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Biomedical subjects

M Rogers

Publications and source records attributed to M Rogers.

At least 19 recordsLinked to original sources
PubMed2006

Efficacy of super-oxidized water fogging in environmental decontamination.

The efficacy of decontamination using Sterilox fog was assessed against meticillin-resistant Staphylococcus aureus (MRSA) and Acinetobacter baumannii. Ceramic tiles were inoculated with the test organisms and, once dried, were subjected to Sterilox fogging using a stationary vaporizing machine sited at a distance of 3m for 10 min and then left for a further hour. In a second experiment using the same organisms, the first 10-min fogging period was followed by a directed fogging period of 30s at a distance of 1m. Organisms were cultured from the tiles, plated on to tryptone soya agar and incubated for 48 h. Initial counts of approximately 10(9) colony-forming units/mL for both organisms were reduced approximately 10(4) fold for MRSA and 10(5.8) fold for A. baumannii when using a single fogging. The second fogging resulted in 10(6.8)-fold reductions for both organisms. Sterilox fog is safe and simple to use, and can reduce levels of nosocomial pathogens by a factor of almost 10(7). It is worthy of clinical evaluation in clinical settings to determine whether it maintains its microbicidal effects against a variety of organisms on different surfaces.

Acinetobacter↗
PubMed2005

A new, recurrent mutation of GJB3 (Cx31) in erythrokeratodermia variabilis.

BACKGROUND: Erythrokeratodermia variabilis (EKV) is an autosomal dominant or recessive genodermatosis characterized by the coexistence of randomly occurring, transient, erythematous patches and hyperkeratosis of the skin. The disorder has been mapped to chromosome 1p35.1 but is genetically heterogeneous. EKV may be caused by pathogenic mutations in one of two neighbouring connexin genes, GJB3 and GJB4, encoding the gap junction proteins Cx31 and Cx30.3, respectively. Twelve distinct mutations identified to date cluster either at the cytoplasmic amino-terminus or in the four transmembrane domains. OBJECTIVES: To report a large family with EKV and an unrelated sporadic case. METHODS: DNA amplification and mutation analysis, followed by denaturing high-performance liquid chromatography to confirm the segregation of the mutations in the two families with EKV. RESULTS: A novel, recurrent GJB3 mutation (625C-->T; L209F) was identified in the family with EKV and in the unrelated sporadic case. CONCLUSIONS: This mutation is the first to affect a conserved residue in the cytoplasmic carboxy-terminus of any connexin gene with a cutaneous phenotype, emphasizing its structural and/or functional importance.

Adult↗
PubMed2003

D4F104S1 deletion in facioscapulohumeral muscular dystrophy: phenotype, size, and detection.

BACKGROUND: The facioscapulohumeral muscular dystrophy (FSHD) locus maps to 4q35 where it is closely linked to D4F104S1 (p13E-11), a probe that recognizes the pathognomonic FSHD deletion involving the subtelomeric D4Z4 tandem repeat array. Extended deletions that include both the more proximal D4F104S1 region and the D4Z4 repeat array proper do, however, occur, albeit rarely, and such deletions can lead to difficulties of interpretation in the diagnostic setting. OBJECTIVE: To devise a means to determine the true frequency of proximally extended deletions in individuals with FSHD. METHODS: Three families selected for this study were originally identified during routine FSHD analysis on the basis that the affected individuals in each family had failed to exhibit a small (<38-kb) EcoRI fragment. High molecular weight DNA from these families was analyzed with both conventional and pulsed-field gel electrophoresis using DNA markers p13E-11, 9B6A, B31, 4qA, and 4qB. RESULTS: Large genomic deletions were identified involving both D4Z4 and D4F104S1. The precise number of D4Z4 repeat units borne by the p13E11 deletion allele was established by the use of an additional restriction enzyme (MseI) digest. All three cases carry different sizes of deletion proximal to the D4Z4 repeat units. With use of a recently described telomeric probe, 4qA, a method was developed that identifies large genomic deletions involving both D4Z4 and D4F104S1 using conventional gel electrophoresis. CONCLUSION: Proximally extended deletions can be found in patients with a normal spectrum of the disease. This assay promises to allow estimation of the true frequency of proximally extended deletions and should improve the accuracy and reliability of molecular diagnostic testing for FSHD.

Adult↗
PubMed2003

Early detection of PrPres in BSE-infected bovine PrP transgenic mice.

Transgenic mouse lines expressing different levels of the bovine prion protein gene (boPrP(C)) were generated. Upon infection with BSE prions, all transgenic lines tested exhibited characteristics of the bovine disease. Typical CNS spongiform degeneration was observed by histopathology and presence of PrP(res) could be detected both by Western blot and immunohistochemistry (IHC) assays, confirming for this model the absence of an interspecies barrier to BSE infection. Differences in incubation times post-inoculation depend upon the expression level of boPrP(C) and the amount of prions in the inoculum. In the absence of clinical signs, pathognomonic markers of disease could be detected as early as 150 or 196 days post-inoculation by IHC and Western blot analysis, respectively. This result indicates that prion infectivity in experimental mouse bioassays can be measured earlier by assessing immunologically the presence of PrP(res) in brains from inoculated animals. Although these transgenic mice were also susceptible to sheep scrapie prion infection, the extent of incubation times was considerably longer and PrP(res) was detected in only 70 % of inoculated mice. Interestingly, transgenic mice-propagated sheep scrapie prions displayed distinct biochemical properties when compared to both the original sheep scrapie and transgenic mouse-propagated BSE inoculum.

Animals↗
PubMed2003

Prevention of incisional hernia after aortic aneurysm repair.

BACKGROUND: Incisional hernia is a common late complication of elective abdominal aneurysm (AAA) repair. This paper describes a technique that could prevent the development of this condition. METHODS: Since Jan 2001, a polypropylene mesh has been sutured prophylactically in the pre-peritoneal space during abdominal closure after elective AAA repair. RESULTS: Twenty-eight consecutive elective procedures were performed. One patient died from a myocardial infarct 13 days after operation. Four patients (14%) had a wound infection (1 deep methicillin resistant Staphylococcus aureus (MRSA) infection and 3 superficial) that were treated successfully with antibiotics and dressings. One additional patient had a positive MRSA wound swab but required no treatment. Two patients required late re-operations. One, who was on warfarin, required an urgent laparotomy for a leaking false aneurysm of the distal anastomoses 3 months after elective repair. A second patient had an anterior resection 18 months after aneurysm repair. Both re-operations were uneventful. No patient has yet developed a clinically evident incisional hernia. CONCLUSIONS: These early data suggest that this mesh technique is a simple, safe and potentially effective method to decrease the incidence of incisional hernia following aortic aneurysm repair.

Abdominal Wall↗
PubMed2003

Cofactor processing in galactose oxidase.

Galactose oxidase (GO; EC 1.1.3.9) is a monomeric 68 kDa enzyme that contains a single copper and an amino acid-derived cofactor. The mechanism of this radical enzyme has been widely studied by structural, spectroscopic, kinetic and mutational approaches and there is a reasonable understanding of the catalytic mechanism and activation by oxidation to generate the radical cofactor that resides on Tyr-272, one of the copper ligands. Biogenesis of this cofactor involves the post-translational, autocatalytic formation of a thioether cross-link between the active-site residues Cys-228 and Tyr-272. This process is closely linked to a peptide bond cleavage event that releases the N-terminal 17-amino-acid pro-peptide. We have shown using pro-enzyme purified in copper-free conditions that mature oxidized GO can be formed by an autocatalytic process upon addition of copper and oxygen. Structural comparison of pro-GO (GO with the prosequence present) with mature GO reveals overall structural similarity, but with some regions showing significant local differences in main chain position and some active-site-residue side chains differing significantly from their mature enzyme positions. These structural effects of the pro-peptide suggest that it may act as an intramolecular chaperone to provide an open active-site structure conducive to copper binding and chemistry associated with cofactor formation. Various models can be proposed to account for the formation of the thioether bond and oxidation to the radical state; however, the mechanism of prosequence cleavage remains unclear.

Binding Sites↗
PubMed2003

Technique for secondary tracheo-oesophageal puncture in difficult necks.

A secondary tracheo-oesophageal puncture is required for voice restoration post-laryngectomy either for reasons of closure of the primary fistula or as a planned secondary procedure. A method of doing this safely is described using an endotracheal tube and a flexible nasopharyngoscope in especially difficult cases.

Esophagus↗
PubMed2003

Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction.

Periodontitis is a complex, multifactorial process affected by bacterial plaque-components and host defense mechanisms. Inflammation of the periodontitium may lead the destruction of the underlying ligament and alveolar bone. Receptor activator of NF-kappaB ligand (RANKL), a novel TNF receptor-related protein is an important factor for osteoclast differentiation and activation. Given osteolysis by osteoclast has been demonstrated in periodontitis, we hypothesized that RANKL expression may be associated with bone destruction in periodontitis. We used semi-quantitative RT-PCR to compare the gene expression of RANKL and osteoprogerin (OPG), a decoy receptor of RANKL, between moderate and advanced periodontitis, and healthy subjects. The level of RANKL mRNA was highest in advanced periodontitis. In contrast, the level of OPG mRNA in both advanced and moderate periodontitis was lower than that in the healthy group. It appears that the ratio of RANKL to OPG mRNA in periodontitis has increased. To determine the localization of RANKL gene transcripts in gingival tissue at the cellular level, in situ hybridization was performed using digoxigenin-labeled specific riboprobes. RANKL mRNA was expressed in inflammatory cells, mainly lymphocyte and macrophages. In addition, proliferating epithelium in the vicinity of inflammatory cells expressed high levels of RANKL mRNA. In short, our data suggest that up regulation of RANKL mRNA in both inflammatory cells and epithelium may be associated with the activation of osteoclastic bone destruction in periodontitis.

Adult↗
PubMed2002

A control model of the movement of attention.

A control model of the movement of the focus of attention is developed and applied to explain its observed effects on single cell activity and to various quantitative features of the Posner benefit paradigm. This supports the presence of an inverse controller and a rules component in the control model. The ability of the control model to explain a range of deficits is then analyzed, as is its relation to other modeling approaches.

Animals↗
PubMed2002

Metallothionein in bovine spongiform encephalopathy.

An increase in metallothionein I and II (MT I/II) mRNA concentrations has been reported in the central nervous system of scrapie-infected rodents. In this study we compared cattle with bovine spongiform encephalopathy (BSE), cattle affected by neurological disease other than BSE, and clinically healthy cattle in respect of MT I/II immunoreactivity in brainstem medullary tissue. Marked astrocytic MT I/II immunolabelling was seen in all BSE-affected animals, in contrast to clinically healthy cases, in which no such labelling was detected. In BSE, MT I/II immunoreactive astrocytes were confined specifically to areas of vacuolation or abnormal prion protein (PrP(BSE)) deposition, or both. MT I/II immunolabelling was also seen in a small number of animals with a neurological disease other than BSE. These findings complement previous studies by demonstrating increased levels of MT I/II in transmissible spongiform encephalopathy (TSE)-infected brain tissue, indicating that MT I/II may play some as yet unidentified role in the response to TSE infection.

Animals↗
PubMed2001

Cholera toxin-induced PGE(2) activity is reduced by chemical reaction with L-histidine.

Mediators of cholera toxin (CT)-induced fluid secretion include 3',5'-adenosine monophosphate (cAMP), prostaglandin E(2) (PGE(2)), and 5-hydroxytryptamine (5-HT). Administration of L-histidine significantly reduced the net secretory response of the small intestine of mice challenged with CT and reduced the capacity of PGE(2) to stimulate Na+ transport in Ussing chambers. We demonstrated that L-histidine chemically modified the structure of PGE(2) but had no direct effect on cAMP or 5-HT. L-Histidine and imidazole reacted with PGE(2) in vitro in cell-free mixtures incubated at 37 degrees C and pH 7.0 under an atmosphere of N(2) with the formation of PGE(2)-imidazole and PGE(2)-histidine covalent adducts. Nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS) analysis of the purified adduct showed that imidazole catalyzed the dehydration of PGE(2). A Michael adduct then was formed between C11 of 11-deoxy-Delta(10) PGE(2) (PGA(2)) and the tau nitrogen in the imidazole ring of L-histidine. Importantly, the isolated PGE(2)-imidazole and PGE(2)-histidine adducts inhibited CT-induced fluid loss and cAMP accumulation in mouse intestinal loops. The protection provided by PGE(2)-imidazole, PGE(2)-histidine, and L-histidine against intestinal fluid loss could provide a basis for future therapy against cholera.

Animals↗
PubMed2001

Clinical manifestations in a cohort of 41 Rothmund-Thomson syndrome patients.

Rothmund-Thomson syndrome (RTS) is a rare autosomal recessive genodermatosis characterized by a poikilodermatous rash starting in infancy, small stature, skeletal abnormalities, juvenile cataracts, and predisposition to specific cancers. We have identified a contemporary cohort of 41 patients to better define the clinical profile, diagnostic criteria, and management of patients with RTS. Patients with the diagnosis of RTS were ascertained by referrals from dermatology, ophthalmology, genetics, and oncology or from direct contact with the patient's family. Medical information was obtained from interviews with physicians, patients, and their parents and a review of medical records. The age range at ascertainment was 9 months to 42 years (28 males and 13 females; M:F, 2:1). All subjects displayed a characteristic rash. Thirteen subjects had osteosarcoma (OS) (32%), eight had radial defects (20%), seven had gastrointestinal findings (17%), two had cataracts (6%), and one had skin cancer (2%). Twenty-two of 28 patients without OS were less than 15 years old and thus remain at significant risk for this tumor. This case-series study reveals a clinical profile of RTS that includes a higher prevalence of OS and fewer cataracts, compared with historical reports. These differences may reflect either allelic or genetic heterogeneity. This study documents the frequency of clinical anomalies in a contemporary cohort of RTS patients and revises guidelines for diagnosis and management of RTS.

Adolescent↗
PubMed2001

Interferon gamma and prostaglandin in BSE-infected cattle.

Suspect field cases of BSE infection (displaying clinical signs) were examined for possible alterations of cytokine/autacoid plasma levels and were compared to control cases (not displaying clinical signs of BSE infection). Interferon gamma (IFN-gamma) plasma levels were demonstrated as being elevated in all suspected field cases of BSE infection (irrespective of BSE status; determined via postmortem histopathological examination). We demonstrated that plasma IFN-gamma levels were significantly (P<0.005) higher in suspect cases of BSE infection than in control cases. BSE-positive prostaglandin-E(2), (PGE(2)) plasma levels were demonstrated as being elevated 1.25-fold above BSE-negative cases and 2.22-fold above control cases. No significant (P>0.5) increase in PGE(2)plasma levels was recorded between BSE-positive and -negative. IFN-gamma and PGE(2)plasma levels were examined using commercially available ELISA assay. The results presented in this publication are the first demonstration of alteration in immune state in animals with BSE.

Animals↗