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Biomedical subjects

W M Carroll

Publications and source records attributed to W M Carroll.

At least 19 recordsLinked to original sources
PubMed2006

Global gene expression analysis of the effects of vinblastine on endothelial cells, when eluted from a thermo-responsive polymer.

In-stent restenosis remains a significant problem associated with bare metal stents. This drawback has prompted research into improving stent design and the development of novel coatings, including drug-eluting stents. A number of drug-eluting stents are currently on the market; however, the success rate of these stents in complex situations has been found to be quite low. Thus, there remains potential for the development of more suitable drug-eluting stents. The aims of this study were to use a thermoresponsive polymer to develop a system to locally deliver vinblastine, an antimitotic agent currently used as an anticancer drug, and in addition, assess the effects of this drug at the gene expression level in vitro. An N-isopropylacrylamide/N-tert-butylacrylamide (NiPAAm/NtBAAm) copolymer solution in the ratio 65:35 was prepared and appropriate volumes of vinblastine were added to generate two final drug concentrations of 22 nanomoles/film or 0.022 nanomoles/film. Stainless steel discs (316) were coated with the copolymer solution or this solution containing drug. Human endothelial cells were cultured on collagen type 1 gels and then incubated with the coated discs for 24 h. Gene expression studies using oligonucleotide microarray analysis and quantitative RT-PCR were then performed. Microarray analysis revealed that vinblastine causes the differential expression of a range of genes involved in a variety of different functions, including cell cycle and apoptosis. The changes in expression of some of these genes culminate in cell cycle arrest and apoptotic pathways.

Animals↗
PubMed2005

Cytocompatibility of novel tin oxide thin films.

The capacity of tin oxide films to support cell growth was investigated. Three substrates were used for the test: glass coverslips, glass coverslips spin coated with tin oxide and commercially available 316 stainless steel. The wettabilities and surface roughness of the three surfaces were measured before seeding 3T3 fibroblasts onto the samples. The behaviour of the cells grown on the tin oxide was compared to the uncoated glass and the steel and results showed that the cell growth on tin oxide compared favourably with the other substrates. The surface wettability appeared to have the strongest effect on cell adhesion to tin oxide.

3T3 Cells↗
PubMed2003

Corrosion behavior of nitinol wires in body fluid environments.

In this study, breakdown potentials were measured for unpolished and mechanically polished nitinol wires in simulated body fluids. These wires are similar to those used in the manufacture of stents. Considerable scatter was observed in the results indicating a variable surface state. After appropriate heat treatments, the measured breakdown values were lower but more reproducible for the mechanically polished samples. Significantly higher breakdown potentials were observed for cross-section wire samples. Some wires were tested in human blood and the breakdown values were higher than in Ringer and 0.9% NaCl solutions. Energy dispersive X-ray analysis of the surface layers indicated that oxide thickening occurred after heat treatments. Dynamic secondary ion mass spectroscopy also revealed thickened surface oxides on the wires. The oxide was predominantly made up of TiO(2) with a very thin layer of NiO at the outer surface. Galvanic corrosion tests were performed on nitinol wires coupled with gold, elgiloy/phynox, and stainless steel. Nitinol was found to be anodic in all cases yet the currents measured were small. In tests in which nitinol-gold couples were immersed in 0.9% NaCl for periods up to 12 months, only very small amounts of nickel (in the part per billion range) were released into solution and scanning electron microscopy examination revealed no corrosion.

Alloys↗
PubMed2002

Passivation of nitinol wire for vascular implants--a demonstration of the benefits.

This study investigated a passivation process for polished nitinol wires and vascular stent components, after being given a typical shape setting heat treatment. Heat treated samples were passivated in a nitric acid solution and a series of corrosion tests, surface analysis and chemical analysis was performed. Potentiodynamic polarization tests demonstrated a significant increase in breakdown potential for passivated samples, compared to heat treated surfaces. Surface analysis indicated that the passivation reduces Ni and NiO content in the oxide and increases TiO2 content. Chemical analysis of passivation solutions suggests that the improvement in corrosion resistance is proportional to the quantity of nickel removed. Long term immersion tests demonstrate that nickel release from the surface of the material decreases with time and the quantity of nickel released is lower for passivated samples. The improved corrosion resistance is maintained after extended periods of immersion in saline solution.

Alloys↗
PubMed1998

Focal accumulation of intra-axonal mitochondria in demyelination of the cat optic nerve.

Mitochondrial accumulation has been reported at sites of degenerating nerve fibres. The reason for focal accumulation of mitochondria within axons has not previously been investigated. The aim of this study was to quantitate changes in mitochondrial concentration within demyelinated axons and determine if these changes were due to obstruction of the free passage of organelles within the fibre. The average number of mitochondria per unit area of axon within axons of normal cat optic nerve and optic nerve in which demyelination had been induced with anti-galactocerebroside (GC) was determined using transmission electron microscopy. Increased numbers of mitochondria were demonstrated at the site of demyelination, peaking at approximately two and a half times the value for normal non-lesioned nerves at 6-7 days after anti-GC administration [0.66+/-0.06 (SD) mitochondria per microm2 of axon compared to 0.28+/-0.04 in controls; P < 0.05]. The mitochondrial concentration gradually decreased over the next 20 days towards normal values. The concentration of mitochondria within non-myelinated axons of cat retina (0.55+/-0.18) was also determined and shown to be comparable to the values for the demyelinated optic axons (0.66+/-0.06). It is proposed that the accumulation of mitochondria within demyelinated axons reflects the adaptive process of the axon during the early restoration of impulse conduction rather than the obstruction of the free passage of organelles within the fibre.

Animals↗
PubMed1998

Identification of the adult resting progenitor cell by autoradiographic tracking of oligodendrocyte precursors in experimental CNS demyelination.

The new population of oligodendrocytes remyelinating an experimental demyelinating optic nerve lesion has been tracked backwards in time. Using autoradiography combined with electron microscopy and immunocytochemistry, serial sections of optic nerves from young adult cats were studied from 42 h (2 days) post-injection to 93 h (4 days) post-injection. The remyelinating oligodendrocyte lineage was found to commence with the single division of a resting progenitor cell residing in a central fascicular location outside the demyelinative lesion. The division of the founding progenitor cell occurs at 2 days post-lesion and results in two motile daughter cells. These cells, previously described by us as precursor cells, migrate to the lesion, closely appose demyelinated axons, produce axon wrapping processes and differentiate to become remyelinating oligodendrocytes. This study confirms that remyelinating oligodendrocytes originate from resting progenitor cells outside the lesion and not from mature oligodendrocytes, and implies that repeated demyelinative injury could exhaust the reparative capacity of such a region.

Animals↗
PubMed1994

Early recruitment of oligodendrocyte precursors in CNS demyelination.

The source of the new population of oligodendrocytes which successfully remyelinates experimentally induced demyelination of the cat optic nerve was studied with a combination of techniques. These included correlative light microscopy, immunocytochemistry, electron microscopy and autoradiography in transverse and longitudinal sections. Extending the analysis from the newly generated oligodendrocyte back to the very early demyelinative phase of the lesion enabled the identification of a glial precursor cell (GPC) outside the lesion which appeared to be readily recruitable and motile. This cell is likely to be the product of the division of a putative resting progenitor cell residing in a central fascicular location of the normal optic nerve surrounding the lesion. On arriving at the fringe of the lesion, GPCs are transformed into vimentin-positive small glial cells (SGCs) possibly by signals from demyelinated axons to which the SGCs become closely apposed. Small glial cells, which together with GPCs share several features in common with O-2A perinatal progenitors of the rodent optic nerve, then differentiate into oligodendrocytes. Together these findings suggest that the events leading to remyelination of adult mammalian optic nerve commence soon after the demyelinating injury and might recapitulate the principal events of developmental myelinogenesis.

Animals↗
PubMed1994

Unilateral asterixis due to a lesion of the ventrolateral thalamus.

A case of unilateral asterixis in a man with a focal ischaemic lesion of the contralateral ventral thalamus is presented. Atypically, the movements were present at rest and had a pattern of activation that resulted in an initial misdiagnosis of epilepsia partialis continua. This case emphasises the importance of electromyographic analysis in establishing the correct diagnosis of involuntary movements before starting specific treatment.

Aged↗
PubMed1994

Unilateral asterixis due to a lesion of the ventrolateral thalamus.

A case of unilateral asterixis in a man with a focal ischaemic lesion of the contralateral ventral thalamus is presented. Atypically, the movements were present at rest and had a pattern of activation that resulted in an initial misdiagnosis of epilepsia partialis continua. This case emphasises the importance of electromyographic analysis in establishing the correct diagnosis of involuntary movements before starting specific treatment.

Aged↗
PubMed1993

In vivo CNS remyelination: HNK-1 labels newly differentiated oligodendrocytes but not precursors.

The possibility that HNK-1 antibody might identify oligodendrocyte precursors in vivo was investigated using a combined immunocytochemical and ultrastructural analysis of remyelination in the cat optic nerve after demyelination induced by local injection of antiserum against galactocerebroside. HNK-1 antibody, in addition to antisera to galactocerebroside, glial fibrillary acidic protein, vimentin and myelin basic protein, was applied to early and late premyelinative lesions within which we have recently identified a putative precursor for the remyelinating oligodendrocyte termed the small glial cell. HNK-1 labelled oligodendrocytes in normal optic nerve and newly differentiated oligodendrocytes within lesions but did not label the small glial cells.

Animals↗
PubMed1992

Late radiation associated neurological injury.

Late radiation-associated neurological injury is a recognised and often fatal complication of therapeutic ionising radiation. This retrospective study outlines its highly variable presentation, radiological findings and prognosis over a 6 year period in a major teaching hospital.

Acute Disease↗
PubMed1991

Saccade onset and offset lambda waves: relation to pattern movement visually evoked potentials.

The lambda (lambda) wave is an occipital EEG potential which occurs when saccadic eye movements are made against an illuminated contrast background. There is some disagreement concerning the presence of sub-components to the lambda-wave, and its relationship to visually evoked potentials. In the present study, lambda-waves were recorded with saccades of different durations (30-110 ms) and compared to VEPs associated with pattern movements of similar durations and velocity. It was found that the lambda-wave consisted of a saccade onset component with positive sub-components at 59 and 100 ms after saccade onset, and a saccade offset component with a positive potential at 74 ms after saccade offset. With small saccades of 30 ms duration or less, these components superimposed to form a single lambda-wave. In the case of pattern movement VEPs, a movement onset component of latency 110 ms following movement onset, and a movement offset component at 89 ms after movement offset, were identified. The similar behaviour of the lambda-wave and VEP under these conditions supports the view that the lambda-wave is a visually evoked potential resulting from movement of the visual field across the retina during a saccadic eye movement.

Adult↗