2 results
Verbal Learning and Memory Enhancement Strategies in Schizophrenia: A Randomized, Controlled Investigation
- Matthew M. Kurtz, Christi L. Trask, Rachel Rosengard, Simone Hyman, Lisa Kremen, Shyle Mehta, Rachel Olfson, Sam Rispaud, Sofia Zaidman, Jimmy Choi
-
- Journal:
- Journal of the International Neuropsychological Society / Volume 23 / Issue 4 / April 2017
- Published online by Cambridge University Press:
- 13 March 2017, pp. 352-357
-
- Article
- Export citation
-
Objectives: Verbal episodic memory is a key domain of impairment in people with schizophrenia with close ties to a variety of aspects of functioning and therapeutic treatment response. A randomized, blinded trial of two mnemonic strategies for verbal episodic memory deficits for people with schizophrenia was conducted. Methods: Sixty-one people with schizophrenia were assigned to one of three experimental conditions: training in a mnemonic strategy that included both visualization and narrative structure (Story Method), a condition in which participants were trained to visualize words interacting with one another (Imagery), or a non-trained control condition in which participants received equivalent exposure to training word lists and other verbal memory assessments administered in the other two conditions, but without provision of any compensatory mnemonic strategy. Participants were assessed on improvements in recall of the word list used as part of training, as well as two, standardized verbal memory assessments which included stimuli not used as part of strategy training. Results: The Story Method produced improvements on a trained word list that generalized to a non-trained, prose memory task at a 1-week follow-up. In contrast, provision of a mnemonic strategy of simple visualization of words produced little improvement on word recall of trained words or on measures of generalization relative to the performance of participants in the control condition. Conclusions: These findings support the inclusion of enriched mnemonic strategies consisting of both visualization and narrative structure in sustained and comprehensive programs of CR for enhancement of verbal episodic memory in schizophrenia. (JINS, 2017, 23, 352–357)
12 - Complement receptors
- Edited by J. S. H. Gaston, University of Cambridge
-
- Book:
- Rheumatic Diseases
- Published online:
- 06 September 2009
- Print publication:
- 28 July 1999, pp 245-276
-
- Chapter
- Export citation
-
Summary
Complement receptor type 1
The primary function of complement receptor (CR) type 1 (CR1, CD35) is phagocytosis and clearance of immune complexes, which is mediated by its capacity to bind complement ligands C3b, iC3b, C4b and C1q and its capacity to inactivate the C3 and C5 convertases of the alternative and classical complement pathways through decay-accelerating and cofactor functions (Fearon, 1979; Iidia & Nussenzweig, 1981; Medof et al., 1982; Klickstein et al., 1997). CR1 is expressed primarily by haematopoietic cells, including erythrocytes, mononuclear phagocytes, eosinophils, B lymphocytes and T lymphocytes. It is also present on glomerular podocytes and follicular dendritic cells (Fearon, 1980; Wilson, Tedder & Fearon, 1983; Gelfand, Frank & Green, 1975; Kazatchkine et al., 1982; Reynes et al., 1985).
Structurally, CR1 is a type I transmembrane glycoprotein (Fig. 12.1). Four CR1 allotypes have been identified (Dykman et al., 1983a,b; 1985; Wong, Wilson & Fearon, 1983; Dykman, Hatch & Atkinson, 1984), with Mr under reducing/non-reducing conditions of ∼250 000/190 000 (A, F), 290 000/220 000 (B, S), 210 000/160 000 (C, F′) and >290 000/250 000 (D) (Wong & Fearon, 1987). All CR1 allotypes share the same transmembrane domain of 25 amino acid residues and a 43 residue cytoplasmic tail. All allotypes have extracytoplasmic domains composed entirely of structural motifs, referred to as short consensus repeats (SCR), or complement control protein (CCP) modules, arranged in tandem. The A(F) allotype comprises 2039 residues, including a 41 residue signal peptide and a 1930 residue extracellular domain composed entirely of 30 SCRs (Klickstein et al., 1988; Hourcade et al., 1988). The amino terminal 28 SCRs are arranged in four long homologous repeats (LHRs) (A–D) of seven SCRs each; two additional SCRs link LHR-D with a 25 residue transmembrane region and a 43 residue cytoplasmic domain (Klickstein et al., 1988).