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Cerebral white matter hyperintensities (WMH) on magnetic resonance imaging (MRI) are part of the spectrum of brain vascular injury accompanying aging and are associated with a substantial risk of stroke and dementia. We investigated the association of cerebral WMH burden on MRI with a DNA methylation-based biomarker of aging, termed DNA methylation age acceleration, which represents the deviation of the DNA methylation-predicted age from the chronologic age.
In this cross-sectional observational study of 713 African-American participants of the Atherosclerosis Risk in Communities study, aged 51–73 years, estimates of predicted age were obtained based on two algorithms (Hannum et al. and Horvath) from DNA methylation measured using the Illumina HM450 array on genomic DNA extracted from blood. Age acceleration, calculated as the residual values from the regression of each of the predicted age measures onto the chronologic age, was significantly associated with WMH burden after accounting for chronologic age and sex, body mass index, systolic blood pressure, hypertension, diabetes, current smoking, and blood cell composition, and results were similar for either Hannum et al.- or Horvath-derived estimates (P=0.016 and 0.026). An age acceleration increase by 1 year was associated with an increase of WMH burden by ~1 grade. To shed light on possible biological mechanisms underlying this association, we conducted a genome-wide association study of age acceleration and identified four loci harboring genes implicated in hemostasis, cell proliferation, protein degradation, and histone methylation. However, none of these loci were associated with WMH burden.
In this population-based study of middle-aged to older African-American adults, we report an association between accelerated epigenetic aging and increased WMH burden, independent of known risk factors, including chronologic age. Additional studies are needed to clarify whether DNA methylation age reflects biological mechanisms implicated in the aging of the cerebral white matter.
The online version of this article (doi:10.1186/s13148-016-0302-6) contains supplementary material, which is available to authorized users.
Cerebral small vessel disease is one of the most common degenerative vessel disorders of the aging brain. White matter hyperintensities (WMH) on brain magnetic resonance imaging (MRI) are typical markers of small vessel disease and are associated with an increased risk of stroke, cognitive and functional impairment, dementia, and death [1]. The prevalence of WMH increases with age, and advancing age is the strongest predictor of WMH severity [2–4]. Chronologic age, however, may not reliably gauge an individual's rate of decline or changes related to the aging process. Thus, development of blood-based biomarkers of aging that could more accurately predict changes in brain morphology and function and their associated neurological outcomes is of long-standing interest.
DNA methylation is a key epigenetic mechanism of regulation of gene expression. Most human tissues and cell types exhibit profound changes in DNA methylation patterns with age [5]. Thus, recent studies have developed a novel biomarker of aging, termed "epigenetic clock", based on DNA methylation levels at specific sites across the genome that are strongly correlated with chronologic age. Using whole blood DNA methylation array data from 656 subjects aged 19 to 101, Hannum et al. developed a predictor of age based on 71 CpG sites [6]. Similarly, using 82 publicly available DNA methylation array data sets comprising 51 healthy tissues and cell types across a range of chronologic ages, Horvath developed a multi-tissue predictor of age based on 353 CpG sites [7]. The deviation of the DNA methylation-predicted age from the chronologic age, defined as "age acceleration", is used as an index of "biological" aging.
Recent studies have shown significant associations between blood DNA methylation-derived measures of accelerated aging and all-cause mortality [8], as well as physical and cognitive fitness late in life [9]. Here, we estimated blood DNA methylation age in African-Americans from the Atherosclerosis Risk in Communities (ARIC) study using, both, Horvath and Hannum et al. methodologies, and examined the cross-sectional association between cerebral white matter hyperintensities on MRI and measures of accelerated epigenetic aging.
The ARIC study is a prospective population-based study of atherosclerosis and clinical atherosclerotic diseases. At its inception (1987–1989), 15,792 men and women, including 4266 African-American participants aged 45 to 64, were recruited from probability samples in four US communities: Suburban Minneapolis, MN; Washington County, MD; Forsyth County, NC; and Jackson, MS (African-Americans only) [10]. Four additional examinations (visit 2: 1990–1992; visit 3: 1993–1995; visit 4: 1996–1998; and visit 5: 2011–2013) have been completed. During the first 2 years of the third ARIC examination, participants aged 55 and older from the Forsyth County and Jackson sites were invited to undergo a cranial MRI. A total of 1920 participants, including 955 African-Americans had usable MRI data. All methods were approved by the institutional review board at each field center and coordinating center, and written informed consent was obtained from the participants.
Details of the MRI scanning and the image interpretation protocols used for this study have been published [11, 12]. General Electric (General Electric Medical Systems) or Picker (Picker Medical Systems) 1.5-T scanners were used for the MRI examination. The scanning protocol included a series of sagittal T1-weighted scans and axial proton density-weighted, T2-weighted, and T1-weighted scans with 5-mm thickness and no interslice gaps. Images were interpreted directly from a PDS-4 digital workstation consisting of four 1024×1024-pixel monitors capable of displaying all 96 images simultaneously. WMH were estimated as the relative total volume of periventricular and subcortical white matter signal abnormality on proton density-weighted axial images by visual comparison with eight templates that successively increased from barely detectable white matter abnormalities (grade 1) to extensive, confluent abnormalities (grade 8). Individuals with no white matter abnormalities received grade 0, and those with abnormalities worse than grade 8 received grade 9.
DNA methylation analysis was conducted with the Infinium HumanMethylation450 BeadChip (HM450) array (Illumina Inc., San Diego, CA) on genomic DNA extracted from blood samples collected at ARIC visit 2 or 3. Assay were performed on 2879 African-American participants who had not restricted use of their DNA and for whom at least 1 μg of DNA and genome-wide genotyping data were available.
Details of assay and QC procedures have been previously published [13]. Briefly, genomic DNA was treated with sodium bisulfite using the EZ-96 DNA methylation kit (Zymo Research Corporation, Irvine, CA) following the manufacturer's protocol. Bisulfite converted DNA was amplified, enzymatically fragmented, purified, and hybridized to the HM450 array in accordance with the manufacturer's directions. Methylation typing at 485,577 CpG sites was performed using GenomeStudio 2011.1 (Illumina Inc., San Diego, CA). Methylation level for each probe was derived as a beta value representing the fractional level of methylation at that location. Quality control analysis was performed using the wateRmelon R package [14]. Probe data were excluded if they had a low detection rate (<95% at P<0.01) and a high missing rate (greater than 1% across all samples). Sample data were excluded based on the following criteria: (1) greater than 5% missing values across all probes; (2) possible gender mismatch based on principal component analysis; and (3) genotype mismatch based on 24 SNPs present on the HM450 array.
A total of 713 participants with, both, a DNA methylation measure and a brain MRI scan are included in these analyses. For each participant, DNA methylation age was estimated from the background-subtracted beta values processed in GenomeStudio. Imputation of missing beta values and data normalization were performed using R codes implemented by Horvath. Specifically, non-normalized beta values were uploaded, and data normalization option was selected. Two estimates of DNA methylation age were derived: The Horvath predicted age based on 353 CpG probes was generated using the online calculator; and the Hannum et al. predicted age based on 71 probes was derived using the regression weights supplied by the authors [6]. Age acceleration estimates were calculated as the residual values from the regression of each of the predicted age measures onto the chronologic age at the time of blood collection.
To reduce the skewness of its distribution, WMH burden was expressed as the natural log-transformed WM grade (log(WMH+1)). Linear regression models were used to estimate the association of WMH burden (log(WMH+1)) with either Horvath or Hannum et al. estimate of age acceleration adjusting for covariates. Covariates were measured at ARIC visit 3 except for blood cell composition, which were estimated from the DNA methylation data as described elsewhere [15, 16]. Model 1 adjusted for age at brain MRI and sex. Model 2 adjusted for age at brain MRI, sex, body mass index, systolic blood pressure, hypertension, diabetes, and current smoking. Model 3 adjusted for covariates in model 2 and blood cell composition (estimated proportions of CD8 and CD4 T cells, natural killer cells, plasma blasts, monocytes, and granulocytes were derived from Horvath algorithm).
To examine whether estimates of age acceleration were associated with greater WMH severity, WMH was classified into three categories: no WMH (grade 0); low WMH burden (grade=1–4); and high WMH burden (grade>=5). Multinomial logistic regression was used to estimate the association of WMH severity categories with estimates of age acceleration adjusting for covariates. The covariate adjustment scheme was the same as that described for the linear models. Statistical analyses were performed using the SAS software v9.4.
Genome-wide genotyping was conducted at the Broad Institute using the Affymetrix 6.0 SNP Array on 3207 African-American participants. Of these, 336 were removed in data cleaning procedures, which included an insufficient call rate, sex mismatch, discordance with previously genotyped markers, first-degree relative of an included individual, and genetic outlier based on allele sharing and principal components analyses. Imputation was performed on the QCed data in two steps: (1) pre-phasing with ShapeIt (v1.r532) and (2) imputation with IMPUTE2 using the 1000 Genomes Phase I v3 reference panel. Measured SNPs used for imputation were restricted to have MAF>0.01, >95% call rate, and Hardy Weinberg Equilibrium P>1×10−6. After frequency and genotyping pruning, there were 806,416 SNPs in the final set used for the imputation.
Statistical analyses modeled the association between the number of minor alleles at each SNP and each measure of age acceleration trait using linear regression, adjusting for chronologic age, gender, study site, blood cell composition and 10 PCs. A P value less than 5×10−8 was considered statistically significant. There were 2216 ARIC participants with both DNA methylation and genome-wide genotyping included in the analyses. Significant epigenetic age acceleration loci were, then, evaluated for their association with WMH using the largest published GWAS of WMH to date [17].
We examined the association of individual CpG probes with WMH burden in the 713 individuals with DNA methylation and brain MRI data. The association between methylation scores at each CpG site and log(WMH+1) was modeled using linear mixed models, adjusting for age at brain MRI, gender, study site, visit, BMI, smoking, blood cell composition, systolic blood pressure, diastolic blood pressure, and technical variables (plate ID, chip ID and chip row). For this analysis, beta values normalized using the BMIQ procedure [18] were used. Probes with poor reliability in our technical replicate analyses [19], probes containing known SNPs, and non-specific probes were excluded [20, 21]. A P value less than 1×10−7, which corresponds to a Bonferroni correction to the total number of CpGs tested of the P=0.05 threshold, was considered statistically significant.
Selected characteristics of the participants are shown in Table 1. In this group of 713 African-Americans aged 51–73 years, 579 (81%) had a WMH grade >0. Pearson correlations between measures of chronologic age, estimates of DNA methylation age, and estimates of age acceleration are shown in Table 2. On average, the Horvath predicted age was lower than the chronologic age, while the Hannum et al. predicted age was higher (mean difference: −1.5 vs. 3.4 years). The Pearson correlation between the chronologic age of the subjects and the Horvath predicted age was ρ=0.51, while the correlation with the Hannum et al. predicted age was ρ=0.62. The correlation between the two sets of predicted age values was ρ=0.69. Age acceleration estimates were not correlated with chronologic age measures. Because a subset of the subjects (N=604) had their blood collection earlier than their MRI scan, we also calculated the Pearson correlation between the participants' chronologic age at which blood was collected and the chronologic age at the time of the MRI scan, which was very high (ρ=0.96). For this subset of subjects, blood collection was on average 2.94±0.28 years earlier than brain MRI examination.
Chronologic age and DNA methylation age were significantly associated with WMH burden (Table 3). Chronologic age explained ~6–8% of the variance in WMH grade (on the log scale) adjusting for known risk factors. The proportion of variance explained was generally higher for Hannum et al. DNA methylation age than for Horvath DNA methylation age (~5 to 8% vs. 3.5 to 5%), but results from the two estimates were more comparable after adjustment for blood cell composition (Table 3, model 3).
Age acceleration, defined as the residual value from the regression of the predicted DNA methylation age onto the chronologic age (at the time of DNA methylation assay), was significantly associated with WMH burden. An age acceleration increase by 1 year was associated with an increase of WMH burden by ~1 grade (0.007 on the log scale) (Table 4). The association of Hannum et al. age acceleration was slightly stronger than that of Horvath, although adjustment for blood cell composition yielded similar results.
When WMH burden was classified into categories (no WMH, low, and high burden), there was a significant association of WMH severity with age acceleration using either the Horvath or Hannum et al. predictor and accounting for age, sex, and known risk factors (Table 5). Further adjusting for blood cell composition did not appreciably change these results. Compared to those with no WMH burden (grade=0), those with high WMH burden (grade=5 or greater) had a significantly greater age acceleration by either predictor (P=0.02, Horvath; P=0.03, Hannum et al.). By contrast, there was no association of age acceleration with low WMH burden.
To further examine whether the relationship between WMH and epigenetic age acceleration reflects biological mechanisms implicated in the aging of the cerebral white matter, we sought to identify genetic loci influencing age acceleration using genome-wide association analysis in 2216 African-American ARIC participants with DNA methylation and genome-wide genotyping data. For age acceleration derived from the Hannum et al. algorithm, we identified two regions with genome-wide significant SNPs: 1q24 (top SNP: rs9332507, P=2.2×10−10) and 5q12 (top SNP: rs115651691, P=1.7×10−8). For age acceleration derived from the Horvath algorithm, we identified two regions with genome-wide significant SNPs: 6p22 (top SNP: rs75407001; P=1.0×10−11) and 17q11 (top SNP: chr17:2736978 I/D, P=3.5×10−23). The chr1q24 locus contained 62 SNPs with P<5×10−8 (Fig. 1a). The top SNP rs9332507 (MAF=0.087) lies within an intron of the F5 gene, which encodes coagulation factor V. Of the 62 chr1q24 SNPs associated with Hannum et al. age acceleration, 12 SNPs, all in high to moderate linkage disequilibrium (LD), were also nominally associated with Horvath age acceleration (P<0.05). The chr5q12 contained three SNPs with P<5×10−8 (Fig. 1b). The three SNP, all in high to moderate LD, lie near KIF2A, encoding the kinesin heavy chain member 2A. All three SNPs were also nominally associated with Horvath age acceleration (P≤0.001). The chr6q22 locus contained 32 SNPs with P<5×10−8 (Fig. 2a). The top SNP rs75407001 (MAF=0.076) lies 425 bp downstream of NHLRC1, which encodes an E3 ubiquitin ligase. None of the chr6q22 was also associated with Hannum et al. age acceleration. The chr17q11 locus contained 18 SNPs with P<5×10−8 (Fig. 2b). The top SNP chr17:2736978 (MAF=0.046) is an indel located 138 bp upstream of PIPOX, encoding pipecolic acid oxidase. Only one of the 18 SNPs in the chr17q11 region (rs140625670) was also nominally associated with Hannum et al. age acceleration (P=0.01). This SNP was located in an intron of NUFIP2, encoding nuclear fragile X mental retardation protein interacting protein 2.
We then examined the association of selected SNPs in each locus with WMH burden in middle-aged to elderly individuals from population-based cohorts of the NeuroCHARGE consortium, including 17,936 participants of European ancestry and 1943 African-Americans [17]. From each region, we selected the SNP that was most significantly associated with both measures of age acceleration (chr1q24, 5q12, and chr17q11) or the topSNP (chr6q22). There was no evidence of an association of age acceleration loci with WMH burden (Table 6). Although rs6703462 on chr1q24 was nominally associated with WMH in Europeans, the direction of association was not consistent with the observed relationship of an increased age acceleration with an increased WMH burden.
Finally, we examined the association of WMH burden with methylation levels of individual CpG probes, first, among the 71 Hannum et al. and 353 Horvath CpGs probes used to estimate DNA methylation (DNAm) age and then genome-wide. Figure 3 shows the Manhattan plot of the epigenome-wide association study (EWAS) of WMH burden in ARIC African-Americans. No probe reached the Bonferroni corrected threshold of significance either in targeted analyses or genome-wide. A more complete description of these results is available as Additional file 1.
In this population-based study of middle-aged to older African-American adults, we report evidence of an association between accelerated epigenetic aging assessed in blood and increased WMH burden and severity, independent of known risk factors, including chronologic age. On average, an increase in WMH burden by one grade was associated with an older epigenetic age by ~1 year. These results are consistent with those of a prior study [22] reporting an association of WMH with leukocyte telomere length, another biomarker of aging, independent of known risk factors; and raise the possibility that mechanisms of accelerated biological aging may be implicated in WMH pathophysiology.
We applied two distinct predictors of DNAm age. While the association of DNAm age acceleration with WMH appeared generally stronger using the blood-based predictor of Hannum et al., adjustment for blood cell composition yielded comparable estimates than those of the multi-tissue predictor of Horvath, which is more robust to the tissue type from which DNA methylation age is derived. Consistency of findings between the two distinct predictors suggest that the relationship between epigenetic age acceleration and cerebral WMH burden does not depend on specific epigenetic signatures but likely reflects the association of WMH with a general biomarker of "biological" aging.
Whether the relationship between DNAm age and WMH reflects biological mechanisms involved in the aging of the white matter remains to be determined. A previous study by Marioni et al. suggested that about 40% of interindividual variation in age acceleration is due to genetic factors and this heritability estimate was similar for both Hannum et al.- and Horvath-derived measures [8]. These data suggest that DNAm age acceleration may capture, in part, biological differences that affect the rate of age-related decline. We, thus, conducted a genome-wide association analysis of age acceleration and identified four loci, which were largely distinct for the two measures. The two loci identified for Hannum et al.-derived age acceleration encompassed genes involved in hemostasis (F5, SELP) and cell cycle and proliferation (KIF2A) and were only nominally associated with the Horvath-derived measure of age acceleration. Two distinct loci were identified for Horvath-derived age acceleration, which encompassed genes involved in protein degradation (PIPOX, NHLRC1), detoxification (TPMT) and histone methylation (KDM1B). None of the SNPs associated with age acceleration were significantly associated with WMH in the largest GWAS of WMH published to date [17], suggesting that loci implicated in age acceleration do not significantly contribute to WMH pathophysiology.
No individual CpG probe reached genome-wide significance for association with WMH in this cohort of middle-aged to older African-American adults. Suggestive associations include cg10262662 (P=4.7×10−6) mapping to the 3′ UTR of the VAC14 gene, which encodes a component of a trimolecular complex that tightly regulates the level of phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2). Mice lacking the Vac14 gene show a significant decrease in cellular levels of phosphatidylinositol polyphosphates, including PI(3,5)P2, and exhibit significant neurodegeneration [23]. Mice carrying a mutation in the Vac14 gene that results in significantly reduced PI(3,5)P2, show an accumulation of membrane-bounded vesicles in neurons of the central nervous system, an early feature of neurodegeneration, astrocytosis, and defective autophagy [24]. Future studies will include additional samples to identify robust associations with WMH.
Several limitations of our study must be acknowledged. First, DNA methylation was measured in blood. It is not clear whether DNAm age estimated from blood can serve as a proxy for that of brain, a likely more relevant tissue for cerebrovascular disease, or whether DNAm age estimates derived from more specific and relevant tissues would provide more accurate estimates of age acceleration and, thus, more robust associations with disease risk. Second, our analyses were cross-sectional, and DNAm was measured as a single time point. Thus, we are unable to examine whether change in DNAm age is associated with change in WMH burden, which would strengthen our findings. Third, we were unable to establish whether the association between epigenetic aging and WMH burden reflects biological mechanisms implicated in aging-related injury to the white matter. Indeed, there was no association between genetic loci influencing age acceleration and WMH burden in the largest GWAS published to date [17]. However, it is worth pointing out that our GWAS of age acceleration was performed in a single study of African-Americans. While the published GWAS of WMH includes a large sample of Europeans, the African-American sample was comparatively small and, thus, may be insufficiently powered to uncover race-specific relationships. Additional studies will be needed to clarify these relationships. Finally, we did not independently replicate the described association between DNAm age acceleration and WMH. Race/ethnicity has been recently associated with epigenetic age acceleration in blood, with African-Americans exhibiting significantly lower age acceleration than whites, especially at older ages [25]. Additional studies, preferably in African-Americans, will be needed to corroborate our findings.
Overall, our study shows that epigenetic aging in blood is associated with WMH burden, suggesting that the epigenetic clock may represent a novel molecular biomarker of vascular and neurodegenerative aging of the brain. Future studies in expanded samples will examine whether the relationship between epigenetic age acceleration and WMH burden reflects biological mechanisms implicated in the aging of the cerebral white matter.
The authors thank the staff and participants of the ARIC study for their important contributions.
This research is supported by grant NS087541 from the National Institutes of Health. The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C), R01HL087641, R01HL59367, and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C.
ARIC genotype data are deposited in dbGaP. http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000280.v3.p1.
AR and XZ carried out the statistical analysis and interpreted the data. MLG, JB, WG, JSP, and EB contributed to the acquisition of the DNA methylation data and critically reviewed the manuscript. RFG and THM contributed to the acquisition of the brain MRI data and critically reviewed the manuscript. MF conceived of the study question, analyzed the data, and drafted the manuscript. All authors contributed to manuscript and read and approved the final manuscript.
The authors declare that they have no competing interests.
Not applicable.
The research was approved by the institutional review board of the University of Texas Health Science Center at Houston and of each ARIC field center and coordinating center. Written informed consent was obtained from all ARIC participants included in this research.
Additional file 1:(195K, pdf) Top 100 CpGs from the epigenome-wide association study (EWAS) of WMH burden in ARIC African-Americans. Association P-value, effect size, and standard error for each probe are shown as well as location(chromosome, position) and probe type. (PDF 195 kb)
Top 100 CpGs from the epigenome-wide association study (EWAS) of WMH burden in ARIC African-Americans. Association P-value, effect size, and standard error for each probe are shown as well as location(chromosome, position) and probe type. (PDF 195 kb)
Abhay Raina, Email: firstname.lastname@example.com.
Xiaoping Zhao, Email: firstname.lastname@example.com.
Megan L. Grove, Email: email@example.com.
Jan Bressler, Email: email@example.com.
Rebecca F. Gottesman, Email: ude.imhj@msettogr.
Weihua Guan, Email: ude.nmu@naugw.
James S. Pankow, Email: ude.nmu@100oknap.
Eric Boerwinkle, Email: firstname.lastname@example.com.
Thomas H. Mosley, Email: ude.cmu@yelsomt.
Myriam Fornage, Email: email@example.com.
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Trip to SylvaPosted Jan 14, 2016
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|Name: _________________________
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This quiz consists of 5 multiple choice and 5 short answer questions through Summary and Analysis For Chapters 6-8.
Multiple Choice Questions
1. What does Oscar talk about concerning the country?
(a) Its noble history.
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5. What is revealed in Mr. Washburn's car when the accident occurs?
(a) Weapons.
(b) Picnic supplies.
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(d) Suitcases.
Short Answer Questions
1. Where are the children allowed off the compound?
2. What is the class preparing to do?
3. What does Anita's brother say when he comes home?
4. What influence does Mr. Smith have on the behavior of some of the families?
5. What does Anita not want her family to discover?
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Andrew Otwell (drawing on Abe Burmeister, Clay Shirky, Christopher Alexander, and it looks like one or two others) has posted his provocative thoughts on the metastatic logic of scalability in urban and interface design. His point, among others, is that practices appropriate to the design of systems for small groups of people - the groups, in other words, in which most of us spend the majority of our lives, certainly the majority of personally meaningful moments - are simply different from those useful in the design of "enterprise-scale" systems.
One implication of this insight is that the hierarchical tree so familiar from org charts and site maps gets improperly imposed on these intimate systems, very much to their disadvantage. Let's take a closer look to see why I wind up only partially agreeing.
the plane of a foolish consistencyIn the case of large-scale systems, I can tell you from daily personal experience, the working information architect is presented with challenges having to do with consistency of experience, with smoothness. We're faced, often enough, with a situation in which the heterogeneous needs of tens of thousands of people inside an organisation communicating with potentially millions of people outside (and vice versa!) are forced through an aperture maybe seven, ten, twelve options wide: the front page of the corporate Web site.
For reasons having primarily to do with economics - that is, with the managed scarcity of resources - we're willy-nilly forced to regularize and rationalize this situation. We devise personae and use cases to account for the majority of anticipated interactions with the site. We design structures - hierarchical trees, generally - to accommodate those interactions. We discount edge cases. The result is repeatable, consistent, relatively easy to reconfigure on the fly. In a word: modular.
Most of the time, it must be said, this arborescent modularity works pretty well. In contrast to the creative ferment that characterized Web design circa 1997-1999, this more-or-less standard interface and deep structure paradigm has become normative precisely because it does treat the majority of interactions efficiently. (It also happens to play nicely to the predilections of software developers used to the nested hierarchical logic imposed by code, whose preferences play a significant role in the outcome of any large-scale Web project. But that, my friends, is a different story.)
It should go without saying, though, that not every Web site, and certainly not every physical space or system of same, faces the same pressures as the ones on which enterprise-scale information architecture is predicated. As I understand it, part of Alexander's argument with tree structures - and, by inference, Andrew's - is that they tend to cut across the relations that mean the most to our conceptions of the good life.
No problem there. If the critique is that a modularity imposed from an inapposite desire for scalability is detrimental to the organic growth of smaller systems, systems neither required nor destined to scale arbitrarily, I'm right there with you. But even this is too simplistic a view: it's not merely the shape of an architecture that determines what sort and richness of activities it can support, but its intelligence as well.
stupid is as stupid does
Intelligence? I'm tempted - OK, I'll surrender to the temptation - to introduce yet another metaphor from network architecture, the "end-to-end network," as a way to understand what may be going wrong in these structures. Because I think it's not necessarily a hierarchical, arborescent, functional modularity that does most to compromise quality of life or experience in designed systems, but their overspecification.
The term arises out of a tension in the theory of network design, going back some twenty-five years now. At that point in time, the programmability of a network, then a novel technical possibility, appeared to offer an attractive solution to seemingly intractable issues of congestion or underuse. A traffic-management function, for example, to allow packets of information moving through the network to change their priority dynamically - to let them redefine themselves as ambulances and fire engines should traffic thicken, as it were - is the kind of elaboration engineers thought might prove useful.
Computer scientists David Reed, Jerome Saltzer, and David Clark advanced a countervailing theory, one whose adoption in time proved essential to the rapid spread and easy extensibility of the Internet. They held that "building complex function into a network implicitly optimizes the network for one set of uses while substantially increasing the cost of a set of potentially valuable uses that may be unknown or unpredictable at design time."
This, ultimately, is the argument behind adopting, instead, a "small pieces loosely joined" architecture. Designing function into the network itself freezes a moment in time, with all its arrangements and priorities and valuations intact. The trouble is, of course, that all of those things change over time, in unpredictable directions. As Reed, Saltzer and Clark rather dryly put it, "enthusiasm for the benefits of optimizing current application needs by making the network more complex may be misplaced."
The model they offered, the "stupid" or "end-to-end" network, pushes functionality outward, to the objects connected to the network. The network itself is intentionally agnostic regarding - even ignorant of - the needs imposed by any given functionality. The result is a relatively unrestrictive specification set for what can be attached to the network. It's this freedom that has let the hundred flowers of the Internet bloom, especially the World Wide Web built on it and through which you are presumably reading these words.
the white zone is for loading and unloading only
Let's jump back across the gulf of metaphor, and think about Modernist-era urban planning practice in this light. City planners used to step right into the pitfall Reed, Saltzer and Clark described, by overdesigning and overspecifying; in architectural terms, one might say they collapsed program and circulation, with "loops" and "zones" dedicated to given functions. (Christopher correctly torpedoes Paolo Soleri's ostensibly organic arcologies as fraudulent in this regard. Drawing a beguilingly biomorphic shape and labeling the voids within "Cultural Center" or "Factories and Utilities" has as much to do with helping a community find its own appropriate shape as Levittown does.)
By contrast, in the end-to-end model, "[m]oving functions and services upward in a layered design, closer to the application(s) that use them, increases the flexibility and autonomy of the application designer to apply those functions and services to the specific needs of the application."
Education, that is, is something that might happen inside a school (or library, or home, or wherever, but at any rate through the interaction of people taking on the roles of student and teacher, respectively), not in a Learning Zone hardwired into the city plan. And why should rest and recuperation not be possible throughout an urban complex, wherever and whenever required? Why force people to haul their weary bones to the Relaxation Zone?
When framed this way, the natural thing is to say, sure, that degree of overspecification and functional differentiation is silly and counterproductive; urban infrastructure should exist solely to facilitate activity ("application") by permitting the free circulation of people within it.
when you get to the bottom you go back to the top
All of which brings us back to that problematic modularity. But in this light, we can see that modularity, and maybe even the apparition of an arborescent framework behind the individual modules, emerges to some extent from below. The repeating, soulless grid of franchises that Abe's talking about here exists simply because people don't want to travel half an hour to the Services Core to fulfill the basic requirements of everyday life. It's an emergent property of the maximum distance people will travel for a given commodity, a quantity which changes from (sub)culture to culture and from commodity to commodity, but in any event rarely exceeds a few kilometers.
In the case of Manhattanites on foot and coffee, say, the maximum displacement may be as short as a single city block, for that is the distance by which many a Starbucks is separated from another hereabouts. They serve different microcommunities, draw from different catchment basins: the traffic from a cluster of two or three office buildings during business hours is probably enough to keep any single outlet operating in the black.
Not only would it appear that this modularity is itself an organic thing, then, and not necessarily something imposed, but it certainly seems superior as an organising principle for the city to others proffered by post-Modern urban planning.
induced anxiety
In the years since the eclipse of High Modernism, and especially since cheap computing power made complexity theory a topic of immediate relevance, the possibility that pleasing forms might be generated algorithmically has seduced many a designer. (Greg Lynn, discussed on v-2 some three years ago, is notable in this regard, though one would surely be remiss in not mentioning the antecedent work of John Cage and Brian Eno in a different realm.)
It was inevitable that someone would turn these methods of production to the design of urban space; Makoto Sei Watanabe's Induction Cities is one such attempt, a long-term research project into the possibilities of generating urban form from algorithms.
The trouble with the Induction City model is that it's just as intellectually bankrupt, just as irrelevant to how life is actually lived by human beings in human communities, as the hyperrationalized Brasilia. As a "tool for the visualization of concepts," fine. But I surely hope nobody is seriously suggesting that these generative maps be seen as any kind of blueprint for cities in which human beings are intended to live.
Far from thinking the status quo is too rigid, Watanabe apparently has a hard time with the sheer unreliability of architecture and urban planning as they're currently practiced: Roughly speaking, the method will work to substantiate "inspiration." It will be able to reduce the probability of "inspiration" turning out to be a failure. The scientific method will come nearer to engineering, and the great master's art will come closer to science.
My problems with this line of thought are several. Not to set the hapless Watanabe up as a strawman for all those working in parallel endeavors, but how can someone sophisticated enough to understand that "a city cannot be designed" and that "[l]iving organisms are not governed by a grand designer" possibly believe that simply setting a few parameters and letting a computer draft a pleasingly fractal shape has anything to do with the real methods by which human communities organize themselves?
"What we need is not critical perceptions of what a city is, but a methodology for creating a city." Really? In a bizarre inversion, what Watanabe is doing here - despite wielding eminently buzzword-compliant, zeitgeisty toys like "a neural network, genetic algorithms and artificial intelligence" - is nothing other than imposing control from above. If anything, the bizarre flows set up by his Induction Cities seem bound to create moments of human isolation and disconnection, without even the justification from efficiency that an imposed arborescent form offers.
The problem, again, isn't the tree per se, and we should resist the temptation to equate it with relations inimical to the development of community or affinity. No, the problem is the imposition of form - any form. It seems to me that humans already know how to create cities just fine by ourselves, without the help of any algorithms other than the ones we're already carrying around upstairs. After all, we do it every day, and have been since before we began recording our efforts and calling it "history."
beyond the will to a system
I mistrust all systemizers and I avoid them.
Here, finally, is one of the tensions I live with, or in. The above lines from Twilight of the Idols are ones that Anne Galloway uses as an epigram of sorts on her site, and they happen to reflect a sentiment that I've long accepted, even reveled in.
Life, living things, organic things: they're messy, they continually flow and leak and fold back on themselves. It takes a certain maturity to accept this, to find beauty in it, especially for those of us who (have been trained to) associate harmony first and foremost with order. It's not easy to let go of the idea - the introduction of which into my own life which I associate with eighth-grade biology's unit on Linnean classification - that the universe of phenomenal objects can be comprehensively named, ordered, and understood.
Nietzsche is here talking primarily about intellectual systems, about ways of organizing knowledge such that anomalies or edge cases must be sawn off to fit. The "lack of integrity" he's talking about I understand to mean the inability to face up to the fact that the world is endlessly varied, and the implications of this heterogeneity. Socially, politically, personally, this mistrust of systematization holds true. Where it breaks down for me is when we begin talking about metadesign, about frameworks and arrangements in which to provide for communication between those smaller-scale chunks of meaning and being.
To return to the original question implied in Andrew's post: what is the language of form appropriate to the design of systems for small groups of people? I think most of the people reading this would agree that, almost without exception, it would be their own language, whatever that would happen to be and whether it produced maps resembling "semilattices," pyramids, Lorenz butterflies, or anything else.
But there does come a place where a systematic approach is called for, and that place is the network that connects these local, heterogeneous, wildly and delightfully variable moments with each other and that facilitates movement between and among them.
I wonder, in a world where many, many small groups of people must coexist with each other, if it couldn't be the case that a degree of systematization, applied with care, actually provides for greater diversity overall? I'm thinking of signage programs, or protocols for the design of thoroughfares: the provisions of a relatively "stupid" end-to-end urbanity, just enough and no more.
Such systematization is all about providing a stable platform for the emergence of what are, I trust, the more interesting sorts of complexity and diversity. Put concretely: would you rather live in a city with a hundred different, locally varying practices for the labeling and coloring and shape and placement of street signs, or one that imposed this one standard on its constituent parts? All of the interesting, complicated stuff still exists in the things connected to the network, but the network is left to do its job.
Maybe this is just a different way of agreeing with Andrew, with Clay Shirky and Christopher Alexander, with everyone who's ever felt that arrangements which make perfect sense at the scale of a city or a global site break down badly on the neighborhood or blog level. Maybe it's yet another misplaced technical metaphor destined to founder on the rocks of lived reality. All I know is that the relatively small situations that matter most to me in life - comfortable cafes and well-provisioned magazine stands, decent repertory cinemas, above all great conversations - are accounted for neither in hierarchical directory structures nor in putative "programs of flow."
It seems strange to me that a quarter-century old paper from network systems theory could provide the most convincing explanation of just how to support the emergence of these things that mean so much to me, but there you have it. I guess I'm just an end-to-end guy.


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The Harp In The South (Compact Disc)
Ruth Park
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Title: The Harp In The South (Compact Disc)
Publication Date: 2011
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An Australian classic, this is the story of the Darcy family who live in the Depression era tenements of Surry Hills, Sydney. Hugh and Margaret Darcy are raising their family in Sydney amid the brothels, grog shops and run-down boarding houses of Surry Hills, where money is scarce and life is not easy. Filled with beautifully drawn characters that will make you laugh as much as cry, this Australian classic will take you straight back to the colourful slums of Sydney with convincing depth, careful detail and great heart.About the Author:
Ruth Park was a New Zealand-born Australian author. Her best known works are the novels The Harp in the South (1948) and Playing Beatie Bow (1980), and the children's radio serial The Muddle-Headed Wombat (1951–1970), which also spawned a book series.
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Brand Label: M S
Available for Purchase Online at Marks and Spencer for £2.00Pin It
Say you are sorry with this simple, straightforward card. The 'Sorry' is written across the top of a white background in silver foil to accentuate. Effective without being over the top, Dimensions: 178 x 127mm, Item details: Cover text: Sorry, Inside text: Blank, Made in UK, Product Contains: White envelope.
Shop other brand label items from M S on FashionStylist.com.
This item was published for sale online by Marks and Spencer on March 9, 2016 12:09 pm and last updated by us October 31, 2016 1:40 pm.
Marks and Spencer Note: This vendor may charge a fee of £3.50 for shipping and handling of this item. See website for further details and/or any volume discounts.
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New promo codes and links offering limited time promotions, sales coupons, and special offers on M S designer fashions and accessories will be posted on each designer label apparel page. For the latest up to date information on this M S Sorry Silver Foil Greetings Card fashion item, including product specifications, ordering options, pricing, shipping details, high resolution pictures, shopper comments, and other sales media, visit the Marks and Spencer Online Store.


text:
Prevent Hair Loss: How To Prevent Alopecia
It might sound easy at times, but preventing hair loss is no small task. Losing even a strand of hair is painful, agonising, heart wrenching. Though we may not project this feeling to everyone around us, deep within we constantly think about how to prevent hair loss and prevent alopecia. That's the reason why we jump to every product and serum and tablet that promises hair loss treatment; but preventing hair loss is a much better plan! Here's how...
Prevent Hair Loss by Not Smoking
Smoking has a major negative impact on the body's circulatory system. So if you want to prevent hair loss and save a substantial amount of money at the same time, invest in a program to quit smoking.
Prevent Hair Loss by Exercise & Live a Stress Full Life
Too much stress can cause your hair to fall out, stall its growth and maybe even lead you to pull out your own strands. Exercise can help you deal with stress and may lessen hair loss caused by it.
Prevent Hair Loss by Proper Diet And Exercise
Many people can greatly improve their diet by simply cutting out sugar overloads from candies, cakes, soft drinks, etc. A balanced diet with correct proportions of fruit, vegetables, cereals, dairy products and protein can have an amazing effect on the health of the scalp and hair production.
Prevent Hair Loss by Quitting / Reduce Smoking & Drinking
Reduce your alcohol and caffeine intake. Eat healthy protein rich food.
Prevent Hair Loss by Protecting Your Hair from UV Rays
Sun exposure also increases hair fall. One could avoid contact of sunlight to his hairs as direct exposure can make you bald because of the harmful UVA and UVB rays.
*Inputs as provided by Dr. Shreepad Khedekar, Clinical Director And Mind Body Expert, Imperial Clinics.
*Image courtesy: © Thinkstock photos/ Getty Images
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We provide an integrated approach to roof and open space management and utilization, including: initial structural and infrared assessment, sensors and ongoing maintenance, and advanced applications to generate revenues
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In June, we have launched the first community solar project in Boston, on top Avid Management's commercial building in Somerville, MA
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"This is a milestone for Somerville and the greater boston community" - Dave Lewis, President, Avid management


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This weekend, President Barack Obama is perfecting his State of the Union address, to be delivered on Tuesday. Just as basketball players watch clips of old stars like Dr. J. or Julius Erving—Obama's boyhood hero—the president might want to download President Bill Clinton's addresses. I would particularly recommend Clinton's 1998 and 1999 speeches. Perhaps by watching this political virtuoso, Obama can get his speechmaking mojo back.
As a rare president who enjoyed both politicking and policy-making, Clinton loved delivering the State of the Union Address. Watching him speak to a packed Congress was like watching Barbra Streisand sing, Michael Jackson moonwalk, Tiger Woods golf, or Steve Jobs pitch a product. For Clinton it was New Year's Day, Thanksgiving Day, Commencement Day, and the Fourth of July all wrapped in one. Each January, he framed a new agenda. He catalogued—and boasted about—the old year's accomplishments. He charted a detailed path infused with a broader purpose. And he celebrated America in the reddest, whitest, and bluest terms.
source: the daily beast


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LOTL : Mardi Gras
19 lotl.com • Lesbians On The Loose Magazine blowback from her community: "thousands and thousands" of tweets criticise her, she tells me. But Velásquez hopes to change those attitudes. "The Latin culture is very male-dominated, but it can be divided into different places. For example, Argentina is forward thinking, very open. In Spain, you can get married, but it's still very judgmental. In Colombia, they are fight- ing hard to have gay marriage. In Venezuela, they are also fighting, but it's not on the top of the list because people are struggling to feed themselves. "If we really go to the root of it, the male domination doesn't come from the men. It comes from us. We're the women, we're the mothers, we're the ones who have the voice at home, and we're not asking them to make their beds, and we're cooking for them, and there's nothing wrong with it, but we are the ones creating this in our homes. So unless we change it at home, it's not going to change." As hard as it is for Velásquez to be attacked by her compatriots, she'll take the heat for the sake of her path. Being dedicated to Kabbalah, which seeks to explain the nature and purpose of existence, Velásquez is convinced that every- thing has a role and everything happens for a reason. "If [coming out] is going to drive people to read the book, and be more inspired, not only within themselves, but to understand others around them, then, you know, let me go through what I have to go through. It's okay. As long as we can plant a little bit of a seed, then it means we are doing the job." And she has a message for women who are not yet out, or who conform to the wishes of others—especially Latinas: "There is a reason why you are who you are, and if you stop being who you are, you will never be happy. Often, when we try to protect other people by not liv- ing the truth, we are indeed hurting them by not living the path. I'm here to tell you it's okay to live your path. It's not easy, it's challenging. But if we don't do it, then who's going to do it? There is a reason why it's us." In the epilogue to Straight Walk, Velásquez writes: "Once I was honest about being gay, I was honest about enjoying being sexy. I was able to accept that everyone who was gay didn't also have to maintain a masculine status, though at times there's a big, butch dyke in me, not just a lipstick lesbian. Now we can embrace our feminine and masculine side, and that's okay. Gay women are beautiful, so with nothing to prove to myself or anyone else, I felt free just to be." After coming out, Velásquez realized she was more than just "glitz and glam and legs": She was a woman with an honest relationship to her family, rather than a celebrity trying to rescue them; she was a giving partner, rather than a demanding one; she was an indigenous woman who could help improve the lives of the indigenous people of Latin America. No, you don't have to come out. After all, there is a lot at stake. "But even if you feel ashamed, or you get rejected, what are you going to do?" she asks me. "Are you going to stay down? No, you're going to get up and do it again. So this is only a challenge for me to say, you know what, we are part of a minority, we are judged, we are looked at as weird, but we still have a job to do. Go out and fight and be proud of who you are." (patriciavelasquez.com) BY WILLIAM SHAKESPEARE DIRECTOR PETER EVANS 20 FEBRUARY – 27 MARCH SYDNEYOPERAHOUSE.COM #Bell2016
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White Angel Sleeping with Teddy Christmas Ornament
Personalized Christmas Ornament
Dimensions: 3" diameter
Material: Glass Ball
ITEM IS HAND PAINTED IN GERMANY. This serene little angel sitting in front of the Christmas tree with her precious teddy bear is waiting for Santa Claus to arrive. This adorable personalized angel ornament is hand-painted by an artist in Germany who believes that all children are angelic, at least when you catch them at the right moment! Asleep in the snow with her teddy bear in her lap, this toddler girl has golden wings and a star on her head. Makes a great gift for a sweet toddler or little angel in your life.
Customer Reviews
Read what our customers say about our Personalized Christmas Ornaments and their shopping experience!Hover over testimonials to stop scrolling
12/14/2016 - "Very pleased. Katherine K."
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text:
Wales lost for the fifth time in a row but George North graduated from schoolboy to national hero with a sizzling debut double.
The 18-yearold wing lived up to his billing as the 'Welsh Jonah Lomu' as he scored two tries and had a hand in a third against South Africa in Cardiff.
It completed a remarkable rise for North, who was playing school-grade rugby in May.
North said: "It was a great debut and fantastic to score two tries.
"It's hard coming from playing schoolboy rugby six months ago to facing the world champions. I hope people now look at me as a player to be relied on at this level."


text:
Keep Calm and watch Eastenders :)
cutest couple ever wish they would get back together
Roxie and Ronnie Mitchell : Eastenders
Although it broke her heart, Jean was left with no choice but to have Stacey sectioned.
Played by Letitia Dean
British Soap Awards: EastEnders' Kellie Bright admits first crush . Girlie see you tv Love you girlie
the character phil mitchell is a famous addict and is the source of the name mhil pitchell
Phil and Grant back together again!
Barbara Windsor returns to EastEnders for a "very special episode", three years after she left the soap.
Fiery Bianca doesn't mince her words. Woe betide you if you get on the wrong side of her.
More ideas
EastEnders is a British soap opera; the first episode was broadcast in the United Kingdom on BBC One on February
'EastEnders': The Women Of Albert Square Dot Cotton (June Brown, Where would we be without Dot's wise words? The laundrette worker has been on hand to offer advice to anyone who needs it, since the show first aired in (BBC)
Maddy Hill plays Nancy Carter in Eastenders
the character phil mitchell is a famous addict and is the source of the name mhil pitchell
Played by Letitia Dean
EastEnders' Queen Vic gets a new landlord as actor Danny Dyer joins the soap
Albert Square from Eastenders
Letitia Dean, Sharon Watts on Eastenders
Red-carpet glamour: EastEnders actors Sam Strike, Kellie Bright, Danny Dyer and Maddy Hill arrive at the TV BAFTAS Maddy and Kelly just blend in x
EastEnders // EastEnders Christmas Tameka Empson as Kim Fox and Diane Parish as Denise Fox .


text:
Shocking video shows 'newborn baby' being tossed around like a rag doll during controversial Indian ceremony
- In the footage a man wearing a woman's saree throws around the 'child'
- A large crowd cheers and claps to music during the sickening dance
- If genuine the powerless baby could face dangerous lifelong injuries
- The video is going viral after it was posted by Indian Atheists group
- Ritual being described as religious ceremony but this cannot be confirmed
Deadly newborn baby rituals were well known in ancient times.
But this outrageous video appears to show in the small corners of the world horrific customs may still be in practice today.
In infuriating footage which is hard to watch to the end a powerless naked 'child' is flung around like a rag doll, in what is believed to be an Indian ceremony to test its strength.
Yet due to the poor quality of the clip, filmed by a member of the large cheering crowd, it is hard to confirm whether the baby is genuine and some commenters are sceptical.
If real the poor child faces the likelihood of developing dangerous lifelong injuries.
In the footage a man, apparently dressed in a woman's saree, violently swings around the newborn to music as onlookers clap their hands.
An outrageous video appears to show a newborn baby being swung around like a rag doll in Indian ceremony
The video can be traced back on YouTube at least as far as 2014, but it has gone viral on social media since being uploaded to the popular Indian Atheists Facebook page.
They wrote: 'Been on the border about posting this. This is extremely disturbing and scary.
'Kindly scroll past if you can't stand it. Video shows a godman handling a baby like a ragdoll.'
Referring to the man as a 'godman' the author of the page then uses the video to attack religion, and many of the commenters follow suit.
Yet it cannot be confirmed whether the thoughtless practice is religious in nature.
In the shocking footage a man dressed in a woman's saree violently swings around the newborn to music
If real the child faces the likelihood of developing dangerous lifelong injuries due to the violence of the ritual
The Indian Atheists, who describe their group as having 'an in-depth and nuanced position on religion', under the 'Nirmukta' tradition, reacted angrily to those who would suggest the ceremony is not religious in nature.
They wrote: 'For those who will run in and ignorantly shout 'Oh! This is not religion. This is superstition' or some s*** like that, Get lost brainless zombies. Go sit in your cave of ignorance and shout mantras.'
But some commenters were unconvinced the footage is even genuine.
Yet due to the poor quality of the clip, filmed by a member of the large cheering crowd, it is hard to confirm whether the baby is genuine and some commenters are sceptical
Another question which the video raises, which has been debated vigorously online, is whether the practice is religious in nature
Ankit Kapil wrote: 'It's not a real baby, look closely. Had it been a real one it would retort back and move or the worst part is the baby is Dead. Anyways this is stupid.'
While Vikram Rana posted: 'First of all he is not a godman he is a thug nothing else.
'Please get this straight it is not problem of religion it is problem of some superstitious lunatics,' he added.
One shocking newborn religious ritual in India that is definitely not false is the custom of tossing babies of a 30ft rooftop temple.
In 2012 it was widely reported that Hindu priests in the state of Karnataka were dropping babies onto a sheet held by men on the ground below, to large crowds of cheering devotees.
The centuries-old custom, carried out by Muslims as well, was staunchly defended by worshippers at the time.
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