1,504 research outputs found
Understanding subjective memory complaints in ageing : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Psychology at Massey University, Wellington, New Zealand
Everyday memory difficulties are a common experience with age, and cause
considerable distress for many people when they are interpreted as potential indicators
of age-related disease. However, research literature examining the relationship between
these difficulties (known as subjective memory complaints; SMCs) and actual memory
performance on neuropsychological tests has shown mixed results, suggesting that
SMCs are not a pure reflection of memory ability, but instead that their aetiology is
complicated and not fully understood. Both psychological and methodological factors
are also implicated, although no research has yet comprehensively examined how a
combination of these factors might predict SMCs.
The current research aimed to test a new aetiological model of SMCs that incorporated
a range of potential confounds. It was hypothesised that SMCs would be predicted by
measures of processing speed and executive functioning, and that this relationship
would be moderated by measures of anxiety and depression.
First, a meta-analysis and systematic review of existing research on the relationship
between subjective and objective memory was conducted as a platform to inform
subsequent analyses. Then, Study A addressed current variation in assessment methods
by describing differences in SMCs when assessed with both an open-ended measure and
a prescriptive questionnaire. Study B examined how these differences in subjective
reports related to objective memory performance. Finally, Study C tested the proposed
aetiological model of SMCs.
Study A showed that different measures of SMCs garnered non-overlapping reports.
SMCs gathered via the open-ended measure were fewer in number, but rated as more
distressing, than those endorsed on the questionnaire. Spontaneous reports appeared to
be more ecologically valid reflections of SMCs, although questionnaire assessments
were by their nature more robust to a “catch 22” situation whereby some endorsed
SMCs were not reported spontaneously (perhaps due to memory failures in themselves).
Study B found that neither method of assessing SMCs produced reports that were
significantly convergent with objective measures of memory functioning. Study C
found partial support for the hypothesised aetiological model. SMCs (as assessed by the
questionnaire) were inversely related to processing speed, but only when depressive
symptoms were relatively high. Collectively, results offer important insights into the
interaction of cognitive and psychological factors in explaining SMCs, and highlight the
previously undelineated context in which processing speed contributes to SMCs
Influence of peptidylarginine deiminase type 4 genotype and shared epitope on clinical characteristics and autoantibody profile of rheumatoid arthritis.
Background: Recent evidence suggests that distinction
of subsets of rheumatoid arthritis (RA) depending on anticyclic
citrullinated peptide antibody (anti-CCP) status may
be helpful in distinguishing distinct aetiopathologies and in
predicting the course of disease. HLA-DRB1 shared
epitope (SE) and peptidylarginine deiminase type 4
(PADI4) genotype, both of which have been implicated in
anti-CCP generation, are assumed to be associated with
RA.
Objectives: To elucidate whether PADI4 affects the
clinical characteristics of RA, and whether it would
modulate the effect of anti-CCPs on clinical course. The
combined effect of SE and PADI4 on autoantibody profile
was also analysed.
Methods: 373 patients with RA were studied. SE,
padi4_94C.T, rheumatoid factor, anti-CCPs and antinuclear
antibodies (ANAs) were determined. Disease
severity was characterised by cumulative therapy
intensity classified into ordinal categories (CTI-1 to CTI-3)
and by Steinbrocker score.
Results: CTI was significantly associated with disease
duration, erosive disease, disease activity score (DAS) 28
and anti-CCPs. The association of anti-CCPs with CTI was
considerably influenced by padi4_94C.T genotype (C/C:
ORadj=0.93, padj=0.92; C/T: ORadj=2.92,
padj=0.093; T/T: ORadj=15.3, padj=0.002). Carriage of
padi4_94T exhibited a significant trend towards higher
Steinbrocker scores in univariate and multivariate
analyses. An association of padi4_94C.T with ANAs
was observed, with noteworthy differences depending on
SE status (SE2: ORadj=6.20, padj,0.04; SE+:
ORadj=0.36, padj=0.02) and significant heterogeneity
between the two SE strata (p=0.006).
Conclusions: PADI4 genotype in combination with anti-
CCPs and SE modulates clinical and serological characteristics
of RA
Cells of the synovium in rheumatoid arthritis. Macrophages
The multitude and abundance of macrophage-derived mediators in rheumatoid arthritis and their paracrine/autocrine effects identify macrophages as local and systemic amplifiers of disease. Although uncovering the etiology of rheumatoid arthritis remains the ultimate means to silence the pathogenetic process, efforts in understanding how activated macrophages influence disease have led to optimization strategies to selectively target macrophages by agents tailored to specific features of macrophage activation. This approach has two advantages: (a) striking the cell population that mediates/amplifies most of the irreversible tissue destruction and (b) sparing other cells that have no (or only marginal) effects on joint damage
Kitasato Symposium 2009: New Prospects for Cytokine Inhibition
The Kitasato Symposium 2009: New Prospects for Cytokine Inhibition was held in Berlin, Germany from 7 to 9 May 2009. The key aims of this meeting were to bring together a group of front-line researchers and rheumatologists to evaluate the use of cytokine blockade and to examine the role of certain cytokines in the pathogenesis of rheumatoid arthritis and other autoimmune diseases. A keynote lecture delivered by Professor Jean-Michel Dayer provided an up-to-date overview of the interactions occurring between the immune system and acute phase proteins. Other speakers discussed the role of cytokines in rheumatoid arthritis, including their role in joint destruction, as well as their regulatory role upon T cells and B cells. The involvement of cytokines in other autoimmune diseases was also addressed
Persistent clinical efficacy and safety of anti-tumour necrosis factor \textgreeka therapy with infliximab in patients with ankylosing spondylitis over 5 years: evidence for different types of response
Background: There is insufficient evidence for the long-term efficacy and safety of anti-tumour necrosis factor therapy in patients with ankylosing spondylitis (AS). This is the first report on the treatment with infliximab over 5 years.Methods: As part of a multicentre randomised trial, 69 patients with active AS at baseline (BL) have been continuously treated with infliximab (5 mg/kg i.v. every 6 weeks)---except for a short discontinuation after 3 years (FU1). The primary outcome of this extension was remission according to the ASsessment in Ankylosing Spondylitis (ASAS) criteria at the end of year 5 of the study (FU2).Results: Of the 43 patients who completed year 3, 42 agreed to continue, 38 of which (90.5%) finished year 5 (55% of 69 initially). Partial clinical remission was achieved in 13 of 38 patients (34.2%) at FU1 and FU2. At FU2, the mean Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) was 2.5±1.9 (BL:6.4, FU1:2.5). BASDAI values <4 were seen in 79% of patients at both, FU1 and FU2. ASAS 20% and 40% responses were seen in 32 (84%) and 24 (63%) patients at FU2, respectively. Most patients classified as non-responders at FU2 were part-time responders, as all but one patient achieved an ASAS 20% response at least once within the last 2 years. Three types of responders were identified. No major side effects occurred during years 4 and 5 of infliximab therapy.Conclusions: Infliximab is safe and efficacious in AS patients over 5 years. The majority of the patients remained on treatment and had rather persistent levels of low disease activity. Different response types could be identified
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