlassian.com/software/jira --------------------------------------------------------------------- To unsubscribe, e-mail: email@example.com For additional commands, e-mail: firstname.lastname@example.com
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text: The Sands IPO likely sparked interest in other big casino names, according to Matt Quinn, senior lodging and gaming analyst at Zack's Investment Research. The company's casino in the Chinese enclave of Macao highlighted broader investor optimism about casino opportunities across the Pacific, Quinn said. (Zack's neither does nor seeks to do business with companies it covers, and Quinn owns no shares of companies he covers.) "People are starting to realize there's strong growth potential in Macao," he said. "Casino companies can benefit from building there. They get a chance to build their brands in Asian markets and hopefully get Asian customers to come over to the U.S." In a filing with the Securities and Exchange Commission, Sands said net income from its Macao casino, which opened in May, was $60.7 million during the third quarter. The company also plans to build a Venetian-branded resort in Macao by 2008. MGM Mirage and Wynn also have plans for Macao casinos, and Merrill Lynch's Anders cited MGM Mirage's long-term prospects in Macao as a factor behind his price target upgrade. Although Quinn is also bullish on the future of Las Vegas and Macao gaming, he's more cautious on the potential for robust casino stock gains in the near term. "I don't see a lot of upside for them at this point," he said. "They looked pretty reasonably valued." Quinn has holds on all the stocks he covers in the large-cap gaming sector, including MGM Mirage, Caesars, Harrah's and Mandalay. The stocks are likely to trade sideways for the next three to six months, but MGM Mirage and Harrah's could see additional upside after that, as benefits from their big mergers begin to appear, Quinn added. Despite the huge gains in Las Vegas Sands since its IPO, Quinn contends its multiple is not out of whack with the market. At recent levels, the company's enterprise value-to-EBITDA multiple is about 9, which is comparable to Aztar Corp. ( AZR) and Boyd Gaming ( BYD), both of which have Vegas properties similar to Sands.


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history of Western painting from its beginnings in prehistoric times to the present. Painting, the execution of forms and shapes on a surface by means of pigment (but see also drawing for discussion of depictions in chalks, inks, pastels, and crayons), has been continuously practiced by humans for some 20,000 years. Together with other activities that may have been ritualistic in origin but have come to be designated as artistic (such as music or dance), painting was one of the earliest ways in which man sought to express his own personality and his emerging understanding of an existence beyond the material world. Unlike music and dance, however, examples of early forms of painting have survived to the present day. The modern eye can derive aesthetic as well as antiquarian satisfaction from the 15,000-year-old cave murals of Lascaux—some examples testify to the considerable powers of draftsmanship of these early artists. And painting, like other arts, exhibits universal qualities that...READ MORE


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Home > Product Categories > Pro-Video > Tripods & Camera Support > Tripods & Fluid Heads > 732
Item #: MIL-732 MFG #: 732
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Item #: MIL-1028
Our Price: $4,682.49
60lb capacity pedestal with Gas assist for prompter payloadsWith a maximum capacity of 60lb, and the ability to support all EFP portable cameras with teleprompters, the Miller Pedestal 60 delivers the performance lift your programs are missing. The gas assist column lift ensures rapid height repositioning, while the sturdy base and 4" castor offer smooth moving across all studio floors.
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text: Ashley & Trey go to a video store wich has a lot of Barney & Barbie videos, then Ashley was surprised when she sees a Barney's Halloween Party DVD, the 2009 print, and try to ask for it, but Trey says "you have many barney things at my house!" then she cryed and bowled, then Trey takes her out, the next day, they go to a toy store where the boy & girl saw a playmobil circus, again, she begs for it, but trey says "no!" then it's up to katherine pully to solve her promblem, then they get the dvd & circus, then the whole family had so much fun!