Psychological processes in chronic embitterment: The potential contribution of rumination.

OBJECTIVE: Chronic embitterment has received considerable attention in terms of its presentation and epidemiology, but there has been relatively little focus on its psychology. The present study aimed to test the hypothesis that embitterment is positively correlated with rumination, and that this effect is influenced by positive beliefs about rumination. METHOD: A convenience sample (N = 79) of staff of a health care facility attending its occupational health service completed questionnaires assessing chronic embitterment, work-related rumination (distinguishing affective rumination and problem solving pondering), positive beliefs about rumination, and depression. RESULTS: Embitterment scores correlated positively with affective rumination and depression. Positive beliefs about rumination correlated positively with problem-solving pondering but not with affective rumination. Regression analysis revealed that affective rumination contributed to embitterment independently of depression. CONCLUSIONS: Previous research has demonstrated that rumination impairs executive functions and problem-solving. The association of affective rumination with embitterment may contribute to the explanation for why embitterment becomes chronic and is often difficult to alleviate. However, this association also opens up possibilities of intervention, in light of research evidence of the effectiveness of rumination-focused therapies. (PsycINFO Database Record

Is there information contained within the sentence-writing component of the mini mental state examination? A retrospective study of community dwelling older people.

OBJECTIVE: To investigate the relationship between features of the MMSE written sentence and cognitive function, depression and disability. METHODS: MMSE sentences from 191 community dwelling individuals without dementia from the Lothian Birth Cohort 1921 (LBC1921) study were: (a) photocopied and (b) typed as written. Sentences were rated for objective criteria: word number and frequency, first person usage, time orientation, and letter case. Twenty healthy raters (50% male, age 20-26 years), blind to all other data, rated each handwritten and typed sentence for subjective criteria: legibility, 'emotional' tone (positive to negative), estimated age, health, and intelligence. As part of the LBC1921 volunteers had results available for cognitive ability tests (from which we extracted a general cognitive ability factor, g), Hospital Anxiety and Depression Score (HADS), and Townsend disability scores. RESULTS: 43.5% of subjects were male, mean age 78.6, SD 0.43 years. There was no significant association between the objective sentence criteria, legibility or tone and measured cognitive ability or physical disability. However, estimates of intelligence from the MMSE written sentence correlated significantly with current cognitive ability (r = 0.29, p < 0.001). There was a trend towards sentences with a negative tone being associated with a higher HADS-depression score (rho = -0.12, p = 0.09). CONCLUSION: In community dwelling people aged around 80 years, despite no association between objectively rated features of the MMSE sentence and intelligence or disability, raters were able to make better-than-chance estimates of subjects' intelligence test scores.

Expression of doublecortin (DCX) and doublecortin-like kinase (DCLK) within the developing chick brain.

Doublecortin (DCX) is a microtubule-associated protein widely expressed in the developing mammalian nervous system and important for neuronal migration. DCX is known to belong to a novel protein family defined by sequence homology and the presence of a conserved microtubule-binding domain, but the functions of other members of this family are still undefined. In this study, we describe the cloning of the chick ortholog of doublecortin-like kinase (DCLK), a member of this family, and assess the expression of DCX and DCLK in the layered regions of the developing chick brain. DCX and DCLK are widely expressed in pallial and subpallial structures, including the telencephalon, optic tectum, and cerebellum, in similar distribution patterns. In addition to their expression in migrating cells, both proteins were also detected in the ventricular zone and in postmigratory Purkinje cells. Finally, DCX and DCLK were found to be coexpressed in all areas examined. In postmigratory Purkinje cells, DCX and DCLK both colocalized to the cell membrane, although DCLK was also distributed more generally throughout the cell soma. These data are consistent with multiple roles for DCX and DCLK in the developing chicken brain and suggest that the chick cerebellum will be an intriguing system to explore the effects of DCX and DCLK on postmigratory neuronal function.

Multisite phosphorylation of doublecortin by cyclin-dependent kinase 5.

Doublecortin (DCX) is a 40 kDa microtubule-associated protein required for normal neural migration and cortical layering during development. Mutations in the human DCX gene cause a disruption of cortical neuronal migration. Defects in cdk5 (cyclin-dependent kinase 5) also cause defects in neural migration and cortical layering. DCX is a substrate for cdk5 in vitro and in vivo and the major site of in vitro phosphorylation is Ser-297. We used a highly developed MS strategy to identify the cdk5 phosphorylation sites and determine the major and minor sites. Several phosphopeptides were identified from a tryptic digest of 32P-labelled, cdk5-phosphorylated DCX using a combination of off-line HPLC and matrix-assisted laser-desorption ionization-MS with alkaline phosphatase treatment. Tandem MS/MS enabled the identification of seven phosphorylation sites for cdk5. Monitoring of 32P label indicated that there was one major site, Ser-28, at the N-terminus, and a major site, Ser-339, in the serine/proline-rich domain at the C-terminus. Five other sites, Ser-287, Thr-289, Ser-297, Thr-326 and Ser-332, were also found in the tail. Site-directed mutagenesis largely supported these findings. Single mutation of Ser-28 reduced but did not abolish phosphorylation. Double, rather than single, mutation for Ser-332 and Ser-339 was required to reduce overall phosphorylation, suggesting an interaction between these sites. Truncations of the tail produced a significant reduction in cdk5 phosphorylation of DCX. These results do not support Ser-297 as the major cdk5 phosphorylation site in DCX, but indicate that DCX is subject to complex multisite phosphorylation. This illustrates the importance of a well-developed MS strategy to identify phosphorylation sites.