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S Green

Publications and source records attributed to S Green.

At least 19 recordsLinked to original sources
PubMed2026

Genomic characterisation of Enterococcus cecorum isolated from broiler chickens in the United Kingdom.

Enterococcus cecorum is an important poultry pathogen associated with lameness and increased mortality, leading to major welfare and economic impacts. Treatment is often challenging because disease is frequently detected late and the organism can localise in bone and joints, limiting antimicrobial efficacy. Presence of antimicrobial resistance (AMR) genes may further complicate treatment. Despite increasing global genomic research, only one recent study has investigated the phylogeny of E. cecorum from conventional UK broiler farms, using limited samples and a restricted time frame. In this study, 283 E. cecorum isolates were analysed, including 158 from the United Kingdom and 125 global non‑UK isolates. UK isolates comprised 123 archived by the Animal and Plant Health Agency (APHA) between 2003 and 2022, predominantly from clinical outbreaks with increased welfare culling and mortality, and 35 isolates from a UK study including clinical and environmental samples. Genome sequencing was used to assess phylogeny, AMR determinants and virulence factors (VFs). Single nucleotide polymorphism phylogenetic analysis identified eight major UK lineages with limited intra‑lineage diversity, indicating that UK isolates were genetically distinct from non‑UK populations. Using a 60‑SNP threshold, APHA isolates formed 18 subclusters, consistent with long‑term persistence and recurrent farm transmission, while multiple subclusters detected on some farms suggested repeated introductions. UK isolates carried fewer AMR genes than non‑UK isolates, with erm(B), lnu(C), tet(M) and tet(L) most prevalent. Screening of VF genes identified nine genes present in all isolates, with the remainder variably distributed. A subset of 60 UK isolates was examined for 13 previously described virulence‑associated genes, with phylogenetic clustering indicating associations between gene presence or absence and clinical status or mortality classification. The capsular polysaccharide gene cpsO was assessed in this subset and most non‑clinical or environmental isolates were cpsO‑negative, although several isolates from high‑mortality outbreaks also lacked this gene. Overall, this study provides insight into the phylogeny, AMR profiles and virulence gene diversity of E. cecorum within the UK broiler sector, supporting targeted surveillance and investigation of pathogenic mechanisms.

Antimicrobial resistance↗
PubMed1992

The ontogeny of peroxisome-proliferator-activated receptor gene expression in the mouse and rat.

The expression of the gene coding for peroxisome-proliferator-activated receptor (PPAR), a novel transacting factor belonging to the steroid superfamily, has been determined in the mouse and rat throughout development using hybridization histochemistry. Messenger RNA is demonstrable in the liver and brown fat from the fetal period onwards and, additionally, in the heart, kidney and gut post-natally. It is proposed that the upregulation of transcription of peroxisomal beta oxidation genes in specific tissues follows binding of the receptor to its natural ligand. Thus PPAR may have an important role in cold adaptation and non-shivering thermogenesis as well as in detoxification.

Adipose Tissue, Brown↗
PubMed1992

The mouse peroxisome proliferator activated receptor recognizes a response element in the 5' flanking sequence of the rat acyl CoA oxidase gene.

Peroxisome proliferators are a diverse group of chemicals, including several hypolipidaemic drugs, that activate a nuclear hormone receptor termed the peroxisome proliferator activated receptor (PPAR). The peroxisomal enzyme acyl CoA oxidase (ACO) is the most widely used marker of peroxisome proliferator action. We have examined the 5' flanking region of the rat ACO gene for sequences that mediate the transcriptional effect of peroxisome proliferators and have identified an element located 570 bp upstream of the ACO gene that confers responsiveness to the hypolipidaemic peroxisome proliferator Wy-14,643. This peroxisome proliferator response element (PPRE) contains a direct repeat of the sequence motifs TGACCT and TGTCCT and binds PPAR. These data therefore indicate an important role of PPAR in mediating the action of peroxisome proliferators including the induction of ACO.

Acyl-CoA Oxidase↗
PubMed1992

Southwest Oncology Group standard response criteria, endpoint definitions and toxicity criteria.

The Southwest Oncology Group, in cooperation with the National Cancer Institute and the other major cooperative oncology groups, has participated in the development of new toxicity criteria for reporting the results of cancer clinical trials. The new criteria (NCI Common Toxicity Criteria) respond to a recognized need to: (1) report toxicities consistently among cooperative groups, particularly for shared 'intergroup' clinical trials; (2) strive for comparability in toxicity reporting among clinical trials; and (3) recognize new toxicities accompanying new classes of anticancer treatment modalities. The Southwest Oncology Group has extended the toxicity criteria, incorporating additional new criteria for biological agents, radiation therapy, surgery, and hormonal agents. In addition, endpoint definitions and response criteria are discussed. These have been developed in response to previous uncertainties in clinical trials objectives, to limitations in the resolution of imaging methods, and to demands for greater rigor in response and endpoint definitions. Toxicity criteria, endpoint definitions, and response criteria are tabulated.

Combined Modality Therapy↗
PubMed1992

Proportional hazards and recursive partitioning and amalgamation analyses of the Southwest Oncology Group node-positive adjuvant CMFVP breast cancer data base: a pilot study.

Several putative prognostic factors have been identified in node-positive breast cancer patients, but their importance needs to be clarified in a uniformly treated population. The objectives of this investigation were: 1) to describe the characteristics of a uniformly treated node-positive data base; 2) to use proportional hazards (Cox) and recursive partitioning and amalgamation (RPA) multivariate models to assess the importance of potential prognostic factors for disease-free and for overall survival; and 3) to define prognostic groups with different disease-free survival and survival outcomes with RPA. A data base of 768 node-positive patients enrolled on 1-year adjuvant CMFVP arms of four SWOG trials was formed. Variables were number of positive nodes, age, age at menopause, menopausal status, ER status, ER and PgR levels (for RPA only), tumor size, race, breast cancer in mother, and obesity index. Independent predictors of both disease-free and overall survival in the Cox models were: number of positive nodes (4-6 worse than 1-3, and better than greater than 6); the age/menopause category (age greater than or equal to 35/premenopausal better than age less than 35/premenopausal and better than postmenopausal); and ER status (patients on ER-negative study worse than others). The RPA for disease-free survival defined four subgroups based on nodes, menopausal status, tumor size, and age at menopause (5-year recurrence-free rates = 73%, 52%, 38%, and 15%). The RPA for survival found four prognostic groups, defined only by the number of positive nodes and ER and PgR levels (5-year survivals = 91%, 72%, 56%, and 37%). Both RPAs suggested interesting refinements of the results of the Cox models. In the RPA for disease-free survival, best node cutoffs differed by menopausal status, tumor size was important only in postmenopausal patients with few positive nodes, and age at menopause emerged as an independent predictor of recurrence potential. And, the RPA for survival showed that node cutoffs differed according to ER level. Thus, these analyses underscore the value of simple, clinically available prognostic factors and suggest the possible need to reconsider the definition of good and poor risk patient groups in future adjuvant trial design.

Adult↗
PubMed1992

Nuclear receptors and chemical carcinogenesis.

A number of non-genotoxic chemical carcinogens can recognize specific intracellular proteins. These cellular targets include members of the nuclear receptor family of ligand-activated transcription factors. Some non-genotoxic carcinogens appear to mimic the action of hormones and growth factors and perturb signal transduction pathways. Their carcinogenic activity may therefore result from the persistent stimulation of such pathways, promoting the growth of initiated cells.

Animals↗
PubMed1992

The molecular mechanism of peroxisome proliferator action: a model for species differences and mechanistic risk assessment.

An increasing number of chemicals that produce tumours in rodent bioassays belong to the non-genotoxic class of carcinogens. There are no suitable tests for these carcinogens and our understanding of their mechanism of action is poor. Importantly, assessment of their potential hazard to man is usually difficult without extensive research. Peroxisome proliferators (PP) are a diverse group of rodent non-genotoxic carcinogens that include hypolipidemic drugs, plasticizers and herbicides. We have reported previously the cloning of a member of the nuclear hormone receptor superfamily and, through the use of chimeric receptors, discovered that it could be activated by PPs. The receptor is therefore termed the PP activated receptor (PPAR). The most widely used marker of PP action is the peroxisomal beta-oxidation enzyme acyl CoA oxidase (ACO). Interestingly, it has been speculated that the hydrogen peroxide produced as a result of ACO activity could lead to DNA damage and tumorigenesis. We have now demonstrated that PPAR recognizes a specific PP response element (PPRE) located in the ACO gene promoter and that the response is dependent upon the presence of receptor and the addition of the PP Wy-14,643. These data therefore support a model in which the mechanism of PP action is mediated by PPAR in a manner similar to that of steroid hormone action. Learning more about the function of PPAR offers a unique opportunity to understand the mechanism of action of some non-genotoxic carcinogens. Furthermore, this knowledge when combined with comparison of receptor expression between rodents and man will be important in providing a framework for a new threshold model of risk assessment based upon receptor-mediated carcinogenesis.

Acyl-CoA Oxidase↗
PubMed1992

A feasibility study of the in vivo measurement of aluminium in peripheral bone.

In summary, it is feasible to construct a neutron source, using the 3H(1H,n)3He reaction and the Dynamitron accelerator, which is suitable for the measurement of aluminium in vivo. It is useful to compare this system with other published data for in vivo aluminium measurement. The important parameters are presented in table 2 where MDL represents the minimum detectable level for the stated local dose. The figures in table 2 are very encouraging since the system described in this paper is at a very early stage of development. Significant improvements in sensitivity (detected 28Al counts per unit dose) should be expected from the combined effects of: (i) Increased NaI detector sizes. (ii) Neutron transport calculations to optimise the irradiation cavity. (iii) Experiments to determine the optimum source energy more precisely. (iv) Better dose delivery (giving the same dose in a shorter time). (v) More sophisticated spectroscopic data reduction. Published data on the amounts of aluminium typically found in hands of patients with renal disease (Ellis and Kelleher 1987) show that aluminium levels are likely to be in the 0.3 to about 15 mg range. Any improvements in system performance could largely be used to reduce the patient dose since the measurement sensitivity reported here is already close to that required for meaningful clinical measurements.

Aluminum↗
PubMed1992

Design studies related to an in vivo neutron activation analysis facility for measuring total body nitrogen.

Design studies relating to an in vivo prompt capture neutron activation analysis facility measuring total body nitrogen are presented. The basis of the design is a beryllium-graphite neutron collimator and reflector configuration for (alpha, n) type radionuclide neutron sources (238PuBe or 241AmBe), so as to reflect leaking, or out-scattered, neutrons towards the subject. This improves the ratio of thermal neutron flux to dose and the spatial distribution of thermal flux achieved with these sources, whilst retaining their advantage of long half-lives as compared to 252Cf based systems. The common problem of high count-rate at the detector, and therefore high nitrogen region of interest background due to pile-up, is decreased by using a set of smaller (5.1 cm diameter x 10.2 cm long) NaI(Tl) detectors instead of large ones. The facility described presents a relative error of nitrogen measurement of 3.6% and a nitrogen to background ratio of 2.3 for 0.45 mSv skin dose (assuming ten 5.1 cm x 10.2 cm NaI(Tl) detectors).

Body Composition↗