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The relevance of group selection to understanding behavior in groups—including in organizations like investment banks—is one of the most hotly-debated topics in human behavioral biology. (For example, see this recent debate on Edge.org). In essence, the debate is between individual selectionists who believe that behavior evolves primarily to benefit individual fitness (genetic survival and reproduction), and group selectionists who believe that behavior evolves to benefit individuals and/or groups. That may sound like a clear-cut debate, but it's actually a very confused one. Unfortunately, a main reason why people argue so much about group selection is because there's so much semantic and conceptual confusion, on both sides of the debate, about what group selection actually means.
To judge whether group selection is useful for understanding behavior in banks, then, we first have to define it clearly, or at least choose one of the three definitions of group selection that are commonly used: the good, the bad, and the cultural.
So are any of these definitions of group selection consistent with the kind of behavior we see in investment banks? If we're choosing between the two genetic kinds of group selection defined above, it's obvious that the "good" definition is realistic, and the "bad" definition is fantastic. That is, bankers work for banks in order to make themselves money, not to sacrifice themselves for the good of the bank. (Yes, this point is obvious, but its very obviousness seems like a good illustration of what's unrealistic about the "bad" definition). What about the cultural definition of group selection —does that apply to banks? In theory it would, if banks were allowed to succeed or fail based on whether their corporate cultures encouraged sustainable organizational competitiveness, as opposed to encouraging employees to gamble away their firm's future in the pursuit of short-term payoffs. In practice, however, government rescue missions have artificially prolonged the lives of banks whose cultures are dysfunctional and self-destructive in the long-term, and have thus interfered with the group selection of more sustainable bank cultures.
(A version of this article will appear as the author's "Natural Law" column in the banking magazine Global Custodian).
Copyright Michael E. Price 2012. All rights reserved.

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Pathological tau burden and distribution distinguishes progressive supranuclear palsy-parkinsonism from Richardson's syndrome
Clinical syndromes associated with progressive supranuclear palsy-tau pathology now include progressive supranuclear palsy-parkinsonism (PSP-P), in addition to classic Richardson's syndrome (RS) and pure akinesia with gait freezing (PAGF). Although pathological heterogeneity of progressive supranuclear palsy (PSP) has also been established, attempts to correlate this with clinical findings have only rarely provided conclusive results. The aim of this study was to investigate whether regional variations in the types of tau lesions or differences in overall tau load may explain the clinical differences between the RS, PSP-P and PAGF. Quantitative tau pathology assessment was performed in 17 brain regions in 42 cases of pathologically diagnosed PSP (22 RS, 14 PSP-P and 6 PAGF). Neurofibrillary tangles, tufted astrocytes, coiled bodies and thread pathology were quantitated and a grading system was developed separately for each region. Using these grades the overall tau load was calculated in each case. To establish a simplified system for grading the severity of tau pathology, all data were explored to identify the minimum number of regions that satisfactorily summarized the overall tau severity. The subthalamic nucleus, substantia nigra and globus pallidus were consistently the regions most severely affected by tau pathology. The mean severity in all regions of the RS group was higher than in PSP-P and PAGF, and the overall tau load was significantly higher in RS than in PSP-P (P = 0.002). Using only the grade of coiled body + thread lesions in the substantia nigra, caudate and dentate nucleus, a reliable and repeatable 12-tiered grading system was established (PSP-tau score: 0, mild tau pathology, restricted distribution; >7, severe, widespread tau pathology). PSP-tau score was negatively correlated with disease duration (Spearman's rho −0.36, P = 0.028) and time from disease onset to first fall (Spearman's rho −0.49, P = 0.003). The PSP-tau score in PSP-P (median 3, range 0–5) was significantly lower than in RS (median 5, range 2–10, Mann–Whitney U, P < 0.001). The two cases carrying the tau-H2 protective allele had the two lowest PSP-tau scores. We have identified significant pathological differences between the major clinical syndromes associated with PSP-tau pathology and the restricted, mild tau pathology in PSP-P supports its clinical distinction from RS. The grading system we have developed provides an easy-to-use and sensitive tool for the morphological assessment of PSP-tau pathology and allows for consideration of the clinical diversity that is known to occur in PSP.
- progressive supranuclear palsy
- Richardson's syndrome
- PSP-parkinsonism
- tau
Progressive supranuclear palsy (PSP) is a degenerative disorder of the central nervous system with protean clinical manifestations. The classic clinical picture, originally described by Richardson is the most common clinical form (Richardson's syndrome or RS), with an insidious onset and relentlessly progressive postural instability and falls, gait disturbance, supranuclear vertical gaze abnormalities, pseudobulbar palsy, rigidity in extension and a dysexecutive syndrome (Richardson et al., 1963; Steele et al., 1964; Litvan et al., 1996a; Williams et al., 2005). We have recently defined a further clinical phenotype, PSP-parkinsonism (PSP-P), in which disease duration is longer and parkinsonism dominates the early clinical picture (Williams et al., 2005). In contrast to RS these patients may show a moderate initial therapeutic response to levodopa, falls are delayed and if gaze palsy or dementia occur at all, they develop late in the course of the disease. PSP-tau pathology may also present as pure akinesia with gait freezing (PAGF), corticobasal syndrome or, exceptionally, with an isolated dementia (Imai et al., 1993; Williams et al., 2005; Tsuboi et al., 2005; Josephs et al., 2006).
The post-mortem diagnosis of PSP is dependent on the identification of neurofibrillary tangles (NFTs) and neuropil threads in basal ganglia and hindbrain structures (Litvan et al., 1996b); tufted astrocytes (TAs) and coiled bodies (CBs) are other highly characteristic findings (Dickson, 1999). PSP is a primary tauopathy, in which tau dysfunction is regarded as central to the pathogenesis (Goedert, 2005). The predominance of 4-repeat tau isoforms in the neuronal and glial tau inclusions is also characteristic, although this is not included in the current operational diagnostic criteria (Komori et al., 1998; Hauw, 2003; de Silva et al., 2003). Pathological heterogeneity of PSP has also been reported (Braak et al., 1992; Hof et al., 1992; Mizusawa et al., 1993; Verny et al., 1996; Halliday et al., 2000; Piao et al., 2002; Williams et al., 2005; Tsuboi et al., 2005; Josephs et al., 2005), but attempts to correlate this with clinical findings in PSP have only rarely revealed definitive correlations (Daniel et al., 1995; Litvan et al.,1996b; Tsuboi et al., 2005). Unlike Parkinson's disease and Alzheimer's disease, cases of 'incidental' PSP-tau pathology are unusual and pathological examples of 'early' PSP are rare, hampering any attempts to develop a pathological staging system. It is unknown whether the pathology in PSP follows a consistent topographical progression or whether a disease 'footprint' of regional susceptibility is established early with subsequent uniform progression of pathology in all affected structures. However, serial imaging studies confirm that the brainstem, in particular the midbrain, and frontal lobes bear the brunt of the disease (Paviour et al., 2006).
We have already demonstrated an increased contribution by 3-repeat tau isoforms to the total insoluble-tau fraction in PSP-P, raising the possibility that biological differences influencing tau pathology may exist between PSP-P and RS (Williams et al., 2005). In this study, we carried out a quantitative survey of different brain regions looking for regional differences in the tau load or variations in the type of tau lesions between the clinical PSP phenotypes. We have also applied a newly developed PSP-tau staging system in order to gain insight into the dynamics of the development of PSP-tau pathology.
Material and methods
We selected 42 cases from 102 pathologically diagnosed as PSP that were archived at the Sara Koe PSP Research Centre in the Queen Square Brain Bank for Neurological Disorders between 1992 and 2002. A systematic case note review was performed and the clinical features were recorded in a standardized fashion and cases were divided into three groups based on previously defined clinical criteria to allow for categorical analysis (Williams et al., 2005). When falls, cognitive dysfunction, supranuclear gaze palsy, abnormalities of saccadic eye movements and postural instability were the predominant clinical features in the first 2 years of illness, RS was retrospectively diagnosed, whereas those without these features and with features including asymmetric bradykinesia of the limbs, a positive initial levodopa response, tremor or limb dystonia, were labelled as PSP-P. PAGF was defined when there was a history of gradual onset of freezing of gait or speech, absent limb rigidity and tremor, no sustained response to levodopa and no dementia or ophthalmoplegia in the first 5 years of disease. We aimed to select approximately equal numbers of cases classified as RS and PSP-P with additional representation of PAGF cases. In the most recent 21 brains, comprising 13 cases of RS, 7 of PSP-P and 1 of PAGF tissue blocks had been selected following a standardized protocol and these were therefore analysed first. A further 21 cases in which as many as possible of the appropriate anatomical areas were available for examination were randomly selected without reference to neuropathological details from a pool of 81 cases separated into RS, PSP-P and PAGF. This second group comprised nine cases of RS, seven cases of PSP-P and five cases of PAGF. In 26 cases tau haplotype data were available, and in 13 there were data regarding tau isoform profile in the pontine base (Williams et al., 2005; Pittman et al., 2005). The protocols for the retention and access to human tissue and clinical records at the Queen Square Brain Bank have approval from the London Multi-Centre Research Ethics Committee.
Pathological methods
Diagnostic procedures
Consent for brain donation was obtained from the patients prior to death and consent for post-mortem examination was obtained from the next of kin after death. The diagnosis of PSP was made using standard methods including immunohistochemical analysis using the AT8 anti-tau antibody (tau phospho-epitope Ser202/Thr205). The preliminary PSP pathological diagnostic criteria were applied which insist on the presence of NFTs, neuropil threads and glial tau pathology (Litvan et al., 1996b).
For this study further neuropathological evaluation with a standardized approach was carried out to document Alzheimer pathology using Bielschowsky's silver impregnation and CERAD (Consortium to Establish a Registry for Alzheimer's Disease) criteria (Mirra et al., 1991). Aβ immunohistochemistry was also performed using an anti-Aβ antibody to document cerebral amyloid angiopathy (Revesz et al., 2003). Tau immunohistochemistry with the AT8 antibody was also used in the hippocampal formation to identify the presence of tau-positive grains in the hippocampal formation (Togo et al., 2002). The frontal lobe, lentiform nucleus and pons were examined for vascular pathology including small vessel atherosclerosis, lipohyalinosis, microaneurysm and arteriolosclerosis and their sequelae, such as lacunes, perivascular rarefaction and diffuse white matter attenuation of Binswanger's disease-type. Vascular pathology was graded as mild (occasional vessels affected), moderate (a significant proportion of the small vessels affected with few or no sequelae noted) or severe (a significant proportion of the small vessels affected with obvious sequelae). The presence of associated Lewy body pathology in the substantia nigra was assessed using α-synuclein immunohistochemistry.
Seven micrometres thick tissue sections were cut from tissue blocks of the anterior and posterior frontal cortex, parietal and temporal cortices, midbrain, pons and cerebellum for immunohistochemical analysis. Immunohistochemical staining for tau, α-synuclein and Aβ peptide (AT8, AutogenBioclear, 1 : 600; α-synuclein, Novocastra, 1 : 50; Aβ peptide, Dako, 1 : 100) was performed using a standard avidin–biotin method.
Regional pathological examination and quantification
In each case quantitative assessment of the tau pathology was carried out by one rater (DRW), blinded to the clinical features, in 17 brain regions that have previously been documented to show variability in PSP or were predicted to contribute to the clinical features of disease. The cortex and white matter in anterior and posterior frontal lobes, parietal lobe and temporal lobe, internal and external globus pallidus, putamen, caudate nucleus, subthalamic nucleus, substantia nigra, pontine nuclei, dentate nucleus and cerebellar white matter were used. In each region AT8 positive NFTs, TAs and oligodendroglial CBs were counted separately in seven randomly placed microscopic fields using a ×20 objective. Thread-like positivity was counted within a 10 × 10 graticule in the same field (×20 objective) and added to the CB score to give a CB plus thread (CB+Th) score. This enabled the classification of all immunoreactive lesions that were not obviously part of NFTs or TAs. Absolute counts were converted to a five-point grading scale that was developed for each region after the distribution of lesion counts was examined. Counted values were plotted along the x-axis and ranges for grades 0 to 4 were assigned on the y-axis. Grade 0 was reserved for when tau-positive pathology was absent. If the distribution of counts fitted a logarithmic curve the upper limit of grade 4 was set as the highest number counted, grade 1 the lowest count above zero and grades 2, 3 and 4 evenly spaced between these markers on a log scale along the y-axis. If the distribution of counts suggested that a linear model was more appropriate the upper limit of grade 4 was set at the highest value counted and grades 1–3 were set at 25, 50 and 75% of this highest value. In regions where the range included less than four values, absolute counts were used.
The repeatability of all counts was assessed by the same rater (DRW) by re-counting four (10%) cases. The intra-rater standard deviation (IRSD) was calculated as follows: IRSD = SD(Rm1 − Rm2)/√2, where SD is standard deviation, Rm1 is median grade at first reading and Rm2 is median grade at second reading.
Regions representative of overall tau severity
All graded data were explored to identify the minimum number of regions that satisfactorily summarized the overall tau severity. Grades from the temporal lobe grey matter were excluded to remove the influence of Alzheimer-type pathology on the analysis. First, the overall tau severity was determined in each case, by adding the grades of all lesions in all regions together. Next, the median grades for NFT, TAs, CBs and CB+Th were calculated for each region in each case (see example, Fig. 1). After choosing regions with the greatest range of grades, different combinations of regions and lesion types were tested for correlation with overall tau severity. It was found that the sum of grades for CB+Th pathology in the substantia nigra, caudate and dentate nucleus best correlated with the overall tau severity (see section 'Results'). This number designated the PSP-tau score (substantia nigra CB+Th grade + caudate CB+Th grade + dentate CB+Th grade) had a range from 0 to 12. The Friedman test was used to assess whether increments in the PSP-tau scores were associated with statistically significant increases in overall tau severity.
Neuropathological grading of tau severity
So that the repeatability of the pathological data used to produce the PSP-tau score could be tested, images representative of grades 1 to 4 of CB+Th pathology for the three regions of interest were obtained and used to produce a visual aid to grading (Fig. 2). This aid only, was used independently by two neuropathologists (TR and JH) as a guide to grading CB+Th pathology in the substantia nigra, caudate and dentate nucleus. While blinded from the clinical details, they were asked to grade the CB+Th pathology in the 34 cases of PSP with a complete data set (RS 21, PSP-P 12 and PAGF 1). The neuropathologists were asked to examine five to seven microscopic fields (×20 objective) in the dentate nucleus, caudate and substantia nigra. They were instructed to consider all sub-regions of the substantia nigra represented in the section and informed that all tau-positive lesions except NFTs and TAs were to be evaluated to give the CB+Th grade. Grade 0 was given when there were no pathological lesions, and was not included on the visual aid. Finally PSP-tau scores were calculated using the sum of median scores from all the three sampled regions (substantia nigra CB+Th grade + caudate CB+Th grade + dentate nucleus CB+Th grade), giving a score with a minimum of 0 and maximum of 12. Agreement between these two raters was assessed by calculating the weighted kappa and applying Landis and Koch's categorization of responses (Landis and Koch, 1977).
Distribution of pathological tau
The regional distribution of PSP-tau pathology was compared between cases of different severity. Cases were separated according to their PSP-tau score (0–1, 2–3, 4–5, 6–7 and >7) and median values of CB+Th were calculated for each brain region in each group.
Statistical methods
Spearman's correlation calculation was used to determine the relationship between the PSP-tau score and disease duration, age of onset, age at death, time from disease onset to first fall and time from disease onset to supranuclear gaze palsy. The correlation between PSP-tau score and the severity of tau lesions in each region (grade and absolute counts) was also examined using Spearman's calculation. The significance level for this test was set at 0.01 because of the multiple comparisons. For other data univariable analyses using χ2 for categorical and two-tailed t test or the Mann–Whitney U test, as appropriate, for continuous variables were applied with a significance level of 0.05. All statistical analysis was performed using SPSS for Windows (version 12.0.1).
Forty-two patients (26 men, 16 women) were included in the study. The mean age of onset was 66.5 years (range 44.4–87.5), the mean age at death was 75.6 years (60.9–95.8) and the mean disease duration was 9.1 years (1.2–17.3). Additional pathological findings are recorded in Table 1. There was no difference between the RS and PSP-P groups in the prevalence or severity of the CERAD plaque score, small vessel pathology, cerebral amyloid angiopathy or prevalence of tau-positive grains.
|CERAD neuritic plaque score
|10 (45)
|6 (46)
|2 (33)
|13 (55)
|7 (54)
|4 (67)
|5 (21)
|3 (23)
|2 (33)
|7 (30)
|3 (23)
|2 (33)
|1 (4)
|1 (8)
|Tau-positive grains
|4 (18)
|6 (46)
|Lewy body pathology
|1 (4)
|Small vessel pathology
|7 (30)
|6 (46)
|6 (26)
|5 (38)
|1 (8)
|1 (4)
|Cerebral amyloid angiopathy
|3 (13)
|3 (23)
|1 (17)
Note: Percentages are shown in brackets.
PSP-tau pathology
The diagnosis of PSP was confirmed in all the cases by the presence of typical PSP-tau lesions including NFTs, TAs, CBs and neuropil threads in the expected distribution. The intra-rater standard deviation of the regional analysis was 0.012, implying that the variability of counting was <2% and was thus highly repeatable.
The number of pathological lesions per microscopic field varied substantially between regions and between cases, although in no case was the subthalamic nucleus, substantia nigra or internal globus pallidus spared. NFTs were most abundant in the basal ganglia and brainstem structures and TAs in the cortices, putamen and caudate nucleus. CB+Th were the major contributor to the overall tau load and were most numerous in the subthalamic nucleus (median 283/microscopic field, range 8–1710), substantia nigra (median 186/microscopic field, range 0–1430) and internal globus pallidus (median 49/microscopic field, range 0–720), and least dense in the cortical regions. In the cases with the lowest density of lesions, tau pathology was limited to the subthalamic nucleus, substantia nigra and internal globus pallidus, with sparse tau immunoreactivity in the posterior frontal cortex and white matter, and few NFTs in these structures. As the severity of CB+Th pathology in the subthalamic nucleus, substantia nigra and internal globus pallidus increased, there was a concurrent increase in the density and severity of tau immunoreactivity in the pontine nuclei, dentate nucleus, cerebellar white matter and frontal cortex. The parietal lobe was not affected in cases with milder tau pathology, but in those with severe CB+Th pathology in the basal ganglia it was severely affected. Alzheimer changes lay within the expected range for the age groups, but Lewy body pathology was less frequent than previously reported (Braak et al., 1992; Tsuboi et al., 2001).
The mean regional tau-severity was higher in RS than PSP-P and PAGF in all brain regions. The difference with PSP-P was significant in all regions except the putamen (Mann–Whitney U test, P = 0.15) and subthalamic nucleus (Mann–Whitney U test, P = 0.77) (Fig. 3). Tau pathology was significantly more severe in RS than PAGF in the parietal cortex (Mann–Whitney U test, P = 0.022), pontine nuclei (Mann–Whitney U test, P = 0.003), dentate nucleus (Mann–Whitney U test, P = 0.01) and cerebellar white matter (Mann–Whitney U test, P = 0.023). Total tau load (∑ of grades for all lesions in all regions) was higher in the RS group (median 155) than in the PSP-P group (median 116, Mann–Whitney U test, P = 0.002) (Fig. 4). The PAGF group was not analysed further because of the small number of cases with a complete data set.
Grading of PSP-tau severity
The PSP-tau score (∑ CB+Th grade in the substantia nigra, caudate and dentate nucleus) correlated significantly with the overall CB+Th severity (∑ CB+Th grades in all 17 regions, Spearman's rho 0.89, P < 0.001) and also highly correlated with the overall lesion severity comprising all lesion types (∑ all lesion grades in all 17 regions, Fig. 5, Spearman's rho 0.93, P < 0.001) in the 34 cases with a complete data set. There was a significant positive correlation (Spearman's rho, P < 0.01) between the PSP-tau score and lesion grades in 70% of regions and lesion counts in 63% of regions (supplementary material). PSP-tau score correlated with NFT grades in 36% of brain regions, CB grades in 100% and CB+Th grades in 94% of regions (all, Spearman's rho P < 0.01). No other combination of regional grades correlated with more regions. Each increment in the PSP-tau score (tau score 0 to 10—this latter being the highest observed) was significantly different from the previous according to the mean ordinal rank of tau severity (Friedman's χ2, 23.7, P = 0.005). The weighted kappa measuring agreement between two independent pathologists using the visual aid and instructions for grading was 0.71, which is 'very' good inter-rater agreement (Landis and Koch, 1977).
The PSP-tau score did not correlate with age at symptom onset or age at death, but there was a negative correlation between PSP-tau score and disease duration (Spearman's rho −0.36, P = 0.028) (Fig. 6). Time from disease onset to first fall (Spearman's rho −0.49, P = 0.003) was negatively correlated with PSP-tau score. There was a modest, but significant correlation between tau isoform ratio (4-repeat tau:3-repeat tau) in the few cases with this data (Spearman's rho 0.56, P = 0.048). The only two cases that did not have the H1/H1 PSP susceptibility genotype (H2/H2 and H2/H1) had the lowest PSP-tau scores (0 and 1, respectively). The three cases homozygous for the H1c haplotype did not have a significantly higher tau score than cases with other genotypes. No cases classified as PSP-P had a PSP-tau score of more than 5 (median 3), and there was a significant difference between the median PSP-tau scores for RS (median 5, versus PSP-P, Mann–Whitney U test, P < 0.001) (Fig. 7).
Distribution of PSP-tau pathology
As our findings suggested that the PSP-tau score (sum of CB+Th grades in substantia nigra, caudate and dentate nucleus) was a reasonable surrogate marker for pathological disease severity with significant clinical correlations, the relationship between this surrogate marker for pathological severity and the distribution of lesions throughout all 17 brain regions was further examined. Cases were grouped according to PSP-tau score (PSP-tau score 0–1, 2 cases; 2–3, 9 cases; 4–5, 16 cases; 6–7, 3 cases; >7, 3 cases) and median values of CB+Th for each region were calculated (Fig. 8). Pathological features noted, in addition to the graphically displayed median data for CB+Th, are discussed according to PSP-tau score.
Scores 0–1: involvement limited to pallido-luyso-nigral distribution with sparse involvement of the pre-motor cortex: Regions caudal to the substantia nigra had little or no tau pathology, including the dentate nucleus, cerebellar white matter and the pontine nuclei. In these cases the parietal cortex was spared from tau lesions and the anterior frontal lobe had very few lesions.
Scores 2–3: moderate involvement of basal ganglia, pontine nuclei and dentate nucleus in the absence of parietal lobe lesions: The severity of the previously described lesions was increased and in particular the number of tau positive lesions in the subthalamic nucleus and globus pallidus was increased. Caudal regions, including the dentate nucleus and pontine nuclei, were affected and in some cases the cerebellar white matter was mildly involved. There were NFTs, TAs and thread pathology in the posterior frontal lobe, but the anterior frontal lobe was rarely involved.
Scores 4–5: more severe involvement of the basal ganglia and dentate nucleus with involvement of the frontal and parietal lobes: Brains with scores of 4 or 5 were most numerous in this study. The internal globus pallidus, subthalamic nucleus, substantia nigra, pontine nuclei, dentate nucleus and cerebellar white matter were more severely affected, but there was no increase in CB+Th pathologies in the external globus pallidus. Cortical regions, including the frontal and parietal lobes, were consistently moderately affected.
Scores 6–7: moderately severe pathology in the basal ganglia, pontine nuclei, parietal and frontal lobes: In the internal globus pallidus numerous NFTs, threads and CBs were present, and the severity of all lesions, except NFTs, was equally severe in the external globus pallidus. The caudate and putamen remained only moderately affected, similar to the lower scored brains, but the involvement of caudal structures was more severe, in particular the cerebellar white matter. In these brains the neocortical regions, except the temporal lobe, had moderately severe NFTs, TAs, thread pathology and CBs.
Score >7: severe involvement of the subthalamic nucleus, substantia nigra, internal globus pallidus as well as neocortical areas, pontine nuclei and cerebellar structures: In the three cases in this category there was severe pathology throughout the regions examined, with the exception of the caudate, putamen and temporal lobe where there was very little increase in the numbers of tau lesions as the score increased above 2.
The higher contribution by 3-repeat tau isoforms to the insoluble tau fraction in PSP-P raised the possibility that the biological differences determining different clinical PSP sub-types might also affect the severity and distribution of the histopathological lesions (Williams et al., 2005). We have indeed demonstrated pathological differences between the two major clinical sub-types, with the RS group having a significantly higher total PSP-tau burden than the PSP-P group. The quantitative data for the overall severity of PSP-tau pathology can be assessed reliably by using a 12-tiered scoring system that takes into account the tau burden in oligodendroglia and threads in three anatomical regions: the substantia nigra, caudate and dentate nucleus. This can also be reproduced consistently when only a visual aid, akin to those used for the CERAD diagnosis of Alzheimer's disease (Mirra et al., 1991) and dementia with Lewy bodies (McKeith et al., 2005), is used for grading. Having assigned a PSP-tau score to each case, an excellent correlation was found with the overall tau-load determined by the morphometric data. Further analysis also revealed important associations between PSP-tau scores and clinical, biochemical and genetic features of the cases. Those with RS had a significantly higher PSP-tau score than the PSP-P cases, and no PSP-P case had a score of more than 5. In addition, we established that with increments in PSP-tau scores tau deposition also becomes more widespread indicating that PSP-P is not only associated with a lower tau burden, but also that this takes place in a topographically more restricted pattern. Disease duration was shortest in patients with the most severe tau pathology, and therefore the highest PSP-tau score and topographically most extensive tau pathology. Tau severity, according to this score, correlated with 4-repeat tau:3-repeat tau ratio. Patients who carried the H2 PSP-protective allele had the lowest tau scores.
Although differences in the severity of pathology in some brain regions have previously been correlated with particular clinical features, heterogeneity in regional tau distribution has made qualitative and quantitative comparisons between pathology and clinical features problematic (Daniel et al., 1995; Verny et al., 1996; Revesz et al., 1996; Bigio et al., 1999; Halliday et al., 2000; Tsuboi et al., 2005; Josephs et al., 2006). We used an unbiased, region-specific and lesion-specific grading system to overcome these difficulties and to allow for regional comparisons to be made. The severity of CB+Th pathologies were the most useful in separating cases of PSP and the PSP-tau score correlated well with the majority of other pathological lesions, but not NFTs in the striatum, substantia nigra or subthalamic nucleus (see supplementary material). Unlike NFTs, there is no convincing evidence that threads, representing accumulation of PSP-tau in both neuronal and oligodendroglial processes (Probst et al., 1988; Ikeda et al., 1994; Dickson, 1999), decrease in density in PSP as the disease progresses (Halliday et al., 2000), making their post-mortem analysis more likely to reflect dynamic changes during the course of the disease.
We have previously shown that amongst the clinical features of patients with PSP-tau pathology, a number of distinct clinical syndromes can be identified (Williams et al., 2005). The close association between the severity of the PSP-tau scores, as a measure of the PSP-tau load, and the clinical sub-types also suggests that they are a sensitive surrogate marker of the functional and structural changes that accompany the underlying neurodegenerative processes and determine the different PSP phenotypes. Others have also found that the severity of tau accumulation, and neuronal loss, in the substantia nigra pars reticulata (Halliday et al., 2000), mesencephalon (Juncos et al., 1991) and the pontine nucleus raphe interpositus (Revesz et al., 1996), is higher in patients with gaze palsy (RS) compared to those without (mostly PSP-P). However, the current findings suggest these localized changes mirror neurodegeneration in a number of other susceptible regions, and are part of more severe and widespread disease in the brain. This notion is supported by several reports of an association between the severity of tau changes in cortical regions and cognitive dysfunction in PSP and by our finding of more severe cortical pathology in RS (Bergeron et al., 1997; Tsuboi et al., 2005; Josephs et al., 2006). In contrast, patients who present with parkinsonism without gaze palsy, early falls and dementia have more moderate pathological tau accumulation, in a more restricted pattern of distribution.
The general pattern of distribution of tau pathology in PSP appears remarkably consistent despite the broad spectrum of clinical features recorded during life. No case of 'incidental' PSP-tau has been included in this analysis, and, to our knowledge, definitive reports of such cases have not been made. In their absence, and without a substantial number of cases with early PSP, attempts to determine the dynamics of topographical evolution of tau pathology cannot be considered. However, we have constructed a model that may represent the disease 'footprint' of relative susceptibility to regional pathological tau accumulation in PSP. This model identifies the subthalamic nucleus, substantia nigra and globus pallidus as the most susceptible regions and that other regions lag behind in severity in a gradient from the posterior frontal lobe, dentate nucleus, cerebellar white matter, pontine nuclei, caudate, to the anterior frontal and parietal lobes. The significant negative correlation between the PSP-tau score and disease duration suggests that more fulminant disease affects more regions, more severely from disease onset and contributes to an earlier death. The factors that influence the severity and extent of PSP-tau pathology are unknown, but the genetic background and, in particular, possession of the H1c tau sub-haplotype, may be important (Baker et al., 1999; Pittman et al., 2005). Our observation that the patients with at least one H2 allele accounted for the two mildest cases of tau accumulation is of interest given recent suggestions that the H2 tau haplotype not only lacks an association with PSP, but also that it contributes to protection from the disease (Pittman et al., 2005). The least severe pathology also tended to have the lowest ratio of 4-repeat tau:3-repeat tau in the pontine base. Recent findings suggest that the presence of the MAPT H1c sub-haplotype favours the increased production of 4-repeat tau in controls and possibly its accumulation in disease (Myers et al., 2006). The small number of cases homozygous for H1c tau sub-haplotype in our study did not have a significantly higher severity of tau pathology implying that other modifying factors may influence the effect of genetic susceptibility.
Our data are also consistent with the notion that regions predicted to be most susceptible to PSP-tau neurodegeneration (subthalamic nucleus, substantia nigra and globus pallidus) have the lowest threshold for disease manifestation and in the context of protective factors, such as the H2 allele for example, may remain the only severely affected regions. Other related tauopathies, such as post-encephalitic parkinsonism and parkinsonism dementia complex of Guam have overlapping pathological features (Geddes et al., 1993), and recent data suggest that genetic factors that contribute to the Guam neurodegenerative disease risk may also, at least in part, be similar to those in PSP (Sundar et al., 2007). The differences in the type, ultrastructural and biochemical characteristics of the tau pathologies of these diseases and PSP that are also documented are, however, consistent with the presumed different aetiologies of these conditions (Geddes et al., 1993; Buee-Scherrer et al., 1995; Litvan et al., 1996b; Mawal-Dewan et al., 1996; Buee-Scherrer et al., 1997; Oyanagi et al., 2001; Oyanagi, 2005; Williams, 2006). Nevertheless the similarities in the distribution of the pathological lesions in post-encephalitic parkinsonism and parkinsonism dementia complex of Guam that overlap with the range described in the present work, raise the possibility of similar factors contributing to regional tau susceptibility in these diseases particularly in the substantia nigra, subthalamic nucleus and pallidum (Geddes et al., 1993; Oyanagi et al., 1997, 2000, 2001).
The grading system used in this study is a practical and sensitive tool for the morphological assessment of PSP-tau pathology and takes into account the clinical, biochemical and genetic diversity that is known to occur in PSP. Although the relationship between neuronal loss and PSP-tau pathology remains to be determined, the proposed model provides a framework for further evaluating the cellular factors that contribute to PSP-tau neurodegeneration, and the clinical and biochemical manifestations of the disease. A pathological distinction between PSP-P and RS can be made, which together with the biochemical differences gives weight to previous attempts of separating these two PSP phenotypes clinically. Future research identifying genetic and other disease markers may also help to underpin the notion that PSP-P is a distinct clinicopathological entity, albeit with a close relationship with RS. In the meantime the pathological distinction between PSP-P and RS emphasizes the need to identify these patients in the clinic and that research in PSP should also take into account the biological differences that exist between these clinical phenotypes.
Supplementary material
Supplementary material is available at Brain online.
The authors would like to thank the patients and their families, without whose support none of this research would have been possible. Aviva Petrie (Eastman Dental Institute, University College London) assisted with the statistical analysis. This work was supported by the Reta Lila Weston Trust and the PSP (Europe) Association. Catherine Strand is funded through a grant from the PSP (Europe) Association. Janice L Holton is partly funded by the Reta Lila Weston Trust.
- Abbreviations:
- Abbreviations:
- coiled body
- neurofibrillary tangle
- pure akinesia with gait freezing
- progressive supranuclear palsy
- progressive supranuclear palsy-parkinsonism
- Richardson's syndrome
- tufted astrocyte
- © The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: firstname.lastname@example.com


text: PhotoMallee farmers are owed millions from Convector ABC Rural Tom Fedorowytsch (ABC News) Wed Sep 18 07:27:20 EST 2013 Farmers in the Victorian Mallee will be watching the outcome of Convector Grain's impending sale, because it will have a bearing on the amount unsecured creditors of the grain handler receive, according to one administrator. Read more. Share Email Facebook Twitter


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plow21jaw's Contributions
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You went and did an internet search for Win Employment Center and stumbled on my video media, it's possible that you are searching for a job opportunity or simply tips on how to earn some cash.
03/28/13 Community Articles
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You probably did specific searches for Win Job Center and came across this video media, its likely you are looking for a job as well as approaches to make some money.
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text:
It may not surprise you that we live in an artistic community.
But it may be a surprise to learn where the Pump House's latest art exhibit came from: La Crosse's elementary and middle schoolers.
Students created a piece in their art classes to fit the "Essence of Color" theme.
On Thursday night, night art lovers had the chance to ask those young artists about their work at an open house.
Art Specialist Maria Mason says the project and the showcase "gives a lot of support to the arts, and shows what students can do and how art can be integrated into other fields. It brings them out and gives them a sense of pride. I think that's really important to uplift them in a non-competitive way."
If you'd like to check out "The Essence of Color" exhibit, it's on display at the Pump House in La Crosse through Jan. 26th.


text:
denote the number of people in each category.
You can do this using Variance Analysis. You can use F-distribution to determine whether there is any significant difference between washing hands and not washing hands. You also can determine whether the number of peeple getting sick and not getting sick in relation to washing and not washing hands.


text:
Clear Light Yoga
- Commitment
- Purification
- Focus
- Cutting through
- Absorption
Chuang Tzu: Discussion On Making All Things Equal
Alfred Pulyan - Letters from a Zen Master, or Why You're Still Suffering
Richard Rose - Monitor Papers & Transcriptions
JJ van der leeuw - Conquest of Illusion
Sivananda Saraswati on Celibacy-Bramacharya
The Surest Path To Mental Clarity
Dried Shit Zen Roshi:
What Is Shingon Magic?
Kukai: Principle Of Attaining Buddhahood With the Present Body
Franz Hartman - Magic White and Black
Éliphas Lévi - Paradox VII: The Will Accomplishes Everything, Which It Does not Desire
Paul Hedderman - Are you a lion or a sheep?
The Six Bardos
- The bardo of the realm of life
- The bardo of the dream state
- The bardo of meditation
- The bardo of the experience of death
- The bardo of the experience of reality
- The bardo of seeking rebirth
Six Doctrines of Naropa
- The mystical heat (tummo)
- The illusory body (mahamaya)
- The dream state (svapnadarsana)
- The clear light (abhasvara)
- The intermediate state (antarabhava)
- The transmission of consciousness (samkranti)
Doctrine of Trikaya - three bodies
- Dharmakaya
- Sambhogakaya
- Nirmanakaya
- Vajrayana "fourth body" = The indivisibility of the Trikaya
Sambhogakaya's Five Manifestations
- Vajrasattva:
mirror-like awareness
- Ratnasambhava:
awareness of equanimity
- Amitaba:
discriminating awareness
- Amoghasiddhi:
spontaneously fulfilling action
- Vairocana:
all-encompassing emptiness
The Five Tathagatas
- Vairocana (center, white)
- Aksobhya (east, blue)
- Ratnasambhava (south, yellow)
- Amitabha (west, red)
- Amoghasiddhi (north, green)
Nine designs of the Supreme Energy
- Vama
- Energy flowing in ida nadi
- Ambika
- Energy flowing in pingala nadi
- Jyestha
- The supreme flow of energy in sushumna nadi
- Raudri
- Protectress of space
- Iccha
- Energy of will
- Jnana
- Energy of knowledge
- Kriya
- Energy of action
- Shanti
- Energy of tranquility
- Para
- Transcendental energy
The starry night sky,a massive bonfire of uncreated wisdom, blazes unceasingly between your ears.
DriedShitZen Roshi
Kill Everything In You
When you've killed everything in you
that might interfere with the Clear Sky (the Dark Expanse)
light and darkness are just the same nothing.
How could anything be different?
It's clearly the same.
How could anything be the same?
It's clearly different.
How could anyone suffer?
Who exists to have a mind
or to become a Buddha?
Cure yourself of sick thinking,
and the un-ease of life is gone.
Gone beyond, utterly beyond,
bo-ji so wa-ka!
Hearing all day long you hear nothing.
Seeing all day long you see nothing.
Laughing you don't laugh.
Crying you don't cry.
You're liberated, and can live as you want
and you don't understand the idea of "bondage"
or getting "caught up in something."
You're always a golden buddha.
You're always a temple in calm starlight.
A demon playing the bamboo flute,
a samurai hiding in the long grass --
whatever! you're always just THAT.
If the darkness comes cut it down.
If the brightness comes cut it away.
If people come don't answer them.
If the Clear Sky comes shatter it completely.
If the Void ever comes, slash it with your sword.
Destroy all thinking, let it go
and both objects and subjects disappear.
What's left can't even be imagined,
so how do you expect me to give it to you?
There isn't any one or any body left anywhere
to experience this,
to pretend or deny IT alone "exists"
or to ever say a single word about anything.
-- D.S.Z. Roshi
The Six Perfections
- Dāna pāramitā - generosity, giving of oneself
- Śīla pāramitā - virtue, morality, discipline
- Kṣānti pāramitā - patience, tolerance
- Vīrya pāramitā - energy, diligence, vigor
- Dhyāna pāramitā - one-pointed concentration, contemplation
- Prajñā pāramitā - wisdom, insight
Knowledge required for the path through the six intermediate realms
- Knowledge of the former place of birth or realm of existence
- Knowledge of dying, of the crossing over of awareness, and new rebirth
- Knowledge of transcending spirit
- Knowledge of all hidden appearances, in the realm of the non-visible
- Knowledge of the six realms of existence
- Knowledge of all liberating capabilities
The Five Pure Lights, pañca-jñāna
- Ādarśa-jñāna
Melong, mirror-like awareness
- Samatā-jñāna
Awareness of sameness, the non-dual method of upāya and prajñā
- Pratyavekṣaṇa-jñāna
Investigative awareness
- Kṛty-anuṣṭhāna-jñāna
Accomplishing activities, spontaneously
- Tathatā-jñāna
Suchness, dharmadātu, universal substrate
Page 111, Secret Doctrines of the Tibetan Books of the Dead, by Detlef Ingo Lauf


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Firstly, happy July 4 to my lovely Americans.
Does it strike you as weird that a number of Brits I know are using it as an excuse to have a Sunday BBQ/party? You know, given what the holiday actually commemorates? That's a bit weird, right?
Maybe I just know too many achingly trendy hipsters.
A couple of the wizard links are "nested" this week so I'll start with them.
Jow waxes awesome on Natural Philosophy
I particularly like his comments about self-ghettoization in the last few paragraphs. That is always a danger with any specialist group but I feel the implications are more acute in an occult setting.
And he was riffing off this spectacular post by John Michael Greer. The part about the "professional advice givers" is neat. I'm sure most of you are in that boat for your circle of friends, colleagues, clients and sometimes just people at the bus stop. I know I am.
The Divine Miss Sugar doles out some truth bombs about toxicity
I think the reason why we are happily, platonically, transatlantically e-married is her continuing desire for (and success at) building magical learnings into her day to day life. Which is right where my head is at the moment, as well.
Jack picks up the toxicity thread here as well. Not literally, of course.
Like so many others, Jacobus makes me feel dumb
Even if, like me, Kabbalah isn't really on your roadmap at the moment, this is an excellent blog to subscribe to. I always get a lot out of it. In this post he talks about a variant of the Ineffable Name that means "God Protect".
If you want a genie, summon a genie
Even then, spirit work requires a bit of a reality check. Balthazar coins a very helpful term: "Genie Syndrome". I like it.
Again, not really a "teaching" link but it's exciting news. Especially as he's getting married in New Zealand... Which, as countries go... Is made for weddings. Mountains, beaches, islands, volcanoes... Take your pick.
The title is a bit hyperbolic (which is probably why I like it), but I share Barrabbas's sentiment on the Tarot. In fact, whenever I play that "what books would you bring to a desert island" thing I always take the really annoying option of saying "a Tarot deck" for at least one of them. Then I argue about what exactly constitutes a book.
Maybe pamphlets will make a comeback?
I love that Frater AIT has done this and I love and agree with his reasons for doing so: laziness, effectiveness, utility, time management.
Scotland's magicians are in crisis
Read it. It will make sense. Plus it's entertaining. The pizza thing is great.


text:
Raymond Dallas McCloud
Raymond Dallas McCloud of Marietta passed away Tuesday (Nov. 5, 2013) at the home of his brother and his wife, Dan and Mariesa McCloud.
He was born Sept. 9, 1939, in Marietta, to Mary (Scarbrough) and Russell McCloud. After high school, Sgt. McCloud enlisted in the U.S. Air Force and was stationed in Alaska, after being discharged he enlisted in the U.S. Army serving during the Vietnam conflict and Desert Storm. He was a highly decorated Green Beret, Special Forces, and Airborne when he retired from the Army. He was stationed in numerous places including Germany, France, Korea, Vietnam, and Fort Bragg.
He is survived by two children, Jeanna Pennington of Mississippi and Teresa Hutchison of North Carolina; three grandchildren, Destin, Tiffanie and Danny; five brothers, Danny (Mariesa) McCloud, Jimmie McCloud, Larry (Tonya) McCloud, Mike (Han Ok) McCloud, and Russell McCloud; four sisters, Janet (Butch) Mclntosh, Dee (Gary) Ward, Randa (Scott) Arrowood, and Kelly (Rich) Howell; stepmother, Jean (Don) Brothers; and numerous nieces and nephews.
He was predeceased by his parents; brother, Russell Jr.; and sisters, Darlene (Ed) Kostolick, Maxine (Bill) Cassady and Leora (Dick) Callihan; stepfather, Jack Cunningham; and closest friend, Jerry Roush.
Calling hours will be from 6 to 9 p.m. Thursday (Nov. 7) with funeral services at 10 a.m. Friday (Nov. 8) at McClure-Schafer-Lankford Funeral Home, with full military honors. He will be interred in Rainbow Cemetery, Lowell. Messages of sympathy may be sent at www.lankfordfh.com.
He was a life member of VFW Post 1508, life member of the Special Forces Association, a member of American Legion Post 159, the DAV, Eagles and Moose. Contributions can be made in his memory to American Legion Post 159, Williamstown.


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Cropp: November dairy situation and outlook
By Bob Cropp, Professor Emeritus
University of Wisconsin-Madison
Milk prices may have peaked for the year in October.
The October Class III price was $21.02/cwt., and it now looks like the November Class III price will be about $20.80/cwt., falling lower in December. Dry whey prices have held up trading in the 60¢-65¢/lb. range, but cheese prices have declined, lowering the Class III price. On the CME, cheddar barrels were as high as $2.08/lb. late October, started Nov. 1 at $2.00/lb., but continued to decline and were $1.7225/lb. as of Nov. 19. The 40-lb. cheddar blocks were as high as $2.12/lb. in late October, started Nov. 1 at $2.11/lb., but also continued to decline and were $1.8250/lb. as of Nov. 19.
The Class IV price was $18.54/cwt. in October and will about $18.70/cwt. for November, and may hold near this level for December. While CME butter averaged $1.9086/lb. in October and will average lower in November at about $1.85/lb., nonfat dry milk prices have strengthened, trading in the $1.49-$1.53/lb. range, giving some strength to the Class IV price.
With lower cheese prices, Class III prices on the futures market also show weaker prices in 2013, falling below $19/cwt. by January, but staying above $18/cwt. through November, with December dropping slightly below $18.00/cwt.
But, there is a good probability that prices could end up higher than this. Recently cheddar cheese production has been below a year ago, with September production 2.7% lower, and total cheese production just 0.3% higher. And, with cheese stocks tighter, along with favorable domestic sales and cheese exports, cheese prices ought to hold at levels above a year ago at least through the first half of the year.
Sept. 30 stocks of American cheese were 4.8% lower than a year ago, with total cheese stocks 4.9% lower.
Cheese prices and other dairy product prices will also be helped by milk production, which is not expected to increase in 2013, and is actually running lower than a year ago in the California, the second-largest cheese producer and largest producer of butter and nonfat dry milk.
In September California's cheese production was 6% lower than a year ago. Some forecaster still have a Class III price in the high $19s/cwt. during much of the first half of 2013, and even reaching above $20/cwt. by summer. Assuming dry whey prices will hold, an average cheese price near $2.00/lb. would give a $20/cwt. Class III price; at $1.90/lb. about $19.45/cwt.; at $1.85/lb. about $18.95/cwt.; and at $1.80/lb., about $18.50/cwt. As of now, cheese prices in the $1.80-$1.90/lb. range seem quite possible for the first half of the year.
Since dairy exports are more than 13% of milk production on a total solids basis, a significant drop in exports could lower dairy product prices and milk prices. With dairy product prices higher than world prices, exports have slowed after peaking in May. However, total exports of all dairy products on a volume basis remain well above a year ago. September cheese exports were 17% higher than a year ago and 21% higher year-to-date. September exports and year-to-date exports for other products were: butterfat, -36% and -22%; nonfat dry milk/skim milk powder, -13% and +6%; dry whey, -21% and - 10%; whey protein concentrate, +21% and +72%; and lactose, -1% and +7%.
But, with milk production running lower in two major exporters, U.S. and the European Union, and world demand holding, U.S. exports should still remain favorable through 2013, especially for milk proteins. USDA estimates exports for 2013 to be just 3.3% lower on a fat basis and 2.3% lower on a skim-solids basis.
If the trend in milk production continues, this will support stronger milk prices than what are currently indicated by Class III futures. USDA's release of U.S. milk production shows production dropping below a year ago for two consecutive months (September down 0.6%, but October down just 0.1%).
Cow numbers started to decline in May and were down 84,000 head as of October, which put the number 0.3% below a year ago. October milk per cow was up just slightly, resulting in the decline in milk production.
As in recent months, the pattern of regional milk production was the same, with the major declines in milk production in the West, and both the Northeast and Upper Midwest with increases. In the West, with the exception of Idaho, which had an increase of 1.6% in milk production compared to a year ago, October milk production was down by 4.5% in Arizona, 3.5% in California, 2.4% in New Mexico and 5.0% in Texas. California cow numbers fell from September and were just 2,000 head more than a year ago. Each of the other states had fewer cows than a year ago. Arizona and Idaho had increases in milk per cow of 1.8% and 1.6% respectively, but milk per cow was 3.6% lower in California, 5.9% lower in New Mexico, and 4.0% lower in Texas.
In the Northeast, increases in October milk production were 2.7% for New York and Michigan, and 2.6% for Ohio; but a decrease of 0.3% for Pennsylvania. Increases in milk production for Upper Midwest states were 2.0% for Iowa, 2.9% for Minnesota, and 4.7% for Wisconsin.
Alfalfa hay prices continue to increase. While still high and above a year ago, both corn and soybean meal prices have softened some. Current milk prices are also higher, but margins remain tight. With higher feed costs and lower milk prices in the West than compared to the Northeast or Upper Midwest, the regional pattern in milk production now experienced will likely continue into 2013.
Robert Cropp
University of Wisconsin-Madison


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I think the Mettenberger kid has potential next year and didn't they bring in one of the top pro style QBs in the nation. They only have to get a little bit better on offence to be a great team. They were awful last year. I think a upgrade at OC and a second year for Mettenberger will do that.
Better then Bama or the Dawgs no most likely not but I think they will be much better. Plus South Carolina I cannot see someone outside the SEC really challenging. Kelly is gone from Oregon and Ohio St. isn't as good as this years record in a over rated big 10.
Last edited by Nate_C; 02-09-2013 at 12:13 AM.
Oh really...lets see they return a ton of people including a QB who threw for 15 TD's and ran for 13 TD's...Urban Meyer pulls out the #2 ranked recruiting class....plus they have a soft schedule, and you dont think they are as good...got news for you they may win it all...and I am no OSU fan
unless the buckeyes trade for tebow.........urban meyer will need 40 days worth of depends prior to the bcs game. incontinence personified!
john mccallie
Then given tosu's likely BCS opponent, Urb's health will start to go south with the opening kickoff, 2009 redux. Only thing worse for bringing on those symptoms would be Saban making him sicker still by moving to Michigan.
LSU's problem isn't coordinators. LSU's problem is the head coach. The players don't respect him because they view him as a buddy, not a leader. That's the difference between him and Saban. Now, I know he has a lot of won games, but a good percentage of his wins were squeezed out, not decisive wins.
"If you like your doctor, you can keep your doctor"
"I dont believe people should be able to own guns."
"I will not sign a healthcare reform plan that adds one dime to our deficits, either now or in the future."
"We've got to make sure that people who have more money help the people who have less money."
"Over the last 15 months, we've traveled to every corner of the United States. I've now been in 57 states? I think one left to go."
B. Hussein Obama


text:
Open Forum
Tom Nash answers:
How is original sin inherited since we do not get our soul from our parents?
The state of Illinois passed a law that allows illegal immigrants to obtain driver's licenses -- why is the Catholic Church in Illinois supporting this?
Luke says that Mary was full of grace, but Acts says that Stephen was full of grace -- why do we say that Mary was immaculately conceived?
Why are scientists hiding proof of God's existence?
Doesn't John 6:53 mean that your salvation is in jeopardy if you are outside the Catholic Faith?
How do you respond to someone who says that it is not fair that we have to suffer the consequences of original sin?
Can a papal bull be rescinded?
Did Paul Ryan commit grave sin by being a part of a ticket that allows exceptions for abortion?
What is Wicca?
The premier magazine of Catholic apologetics and evangelization for more than two decades, Catholic Answers Magazine helps build your faith—and your ability to defend it. Its lively articles are written by some of the best Catholic thinkers in the U.S. Church.


text:
Homestead to launch Burlington House collection
April 16, 2008-- Home Textiles Today,
New York – Homestead, the home fashions division of Li & Fung USA, has entered into an agreement with Burlington House, the decorative fabric and interior textiles unit of International Textile Group, to launch a re-branded home lifestyle collection.
"We are please to have reached this agreement with Burlington House and are looking forward to working with its portfolio of brands," said Rick Darling, president, Li & Fung USA.
"The heritage and appeal of Burlington House transcends generations," said Derrill Rice, president of Burlington House, which traces its history as a textiles and softlines pioneer back to 1923.
The nature of the agreement grants Homestead the Burlington House master home license for all categories other than floor coverings.
Related Content By Author
Sponsored Content
Sponsored Links
Featured Video
Previewing Heimtextil 2017


text:
|Tice with a J's Journal
5 most recent entries
I opened an account here when Scans_Daily opened an account here. Well, I've since stopped caring about Scans_Daily, and as you can see, I don't care about my personal journal here either. So if you want to see where I do care:
For now, anyway. Is anyone else alive on this thing?
A comic on the internet, of course! Behold its feeble majesty!
Alors! C'est la Journée Mondiale du Ninja! Célébrez en silence!
It seems that there are many places on the 'net to post your words, and this place is one of them. I already have an account on LJ, but I thought I'd get one here, too. I may regret this, but we'll see.


text:
A 50-year-old abalone fisherman is in a critical condition after he was dragged from the water unconscious at Trigg Beach this morning.
A City of Stirling beach inspector rescued the fisherman, who had fallen from reef about 30m offshore, about 7.20am after being alerted by the screams for help from another beachgoer.
The inspector tried to resuscitate the man in the water before Fisheries officers helped him drag the unconscious man to the beach where the beach inspector did CPR onshore.
Paramedics were called and rushed the man to Sir Charles Gairdner Hospital.
It is understood his friends told rescuers the man could not swim.
Two abalone fishermen have drowned this season in separate incidents.
On December 30, a man in his early 40s drowned while diving for abalone with friends near Cape Leeuwin, near Augusta in WA's South West.
A 20-year-old Malaysian man was swept away while looking for the delicacy at Yanchep on the first day of the heavily restricted metropolitan recreational fishing season in November.
He was caught in a strong rip in treacherous conditions in Yanchep Lagoon.
The tragedy triggered calls for metropolitan abalone fishing spots to be closed in dangerous weather.
Conditions this morning were not considered dangerous.


text:
For a limited time you can save $10 off our range of accessories by booking online!
Not valid with any other offer.
We don't just claim to use only the best parts in your phone, we back it up with a lifetime warranty.
If you find a cheaper like for like price from a specialised local repairer, we'll match it! So you know you're always getting the best deal. Conditions apply.
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What is in this article?:
- South Texas ranchers feeding cactus to keep from liquidating herds
- Water problems
• The unrelenting drought is taking its toll on South Texas cattle ranchers.
• Some ranchers are using 18th century techniques to keep cattle healthy.
• South Texas drought taking its toll on cattle ranchers.
More About:
BILL BARFIELD, a South Texas cattle rancher near the Jim Hogg and Starr County line, burns needles off cactus pads to feed parched cattle.
The unrelenting drought is taking its toll on South Texas cattle ranchers who are resorting to a centuries-old emergency method of feeding cattle, according to a Texas A&M AgriLife Extension Service agent.
"Ranchers down here commonly refer to it as 'chamuscando,' the Spanish word for the process of burning off spines from prickly pear cactus so cattle can eat the pads for food and water," said Omar Montemayor, an AgriLife Extension agent in Starr County. "For many of our aging ranchers, chamuscando (pronounced chah-moos-KAHN-doh) and hauling hay and water to their livestock are last ditch efforts to stay in the cattle business."
Burning cactus is a practice that dates back to the mid-1700s when Spanish settlers moved here from Mexico City and raised cattle for sustenance along both sides of the Rio Grande, Montemayor said. The pioneers burned cactus over mesquite fires, which eventually gave way to kerosene burners until the 1950s when ranchers switched to butane then propane.
"In times of drought, when pastures have no grass or hay for cattle to feed on, ranchers use a propane-fueled torch to burn the needles off nopal, or cactus. The pads or stems of the plant contain moisture and fiber, but very little protein. Ranchers supplement their cattle's diets with protein pellets called range cubes."
Chamuscando and hauling supplemental feed, hay and water to cattle are costly measures, Montemayor said, but for many South Texas ranchers, time may be too short to sell their herds now and rebuild if and when the drought breaks.
"Many of our ranchers are in their late 60s and 70s," he said. "If they sell their cattle and the drought ends next year, they'll have to buy young cattle back. If a rancher pays $2,400 for a 'pair,' a cow and a young calf, he or she will have to wait four to five years to sell four or five calves just to recoup their investment.
"For a lot of ranchers, that's time they think they may not have, so they're doing everything they can to keep their cattle alive now. But it's hard work and very expensive."
Once cattle start eating burned cactus, a rancher has to have a plentiful supply on hand.
"When ranchers burn cactus, they have to burn at least a two-day supply because cattle used to eating cactus will eat it with spines and all if the burned cactus runs out. That results in mouth injuries, they stop eating and a rancher has a whole new set of problems."
At an average cost of $3.50 per gallon of propane, a rancher with 30 head of cattle will spend about $35 per day just on the fuel to burn cactus, Montemayor said.
"Hopefully, a rancher has plenty of cactus on his ranch land. Then there's the cost of the protein supplement. Some set out molasses tubs which help with the livestock's hydration and digestive process."


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Did You Know: There Are LOTS of PCH Winners!
PCH Staff
12:00 am | 212 Comments »
Greetings, fans and friends! Today, I have 2 really cool facts to share with you, which you might have seen on the PCH Fan Page on Facebook : Did You Know that PCH has around 300 winners every day? 2. Did you know that PCH has made over 5 MILLION winners since 1967? Given that [read more…]


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Nintendo Land review
The good:
A land of potential
It manages to show off the capabilities of the WiiU's controller well enough to make you wonder how developers are going to utilize it. In a group setting, this game is a lot of fun.The bad:
The lack of online play is a missed opportunity. Most of the single player games are passable if not a bit lacking, and one of them is pretty much broken. So really, it's only fun with a group of people. Hope your friends have Wiimotion Plus Wiimotes... Oh, and there are some calibration issues here and there.Summary:
Released in 2012 by Nintendo, Nintendo Land is a collection of mini games that, in some way, shape or form, utilizes the features on the game pad. Whether it's motion control, the touch screen or the fact that games on the WiiU can also be viewed on said touch screen, every feature gets a chance to demonstrate themselves. So as a tech demo, it's actually not too bad, but unfortunately, I'm not reviewing it just as that - I'm also reviewing it on the merits of being a retail game. You know, a game you buy in a store, not a game that's packaged with the console! On those merits, Nintendo Land is decent and even a lot of fun under the right circumstances, but more often than not, it's just that game you play for about an hour or so before you go and do something else, like mow the lawn, head out to the beach or play a better game.
Nintendo Land has 12 attractions, which are grouped into three categories - Competitive, Team and Solo. To start this on a weaker note, the Solo attractions are pretty lackluster and only really serve to show what kind of potential the WiiU has. This is no more evident than in Octopus Dance. The idea is to either move the analogue sticks, tilt the controller or shake it when the onscreen dance instructor prompts you to do so. He'll show you the moves first, and then you'll need to do them in time with him and the music. Now, where this attraction loses me is when it expects you to use the motion controls. See, the controller can't seem to properly recognize whether you're tilting or shaking it if you tilt it quickly, which is what you're inevitably going to do because you'd want to keep up with the beat. As a result, when it asks you to tilt it and it inevitably recognizes it as shaking, you're going up a choppy river without a lifeboat. Because of this, Octopus Dance is easily the worst attraction.
There are two more that utilize motion control – Donkey Kong's Crash Course, and Captain Falcon's Twister Race. Donkey Kong's Crash Course involves you moving a trolley from Point A to Point B by tilting the controller. This reminds me of Super Monkey Ball where you have to tilt the level so that you can move the ball around, but oh man, I don't remember that game going from manageable to a whole heap of bullshit within the first ten seconds! You'll eventually find a segment where you'll lose a lot of lives until you realize "I need to go this quickly and tilt the controller at that exact moment". The calibration is fine on this one; at least the course tilts with your controller, the shoulder buttons at least manage to activate the movable platforms and you can at least blow on the microphone to activate the fans. It's just how much you're willing to tolerate constant failure due to minute speeding errors.
As for Captain Falcon's Twister Race, you're racing through twelve increasing difficult parts of a long race track, dodging obstacles along the way. For a while, this was my favorite because while I had to turn the controller around like a steering wheel, there was plenty of fun to be had in swerving around tight corners like Captain Falcon. But then I notice some calibration issues after making some particularly tight turns... and when I hold it straightly, I'm turning a bit in the opposite direction! Ouch! There are some methods like pressing up or down on the D-pad, and a lot of it is due to wildly turning it to get around those sharper corners, but with all that's said and done, it's all a natural response to these kinds of situations and, unless you're willing to constantly recalibrate during downtime, it's an outright pain in the ass. Doesn't help that you're on a time limit – if it hits zero (or if you blow up by crashing into an explosive), it's game over and you have to start again. Imagine if it's all because of calibration issues! So a favorite stops being a favorite because of an oversight on Nintendo's part. Double ouch.
The other three Solo attractions make use of the touch screen, rather than motion control. For instance, Takamaru's Ninja Castle (remember Takamaru? No? Well, he's from some Japanese-only game called Nazo no Murasame Jo) has you throwing ninja stars by stroking the screen either quickly for a quick throw, or slowly for a slower, lower throw. The idea is to take out all of the ninjas before they manage to hit you three times. This one is actually a lot of fun as it gets more frantic with more ninjas to take down and they're not afraid to take you down either. If you're willing to get used to the flick controls, this game will be a potential favorite for when you just want to kill a few minutes.
Then there's Yoshi's Fruit Cart, where you'll need to draw a path for Yoshi to follow, gathering up the fruit in the order shown on screen... the TV screen, that is, without falling down any holes. The touch screen won't show crap, so you'll need to use the TV screen to make reference points. Early on, it's easy enough, but later on, it becomes a bit trickier as you absolutely have to get the numbered fruit in numeric order, without falling into holes AND while making it to the door at the end. There aren't any technical issues as it follows the path you've drawn finely and whatever fruit you miss is entirely your fault – don't be such a sloppy drawer – and it can be refreshingly addicting if you're a sucker for puzzle games, and hey, if they added some sexually explicit anime characters, they can pitch it to Atlus as their newest hentai dating sim!
Okay, teasing aside, there is one last Solo attraction, and that's Balloon Trip Breeze. You use the touch screen as a means of creating a small breeze of wind for your balloon fighter to fly by. Said touch screen gives you a zoomed in view of the action while the TV screen is zoomed out. This one's alright, but having to constantly switch between the touch screen and the TV screen is a bit of a pain, and there isn't much to really keep your interest. The touch controls are fine, but the physics are a bit stiff and it's a bit too easy to die because of one slightly misdirected breeze, but maybe it's just because it's a bit too dull that I can notice something like that before moving onto a different attraction.
Better yet, it might entice you to bring over friends to try out the Competitive attractions! These ones can only be done with 2-5 players, so hope that said four people brought over their Wiimotion Plus Wiimotes... because that's the only Wiimote the WiiU will accept and there's no option for classic controller usage. Let's start with Mario Chase. The idea is that the person using the WiiU controller, playing as Mario, runs away from the people or "Toads" using the Wiimotes. Now, this sounds like a great idea for a simple, fun competitive game – have the rowdy Toads drunkenly bumble about trying to find Mario while he does his best impression of Sam Fisher by staying in hiding. The execution is hit and miss. For one thing, if you have less than five players, their Toads will be replaced by robotic Yoshis with... random AI, so to speak. Sometimes, they're relentless in their pursuit; at other times, they're complete idiots who couldn't catch a cold. Unless you're all rowdy and/or the TV is turned down reasonably low, the robotic Nintendo Land guide Monita will tell the others where Mario happens to be. Given that the best Mario has at his disposal is a star that appears after a while to make him run faster, this is unfair.
Luigi's Ghost Mansion is the opposite – the idea is for the person with the WiiU controller to frighten the torch wielding Wiimote using Luigis while said Luigis shine a light on the ghost to capture it. Where it's Mario Chase's opposite is in the fact that human players are a necessity in order to capture the ghost because the Monitas that replace the Luigis are more braindead than Patrick from Spongebob Squarepants. Theoretically, they're meant to spin around when they find a ghost, but they seem to spin around because... why not? The only real advantage that humans have is that they can revive Luigis that... crapped their pants in such fear that they can't move anymore. Overall, you absolutely need plenty of human players to actually have any fun with this, particularly a rowdy group of friends.
Oh wait, there is one more Competitive attraction that I forgot to mention, and that's Animal Crossing: Sweet Day. The idea is that the animals, controlled by the Wiimotes, have to collect the candy and drop them off at score zones while the guards, controlled by the WiiU controller, have to capture said animals three times while protecting said score zones. Keep in mind that the more candy the animals have, the slower that they go, so keep an eye out for any that are taking on more than they can handle... if you can. See, if you're controlling the guards, you may go a bit cross eyed as you're controlling two at the same time using both analogue sticks. If you've noticed a pattern, it's that all of these Competitive attractions are a glorified form of tag. Not that it's a bad thing or anything, it's just something I thought was amusing enough to point out.
Which leads us to the Team attractions, which are most definitely the highlight of the game. These, you can either play on your own or with a group of friends, but either way, they're vasty superior to the other two types of attractions. First up is The Legend Of Zelda: Battle Quest. In this one, the person with the WiiU controller uses a bow and arrow while everyone with Wiimotes uses a sword each. For the WiiU controller, you tilt it in the direction that you want to aim, and then hold down the left or right analogue stick to charge a shot before letting go to fire, and reloading is as simple as tilting it down pretty low. For Wiimote users, you swing the Wiimote around and the sword will swing with you. Holding it up will charge up your next strike. The quest is on rails though, meaning that you can't move at your own pace, so pay attention for enemies that charge towards you and above all else, back each other up! If anybody dies, it's game over! But honestly, this is so much fun to go through – taking down enemies, especially big bosses, always feels so satisfying, especially amongst company that helps you out, but even on your own with just your bow and arrows, there's always plenty to shoot and some strategy that's necessary to ensure that you survive long enough to get the Triforce. Thankfully, it's split into stages and they aren't all that long, but not to worry, as they get progressively harder, forcing you to prioritize and aim better.
Next up is Pikmin Adventure, which... well, it's fun if you're using the WiiU controller as you get to control Captain Olimar, master of all Pikmin that he plucks out of the ground. I'd hate to be the one using a Wiimote in this game – Wiimote users control one of the Pikmin. Granted, these will have more room to do what they need to in order to progress than those ordered by Olimar, but not by much. Sure, they're bigger, but other than that, they're as much Olimar's slaves as the smaller Pikmin. There wasn't much thought put into this one as far as a Team attaction goes. It feels more like a Solo attraction and when you play it by yourself, it definitely feels more natural. But anyway, the idea is to get the Pikmin to destroy obstacles and kill enemies in order to get to the boss at the end, defeat it and move on to the next stage. It's still fun to go through, but more on your own than with friends.
Finally, there's Metroid Blast, my absolute favorite attraction in the entire game and one that'll most definitely be yours too! The person using the WiiU controller will control a gunship, using the analogue sticks to move around, motion controls to aim and buttons to fire. Now, this will feel unwieldy for a while, but once it clicks, it sticks, and when it sticks, this attraction will be so much fun that you wouldn't believe it! There are plenty of enemies to shoot down in this attraction – at first, the most that they'll do is nonchelantly float towards you, but eventually, you'll get ones that shoot at you and will put up quite a fight. Thankfully, the Team part of this attraction is fairly balanced like the Zelda attraction. The Wiimote users will be on the ground, backing you up... I would hope so, anyway. The only problem is that some of the later levels' designs favor the gunship as there's some convoluted navigation for the ground troops. Bit of a shame that there has to be at least one problem beyond the learning curve for the gunship's controls. But yeah, once things get rolling, they most certainly get rolling and unless you have a full force, it becomes an intense festival of staying alive against impossible odds, like a battle in one of the Lord Of The Rings movies... only with laser beams instead of swords and arrows.
I would talk about Nintendo Land itself, but all it is, is just a means of getting into the attractions in an easy to navigate manner, maybe with some prizes that tell you fun facts about various Nintendo franchises. There would be something to say if there was online multiplayer... then you could set up rooms to play the multiplayer attractions with people from across the world. But alas, that'd go against what Nintendo had set out to do with this game, which is to test out the capabilities of the WiiU's controller and see how well Wiitmotes work on the console. Oh well, I mean, I'd love to play the Competitive attractions with people online because it could make things even more rowdy, or maybe there'd be some people willing to work with me while I play the Team attractions! Not everybody is in a position to get together four of their real life friends for some video games – this is why online multiplayer was invented in the first place!
Nintendo Land looks pretty good. The most that it shows off about the WiiU's graphical capabilities is that at least it looks crispy and sharp, not at all low quality. The visuals themselves are cartoony with plenty of colors to keep your eyes on the prize, although a lot of the character modelss do appear to have a coat of wax smeared all over them. Not that it hurts the game in any way nor is it all that distracting, but when Monita the robot appears more human than the supposedly human characters, it's just a bit weird to me. I have noticed some issues with objects popping up as you walk near them in the main park, but unless you want some fun facts, it's not even noteworthy since you'd hardly be in the main park anyway – not much if anything suddenly pops up in the games. So while it doesn't make you go "WOW check out these phat graphics on this spiffy new HD console", it at least shows that the WiiU has the potential for high definition graphics.
The sound design is nothing to write home about. A lot of the songs are chippy and upbeat to get you into the fun of playing a bunch of carnival games, but unfortunately, none of these songs are memorable in the slightest. They just sound like generic uptempo songs that do little to stand out or even get you all that chipper. It's almost like listening to feel good elevator music, it's that bland and forgettable. The sound effects aren't much better – they're either 8-bit sound effects to try and niggle at your nostalgia bone, or they just sound like what they ought to. Monita's voice is the only thing that works. It's robotic, yet her voice is strangely welcoming, which is what a tour guide ought to be.
Something that I've stated throughout the review is "it at least shows *insert feature here*'s potential", and that's all Nintendo Land really is. It's a platform on which they can experiment with what the WiiU has to offer. They did do this with Wii Sports on the Wii and Sega did this with Altered Beast, but the reason I'm stressing this with Nintendo Land is because it's more blatant about it than those games. Outside of the Zelda and Metroid attractions and maybe the Takamaru's Ninja Castle attraction, nothing really stands out as more than adequate on their own terms, relying more on human interaction than the actual playing of the game to hide underdeveloped designs and blatant tech demo-isms. Perhaps I am unfairly criticising a game that comes packaged with a console, but at the same time, that's the only condition on which this game is ever anywhere near your collection – because it came with your console! There's no real reason to have this game otherwise because only a few attractions are worth playing as games rather than just as a social activity!
Gameplay - 6/10 – A lot of the attractions feel somewhat underdeveloped, like they really wanted to make games that just tested how everything worked. There are some that are legitimately fun to play through, but others are just time killers. It's not worth rating it highly just because of two very good attractions when the other ten were a mixed bag.
Controls - 3.5/5 – There are some calibration issues to be found in a few attractions – whether it doesn't straighten out completely or recognize the difference between quick tilts and shaking, there's definitely some room for improvement. The normal controls work finely as you can move with them just finely, it's the motion controls that need some work.
Graphics – 4/5 – Everything looks fine as they're crispy enough, although pop up is a bit weak.
Sound – 2.5/5 – Bland and unmemorable. Remembering a single track takes a lot more brainpower than I'm willing to expel. At least Monita sounds like what you'd expect and sounds good doing so.
Overall - 6/10 – As a tech demo, it somewhat succinctly demonstrates what the WiiU can do; as a game, it's alright, but unless you absolutely need a time killer to play with friends, I'd advise on skipping this one and going straight to Mario.
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Sign up
We're looking for enthusiastic individuals from all across the UK who are keen to create change where they live. If you need some inspiration to make it happen, come on a journey with us.
Sign up to apply for a place on the programme and for the opportunity to come on one of our residential camps at the Eden Project.
Inspirational events
We're giving people the chance to take part in a series of events – to help you meet others, boost your creative thinking, and pick up some of the skills to start making a difference where you live.
Hosted at the Eden Project, Cornwall, and across the UK, these are your introduction to a fantastic group of people, chosen from around the country, who are looking to do similar things as you in their own neighbourhood.
Participants have told us that the overwhelming take-away for them was 'a feeling of not being alone' (the number one impact for 48% of them), as well as 'motivation' (25%) and 'new ideas' (20%).
Support from others
Our regional roadshows and residential 'camps' at the Eden Project, as we call them, are just one part of the journey. When you return to your community, we'll stay in touch so that we can hear how your initiatives are progressing and can help you maintain momentum.
We'll also invite you to other relevant, regional events, point you in the direction of useful resources for your projects – and help you keep in contact with other participants through our online forum.
It was great to meet up with so many inspiring community volunteers.
Is Big Lunch Extras for you?
Learn a bit more about what's involved before you sign up. We think we've got most of your questions answered here, but if you've got any more or would like to have a quick chat, just contact us.
- Who is Big Lunch Extras for?
- Big Lunch Extras is for individuals in the UK wishing to start a community initiative or take existing projects to the next level. When you apply to join the programme, we ask you to tell us a bit about yourself so we can make sure it's right for you.
It's not designed for professionals working within the sector, but we're always interested in hearing about potential speakers at our events!
If you are interested in attending one of our Community camps, you must apply during the 'applications open' period. Selection is at the discretion of The Big Lunch Programme team, and is based on an individual's suitability for each event. You may only attend a Community camp once. We will not accept repeat applications. All personal belongings brought to the camps are the responsibility of the individual attending. The Big Lunch Programme or the Eden Project cannot accept responsibility for lost or stolen belongings.
You don't need to have taken part in or held a Big Lunch before to join the Big Lunch Extras.
- What happens throughout the programme?
- As well as coming along to our events to make them a great success, you'll be able to:
- keep in touch with us about the progress you're making on your community initiatives
- join our online forum where you can swap advice on community issues with other Big Lunch Extras partcipants and people across the UK who are in the same boat
- What would I learn on an event?
- Each of our events is unique, but we have designed the series to always include a range of practical activities, facilitated sessions and networking opportunities which help you increase your knowledge of a certain area (for example, funding or social media), offer you practical ideas to engage people where you live (such as outdoor play or community art), and give you the chance to talk to people who are in the same boat as you (fellow participants from around the UK).
- Where do the events take place?
- Big Lunch Extras camps take place at the Eden Project in Cornwall, the educational charity behind the project, which offers a fantastic place to learn. Each participant will have the opportunity to deepen their involvement with the programme through an event at the Eden Project. You may also be invited to our regional roadshows across the UK, where you can network with others in your area.
- How long are the events?
- A typical Big Lunch Extras event takes place across a long weekend (from a Friday evening until a Monday morning) and our regional roadshows are either one or two days.
- Can more than one person take part from the same community?
- We know it's great to have an ally when you go back to where you live, to help spread the word about what you've learnt. We are happy to welcome two members from the same community to apply to take part in the programme – but we want as many communities to benefit from the programme as possible, so we hope you'll understand if we can't always offer this.
- When are the events?
- We run Big Lunch Extras events regularly. You can see a full list on our Events page.
- How much does it cost to take part?
- Thanks to the Big Lottery Fund, nothing! The events themselves are free to attend. For camps at the Eden Project, participants' travel and food is also included throughout the event – as well as accommodation for those who need it.
- Where do people stay?
- During events at the Eden Project, our team arranges free accommodation onsite or in a nearby hotel for participants who are unable to travel to the venue from home each day.
- How would I get there?
- For events at the Eden Project, our team can arrange your travel to the venue – or reimburse your travel costs if we agree it with you beforehand. We are also able to cover transport costs to regional events, agreed beforehand.
- Would I get a qualification?
- We aren't offering a formal qualification to participants, but we know you'll pick up all sorts of useful skills from taking part.
- Can you help me deliver my community project?
- Our aim is to try to give you the ideas, confidence, motivation, skills, tools and contacts to make good things happen where you live. Our events, online forum and web resources are all there to help you. We unfortunately can't get involved in delivering, endorsing, publicising or funding your project or event.
I'm completely inspired and motivated to get on and make my project work!
How to join in
If you think Big Lunch Extras sounds like your cup of tea, you can get involved by following these two steps:
- Create an account – this gives you access to the Community Chat area to talk to others online, allows you to apply to get a funded place on our programme, and adds you to our newsletter mailing list.
N.B. If you're on The Big Lunch mailing list you'll already have an account with us; you just need to activate it. You simply need to request a new password. You'll then receive an email with instructions on how to set up a password for yourself. You can use this account to complete step two, below. By activating your account you will be accepting Big Lunch Extras' terms and conditions.
- Apply to join the Big Lunch Extras programme – you'll be asked to complete a simple form to help us to ensure the programme is right for you, and to check that you're eligible for a funded place. If you're accepted on to the programme (you'll hear back by email within a few days) you will then be able to book a specific event to attend.
- If you are accepted onto the programme, apply to attend an inspirational event. Logged in, you'll be able to see a form on each event page, which you should complete with practical details.


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Only two community members showed up yesterday at a Toledo Board of Community Relations hearing aimed at helping a North Toledo neighborhood heal after a melee Oct. 15.
The other 14 people at the session at the West Toledo branch of the Toledo-Lucas County Public Library were BCR members and city employees.
"I just think [people in the community] have had enough of this issue. Now they want to heal," said Juanita Greene, BCR executive director.
"We put 250 flyers out. We put out press releases. But only two people not associated with the board came."
Ms. Greene said she would continue holding the sessions, because "even if just one person comes in, that's one person we can help."
Both community members at the public hearing had insights to share about what they view as necessary to prevent such outbreaks of violence.
Craig Wescoe, 22, a University of Toledo graduate student, said police need to sit down with representatives of community youth to "get past some biases that [police] may have."
Mitch Balonek, an English teacher at Scott High School, agreed that bias is an issue, and said police need additional multicultural diversity training.
"[But] until we address the bigger issues, we can micromanage all we want without achieving much," Mr. Balonek said.
The issues are not only the lack of jobs for youth, but the need for recreational and educational programs for them, he said.
A date for the next session has not been set.


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Vermont to Participate in Second National Take-Back Day
For Immediate Release: October 7, 2011
Media Contact: Communication Office
Vermont Department of Health
BURLINGTON – Expired, unwanted or unused prescription drugs can be dropped off for proper disposal at collection sites throughout Vermont on Saturday, Oct. 29, 10 a.m. to 2 p.m. as part of the U.S. Drug Enforcement Administration's second National Prescription Drug Take-Back Day.
The Burlington Police Department on North Avenue, the Price Chopper parking lot on Shelburne Road in Burlington, the Colchester Police Department, and the University Mall parking lot in South Burlington are the four collection sites in Chittenden County. Sites will be set up throughout the state. Forty sites were set up in 2010 in all 14 counties in Vermont.
Prescription drug abuse is a vital public safety and public health issue. The one-day effort will bring national focus to the issue of prescription drug abuse. The service is free and anonymous.
"Drug diversion, when a person gets narcotics from their families', friends' or neighbors' medicine chests, is more common than most people think," said Barbara Cimaglio, deputy commissioner of the Health Department's Alcohol & Drug Abuse Programs. "We have to continually educate people on safe storage and disposal of prescription drugs."
Last September, more than 242,000 pounds — 121 tons — of prescription drugs were collected for disposal at nearly 4,100 sites nationwide operated by approximately 3,000 of the DEA's state and local law enforcement partners.
To find the nearest disposal site in your area visit http://www.justice.gov/dea/index.htm.
Follow the Health Department on Twitter and join us on Facebook for up-to-date news, alerts and health information.
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