Ordering our world: the quest for traces of temporal organization in autobiographical memory

An experiment examined the idea, derived from the Self Memory System model (Conway & Pleydell-Pearce, 2000), that autobiographical events are sometimes tagged in memory with labels reflecting the life era in which an event occurred. The presence of such labels should affect the ease of judgments of the order in which life events occurred. Accordingly, 39 participants judged the order of two autobiographical events. Latency data consistently showed that between-era judgments were faster than within-era judgments, when the eras were defined in terms of either: (a) college versus high school, (b) academic quarter within year, or (c) academic year within school. The accuracy data similarly supported the presence of a between-era judgment effect for the college versus high school dichotomy

Mnemic neglect : selective amnesia of one's faults

The mnemic neglect model predicts and accounts for selective memory for social feedback as a function of various feedback properties. At the heart of the model is the mnemic neglect effect (MNE), defined as inferior recall for self-threatening feedback compared to other kinds of feedback. The effect emerges both in mundane realism settings and in minimal feedback settings. The effect is presumed to occur in the service of self-protection motivation. Mnemic neglect is pronounced when the feedback poses high levels of self-threat (i.e., can detect accurately one’s weakness), but is lost when self-threat is averted via a self-affirmation manipulation. Mnemic neglect is caused by selfthreatening feedback being processed shallowly and in ways that separate it from stored (positive) self-knowledge. For example, mnemic neglect is lost when feedback processing occurs under cognitive load. The emergence of mnemic neglect is qualified by situational moderators (extent to which one considers their self-conceptions modifiable, receives feedback from a close source, or is primed with improvement-related constructs) and individual differences moderators (anxiety, dysphoria, or defensive pessimism). Finally, the MNE is present in recall, but absent in recognition. Output interference cannot explain this disparity in results, but an inhibitory repression account (e.g., experiential avoidance) can: Repressors show enhanced mnemic neglect. The findings advance research on memory, motivation, and the self

The waxing and waning of mnemic neglect.

The mechanisms underlying mnemic neglect (MN) and the conditions under which it waxes and wanes are not yet fully understood. The research in this article examined conditions during both encoding and recall that could potentially moderate the MN effect and that could provide cues about the cognitive mechanisms that contribute to the effect. Results showed that MN: (a) emerged after recall was delayed (Study 1); (b) could not be attributed to differential behavior looking time (Study 2); (c) did not emerge under cognitive load (Study 3); and (d) was not linked to the perceived extremity, importance, or evaluations of the behaviors. However, how informative the behaviors were perceived for personality may contribute to the effect (Study 4). Finally, results from Study 3 and Study 4 showed that when participants were cognitively occupied during encoding, the MN effect waned. Implications of these collective findings for the MN phenomenon were discussed

Mnemic Neglect for Behaviors Enacted by Members of One’s Nationality Group

People exhibit impaired recall for highly self-threatening information that describes them, a phenomenon called the mnemic neglect effect (MNE). We hypothesized that the MNE extends to recall for information that highly threatens an individual’s important ingroup identity. We tested our hypothesis in two experiments in which participants read behaviors depicted as enacted by either ingroup members (Experiment 1 = American; Experiment 2 = British) or outgroup members (Andorrans). Participants recalled identity-threatening behaviors poorly when enacted by ingroup members, but not when enacted by outgroup members. Additional results evinced ingroup favoritism in: (1) evaluations of the two groups, and (2) trait judgments made from the behaviors, but only on traits central to the self. Finally, mediational analyses suggested that the group-driven memory differences are plausibly due to the global between-group evaluation differences, but not the perceived between-group trait judgment differences

1968

Maintenance of Golf Carts by Thomas Pepe (page 1) Why a Golf Course Superintendent Should Play Golf by Stephen Skowronski (2) Tree Pruning by Martin Walsh (3) Golf Course Labor: A Dilemma by Robert Barber (5) Turf Problems by Alexander M. Radko (A-1) 1967 Turfgrass Problems by Lee Record (A-3) Southern Turfgrass Production and Problems by Ralph W. White Jr. (A-5) Canadian Turf Grass Production and Problems by David Moote (A-8) Turf Research Abroad by C.R. Skogley (A-13) Turf Research at Home by Victor B. Younger (A-14) Turfgrass Research - An Industrial Approach by J. A. Simmons (A-16) Cutting Labor Costs in Turfgrass Managemnt by Tom Mascaro (A-24) The Reluctant human by John W. Denison (A-28) The Problem Drinker - Management Responsibility by G.E. Osburn (A-31) Contemporary Design Standards by Geoffrey S. Cornish (A-34) Construction - Superintendents\u27 Viewpoint by Robert E. Grant (A-36) Construction b Contract and the Role of the Superintendent by David Canavan (A-39) Seed Production by Robert J. Peterson (A-41) Cemetery Turf Maintenance on a High and Low Budget by Stanley Sosenski (A-45) Ten Steps to a Good Lawn by John Zak (A-49) Review of Herbicides for Turf Weed Control by Alvin A. Baber (A-53

Influenza activity in Europe during eight seasons (1999–2007): an evaluation of the indicators used to measure activity and an assessment of the timing, length and course of peak activity (spread) across Europe

<p>Abstract</p> <p>Background</p> <p>The European Influenza Surveillance Scheme (EISS) has collected clinical and virological data on influenza since 1996 in an increasing number of countries. The EISS dataset was used to characterise important epidemiological features of influenza activity in Europe during eight winters (1999–2007). The following questions were addressed: 1) are the sentinel clinical reports a good measure of influenza activity? 2) how long is a typical influenza season in Europe? 3) is there a west-east and/or south-north course of peak activity ('spread') of influenza in Europe?</p> <p>Methods</p> <p>Influenza activity was measured by collecting data from sentinel general practitioners (GPs) and reports by national reference laboratories. The sentinel reports were first evaluated by comparing them to the laboratory reports and were then used to assess the timing and spread of influenza activity across Europe during eight seasons.</p> <p>Results</p> <p>We found a good match between the clinical sentinel data and laboratory reports of influenza collected by sentinel physicians (overall match of 72% for +/- 1 week difference). We also found a moderate to good match between the clinical sentinel data and laboratory reports of influenza from non-sentinel sources (overall match of 60% for +/- 1 week). There were no statistically significant differences between countries using ILI (influenza-like illness) or ARI (acute respiratory disease) as case definition. When looking at the peak-weeks of clinical activity, the average length of an influenza season in Europe was 15.6 weeks (median 15 weeks; range 12–19 weeks). Plotting the peak weeks of clinical influenza activity reported by sentinel GPs against the longitude or latitude of each country indicated that there was a west-east spread of peak activity (spread) of influenza across Europe in four winters (2001–2002, 2002–2003, 2003–2004 and 2004–2005) and a south-north spread in three winters (2001–2002, 2004–2005 and 2006–2007).</p> <p>Conclusion</p> <p>We found that: 1) the clinical data reported by sentinel physicians is a valid indicator of influenza activity; 2) the length of influenza activity across the whole of Europe was surprisingly long, ranging from 12–19 weeks; 3) in 4 out of the 8 seasons, there was a west-east spread of influenza, in 3 seasons a south-north spread; not associated with type of dominant virus in those seasons.</p

Development of β-globin gene correction in human hematopoietic stem cells as a potential durable treatment for sickle cell disease

Sickle cell disease (SCD) is the most common serious monogenic disease with 300,000 births annually worldwide. SCD is an autosomal recessive disease resulting from a single point mutation in codon six of the β-globin gene (HBB). Ex vivo β-globin gene correction in autologous patient-derived hematopoietic stem and progenitor cells (HSPCs) may potentially provide a curative treatment for SCD. We previously developed a CRISPR-Cas9 gene targeting strategy that uses high-fidelity Cas9 precomplexed with chemically modified guide RNAs to induce recombinant adeno-associated virus serotype 6 (rAAV6)-mediated HBB gene correction of the SCD-causing mutation in HSPCs. Here, we demonstrate the preclinical feasibility, efficacy, and toxicology of HBB gene correction in plerixafor-mobilized CD34+ cells from healthy and SCD patient donors (gcHBB-SCD). We achieved up to 60% HBB allelic correction in clinical-scale gcHBB-SCD manufacturing. After transplant into immunodeficient NSG mice, 20% gene correction was achieved with multilineage engraftment. The long-term safety, tumorigenicity, and toxicology study demonstrated no evidence of abnormal hematopoiesis, genotoxicity, or tumorigenicity from the engrafted gcHBB-SCD drug product. Together, these preclinical data support the safety, efficacy, and reproducibility of this gene correction strategy for initiation of a phase 1/2 clinical trial in patients with SCD

A Prospective Study of Plasma Vitamin D Metabolites, Vitamin D Receptor Polymorphisms, and Prostate Cancer

BACKGROUND: Vitamin D insufficiency is a common public health problem nationwide. Circulating 25-hydroxyvitamin D(3) (25[OH]D), the most commonly used index of vitamin D status, is converted to the active hormone 1,25 dihydroxyvitamin D(3) (1,25[OH](2)D), which, operating through the vitamin D receptor (VDR), inhibits in vitro cell proliferation, induces differentiation and apoptosis, and may protect against prostate cancer. Despite intriguing results from laboratory studies, previous epidemiological studies showed inconsistent associations of circulating levels of 25(OH)D, 1,25(OH)(2)D, and several VDR polymorphisms with prostate cancer risk. Few studies have explored the joint association of circulating vitamin D levels with VDR polymorphisms. METHODS AND FINDINGS: During 18 y of follow-up of 14,916 men initially free of diagnosed cancer, we identified 1,066 men with incident prostate cancer (including 496 with aggressive disease, defined as stage C or D, Gleason 7–10, metastatic, and fatal prostate cancer) and 1,618 cancer-free, age- and smoking-matched control participants in the Physicians' Health Study. We examined the associations of prediagnostic plasma levels of 25(OH)D and 1,25(OH)(2)D, individually and jointly, with total and aggressive disease, and explored whether relations between vitamin D metabolites and prostate cancer were modified by the functional VDR FokI polymorphism, using conditional logistic regression. Among these US physicians, the median plasma 25(OH)D levels were 25 ng/ml in the blood samples collected during the winter or spring and 32 ng/ml in samples collected during the summer or fall. Nearly 13% (summer/fall) to 36% (winter/spring) of the control participants were deficient in 25(OH)D (<20 ng/ml) and 51% (summer/fall) and 77% (winter/spring) had insufficient plasma 25(OH)D levels (<32 ng/ml). Plasma levels of 1,25(OH)(2)D did not vary by season. Men whose levels for both 25(OH)D and 1,25(OH)(2)D were below (versus above) the median had a significantly increased risk of aggressive prostate cancer (odds ratio [OR] = 2.1, 95% confidence interval [CI] 1.2–3.4), although the interaction between the two vitamin D metabolites was not statistically significant (p (interaction) = 0.23). We observed a significant interaction between circulating 25(OH)D levels and the VDR FokI genotype (p (interaction) < 0.05). Compared with those with plasma 25(OH)D levels above the median and with the FokI FF or Ff genotype, men who had low 25(OH)D levels and the less functional FokI ff genotype had increased risks of total (OR = 1.9, 95% CI 1.1–3.3) and aggressive prostate cancer (OR = 2.5, 95% CI 1.1–5.8). Among men with plasma 25(OH)D levels above the median, the ff genotype was no longer associated with risk. Conversely, among men with the ff genotype, high plasma 25(OH)D level (above versus below the median) was related to significant 60%∼70% lower risks of total and aggressive prostate cancer. CONCLUSIONS: Our data suggest that a large proportion of the US men had suboptimal vitamin D status (especially during the winter/spring season), and both 25(OH)D and 1,25(OH)(2)D may play an important role in preventing prostate cancer progression. Moreover, vitamin D status, measured by 25(OH)D in plasma, interacts with the VDR FokI polymorphism and modifies prostate cancer risk. Men with the less functional FokI ff genotype (14% in the European-descent population of this cohort) are more susceptible to this cancer in the presence of low 25(OH)D status