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Biomedical subjects

Mike Jackson

Publications and source records attributed to Mike Jackson.

5 recordsLinked to original sources
PubMed2005

Tissue edema does not change gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T1 relaxation times of viable myocardium.

PURPOSE: To determine whether tissue edema changes gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T1 relaxation times of the viable myocardium. MATERIALS AND METHODS: A total of 16 isolated pig hearts were divided into four groups (N=4/group) and perfused in a Langendorff apparatus. Gd-DTPA was injected into the aortic perfusion line. Tissue edema was then induced by two hours of simultaneous arterial/venous perfusion (SAVP). Myocardial water content and T1 relaxation times were monitored throughout SAVP. The volumes of the extracellular and intracellular compartments were assessed using 31P MRS-detectable markers, phenylphosphonic acid (PPA) and dimethyl methylphosphonate (DMMP). RESULTS: Tissue water content in both viable and infarcted myocardium increased significantly during two-hour SAVP. However, Gd-DTPA-enhanced T1 relaxation times of the viable myocardium remained relatively unchanged. Infarcted myocardium, on the other hand, exhibited significant T1 shortening during SAVP. Furthermore, SAVP resulted in significant expansions of both extracellular and intracellular compartments, but the ratio of the volumes of the two compartments remained relatively constant. CONCLUSION: Tissue edema in the viable myocardium does not increase the relative distribution volume of the contrast agent. As a result, edema does not change Gd-DTPA-enhanced T1 relaxation times of the viable myocardium.

Analysis of Variance↗
PubMed2004

A giant novel gene undergoing extensive alternative splicing is severed by a Cornelia de Lange-associated translocation breakpoint at 3q26.3.

Cornelia de Lange syndrome (CdLS) is a rare developmental malformation syndrome characterised by mental handicap, growth retardation, distinctive facial features and limb reduction defects. The vast majority of CdLS cases are sporadic. We carried out a high density bacterial artificial chromosome (BAC) microarray comparative genome hybridisation screen but no evidence was found for a consistent pattern of microdeletion/microduplication. As an alternative, we focused on identifying chromosomal regions spanning associated translocation breakpoints. We prioritised the distal 3q region because of the occurrence, in a classical CdLS patient, of a de novo balanced translocation with a breakpoint at 3q26.3 and of reports of phenotypic overlap between cases of mild CdLS and individuals trisomic for the 3q26-q27 region. We show that the 3q26.3 breakpoint severs a previously uncharacterised giant gene, NAALADL2, containing at least 32 exons spanning 1.37 Mb. Northern blot analysis identified up to six different transcripts in the 1-10 kb range with strongest expression in kidney and placenta; embryonic expression was largely confined to duodenal and stomach endoderm, mesonephros, metanephros and pancreas. Transcript analysis identified extensive alternative splicing leading to multiple 5' and 3' untranslated regions and variable coding sequences. Multiple protein isoforms were defined by different N-terminal regions (with at least four alternative initiating methionine codons), and by differential protein truncation/use of alternative C-terminal sequences attributable to alternative splicing/polyadenylation. Outside the N-terminal regions, the predicted proteins showed significant homology to N-acetylated alpha-linked acidic dipeptidase and transferrin receptors. Mutation screening of NAALADL2 in a panel of CdLS patient DNA samples failed to identify patient-specific mutations. We discuss the possibility that the 3q26.3 translocation could nevertheless contribute to pathogenesis.

Alternative Splicing↗
PubMed2003

Quality of life in schizophrenia: a grounded theory approach.

BACKGROUND: Research into health related quality of life (HRQoL) in schizophrenia has predominantly been conducted using lengthy interviewer administered questionnaires, many of which have not been validated for use with schizophrenic samples. The present study seeks to address the dearth of qualitative research by conducting a small-scale qualitative exploration of the impact of schizophrenia on HRQoL. METHOD: The study was conducted using the qualitative approach of grounded theory. Six individuals with a diagnosis of schizophrenia participated (3 men, 3 women). Mean age of participants was 33.3 years (range 20-55), mean length of illness was 12 years (range 2-38 years) and average length of interviews was 47 minutes (range 20-70). RESULTS: Ten HRQoL domains were identified as being important: (1) barriers placed on relationships; (2) reduced control of behaviours and actions; (3) loss of opportunity to fulfil occupational roles; (4) financial constraints on activities and plans; (5) subjective experience of psychotic symptoms; (6) side effects and attitudes to medication; (7) psychological responses to living with schizophrenia; (8) labelling and attitudes from others; (9) concerns for the future and (10) positive outcomes from experiences. CONCLUSIONS: Domains identified by participants encompassed a wide range of factors that may be expected to contribute generally to engaging in a positive quality of life. Participants identified that it was the loss of these things as a direct consequence of having schizophrenia that influenced their HRQoL. It would appear that in the main, factors that are secondary to the experience of schizophrenia are of most importance to participants. Suggestions are also made in the discussion for future research.

Adult↗
PubMed2002

Abnormal spine morphology and enhanced LTP in LIMK-1 knockout mice.

In vitro studies indicate a role for the LIM kinase family in the regulation of cofilin phosphorylation and actin dynamics. In addition, abnormal expression of LIMK-1 is associated with Williams syndrome, a mental disorder with profound deficits in visuospatial cognition. However, the in vivo function of this family of kinases remains elusive. Using LIMK-1 knockout mice, we demonstrate a significant role for LIMK-1 in vivo in regulating cofilin and the actin cytoskeleton. Furthermore, we show that the knockout mice exhibited significant abnormalities in spine morphology and in synaptic function, including enhanced hippocampal long-term potentiation. The knockout mice also showed altered fear responses and spatial learning. These results indicate that LIMK-1 plays a critical role in dendritic spine morphogenesis and brain function.

Actin Cytoskeleton↗