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Biomedical subjects

E M Hicks

Publications and source records attributed to E M Hicks.

14 recordsLinked to original sources
PubMed2005

Biological applications of localised surface plasmonic phenomenae.

Researchers and industrialists have taken advantage of the unusual optical, magnetic, electronic, catalytic, and mechanical properties of nanomaterials. Nanoparticles and nanoscale materials have proven to be useful for biological uses. Nanoscale materials hold a particular interest to those in the biological sciences because they are on the same size scale as biological macromolecules, proteins and nucleic acids. The interactions between biomolecules and nanomaterials have formed the basis for a number of applications including detection, biosensing, cellular and in situ hybridisation labelling, cell tagging and sorting, point-of-care diagnostics, kinetic and binding studies, imaging enhancers, and even as potential therapeutic agents. Noble metal nanoparticles are especially interesting because of their unusual optical properties which arise from their ability to support surface plasmons. In this review the authors focus on biological applications and technologies that utilise two types of related plasmonic phenomonae: localised surface plasmon resonance (LSPR) spectroscopy and surface-enhanced Raman spectroscopy (SERS). The background necessary to understand the application of LSPR and SERS to biological problems is presented and illustrative examples of resonant Rayleigh scattering, refractive index sensing, and SERS-based detection and labelling are discussed.

Biology↗
PubMed1999

Psychological management of intractable seizures in an adolescent with a learning disability.

Psychological interventions aimed at seizure management are described with a 14-year-old boy with a learning disability and intractable epilepsy. Baseline records suggested that a majority of tonic seizures and 'drop attacks' were associated with going off to sleep and by environmental 'startles'. Psychological formulation implicated sudden changes in arousal levels as an underlying mechanism of action. Cognitive-behavioural countermeasures were employed to alter arousal levels and processes in different ways in different 'at-risk' situations. A multiple baseline design was used to control for non-specific effects of interventions on non-targeted seizures. Results suggested significant declines in the number of sleep onset and startle-response seizures were attained by these methods. Gains were maintained at 2-month follow-up.

Adolescent↗
PubMed1999

Mammary tumor formation in p53- and BRCA1-deficient mice.

The inheritance of a mutant copy of the BRCA1 gene greatly increases a woman's lifetime risk for ovarian and breast cancer. While a homologous gene has been identified in mouse, mice carrying mutations in this gene do not display a detectable increase in tumor formation. To determine whether mutations in p53 might increase the incidence of tumors associated with the loss of BRCA1 function in mice, we have generated mice carrying mutations at both of these loci. We report here that the presence of a mutant Brca1 allele does not alter survival of either p53-/- or p53+/- mice. Although the tumor spectrum was not dramatically altered, an increased incidence of mammary tumors was observed in the Brca1+/-p53-/- mice. Four mammary tumors were seen in the Brca1+/-p53-/- group whereas only one such tumor was seen among the p53-/- control group. In addition, although the presence of a mutant Brca1 allele did not alter the survival rate or the incidence of most tumor types in the p53+/- mice, 5 of the 23 tumors isolated from the Brca1+/-p53+/- mice treated with ionizing radiation were of mammary epithelial origin, and 3 of these had lost expression of the wild-type Brca1 gene. In contrast, no such tumors were observed in the irradiated p53+/- controls. Although the number of mammary tumors observed in these animals is small, these results are suggestive of a role for BRCA1 in mammary tumor formation after exposure to specific DNA damaging agents.

Animals↗
PubMed1998

New form of autosomal-recessive axonal hereditary sensory motor neuropathy.

Two siblings, a male and a female, had severe axonal neuropathy and sideroblastic anemia. Despite a distinct clinical picture with areflexia, ataxia, hypotonia, optic atrophy, and progressive sensory neural hearing loss, no definite diagnosis could be reached and the older sibling died at 6 years of age of respiratory failure. It is proposed that the two affected siblings have a new form of autosomal-recessive axonal hereditary sensory motor neuropathy.

Anemia, Sideroblastic↗
PubMed1998

The relationship of chronic mucin secretion to airway disease in normal and CFTR-deficient mice.

In the cystic fibrosis (CF) patient, lung function decreases throughout life as a result of continuous cycles of infection, particularly with Pseudomonas aeruginosa and Staphylococcus aureus. The mechanism underlying the pathophysiology of the disease in humans has not been established. However, it has been suggested that abnormal, tenacious mucus, resulting perhaps from improper hydration from loss of Cl- secretion via the cystic fibrosis transmembrane conductance regulator (CFTR) protein, impairs clearance of bacteria from the CF airway and provides an environment favorable to bacterial growth. If this hypothesis is correct, it could explain the absence of respiratory disease in CFTR-deficient mice, since mice have only a single submucosal gland and display few goblet cells in their lower airways, even when exposed to bacteria. To test this hypothesis further, we induced allergic airway disease in CFTR-deficient mice. We found that induction of allergic airway disease in mice, unlike bacterial infection, results in an inflammatory response characterized by goblet cell hyperplasia, increased mucin gene expression, and increased production of mucus. However, we also found that disease progression and resolution is identical in Cftr-/- mice and control animals. Furthermore, we show that the presence of mucus in the Cftr-/- airway does not lead to chronic airway disease, even upon direct inoculation with S. aureus and P. aeruginosa. Therefore, factors in addition to the absence of high levels of mucus secretion protect the mouse from the airway disease seen in human CF patients.

Animals↗
PubMed1996

The prevalence of inherited neuromuscular disease in Northern Ireland.

A comprehensive study of inherited neuromuscular disease was carried out in Northern Ireland between 1 February 1993 and 30 June 1994. Cases were ascertained from eight different sources and investigations and diagnoses were reviewed. Five hundred and forty three individuals were identified giving an overall prevalence of inherited neuromuscular disease of 1 in 2900 of the population. The prevalence of myotonic dystrophy was higher than that in most previously reported studies and accounted for 25% of all cases. Congenital myopathies were also found more frequently than expected. The overall prevalence compares well with that estimated by Emery from the reported prevalence rates of individual diseases.

Adolescent↗
PubMed1995

Infantile spasms associated with theophylline toxicity.

We report on a 6-month-old infant with asthma who developed spasms and hypsarrhythmia on the electroencephalogram (EEG) shortly after starting oral theophylline medication. Theophylline levels at that time were just above the upper normal range. The spasms stopped and the EEG normalized when theophylline was discontinued and nitrazepam therapy started. On follow-up over the next 3 years there was no recurrence of seizures and the child's neurodevelopment has been normal. Nitrazepam was stopped at 10 months and the waking and sleeping EEG were normal at 14 months. We believe that the infantile spasms were caused by theophylline.

Electroencephalography↗
PubMed1993

Progressive neuronal degeneration of childhood (Alpers syndrome) with hepatic cirrhosis.

Four children, from two families, suffered from fatal degeneration of the cerebral grey matter. Their disease was characterised by intractable epilepsy, epilepsia partialis continua, progressive deterioration, and terminal hepatic dysfunction. EEG showed marked and distinctive slow wave abnormality, visual evoked responses were diminished, and cerebral atrophy was seen on CT scan. Pathological findings were of neuronal loss and hepatic cirrhosis. The combination of cerebral degeneration, hepatic disease and familial occurrence suggests an inborn error of metabolism with autosomal recessive inheritance. The features described are those of Alpers syndrome, especially the recently delineated subgroup with progressive neuronal degeneration and liver disease.

Brain↗
PubMed1990

Power spectral analysis of the EEG of term infants following birth asphyxia.

The aim of this pilot study was to perform power spectral analysis of the EEGs of term infants following birth asphyxia, to establish its value as a prognostic indicator. 16 term infants were studied over an 18-month period. Power spectral analysis was performed on the EEGs of babies with signs of hypoxic-ischaemic encephalopathy at regular intervals during the first five days of life. It showed distinct changes following birth asphyxia, which were related to the eventual outcome of the babies. Absolute power was significantly reduced in the babies with poor outcome compared with those with good outcome, particularly in the delta bands.

Asphyxia Neonatorum↗
PubMed1987

Reye's syndrome: assessment of intracranial monitoring.

Direct measurements of arterial blood pressure and intracranial pressure were recorded in 39 patients aged 3.6 months to 5 years 11 months with Reye's syndrome judged to be stage 2 or beyond. Of 33 patients who survived, 27 made a full recovery and six were severely handicapped. Measurement of cerebral perfusion pressure, which is greatly reduced in the more severe forms of Reye's syndrome, was a better guide to prognosis and management than intracranial pressure alone. The findings emphasise that maintenance of cerebral perfusion pressure is essential if mortality and morbidity are to be reduced. Intracranial monitoring is mandatory in all but the mildest cases of Reye's syndrome.

Blood Pressure↗
PubMed1985

Reye's syndrome.

Reye's syndrome, an uncommon childhood encephalopathy of uncertain aetiology, is an important cause of mortality and permanent handicap. Since its recognition treatment has changed, current management focusing upon prevention or control of raised intracranial pressure. Prognosis is radically improved by early recognition and prompt transfer to a specialist centre.

Cerebrovascular Circulation↗
PubMedDate not supplied

Cranial computed tomography in the under twos.

One hundred consecutive cranial computed tomographic scans were reviewed in children aged 0-2 years, presenting to the Royal Belfast Hospital for Sick Children. The mean age at scanning was 8.3 months and 73% of the scans were abnormal. The majority of scans were performed electively (78%). The commonest indication for a scan was seizures (31) and the diagnostic yield was highest where they were associated with other neuro-developmental symptoms. The usefulness of the CT scan was not limited to the abnormal studies but contributed to management in children with normal scans by excluding important intracranial pathology. Developmental CNS malformation (16 scans) and cerebral atrophy (15 scans) were the most frequent CT abnormalities encountered.

Brain↗