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This is part of a series of posts that were prompted by an article written by the Leading Edge Forum entitled The 7 Digital Habits of Highly Effective People.
So far in this series we've talked quite a bit about the changes that you can make in your own working practice to build a set of digital habits. We've talked about the tools and techniques available to enable us to understand what is going on around us. We each have a personal brand and we've talked about how we can proactively manage that. There are new techniques and tools available all the time and we've discussed how to keep a sharp edge and how to avoid all the distractions. We've even highlighted the role of the digital synergist.
These new techniques and tools are only as good as the amount of change they're able to make to ways we and our teams work. A powerful way of bringing about change is to model the changes through leading by example. This brings us to the sixth digital habit.
From The 7 Digital Habits of Highly Effective People:
HABIT 6 – Lead by being a digital example – we need to be the change we want to see in our people, so we need to be clear on our own reasons or "whys" for becoming a 21st Century Human and make what we call a Digital Decision to follow through. This links to the [Stephen] Covey habit of "Begin with the end in mind." That is being clear on what you want by understanding your mission, your values, your goals. Doing the regular goal setting and reviews, so that they are front and centre to combat the distraction issue covered by Habit 4. Getting a digital coach to help is also we believe key to support leaders' efforts in this area.
Leading ourselves into change
When I say lead here, I mean it in the broadest sense. I'm not talking about organisational hierarchies, I'm talking about all the people that you and I influence. You might be "leading" your organisational manager. Or, you may be leading someone who regards you as a mentor. Your leadership may apply broadly to a team that you work within. Technology has allowed leadership to happen in many ways and in many different directions.
The primary leadership that we have, though, is of ourselves — so we'll start there. A significant factor in leading ourselves into a set of changed habits is to have a clear understanding of why we want to make the change and to continuously reinforce that foundation. For most of us, we need a tangible reason to make a change and for that change to stick. You'll need to find that reason for yourself, but here are some of my motivators for change:
- Emerging technologies are making many things that were previously impossible, attainable, and that's an exciting place to be. The exploitation of these technological capabilities requires each of us to evolve our skills on a continuous basis.
- Automation is changing what we regard as work, making some jobs redundant and radically changing others. This creates a whole new set of opportunities, but only for those with the ability to see them coming — and I'd like to be one of those people.
- Many people are overwhelmed with the amount of information that they are expected to process on a daily, even hourly, basis. Adopting the right set of tools and practices can have a significant impact on that overload.
- Change is inevitable, which, for me, is exciting. I quite like change.
Perhaps you have different reasons, and that's fine. You just need to know what they are. Then, from that foundation, you can decide on your initial mission and goals.
Agile personal change mindset
One of the practices synonymous with "digital" is an Agile mindset, a term that has grown out of the Agile Manifesto created in 2001 for software development (though the fundamentals of these principles are even older). Since then, the principles have been applied in many different scenarios — and that's how I view the adoption of the Digital Habits. Let me explain . . .
Many organisations have defined people development cycles — including annual reviews and mid-term reviews — that align to the Waterfall approach to project management. You define a goal out in the future, perhaps 12 months away, and aim for it. That may be fine for someone who is training to be a physician, but it doesn't really work in the changing world of technology.
In an Agile world, things are planned in sprints lasting only a few weeks, and the content of each sprint is based on items collected into a backlog. At the start of each sprint you decide what you are going to tackle based on the items in the backlog. That's kind of how I now plan my personal and professional development.
Working this way has several advantages:
- It allows me to try something out as a kind of personal development experimentation to see if I've got an aptitude for it.
- I can see the value of each sprint in a skill learnt or an understanding gained. That's quite motivating.
- The cost of change is very low. If I try something I don't connect with, I don't have to go any further with it.
- The backlog provides a place to store all the things that look interesting as I come across them. I don't have to investigate them immediately, which helps me to maintain focus.
- It's easy to adjust my course when things change — which they do, regularly — as the priority of each item in the backlog is revisited at the start of each sprint.
Getting the practice in
There's never been a time when good quality training has been so accessible. Learning platforms like Udemy provide access to professional training for the cost of a book, and most of the digital capabilities are supported by extensive training capabilities. Then there's the ultimate source of thousands of hours of expertise — YouTube.
But for me there's little point in doing training without also implementing that learning. Fortunately, the digital change that we are going through provides many ways to have a go as we practice. Take collaboration as a great example — you don't have to procure a collaboration platform and wait six months to have it implemented. The most popular collaboration platforms are based on consumer models that allow a small team to get started for free or for a very low investment.
Both Microsoft Teams and Slack enable you to start with a small team and build out from that point. If this works for your team during a sprint, carry on, grow from there. If it doesn't, then try to understand, learn and move forward in a different way.
Perhaps you want to understand how a Kanban approach may work. Trello provides free access to experiment.
There are many other examples: Amazon Web Services provides a free tier. Microsoft Azure provides free credits. Google Cloud Platform has a free tier also. GitHub allows you to create your own project (in public) for no charge. The list goes on.
Being the change you want to see
There isn't a certificate that you and I can take to prepare us for the digital future. We each need to work our way through this change as it evolves and mutates. My plan is to be the change that I want to see in sprints — adding to my skills and changing my practice in increments and leading others along the journey.
Just as important as being an out-in-front leader is for us to be supporting leaders, encouraging others in their experimenting. We have so much to learn from each other and being an active participant who is leading by example can be just as powerful as being the official driver of change.
Graham Chastney is a senior principal technologist in DXC. He has worked in the arena of workplace technology for nearly 30 years, starting as a sysprog supporting IBM DISOSS and DEC All-in-1. Latterly Graham has been working with DXC's customers to help them understand how they exploit the changing world of workplace technology. Graham lives with his family in the United Kingdom.
Twitter: @grahamchastney


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Added to Your Shopping Bag
The Kansas City Royals Core Classic 9TWENTY Adjustable is a lightly structured cotton 9TWENTY that displays the Royals logo embroidered on the front panels offset by the New Era flag embroidered on the left wear side in team color embroidery. Completing this style is a woven tab displaying the team logo on the cap rear adjacent to the cloth strap closure.
Made of 100% Cotton Woven
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subset: commoncrawl


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Jeopardy! category: CONTINENTS (8-11-2005)
FJ! Clue: This continent has the lowest high point & the highest low point, less than a 7,500′ difference
The gist: It's mostly flat.
The highest point on Australia is the 2228-metre Mount Kosciuzsko in the country's southeast corner, near the border with Victoria. Its lowest (natural) point is Lake Eyre in South Australia, which dips down to just fifteen metres below sea level. Mt. Kosciuzsko (named for Polish patriot and American Revolutionary fighter Tadeusz Kościuszko, and also known by several Aboriginal names that mean "Table Top Mountain") is a peak in the Great Dividing Range, Australia's most substantial mountain range. It runs along the coutnry's eastern shore, and is most prominent in the southeastern portion. At just about a quarter of the height of Mount Everest, reaching the summit of Kosciuzsko isn't much of an ordeal, and it even has chairlifts and walkways to support climbers. Lake Eyre (or Kati Thanda in the local Arabana Aboriginal language) is the deepest part of its namesake Lake Eyre Basin, and as such collects rainfall from the Basin's 1 200 000 square kilometres of land. But even with that much area the lake rarely fills, as average rainfall in the central Australian is just a few inches (from about four to about twelve, depending on where exactly you're looking) per year. Some years there is so little rain that no water reaches the lake at all, and it remains dry throughout the year. Still, a few times a decade it will reach depths of a few metres, and in strong La Niña years it can reach about six metres. When wet it rapidly gains salinity, and resulting algae gives the water a distinct pink hue. The continent managed to end up so flat because its major tectonic and volcanic activity took place way back in its Gondwana days, about 500 million to 180 million years ago, meaning there's been plenty of time for erosion to wear down the mountains, and silting to fill in the valleys.
The clue: This isn't the sort of FJ! clue that you'd normally just know. Instead, it's one you might be able to work out in your head – although only one of the contestants got it right. First, it's probably going to be a smaller continent, since the larger the landmass the more varied its terrain, and the more likely there is to be variations in altitude. Second, if you've got any idea of how tall a mountain like, say, Everest of Kilimanjaro are (over 20 000 feet), you can easily eliminate their continents, plus any other continents where you're familiar with the highest point – Mount McKinley in Alaska is another well known one. Finally, even without knowing any specific mountains, you should be able to eliminate most of the continents – you probably know that the Andes in South America, or Europe's Alps, can get pretty big, and probably bigger than 7500 feet. The way I see it, that process leaves Australia and Antarctica – both of which were given by a contestant. I'm fairly certain I've seen pictures of big mountains in Antarctica, so that might have eliminated it for me, but to be honest I'm not entirely sure if or how I'd settle on Australia on the show.
In Jeopardy!: Australia is in many, many clues in the J!Archive, so we'll focus on Mount Kosciuzsko and Lake Eyre instead. "Kosciuszko" is in six clues, four about the Polish patriot and two about the mountain. Both of the latter have Australia as the correct response, as do all five clues about Lake Eyre. If you're interested in learning some Australian geography, much better to start with the states and capitals than concentrate on its geology too much.


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Callistasia Anggun WijayaThe Jakarta Post
Jakarta Governor Basuki "Ahok" Tjahaja Purnama sits on the defendant's chair at the start of his trial hearing at North Jakarta District Court in Jakarta on Tuesday. Ahok is on trial for an accusation of blasphemy following his remark about a passage in the Quran. (AP/Tatan Syuflana, Pool)
Jakarta Governor Basuki "Ahok" Tjahaja Purnama shed tears when he read out his statement against prosecutors' indictments in a hearing at the North Jakarta District Court on Tuesday morning.
Ahok told the court's judges that he has always had a harmonious relationship with Muslims. He attended Muslim schools, and he has Muslim friends who he considers his own family.
Ahok further said it was Analta Amir, his Muslim brother, who paid his tuition fee when he got his Master's degree at Prasetya Mulya University.
"I am so sad about being accused of insulting Islam because it means that I have defamed my own Muslim family whom I really love," Ahok said, weeping before the judges.
The non-active governor later mentioned several pro-Muslim programs, which had been implemented under his leadership as an East Belitung City Council member, East Belitung Regent and later Jakarta governor.


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You don't need to fight fires to be cool with this iPad or tablet case from Elvis & Kresse. Made from genuine decommissioned fire-hose it is extremely hard wearing, offering ultimate protection to your iPad. The lining is reclaimed parachute silk, ensuring that your iPhone screen stays protected.


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Author Affiliations
- Jayaram Vijayakrishnan and
- Richard S. Houlston⇓
- Correspondence: Richard S Houlston, Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, SM2 5NG, UK. Phone: international +44.02087224175. Fax: international +44.02087224365. E-mail: Richard.houlston{at}icr.ac.uk
To evaluate the contribution of candidate gene association studies to the understanding of genetic susceptibility to childhood acute lymphoblastic leukemia we conducted a systematic review and meta-analysis of published studies (January 1996–July 2009). Studies had to meet the following criteria: be case-control design, be studied by two or more studies, not be focused on HLA antigen genetic markers and be published in English. We identified 47 studies of polymorphic variation in 16 genes and acute lymphoblastic leukemia risk. To clarify the impact of individual polymorphisms on risk, pooled analyses were performed. Of the 25 polymorphic variants studied, significant associations (P<0.05) were seen in pooled analyses for eight variants: GSTM1 (OR =1.16; 95%CI: 1.04–1.30), MTRR A66G (OR=0.73, 95%CI:0.59–0.91), SHMT1 C1420T (OR=0.79, 95%CI: 0.65–0.98), RFC1 G80A (OR=1.37, 95%CI: 1.11–1.69), CYP1A1*2A (OR=1.36, 95%CI:1.11–1.66), CYP2E1*5B (OR=1.99, 95%CI:1.32–3.00) NQO1 C609T (OR=1.24, 95%CI:1.02–1.50) and XRCC1 G28152A (OR=1.78, 95%CI:1.32–2.42). These findings should, however, be interpreted with caution as the estimated false-positive report probabilities (FPRP) for each association were not noteworthy (i.e. FPRP>0.2). While candidate gene analyses are complementary to genome-wide association studies, future analyses should be based on sample sizes commensurate with the detection of small effects and attention needs to be paid to study design.
Acute leukemia is the major pediatric cancer in developed countries, affecting between 30–45 per 1,000,000 children each year.1 Dysregulated immune response to infection may be a cause of childhood acute lymphoblastic leukemia (ALL)2 and epidemiological data are consistent with transplacental carcinogen exposure as a basis for infant leukemia associated with MLL gene fusion,3 but the role of environmental carcinogenesis in ALL is currently undefined. It is, however, likely that the risk of ALL from environmental exposure is influenced by co-inheritance of multiple low-risk variants.
The commonest method for identifying common low-risk variants is through association studies. These are based on comparing the frequency of polymorphic genotypes in cases and controls. Alleles positively associated with the disease are analogous to risk factors in epidemiology and may be causally related to disease risk or in linkage disequilibrium with disease-causing variants. There are a number of different methods of analyzing the risk associated with a specific variant. For simple bi-allelic polymorphisms, the odds ratio of disease can be derived by comparing allele frequencies in cases and controls. This approach is, however, less powerful than a comparison of frequencies of the three genotypes among cases and controls using homozygosity of the "wild-type allele" as the reference group. Where homozygotes are rare, it is common to combine the heterozygotes and homozygotes together; but this is only appropriate if a dominant model can be presumed. Similarly, combining heterozygotes with wild-type homozygotes is only appropriate if alleles act recessively.
Excluding HLA, the genetic candidates that have been evaluated as susceptibility genes for childhood ALL to date can be broadly delineated into those coding for carcinogen metabolism enzymes, folate metabolism enzymes, DNA repair proteins, and others. Table 1 details the candidate gene polymorphisms that have been reviewed. For clarity the position and standard nomenclature of each polymorphism is provided.
Carcinogen metabolism genes
Children may be particularly vulnerable to environmental toxins because of their greater relative exposure, immature metabolism and higher rate of cell division and growth.4 In this context, functional polymorphisms in xenobiotic metabolizing enzymes have been postulated to be of relevance in determining susceptibility to ALL.4
The first and obligatory step in the activation of arylamines is N-hydroxylation by phase-I enzymes that include cytochrome P4501A1 (CYP1A1; MIM 108330).5,6 The glutathione S-transferases are a family of phase-II enzymes responsible for the detoxification of mutagenic electrophiles including polyaromatic hydrocarbons (PAHs). Homozygotes for null alleles (deletion) of GSTM1 (MIM 138350) and GSTT1 (MIM 600436) have absent activity of the respective enzyme. DNA-adduct formation and rates of somatic mutation have been reported to be increased in carriers of null alleles.7
Other metabolic gene variants that have been investigated as risk factors for ALL include polymorphisms in NQO1 (NADPH:quinone oxidoreductase; MIM 125860) a cytosolic enzyme catalyzing reduction of quinones and prevention of their participation in redox cycling and thus in oxidative stress.8 Variation in MDR1 (MIM 171050) which encodes the P-glycoprotein (P-gp) has also been studied as a possible risk factor for childhood ALL on the basis that it provides a cellular defense against toxic xenobiotic compounds.9
Folate metabolism genes
Leukemia commonly arises as a result of DNA translocation, inversions or deletions in genes regulating lymphocyte development. The formation of translocations in leukemia are thought to involve DNA double-strand break formation by means other than aberrant V(D)J recombinase activity.10 Folate deficiency has been associated with uracil misincorporation into DNA and double strand breaks during uracil excision repair thus potentially increasing the risk of chromosomal aberration.11 Pregnancy is a time of extreme folate requirement and supplementation in pregnancy has been reported to afford protection against childhood ALL.12 Dysfunctional folate metabolism is, therefore, an attractive candidate in the etiology of ALL as the most common translocations in infant leukemia (MLL-AF4) and in common childhood ALL (TEL-AML1) occur in utero in most, if not all, patients.13 Central to folate metabolism are the enzymes 5,10-methylenetetrahydrofolate reductase (MTHFR; MIM 607093), methionine synthase (MTR alias MS; MIM 156570) and methionine synthase reductase (MTRR; MIM 602568). These genes are characterized by functional polymorphisms and it has been postulated that these variants may impact on ALL risk through affecting folate metabolism. A similar rationale for evaluating variants of serine hydroxymethyltransferase (SHMT; MIM 182144), thymidylate synthetase (TS; MIM 188350) and reduced folate carrier 1 (RFC1, alias SLC19A1; MIM 600424) as risk factors for ALL has also been advanced.
DNA repair genes
XRCC1 (X-Ray repair-cross complementing group 1; MIM 194360) is believed to play a role in DNA single strand repair by forming protein complexes with DNA repair associated proteins.14 Polymorphic variants in XRCC1 may, therefore, play a role in ALL through aberrant DNA repair. Polymorphic variants in other DNA repair genes, including ERCC2 (excision repair-complementing group 2; MIM 126340), mutations which cause xeroderma pigmentosum (MIM 278700), trichothiodystrophy (MIM 601675) and Cockayne syndrome (MIM 216400)15 have also been evaluated as risk factors for ALL for similar reasons.
Although some polymorphic variants have only been examined once, most have been evaluated as risk factors in several studies but often with discordant findings. Furthermore, many of the studies have been based on small sample sizes with limited power to robustly demonstrate a relationship with ALL risk. To gain better insight into the impact of polymorphic variants on risk of childhood ALL, we have undertaken a systematic review of published studies and used standard meta-analysis techniques according to Cochrane16 and PRISMA17 guidelines to derive a more precise estimate of the individual variants. The implications of findings for future research on predisposition to ALL are discussed.
Design and Methods
Study identification
A literature search for studies reporting on the association between polymorphic variants and risk of childhood ALL was conducted using the electronic database PubMed from January 1996 up to the end of June 2009 (www.ncbi.nml.nih.gov/pubmed). The search strategy used the key words "acute lymphoblastic leukemia, genetic, association, case, control, polymorphism, risk". We searched for any additional studies in the bibliographies of identified publications, including previous review articles and meta-analyses.18–22
Selection criteria
Studies were eligible if they were based on unrelated individuals and examined the association between childhood ALL and polymorphic genotype. Only studies published as full-length articles or letters in peer-reviewed journals in English were included in the analysis.
Data extraction
Data for analyses, including study design, sample size, ethnicity, as well as allele and genotype frequencies, were extracted from the published articles and summarized in a consistent manner to aid comparison. When a study reported results on different sub-populations according to ethnicity, we considered each sub-population as a separate study in the meta-analyses.
Statistical analysis
Raw data of genotype frequencies, without adjustment, were used for calculation of the study-specific estimates of odds ratio (OR) and 95% confidence interval (CI). Cochran's Q statistic was used to test for heterogeneity, and the percentage variability of the pooled OR attributable to heterogeneity between studies was quantified using the I2 statistic; large heterogeneity is typically defined as I2 ≥ 75%. A P value of >0.05 for the Q test was considered to indicate a lack of heterogeneity across studies and for these analyses the pooled estimation of ORs of each study was calculated by the fixed effects model (Mantel-Haenszel methods).23 For results showing high heterogeneity, the random effects model (DerSimonian and Laird's method)24 was used. The significance of the pooled OR was determined by the z-test and P<0.05 was considered as statistically significant. An estimate of the potential publication bias was conducted by examination of funnel plots. An asymmetric plot is reflective of publication bias. The funnel plot symmetry was assessed by Egger's test25 based on inverse-variance weighted regression of the standardized effect sizes (OR/standard error (SE) of OR) on their precision (1/SE) to test whether the intercept deviates significantly from zero; P<0.05 was considered indicative of statistically significant publication bias.
To test for population stratification, the distribution of genotypes in control subjects of each individual population was tested for departure from Hardy-Weinberg equilibrium [HWE] by means of the χ2 test.26
For each statistically significant association identified, we estimated the false positive reporting probability (FPRP).27 The FPRP value is determined by the P value, the prior probability for the association, and statistical power. We calculated FPRP assuming a prior of 0.001 as previously proposed for candidate gene analyses.28 Statistical power was based on the ability to detect an OR of 1.2 and 1.5 (or reciprocal), with α equal to the observed P value. To evaluate whether the association was noteworthy, we imposed an FPRP cut-off value of 0.2, advocated for summary analyses.27 Hence, FPRP values less than 0.2 were considered to indicate robust associations.
All statistical analyses were undertaken using STATA version 10.0 (Stata Corporation, College Station, TX, USA).
Characteristics of published studies
We retrieved 267 published studies using our search criteria (Figure 1). Forty-seven of these studies met our predetermined criteria for inclusion. These 47 publications detailed 25 polymorphisms in 16 genes (Table 1). All the studies were essentially of similar design, although different types of controls have been analyzed (Online Supplementary Table S1). In the final group, three studies29–31 sub-grouped cases and controls according to ethnicity and seven studies32–38 grouped subjects according to ethnicity but did not present data on genotype and risk for the different subgroups. We did not identify any overlapping studies. The ORs of ALL associated with each polymorphism in individual studies are detailed in the Online Supplementary Table S2.
Pooling data from the 17 studies29,33,38–51 which have examined MTHFR C677T provided no evidence for a relationship between genotype and risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). There was evidence of population stratification in the studies reported by Wiemels et al.38 and Balta et al.,40 as controls showed evidence of departure from HWE (P=0.02, 0.05). The pooled ORs were, however, unchanged excluding these studies from the meta-analysis. MTHFR A1298C has been evaluated in 14 studies.29,33,38,39,42,44–51 Pooled analysis provided no evidence for a relationship between A1298C and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). Similarly pooling data from the four studies of the MTR A2756G polymorphism42,44,47,52 provided no support for a relationship between A2756G genotype and risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
The MTRR A66G polymorphism had been evaluated in three studies (Online Supplementary Figures S1 and S2; Online Supplementary Table S2).42,47,52 Pooling data from the three studies (Table 2) there was a significant association between A66G genotype and decreased risk; ORs for heterozygosity 0.76 (95% CI: 0.60–0.96, P=0.02; P heterogeneity (Phet) =0.85, I2=0%), homozygosity 0.67 (95% CI: 0.52–0.88, P=0.003; Phet=0.84, I2=0%) and carrier status 0.73 (95% CI: 0.59–0.91, P=0.005; Phet=0.82, I2=0%). Genotype frequency of controls in the study reported by Gast et al.,52 however, showed deviation from HWE (P=0.05) and excluding this study provided no evidence for an association between MTRR A66G and ALL risk (data not shown).
SHMT1 C1420T has been studied as a risk factor for ALL in two studies.42,52 Pooling data from both studies provided evidence for an association between the heterozygosity and risk (OR=0.79, 95% CI: 0.65–0.98, P=0.028; Phet=0.46, I2=0%). There was, however, no evidence for an association with homozygosity or carrier status (Table 2; Online Supplementary Figures S1 and S2; Online Supplementary Table S2).
RFC1 G80A has also been evaluated in two studies (Online Supplementary Figure S2; Table 2; Online Supplementary Table S2).42,52 One study showed heterozygosity, homozygosity and carrier status to be associated with an increased ALL risk (Table 2; Online Supplementary Table S2). Pooling all studies, ORs were: 1.37 (95% CI: 1.10–1.72, P=0.005; Phet=0.87, I2=0%), 1.36 (95% CI: 1.02–1.81, P=0.04; Phet=0.02, I2=81%) and 1.37 (95% CI: 1.11–1.69, P=0.003; Phet=0.49, I2=0%), respectively (Online Supplementary Figures S1 and S2). Evidence for an association between homozygosity and risk was not apparent under a random effects model (OR=1.44, 95% CI: 0.74–2.8).
The four studies42,43,47,52 of the TS 2R>3R provide no evidence for a relationship between this polymorphism and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
Seven studies35,36,53–57 have evaluated NQO1 C609T as a risk factor for ALL (Table 2; Online Supplementary Figure S1; Online Supplementary Table S1). The study by Lanciotti et al.53 only provided data on 609T carrier status. One study57 showed a significant relationship between heterozygosity and risk while two studies showed a significant association for carrier status36,57 (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). Pooling data from all seven studies, however, provided no evidence of a relationship between NQO1 C609T genotype and risk (Online Supplementary Figure S1). Controls in the study by Sirma et al.56 showed evidence of population stratification (P=0.01). In pooling data from the six other studies (Table 2; Online Supplementary Figure S2), there was evidence for a relationship between carrier status and risk (1.24, 95% CI: 1.02–1.50, P=0.03; Phet=0.49, I2=0%) but no relationship with either hetero- or homozygosity (data not shown).
Two studies54,57 have examined the relationship between NQO1 C465T and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2); pooled analyses provided no evidence for a relationship between genotype and risk (Online Supplementary Figure S1).
Fifteen studies30–32,35,37,40,58–64 have examined the relationship between GSTM1 and GSTT1 and ALL risk (Table 2; Online Supplementary Figures S1 and S2; Online Supplementary Table S2). Five of the studies reported a statistically significant increased risk associated with GSTM1 deletion. The pooled OR for GSTM1 was significant (Online Supplementary Figure S2), under both fixed (OR=1.16, 95%CI: 1.04–1.30, P=0.008; Phet<0.01, I2=13%) and random effects models (OR=1.26, 95% CI: 1.05–1.51). There was, however, evidence of publication bias (P<0.01), with four of the smallest studies showing a significant association but with no effect being observed in the larger studies (Online Supplementary Figure S3). Across all studies no evidence for a relationship between GSTT1 null genotype and ALL risk was shown (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
Seven studies32,35,37,40,53,65,66 have examined GSTP1 A1578G and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). Pooling data from the seven studies provides no evidence of a relationship between genotype and risk (Online Supplementary Figure S1; Table 2). Similarly, pooling of data from the two studies which have examined GSTP1 C2293T as a risk factor provides no support for an association between this variant and ALL (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
CYP1A1*2A (T6235C) heterozygosity and carrier status was associated with a significant increased risk in two of seven studies32,35,40,59–61,67 (Table 2; Online Supplementary Figures S1 and S2; Online Supplementary Table S2). A relationship between genotype and risk was supported by pooled analysis; ORs for heterozygosity and carrier status were: 1.38 (95% CI: 1.12–1.70, P=0.002; Phet=0.06, I2=51%), and 1.36 (95% CI: 1.11–1.66, P=0.003; Phet=0.04, I2=54%), respectively (Online Supplementary Figure S2). While there was evidence of between study heterogeneity, an association was still shown under a random effects model, with respective ORs of 1.38 (95% CI: 1.03–1.40) and 1.36 (95% CI: 1.01–1.84).
Of the three studies60,61,67 which evaluated CYP1A1*2B (A4889G) as a risk factor, one study showed a significant association between the A4889G and increased risk (Online Supplementary Figure S1; Online Supplementary Table S2). Pooled data from the three studies, however, provided no evidence for relationship between CYP1A1*2B genotype and risk (Table 2).
None of the three studies59–61 of CYP2D6*4 (G1934A) showed a relationship with ALL risk (Online Supplementary Figure S1; Online Supplementary Table S2). Similarly, pooling data from the three studies provided no evidence for an association (Table 2; Online Supplementary Figure S1). Two studies of CYP2D6*3 (del 2637) also found no evidence for a relationship between this polymorphism and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
Two of the four studies32,59,61,68 of CYP2E1*5B showed evidence of a statistically significant association between heterozygosity/carrier status and increased risk (Online Supplementary Figure S1; Online Supplementary Table S2). Pooling data from all four studies (Table 2; Online Supplementary Figure S2), respective ORs were 2.03 (95% CI: 1.34–3.06, P=0.001; Phet=0.28, I2=22%) and 1.99 (95% CI: 1.32–3.00, P=0.001; Phet=0.24, I2=29%).
Five studies34,69–72 have evaluated the synonymous MDR1 C3435T polymorphism as a risk factor (Online Supplementary Figure S1; Online Supplementary Table S2). Homozygosity for TT was associated with a statistically significant increased risk in one study.69 In the pooled analysis there was, however, no evidence of an association with risk (Table 2). While the controls analyzed by Jamroziak et al.70 showed evidence of departure from HWE (P=0.04), findings were unaffected excluding this study from the meta-analysis (data not shown).
Pooling data from the two studies34,70 of the triallelic variant MDR1 G2677T/A provides no evidence for a relationship between this variant and ALL risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
Three studies73–75 have evaluated XRCC1 polymorphisms C26304T and G28152A (Online Supplementary Figure S1; Online Supplementary Table S2). A significant association between XRCC1 C26304T carrier status/homozygosity and elevated risk was shown in two studies.74,75 Pooling data from the three studies did not, however, provide evidence of a relationship between the C26304T genotype and risk (Table 2; Online Supplementary Figure S1). Two of the three studies showed evidence of an association between XRCC1 28152A and increased risk (Online Supplementary Figure S1). Pooling data from all three studies (Table 2; Online Supplementary Figure S2), respective ORs were 1.78 (95% CI: 1.30–2.46, P<0.001; Phet=0.20, I2=37%) for heterozygosity and 1.78 (95% CI: 1.32–2.42, P<0.001; Phet=0.10, I2=37%) for carrier status. No significant association between XRCC1 G27466A genotype and ALL risk was shown in the two case-control studies74,75 and pooling data also provided no evidence of a relationship (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). Similarly no significant association between ERCC2 G23591A and A35931C genotype and risk was shown in two studies73,75 (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
Acute lymphoblastic leukemia is genetically heterogeneous, hence some associations may be subtype specific. Only five studies examined the relationship between B-cell ALL and risk.30,40,41,44,64 Among the three studies40,41,44 that looked at MTHFR C677T and risk, one study had irregularities in the genotype data presented40 hence data from the study could not be pooled. Combining data from the other two studies showed that C677T was not significantly associated with risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2). Of the three studies30,40,64 which examined the relationship between GSTM1 and risk of B-cell ALL, only two30,40 had extractable genotype data. One of the studies was significantly associated with risk. Pooling data from both studies the OR was 0.80 (95% CI: 0.66–0.99, P=0.037; Phet<0.001, I2=92%). However, the association was not significant (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2) under a random effects model (OR=1.22, 95% CI: 0.38–3.89, P=0.742). Two studies30,40 evaluated GSTT1 and risk of B-cell ALL and pooling data from these showed no evidence of an association with risk (Table 2; Online Supplementary Figure S1; Online Supplementary Table S2).
To evaluate the robustness of the 16 significant findings from the pooled analyses, we calculated FPRP conditional on a pre-specified prior probability of 0.001. None of the results can be considered noteworthy on the basis of assumptions (Table 2). For example, although the summary OR from the pooled analysis of XRCC1 G28152A indicated a statistically significant positive association with risk (OR, 1.78; 95% CI, 1.32–2.42), the FPRP was 0.63 which was much higher than our cut off for noteworthiness (<0.2) for pooled analyses.27
It is clear that substantial research has been carried out evaluating polymorphic variants in a number of specific genes as susceptibility alleles for ALL. Has this been worthwhile? While our meta-analysis provides support for variation at GSTM1, MTRR, SHMT1, RFC1, CYP1A1, CYP2E1, NQO1 and XRCC1 as risk determinants for ALL, these data should be interpreted with caution as the associations are not robust on the basis of FPRP estimates.
It is possible to draw a number of conclusions from the current data. Of the 25 variants examined to date, few have been reported as statistically significant, defined by a P value of 0.05, in more than one study. Given the issue of multiple testing in many reports, it is clearly advantageous when interpreting any purported association to have been replicated in an independent series. In some studies, the failure to demonstrate a relationship may be due to a lack of power. Genome-wide association (GWA) studies of cancer have demonstrated that the risk associated with individual polymorphic variants is quite modest (point estimates between 1.1 and 1.6 for an additive mode of inheritance).76 Fewer than 20% of the studies we reviewed had 80% power to demonstrate a 2-fold difference in risk at the 0.05 significance level. To overcome this lack of power, we have undertaken a meta-analysis pooling the data from the published studies. There are, however, caveats to this statistical procedure. In any systematic review, publication bias is clearly of great concern. The most common scenario is that negative findings may go unreported. Furthermore, many studies do not describe the ethnicity of cases or controls, and it is assumed that each polymorphism is functional with respect to risk in each study population. These are likely to be the case with MTHFR C667T, and presumably also for GSTM1 and GSTT1, since the functional role of the variants are better characterized. If, however, the polymorphism is a neutral marker for another variant, the assumption may well not apply, since LD is often population dependent.
An important lesson from current studies is that greater attention should be paid to design of future studies. Considering the issues of concomitant disease, a number of the studies were based on a comparison of cases and hospital based controls. The use of healthy population controls is preferable, since it is conceivable that the polymorphism might confer susceptibility to non-cancer diseases. The issue of population stratification in case-control studies and resulting false positive results is also of great concern. If population subdivisions exist, it is possible that associations will be found between disease and arbitrary markers that are unlinked to causative loci. Such associations occur because of population subdivision and non-random mating, leading to variation in the marker frequency within the population as a result of founder effects and/or genetic drift. The severity of spurious association becomes an increasing problem with increasing study size. To avoid this problem, it is essential that any potential confounding effect of population stratification be allowed for in the design and analysis of the study. This requires the identification of sub-populations in terms of factors that can influence both disease and marker allele frequencies. Provided cases and controls are well matched, differences in the frequency of genotypes will only be seen at predisposition loci. Hence, stratification can be detected by typing a series of unlinked markers chosen from a panel known to exhibit differences in allele frequency between populations.77
The focus of this meta-analysis was strictly on results from candidate-gene association studies and did not take into account results from other analyses. We have attempted to review published analyses of the relationship between polymorphic variation and risk of ALL through several iterations of search criterion; it is, however, possible that we have missed some reported studies. As the number of articles on genetic variation on risk of ALL published in the past decade has increased considerably and continues to grow, we fully accept that this review will not long remain current but provides a snapshot of progress to date in the field.
The choice of tissue used in the 47 studies selected for analysis varied widely. The majority of them29–35,40–44,46–48,51–56,59,60,62,63,65,67,68,70,71,74 were DNA extracted from peripheral blood, bone marrow or buccal samples collected at the time of diagnosis at the study center or with unspecified patient status. Five studies included samples from remission and those collected at diagnosis.36–39,49,69 Only six studies45,57,61,72,73,75 clearly stated that the samples were collected when the patients were in remission. The tissue origin for these studies varied from bone marrow, buccal swabs, Guthrie cards and peripheral blood. Four studies50,58,64,66 gave no clarification pertaining to sample origin. Studies that are based on DNA extracted from peripheral blood or bone marrow tissue obtained from non-remission patient samples may potentially contain somatic mutations that have the potential to confound association studies. Hence the results of such studies should be reassessed and accepted with caution. Due to the small number of studies that only used remission samples, such a screening criterion was not used in our current study selection.
Acute lymphoblastic leukemia is heterogeneous with respect to its underlying cellular and molecular biology, acquired genetic abnormalities and associated clinical responses to combination chemotherapy.78,79 It is, therefore, suspected that subtypes of B- or T-cell precursor ALL may not share a common etiology. To date only a very few studies have examined the relationship between variants and risk by subtype. Additionally these studies invite the issue of post hoc analysis.
All of the studies we have reviewed have been based on a candidate gene approach. It is becoming increasing clear from studies of cancer that without a clear understanding of tumor causalities the definition of what constitutes a candidate gene is inherently problematic, making an unbiased approach to loci selection highly desirable.
The availability of high resolution LD maps and comprehensive sets of tagging SNPs, coupled with the development of highly efficient analytical platforms, allow GWA studies for disease associations to be conducted cost effectively. This approach is unbiased and does not depend upon prior knowledge of function or presumptive involvement of any gene in disease causation. Moreover, it avoids the possibility of missing the identification of important variants in hitherto unstudied genes. Very recently, results from the first GWA studies of ALL have become available and these studies have identified risk loci for ALL at IKZF1, ARID5B and CEBPE.80,81 The substantial evidence supporting these variants, including sizeable power and replication in large samples, indicates that the associations are highly robust. These data thus provide the first unambiguous evidence that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL. Furthermore, they provide novel insight into disease causation of ALL; notably all of the risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors. Given sub-optimal LD between many polymorphisms with tagging SNPs, especially those with low minor allele frequencies [MAF], the findings provide a strong rationale for directly evaluating variation in other B-cell developmental genes as risk factors.
Of the eight associations from the current meta-analysis which were nominally significant at the 5% threshold, one was a deletion. Of the seven SNPs one was directly genotyped as part of our GWA study of ALL (rs1051266; RFC1 G80A) and the CYP2E1*5B SNP rs3813867 was tagged by rs10857733 (R2=0.88). Both SNPs showed no association with risk (respective P values =0.81 and P=0.84).81
The search for polymorphic variants influencing the risk of ALL is a worthy enterprise; however, the studies that have been conducted to date have important lessons for the design and execution of future studies. Candidate gene analyses should be viewed as complementary to GWA studies, as they offer considerable advantages both in terms of statistical power and an ability to identify low frequency risk variants. Furthermore, many functional variants, such as the small scale insertion and deletions in carcinogen metabolism genes, are poorly captured by the tagging SNPs used in GWA studies. It is, however, clear that in addition to conducting studies using sample sizes commensurate with the detection of polymorphic risk factors, attention should be paid to study design to avoid problems of population stratification and other sources of potential bias in order to maximize the output of any study.
we are grateful to Phillip Twiss for careful data checking and to Mel Greaves for constructive criticism.
Funding: the work in the authors' laboratory is supported by grants from Leukemia Research Fund and Cancer Research UK.
The online version of this article has a supplementary appendix.
Authorship and disclosures
RSH study conception, drafting of manuscript; JV literature review, statistical analysis and drafting of manuscript.
The authors reported no potential conflicts of interest.
- Received January 8, 2010.
- Revision received March 1, 2010.
- Accepted March 4, 2010.
- Copyright© Ferrata Storti Foundation
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text:
"Much is different between Massachusetts and North Carolina — our geography, our industries, our crops and our problems. You have sent us your hurricanes — and taken our textiles mills in exchange. "Much is different — but much more is the same. Our borders and your borders extend back to the Atlantic. Our history and […]
Archive for May 20th, 2014
JFK among believers in Meck Dec?
Posted in Just A Bite, tagged mecklenburg declaration, nc democratic club, sen john f kennedy on May 20, 2014 | Leave a Comment »


text:
Go buy Anatomy of Deceit . Don't update agressively. And don't expect a transcript.
Judy back. Looks like she's doing breathing exercises, pouring herself water. Got out of chair and is now back. Gets more water. Thanks person who brings more. Looking around cautiously. Closes eyes. Breathes. Breathes out. Looking straight foward. Head darts nervously. Staring forward. Shifts in chair. Looks toward Libby's team? Looks towawrd lawyers. Adjusts blouse. Looks at lawyers again. looks down, folds arms. Looks down. Looks toward Libby's team. Folds arms, leans back, turning in swivel chair. Takes glasses off. Looks for tissue to wipe her hands.
This is not the picture of someone who is relaxed.
Jury back in.
Jeffress back up.
J Let's go back to the beginning of the investigation that began–do you recall when it began?
M I don't recall, I don't remember when the Taubman discussion was
J Did it occur to you to think whether you were somebody to whom such a leak had been attempted.
M I was concerned [pasue] sir
J Did you remember that meeting.
M I don't remember what I remembered then.
J You were issued a subpoena, you retained counsel or NYT retained counsel, did you think, what you would say if they asked you questions
M I wasn't being asked what I remembered at that time, sir
J Did you remember at that time your June 23 meeting
M I don't know, I discussed my meetings with Libby within my newspaper
J Did you discuss the June 23 meeting within your newspaper
M I discussed a series of meetings I don't recall referring to that specific meeting, I discussed my concern about possibly receiving a subpoena. I was not thinking about what conversations before I received the subpoena,
J When was the subpoena
M Sir, the subpoena asked for meetings and discussions from July. My counsel asked me to review my notes pertinent to July, that's the information I reviewed, I didn't look at info before or after
J Did you think about it?
[Jeffress keeps screwing up date, Judy and Jeffress sharing a laugh]
M I know I expressed concern to in-house counsel, I don't believe we discussed a specific date. I was subpoenaed from July until the Novak column appeared
J Isn't it true that you didn't remember
M Between time I received the subpoena and time I
M I did not
J Did you remember any conversation between time you got subpoena to time of tha meeting
J Is the answer to my question that you didn't remember meeting with Libby on June 23
Walton–I don't think she said that rephrase
J Did you remember meeting with Libby on June 23, you didn't remember it after, when you were fighting the appeal.
M No, I didn't remember a specific meeting
J Did you think about this matter while you were there in Alexandria Jail
M I thought about importance of protecting confidentiality of Mr Libby until I ever got a waiver. I thought about how I would be sure that Prosecutor wouldn't be conducting a fishing expedition.
J You didn't remember when you were in jail, when you got out of jail, you went before the GJ, you swore to tell the truth, you were asked, when you went into the GJ, do you recall if you met with Libby in late June, by first meeting with Asst Jenny. The first GJ at page 11.
GJ transcript on screen
Judy trying to follow sidebar. Then she loks toward Libby. Swallowing hard, She IS ONE STRESSED person. Looks to lawyers. Tries to look at sidebar. Arms folded, looking hard to her right. Looking for something, looks like she's sweating under her eyes. Looking for tissue or something, Rubbing nose with back of sleeve. Unlucky Judy, just when she gets her tissue.
Now bringing up GJ testimony.
And do you recall if a few weeks earlier you had met with Mr. Libby some time in late June, by first meeting with his assistant, Jennifer or Jennie.
I have a very, I don't know if I met with him. I remember meeting with Jennie.
J You didn't go into the GJ to lie.
M I did not remember it. I didn't remember that it even occurred.
J You've testified to his demeanor, very particular things that he said, said the wife "works in the bureau."
M Sir, having reviewed my notes, I have a memory of it.
M [With gusto] No, I have a MEMORY of it.
J Do you recall testifying to te GJ that
Now she's got a pissed look on her face.
J Did you say to the GJ:
I really have to rely on my notes because my memory is not good
M Sir, I'd like to see the context of that.
J Were you asked the following question.
Judy swallowing nervously.
And is it fair to say that in describing Wilson's wife, your best recollection is he did not refer to her by name?
J You remember bureau today even though you forgot about it for three years. So you don't need your notes to remember Mr Libby said Wife Works in Bureau, but you would need notes to remember anything else about the meeting
J Do your notes say "irritated"
M No I read my notes and I remembered
J Do you have a good memory
M About some things
J Do you remember appearing on Digital age, do you remember saying "Wilson's wife didn't mean a thing to me"
M I remember saying one tends to remember things one writes about
J You didn't have a good memory because it wasn't important to you
M I think what I was trying to indicate, I was focused on what had happened was what happened to intell
Jeffress plays one minute clip from program
Judy watching Judy, she nods when she sees herself saying "It didn't mean anything to me." She nods vigorously.
J What did you mean when you said it only bc important when this blew up
M When subpoenas were being issued
J and it was important to you when you got a subpoena, but you didn't remember that meeting
M Counselor I've already said, I just didn't remember it. [waves hand, has her indignant voice on]
J You remember being asked. Let me go back, set the stage. After you didn't remember this meeting at all, you went back after finding that there had been a meeting. What date did it say
J But you know there was a meeting on June 23
M I don't know what was in Mr Libby's calendar
J After you found that notebook, you gave it to your lawyer, you testified a second time, you testified about that conversation
M yes (meek)
J Do you remember that you told the GJ on that occasion, you had now produced all of your notes?
(no audible response–she must have nodded)
J Did you tell GJ your memory is sparked by notes
M I think in certain contexts I said something like that.
J That was a general question
M Generally I'm note driven and they bring back a memory. [realizes she has testified that she doesn't know who told her the name] Or they don't.
J Do you remember my question
M Sighs.
J Your memory is note driven and you don't have an independent memory. You said, you just have to be specific about this because my memory is note-driven. Is that true. [raises voice]
M Yes it's true
J Without using a single note you told the GJ all these details
M I've thought about those meetings, reading those notes brought back my memory about those memories.
J Your memory is largely note-drive
M Largely note-driven
J Do you recall that before ever meeting with Libby on June 23 you had been looking at the stoyr about uranium
J Did you have his name Joe Wilson and his telephone number and extension.
J So who did you talk to about Joe Wilson
M I don't remember
J Do you remember talking about Joe Wilson
J You told that someone had talked to you about Joe Wilson but you don't remember too.
J Do recall telling the GJ that his name was in your notes before June 23, So someone may have told me, but I don't remember.
M reading, GJ up on sccreen.
J was that your testimony.
M Looks closely at screen, follows with her finger
J How many people did you talk to, it was lots, wasn't it
M There were many people I talked to about WMD, and I have a vague memory of talking to them about it.
J What is "it"
M Joe Wilson
J There were several people you talked to about Wilson and Plame, before Novak's columne ever came out.
J You may have talked to someone about it before Mr. Libby
M I Don't remember talking about his wife before talking to Mr Libby
J You have no memory about that
J You testified that you didn't read newspaper
M Yes
J You started reading when you came back Did you read your own newspaper?
M Not particularly. I read the competition.
J So if an article appeared in NYT on WMD after you returned, you likely would have read it.
Putting exhibit up. White House in Denial–Kristof's article
J That's an article by Kristof
M Yes (sounds weak)
J Do you recall seeing that article at the time it was published
M No I don't
J Do you recall reading or hearing at the time about an unnamed ambasador?
M Yes
J Mr. Kristof writes on June 13, less than a week after you got back from Iraq, highlight first two paragraphs
Judy is reading
J Do you remember hearing about this (Condi's MTP appearance)
M mmmm hmmm, I remember hearing about it.
J It would be pretty surprising if true that something had been flatly discredited,
M [pause] Yes
J Goes onto the Wilson section of trip. Reading more of Kristof
J You came to find out that not only did Wilson not report any documents,
M I Don't know what Wilson saw and didn't see
M Libby complained about quality of Wilson's investigation
J Did you read Tenet's statement
M I probably did
J Did you read other articles concerning forgeries.
J Okay, you do remember, you do remember (in his soothing voice)
M I remember what has been claimed on all sides, but since I didn't interview Mr Wilson I don't know what he said or didn't say.I know what he said in his book.
J Oh, you read his book.
M I glanced at it.
[Media room erupts]
J Did you have any notes of meetings with Libby while you were in jail.
M No
J Concerning your decision to resist that subpoena. You decided to resist it originally and to assert what's called a journalist's privilege. You knew… did you know that SCOTUS had decided that there generally was not any privilege.
M That's one interpretation of Branzberg decision, sir
J that's one interpretation?
M Yes
J Did they show you a waiver and request to testify from Libby. Did the govt inform you that Libby had waived confidentiality.
M The govt did not assert that.
J Did you go to jail for 85 days before you didn't believe Mr Libby had signed a waiver
M I went to jail because the waiver my lawyer told me
J that's hearsay.
Judy is shaking her head in frustration.
I'm going to start a new thread.
Liveblogging continues in Judy Three.


text:
Atomic is a classic song from Blondie. Released in 1980, it was in fact the third single from their album Eat to the Beat. It reached number one in the UK and stayed there for 2 weeks.
But enough about that - lets talk about the song itself. This is a real stomper of a song. Blondie were of an undefined genre at the time - neither rock, punk or disco, but somehow melded all those styles in absolutely original sounds. You can tell this is a Blondie song as soon as it kicks in.
That familiar instrumental, mainly bass guitar starts up, which I am confident most of us will recognise as this song has been well used in TV and film - most memorably when it was covered and used in the film Trainspotting! Then Debbie Harry kicks in and her beautiful voice takes the song to a different place than you think it is going.
This is now a club classic, and the beat that kicks in the background still sounds both raunchy, daring and modern. Debbie Harry almost growls the title "Atomic", and the result is a sexy prowl through a pacy record. This to me is the most exciting of the Blondie product. Its uplifting and dark at the same time.
Whilst this is a 1980 song, it stands out from the other music of the time. It doesn't have that dated feel to it. This is also the song that propelled Harry into the consciousness (if she were not already) of a league of new fans by wearing a "garbage bag" in the video - intended to look futuristic. However, this spawned fans who proclaimed her to be so beautiful she could even look good in a bin bag!!
I have listened to 2 other Blondie singles so far this week - Heart of Glass and Call Me. This one though is my favourite by far. I have even added it to my playlist. It sticks in your head. I am really enjoying my revisit to this bands music - join in if you like and go and have yourself a listen. Enjoy. x
Saturday, 11 January 2014
Blondie - Atomic - today's single pick
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text:
onsdag 20. oktober 2010
Babyguttekort / Babyboycard
A little babycard for a little boy..
Dette har brukt... This is what i used...
Blomster/Flower: hjemmelaget/homemade, Prima and Wild Orchid
Image: from Digi Doodle and colored with promarkers
Sentiment and the little body is cut on my silhouette
Whit this card i take part in the following challanges:
Wild Orchid Challange wanted pastels
Karber Weekly challange asked for kids and babies
Tuesday Throwdown has anything goes
Paper Sundaes want something for someone little
Digi Doodle wanted peeps
Craftalicious have anything goes
Hope you like it... :)
10 kommentarer:
Lovely and oh so cute. Love the layout. Thank you for sharing with us at Digi Doodle Shop's Best.SvarSlett
So sweet! Lovely coloring job on the image and I love your flowers and that beautiful "Baby" title. Thanks so much for joining us this week at Digi Doodle Shop's Best!SvarSlett
So cute card! Thank you for Playing the Karber Weekly Challenge :)SvarSlett
Super sweet card! This in one of my favorite images from the Digi Doodle Shop. Thanks for joining us for the challenge at Digi Doodle Shop's BestSvarSlett
pretty card. Thanks for joining us at Paper Sundaes this week.SvarSlett
Adorable!Such lovely shades of blue and love the banner created out of baby vests.Thanks for joining us at Digi Doodle Shop's Best :DSvarSlett
Lisa x
I love this!! Such a sweet card! Any mother would treasure this forever. Thanks for joining us this week at Digi Doodle Shop's Best!SvarSlett
Absolutely gorgeous. Thanks for joining us at Craftalicious for our challenge this time. luv gina xxSvarSlett
What a cute image and beautiful flowers! Thank you for joining us at Paper Sundaes - we hope to see you again next week!SvarSlett
so sweet! The image is very cute and the flowers lovely!SvarSlett
Thanks for joining us at Paper Sundaes this week!


text:
Shaping the day : a history of timekeeping in England and Wales 1300-1800 / Paul Glennie and Nigel Thrift.
By: Glennie, Paul.
Contributor(s): Thrift, N. J.Material type: BookPublisher: Oxford : Oxford University Press, c2009Description: xiv, 456 p., [8] p. of plates : ill., facsims, maps, plans ; 25 cm.ISBN: 9780199278206; 0199278202.Subject(s): Time measurements -- History | Clocks and watches -- England -- History | Time -- HistoryDDC classification: Online resources: Table of contents only
Introduction : the measured heart -- Clocks, clock times, and social change -- 'Not everyone occupies the same now' : reconceptualizing clock time -- Clock times in medieval and early modern Bristol -- The provision of clock time in pre-modern England -- Clock times in everyday lives -- Precision in everyday lives -- 'Posted within shot of the grave' : seafaring times -- The pursuit of precision -- Clocks from nowhere? : John Harrison in context -- Some concluding remarks.
|Item type
|Current location
|Call number
|Date due
|Science Museum London Dana Research Centre Library: Books
|Science & Technology Studies Collection
|529.7:93 GLENNIE (Browse shelf)
|Checked out
Includes bibliographical references (p. [419]-449) and index.
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text:
Apple had so much to announce at the 2017 edition of its annual Worldwide Developer Conference that it had to swallow important bits like the customary updates on status of various verticals. Still it ended up being a two-and-half hour keynote, which CEO Tim Cook tried to summarise into six different heads. But through the course of the eventful presentation it was clear this was a show squeezed into the time slot available — apparently about one hour of presentation had to be forgone or put on fast forward.
The highlight clearly was how Apple's latest iOS 11 will make machine learning integral, while making augmented reality more accessible. Apple's version of machine learning is woven into what its users would do on a daily basis across the operating system, right from understanding faces to suggesting apps based on incoming messages. But it also wants to give a big boost to augmented reality by opening up its ARKit for developers. That, the company says, will make it the largest AR platform in the world.
There is some serious Virtual Reality also coming to the MacBooks, which will get upgraded to macOS High Sierra soon. In fact, Apple showcased VR demos using the MacBook with some external graphics support, and HTC Vive hardware. Apple is upgrading its MacBook range with Intel's new Kaby Lake processors, twice the memory and better graphics.
The iMac range too got upgrades with better displays, but a sneak peek of the $4,999 iMac Pro with unprecedented processing power and graphics capabilities really captured the attention of the audience. The iPad Pro range, meanwhile, got a new 10.5-inch variant which Apple seems to be pushing to replace the older 9.7-inch model. The iPad Pro has actually become cheaper while adding more muscle in processing, screen rates and display quality.
Among the other software announcements, the entry of Amazon Prime — which Cook called a creator of great original content — into Apple TV was significant. The watchOS will soon have a Siri watchface and a Music app that is easier to navigate. Apple also announced a redesign of the App Store, which clocks over 500 million visitors a month on the iOS platform.
There was one last thing, a whole new segment for Apple. It wants to revolutionise home music with the HomePod, a smart speaker for the home. Apple's vision for the speaker is very similar to Amazon and Google's vision for their smart speakers and hence comes with full access to the Siri virtual assistant. The difference, on the other hand, will be the ability to play the music better, with spacial context and access to the entire Apple Music store. The HomePod will start shipping in December, but India is not in the first wave.
Disclaimer: The author is attending Apple's WWDC in San Jose at the invite of Apple India, which is paying for travel, accommodation.
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Hormones often get a bad reputation because when they are out of whack, we feel so powerless. While we may not be able to completely control the ups and downs of our hormones, we can start paying better attention and help them out a little. In the first installment of the naturally healthy hormone series, Caitlin shares a personal story about a time when she was a little "hormonal." She also gives a brief overview of the endocrine system and shares 5 areas you can focus on to begin to take control of your hormonal health naturally.
As with any change, balancing your hormones naturally may take a little work, but the work pays off. And in Caitlin's words, "Trust me…trading out refined sugar for a piece of fruit will be worth it when you're not road-raging at the driver in front of you because he didn't use his blinker!"
CLICK HERE to read Pull Yourself Together: 5 Ways To Start Taking Control of Your Hormonal Health over at The Locust & Honey, and start taking control of your hormones today!
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It seems like I just took down my Christmas tree from last year, and now the holidays are upon us once again – which means some great profit opportunities are here as well.
A lot of investors will hunt for trades in retail and transportation. The holiday season is traditionally good for those sectors. But that's not the full story of where you can get the biggest opportunities.
When you look closer at how stocks actually trade in December, you'll see the most consistent performers during the holidays are not always who you'd expect.
That's why I use stocks' historical patterns to uncover the best potential winners. History tends to repeat, particularly when it produces the same result consistently over longer periods. It's your best guide to predicting the future movement of stocks.
Today I'll show you seven stocks with 100% historical accuracy. That means that if history repeats yet again, these trades can drop profits into your pockets for the holidays…
About the Author
Tom Gentile is widely known as America's #1 Pattern Trader thanks to his nearly 30 years of experience spotting lucrative patterns in options trading. Now, he's diving into the biggest market in the world - one that almost no one has heard of before.


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It's hot hot hot! Ideal for becoming dehydrated, suffering from heatstroke and getting sunburnt… but not so good for enjoying long runs or running fast. But luckily we SJs are a hardy bunch and we also have lots of fantastic shady woodland to run through.
We'll have the full results from the July Handicap next week but here's a brief summary. It was hot…. and Jim Laidlaw was first to finish on a hot night which was not conducive to PB running so well done to the three members who did post a fastest time on the four mile run.
Wednesday Lisa hale ran Helen Windsor 10k at Greetland near Halifax in the North of England in 45:04. This great time bagged her 3rd position in the Senior W35 category. The race doubled as the Yorkshire Vets 10k Championships.
Friday saw Richard Boese and Leon Hicks contest a 100m sprint… only joking it was actually a marathon within the Dinton Pastures Sundae Challenge. The event was a 6 hour timed challenge where you could run as many or as few 2.6 mile laps as you wanted. 10 laps for a marathon, 5 for a half, 11+ for an ultra and 1 or more to be a finisher and get a medal and create your own sundae with a serving of ice cream and choice of sauces and toppings. The weather well and truly cooperated with the ice cream theme.
Rushmoor was closed again this week so Frimley Lodge was very busy with 617 runners! Mark Pattrick was first to finish for the club in 20:28 which is his best time since 2015. Dave O'Toole was next member to finish showing incredible consistency finishing in exactly the same time as last week with 22:10.
Over at Bracknell there was a great turnout by the recent Pure Beginners graduates. Sophie Le Saux scored her best time on the course with 32:27. Three PBs with Jacqueline Hudson logging her best Parkrun time ever with 34:57, Jonathan Evershed with 37:23 and Michelle Williams in 42:36. Sophie Pibworth, Julie Maxwell and Natalie Wilkinson all ran for the first time this week.
On the Parkrun tourism front. Dave Bartlett and Sarah Alexander made the short trip to Woodley. John Tovell ran at home venue Crane Park. Lisa Hale, Phil Turner and Alurie Dutton visited Homewood. Stephen Casey ran (and paid £1.80 for parking!) at Alice Holt. Yvette Glacken ran her home race at Luton Wardown.
Don't forget to add Sandhurst Joggers as your club in your Parkrun profile to help us keep track of your achievements.
Lina Johnson took part in The Corporate Games in Nottingham which consisted of a 10k followed later in the day by a relay in which all members of the team completed one mile. Both races were run off in hot conditions and the 10k was particularly hilly using the same venue as the 2017 National XC Championship.
Nigel Evans took on the Westminster British 10k on a course around many of the London landmarks that provided the backdrop to his marriage proposal (and Virgin London Marathon finish) back in April. He finished in a time of 54:14.
This week we had a new Queen of Strava with Kathryn Carney topping the leaderboard with a total of 71.4km. Krzysztof Zielinski was second with 63.5km, while I was third with a paltry 61.5km. Sixty-one members logged runs this week. To take part in this just create a free Strava account and link it to the club in your profile.
As always, please let me know if I've missed anything and share your results and achievements in the future so the rest of the club know what you are up to.
As always keep a look out on Facebook for details of the weekday evening runs.
Monday: Patrick will be leading the usual Monday night chatfest leaving Sandhurst Sports Centre at 7:30pm.
Tuesday: There will be multiple groups running on Tuesday from Sandhurst Memorial Park this week starting at 6:30pm. Later the interval sessions will meet at The TYTHINGS in Yateley at 8pm but don't overdo it if you are racing on Wednesday!
Wednesday: This week is Race 2 of the Yateley 10k Road Race series with lot's of members running and many more volunteering. If you aren't already involved but can spare some time on Wednesday evening please let Roger know.
Thursday: This week the threshold/improvers run will be on the off road, Nikki will have more details later in the week and soon we'll have a route schedule planned out.
Friday: Track is still free and the THREE coaches have some great sessions planned for all abilities to improve fitness and technique. The Track Challenge is coming up on Friday 21st July so these sessions are a fantastic opportunity to practice ahead of the big night!
Sunday: Anybody not racing can join the crowd running from The Lookout at 9am. It's a flexible run to suit everybody's needs and is either adapted to fit with distance targets or multiple groups are formed. The three 'Cs' of Coffee, cake and chat are enjoyed in the cafe post-run.


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As we all know, music is the universal language. No matter who we are or where we come from, music has the unique power to stir up a well of emotions quickly. We can rock out to a great pop song, find comfort in a mournful ballad or marvel at a beautiful symphony. If you're happiest when you're strumming a guitar or belting an aria then music is likely the academic path you seek!
If you decide to major in music, you'll certainly get a great overview of the subject. Indeed, most departments take both a practical and analytical approach. This will allow you to hone your ear, develop a greater understanding of the evolution of music and enhance your appreciation of the art form. You will take classes ranging from the music of Asia and Miles Davis to film scoring and steel drumming. Though some programs offer a general music degree, many ask their undergrads to choose a specific concentration. These are often divided into categories like music history, performance, theory/composition, cultural musicology and jazz. Regardless of concentration, most schools also require their students to participate in some type of music ensemble and to take instrument or vocal lessons. Lastly, you can expect to complete a senior project. These often entail either the presentation of an original composition or a recital/performance of sorts.
Undergrads who pursue a music major tend to be creative types, armed with a good ear and a great sense of rhythm. They are also adept at handling abstract concepts and have solid communication skills. Moreover, they are dedicated to their craft and don't mind logging lots of hours in the rehearsal room. Finally, they are usually able to make marching band uniforms looks (somewhat) cool.
As a music major, you will have the opportunity to engage with all sorts of genres in classes such as: Introduction to Listening, Classical Music in Western Culture, Jazz Performance Workshop, Music Theory I, Contemporary Popular Composition and Arranging, American Musical Theater, Music of Brazil, Choral Literature, Advanced Harmony, African Drumming Ensemble, Instrumentation and Orchestration, Tonal Forms and Post-Tonal Techniques and The Romantic Period.
Music majors are obviously passionate about their chosen discipline and thus love to study all applications of it. Therefore, they might also be interested in majoring in music history, music therapy, musical theater, dance, journalism, music education, art history and criticism, conducting, jazz studies, radio/television/film, music performance, opera studies, ethnomusicology, percussion, voice, piano, strings and woodwinds.
All right – so music majors cannot bank on becoming the next Leonard Bernstein or Wagner or even the next Bono. However that doesn't mean they need to lock their trumpet in the closet and shelve their musical aspirations as soon as they cross the graduation threshold. Certainly, music majors have a number of professional paths open to them. While many might hope to become working musicians, some grads earn a living as arrangers, accompanists or transcribers. Others might enter the field of arts management or find gainful employment within the music licensing business. Additional possibilities include becoming an agent, journalist or critic. Some also flock to music publishing or instrument repair. Audio production is another popular field and majors can find positions ranging from audio and recording engineer to producer, music director and studio manager. And of course, a larger number ultimately become teachers, working anywhere from public schools to private lessons. No matter what you ultimately decide, rest assured your life can always be filled with music.
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text: "Blouses are our passion. And we want to create gorgeous blouses for all women who share this passion with us. Blouses that are casually and naturally worn like a shirt. Blouses, their clear cut, refined details and top-notch materials. Often in crisp white or decorated in neutral tones, blouses of Lareida are timeless, they have a perfect fit and a cool look."


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Last week, Walt Disney World kicked off their 75 day "International Food and Wine Festival" at WDW's Epcot! The festival has 30+ marketplace booths from all around the World (Showcase), nightly concerts, as well as "The Festival Center."
The Festival Center will be playing host to tons of seminars, the official festival merch, as well as my new favorite exhibit, "The Chocolate Experience: From The Bean To The Bar" presented by Ghirardelli Chocolate Company!
That's not all! Joining in on the festivities this year, 6 teams of Disney Pastry Chefs from around the WDW Resort were each tasked with making one of the six chocolate statues that will be on display during the festival.
While I was at Walt Disney World, I was lucky enough to attend opening day of the festival and got to check out the statues in-person. Each statue is completely made out of chocolate and they look incredible…and delicious.


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Ascetic Limited presents its first compilation. Barcelona based Glaswegian DeepbassÊsupplies his deep ambient techno soundscapes. Italian Techno Dj and producer Dorian Gray's is focusing on beautiful choirs and drones while Hobi takes a darker side with fast tribal beats and voice-like textures. Finally Lanthan.Audio owner Christian Gerlach brings deep and hypnotic techno track on B2.
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Milly scratched her chin with the gun in her hand. She had to come up with a way to get in touch with Giuseppe. And she had to get a nice little ransom for Josh. But how? Milly wasn't a seasoned kidnapper. She didn't have a criminal mind, no criminal energy. She had slid in with the wrong crowd, and now she was in a right mess. And her side hurt. She didn't want to let on that a bullet had hit her, but she felt the blood flowing out of the wound. It was soaking her shirt.
"We need to stop for supplies," Milly announced. She put her gun in her bag and winced again.
"You okay?" Josh asked. His kidnapper grew paler by the minute. It would have been easy to stop and get rid of her. But he was concerned about Milly. And intrigued as well. He wanted to hear her story. She seemed kind enough, even while she was pointing a gun at him. And so he decided to stay and help her as best as he could.
"Pull over there," Milly ordered Josh to pull up to a parking lot of a grocery store. "We need some food and other things."
Josh parked and got around to open Milly's door. She blinked, ready for an attack, but it didn't come. Josh held out his hand, and Milly blinked again.
"We should split? I am sure Henry called the cops. Or a neighbor did. After all, there was a shot." Josh took Milly's bag. She didn't say anything, just held her side with one hand. She didn't dare to look down. She didn't want to see how bad it was. "Or we go together, and you tell me what to get?" That option was more to Milly's liking, and she nodded.
"Let's do that," she croaked. "And after that, we will find us a motel or something." She wanted to sound in charge, but her injury made it hard to think about anything else than the hole in her.
"You could also wait here? I promise to be back," Josh offered, but Milly shook her head. "I am okay, let's go." At the store, they stocked up on convenience food and snacks. Josh sneaked medical supplies into the cart, and he insisted they buy a set of clothes to change into for them both. Milly agreed, and she didn't bicker when Josh stood in the beauty aisle and chose deo and shampoo. Their shopping trip only took them twenty minutes, powering from isle to isle, always checking if no one was looking at them funnily. People were watching them, of course. They were an odd couple, and even a blind person could have seen that Milly was not well.
At the checkout, Josh put an arm around her. She tried to shake him off, but he didn't let go. "Are you okay, Miss?" the cashier asked. Milly merely nodded. "Cramps," she replied with a tortured smile. "Nothing a hot bath and lots of chocolate can't cure." The cashier smiled emphatically while Josh paid her. Milly had not reacted to the things he had added to their shopping. He took the bags and guided Milly back to the car.
"You've been shot," he finally said.
"I am okay," she replied through clenched teeth, getting into the car.
"Let me take a look!" Josh didn't wait for her affirmation, and already he was pulling at her shirt. Milly didn't like it at all, and with a mighty punch, she let Josh know it too. "Let's get this straight, don't you ever touch me again," she threatened.
"I don't need to be here. I could have run a while ago and left you." Josh shot back.
"Why didn't you?" Milly groaned and hid her face behind her hands. "I am the world's worst kidnapper."
"I don't know. Maybe I want to get back at my father too." Josh finally admitted. He pulled out of the parking lot, and both stayed silent for a long time. The silence was comforting, as was the sound of the car. Before long, pain and exhaustion got the best of Milly, and she fell asleep.


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The 2018 Ford Taurus from Briggs Ford of Fort Scott, KS, serving Pittsburg, Iola, and Chanute, is a practical sedan for the top-notch driver. You deserve a vehicle that answers to your needs, so you need a 2018 Ford Taurus. With all the modern features you could dream of and the powerful, 288-horsepower 3.5L engine, you'll enjoy every drive. Soft-touch, high-quality materials fill the cabin and delight your senses. The available Sony audio system takes your music up a notch, and with the available SYNC 3 system you'll have access to Apple CarPlay and Android Auto, so you can use your favorite smartphone apps without touching your device. SHO and Limited models boast standard ambient lighting, and all models have dual-zone climate control to keep each row at the perfect temperature. With the available active park assist, you'll always have the best parking job in the lot.
Right now is the best time to buy a new Ford! We have an outstanding selection of the new 2018 models and amazing deals to satisfy your wallet. Schedule your test drive today by calling 866-798-1640, or stop by our location at 1819 South Main Street, Fort Scott, KS. Drive home the new 2018 Ford Taurus you've always dreamed of!
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Intelligent AWD sensors balance torque between the front and rear wheels to enhance handling and maximize traction, typically before wheelslip can even occur. Standard on SHO and available on SEL and Limited.
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Superior styling and craftsmanship are evident in every detail of the Taurus interior. Soft-to-the-touch, high-quality materials are used throughout the cabin, including cloth-wrapped front, center and rear pillars. Design aficionados will appreciate the clean, elegant lines and refined color palette. And for that sense of quiet comfort, Taurus features insulation in the engine compartment as well as the cabin to isolate engine and external noise to provide you and your passengers with an enjoyable ride
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Our recently renovated Utilities Operations Center (UOC) is a multi-purpose building in which our operations team provides steam generation and compressed air for our primary campus. UOC staff also provides remote monitoring of campus utilities and building controls, and handles off-hours call service for our Customer Service Center.
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For immediate assistance or emergencies, contact us immediately at 336.758.4255.


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Nuno: Wolves will emerge stronger
Nuno Espirito Santo believes Wolves will emerge stronger from their poor run as he looks to engineer a shock win against Chelsea tomorrow.
Wolves are enduring their worst run under Nuno, while the boss is on the worst run of his managerial career.
Five defeats in six have seen the team drop to 12th in the table.
But Nuno said at today's pre-match press conference: "I believe we'll come (out) stronger.
"What's important is how we approach the situation.
"We're not being so solid. When you have this balance, you have to try and find the solution offensively and defensively.
"The only game we weren't on our standards was Huddersfield at home.
"Giving up is not an option – we must fight for every moment, every match.
"First you have to know what's happening, then the approach cannot change because you believe in the things you do.
"We cannot be obsessed with a big performance to get us out of trouble. No, we have to go step by step, game by game. We have to fix the other things, keep building and working hard.
"I don't sense a lack of confidence, it has to do with performance
"A team is like a player, ups and downs, you have to find solutions to help them, give them good advice and have a good game-plan.
"It has to do with so many aspects, technical, tactical, mental."
Chelsea are third in the table having only lost once this season, to Spurs last month.
Nuno said Wolves wouldn't change their approach for any team.
"Chelsea is a very good team, the way they play, its going to be a big challenge," he said.
"They have a very good manager with a very good idea of how to play football.
"We approach always the same, no matter what the opponent. Always the same approach but it's a big, big challenge."
Some fans have called for Nuno to change his usual 3-4-3 formation but the boss said: "It's what you believe. When you want to build something and you're really onto it, something that started more than a year and a half ago, sticking to a shape we believe can deal with any opponent, you have to stick on it.
"It's not about changing, it's adapting and being versatile. The same shape but change details that can help us."
Nuno says he's already chosen his XI for tomorrow night.
Ruben Neves will miss out as he's suspended after earning his fifth booking of the season against Cardiff.
The Portuguese midfielder was suspended on three occasions last season – twice for bookings and once for being sent off at Middlesbrough – but Nuno doesn't want the 21-year-old to cut down on tackling.
On the contrary, he said: "If a foul can help a team, let's do it, because it's important.
"I speak with Neves every day, if we analyse the bookings some of those were helpful for the team and part of the tasks he has, even if he causes a problem that he cannot be on the pitch (due to suspension).
"I won't accept yellow cards by insulting or strange words to referees or opponents, that doesn't make sense.
"But if its a foul that can help the team, he must do it."
Ryan Bennett was dropped in favour of Romain Saiss at Cardiff on Friday.
Nuno said of the decision: "It's not an individual issue.
"We wanted a different approach individually on that specific position with Saiss.
"What Bennett gives us, what Saiss gives us, we balanced that and decided for Cardiff."
Most Read


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Our famous Transition Week gives all of the Year 6 children who will be starting here in September a chance to settle in, make new friends, and have fun here at Shuttleworth. Every child works within a small group to develop ideas, learn skills, and make new friends.
Miss. Roach, our Transition Lead, and Mr. Turner, the Year 7 Pastoral Leader, work tirelessly to create a great environment that promotes a smooth and stress-free transition from primary school to secondary school. They are both excited to have so many brilliant young people coming to our school!
Our student ambassadors help too; guiding new students around the school and assisting our teachers. We're very proud of them for setting such a fantastic example for our new students.


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The girls, varsity soccer team, in preparation for the upcoming season, had a practice game against York, at York High School, on Saturday August 18th.
The Eagles started this one strong with great teamwork, moving the ball up and down the field, putting the pressure on. Windham had excellent communication and did an outstanding job of keeping the ball moving towards the York half of the field early on in the game. Windham had tough offense and defense throughout the game, although, in the first half, York did score. Windham made up for it later in the game.
|Riley Beam
Windham players were taking multiple shots on York's goal, giving it all, showing they came to play and win. Windham's goalie, Riley Silvia, had several impressive stops and saves throughout the entire game.
Shortly before the end of the first half, Riley Beem got one by York's goalie tying the game at 1.
The girls hit the field ready to get it done in the second half. Windham kept up the intensity and had tight offense and defense, keeping the ball on York's side of the field. The Eagles took multiple shots on York's goal. Windham continued going strong the entire second half, not letting up. Their hustle and teamwork were really putting the pressure on York. With the clock winding down in the second half, both teams were looking to break the tie.
There was roughly a minute left on the clock, when the ball was passed to Meghan Hoffses. She took it up the field toward York's goal and the goalie charged out to block the shot. Hoffses had a clear shot at the goal and scored!
Windham won 2-1.
"We play right to the end, we play with a lot of heart…that competitive edge right to the end will help us throughout the season," said coach Deb Lebel.


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Dell outlet has been one of the biggest success stories amongst big companies using social media. For those unaware, @DellOutlet is a Twitter account owned by Dell that tweets out major discounts for Dell computers and products. All of the deals on @DellOutlet are Twitter-exclusive.
It has gained quite a following (15lac+ followers) and sold a lot of computers – at the end of last year, they surpassed $1 million in revenue, after about a year and a half's worth of tweeting.
Well throw those numbers out the window, because Twitter's phenomenal growth and Dell's social savvy have pushed sales from Dell Outlet to over $2 million, in 1/3 the time needed to pass the first milestone. And @DellOutlet is still on the rapid rise.
It took nearly two years to reach $2 million in Twitter-based revenue, and only six months to go from $1 million to $2 million.
@DellOutlet still is fundamental proof that Twitter can be a lucrative platform for companies big and small. It's a win-win for both the consumer (who get a great deal) and the company (who makes more money).


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Take an egg. Or, take two if you feel.
The urge to spend All the time you would like to have.
With care knowing the secret within,
Break open heaven's door and behold the gold of sacrifice.
Take time to begin to know gold and liquid – surrounded in clarity;
Then, faithfully, hold eternity in your hand.
The life-promise to light.
Take care to let go of the transparent, to reveal the essence of life.
The sacrifice has begun. Now enfold wine with golden yolk. It must be part of the sacrifice.
Then add drops of lavender oil. Creation is closer now than at first.
Say the prayer of eternity. "Behold, it is very good."
Reach out your hand and take the color that calls you by name.
On the white virgin surface you are the Creator's heart with each beat, paint what needs creating
Made new and do not forget.
Amen. A prayer to be said before unknowing Jeff Sells, 2014
This is what icon painting techniques are to me. The soft flow of layer upon layer of paint. The meditation that goes hand in hand with the icon painting techniques being taught and learned. These are the things I try to show my students; followers and those who appreciate these icon painting techniques.


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Good Morning all,
we are troubleshooting some quiesce problems. I see on 2 VMs ( running on nutanix ahv ) that the VMs have 2 Providers:
vssadmin 1.1 - Volume Shadow Copy Service administrative command-line tool(C) Copyright 2001-2013 Microsoft Corp.
Provider name: 'Microsoft File Share Shadow Copy provider' Provider type: Fileshare Provider Id: {89300202-3cec-4981-9171-19f59559e0f2} Version: 22.214.171.124
Provider name: 'Microsoft Software Shadow Copy provider 1.0' Provider type: System Provider Id: {b5946137-7b9f-4925-af80-51abd60b20d5} Version: 184.108.40.206
as i know when an hardware provider is installed and running on the server like netapp ontap dsm driver or something like this windows will fokus this provider first. In my case i have 2 software providers.
I know with the windows filesystem agent there is an regkey to force the ms software provider but for vsa baackup ?
so i have 2 questions:
1) is there any posibility to check wich vss provider was used during the vsa backup ?
2) can i force the default provider 'Microsoft Software Shadow Copy provider 1.0' during vsa backup ?
thanks for your help
In the case of most vsa backups the actual quiescing is handled by the guest tools. So in the case of AHV it is handled by NGT (Nutanix Guest Tools). There may be some ways to force which provider is getting used, but you just have the default providers listed there so i don't expect that to really be the issue.
What I would suggest doing there is checking the Program Files\Nutanix\logs\guest_agent_service.log for messages about the quiesce operation. You may also want to enable vss tracing inside the VM to get more insight into the quiesce operation.