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Biomedical subjects

E Reid

Publications and source records attributed to E Reid.

At least 19 recordsLinked to original sources
PubMed2007

Biomass effects on oxygen transfer in membrane bioreactors.

Ten biomass samples from both municipal and industrial pilot and full scale submerged membrane bioreactors (MBRs) with mixed liquor suspended solids concentrations (MLSS) ranging from 7.2 to 30.2g L(-1) were studied at six air-flow rates (0.7, 1.3, 2.3, 3, 4.4 and 6m(3)m(-3)h(-1)). Statistical analyses were applied to identify the relative impacts of the various bulk biomass characteristics on oxygen transfer. Of the biomass characteristics studied, only solids concentration (correlated with viscosity), the carbohydrate fraction of the EPS (EPS(c)) and the chemical oxygen demand (COD) concentration of the SMP (SMP(COD)) were found to affect the oxygen transfer parameters k(L)a(20) (the oxygen transfer coefficient) and alpha-factor. The relative influence on k(L)a(20) was MLSS>aeration>EPS(c)>SMP(COD) and on alpha-factor was MLSS>SMP(COD)>EPS(c)>aeration. Both k(L)a(20) and alpha-factor increased with increasing aeration and EPS(c) and decreased with increasing MLSS and SMP(COD). MLSS was found to be the main parameter controlling the oxygen transfer.

Biomass↗
PubMed2005

Anti-tumour activity in non-small cell lung cancer models and toxicity profiles for novel ruthenium(II) based organo-metallic compounds.

Novel ruthenium(II) organo-metallic compounds are active in ovarian cancer models [Aird RE, Cummings J, Ritchie AA, Muir M, Morris RE, Chen H, et al. In vitro and in vivo activity and cross resistance profiles of novel ruthenium(II) organometallic arene complexes in human ovarian cancer. Br J Cancer 2002;86(10):1652-7]. [(eta6-C6H5C6H5)Ru(en)Cl]+ (as a PF6 salt, where en=ethylenediamine (RM175)) has been evaluated in a 13-cell line panel. Particular sensitivity (approximately 10-fold lower than mean IC50) was noted in breast cancer and non-small cell lung cancer cell lines. In addition, IC50 in the A549 was 2 microM and RM175 (25 mg kg-1, days 1 and 5, i.p.) caused a significant (p=0.004) growth delay in a xenograft model. HC11 [(eta6-tetrahydroanthracene)Ru(en)Cl]PF6 was more potent in the A549 cell line (IC50 0.5 microM). HC11 (25 mg kg-1, days 1, 8 and 15, i.p.) was also active in vivo. Following RM175 25 mg kg-1, days 1 and 5, and 15 mg kg-1, days 1-5, HC11 25 and 40 mg kg-1, day 1, elevated alanine transaminase levels were detected, suggesting hepatotoxicity. No changes were observed in kidney or haematological parameters. In liver sections, multi-focal hepatic necrosis was seen, becoming confluent at high doses of HC11. In vitro studies confirmed that HC11 was more toxic than RM175 to fresh human hepatocytes and equitoxic to mithramycin. Liver toxicity may be related to the arene ligand and modification may reduce the potential for hepatic toxicity, while maintaining the anti-tumour activity seen.

Alanine Transaminase↗
PubMed2004

X-linked adrenoleukodystrophy presenting as autosomal dominant pure hereditary spastic paraparesis.

We present a family in which an initial clinical diagnosis of autosomal dominant pure hereditary spastic paraparesis (HSP) was made on the basis of a three generation pedigree in which both males and females presented with a spastic paraparesis. Subsequent biochemical and genetic analysis revealed that the family was in fact affected by the adrenomyeloneuropathy subtype of X-linked adrenoleukodystrophy. In the family described, both males and females were affected by a spastic paraparesis, and there was no male to male transmission, consistent with both autosomal dominant and X-linked inheritance. This report illustrates the importance of assaying very long chain fatty acids (VLCFAs) in any HSP family where there is no male to male transmission.

Adrenoleukodystrophy↗
PubMed2003

Screening of patients with hereditary spastic paraplegia reveals seven novel mutations in the SPG4 (Spastin) gene.

Hereditary spastic paraplegia (HSP) is a heterogeneous condition characterised in its pure form by progressive lower limb spasticity. Mutations in SPG4 (encoding spastin) may be responsible for up to 40% of autosomal dominant (AD) cases. A cohort of 41 mostly pure HSP patients from Britain and Austria, 30 of whom displayed AD inheritance, was screened for mutations in SPG4 by single strand conformation polymorphism (SSCP) analysis followed by sequencing of samples with mobility shifts. We identified eight SPG4 mutations in pure AD HSP patients, seven of which were novel: one missense mutation within the AAA cassette (1633G>T), two splice site mutations (1130-1G>T, 1853+2T>A) and four frameshift mutations (190_208dup19, 1259_1260delGT, 1702_1705delGAAG, 1845delG). A novel duplication in intron 11 (1538+42_45dupTATA) was also detected. We report the HUGO-approved nomenclature of these mutations as well. Furthermore, we detected a silent change (1004G>A; P293P), previously reported as a mutation, which was also present in controls. The frequency of SPG4 mutations detected in pure AD HSP was 33.3%, suggesting that screening of such patients for SPG4 mutations is worthwhile. Most patients will have unique mutations. Screening of SPG4 in apparently isolated cases of HSP may be of less value.

Adenosine Triphosphatases↗
PubMed2003

Practice development in psychological interventions: mental health nurse involvement in the Conversational Model of psychotherapy.

This paper describes a mental health nurse led practice development initiative in psychotherapy. Four mental health nurses have been trained to deliver the Conversational Model of psychotherapy (also known as psychodynamic-interpersonal (PI) psychotherapy) a non-cognitive behavioural therapy (CBT) with a robust evidence base. We report on the robust range of both processes and outcome measures being used to evaluate this initiative. We conclude that good quality evidence-based practice requires careful planning and preparation, adequate financial resources from Trusts, as well as commitment and motivation from the staff expected to be involved in such initiatives.

Behavior Therapy↗
PubMed2003

Personal reflections of mental health nurses training to use Hobson's Conversational Model (psychodynamic-interpersonal) of psychotherapy.

Current mental health policy documents highlight the need for mental health nurses to become increasingly involved in the delivery of evidence-based psychological interventions. However, substantial evidence exists indicating that there is a paucity of training to adequately equip nurses to deliver these interventions and, even when training is available, there are barriers to their implementation into routine clinical practice. This paper reports on the personal reflections and experiences of a group of four mental health nurses undertaking training in the Conversational Model of psychotherapy (also known as psychodynamic-interpersonal 'PI' psychotherapy). These reflections highlight the rewards and challenges arising from the effort to undertake training in an evidence-based model of psychological intervention and from attempting to implement and sustain this training into routine practice.

Attitude of Health Personnel↗
PubMed2003

Pseudo-isolated FSH deficiency caused by an inhibin B-secreting granulosa cell tumour: case report.

Isolated FSH deficiency due to a mutation in the FSHbeta subunit is characterized by an extremely low serum FSH concentration. We report a patient who presented with an FSH of 0.8 mIU/ml and infertility associated with anovulation. Endocrinological assessment and immunohistochemistry revealed that a granulosa cell tumour was secreting inhibin B and suppressing FSH; however, LH and estradiol were within their normal ranges. Upon removal of the tumour, inhibin B decreased and FSH levels rose to normal values. The patient subsequently conceived and delivered successfully. Based on this case and on those previously described in the literature, we suggest that inhibin B levels should be evaluated in anovulatory patients having a clinical presentation consistent with functional hypothalamic amenorrhoea and very low to normal values of FSH.

Adult↗
PubMed2003

Coeliac disease: investigation of proposed causal variants in the CTLA4 gene region.

Coeliac disease (CD) is an immune-mediated enteropathy triggered by gluten in genetically predisposed individuals. Patients with CD have an increased prevalence of other autoimmune disorders, including type 1 diabetes (T1D) and Graves' disease (GD). CD shares with these conditions certain HLA susceptibility alleles. A number of studies have also shown association of autoimmune diseases, including CD, with the CD28-cytotoxic T lymphocyte antigen 4 (CTLA4)-inducible costimulator (ICOS) region of chromosome 2q33, but until recently the precise causal variant has remained unknown. Recently, it was shown that, in GD, CT60 (+6230G>A), a single nucleotide polymorphism (SNP) at the end of the CTLA4 transcript, is associated with an alteration in the ratio of splice forms of the CTLA4 gene and that this ratio affects disease susceptibility. A similar but weaker association was found with T1D. There is also an independent association of GD and T1D with the SNP MH30 (-23 327G>C), which possibly affects promoter region function. Hypothesizing that CT60 and MH30 may be causal variants in other autoimmune disorders, we investigated these SNPs in CD using 149 family trios and 100 unrelated/unaffected controls. No association was detected with either SNP using both the transmission disequilibrium test (TDT) and case-control methods. Our study appears to have good power to detect moderate genetic effects, but possibly these SNPs exert too weak an effect on risk of CD to have been detected in our sample. Alternatively, the previously noted association of CD with the CTLA4 gene region may be due to different causal variants. Unlike T1D and GD, CD is not a true autoimmune disease, and CD has different associations at the CTLA4 exon 1 SNP +49G>A from all other autoimmune disorders. MH30, CT60, and other SNPs in the region may still warrant further investigation in other CD samples.

Antigens, CD↗
PubMed2003

Science in motion: common molecular pathological themes emerge in the hereditary spastic paraplegias.

The hereditary spastic paraplegias are a group of neurodegenerative conditions that all share the principal clinical feature of progressive lower limb spastic paralysis, caused by either failure of development or progressive degeneration of the corticospinal tract. The conditions are characterised by extreme genetic heterogeneity, with at least 20 genes involved. Until recently, no functional overlap was apparent in the associated molecular pathological mechanisms. However, with recent progress in hereditary spastic paraplegia gene identification, common pathological themes are now emerging.

ATPases Associated with Diverse Cellular Activitie↗
PubMed2001

The Escherichia coli CcmG protein fulfils a specific role in cytochrome c assembly.

In Escherichia coli K-12, c-type cytochromes are synthesized only during anaerobic growth with trimethylamine-N-oxide, nitrite or low concentrations of nitrate as the terminal electron acceptor. A thioredoxin-like protein, CcmG, is one of 12 proteins required for their assembly in the periplasm. Its postulated function is to reduce disulphide bonds formed between correctly paired cysteine residues in the cytochrome c apoproteins prior to haem attachment by CcmF and CcmH. We report that loss of CcmG synthesis by mutation was not compensated by a second mutation in disulphide-bond-forming proteins, DsbA or DsbB, or by the chemical reductant, 2-mercaptoethanesulphonic acid. An anti-CcmG polyclonal antibody was used in Western-blot analysis to probe the redox state of CcmG in mutants defective in the synthesis of other proteins essential for cytochrome c assembly. The oxidized form of CcmG accumulated not only in trxA or dipZ mutants defective in the transfer of electrons from the cytoplasm for disulphide isomerization and reduction reactions in the periplasm, but also in ccmF and ccmH mutants. The requirement of both CcmF and CcmH for the reduction of the disulphide bond in CcmG indicates that CcmG functions later than CcmF and CcmH in cytochrome c assembly, rather than in electron transfer from the membrane-associated DipZ (also known as DsbD) to CcmH. The data support a model proposed by others in which CcmG catalyses one of the last reactions specific to cytochrome c assembly.

Antibodies↗
PubMed2001

Nursing at the edge of the world: nurses on St Kilda.

In the early twenty-first century geographically isolated communities continue to experience unequal access to health care. The advent of new technologies such as telemedicine do not overcome the financial constraints of employing professionals such as health visitors or district nurses to meet the needs of these remote areas. In late nineteenth century Britain there were few more isolated communities than the St Kildans. Although it is 70 years since St Kilda was evacuated it continues to capture the popular imagination. This archipelago of islands lies less than 50 miles west of the Outer Hebrides yet remains inaccessible by sea except on the calmest of summer days. Isolation such as this may have been acceptable, even desirable, to the islanders for generations but became problematic with their increasing reliance on supply boats for food. As the population dwindled it became more difficult to be self-sufficient, with few able-bodied men to row to the nearby rocks and climb to harvest the seabirds that were their staple diet. The rocks, or stacs, as they are known, have sheer cliff faces rising spectacularly from the sea. It would be logical to assume that the population had difficulty expanding due to the high male mortality rate from accidents on the these pinnacles. But it was not the skillful rock climbers that were dying in large numbers, it was their babies. Sustained infant mortality rates of between 50-70 per cent during the nineteenth century contributed to the consistently low population levels which led to the eventual death of the community. It is surprising in this context to learn that the first nurses to serve the St Kildans were ostracised and rejected by the islanders.

Community Health Nursing↗
PubMed2000

Prescribing costs. Braking point.

A joint hospital, health authority and PCG initiative to improve prescribing has produced significant savings in the PCG involved. The venture included the appointment of a medicines management pharmacist to work with practices, and a survey to ascertain GPs' prescribing needs. GPs considered the most important issues to be developing local disease management guidelines, education and repeat prescribing. Guidelines on dyspepsia management have resulted in a 4.9 per cent reduction in the cost of prescribing gastrointestinal drugs. Antibiotic prescribing has also fallen.

Anti-Bacterial Agents↗
PubMed2000

A locus for autosomal dominant "pure" hereditary spastic paraplegia maps to chromosome 19q13.

Genetic loci for autosomal dominant pure hereditary spastic paraplegia (ADPHSP) have been mapped to chromosomes 2p, 8q, 12q, 14q, and 15q. We undertook a genomewide linkage screen of a large family with ADPHSP, for which linkage at all previously identified ADPHSP loci was excluded. Analysis of markers on chromosome 19q gave a peak pairwise LOD score of 3.72 at D19S420, allowing assignment of a novel ADPHSP locus (which we have termed "SPG12") to this region. Haplotype construction and analysis of recombination events narrowed the SPG12 locus to a 16.1-cM region between markers D19S868 and D19S902.

Adolescent↗
PubMed2000

Mutation analysis of the spastin gene (SPG4) in patients with hereditary spastic paraparesis.

BACKGROUND: Hereditary spastic paraparesis is a genetically heterogeneous condition. Recently, mutations in the spastin gene were reported in families linked to the common SPG4 locus on chromosome 2p21-22. OBJECTIVES: To study a population of patients with hereditary spastic paraparesis for mutations in the spastin gene (SPG4) on chromosome 2p21-22. METHODS: DNA from 32 patients (12 from families known to be linked to SPG4) was analysed for mutations in the spastin gene by single strand conformational polymorphism analysis and sequencing. All patients were also examined clinically. RESULTS: Thirteen SPG4 mutations were identified, 11 of which are novel. These mutations include missense, nonsense, frameshift, and splice site mutations, the majority of which affect the AAA cassette. We also describe a nucleotide substitution outside this conserved region which appears to behave as a recessive mutation. CONCLUSIONS: Recurrent mutations in the spastin gene are uncommon. This reduces the ease of mutation detection as a part of the diagnostic work up of patients with hereditary spastic paraparesis. Our findings have important implications for the presumed function of spastin and schemes for mutation detection in HSP patients.

Adenosine Triphosphatases↗